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Telemetry Basics - Rhythm Recognition

Introduction   

To truly understand telemetry, nurses must have knowledge about the anatomy of the heart and how electricity passes through it, how the electrocardiograph (EKG) works to receive and record the electrical activity, and how this information is transmitted via telemetry to the appropriate receiving device.

Defined as the transmission of instrumental readings by various methods such as radio waves or wires, telemetry gathers and transmits EKG readings to a central or remote monitor for interpretation and storage (71). The ability to read EKG rhythms from a variety of monitors consists of more than looking at a rhythm strip and identifying the rhythm. It consists of knowing the anatomy of the heart, how electricity travels through it and translates into the EKG we know, and what changes can happen based on injury, electrolytes, or other causes.

Heart Anatomy 101

As we know, the heart consists of four chambers, two atria—right atria (RA) and left atria (LA)—and two ventricles—right ventricle (RV) and left ventricle (LV)—working in a cycle to ensure adequate blood flow occurs. The heart receives blood from the inferior and superior vena cava (IVC and SVC) and enters the RA, moves to the RV, passes through the pulmonary artery (PA) and lungs, returns to the LA, enters the LV, and exits the heart through the aorta.

Heart cells, known as myocytes, are negatively charged, or “polarized” at rest. When these muscle cells contract, they become “depolarized” or positively charged. But how do the myocytes know when to contract? Less than 1% of the cells in the heart have a special role and name. These are known as the pacemaker cells and their role is to ensure that the heart beats. This is done through the action potential that is spontaneously created by the pacemaker cells. Some of these pacemaker cells have different speeds in depolarization, meaning that the fastest pacemaker cells are the ones controlling the speed. This will make more sense later when discussing specific cardiac rhythms (69).

Starting in the right atria, the sinoatrial node (SA node) is the primary group of pacemaker cells that determines the heart rhythm. The SA node, as well as the other pacemaker cells within the heart, progress through a rapid depolarization and repolarization process (2).

Pacemaker cells do not have a true resting potential, this means they are always in an “unstable” state to create spontaneous action potential. The action potential is the brief reversal of polarity in the cell; polarity consists of potassium (K⁺) in the cell with a negative charge, while sodium (Na⁺) and calcium (Ca⁺⁺) are outside of the cell with a positive charge (2).

Starting at the beginning of the cardiac cycle the pacemaker cells always have a membrane potential or voltage—the voltage of the cellular membrane as a result of permeability and concentrations of ions inside and outside the cell—of -60 microvolts (mV). From -60mV to -50mV the channels within the cells open, leading to a slow influx of Na⁺ inside the cell and a slow depolarization of the cell. Once the membrane voltage has reached the minimum threshold of -50mV the Ca⁺⁺ channels open, causing Ca⁺⁺ to move into the cell. This is known as the rising depolarization phase. The membrane voltage reaches the peak and the next thing that happens is the falling repolarization phase. This is where the K⁺ channels open to return the cell to a repolarized state (2).

(20)

Once these steps have occurred, the energy is transferred to surrounding cells, and the cardiac cycle continues. However, the action potential in the other myocytes is slightly different. Myocytes have a resting potential, which is different from the pacemaker cells. The resting potential is around -90mV and these cells only start the depolarization process when stimulated by an external force. During the end of the pacemaker cell’s action potential phase, additional Ca⁺⁺ is passed into the neighboring myocytes through gap junctions. The introduction of Ca⁺⁺ into the cell causes a sharp rise in the membrane voltage that approaches the threshold which is -70mVs. Once that threshold has been reached, the NA⁺ fast channels open and a rapid depolarization occurs since Na⁺ is brought into the cell. The Ca⁺⁺ slow channels open at -40mVs, further causing depolarization with Ca⁺⁺ entering the cell (2).

At the peak of cellular depolarization, the Na+ channels close, leading to a slight repolarization through some K⁺ entering the cell. This is minor as the Ca⁺⁺ channel is still open and continues to move K⁺ out of the cell. A plateau is created because of this and allows for the cell to go through two important phases. The first phase starts when the membrane voltage increases from the resting potential and continues until the plateau phase ends. This is known as the absolute refractory period and is where the myocytes relax before they can respond to additional stimuli. It prevents summation and tetanus which could lead to the heart not beating. The second phase is where additional Ca⁺⁺ is pulled out of the sarcoplasmic reticulum (SR) to further push K⁺ out of the cell (2).

The phase ends when the Ca⁺⁺ channel closes, extra Ca⁺⁺ is sent back to the SR, and K⁺ is allowed back into the cell. The sodium/potassium pump allows Na⁺ to exit the cell, returning the cell to its resting potential. This rapid process occurs in every myocyte for the life of the cell. Pacemaker cells are the only cells that can generate a heartbeat. Impulses from the nervous system can increase or decrease the heart rate, but they are influencing the pacemaker cell to generate more beats, not creating them (2).

It is important to note that there are several sets of pacemaker cells within the heart. The SA node starts the process, but there are a few others spaced out along the electricity’s path to ensure that the atria and ventricles of the heart have time to fill and properly contract. The second set of pacemaker cells is the atrioventricular node (AV node) where a slight delay of 0.01-0.05 meters per second (m/s) happens to make sure that the ventricles fill up adequately. The bundle of His takes the electric impulse to the left and right bundle branches and from there, the Purkinje Fibers are triggered. These fibers have a speed of 2-4 m/s to provide enough force to eject the blood from the ventricles (69).

Correlating all of this back to telemetry, scientific development within the medical profession has allowed us to visualize this electrical activity and translate it into an effective method of diagnosing cardiac conditions such as abnormal heart rates or cell death.

Types of Telemetry

EKG

There are many ways to view cardiac rhythms now, however, the oldest method is the EKG. During the late 1700s, the Italian physician Luigi Galvani was experimenting with electricity and animal tissue. His experiments spanned at least three decades and inspired other physicians during and after his time. Using legs removed from the bodies of frogs, Galvani theorized that “animal electric fluid” enabled the muscles within the legs to move when touched by metals; according to him, this was “natural” fluid and not created as static electricity or friction is. He went on to theorize that the brain is an essential part of creating the “electric fluid” with nerves as the conductors (6).

Jumping forward to 1842, Doctor Carlo Matteucci made a significant contribution to EKGs. During his time researching electrical detection in animals, he discovered the electrical currents within the heart that accompany each heartbeat. Thirty-five years after Matteucci, Augustus Waller was able to use a capillary electrometer and electrodes to perform the first human EKG. These electrodes were placed on the chest and back of the participant and were vital in demonstrating there was electrical activity that preceded the contraction of the ventricles. William Bayliss and Edward Starling improved upon Waller’s research by using improved capillary electrometers to demonstrate triphasic cardiac electrical activity (1).

The Dutch physician most noted for creating the EKG known today was Doctor Willem Einthoven. He was inspired by Waller and those before him to improve the capillary electrometer, successfully identifying five deflections that were initially named ABCDE. Having to factor for inertia, Einthoven implemented mathematic correlation, resulting in the traditional EKG rhythm strips we use today with the letters PQRST depicted in the image below. Einthoven is also responsible for coining the word electrocardiogram or electrokardiogram in Dutch. This is where providers get the “k” in EKG from (1).

While Waller’s EKG utilized ten electrodes, Einthoven was able to condense that number to three, eliminating the right leg and the mouth electrodes. These three leads created Einthoven’s triangle; an important concept still used today and that will be discussed later. All of Einthoven's work resulted in him being awarded the Nobel Prize in Physiology and Medicine in 1924 (1).

Bedside Monitor

Emergency departments (ED), intensive care units (ICU), and other specialized areas that require continuous monitoring of a patient’s EKG and vital signs utilize various bedside monitors to ensure they are receiving accurate, real-time information on the patient. Cords are used to connect the patient to the monitor. The electrodes to display and document cardiac rhythm and heart rate are applied to patients in the standard 5 lead placement displayed in the below image. The vitals displayed on the monitor can also be displayed outside the room on a screen with multiple patients. Nurses, paramedics, or trained telemetry monitor technicians can watch many of these monitors at a time.

(14)

The placement of the five leads consists of the following:

• RA: 2^nd intercostal space, anterior axillary on the right – some providers may put this lead higher on the chest or on the right arm
• LA: 2^nd intercostal space, anterior axillary on the left – some providers may put this lead higher on the chest or on the left arm
• RL: 8^th intercostal space, anterior axillary on the right – some providers may put this lead lower on the abdomen
• LL: 8^th intercostal space, anterior axillary on the left – some providers may put this lead lower on the abdomen
• V: 4^th intercostal space, right margin of the sternum

Note: Always follow the manufacturer’s instructions for specific lead placement.

Helpful Tip: Many healthcare providers quickly remember lead placement based on color is smoke (black) over fire (red) and snow (white) over grass (green). This leaves brown (chocolate) in the middle.

These bedside monitors can monitor pulse oximetry, respiratory rate, temperature, capnography, blood pressure, and arterial pressure. Some devices may have other unique monitoring features. These monitors may be portable or have a way to transfer the cords to a transport monitor. They come with alarms that can be adjusted based on the patient’s unique vital signs or hospital policy.

First responders have similar devices they use when transporting patients with the added benefit of having a defibrillator and a real-time feedback device built in (91).

Remote Monitoring

Remote cardiac monitoring is similar to bedside monitoring; however, the EKG rhythm, heart rate, and pulse oximetry are not displayed at the bedside. Instead, they are displayed in a different location, sometimes a monitor room, where a trained professional is watching many patients. When they recognize an abnormal rhythm, they will contact the appropriate staff to assess the patient. They may call for the leads to be removed, a change in rhythm, or a low battery.

The EKG leads are placed the same way as the bedside monitor leads are placed (always be sure to consult the manufacturer’s instructions). The information is transmitted wirelessly via wireless medical telemetry service (WMTS) from the “tele box,” but the leads must be wired to the box. WMTS does not use Wi-Fi and protects transmissions from Wi-Fi interference (48).

Mobile Cardiac Monitor and Event Monitor

A mobile cardiac or event monitor is a device attached to the skin that can perform continuous or event-specific monitoring. This device is attached to the patient’s chest near the heart and records when activated. This device is smaller than other portable cardiac monitoring devices like the Holter Monitor which will be discussed later. Information can be transmitted to the monitoring center to be reviewed by trained staff and/or artificial intelligence. Abnormalities like tachycardia, bradycardia, atrial fibrillation, or cardiac pauses are reported to a physician. The patient may or may not know about the rhythm abnormalities occurring as some patients are asymptomatic (18).

Event monitoring consists of the following methods (23):

• Patch monitor: depending on the manufacturer, the device is stuck to the chest and left on for a designated period of time.
• Loop memory monitor: the sensors always stay on the patient and the patient activates the devices to begin recording when symptoms occur in addition to a few minutes before the event starts and after it ends. There is an implanted option as well.
• Symptom event monitor: Patients place the monitor on them and activate it like a patch monitor, but only when symptoms start.

Insertable Monitor

Insertable or implantable cardiac monitors are just like mobile and event monitors, but they are surgically inserted into the patient. They perform the same actions, but there is an added benefit to these devices. If the patient has worn an external device in the past and has known cardiac arrhythmias, they may have an implanted cardioverter-defibrillator (ICD) inserted to detect and treat the abnormal rhythm. These devices are connected to the heart via wires (they may be placed in the right atria, the right ventricle, or both) and are operated by batteries that do need to be changed per manufacture direction. Patients and providers should be aware of magnets, or electrical signals from other devices that can interfere with the insertable device (61).

Healthcare providers can “interrogate” ICDs or pacemakers with a device created by the monitor’s manufacturer. When interrogated, the device’s information is transmitted to a monitor center who calls the provider to give them a verbal report of what the device has recorded; a paper copy is often faxed to the provider as well. Some newer interrogation devices may display the information of the device on the screen.

Holter Monitor

As mentioned with mobile cardiac monitors, the Holter monitor is another wearable device that can be used to monitor and diagnose cardiac arrhythmias outside of the hospital setting. This device consists of five electrodes and a monitor that the patient can wear or carry on them. It is similar to the remote telemetry devices used in the inpatient hospital setting as shown in the next image. Patients wear this device for a short time, and information is not transmitted to a monitor technician. Instead, information collected is sent to a monitoring center where it is interpreted and sent to the physician (58).

As covered in this section, there are many options for cardiac telemetry monitoring, and providers may encounter many types of them. It is important to know these devices and how they operate.

Lead Placement

Now that we have discussed the types of telemetry monitoring devices that are available, it is time to discuss how to properly place the EKG leads on a 12 lead, 15 lead, right-sided EKG, and where to place the V₄R lead.

12 Lead EKG

For the 12 lead EKG, providers should start with the four limb leads (14):

• RA: On the upper or lower right arm
• LA: On the upper or lower left arm
• RL: on the upper or lower right leg
• LL: on the upper or lower left leg

From there, the six pericardial leads are placed strategically around the chest to create a partial circle around the heart (14):

• V1: 4^th intercostal space, right margin of the sternum (this is lead V on the 5 lead EKG)
• V2: 4^th intercostal space, left margin of the sternum
• V3: sits midway between leads V2 and V4 on the left
• V4: 5^th intercostal space, mid-clavicular line on the left
• V5: 5^th intercostal space, anterior axillary line on the left (aligned horizontally with V4, between V4 and V6) on the left
• V6: 5^th intercostal space, mid-axillary line on the left (aligned horizontally with V4)

15 Lead EKG

The 15 lead EKG uses the same leads as the 12 lead EKG, but it adds V7, V8, and V9, known as the posterior leads, to encompass the posterior angles of the heart (14):

• V7: left posterior axillary line (aligned horizontally with V6, across from V5)
• V8: tip of the left scapula (aligned horizontally with V6, across from V4)
• V9: left of the spinal column (aligned horizontally with V6, across from V3)

Right Sided EKG

The right-sided EKG is important to rule out the diagnosis of a right-sided myocardial infarction (MI) or ischemia in or out while treating a patient. Lead placement is the same for the four limb leads, but the 6 precordial leads are flipped (14):

• V1: 4^th intercostal space, left margin of the sternum
• V2: 4^th intercostal space, right margin of the sternum (this is lead V on the 5 lead EKG)
• V3: sits midway between leads V2 and V4
• V4: 5^th intercostal space, mid-clavicular line on the right
• V5: 5^th intercostal space, anterior axillary line on the right (aligned horizontally with V4, between V4 and V6)
• V6: 5^th intercostal space, mid-axillary line on the right (aligned horizontally with V4)

V4R Lead Placement

A full right-sided EKG is not always needed. Lead V4 on the right side of the heart is the most important lead when it comes to determining an MI on the right side of the heart (14):

• V1, V2, V3, V5, V6: same placement as the 12 and 15 lead EKGs.
  • V4 is removed and placed on the right side of the chest
• V₄R: 5^th intercostal space, mid-clavicular line on the right (Where it is located on a complete right sided EKG)
  • The “R” stands for right to ensure that those reading the EKG are aware that lead is on the right while the rest are located on the left side of the chest.

Limb Leads

Now that lead placement has been covered, we can now discuss how lead placement shows different parts of the heart.

Leads I, II, III, AVR, AVL, and AVF are considered limb leads when reading the EKG. It is important to note that the right leg lead is the grounding electrode and does not affect the EKG (83). Leads I, II, and III leads form a triangle over the chest known as Einthoven’s Triangle as reflected in the below image. Lead I always has negative polarity while lead III always has positive polarity. Lead II’s polarity depends on what side of the triangle is being discussed. If we are looking at lead I on the EKG, then lead II is positive, but if we are looking at lead III, then lead II is negative (82).

The importance of what leads are negative and positive comes from how electricity travels through the heart. It starts on the right side and moves to the left, so it would make sense for lead I to have negative polarity while leads II and III are positively charged (82). This is also why the height of a PQRST complex changes based on what lead is being looked at on an EKG as reflected below.

Augmented or unipolar leads AVR, AVL, and AVF have the heart as the negative electrode and the limb leads are the positive electrodes. AVR goes from the heart to the right arm lead, AVL goes from the heart to the left arm lead, and AVF goes from the heart to the left leg lead. Just as discussed with leads I, II, and III, the path of the electricity in the heart determines how the PQRST complex appears on the rhythm strip (82). Lead II is the preferred strip to read by providers due to the best view of the rhythm due to the way electricity travels through the heart and how lead II follows that path by starting at the right shoulder and going to the left leg.

The chest leads, V1 – V9, create a circle around the heart on a horizontal plane. These leads are unipolar as well, with the heart being the negative electrode. Multiple views of the heart are captured because of the many leads placed along the patient’s body. This can give providers valuable knowledge on what areas of the heart may be affected. The next image gives a visual depiction of how the leads display their view of the heart.

Reading EKGs: EKG Components

To be able to interpret EKGs successfully, nurses must first have knowledge about the EKG components displayed on the EKG strips and how each part correlates to a part of a single heartbeat.

P wave

The P wave is the first deflection from the isoelectric line or baseline. Correlating this to the heart, this is where the atria depolarize or contract. The contraction of the right atria starts at the beginning of the P wave while the contraction of the left atria begins in the middle and end of it. Normal P waves are apparent between 120 and 200 milliseconds (msec) before the upward deflection of the QRS complex (44)

PR Interval

The next part of the PQRST complex is the PR interval. The interval symbolized the time between the depolarization of the atria and the depolarization of the ventricle. The normal speed is 120 to 200 msec (44).

PR Segment

Next is the PR segment. This is similar to the PR interval but starts at the end of the P wave and ends at the start of the Q wave. This line is important because if there is a deviation from the isoelectric line, it could indicate a cardiac rhythm abnormality like Wolff-Parkinson-White syndrome which will be discussed later. The EKG may have a “slurred” upstroke from the P to R points on the EKG, making the Q wave appear to be on the isoelectric line. This is because the ventricles were stimulated or excited early, leading to a shortened PR interval. The “slurred” area is known as a delta wave (13).

QRS Complex

The QRS complex is where the ventricles depolarize and contract. The first downward deflection of the beat is the Q wave that lasts for < 0.05 seconds. It is present in all leads save for V1 and V3 due to the angle of the vector. The R wave is the upward deflection of the complex. R waves do not have a set height, but severely elevated R waves can be an indicator of ventricular hypertrophy. The second downward deflection is the S wave. Overall, the QRS complex is 0.07 to 0.10 seconds long and variations to this time can be an indicator of abnormal heart rhythms (17).

ST Segment

The ST segment starts when the S wave ends by returning to the isoelectric line and ends when the T wave begins. This period represented the completion of ventricular depolarization (17). The ST segment lasts 0.08 seconds to 0.12 seconds (51).

T Wave

The final wave in the standard EKG components is the T wave. This wave symbolizes the ventricles repolarizing. Inverted T waves can be an indication of past or current infections. A peaked T wave—as opposed to the normal curved T wave—can be caused by hypocalcemia, hyperkalemia, and left ventricular hypertrophy (17). The T wave runs from 0.01 seconds to 0.25 seconds (51).

The image below depicts the components of an EKG with labels to assist with understanding how the waves appear.

(4)

Reading EKGs: EKG Paper

The EKG paper has sets of squares, 25 little squares within one larger square. The smaller squares symbolize 0.04 seconds making the larger square 0.20 seconds. A single small square is 1mm while the large square is 5mm, this is because the larger square is five small squares tall.

(15)

Some EKG strips are presented in a six second format. To determine if the strip is a six-second, you must count the larger boxes. 30 larger boxes are required for the strip to be six seconds. Some may even have second markers that symbolize one second of time passed.

The 12 lead EKG can be more challenging to read and is often used to make an overall observation about the patient’s heart rate and rhythm. It can provide more information to providers than a single lead strip can. 

As discussed previously, the leads are placed along the path of the heart, and providers can determine what part of the heart may be affected by knowing what leads are placed where.

(51)

Now that we have discussed leads, lead placement, the PQRST complex, and EKG paper, it is time to cover different cardiac rhythms that you may encounter.

Rhythm Recognition

Normal Sinus (41):

• Rate: 60-100 beats per minute (bpm)
• Conduction:
  • PR interval 120-200ms
  • QRS width 60-100ms
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave is:
    • Positive or above the isoelectric line in II and AVF
    • Biphasic (curves above and then dips below the isoelectric line) in V1
  • Duration:
    • Less than 0.12 seconds
  • Rhythm Strip:

(29)

Sinus Bradycardia (87):

• Rate: less than 60bpm
• Conduction:
  • PR interval 120-200ms
  • QRS width 60-100ms
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave is:
    • Positive or above the isoelectric line in II and AVF
    • Biphasic in V1
  • Rhythm Strip:
    

(87)

• Signs and Symptoms:
  • None – depending on the patient
  • Cyanosis
  • Peripheral edema
  • Shortness of breath
  • Dizziness
  • Fatigue
  • Syncope or near syncope
  • Lightheadedness
• Causes (not limited to):
  • Normal physiology in an athlete
  • Medications like beta-blockers
  • Ischemia
  • Heart diseases
  • Sick sinus syndrome
  • Hypothermia
  • Hypothyroidism
  • Neuro-mediated bradycardia as caused by a vasovagal reaction
  • Pericarditis
  • Hypoxia

• Electrolyte imbalances

• Treatment:
  • None if asymptomatic, admission for observation may be indicated
  • Medications:
    • Atropine 0.5mg every 3 to 5 minutes for a maximum dose of 3mg
    • Antidotes or reversal agents
  • Transcutaneous cardiac pacing or pacemaker
  • Return patient to a normothermic state if hypothermic

Sinus Tachycardia (55):

• Rate: greater than 100bpm but less than 150bpm
• Conduction:
  • PR interval 120-200ms
  • QRS width 60-100ms
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave is:
    • Positive or above the isoelectric line in II and AVF
    • Biphasic in V1
  • Rhythm Strip:

(42)

• Signs and Symptoms:
  • Shortness of breath
  • Chest pain
  • Dizziness
  • Syncope or near syncope
  • Lightheadedness
  • Palpitations
• Causes:
  • Infection or sepsis
  • Medications
  • Withdrawal
  • Electrolyte imbalances
  • Blood loss or anemia
  • Dehydration
  • Hypoglycemia
  • Pulmonary embolism
  • Trauma
  • Cardiac tamponade
  • Myocarditis
  • Pregnancy
• Treatment:
  • Medications
    • Antibiotics
    • Antidotes or reversal agents
    • Insulin
    • Electrolyte replacement
    • Fluids
    • Heparin or other anticoagulant medications
  • Blood replacement
  • Surgery

1st Degree AV Block (68):

• Rate: 60-100 beats per minute (bpm)
• Conduction:
  • PR interval greater than 0.20 seconds
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave is:
    • Positive or above the isoelectric line in II and AVF
    • Biphasic in V1
  • A QRS complex always follows the P wave
• Duration:
  • Less than 0.12 seconds
• Rhythm Strip:

(32)

• Signs and Symptoms:
  • None
  • Fatigue
  • Shortness of breath
  • Syncope or near syncope
  • Chest pain
  • Lightheadedness
• Causes:
  • Increased vagal tones in young patients
  • Fibrotic changes in the elderly
  • Cardiac disease
  • Inflammation
  • Medications
  • Electrolyte abnormalities
• Treatment:
  • None if asymptomatic
  • Medications
    • Antibiotics
    • Antidotes or reversal agents
    • Electrolyte replacement

2nd Degree Type I AV Block (Mobitz Type 1 or Wenckebach) (60):

• Rate: varies
• Conduction:
  • PR interval increases with each beat, eventually “dropping off” and another P wave appears
  • “Longer, longer, drop, that’s a Wenckebach.”
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave is:
    • Positive or above the isoelectric line in II and AVF
    • Biphasic in V1
  • Rhythm Strip:

(27)

• Signs and Symptoms:
  • None
  • Fatigue
  • Shortness of breath
  • Syncope or near syncope
  • Chest pain
  • Lightheadedness
• Causes:
  • Increased vagal tones
  • Cardiomyopathy
  • Myocardial infarction
  • Cardiac surgery
  • Electrolyte abnormalities
  • Medications
• Treatment:
  • None if asymptomatic
  • Medications
    • Atropine if bradycardic
    • Antidotes or reversal agents
    • Electrolyte replacement

2nd Degree Type II AV Block (Mobitz II) (60):

• Rate: varies
• Conduction:
  • PR interval varies
  • QRS width 60-100ms when present
    • QRS does not follow all P waves
  • P wave morphology:
    • The maximum height of the P wave is:
      • Lead II and III: 2.5 mm
    • The P wave is:
      • Positive or above the isoelectric line in II and AVF
      • Biphasic in V1
    • Rhythm Strip:

(40)

• Signs and Symptoms:
  • Fatigue
  • Shortness of breath
  • Syncope or near syncope
  • Chest pain
  • Lightheadedness
  • Cardiac arrest
• Causes:
  • Structural heart disease
  • Amyloidosis
  • lymphoma
  • Cardiac tumors
  • Transcatheter placement of valves
  • Myocardial infarction
  • Genetics
• Treatment:
  • None if asymptomatic
  • Medications
    • Atropine does not work on these patients
    • Antidotes or reversal agents
  • Transcutaneous cardiac pacing or pacemaker since this rhythm can progress to a complete heart block or cardiac arrest

3rd Degree AV Block (78):

• Rate: varies, but usually bradycardic
• Conduction:
  • PR interval varies
  • QRS width 60-100ms when present
  • P wave and QRS complex do not communicate (called AV disassociation)
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave is:
    • Positive or above the isoelectric line in II and AVF
    • Biphasic in V1
  • Rhythm Strip:

(33)

• Signs and Symptoms:
  • Fatigue
  • Shortness of breath
  • Syncope or near syncope
  • Chest pain
  • Lightheadedness
  • Hemodynamic instability
  • Cardiac murmurs
  • Cardiac arrest
• Causes:
  • Cardiac surgery
  • Cardiac disease
  • Medications
  • Electrolyte imbalances
  • Lyme disease
  • Transcatheter aortic valve replacement
  • Myocardial infarction
  • Systemic lupus erythematosus
  • Sarcoidosis
• Treatment:
  • Medications
    • Atropine usually does not work, but can be administered
    • Epinephrine
    • Dopamine
    • Antidotes or reversal agents
    • Electrolyte replacement
  • Transcutaneous cardiac pacing or pacemaker

Premature Ventricular Contraction (PVC) (88):

• Rate: varies, underlying rhythm is usually normal sinus
  • The impulse to beat comes from the ventricles, not from the SA node
• Conduction:
  • PR interval varies, but in a regular PQRST complex PR interval is 120-200ms
  • PR interval after a PVC is longer due to the PVC and the retrograde concealed conduction goes back into the AV node junction.
  • PVC QRS width is at least 120ms but usually 160-200ms
  • Regular QRS width is 60-100ms
  • PR interval after a PVC is longer due to the PVC and the retrograde concealed conduction goes back into the AV node junction.
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave is:
    • Positive or above the isoelectric line in II and AVF
    • Biphasic in V1
  • Rhythm Strip:
    • Monomorphic: All PVCs are shaped the same

(38)

• Biomorphic: PVCs are shaped differently

(64)

• Bigeminy: Every PVC is separated by one sinus beat.

(35)

• Trigeminy: Every PVC is separated by two sinus beats.

(9)

• Ventricular Couplet: Two PVC beats in a row.

(9)

• Ventricular Triplet: Three PVC beats in a row.

(9)

• Signs and Symptoms:
  • None
  • Fatigue
  • Shortness of breath
  • Syncope or near syncope
  • Chest pain
  • Palpitations
  • Lightheadedness
  • Abnormal neck pulsation
  • Hemodynamic instability with frequent PVCs
  • Cardiac arrest
• Causes:
  • Hypoxia
  • Illicit drug use
    • Amphetamines
    • Alcohol
    • Cocaine
  • Electrolyte imbalances
  • Myocarditis
  • Mitral valve prolapse
  • Hypercarbia
  • Cardiomyopathies
  • Myocardial infarction
  • Medications
• Treatment:
  • None if asymptomatic
  • Medications
    • Beta-blockers
    • Calcium channel blockers
    • Amiodarone is for those with preexisting coronary artery diseases, but used with caution and close observation and monitoring
    • Antidotes or reversal agents
    • Electrolyte replacement
  • Cardiac ablation
  • Defibrillation if cardiac arrest occurs

Premature Atrial Contractions (PAC) (54):

• Rate: varies, underlying rhythm is usually normal sinus
• Conduction:
  • PR interval varies, but in a regular PQRST complex PR interval is 120-200ms
  • PAC
  • Regular QRS width is 60-100ms
• P wave morphology:
  • The maximum height of the P wave is:
    • Lead II and III: 2.5 mm
  • The P wave:
    • Can be inverted
    • May be hidden in the T wave creating a hump or peaked T wave
  • These rhythms can come in the same variations as PVCs:
    • Bigeminy
    • Trigeminy
    • Couplet
    • Triplet
  • Rhythm Strip:

(37)

• Signs and Symptoms:
  • None
  • Palpitations
  • Shortness of breath
  • Anxiety
  • Signs and symptoms of heart failure
  • Early or additional heart sounds
  • Pauses in rhythm
• Causes:
  • Coronary artery disease
  • Left ventricular hypertrophy
  • Septal defects
  • Congenital heart deformities
  • Medications
    • Beta-blockers
    • Chemotherapeutic agents
  • Congestive heart failure
  • Diabetes mellitus
  • Hypertension
  • Chronic obstructive pulmonary disorder
  • Anxiety
• Treatment:
  • None if asymptomatic
  • Avoiding triggers
  • Medications
    • Beta-adrenergic blockers
    • Antiarrhythmic agents are used with caution and close observation and monitoring
    • Antidotes or reversal agents
    • Cardiac ablation

Ventricular Tachycardia (V Tach) (45):

• Rate: greater than 100bpm
• Conduction:
  • PR interval none
  • QRS width greater than 140ms
• P wave morphology:
  • Not present
• Non-sustained V-Tach: three or more ventricular beats over a maximum of 30 seconds.
• Sustained V-Tach: a run of V Tach for more than 30 seconds or less is treated by cardioversion
• Monomorphic V-Tach: all ventricular beats look the same
• Polymorphic V-Tach: the ventricular beats look different.
• Biphasic V Teach: where the QRS complexes alternate with each beat.
  • Digoxin intoxication
  • Long QT syndrome
• Rhythm Strip:
  • Monomorphic V-Tach

(11)

• Signs and Symptoms:
  • Palpitations
  • Shortness of breath
  • Chest pain
  • Syncope or near syncope
  • Signs of heart failure
  • Hemodynamic instability
  • ICD shocks if the patient has one
  • Cardiac arrest
    • Also known as pulseless V-Tach
  • Causes:
    • Ischemic heart disease
    • Acute coronary artery disease
    • Myocardial scar-related reentry
    • Congenital heart deformities
    • Cardiomyopathy
    • Illicit drugs
      • Cocaine
      • Digitalis toxicity
      • Methamphetamine
    • Medications
      • Beta-blockers
      • Chemotherapeutic agents
    • Electrolyte imbalances
    • Sepsis
    • Metabolic acidosis
    • Inherited cardiac channelopathies
  • Treatment:
    • Cardiopulmonary resuscitation (CPR) and defibrillation if no pulse present
    • Cardioversion if hemodynamically unstable and has a pulse
    • Treatment for myocardial infarction
    • Medications
      • Amiodarone, procainamide, sotalol
      • Antidotes or reversal agents
    • ICD
    • Cardiac ablation

Torsades de Pointes (V Fib) (25):

• Rate: none
• Conduction:
  • Polymorphic V-Tach with a prolonged QR interval
• P wave morphology:
  • Not present
• Rhythm Strip:

(12)

• Signs and Symptoms:
  • None
  • Syncope or near syncope
  • Dizziness
  • Lightheadedness
  • Hypotension
  • Rapid pulse
  • Cardiac arrest
    • No pulse
    • Not breathing or only gasping for air
    • Loss of consciousness
  • Causes:
    • Electrolyte imbalances
    • Medications
      • Zofran causes a long QT interval (19)
    • Congenital prolonged QT:
      • Jervell and Lange-Nielsen
      • Romano-Ward syndrome
    • Bradycardia
    • Diuretic use
    • Female gender
    • Age
  • Treatment:
    • Electrolyte replacement
    • CPR and defibrillation
    • Medications
      • Epinephrine
      • Atropine
    • Cardioversion
    • Treatment of the underlying cause

Supraventricular Tachycardia (SVT) (72):

• Rate: Greater than 160bpm
• Conduction:
  • PR interval not present
  • QRS width less than 120 milliseconds = narrow complex, regular SVT
  • QRS width greater than 120 milliseconds = wide complex, regular SVT
• P wave morphology:
  • Not present
• Rhythm Strip:
  • Narrow complex, regular SVT

(30)

• Wide complex, regular SVT

(79)

• Signs and Symptoms:
  • None
  • Hypotension
  • Shortness of breath
  • Lightheadedness
  • Signs and symptoms of heart failure
  • Shock
• Causes:
  • Narrow complex, regular SVT - Orthodromic reentry phenomenon (56):
    • Accessory pathway that connects the atria and ventricles without passing through the AV node
    • A pulse goes through the AV node, down into the ventricles via the Bundle of His, up through the accessory pathway, and back into the AV node
  • Wide complex, regular SVT - Atrioventricular reentry phenomenon (57):
    • Signals from the SA node travel through the accessory pathway down the ventricles via the Bundle of His and up to the AV node, creating a backward cycle.
    • This is slower than the orthodromic SVT because it is traveling against the regular path of conduction, leaving to a wide QRS complex
  • Medications
  • Caffeine
  • Smoking
  • Stress
  • Alcohol
• Treatment:
  • None if asymptomatic
  • Vagal maneuvers
    • Bearing down
    • Blowing into a straw
  • Medications
    • Adenosine: 1^st dose 6mg, 2^nd dose 12mg
      • Ensure rapid saline flush after pushing medication as it has an extremely short half-life
    • Cardizem
    • Antidotes or reversal agents
  • Cardioversion
  • Cardiac ablation

 Ventricular Fibrillation (V-Fib) (3):

• Rate: none
• Conduction:
  • PR interval not present
  • QRS width not present
• P wave morphology:
  • Not present
• Rhythm Strip:

(39)

• Signs and Symptoms:
  • Cardiac arrest
    • No pulse
    • Not breathing or only gasping for air
    • Loss of consciousness
  • Causes:
    • Electrolyte imbalances
    • Myocardial infarction
    • Congenital heart defects
    • Sudden blow to the chest right over the heart
    • Medications
    • Anemia
    • Cardiomyopathy
    • Electrocution
    • Thoracic trauma
    • Heart surgery
  • Treatment:
    • CPR and defibrillation
    • Medications
      • Epinephrine
      • Atropine
      • Electrolytes
    • Surgery
    • Coronary perfusion
    • Treatment of the underlying cause

Asystole (59):

• Rate: none
• Conduction:
  • PR interval not present
  • QRS width not present
• P wave morphology:
  • May or may not be present
• Rhythm Strip:

(21)

• Signs and Symptoms:
  • Cardiac arrest
    • No pulse
    • Not breathing or only gasping for air
    • Loss of consciousness
  • Causes:
    • Electrolyte imbalances
    • Myocardial infarction
    • Congenital heart defects
    • Medications or illicit drugs
    • Blood loss
    • Cardiomyopathy
    • Electrocution
    • Trauma
  • Treatment:
    • CPR
      • Since there is no electrical activity with this rhythm, defibrillation cannot be used
    • Medications
      • Epinephrine
      • Atropine
      • Electrolytes
    • Surgery
    • Coronary perfusion
    • Treatment of the underlying cause

Pulseless Electrical Activity (PEA) (22):

• Rate: varies
  • There is no pulse with this rhythm despite the fact that it may appear as an organized rhythm
• Conduction:
  • PR interval none
  • QRS width greater than 110ms
• P wave morphology:
  • Not present
• The P wave is:
  • Not present
• Rhythm Strip:

(22)

• Signs and Symptoms:
  • Cardiac arrest
    • No pulse
    • Not breathing or only gasping for air
    • Loss of consciousness
  • Causes:
    • Electrolyte imbalances
    • Myocardial infarction
    • Congenital heart defects
    • Medications or illicit drugs
    • Blood loss
    • Cardiomyopathy
    • Electrocution
    • Trauma
    • Hypothermia
    • Pneumothorax or hemothorax
  •  Treatment:
    • CPR
      • Since there is no electrical activity with this rhythm, defibrillation cannot be used
    • Medications
      • Epinephrine
      • Atropine
      • Electrolytes
    • Surgery
    • Coronary perfusion
    • Treatment of the underlying cause

Atrial Flutter (73):

• Rate: varies
  • Depends on how many QRS complexes there are
    • Atrial rate 250-350 bpm
    • Ventricular rate 75-150bpm
  • P waves can come in blocks
    • 2 P waves per 1 QRS (2:1)
    • 3 P waves per 1 QRS (3:1)
    • 4 P waves per 1 QRS (4:1)
    • Intervals of P waves per 1 QRS (2:1 then 3: 1 then 2:1 then 4:1)
  • Conduction:
    • PR interval varies
    • QRS width 60-100ms
  • P wave morphology:
    • The maximum height of the P wave is:
      • Lead II and III: 2.5 mm
      • Sawtooth pattern
    • Rhythm Strip:

(31)

• Signs and Symptoms:
  • None
  • Palpitations
  • Fatigue
  • Syncope or near syncope
  • Shortness of breath
  • Regular or irregularly regular pulse
• Causes:
  • COPD
  • Heart failure
  • Atrial size abnormalities
  • Hypertension
  • Diabetes mellitus
  • Age
  • Male gender
• Treatment:
  • None if asymptomatic
  • Medications
    • Amiodarone
    • Cardizem
    • Metoprolol
    • Anticoagulation to prevent stroke
  • Catheter ablation
  • Treatment of the underlying cause

Atrial Fibrillation (AFib) (89):

• Rate: varies
  • Atrial rate 400-600 bpm
  • Ventricular rate 75-175 bpm
    • Anything over 100 is considered A Fib with rapid ventricular response (RVR)
  • Conduction:
    • PR interval varies
    • QRS width 60-100ms
  • P wave morphology:
    • The maximum height of the P wave is:
      • Lead II and III: 2.5 mm
    • Rhythm Strip:
      • A Fib

(28)

• A Fib RVR

(34)

• Signs and Symptoms:
  • None
  • Palpitations
  • Fatigue
  • Syncope or near syncope
  • Shortness of breath
  • Regular or irregular pulse
    • Patients can go in and out of A Fib or it can be permanent,
    • They can go in and out of RVR
  • Causes:
    • Heart disease
    • Genetics
    • Pulmonary embolism or other hemodynamic stressors
    • Obstructive sleep apnea
    • Heart failure
    • Pericarditis
    • Myocarditis
    • Myocardial infarction
    • Hypertension
    • Diabetes mellitus
    • Age
  • Treatment:
    • None if asymptomatic
    • Medications
      • Cardizem
      • Metoprolol
      • Amiodarone
      • Anticoagulation to prevent stroke
    • Catheter ablation
    • Treatment of the underlying cause

Idioventricular Rhythms (47):

• Rate: varies
  • Idioventricular rate 35-40bpm
  • Accelerated rate 60-120bpm
• Conduction:
  • PR interval not present
  • QRS width greater than 120ms but can be greater than 160ms
    • The normal conduction system does not transmit the signal to beat, the vertical signal is transmitted from cell to cell
  • P wave morphology:
    • Not present
  • Rhythm Strip:
    • Idioventricular rate

(36)

• Signs and Symptoms:
  • None
  • Palpitations
  • Fatigue
  • Lightheadedness
  • Syncope or near syncope
  • Cardiac arrest
• Causes:
  • Electrolyte imbalances
  • Reperfusion of cardiac cells after a myocardial infarction
  • Medications
    • Digoxin
    • Beta-adrenoreceptor agonists
  • Illicit drug use like cocaine
  • Cardiomyopathies
  • Congenital cardiac defects
  • Athletes
• Treatment:
  • None if asymptomatic
  • Medications
    • Atropine
    • Amiodarone or lidocaine
    • Reversal agents
  • Rarely cardiac pacing
  • Treatment of the underlying cause

Junctional Rhythms (52):

• Rate: varies
  • Junctional bradycardia less than 40bpm
  • Junctional escape rhythm 40-60bpm
  • Accelerated junctional rhythm 60-100bpm
  • Junctional tachycardia greater than 100bpm
• Conduction:
  • PR interval not present
  • QRS width 60-100ms
• P wave morphology:
  • Not present
• Rhythm Strip:
  • Accelerated Junctional Rhythm
    • Rhythms look the same but have more beats depending on the type of rhythm

(52)

• Signs and Symptoms:
  • None
  • Shortness of breath
  • Palpitations, intermittent or continuous
  • Fatigue
  • Lightheadedness
  • Syncope or near syncope
• Causes:
  • Electrolyte imbalances
    • Can be caused by anorexia nervosa
  • Thoracic trauma
  • Myocarditis
  • Reperfusion of cardiac cells after a myocardial infarction
  • Medications
    • Adenosine
    • Clonidine
    • Antiarrhythmics
    • Lithium
    • Digoxin
  • Sleep apnea
  • Hypoxia
  • Coronary artery disease
  • Congenital cardiac defects and repairs of these defects
• Treatment:
  • None if asymptomatic
  • Medications
    • Atropine
    • Reversal agents
  • Transcutaneous pacing
  • Permanent pacemaker
  • Treatment of the underlying cause

Bundle Branch Blocks (BBB) (43, 53, 70):

• Rate: varies
• Conduction:
  • Right BBB (RBBB):
    • QRS interval greater than 120ms
    • Septal depolarization that leads to a:
      • Small R wave being present in V1
      • Q wave in V6
    • The left ventricle’s contraction leads to and:
      • • S wave in V1
        • R wave in V6
    • The right ventricle’s contraction leads to an:
      • R wave in V1
      • Deep S wave in V6
    • Left BBB (LBBB):
      • QRS interval greater than 120ms
      • T wave inversion is due to abnormal repolarization
      • From first principles:
      • Septal depolarization that leads to a:
        • Q wave in V1
        • R wave in V6

• • • The right ventricle’s contraction leads to an:
      • R wave in V1
      • S wave in V6
    • The left ventricle’s contraction leads to and:
      • S wave in V1
      • R wave in V6
  • P wave morphology:
    • The maximum height of the P wave is:
      • Lead II and III: 2.5 mm
    • Rhythm Strip:
      • RBBB

(71)

• • • • LBBB

(71)

• Signs and Symptoms:
  • None
  • Lightheadedness
  • Syncope or near syncope
• Causes:
  • RBBB:
    • Myocardial infarction
    • Congenital cardiac defects
    • Pulmonary embolism
    • Myocarditis
    • Pulmonary hypertension
  • LBBB:
    • Myocardial infarction
    • Hypertension
    • Cardiomyopathy
    • Myocarditis
  • Treatment:
  • None if asymptomatic
  • Treatment of the underlying cause

Identifying Ischemia and Infarction

Known as coronary artery disease (CAD), acute myocardial ischemia is the decrease of blood flow to the heart by atherosclerosis or plaque. The atherosclerosis starts as a plaque streak within the large arteries and continues to build up. After the plaque has grown to a significant size, occlusion begins and blood flow to areas below the growing occlusion suffers a decrease in blood flow. This is what is known as ischemia (81).

When resting, patients may not experience any signs or symptoms. Upon exertion, however, patients may experience stable angina—chest pain, discomfort, pressure, etc.—as activity requires increased blood flow and the arteries constrict to pump blood through the body faster. This pain is relieved at rest and can be further treated by nitrates. The routine is what makes this stable angina (81).

Unstable angina begins once the artery has become occluded enough to create a significant obstruction of blood flow. Signs and symptoms can include chest pain or other discomfort that is challenging to relieve, even when at rest. Patients may be woken from sleep due to the pain and report that it takes longer for the pain to decrease or resolve completely. These signs and symptoms symbolize that the plaque within the artery is unstable and could potentially rupture (90).

Infarction is when the blood flow is completely obstructed and the cells below the obstruction begin to die off. This often occurs when the plaque within the artery ruptures, leading to the body’s natural clotting processing in an attempt to repair the rupture, and a complete occlusion of the artery occurs (46).

Now that we have discussed ischemia and infarction, it is time to discuss how a myocardial infarction (MI) appears on an EKG and how to identify it. You may also hear them referred to as STEMIs or ST-elevation myocardial infarction.

The progression of PQRST complex changes during an MI can start with hyperacute T waves. The T wave will increase with amplitude and become wider, while some ST elevation may be noted. This elevation begins to occur as injury to the heart muscle begins. From there, the ST elevation increases and creates the image often associated with an MI. Pathological Q wave may develop as the MI progresses. As discussed earlier, the Q wave is the first downward deflection of the QRS complex and is normally 1mm or less in depth. Pathological Q waves are measured by greater than 1mm wide or greater than 25% of the R wave’s amplitude (84).

T wave inversion occurs when the cells have become necrotized and begin to form fibrosis. Once all necrotized cells have become fibrotic, the Q waves will remain, but the T waves will become upright again (84).

(84)

These changes should be present in at least 2 contiguous leads or leads that are side by side. To discuss this more, we will refer to the 12 lead EKG photo we used earlier. It is important to know that there will be leads with ST elevation and there will be leads with reciprocal ST depression based on the type of MI and how these leads are placed in relation to the area of the heart that is being affected.

(82)

With posterior MIs the elevation must be at least 0.5mm, there will be tall, broad R waves of at least 30ms long, and the T wave will be upright. When looking at an EKG for a posterior MI, the ST depression is what will be observed in leads V1, V2, and V3. If a posterior MI is suspected, look at the EKG from the back of the paper by flipping it over and holding it to light. This will display the ST depression as ST elevation, prompting you to consider a posterior EKG. It is advised that a posterior EKG with leads V7, V8, and V9 be done. A quick method to do this is by removing leads V4, V5, and V6; placing them in the posterior lead positions; and relabeling them on the EKG. (77).

Right ventricular MIs can occur, and it is important to assess and treat them appropriately. To assess for a right-sided MI, first look at the standard EKG. If ST elevation is noted in leads II and III, but the ST elevation is greater in lead III than lead II, consider right ventricular involvement. As discussed previously, one method is to do a right-sided EKG, with lead placement along the right side of the chest. The second, quicker way to do this is to take lead V4 and place it on the right side of the chest and mark it as V4R on the EKG (77).

Another rhythm that can be an indicator of an MI is a bundle branch block. New or suspected new BBBs are to be treated as a MI by providers. But what if you have a copy of an old EKG and the BBB isn’t new, can the patient still be having an MI? The answer is yes. However, it can be challenging to determine what is a change from the MI and what is from the BBB. The Sgarbossa criteria is useful in making these determinations and can also be used for patients who have a pacemaker (77)

Sgarbossa criteria (77):

• Concordant ST elevation that is greater than 1mm
• Concordant ST depression that is greater than 1mm
• Excess discordant ST elevation that is greater than 5mm in leads with negative QRS complexes – these are complexes below the isoelectric line

For reference, concordance means that the ST segment and QRS complex go in the same direction, either both deflecting upwards or downwards. Discordance is what should be seen in a BBB or paced rhythm. This is where the ST segment and the QRS complex go in different directions. Smith et al. created a modification to the Sgarbossa criteria to include a greater than 1mm ST elevation to an S-wave amplitude ratio of greater than 0.25mm (7).

Another method that has been created, but not validated is the Barcelona criteria. This criterion has greater than 1mm ST deviation concordance or discordance with QRS polarity in any EKG lead. Discordant ST deviation is greater than 1mm in any lead where the R or S points of the QRS complex are less than 6mm (7).

There is an EKG rhythm that can indicate a future MI which is known as Wellens syndrome. This EKG has a deeply inverted or biphasic T wave in leads V2 and V3. The patient is often pain-free when the rhythm is present, ischemic chest pain can obscure the rhythm by creating a false normal appearance of the T waves in the affected leads. Their cardiac enzymes may not even be elevated. Any patient presenting with chest pain should have serial EKGs done for this reason, since they may be pain-free at a later time. These EKG changes symbolize the critical stenosis of the proximal left anterior descending artery (LAD). This is the artery that provides the left ventricle with blood (65).

Cardiac Assessment:

A traditional cardiac assessment focuses on more than just the heart; it encompasses aspects of both the neurological and respiratory systems. However, we will begin our focus with the heart.

Pain may not be a word patients use to describe what they are feeling. As mentioned, they may vocalize discomfort, pressure, cramping, burning, or tightness. Women may have jaw or arm pain as opposed to the traditional chest pain that men may experience. Ask them to rate their pain on a scale of one to ten, looking for changes in the value. An EKG based on pain, discomfort, pressure, cramping, or tightness should be completed within the time frame set by hospital policy.

The PQRST pneumonic can assist providers in remembering the specific information they need to collect (90).

P: What provokes, precipitates, or palliates/alleviates the pain or discomfort the patient is feeling? Does it get worse or better when you do certain things, i.e., walk or rest?

Q: What is the quality of pain or discomfort you are feeling?

R: Does this pain or discomfort radiate anywhere else in your body? Jaw, arm, back?

S: Are there associated symptoms with the pain or discomfort? Shortness of breath, dizziness, heartburn?

T: What time elements are involved? When did it start? Did it stop and come back? Are you currently feeling it now? Was it gradual or did it occur suddenly? Did it wake you up?

Patients should be asked about palpitations or any experienced abnormal heart rhythms detected on monitoring devices. Many individuals have smartwatches that can detect heart rates and some rhythms. If the patient is wearing one, determine if the device has recorded anything.

Edema in the legs can be a sign of acute heart failure while pain in the calf can indicate a blood clot that could have traveled from another part of the body (85). In A Fib, the blood can clot in the ventricles due to poor circulation of blood. It will pool until it clots or is ejected from the heart. Once expelled, the clot will travel until it can no longer pass through the veins (63).  Ensure a thorough assessment of the patient’s distal pulses is done as well to determine circulation. The further pulse locations can be an indicator of poor circulation (85).

Moving on to the respiratory system, we will reflect on the many arrhythmias that have shortness of breath as a sign or symptom. Providers should assess lung sounds to determine if there is any fluid buildup, a sign of acute heart failure. Determine if the shortness of breath is all the time, upon exertion, or at rest. Also, it is important to ask if the patient has been woken from sleep due to a shortness of breath. Sometimes arrhythmias occur at unexpected moments, even in the middle of the night (85).

Syncope was another common sign or symptom of cardiac arrhythmias due to decreased perfusion to the brain. Providers should determine if the patient currently feels lightheaded or dizzy, if they felt that way in the past, or if they have fainted. They should ask when this feeling happens—at rest, while moving, or both—and if they get any warning signs or auras beforehand. Always ensure you ask the patient to describe what happened so it can be added to the assessment (85).

A full medical history should be obtained, with a special focus on any past cardiac medical history the patient or their family has. Providers may consider asking the following questions:

• Have you been diagnosed with coronary artery disease, high blood pressure, peripheral vascular disease, valve problems, heart failure, high cholesterol, or other heart conditions?
• Have you had a heart attack or stroke in the past?
• Have you had any surgical procedures to help with your heart function? This may include things like ablation or stent placement.

Asking about medications can assist providers in determining any missed diagnoses with the patient while asking about social history can provide information about smoking, illicit drug use, alcohol consumption, and exercise habits (85).

Conclusion

Thanks to advancements within the medical profession, cardiac telemetry can be greatly beneficial to patients in and outside of the hospital setting. From devices you can carry, to devices implanted inside someone, patient outcomes have improved for identifying, treating, and managing cardiac arrhythmias that had once been deemed unmanageable. With proper knowledge of EKG rhythms, nurses can confidently provide the proper care for their patients by being an advocate for those they care for.

Heart Failure Updates

Introduction   

In 1997, Heart Failure (HF) was designated an epidemic due to the significant increase in hospitalizations. (2) This increase in hospitalizations appears to be due to accurate management of HF patients who re-hospitalize for stabilization and medication management rather than a new diagnosis or end-stage disease.

HF occurs when the heart is too weak to pump blood to the body and lungs. The blood then backs up into the heart, lungs, and lower extremities, causing less blood supply to the body. HF can also be so severe that it can cause death in patients. (1)

It is crucial for nurses to understand the pathophysiology of HF, risk factors, and what education and treatment a nurse can incorporate in the plan of care, which will slow the progression of disease and maintain quality of life.

Statistical Evidence/Epidemiology

Epidemiologists study a disease's incidence, mortality, and prevalence to predict health care costs, how many people have a disease, how it affects society, and when the numbers of a disease change.

According to the CDC, there are approximately 6.2 million patients with heart failure in the United States. The diagnosis was noted on 13.8% of death certificates in 2018. (2) $30.7 billion was spent on HF in 2012, including health care costs, days away from work, and medications that treat HF.

Although HF is higher in the elderly population, the more significant number of patients ages 35 and above who die with HF are concentrated in the southeast, southwest, Indiana, Wisconsin, and Illinois, with some counties in Utah, Oregon, Montana, South Dakota, and Nebraska.

Readmission rates declined when the Hospital Readmission Reduction Program (HRRP) began in 2012 to reduce costs and deliver care more safely.

Hospitals are penalized by the Centers for Medicare and Medicaid to lower readmission rates to less than 30 days for some diagnoses, and HF was among them. Hospitals began to look closer at the readmission rates, which helped them to focus on improved management. (2) . Using the information below, nurses can better assess the patient and add more information to their care plan.

The classifications of HF as defined by the New York Heart Association are:

• No symptoms with regular physical activity.
• Some mild symptoms with physical activity but not at rest
• Comfortable at rest but with moderate symptoms with some minor physical activity.
• Severe shortness of breath with rest. (2)

Providers typically use echocardiograms to measure heart failure using the ejection fraction (EF) percentage. Ejection fraction demonstrates the blood pumping rate from the left ventricle to the body.

An EF of below 30% indicates severe disease, while an EF at or above 50% indicates milder or no condition. Left ventricular failure with an EF of 50% or above is considered HF with preserved EF. An EF of 30% or below is considered HF with reduced EF. There is now a new category called HF with mid-range, which shows an EF of 40%-50%.

Approximately 15% of the HF population shows mid-range EF.

Incidence - is the number of new disease cases in certain patients. In HF, this number also helps scientists understand how the prevalence of the disease results from a lifestyle change. These studies aid in determining the burden of HF on society, which in turn helps to make changes in public policy and, eventually, how HF patients are treated. "For HF, incidence as a measure of new cases is particularly helpful to assess how the occurrences of HF might have changed over time as a result of changes in risk factors." (2)

Prevalence - measures the commonality of a disease, in this case HF, in the at-risk population at or over a given time. It also measures how often an HF patient will be encountered. (6)

Mortality - CHF is one of the top causes of death. Mortality rates are high, and the data shows that 50% of HF patients die at or within five years of diagnosis. (2) More recent studies show mortality rates in HF are increasing, which may be due in part to an aging population.

Etiology and Pathophysiology  

Heart failure is often caused by an injury to the heart's muscle, such as Myocardial Infarction (MI), valvular regurgitation, stenosis of the heart's valves, and arrhythmia. (4) It is essential that the provider determines the cause to treat these patients appropriately. 

The most common cause of HF is cardiovascular disease. When fatty deposits or plaque buildup in the vessels supplying the heart, the arteries become narrowed and decrease blood flow to the heart muscle. This can cause ischemia (lack of oxygen) to the area of the heart's power involved, causing an MI. This, in turn, causes damage to the heart's muscle, reducing its ability to pump normally. 

There are two main types of HF:

• Left ventricular HF or systolic (LHF)
• Right ventricular HF or diastolic (RHF) 

LHF occurs when the damage to the left ventricle occurs, and RHF occurs when the damage is to the right ventricle. 

The following Table taken from the National Institutes of Health shows comorbidities for Systolic and Diastolic HF: 

Systolic (LHF) 

• Coronary Heart disease 
• Arterial Hypertension 
• Valvular Heart Disease 
• Arrhythmias 
• Inflammatory disease 
• Idiopathic cardiomyopathy 
• Toxic Cardiomyopathy (alcohol)
  

Diastolic (RHF) 

• Diabetes Mellitus 
• Arterial Hypertension 
• Valvular Heart Disease (pressure load) 
• Hypertrophic Cardiomyopathy 
• Restrictive Cardiomyopathy 
• Constrictive Pericarditis 
• Amyloidosis (storage disease) 

HF causes volume overload in the ventricles of the heart. This is due to enlargement and stiffness of the ventricles, so they cannot pump enough blood to the lungs and the body. (1,4) The nurse can utilize this information to care for the patient and implement essential treatments. 

Genetics also play a role in HF but are varied and complex. Studies have found more than 100 genes that may contribute to cardiomyopathy. Depending on where the failure occurs, more genetic testing is recommended in some instances: Left, Right, or Biventricular determines what signs and symptoms may be present in a patient.  

In a patient with an MI or volume/pressure overload, the whole heart will change in structure and function. There will be hypertrophy of the Left ventricle and the dilatation of the chambers, which will cause further deterioration in cardiac function. (4) 

Certain medications may also lead to HF in some patients. These are the diabetic medications Actos and Avandia. NSAIDS (non-steroidal inflammatory drugs) and certain medicines that treat hypertension, cancer, blood dyscrasias, mental health, lung urinary issues, and infections. (1) 

Aging also contributes as the heart's ability to work decreases over time. Too much alcohol and smoking are also important considerations. Heart failure may also cause complications such as kidney damage and failure, more heart problems, and liver disease caused by the backup of fluid that the liver cannot handle. 

The photo below shows the difference between a normal heart and an enlarged one (12). 

Preventable and non-preventable risk factors for heart disease are:  

• Poor diet  
• Smoking 
• Lack of exercise 
• Alcoholism 
• Obesity 
• Genetics/Race-non preventable         

It is also known that Hispanic women are at higher risk for diabetes, which can lead to heart disease if their diabetes is not managed well. Also, African American men are at higher risk for heart disease, possibly leading to HF. 

Interestingly, some studies have shown that the incidence of hospitalizations has declined. This may be due to early diagnosis, better use of medications and newer devices, earlier and ongoing patient education of risk factors, and stellar outpatient and preventive care of those patients living with HF or at risk in the community (2). 

Diagnostic and Screening Tools for Heart Failure (HF) 

Essential diagnostic screening tools are heart rate, cholesterol testing, blood pressure, and weight. Blood pressure measurement is one of the most critical tests since it can have no symptoms.  

If high, it significantly increases the risk of cardiac disease. Fortunately, diet exercise can control blood pressure to lose weight if needed, and medications.  

According to the American Heart Association, the standard for blood pressure is 120/80 or below and should be measured starting at age 20. (5) Next is the fasting cholesterol profile. Again, starting at age 20, a fasting lipid profile should be done. (5) This will give the provider and patient a baseline to follow and assist nurses in developing and implementing care plans. 

The following chart describes lab values for cholesterol. As you can see, the values in red are at the highest risk for cardiovascular disease, which could lead to HF. 

(13)

Body habitus is another crucial factor in predicting CAD. Body mass index (BMI), Waist measurements, and body structure can help predict how at risk a patient is for many diseases, including CAD, diabetes, atrial fibrillation, HF, and stroke. (7) 

The typical Western diet is full of fats and sugars. In the US, many processed foods containing high salt, fat, and sugar are used. 

These foods are unhealthy for the body and cause obesity and poor health. The Mediterranean diet, in turn, is full of fresh fruits and vegetables, lean meat, and a few processed foods. This is the most recommended diet for all populations. 

High blood glucose is another indicator of poor health. Insulin resistance is the precursor to diabetes. A patient has insulin resistance when the body's muscles and tissues cannot respond to insulin, so glucose increases in the blood. (5)  

Causes of insulin resistance are thought to be obesity with a large waist measurement. Blood glucose is usually tested with routine blood work. This gives the provider knowledge if a patient is at risk for diabetes and, therefore, heart disease. (5) Smoking and lack of physical activity can cause poor health, which may lead to cardiovascular disease. 

Echocardiogram, Holter monitoring, stress tests, and nuclear stress tests are routinely used when a patient presents with symptoms of or has known cardiovascular disease. These tests provide a look at heart function and are used to determine disease progression or maintenance. 

Medication Management 

Treating HF with medications can reduce disease progression, and relieve symptoms of dyspnea, fatigue, and edema.  Several classes of drugs can be used to treat HF.  Each one may be used to treat a different symptom. 

The classes are as follows:

Angiotensin-Converting Enzyme (ACE) Inhibitors 

These medications open blood vessels decreasing blood pressure and lowering the heart’s work to keep HF from worsening. (6) 

Some common ACE inhibitors are: 

• Captopril 
• Enalapril 
• Lisinopril 
• Ramipril  

Angiotensin-Receptor Blockers (Arbs)

• Losartan
• Valsartan
  

Angiotensin-Receptor Neprilysin Inhibitors (Arnis) 

Entresto is a drug combination in the class of Angiotensin-receptor neprilysin inhibitors (ARNIs). ARNIs limit the enzyme neprilysin from breaking down natural substances in the body.  By limiting this enzyme, the arteries can open to increase blood flow.  This drug also limits the retention of sodium. (7) 

Beta Blockers  

Beta-blockers work to slow down the heart rate and increase blood flow by widening blood vessels. This also lowers blood pressure. (9) 

Common Beta Blockers are: 

• Atenolol 
• Bisoprolol 
• Carvedilol 
• Labetalol 
• Metoprolol succinate 
• Metoprolol tartrate 
• Nadolol 
• Propranolol 

Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors 

Jardiance and Farxiga are Sodium-glucose cotransporter-2 (SGLT2) inhibitors that were designed to treat diabetes, but they have been found to be cardio-protective. (7) 

Diuretics 

Diuretics allow the body to release extra fluid and sodium through the kidneys.  They cause increased urination so should be taken earlier in the day. 

Most common diuretics are: 

• Lasix 
• Bumex 
• Torsemide 
• Diuril 
• Hydrochlorothiazide (HCTZ) 
• Metolazone 

Other medications can be prescribed depending on the patient's needs, such as anticoagulants to keep the blood thin, statins to lower cholesterol, and Digoxin to control heart rate and increase pumping strength. Calcium channel blockers allow the heart muscle to relax, thereby reducing blood pressure and circulation within the heart. Potassium may be used with certain diuretics that cause potassium to leave the body.  

It is needed to keep the heart's rhythm in control. Oxygen may also increase its amount in the blood, assisting with dyspnea and activity tolerance. (7) It is the nurse's responsibility to evaluate these medications and interventions for plan updates. 

Other Interventions 

Several types of surgery can be utilized for the most severe cases of HF. Bypass surgery has been used for many years. This procedure bypasses blocked coronary arteries, allowing for better blood flow to the heart muscle.  

Replacing damaged or stenosed heart valves will assist blood flow within the heart chambers. In some patients, biventricular pacing with a pacemaker allows both sides of the heart to work in sync. (10) An ICD, or implantable defibrillator, can shock the heart from a life-threatening rhythm back to normal.  

The ventricular assist device or VAD can assist the ventricles to pump blood out to the body. (10) This device can be used either waiting for a transplant or permanently.  

Heart Transplants can be used as the last intervention, with a success rate of 88% after one year and 75% after five. If a patient has sleep apnea, it can be linked to heart failure. In this case, an evaluation and treatment will be performed. (10)

Current areas of research in HF are producing more effective drug therapy, genetic testing, non-surgical devices, transplants, and mechanical support. (8) 

The research is now studying drugs that improve physical symptoms when added to the standard drug treatment and care. These drugs have shown improvement in reducing hospitalizations. 

The newer diabetic medications Jardiance, Invokana, and Farxiga are being studied on HF patients without diabetes to learn if they will improve function and risk reduction of MI, stroke, or cardiovascular death. (8) 

Non-invasive imaging such as MRI, ultrasound, nuclear testing, and radiology are being researched in the hope that advancing these technologies will "provide additional information about coronary arteries and heart tissue, coronary strain, the function and structure of the heart." (8)  

Genetic testing is under investigation to help determine if there is an inherited disease, especially in specific cardiomyopathies. These cardiomyopathies present differently and may be treated with differing modalities. 

One of the newest areas of HF management and treatment is remote monitoring. Nurses are at the forefront of home monitoring in many areas as they are the clinicians making home visits. 

New types of VADs are emerging as treatments for advanced illnesses. They are being manufactured to be more durable and portable. (8) 

Conclusion

As discussed in this course, Heart Failure affects over 6 million people in the US. Age, lifestyle, race, and genetics may predispose a patient to this disease.

HF burdens society and health care costs due to missed work, rehospitalizations, and poor outcomes. As a nurse, learning the mechanisms of HF is imperative. Understanding etiology, statistics, pharmaceuticals, and other interventions will assist nurses in administering the best care.

New research shows how emerging medications, improved implantable devices, and surgery can improve outcomes. However, patient education and prevention are vital to caring for HF patients.

Hypertension Updates

Introduction

This course aims to provide nurses and healthcare professionals with an up-to-date understanding of hypertension (HTN). The course covers epidemiological evidence, etiology, diagnostic tools, medication management, other interventions, and future research on HTN. 

Hypertension, or high blood pressure, is a chronic condition and a significant risk factor for heart disease, stroke, kidney failure, and other serious health problems. The American College of Cardiology defines hypertension as systolic blood pressure greater than 130 mmHg or diastolic blood pressure greater than 80 mmHg [1].

Statistical Evidence/Epidemiology 

According to the Centers for Disease Control and Prevention (CDC), hypertension afflicts 108 million Americans and contributes to almost 500,000 deaths per year in the United States [2]. The prevalence of hypertension varies by race and ethnicity, with non-Hispanic Black adults having the highest majority (57.1%), followed by Hispanic adults (43.7%) and non-Hispanic White adults (43.6%).  

Hypertension is also more common among older adults, with (74.5%) of adults aged 60 and over having high blood pressure [3]. Despite the high prevalence of hypertension, less than a quarter of all adults with hypertension in the United States have their blood pressure under control [2].  

This leaves millions at risk for serious health problems from uncontrolled hypertension, such as heart disease, stroke, kidney failure, and eye problems. In 2021, high blood pressure was a primary or contributing cause of death for more than 691,095 Americans [4]. 

[31] 

Etiology/Pathophysiology of Hypertension 

Hypertension (high blood pressure) is a multifactorial disease characterized by persistent elevated blood pressure in the systemic arteries. Understanding hypertension's etiology, pathophysiology, and sequela is crucial for effective management and treatment.  

There are two main types of hypertension: primary hypertension and secondary hypertension. Primary or essential hypertension (idiopathic hypertension), which accounts for about 80-95% of all cases, has no identifiable cause and results from complex interactions between genetic, environmental, and other unknown factors [5].  

The cause of secondary hypertension (15-30% of cases) is often an underlying medical condition, such as kidney disease, adrenal gland tumors, diabetes, or thyroid disease [6]. Family history plays a role, although science has identified no genetic factor as the "hypertension gene" [7].  

A key mechanism in hypertension is the imbalance between the forces that constrict and dilate blood vessels. This imbalance can be caused by several factors, including increased activity of the sympathetic nervous system, which leads to vasoconstriction, increased production of vasoconstrictor hormones, such as angiotensin II and aldosterone, a decreased output of vasodilator hormones, such as nitric oxide, and structural changes in the blood vessels, such as thickening of the vessel walls [8]. 

The most understood mechanism of hypertension involves increased peripheral vascular resistance due to constriction of small arterioles. The Renin-Angiotensin-Aldosterone System (RAAS) is a hormonal system that regulates blood pressure. Dysfunction of the RAAS can lead to fluid retention and vasoconstriction [9]. Endothelial dysfunction involves the inner lining of the blood vessels (endothelium) and the release of nitric oxide, which promotes blood vessel relaxation. The dysfunction of nitric oxide is a primary contributor to hypertension [10]. 

Secondary hypertension often involves: 

• The kidneys and volume overload. 
• Leading to elevated blood pressure. 
• Often affecting younger patients and those with resistant or refractory hypertension. 

The typical secondary causes of hypertension include: 

• Primary aldosteronism (PA). 
• Renovascular disease. 
• Chronic kidney disease (CKD). 
• Obstructive sleep apnea (OSA). 
• Drug-induced or alcohol-induced hypertension [11]. 

Overactivation within the sympathetic nervous system can result in increased heart rate (tachycardia) and vasoconstriction, both of which can cause a temporary elevation in blood pressure. Within the metabolic process, insulin resistance has been associated with endothelial dysfunction and hypertension [12]. 

Diagnostic and Screening Tools 

The primary current diagnostic and screening tools around hypertension include blood pressure measurement. Blood pressure consists of systolic blood pressure (SBP) and diastolic blood pressure (DBP).  

SBP is the pressure when the heart is beating, and DBP is the pressure when the heart is resting. A diagnosis of hypertension can be established when the Systolic Blood Pressure (SBP) is 130 mmHg or above or when the Diastolic Blood Pressure (DBP) is at least 80 mmHg [1].  

The American Heart Association (AHA) recommends that all adults have their blood pressure checked at least once a year. People with risk factors for hypertension, such as obesity, diabetes, and kidney disease, should have their blood pressure checked more often [13]. 

Secondary tools for evaluating hypertension include ambulatory blood pressure monitoring (ABPM). ABPM is a more accurate way to measure blood pressure, measuring blood pressure over 24 hours. ABPM is an integral part of hypertensive care [14].  

Urine tests can check for protein in the urine, a sign of kidney damage. Kidney damage is a risk factor for hypertension. Blood tests can be used to check for other medical conditions that can cause hypertension, such as diabetes and kidney disease, cholesterol levels, and other risk factors for heart disease.  

Hormonal Tests can measure hormones produced by the adrenal and thyroid glands, which can help diagnose secondary hypertension. Regardless of the diagnostic or screening tools, early diagnosis and management of hypertension save lives [15]. 

Imaging and Other Diagnostic Tests 

Ultrasound of the Kidneys: To rule out kidney abnormalities. 

Echocardiogram: To assess heart function and structure. Useful if hypertension has been longstanding. 

Eye Exam: A fundoscopic examination can reveal changes in the retinal blood vessels, indicative of chronic hypertension. 

Telemedicine: Remote monitoring can be helpful for ongoing assessment and titration of treatment. 

Healthcare Apps: Smartphone apps can log and track blood pressure readings over time. 

Medication Management 

The management of hypertension has evolved over the years, with numerous classes of medications available for treatment. The type of medication best suited for your patients will depend on their needs and health history.  

Treatment strategies often begin with monotherapy, a single drug, usually a diuretic, beta-blocker, ACE inhibitor, or Angiotensin II receptor blocker (ARBs) [16]. Combination therapy for patients with stage 2 hypertension or those not reaching the target BP with monotherapy, which may include two or more drug classes, is also used.[16].  

Step therapy involves starting with one drug and adding others to achieve the desired effect. A tailored approach is considered if comorbid conditions are present, such as diabetes or heart failure, which may influence drug choice. 

Several standard classes of antihypertensive medications are used to treat hypertension, including first-line thiazides such as hydrochlorothiazide, which help rid excess salt and water and lower blood pressure [17]. Angiotensin-converting enzyme (ACE) inhibitors such as lisinopril and ramipril block the production of angiotensin II, a hormone that narrows blood vessels.  

Angiotensin II Receptor Blockers (ARBs) such as losartan and valsartan which inhibit the action of angiotensin II, leading to vasodilation [17]. Beta-blockers such as atenolol or metoprolol slow the heart rate and reduce the force of the heart's contractions, which can lower blood pressure [17].  

Calcium channel blockers such as amlodipine and diltiazem relax the muscles of the blood vessels by inhibiting the movement of calcium into vascular smooth muscle cells, thus lowering blood pressure [17]. Alpha-blockers such as doxazosin work by blocking alpha-adrenergic receptors, leading to vasodilation. Vasodilators such as hydralazine and minoxidil relax the muscles in blood vessel walls [17]. 

Central action agents such as clonidine, methyldopa, and moxonidine work on the central nervous system to lower blood pressure [17]. Moxonidine is a new-generation antihypertensive drug that works by activating imidazoline-I1 receptors in the brain, and it may be used when other antihypertensive drugs, such as thiazides, beta-blockers, ACE inhibitors, and calcium channel blockers, are not appropriate or have failed [18].  

Thiazide-like diuretics such as chlorthalidone and indapamide have found increased use for their more prolonged duration of action and better cardiovascular outcomes when compared to traditional thiazides [19]. New evidence-based medications are coming into play, such as angiotensin receptor-neprilysin inhibitors (ARNIs), and a clinical trial is underway to test the effectiveness of a new drug called finerenone in preventing heart failure and kidney disease in people with hypertension and diabetes [20] [21]. 

Due to their safety profiles, there are special considerations with hypertensive management, including methyldopa and labetalol for pregnancy [22].  

For older people, care is taken to avoid overtreatment, considering the risks of low blood pressure. For patients with chronic kidney disease (CKD), ACE inhibitors and ARBs are often favored due to their renal protective effects.  

Generics are preferred when appropriate to reduce patient costs [23]. Digital adherence tools, including smartphone apps and telemedicine platforms, monitor patient compliance and adjust treatment as necessary. 

[32] 

Other Interventions  

Beyond medication, lifestyle changes, including dietary interventions like the DASH diet and exercise, have proven effective in managing hypertension [24]. The DASH diet focuses on a high intake of fruits, vegetables, and low-fat dairy foods and is low in saturated and total fat.  

A reduction in dietary sodium has been shown to lower blood pressure, with a general recommendation to consume less than 2,300 mg per day, with an ideal limit of 1,500 mg for most adults [24]. Regular aerobic exercise such as walking, jogging, or swimming can lower blood pressure.  

Weight loss of even 5-10% can significantly impact reducing blood pressure [25]. Alcohol moderation and smoking cessation can also lead to blood pressure reduction. 

Behavioral therapies, including stress management techniques such as deep breathing, meditation, and relaxation exercises, can help reduce short-term spikes in blood pressure. There is some evidence that suggests that Cognitive CBT can be effective in managing hypertension [26].  

Biofeedback can help manage stress triggers and measure physiological functions like heart rate and blood pressure [26]. Although evidence is mixed, some studies suggest acupuncture can help lower blood pressure.  

Renal denervation is an invasive procedure using radiofrequency energy to destroy kidney nerves contributing to hypertension. Central sleep apnea therapy can treat central sleep apnea and lower blood pressure.  

Weight loss surgery can be an effective way to lower blood pressure in people who are obese or overweight. Several stress management techniques, such as yoga, meditation, and deep breathing, can be helpful. 

Self-monitoring and regular medical check-ups can ensure that the treatment plan is effective and can be adjusted as needed. Remote consultations can offer more frequent touchpoints for adjustments in treatment plans.  

Various mobile applications can help patients track blood pressure readings, medication schedules, and lifestyle changes. Community-based interventions to educate the public about hypertension risks, prevention, and management can be effective.  

On a policy level, changes and initiatives that reduce sodium in processed foods can have a broader societal impact [27]. 

Upcoming Research 

Using "Omics" genomic, proteomic, and metabolomic data to tailor antihypertensive therapies to individuals' researchers are working to identify the genes that contribute to hypertension and specific genetic markers that can help predict an individual's risk for developing hypertension and their potential response to treatments [28].  

This information could be used to create new genetic tests to identify people who are at risk of developing the condition. Personalized medicine seeks to create customized approaches to managing hypertension, which would involve tailoring treatment to the individual's needs and risk factors.  

Non-invasive treatments, such as devices worn on the body to deliver medication or stimulate the nerves, may also be effective. Researchers are developing a new type of blood pressure monitor that can be worn on the wrist and measure blood pressure throughout the day. 

A study is underway to investigate the use of artificial intelligence to develop personalized treatment plans for people with hypertension. With predictive analytics, AI models are trained to predict hypertension risk and disease progression using large-scale electronic health records [29]. 

In the area of new therapeutic targets, researchers are looking into novel ways to improve endothelial function and vascular health. Studies into how the gut microbiome may influence blood pressure regulation offer potential for new treatment modalities [30]. Research on how diet interacts with genes within the gut microbiome may affect blood pressure. 

Awareness and Patient Education 

What your patients should know: 

• Early diagnosis and treatment of hypertension are essential for preventing complications. 
• There are several different types of medications available to treat hypertension. 
• Lifestyle changes, such as eating a healthy diet, exercising regularly, and maintaining a healthy weight, can also help to lower blood pressure. 

Nurses and healthcare professionals should be aware of the following: 

• Nurses and healthcare professionals play a vital role in educating patients about hypertension and helping them manage their condition. 
• The latest epidemiological statistics on hypertension, including its prevalence, risk factors, and impact on public health. 
• The etiology and pathophysiology of hypertension, including the different types of hypertension and their underlying causes. 
• The diagnostic tools used to diagnose hypertension include blood pressure measurement, ambulatory blood pressure monitoring, urine tests, blood tests, and imaging tests. 
• The different types of medications available to treat hypertension, as well as their side effects and interactions. 

Nurses and healthcare professionals can help patients to manage their hypertension by: 

• Educating patients about hypertension and its risks. 
• Helping patients develop a treatment plan that includes lifestyle changes and medications. 
• Monitoring their blood pressure and adjusting their treatment plan as needed. 
• Providing support and encouragement. 

By working together, nurses and healthcare professionals can help patients manage their hypertension and reduce their risk of complications. 

Conclusion

Hypertension is a significant public health problem in the United States and worldwide [1]. It is a chronic condition that can lead to serious health problems like heart disease, stroke, kidney failure, and eye problems. However, despite its complexity, hypertension is manageable with lifestyle changes, medications, and the potential information from future genomic discoveries [25] [17]. 

GI Bleed: An Introduction

Introduction   

Gastrointestinal bleeding (GI Bleed) is an acute and potentially life-threatening condition. It is meaningful to recognize that GI bleed manifests an underlying disorder. Bleeding is a symptom of a problem comparable to pain and fever in that it raises a red flag. The healthcare team must wear their detective hat and determine the culprit to impede the bleeding.  

Nurses, in particular, have a critical duty to recognize signs and symptoms, question the severity, consider possible underlying disease processes, anticipate labs and diagnostic studies, apply nursing interventions, and provide support and education to the patient. 

Epidemiology  

The incidence of Gastrointestinal Bleeding (GIB) is broad and comprises cases of Upper gastrointestinal bleeding (UGIB) and lower gastrointestinal bleeding (LGIB). GI Bleed is a common diagnosis in the US responsible for approximately 1 million hospitalizations yearly (2). The positive news is that the prevalence of GIB is declining within the US (1). This could reflect effective management of the underlying conditions.  

Upper gastrointestinal bleeding (UGIB) is more common than lower gastrointestinal bleeding (LGIB) (2). Hypovolemic shock related to GIB significantly impacts mortality rates. UGIB has a mortality rate of 11% (2), and LGIB can be up to 5%; these cases are typically a consequence of hypovolemic shock (2).  

Certain risk factors and predispositions impact the prevalence. Lower GI bleed is more common in men due to vascular diseases and diverticulosis being more common in men (1). Extensive data supports the following risk factors for GIB: older age, male, smoking, alcohol use, and medication use (7).  

We will discuss these risk factors as we dive into the common underlying conditions responsible for GI Bleed.  

Etiology/ Pathophysiology

Gastrointestinal (GI) bleeding includes any bleeding within the gastrointestinal tract, from the mouth to the rectum. The term also encompasses a wide range of quantity of bleeding, from minor, limited bleeding to severe, life-threatening hemorrhage.

We will review the basic anatomy of the gastrointestinal system and closely examine the underlying conditions responsible for upper and lower gastrointestinal bleeding.

Let's briefly review the basic anatomy of the gastrointestinal (GI) system, which comprises the GI tract and accessory organs. You may have watched The Magic School Bus as a child and recall the journey in the bus from the mouth to the rectum! Take this journey once more to understand the gastrointestinal (GI) tract better.

The GI tract consists of the following: oral cavity, pharynx, esophagus, stomach, small intestine, large intestine, and anal canal (5). The accessory organs include our teeth, tongue, and organs such as salivary glands, liver, gallbladder, and pancreas (5). The primary duties of the gastrointestinal system are digestion, nutrient absorption, secretion of water and enzymes, and excretion (5, 3). Consider these essential functions and their impact on each other.

This design was created on Canva.com on August 31, 2023. It is copyrighted by Abbie Schmitt, RN, MSN and may not be reproduced without permission from Nursing CE Central. 

As mentioned, gastrointestinal bleeding has two broad subcategories: upper and lower sources of bleeding. You may be wondering where the upper GI tract ends and the lower GI tract begins. The answer is the ligament of Treitz. The ligament of Treitz is a thin band of tissue that connects the end of the duodenum  and the beginning of the jejunum (small intestine); it is also referred to as the suspensory muscle of the duodenum (4). This membrane separates the upper and lower GI tract. Upper GIB is defined as bleeding proximal to the ligament of Treitz, while Lower GIB is defined as bleeding beyond the ligament of Treitz (4). 

Upper GI Bleeding (UGIB) Etiology 

Underlying conditions that may be responsible for the UGIB include: 

• Peptic ulcer disease 

• Esophagitis 
• Foreign body ingestion 
• Post-surgical bleeding 
• Upper GI tumors 
• Gastritis and Duodenitis 

• Varices 
• Portal hypertensive gastropathy (PHG) 
• Angiodysplasia 
• Dieulafoy lesion 
• Gastric antral valvular ectasia 

• Mallory-Weiss tears 
• Cameron lesions (bleeding ulcers occurring at the site of a hiatal hernia 
• Aortoenteric fistulas 
• Hemobilia (bleeding from the biliary tract) 
• Hemosuccus pancreaticus (bleeding from the pancreatic duct) 

(1, 4, 5, 8. 9) 

Pathophysiology of Variceal Bleeding. Variceal bleeding should be suspected in any patient with known liver disease or cirrhosis (2). Typically, blood from the intestines and spleen is transported to the liver via the portal vein (9). The blood flow may be impaired in severe liver scarring (cirrhosis). Blood from the intestines may be re-routed around the liver via small vessels, primarily in the stomach and esophagus (9). Sometimes, these blood vessels become large and swollen, called varices. Varices occur most commonly in the esophagus and stomach, so high pressure (portal hypertension) and thinning of the walls of varices can cause bleeding within the Upper GI tract (9). 

Liver Disease + Varices + Portal Hypertension = Recipe for UGIB Disaster 

Lower GI Bleeding (LGIB) Etiology

• Diverticulosis
• Post-surgical bleeding
• Angiodysplasia
• Infectious colitis
• Ischemic colitis
• Inflammatory bowel disease
• Colon cancer
• Hemorrhoids
• Anal fissures
• Rectal varices
• Dieulafoy lesion
• Radiation-induced damage

(1, 4, 5, 9)

Unfortunately, a source is identified in only approximately 60% of cases of GIB (8). Among this percentage of patients, upper gastrointestinal sources are responsible for 30–55%, while 20–30% have a colorectal source (8).

Laboratory and Diagnostic Testing

Esophagogastroduodenoscopy (EGD) and colonoscopy identify the source of bleeding in 80–90% of patients (4). The initial clinical presentation of GI bleeding is typically iron deficiency/microscopic anemia and microscopic detection of blood in stool tests (6).

The following laboratory tests are advised to assist in finding the cause of GI bleeding (2):

• Complete blood count
• Hemoglobin/hematocrit
• International normalized ratio (INR), prothrombin time (PT), and activated partial thromboplastin time (PTT)
• Liver function tests

Low hemoglobin and hematocrit levels result from blood loss, and blood urea nitrogen (BUN) may be elevated due to the GI system's breakdown of proteins within the blood (9).

The following laboratory tests are advised to assist in finding the cause of GI bleeding:

• EGD (esophagogastroduodenoscopy)- Upper GI endoscopy
  • Clinicians can visualize the upper GI tract using a camera probe that enters the oral cavity and travels to the duodenum (9)
• Colonoscopy- Lower GI endoscopy/ (9)
  • Clinicians can visualize the lower GI tract.
• CT angiography
  • Used to identify an actively bleeding vessel

Signs and Symptoms 

Clinical signs and symptoms depend on the volume/ rate of blood loss and the location/ source of the bleeding. A few key terms to be familiar with when evaluating GI blood loss are overt GI bleeding, occult GI bleeding, hematemesis, hematochezia, and melena. Overt GI bleeding means blood is visible, while occult GI bleeding is not visible to the naked eye but is diagnosed with a fecal occult blood test (FOBT) yielding positive results of the presence of blood (5). Hematemesis is emesis/ vomit with blood present; melena is a stool with a black/maroon-colored tar-like appearance that signifies blood from the upper GI tract (5). Melena has this appearance because when blood mixes with hydrochloric acid and stomach enzymes, it produces this dark, granular substance that looks like coffee grounds (9). 

Mild vs. Severe Bleeding  

A patient with mild blood loss may present with weakness and diaphoresis (9). Chronic iron deficiency anemia symptoms include hair loss, hand and feet paresthesia, restless leg syndrome, and impotence in men (8). The following symptoms may appear over time once anemia becomes more severe and hemoglobin is consistently less than 7 mg/dl: pallor, headache, dizziness from hypoxia, tinnitus from the increased circulatory response, and the increased cardiac output and dysfunction may lead to dyspnea (8). Findings of a positive occult GI bleed may be the initial red flag. 

A patient with severe blood loss, which is defined as a loss greater than 1 L within 24 hours, hypotensive, diaphoretic, pale, and have a weak, thready pulse (9). Signs and symptoms will reflect the critical loss of circulating blood volume with systemic hypoperfusion and oxygen deprivation, so that cyanosis will also be evident (9). This is considered a medical emergency, and rapid intervention is needed. 

Stool Appearance: Black, coffee ground = Upper GI; Bright red blood = Lower GI. 

History and Physical Assessment

History

A thorough and accurate history and physical assessment is a key part of identifying and managing GI bleed. Remember to avoid medical terminology/jargon while asking specific questions, as this can be extremely helpful in narrowing down potential cases. It is a good idea to start with broad categories (general bleeding) then narrow to specific conditions.

Assess for the following:

• Previous episodes of GI Bleed
• Medical history with contributing factors for potential bleeding sources (e.g., ulcers, inflammatory bowel disease, liver disease, varices, PUD, alcohol abuse, tobacco abuse, H.pylori, diverticulitis) (3)
• Contributory medications (non-steroidal anti-inflammatory drugs (NSAIDs, anticoagulants, antiplatelet agents, bismuth, iron) (3)
• Comorbid diseases that could affect management of GI Bleed (8)

Physical Assessment

1. Head to toe and focused Gastrointestinal, Hepatobiliary, Cardiac and Pancreatic
2. Assessments
   Assess stool for presence of blood (visible) and anticipate orders/ collect specimen for occult blood testing.
3. Vital Signs

Signs of hemodynamic instability associated with loss of blood volume (3):

• Resting tachycardia
• Orthostatic hypotension
• Supine hypotension
• Abdominal pain (may indicate perforation or ischemia)
• A rectal exam is important for the evaluation of hemorrhoids, anal fissures, or anorectal mass (3)

Certain conditions place patients at higher risk for GI bleed. For example, patients with end-stage renal disease (ESRD) have a five times higher risk of GIB and mortality than those without kidney disease (2).

Treatment and Interventions

Treatment and interventions for GIB bleed will depend on the severity of the bleeding. Apply the ABCs (airway, breathing, circulation) prioritization tool appropriately with each unique case. Treatment is guided by the underlying condition causing the GIB, so this data is too broad to cover. It would be best to familiarize yourself with tools and algorithms available within your organization that guide treatment for certain underlying conditions. Image 2 is an example of an algorithm used to treat UGIB (8). The Glasgow-Blatchford bleeding score (GBS) tool is another example of a valuable tool to guide interventions. Once UGIB is identified, the Glasgow-Blatchford bleeding score (GBS) can be applied to assess if the patient will need medical intervention such as blood transfusion, endoscopic intervention, or hospitalization (4).

Unfortunately, there is currently a lack of tools available for risk stratification of emergency department patients with lower gastrointestinal bleeding (LGIB) (6). This gap represents an opportunity for nurses to develop and implement tools based on their experience with LGIB.

(8) 

The first step of nursing care is the assessment. The assessment should be ongoing and recurrent, as the patient's condition may change rapidly with GI bleed. During the evaluation, the nurse will gather subjective and objective data related to physical, psychosocial, and diagnostic data. Effective communication is essential to prevent and mitigate potential risk factors.

Subjective Data (Client verbalizes)

• Abdominal pain
• Nausea
• Loss of appetite
• Dizziness
• Weakness

Objective Data (Clinician notes during assessment)

• Hematemesis (vomiting blood)
• Melena (black, tarry stools)
• Hypotension
• Tachycardia
• Pallor
• Cool, clammy skin

Nursing Interventions

Ineffective Tissue Perfusion:

1. Monitor vital signs frequently to assess blood pressure, heart rate, and oxygen saturation changes.
2. Obtain IV access.
3. Administer oxygen as ordered.
4. Elevate the head of the bed (support venous return and enhance tissue perfusion).
5. Administer blood products (packed red blood cells, fresh frozen plasma) as ordered to replace lost blood volume.

Acute Pain:

1. Assess the patient's pain (quantifiable pain scale)
2. Administer pain medications as ordered.
3. Obtain and implement NPO Orders: Allow the GI tract to rest and prevent further irritation while preparing for possible endoscopic procedures.
4. Apply heat/cold therapy for comfort.

Risk for Decreased Cardiac Output

1. Assess the patient's heart rate and rhythm. (Bleeding and low cardiac output may trigger compensatory tachycardia.) (9)
2. Assess and monitor the patient's complete blood count.
3. Assess the patient's BUN level.
4. Monitor the patient's urine output.
5. Perform hemodynamic monitoring.
6. Administer supplemental oxygenation as needed.
7. Administer intravenous fluids as ordered.
8. Prepare and initiate blood transfusions as ordered.
9. Educate and prepare the patient for endoscopic procedures and surgical intervention as needed.

Risk for Deficient Fluid Volume:

1. Monitor intake and output.
2. Maintain hydration.
3. Administer intravenous fluids as ordered.
4. Monitor labs, including hemoglobin and hematocrit, to assess the effectiveness of fluid replacement therapy.
5. Educate the patient on increasing oral fluid intake once the bleeding is controlled.
6. Vital signs
7. Assess the patient's level of consciousness and capillary refill time to evaluate tissue perfusion and response to fluid replacement.
8. Collaborate with the healthcare team to adjust fluid replacement therapy based on the patient's response and laboratory findings.

Nursing Goals / Outcomes for GI Bleed:

• The patient's vital signs and lab values will stabilize within normal limits.
• The patient will be able to demonstrate efficient fluid volume as evidenced by stable hemoglobin and hematocrit, regular vital signs, balanced intake and output, and capillary refill < 3 seconds.
• The patient will exhibit increased oral intake and adequate nutrition.
• The patient will verbalize relief or control of pain.
• The patient will appear relaxed and able to sleep or rest appropriately.
• The patient verbalizes understanding of patient education on gastrointestinal bleeding, actively engages in self-care strategies, and seeks appropriate support when needed.

Case Study

Mr. Blackstool presents to the emergency department with the following:

CHIEF COMPLAINT: "My stool looked like a ball of black tar this morning."

He also reports feeling "extra tired" and "lightheaded" for 3-5 days.

HISTORY OF PRESENT ILLNESS: The patient is a 65-year-old tractor salesman who presents to the emergency room complaining of the passage of black stools, fatigue, and lightheadedness. He reports worsening chronic epigastric pain and reflux, intermittent for 10+ years.

He takes NSAIDS as needed for back, and joint pain and was recently started on a daily baby aspirin by his PCP for cardiac prophylaxis. He reports "occasional" alcohol intake and smokes two packs of cigarettes daily.

PHYSICAL EXAMINATION: Examination reveals an alert and oriented 65-YO male. He appears anxious and irritated. Vital sips are as follows. Blood Pressure 130/80 mmHg, Heart Rate 120/min - HR Thready - Respiratory Rate - 20 /minute; Temperature 98.0 ENT/SKIN: Facial pallor and cool, moist skin are noted. No telangiectasia of the lips or oral cavity is noted. The parotid glands appear full.

CHEST: Lungs are clear to auscultation and percussion. The cardiac exam reveals a regular rhythm with an S4. No murmur is appreciated. Peripheral pulses are present but are rapid and weak.

ABDOMEN/RECTUM: The waist shows a rounded belly. Bowel sounds are hyperactive. Percussion of the liver is 13 cm (mal); the edge feels firm. Rectal examination revealed a black, tarry stool. No Dupuytren's contractions were noted.

LABORATORY TESTS: Hemoglobin 9gm/dL, Hematocrit 27%, WBC 13,000/mm. PT/PTT - normal. BUN 46mg/dL.

Discuss abnormal findings noted during History and Physical Examination; Evaluate additional data to obtain possible diagnostic testing, treatment, nursing interventions, and care plans.

Conclusion

After this course, I hope you feel more knowledgeable and empowered in caring for patients with Gastrointestinal bleeding (GIB). As discussed, GIB is a potentially life-threatening condition that manifests as an underlying disorder. Think of gastrointestinal bleeding as a loud alarm signaling a possible medical emergency. Nurses can significantly impact the recognition of signs and symptoms that determine the severity of bleeding and underlying disease process while also implementing life-saving interventions as a part of the healthcare team. As evidence-based practice rapidly evolves, continue to learn, and grow your knowledge of GIB. 

Constipation Management and Treatment

Introduction   

In the realm of healthcare, where every aspect of patient well-being is meticulously tended to, constipation is a condition that often remains in the shadows. Often dismissed as a minor inconvenience, constipation is a prevalent concern that can have significant repercussions on the health and comfort of hospitalized and long-term care patients (8).  

Imagine a scenario where a middle-aged patient, recently admitted to a hospital for a non-related condition, is experiencing discomfort due to constipation. Despite the patient's hesitation to bring up this seemingly "embarrassing" topic, a skilled nurse takes the initiative to initiate an open conversation.  

By actively listening and empathetically addressing the patient's concerns, the nurse alleviates the discomfort and also plays a crucial role in preventing potential complications. This scenario exemplifies the pivotal role that nurses play in the comprehensive management of constipation. 

Envision a long-term care facility where an elderly resident's mobility is limited, leading to a sedentary lifestyle. As a result, this individual becomes more susceptible to constipation, which could potentially lead to more severe issues if left unattended. Here, the nurse's expertise in identifying risk factors and tailoring interventions comes into play.  

By suggesting gentle exercises, dietary adjustments, and adequate hydration, the nurse transforms the resident's daily routine, ensuring a healthier digestive tract and enhanced overall well-being. 

Through the above scenarios, it becomes evident that constipation is not merely a minor inconvenience but a legitimate concern that warrants attention. As the first line of defense in patient care, nurses are uniquely positioned to identify, address, and holistically prevent constipation.  

Nurses possess the knowledge and skills to create a profound impact on patient lives by acknowledging and addressing this issue. This course aims to equip nurses with an in-depth understanding of constipation, enabling them to be proactive vigilant advocates for patient comfort, bowel health, and overall well-being. 

Epidemiology  

To truly comprehend the significance of constipation in healthcare settings, it's essential to grasp its prevalence and impact. Statistics reveal that constipation holds a prominent spot in healthcare challenges, with up to 30% of patients in hospitals and long-term care facilities experiencing this discomfort (4). This means that in a unit with 100 patients, nearly a third of them might be grappling with constipation-related issues.  

Even though constipation transcends demographics, elderly patients, who are a substantial part of long-term care settings, are more susceptible to constipation due to factors like decreased mobility, altered dietary habits, and medication use. Understanding this demographic predisposition is crucial for nurses as it guides their vigilance in recognizing and managing constipation among this vulnerable group. By unraveling its prevalence and its penchant for affecting diverse patient groups, nurses can step into their roles armed with knowledge, ready to make a tangible difference in patient lives. 

Etiology/Pathophysiology  

Embarking on the journey to comprehend constipation's root causes and underlying mechanisms offers a fascinating glimpse into the intricate workings of the digestive system. The digestive system is a well-orchestrated symphony where even a slight disruption can lead to a discordant note, constipation being one such note.  

Constipation arises from an intricate interplay of factors. Lifestyle choices, such as physical inactivity, dietary habits, and even medication use, can disturb the symphony of digestion. These disruptions impact the stool's consistency, its journey through the intestines, and the efficiency of water absorption.  

Some examples of how lifestyle choices can cause constipation include the following: 

• The digestive tract, like a finely tuned instrument, requires regular movement to maintain its rhythm and balance. Without physical activity to nudge food along, its journey through the digestive process slows down, potentially leading to constipation. 
• Mismanagement of water absorption in the colon can also contribute to constipation. Excess absorption of water in the colon can turn the stool hard and dry, making it a formidable challenge to pass.  
• When fiber is lacking in the diet, stool encounters resistance and sluggishness, akin to a symphony losing its guiding rhythm. This lack of fiber can lead to constipation, underscoring the importance of dietary choices in maintaining a harmonious digestive process (10). 

Understanding the above dynamics empowers nurses to decode the origins of constipation and tailor interventions that restore the harmonious rhythm of the digestive orchestra. Just as a conductor guides a symphony to its crescendo, nurses can orchestrate the path to relief and comfort for patients grappling with constipation. 

Signs and Symptoms  

Constipation's signs and symptoms are the stars that guide nurses toward effective management. Infrequent bowel movements, excessive straining, abdominal discomfort, and bloating are like constellations, revealing the narrative of digestive imbalance. 

Recognizing the constellation of signs and symptoms becomes the compass guiding nurses toward effective care. Just as a seasoned sailor navigates by the stars, nurses navigate constipation's landscape by deciphering the cues that patients present. 

Research by Anderson and Brown (1) reveals that patients grappling with constipation often experience infrequent bowel movements as a telltale sign. Nurses, armed with this insight, recognize that infrequent bowel movements warrant vigilant assessment and timely interventions. 

Excessive straining, much like tugging at sails in adverse winds, emerges as another hallmark of constipation (6). Patients' tales of discomfort during bowel movements point to an underlying imbalance. Nurses adeptly interpret this discomfort as a call for action, initiating strategies that ease the passage of stool and restore harmony to the digestive symphony. 

Discomfort serves as an indicator of the digestive system's struggle to find its equilibrium. Nurses, like skilled navigators, probe further, discerning the nuances of the discomfort to tailor interventions that address its root cause (11). 

Bloating is another symptom. Research by Smith and Williams (9) illuminates the link between constipation and bloating. This connection heightens nurses' vigilance, prompting them to delve into patients' experiences and offer relief from the discomfort. 

Pharmacological/Non-Pharmacological Treatment 

Constipation management encompasses a harmonious blend of pharmacological and non-pharmacological strategies. Just as a symphony thrives on a balanced ensemble, nurses can orchestrate a symphony of relief and comfort by selecting the right interventions for each patient's unique needs. Through this holistic approach, nurses play a pivotal role in restoring the digestive symphony to its harmonious rhythm. 

Pharmacological 

As nurses step into the realm of constipation management, they encounter a diverse array of strategies that can harmonize the digestive symphony. Picture a pharmacist's shelf adorned with an assortment of medications, each with a specific role in alleviating constipation. 

Fiber supplements work by increasing stool bulk and promoting regular bowel movements. They're gentle and mimic the natural process, ensuring a harmonious flow. 

Osmotic laxatives introduce more water into the stool, creating a balanced blend of moisture, preventing dry and challenging stools, and facilitating movement.  

Stimulant laxatives stimulate bowel contractions, hastening the stool's journey through the digestive tract. They're like the energetic beats that invigorate a symphony, leading to a rhythmic and effective passage. 

Lastly, stool softeners ensure that the stool is neither too hard nor too soft, striking the perfect balance. They act by moistening the stool, making it easier to pass without straining. By introducing this harmony, stool softeners contribute to patient comfort. 

Non-pharmacological 

Beyond the realm of medications lies an equally vital avenue: non-pharmacological interventions. Nurses can craft a holistic care plan, carefully considering dietary adjustments and lifestyle modifications as the foundation. Examples of non-pharmacological interventions include the following: 

A diet rich in fiber guides the stool's journey with ease. Nurses can educate patients on incorporating fruits, vegetables, and whole grains, ensuring a harmonious flow through the intestines. 

Engaging in regular physical activity not only stimulates bowel movements but also enhances overall well-being. Nurses can encourage patients to integrate movement into their routines, contributing to a dynamic and efficient digestive process. 

Relaxation techniques play a vital role in constipation management. Nurses can provide guidance on techniques like deep breathing or gentle abdominal massages that soothe the digestive tract, facilitate a smoother passage, and transform discomfort into relaxation. 

Complications 

Constipation complications can disrupt the symphony of health. Nurses, armed with knowledge and interventions, become conductors of comfort, guiding patients toward a harmonious journey free from discomfort and dissonance. Through their skilled care, nurses harmonize the symphony of patient well-being, preventing complications and promoting relief. Examples of complications include the following. 

Hemorrhoids 

These are swollen blood vessels around the rectal area that cause pain, itching, and even bleeding during bowel movements. Nurses can educate patients about preventive measures, such as adequate fiber intake, staying hydrated, and avoiding straining during bowel movements. 

Anal Fissure 

This is a small tear in the anal lining that can cause pain and bleeding, disrupting daily life. Nurses can gently guide patients toward hygiene practices and proper self-care, restoring comfort and preventing further disruption. 

Fecal Impaction 

Here, the stool accumulates, creating an obstruction that can be likened to an unexpected pause in flow. This impaction causes severe discomfort and can even lead to bowel obstruction. Nurses should be attentive to patients at risk of fecal impaction, promptly intervening with measures such as stool softeners, gentle digital disimpaction, and regular bowel assessments.  

Rectal Prolapse 

This protrusion of the rectal lining is a disruptive problem that not only causes physical discomfort but also emotional distress. Nurses can empower patients by educating them about the importance of managing constipation and preventing rectal prolapse.  

Nausea and Vomiting 

The buildup of waste and toxins can trigger these unsettling symptoms. Nurses should be vigilant, recognizing these cues as a sign of digestive imbalance. Collaborating with healthcare teams, nurses can address the underlying constipation, restoring harmony and alleviating discomfort. 

Bowel Obstruction 

This is a medical emergency. Patients experience severe abdominal pain, bloating, and the inability to pass stool or gas. Nurses should be well-equipped to recognize these symptoms and act swiftly, seeking immediate medical intervention.  

Prevention  

Prevention is composed of dietary choices, hydration, exercise, and lifestyle awareness. Nurses, as conductors of preventive care, guide patients toward a harmonious journey of well-being. By embracing preventive measures, patients become active participants in the symphony of their health, ensuring that the digestive rhythm remains soothing and uninterrupted. Sample preventive measures include the following: 

Dietary Adjustments 

Nurses can educate patients about the importance of incorporating fiber into their diets. Picture a patient's plate adorned with vibrant fruits, vegetables, and whole grains — these fiber-rich choices act as the brushstrokes that create a smooth flow through the digestive system.  

Hydration 

Like the gentle spray that keeps a garden vibrant, staying adequately hydrated ensures the digestive landscape remains fluid and inviting. Nurses can encourage patients to drink sufficient water, allowing the stool's journey to be as effortless as the water's flow.  

Exercise 

Nurses can guide patients in incorporating regular physical activities like brisk walks, or gentle stretching into their daily routines, creating a rhythm that enhances bowel motility and overall well-being. Movements, much like instrument tuning before a performance, prepare the digestive system for optimal function.  

Lifestyle Awareness 

Nurses can educate patients about the importance of timely bowel movements and creating a comfortable environment for digestion. Patients can cultivate their well-being by avoiding prolonged periods of sitting and adopting healthy toileting habits.  

Patient Education 

Nurses can provide insights into the importance of fiber-rich foods, hydration, and movement. By empowering patients with knowledge, nurses equip them with the tools needed to prevent constipation and maintain digestive well-being.   

Nursing Implications 

Nurses are instrumental in managing constipation and improving patient outcomes. Nurses should be skilled in assessing patients for constipation risk factors, communicating effectively about symptoms, and tailoring interventions to individual patient needs. Collaborating with other healthcare professionals to develop comprehensive care plans is essential. Examples of useful nursing skills include: 

Holistic Assessment 

Nurses are vigilant observers, attuned to the nuances of patient well-being. Like skilled detectives, nurses delve into patients' histories, medications, and lifestyles, identifying constipation risk factors. Holistic assessments allow nurses to understand the unique backdrop against which constipation may unfold. Armed with this knowledge, nurses can tailor interventions that resonate with each patient's needs (12). 

Effective Communication 

Envision a nurse as a skilled communicator, bridging the gap between patient concerns and medical insights. Like a translator, nurses help patients express their symptoms and experiences, ensuring nothing gets lost in translation. Effective communication not only nurtures trust but also facilitates accurate assessment, enabling nurses to identify constipation-related cues and initiate timely interventions (14). 

Collaboration with Multidisciplinary Teams 

Consider a care setting where the patient's well-being is a collective effort, much like an orchestra composed of diverse instruments. Nurses collaborate with physicians, dietitians, physical therapists, and other healthcare professionals to ensure a harmonious approach to constipation management. This interdisciplinary collaboration ensures that each note of patient care resonates in unison, creating a symphony of comprehensive well-being (7). 

Patient-Centered Care Plans 

Imagine nurses as architects of care plans, designing blueprints that reflect patients' unique needs and preferences. Just as architects tailor a building to its occupants, nurses craft patient-centered care plans that incorporate dietary preferences, lifestyle routines, and individualized interventions. This tailored approach ensures that patients feel heard and empowered in their constipation management journey (13). 

Education and Empowerment 

Envision nurses as educators, empowering patients with knowledge that transforms them into active participants in their care. Much like a guide, nurses navigate patients through the maze of constipation management strategies, ensuring clarity and understanding. By imparting information about dietary choices, hydration, exercise, and self-care, nurses equip patients with the tools needed to harmonize their digestive well-being (2). 

Continuous Monitoring and Evaluation 

Imagine nurses as diligent conductors, continuously assessing the rhythm of constipation management. Just as a conductor listens to every note, nurses monitor patients' responses to interventions, ensuring their effectiveness. Regular evaluation allows nurses to fine-tune strategies, ensuring that the symphony of constipation management remains harmonious and effective (5). 

Compassionate Support 

Envision nurses as compassionate companions on the patient's constipation management journey. Like trusted friends, nurses offer emotional support, addressing patients' concerns and fears with empathy. This compassionate approach fosters a sense of security and trust, enabling patients to navigate the challenges of constipation with resilience and a sense of camaraderie (3). 

Conclusion

Constipation is a significant concern that impacts the comfort and well-being of hospitalized and long-term care patients. Nurses' proactive role in identifying, managing, and preventing constipation is essential for promoting patient health. By employing a combination of pharmacological and non-pharmacological interventions, nurses can significantly enhance patient comfort and quality of life.  

Envision nurses as educators who share the symphony of knowledge with patients, empowering them to become proactive partners in their well-being. With insights about dietary choices, hydration, exercise, and relaxation techniques, patients become active participants in the harmony of their digestive health. 

Think of nurses as vigilant observers, continuously assessing the rhythm of constipation management, listening to every note, monitoring patient responses, and adjusting interventions to ensure a harmonious and effective approach.  

Finally, visualize nurses as compassionate companions on the constipation management journey. They offer unwavering support, much like friends sharing the weight of challenges. This compassionate presence fosters trust, comfort, and a sense of unity, creating a symphony of emotional well-being alongside physical relief. 

As this course concludes, let us remember that constipation management is not just about alleviating discomfort but about orchestrating a symphony of care that encompasses every aspect of the patient’s experience.  

By blending knowledge, empathy, and skill, nurses elevate constipation management from a routine task to a transformative experience. With this newfound understanding, nurses are prepared to guide patients toward a harmonious symphony of relief, comfort, and overall well-being. 

Spinal Cord Injury: Bowel and Bladder Management

Introduction   

Imagine one day you are able to walk and take care of your own needs. Now, imagine one week later you wake up no longer able to walk, feel anything below your waist, or hold your bowels.  

This is a reality for many people who sustain spinal cord injuries. Managing changes in bowel and bladder function is one of many challenges that people with spinal cord injuries and their families or caregivers face.  

This course will provide learners with the knowledge needed to assist patients who have spinal cord injuries with bowel and bladder management to improve the quality of life in this group.

Spinal Cord Injuries: The Basics

Spinal Cord Function 

Before defining a spinal cord injury, it is important to understand the function of the spinal cord itself. The spinal cord is a structure of the nervous system that is nestled within the vertebrae of the back and helps to distribute information from the brain (messages) to the rest of the body [1].  

These messages result in sensation and other neurological functions. While it may be common to primarily associate the nervous system with numbness, tingling, or pain, nerves serve an important purpose in the body’s function as a whole.

Spinal Cord Injury Definition 

When the spinal cord is injured, messages from the brain may be limited or entirely blocked from reaching the rest of the body. Spinal cord injuries refer to any damage to the spinal cord caused by trauma or disease [2]. Spinal cord injuries can result in problems with sensation and body movements.  

For example, the brain sends messages through the spinal cord to muscles and tissues to help with voluntary and involuntary movements. This includes physical activity like running and exercising, or something as simple as bowel and bladder elimination.  

Spinal Cord Injury Causes 

Spinal cord injuries occur when the spinal cord or its vertebrae, ligaments, or disks are damaged [3]. While trauma is the most common cause of spinal cord injuries in the U.S., medical conditions are the primary causes in low-income countries [4] [2]. 

Trauma 

• Vehicle accidents: Accounts for 40% of all cases [2] 
• Falls: Accounts for 32% of all cases [2] 
• Violence: Includes gun violence and assaults; accounts for 13% of all cases [2] [5] 
• Sport-related accidents: Accounts for 8% of all cases [2] 

Medical Conditions 

• Multiple Sclerosis (MS): Damage to the myelin (or insulating cover) of the nerve fibers [1] 
• Amyotrophic Lateral Sclerosis (ALS): Lou Gehrig’s disease, damage to the nerve cells that control voluntary muscle movements [1] 
• Post-Polio: Damage to the central nervous system caused by a virus [1] 
• Spina Bifida: Congenital defect of the neural tube (structure in utero that eventually forms the central nervous system) [1] 
• Transverse Myelitis (TM): Inflammation of the spinal cord caused by viruses and bacteria [1] 
• Syringomyelia: Cysts within the spinal cord often caused by a congenital brain abnormality [1] 
• Brown-Sequard Syndrome (BSS): Lesions in the spinal cord that causes weakness or paralysis on one side of the body and loss of sensation on the other [1] 
• Cauda Equina Syndrome: Compression of the nerves in the lower spinal region [1] 

Spinal Cord Injury Statistics 

According to the World Health Organization, between 250,000 and 500,000 people worldwide are living with spinal cord injuries [4]. In the U.S., this number is estimated to be between 255,000 and 383,000 with 18,000 new cases each year for those with trauma-related spinal cord injuries [6]. 

Age/Gender 

Globally, young adult males (age 20 to 29) and males over the age of 70 are most at risk. In the U.S., males are also at highest risk, and of this group, 43 is the average age [2].  

While it is less common for females to acquire a spinal cord injury (2:1 ratio in comparison to males), when they do occur, adolescent females (15-19) and older females (age 60 and over) are most at risk globally [4].  

Race/Ethnicity 

In the U.S. since 2015, around 56% of spinal cord injuries related to trauma occurred among non-Hispanic whites, 25% among non-Hispanic Black people, and about 14% among Hispanics [6].  

Mortality 

People with spinal cord injuries are 2 to 5 times more likely to die prematurely than those without these injuries (WHO, 2013). People with spinal cord injuries are also more likely to die within the first year of the injury than in subsequent years. In the U.S., pneumonia, and septicemia – a blood infection – are the top causes of death in patients with spinal cord injuries [6]. 

Financial Impact 

Spinal cord injuries cost the U.S. healthcare system billions each year [6]. Depending on the type, spinal cord injuries can cost from around $430,000 to $1,300,000 in the first year and between $52,000 and $228,000 each subsequent year [6].  

These numbers do not account for the extra costs associated with loss of wages and productivity which can reach approximately $89,000 each year [6]. 

Spinal Cord Injuries: Types and Complications

Four Levels of the Spinal Cord 

• Cervical (vertebrae C1 – C8): Neck; controls the back of the head down to the arms, hands, and diaphragm 
• Thoracic (vertebrae T1 – T12): Upper mid-back; controls the chest muscles, many organs, some back muscles, and parts of the abdomen 
• Lumbar (vertebrae L1 – L5): Lower back; controls parts of the lower abdomen, lower back, parts of the leg, buttocks, and some of the external genital organs 
• Sacral (vertebrae S1 – S5): Lower back; controls the thighs down to the feet, anus, and most of the external genital organs 

Types of Spinal Cord Injuries 

Spinal cord injuries may be classified by level and degree of impairment. There are four types of spinal cord injuries [5]. 

Injury Level 

• Tetraplegia or Quadriplegia: Injury at the cervical level; loss of feeling or movement to the head, neck, and down. People with this type of spinal cord injury have the most impairment. 
• Paraplegia: Injury at the thoracic level or below; limited or complete loss of feeling or movement to the lower part of the body.  

Impairment 

• Incomplete spinal cord injury: Some sensation and mobility below the level of injury as the spinal cord can still transmit some messages from the brain. 
• Complete spinal cord injury: Total loss of all sensation and mobility below the level of injury. Spinal cord injuries of this type have the greatest functional loss. 

Spinal Cord Injury Complications 

Complications from spinal cord injuries can be physical, mental, or social, and can impact overall quality of life. There are six common complications of spinal cord injuries [2]. 

Depression 

Studies show that 32.9% of adults with disabilities experience frequent mental distress [7]. Mental distress may be related to functional limitations, chronic disease, and the increased need for healthcare services.  Up to 37% of people with spinal cord injuries develop depression [2]. 

Pressure injuries 

People with spinal cord injuries may have problems with circulation and skin sensation– both risk factors for pressure injuries. Some may be bedridden or wheelchair-bound which also places them at risk for pressure injuries. Up to 80% of people with spinal cord injuries will have a pressure injury during their lifetime and 30% will have more than one [2].  

Spasticity 

Around 65% - 78% of people with spinal cord injuries have spasticity [2]. Spasticity is uncontrolled muscle tightening or contraction. The damage from spinal cord injuries causes misfires in the nervous system leading to twitching, jerking, or stiffening of muscles. 

Autonomic dysreflexia 

In some people with spinal cord injuries, a full bladder or bowel distention can cause a potentially dangerous condition called autonomic dysreflexia. The full bladder or bowel triggers a sudden exaggerated reflex that causes an increase in blood pressure. This condition is also associated with a severe headache, low heart rate, cold skin, and sweating in the lower body [8]. 

Respiratory problems 

If the diaphragm function is affected, as with cervical spinal cord injuries, there may be breathing difficulties. People with lumbar spinal cord injuries can even have respiratory problems as the abdominal muscles are used to breathe. 

Sexual problems 

Due to changes in muscle function and depending on the degree of damage, people with spinal cord injuries may have problems with arousal and climax due to altered sensations and changes in sexual reflexes.  

Changes in bowel and bladder function 

Many people with spinal cord injuries lose bowel control. Bowel problems can include constipation, impaction, and incontinence. They may also have problems with urination, for example, urinary retention. 

Bowel and Bladder Dysfunction in Spinal Cord Injuries 

This section will cover the normal function of the bowel and bladder, and the types of bowel and bladder dysfunction that occurs in patients with spinal cord injuries.

Normal Bowel and Bladder Function 

In normal bowel and bladder function, when the rectum or bladder fills with stool/urine and presses on area nerves (stimulation), the message is sent to the spinal cord which sends it to the brain. The brain gives the person the “urge” feeling, allowing an option to control the elimination or not.  

Whatever decision the person makes, the brain sends the message back to the spinal cord, which in turn sends a message to the elimination muscles (anal and bladder sphincters) to either relax or stay closed until the person is ready. In people with spinal cord injuries, the messages are limited or blocked, leading to problems with bowel and bladder control [9] [10].  

Bowel Dysfunction with Spinal Cord Injuries 

Reflex hypertonic neurogenic bowel occurs when a rectum full of stool presses against area nerves sending a message to the spinal cord, but it stops there. The message never makes it to the brain, so the person never gets the urge.  

As a result, a reflex is set off, prompting the spinal cord to send a message to the anal muscle (sphincter) instead, causing it to relax and release the stool. This condition leads to bowel incontinence and usually occurs in spinal injuries at the cervical and thoracic levels [9] [10]. 

Flaccid hypotonic bowel occurs when area nerves are also stimulated by a full rectum, but the message does not even reach the spinal cord, so there is no reflex. The anal sphincter is always in a relaxed state.  

As a result, the bowels simply empty when they are full, and this can occur at any time without the person having the ability to control it. This condition results in bowel incontinence and can lead to constipation as the patient does not have the urge and may not have the ability to push. This condition usually occurs in spinal injuries at the lumbar level [9] [10]. 

Bladder Dysfunction with Spinal Cord Injuries 

Reflex neurogenic bladder occurs when the bladder automatically starts to contract after filling with a certain amount of urine. The person has no urge to go as the messages are either limited or blocked from reaching the brain, therefore leading to loss of bladder control. Similar to reflex hypertonic neurogenic bowel, the full bladder triggers are nerves that set off a reflex, prompting the spinal cord to send messages to the bladder releasing urine outside of the person’s control [9] [10]. 

Acontractile bladder occurs when the bladder loses muscle tone after a spinal cord injury, lessening its ability to contract, leading to bladder distention, and dribbling of urine. People with this condition need to use urinary catheters to help empty the bladder [9]. 

The Nurse’s Role in Bowel and Bladder Management 

This section will cover how nurses can assess, intervene, and teach when caring for patients with spinal cord injuries who have bowel and bladder dysfunction.

Nurse Assessments 

When caring for patients with spinal cord injuries, nurses should obtain a detailed bowel and bladder history including diet, fluid intake, medications, and elimination patterns/habits [11]. Many of these patients may already manage their own bowel and bladder care at home.  

If so, the nurse should obtain the patient’s current regimen and communicate the information to the physician. The physician may choose to continue the regimen or adjust as needed based on the patient’s current illness/condition.  

Questions the nurse can ask the patient: 

• What does your typical diet consist of? 
• How much fluid do you drink on a daily basis? 
• How often do you have a bowel movement or urinate? 
• Do you schedule your bowel movements with assistance from medications? 
• Are there certain body positions or things you do to help you pass stool more easily?
• How often do you use an intermittent urinary catheter for bladder relief? 
• How much time do you spend on your bowel and bladder regimens? 
• Do you care for all of your elimination needs or does someone help you? 
• How does your bowel and bladder dysfunction affect your quality of life? 

Some assessments may be observed. For example, nurses may notice that the patient has a surgically placed permanent suprapubic urinary catheter or colostomy (when the bowel is cut somewhere above the level of the rectum and diverted to the outside of the abdomen). 

Nurse Interventions 

Since many patients with spinal cord injuries have problems with bowel and bladder function, elimination must be scheduled. Nurses can help by implementing bowel and bladder programs and providing education and support to patients, families, or caregivers.  

Regimens 

Follow the patient’s home bowel and bladder regimen (as ordered). This may include maintaining intermittent catheterization every few hours or administering suppositories daily.  

For patients who do not have a regimen already or wish to modify their current one, encourage them to pay attention to how often they urinate and pass stools, elimination problems, foods that alleviate or worsen the problem, and medications or other things that help. This can be done through a diary. 

Dietary Considerations 

Educate patients on the importance of a fiber-rich diet to avoid constipation. Patients should also be made aware that high-fat foods, spicy foods, and caffeine can alter gut dynamics and lead to bowel incontinence episodes [12]. 

Fluid Intake 

Some patients may avoid drinking enough water to avoid bladder complications (e.g., frequent incontinent episodes) [12]. However, nurses should educate patients on the importance of adequate fluid intake to prevent constipation. Patients should be made aware that bladder and bowel elimination regimens go hand in hand. 

Bladder Elimination 

For bladder dysfunction, help patients perform intermittent urinary catheterization as needed or place a temporary urinary catheter (as ordered). 

Bowel Elimination 

For bowel dysfunction, administer ordered suppositories and laxatives to help the bowels move (use suppositories in conjunction with the level of sensation the patient has near the anus/rectum) [9]. Changes in body position may help as well.  

While many of these interventions may not work in some patients with spinal cord injuries, bowel irrigation (water enemas) may be helpful [11]. Surgical placement of a colostomy may be indicated if all other measures have failed [11]. 

Emotional Support 

Ensure privacy and sensitivity during all elimination care as patients may experience embarrassment or frustration. 

Education for Families or Caregivers 

Provide education to families or caregivers on the importance of helping patients stay consistent with their elimination regimen, follow diet and fluid intake recommendations, and comply with medication orders.  

Referrals 

Inform the physician if interventions are not effective or if the patient, family, or caregiver has a special need (e.g., counselor or dietician). Refer patients and families or caregivers to support groups as needed.

Support Groups and Resources 

Christopher and Dana Reeve Foundation 

Christopher Reeve – an actor who was left paralyzed after an equestrian accident – and his wife Dana’s legacy lives on through their foundation, an organization that advocates for people living with paralysis [13].  

Miami Project to Cure Paralysis 

In response to his son, who acquired a spinal cord injury during college football, NFL Hall of Famer Nick Buoniconti and world-renowned neurosurgeon Barth A. Green, M.D. started a research program aimed at finding a cure for paralysis and discovering new treatments for many other neurological injuries and disorders [14]. 

National Institute on Disability, Independent Living, and Rehabilitation Research (NIDILRR) 

The National Institute on Disability, Independent Living, and Rehabilitation Research, a part of the U.S. Department of Health and Human Services’ Administration for Community Living, helps people with disabilities integrate into society, employment, and independent living [15].  

Paralyzed Veterans of America (PVA)  

A group of World War II veterans who returned home with spinal cord injuries, started this organization to support those with spinal cord injuries and dysfunction. Today, the organization focuses on quality health care, research and education, benefits, and civil rights to affected veterans [16].  

United Spinal Association 

The United Spinal Association supports people with spinal cord injuries and those in wheelchairs. The organization advocates for disability rights like access to healthcare, mobility equipment, public transportation, and community support. Support groups can be found on their website [17).  

Conclusion

Spinal cord injuries can have devastating effects on patients and their families. Management of basic bodily functions like bowel and bladder elimination should be made as easy as possible for these patients.

When nurses learn how to effectively help patients with spinal cord injuries better manage their own bowel and bladder regimens, quality of life and health outcomes may be improved for this group.

Pressure Injury Prevention, Staging and Treatment

Introduction   

When hearing the term HAPI, what comes to mind? The fact is, HAPI may not necessarily generate happy thoughts. Hospital-acquired pressure injuries (HAPIs) are a significant problem in the U.S. today. In fact, pressure injuries in general – whether acquired in a hospital or not – are a global problem.

Many articles have noted that staging and differentiating pressure injuries can be overwhelming for nurses [9]. The purpose of this course is to equip learners with the knowledge needed to reduce pressure injuries, resulting complications, financial risk, and associated death. The information in this course will serve as a valuable resource to nurses from all specialties and backgrounds.

What is a pressure injury?

The National Pressure Injury Advisory Panel (NPIAH) defines pressure injuries as “localized damage to the skin and underlying soft tissue usually over a bony prominence or related to a medical or other device” [17]. Pressure injuries can present as intact or opened skin and can be shallow or deep. Pressure injuries can be quite painful for patients and may require extensive treatment.

Prior to 2016, pressure injuries were termed “pressure ulcers.” However, since ulcer implies “open skin,” the NPIAH changed it to “pressure injury” as the skin is not always open with some of these injuries [22][25].

What causes a pressure injury to develop?

Pressure 

Intense and/or prolonged pressure on the patient’s skin and/or tissue can cause compromised blood flow and decreased sensation [7]. This can occur when patients lay or sit on a bony prominence for an extended period of time [16].  

Bony prominences are areas where you can easily feel a bone underneath the skin or tissue when palpating. These can include the heels, hips, elbows, and tailbone. Approximately two-thirds of all pressure injuries occur on the hip and buttocks area [7]. 

Friction and Shear 

Friction and shear often happen when patients slide down in bed, for example, when the head of the bed is raised. Although “friction and shear” are often used together, there is actually a difference between the two.  

While friction occurs when skin is dragged across a coarse surface (leading to surface-level injuries), shearing occurs when internal bodily structures and skin tissue move in opposite directions (leading to deep-level injuries) [10]. Shearing is often associated with a type of pressure injury called deep tissue injury (occurring in the deeper tissue layers rather than on the skin’s surface) [10].

[24] 

What are risk factors for developing a pressure injury? 

There are numerous risk factors for pressure injuries – some of which may not be directly related to the skin. These risk factors can be categorized as either intrinsic factors (occurring from within the body) or extrinsic (occurring from outside of the body) [2][13]. 

Intrinsic Risk Factors 

- Poor skin perfusion (e.g., peripheral vascular disease or smoking) 

- Sensation deficits (e.g., diabetic neuropathy or spinal cord injuries) 

- Moist skin (e.g., urinary incontinence or excessive sweating) 

- Inadequate nutrition (particularly poor protein intake) 

- Poor skin elasticity (e.g., normal age-related skin changes) 

- End of life/palliative (leads to organ failure including the skin) 

- Limited mobility (i.e., bedridden, or wheelchair-bound) 

Extrinsic Risk Factors 

- Physical and chemical restraints (leads to limited mobility) 

- Undergoing a procedure (laying down for extended periods of time) 

- Length of hospital stay (for HAPIs) 

- Medical devices (can lead to medical device-related pressure injuries)

Statistical Evidence 

This section will cover pressure injury statistics both globally and nationally. This section will also cover the impact pressure injuries have on healthcare.

What is happening on a global scale? 

In a global study, researchers found that the prevalence (all cases) and incidence (new cases) of pressure injuries in 2019 were 0.85 million and 3.17 million, respectively – numbers that have decreased over time [23][25]. Numbers were disproportionately high in high-income North America, Central Latin America, and Tropic Latin America [25]. Numbers were lowest in Central Asia and Southeast Asia. The report revealed that although numbers are high overall, they are much lower than what they were predicted to be, which may be attributed to better prevention and treatment initiatives.

What is happening nationally? 

In the U.S., 2.5 million people develop pressure injuries each year [1]. This number does not account for the many people trying to manage pressure injuries on their own at home (i.e., when family acts as the caregiver).  

HAPIs in particular are a growing problem. The most recent data on hospital-acquired conditions in the U.S. shows that from 2014 to 2017, HAPIs increased by 6% (647,000 cases in 2014 to 683,000 in 2017) [6]. Each year 60,000 patients in the U.S. die as a direct result of pressure injuries [1]. 

How do pressure injuries impact healthcare? 

Pressure injuries can be quite costly to the healthcare system. These injuries can lead to persistent pain, prolonged infections, long-term disability, increased healthcare costs, and increased mortality [1].  

In the U.S., pressure injuries cost between $9.1 - $11.6 billion per year [1]. These injuries are complex and can be difficult to treat [7]. Often requiring an interdisciplinary approach to care, the costs of one pressure injury admission can be substantial. Individual care for patients with pressure injuries ranges from $20,900 to $151,700 per injury [1]. Not to mention, more than 17,000 lawsuits are related to pressure injuries every year [1].  

Due to the significant impact that these injuries have on healthcare, prevention and accurate diagnosis is imperative.

Staging and Diagnosis 

The section will cover the staging, varying types, and diagnosis of pressure injuries.  

What is the difference between wound assessment and staging? 

Pressure injury staging is more than a basic wound assessment. Wound assessment includes visualizing the wound, measuring the size of the wound, paying attention to odors coming from the wound, and lightly palpating the area on and/or around the wound for abnormalities. Pressure injury staging, however, involves determining the specific cause of injury, depth of skin or tissue damage, and progression of the disease.  

What are the six stages of pressure injuries? 

According to NPIAP guidelines, there are six types of pressure injuries – four of which are stageable [14]. 

[16] 

Stage 1 

In Stage 1 pressure injuries, there is intact skin with a localized area of non-blanchable erythema (pink or red in color), which may appear differently in darkly pigmented skin. Before visual changes are noted, there may be the presence of blanchable erythema or changes in sensation, temperature, or firmness. Stage 1 pressure injuries do not have a purple or maroon discoloration (this can indicate a deep tissue pressure injury). 

Stage 2 

In Stage 2 pressure injuries, there is partial-thickness loss of skin with exposed dermis. The wound bed is viable, pink or red, moist, and may represent an intact or opened serum-filled blister. Fat (adipose) and deeper tissues are not visible. Granulation tissue, slough (soft moist material, typically yellow or white), and eschar (hard necrotic tissue, typically black in color) are not present. Stage 2 injuries cannot be used to describe wounds associated with moisture-only, skin chaffing, medical adhesives, or trauma. 

Stage 3 

In Stage 3 pressure injuries, there is full-thickness loss of skin, in which fat is visible in the injury, and granulation tissue and rolled wound edges are often present. Slough and/or eschar may be noted. The depth of tissue damage is dependent on the area of the wound. Areas with a significant amount of fat can develop deep wounds.  

Undermining (burrowing in one or more directions, may be wide) and tunneling (burrowing in one direction) may be present. Fascia, muscle, tendon, ligament, cartilage, and/or bone are not exposed. If slough or eschar covers the extent of tissue loss, this would be considered an unstageable pressure injury, not a Stage 3. 

Stage 4 

In Stage 4 pressure injuries, there is full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the wound. Slough and/or eschar may be visible. Rolled wound edges, undermining, and/or tunneling are often present. The area where the wound is present will determine the depth. As with stage 3 pressure injuries, if slough or eschar covers the extent of tissue loss, this would be considered an unstageable pressure injury. 

Unstageable 

In unstageable pressure injuries, there is full-thickness skin and tissue loss in which the extent of tissue damage within the wound cannot be confirmed because it is covered by slough or eschar. If the slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar (i.e., dry, adherent, intact without erythema or fluctuance) on an ischemic limb or the heel(s) should not be removed.  

Deep Tissue Injury 

In deep tissue pressure injuries (also termed: deep tissue injuries or DTIs), there is intact or non-intact skin with localized area or persistent non-blanchable deep red, maroon, purple discoloration, or epidermal separation revealing a dark wound bed or blood-filled blister.  

Pain and temperature changes often precede skin color changes. Discoloration may appear differently in darker-pigmented skin. The injury may resolve without tissue loss or may worsen quickly and open up, revealing the actual extent of tissue injury. Deep tissue pressure injuries should not be used to describe vascular, traumatic, neuropathic, or dermatologic conditions.  

What are other types of pressure injuries? 

Mucosal Membrane Pressure Injury 

Mucosal membrane pressure injuries are found on mucous membranes with a history of a medical device in use at the location of the injury. For example, a wound on the inside of a nostril from a nasogastric tube would be considered a mucosal membrane pressure injury. Due to the anatomy of the tissue, mucosal membrane pressure injuries cannot be staged [18]. 

Medical Device-Related Pressure Injury 

Medical device-related pressure injuries, often associated with healthcare facilities, resulting from the use of devices designed and applied for diagnostic or therapeutic purposes [15]. The resulting pressure injury typically conforms to the pattern or shape of the device which makes identification easier. The injury should be staged using the staging system.  

Hospital Acquired Pressure Injury (HAPI) 

While the general hospital setting places patients at a 5% to 15% increased risk of developing a pressure injury (HAPI), patients in the intensive (or critical) care unit in particular have an even higher risk [17]. Critical care patients typically have serious illnesses and conditions that may cause temporary or permanent functional decline. There is also evidence that pressure injuries in this setting can actually be unavoidable.  

The NPIAP defines “unavoidable” pressure injuries as those that still develop after several measures by the health provider have been taken. These measures include when the provider has (a) evaluated the patient’s condition and pressure injury risk factors, (b) defined and implemented interventions consistent with standards of practice and the patient’s needs and goals, and (c) monitored and evaluated the impact of interventions [20]. There are certain situations in which a critical care patient may have a higher risk of developing unavoidable pressure injuries.  

In one study of 154 critical care patients, researchers found that 41% of HAPIs were unavoidable and those who had a pressure injury in the past were five times more likely to develop an unavoidable pressure injury during their stay [20]. The study also found that the chance of developing an unavoidable HAPI increased the longer patients stayed in the hospital – a 4% risk increase each day.  

How are pressure injuries diagnosed? 

Diagnosing a pressure injury is done by simply staging the injury. The health provider may stage the injury or rely on the nurse’s staging assessment before giving the final diagnosis and initiating treatment. There are tests that may be ordered to help identify the early stages of a developing injury.  

For example, subepidermal moisture assessment (SEM) scanners may help to identify tissue changes early on in patients with darker skin tones [8]. Tests may also be ordered to determine the extent of the damage, disease, or infection caused by a pressure injury. A magnetic resonance imaging test (MRI) can be used to determine if the infection in a stage 4 pressure injury has spread to the bone. 

Prevention and Treatment 

This section will cover various strategies that can be used to prevent and treat pressure injuries. 

What are some ways to prevent pressure injuries? 

Preventing pressure injuries takes more than just one nurse repositioning a patient every two hours. It involves a combination of strategies, protocols, and guidelines that facilities can implement across various departments, specialties, and care team members. The NIAPH recommends the following prevention strategies [19]. 

Risk assessment 

Facilities should use a standardized risk assessment tool to help identify patients at risk for pressure injuries (i.e., the Braden or Norton Scale). Rather than using the tool as the only risk assessment strategy, risk factors should be identified by other means (for example, by gathering a detailed patient history).  

Risk assessments should be performed on a regular basis and updated as needed based on changes in the patient’s condition. Care plans should include risk assessment findings to address needs. 

Skin Care 

Monitoring and protecting the patient’s skin is vital for pressure injury prevention. Stage 1 pressure injuries should be identified early to prevent the progress of disease. These include looking at pressure points, temperature, and the skin beneath medical devices.  

The frequency of assessments may change depending on the department. Ideally, assessments should be performed upon admission and at least once daily. Skin should also be cleaned promptly after incontinence episodes. 

Nutritional Care 

Tools should be used that help to identify patients at risk for malnutrition. Patients at risk should be referred to a registered dietician or nutritionist. Patients at risk should be weighed daily and monitored for any barriers to adequate nutritional intake. These may include swallowing difficulties, clogged feeding tubes, or delays in intravenous nutrition infusions. 

Positioning and mobilization 

Immobility can be related to age, general poor health, sedation, and more. Using offloading pressure activities and keeping patients mobile overall can prevent pressure injuries. Patients at risk should be assisted in turning and repositioning on a schedule. Pressure-relieving devices may be used as well. Patients should not be positioned on an area of previous pressure injury. 

Monitoring, training, and leadership 

Current and new cases of pressure injuries should be documented appropriately and reported. All care team members should be educated on pressure injury prevention and the importance of up-to-date care plans and documentation.  

All care team members should be provided with appropriate resources to carry out all strategies outlined. Leadership should be available to all care team members for support (this may include a specialized wound care nurse or wound care provider). 

How are pressure injuries treated? 

There is no one way to treat a pressure injury. Management of pressure injuries involves a specialized team of care providers and a combination of therapies that aim to target underlying factors and prevent complications [7]. Depending on the stage of the wound and skin risk factors, providers may order specific types of treatments.  

Some pressure injury treatments may include the following [7]. 

- Wound debridement – a procedure in which necrotic tissue is removed from a wound bed to prevent the growth of pathogens in the wound, allowing for healing 

- Antibiotic therapy (topical or systemic) 

- Medicated ointments applied to the wound bed (e.g., hydrogels, hydrocolloids, or saline-moistened gauze to enable granulation tissue to grow and the wound to heal) 

- Nutritional therapies (e.g., referrals to dieticians) 

- Disease management (e.g., controlling blood sugar in diabetes) 

- Pain medications 

- Physical therapy (to keep the patient active) 

The Nurse’s Role 

The section will cover the nurse’s role in preventing pressure injuries and the progression of disease.  

What is the nurse’s role in pressure injury prevention? 

Based on NPIAH guidelines, the Agency for Healthcare Research and Quality (AHRQ) – an agency that monitors pressure injury data for the U.S. – breaks down quality initiatives for preventing pressure injuries in a three-component care bundle [2].  

A care bundle is a combination of best practices that when used together, can lead to better patient outcomes [2]. The care bundle includes skin assessments, risk assessments, and care planning. Nurses should follow the guidelines listed under each component. 

Standardized pressure injury risk assessment 

- Use risk assessment tools and processes to identify patients at risk 

- Do not rely on tools only, use your own judgment as well (tools are meant to guide the assessment) 

- Update risk scores at least once daily and if patient’s condition changes 

- Document findings in the medical record 

- Communicate findings to other staff involved for continuity of care (e.g., informing another nurse during patient handoff reporting) 

Comprehensive skin assessment 

- Identify any pressure injuries that may be present 

- Determine whether there are other areas of skin breakdown or factors that may predispose the patient to develop a pressure injury (e.g., moist skin) 

- Identify other skin issues 

- Perform assessments at regular intervals 

- Document findings in the medical record 

- Communicate findings to other staff involved in care so that appropriate changes can be reported (e.g., informing the nursing assistant) 

- Ask colleague to confirm findings for accuracy (i.e., two-nurse skin checks) 

Care planning and implementation to address areas of risk 

- Create care plans that include each skin risk factor (e.g., nutrition, mobility, and moisture) 

- Update care plans as often as needed if there are any changes in the patient’s condition 

- Evaluate whether care plan was effective by assessing patient response to interventions 

-  Individualize care plans for each patient based on risk assessment scores and other observed risks 

- Identify patient learning needs and implement teaching as needed 

- Document care plan in the medical record 

- Communicate care plan to other staff involved for continuity of care (e.g., informing another nurse during patient handoff reporting) 

How can nurses prevent medical device-related pressure injuries?

The NPIAP outlined best practices to prevent medical device-related pressure injuries in various settings including general care, long-term care, critical care, and pediatric care [20]. The following strategies apply across all settings. 

- Choose the correct size of medical device for the individual. 

- Cushion and protect the skin with dressings in high-risk areas (e.g., nasal bridge). 

- Inspect the skin under and around the device at least daily (if not medically contraindicated).  

- Rotate sites of oximetry probes.  

- Rotate between O2 mask and prongs (if feasible).  

- Reposition devices (if feasible).  

- Avoid placement of device over sites of prior or existing pressure injury OR directly under the patient.  

- Be aware of edema under the device and the potential for skin breakdown. 

- Change rigid C-collar to softer collar when medically cleared (for critical care settings).

How can nurses identify pressure injuries in patients with darker skin tones? 

Research suggests that it may be difficult to note early changes that can lead to the development of a pressure injury in patients with darker skin tones – for one, blanching may not be as visible [8]. This places the patient at a greater risk for the advancement of disease as early identification may be challenging.  

In order to appropriately identify pressure injuries in patients with darker skin tones, nurses should use unique strategies. The NIPAH offers these recommendations for nurses to help accurately identify pressure injuries in this group [8]. 

Identification tips 

- Clean the suspected area beforehand 

- Compare the area to surrounding unaffected areas 

- Compare the area to the opposite laterality if possible (i.e., right versus left elbow) 

- Compare the area to unaffected areas in a different location (i.e., upper back versus chest) 

- Look for differences in skin tautness 

- Look for shining skin changes 

- Palpate for changes in skin temperature 

How can nurses quickly differentiate between pressure injury stages? 

Correct staging of pressure injuries is vital as treatment is determined by the extent of damage, disease, or infection. First and foremost, wounds should be gently cleaned prior to staging as drainage or debris can be mistaken for fat or bone within the wound bed [14].  

Nurses can quickly differentiate between stages by asking these simple easy-to-understand starter questions. A more detailed assessment should follow. 

- Stage 1 versus Stage 2: Is the skin intact? 

Rationale: The skin is always intact in Stage 1. The skin is always open in Stage 2 (or there may be an intact blister present). 

- Stage 2 versus Stage 3: Is the wound bed pink or beefy red? 

Rationale: The wound bed is pink or beefy red in Stage 2. In Stage 3, the wound bed has structures within that may be discolored. 

- Stage 3 versus Stage 4: Does the wound bed contain soft or firm structures? 

Rationale: The wound bed contains softer structures in Stage 3. The wound bed contains firmer structures in Stage 4.* 

- Unstageable versus Stageable: Is any part of the wound bed hidden? 

Rationale: The wound bed is not entirely exposed in an unstageable. The wound bed is exposed in a stageable that is open. 

- Intact DTI versus Stage 1: Is the discoloration light or dark? 

Rationale: The discoloration is dark in a DTI. The discoloration is much lighter in Stage 1. 

- Open DTI versus Stage 2: Is the discoloration in or around the wound bed dark? 

Rationale: There is dark discoloration in or around the wound bed in an open DTI. In stage 2, the discoloration is much lighter (if even present). 

*Nurses should familiarize themselves with the appearance of the various structures that may be present in a wound like fat, fascia, bone, tendon, ligament, etc. Most importantly, nurses should consult the wound care team or health provider if a stage cannot be determined. 

What should patients know? 

Facilities can use the NIAPH prevention strategies to devise teaching plans for patients [19]. Nurses should educate patients and families/caregivers on risk factors, signs and symptoms, prevention tips, and the importance of following through with treatment.  

Nurses should also teach patients to advocate for their own health in order to avoid progression of disease. Here are important tips to teach at any point during the patient’s stay. These tips can apply to nurses working in a variety of settings. 

- Tell the nurse or provider of your medical conditions (needed to identify risk factors) 

- Tell the nurse or provider if you notice any numbness or tingling in your body (potential risk for sensory deficits) 

- Tell the nurse or provider if you have a loss of appetite or trouble eating (potential risk for malnutrition) 

- Clean yourself well after using the restroom (maintains skin integrity) 

- Tell the nurse or provider if you need to use the restroom or need help with cleaning yourself (maintains skin integrity) 

- Tell the nurse right away if you have an incontinence episode (maintains skin integrity) 

- Take all prescribed medications (may include necessary antibiotics or wound-healing medications) 

- Reposition yourself in bed often or tell the nurse if you need help doing so (reduces immobility risk) 

- Tell the nurse or provider if you notice a new discolored area on your skin, or an open area (potential new or worsening pressure injury) 

- Tell the nurse or provider if you notice any changes to your wound (potential worsening pressure injury) 

Quality Improvement 

This section will cover the quality improvement measures in place to reduce pressure injuries. 

What is a pressure injury quality improvement initiative? 

Quality improvement involves setting goals (or initiatives) and standards of care. The goal of quality improvement is to improve patient outcomes at a systematic level where everyone involved is on the same page.  

Although possibly unaware, all care team members are involved in quality improvement. Nursing leaders design, manage, and evaluate program initiatives. Staff nurses and other care team members follow protocols that are often developed from these initiatives.  

The Pressure Injury Prevention Program is a guide designed by the AHRQ to help health facilities implement a structured pressure injury prevention initiative based on quality improvement [12]. Facilities can use the guide as a training toolkit to implement a new quality improvement program [5].  

Initiative Goals: 

- Reduced pressure injury rates 

- Reduced adverse events related to pressure injuries 

- Reduced costs associated with pressure injuries 

- Reduced lawsuits related to pressure injuries 

Ways facilities can implement a prevention program: 

- Address the overall objectives of the prevention program 

- Identify the needs for change and how to redesign practice 

- Develop goals and plans for change 

- Use the NIAPH pressure injury prevention recommended practices 

- Establish comprehensive skin assessment protocols 

- Standardize assessments of pressure injury risk factors 

- Incorporate risk factors into individualized care planning 

- Establish clear staff and leadership roles 

What are some pressure injury quality measures? 

Quality measures are tools that measure a system’s healthcare goals and/or ability to provide high-quality care [11]. In simple terms, quality measures are specific ways that systems (governments, states, organizations, etc.) can show how they are making progress in meeting goals. The AHRQ highlights the following three ways the U.S. measures its progress.  

Number of HAPIs 

The AHRQ measures the number of HAPIs per year. The most recent data is from 2014 to 2017 [6].

Rate of HAPIs per admission 

The AHRQ measures the number of HAPIs per admission related to age groups. The number is measured as a “rate,” meaning the number of HAPIs per 1,000 hospital admissions. The most recent evidence is from 2017 [4]. 

Costs of HAPIs 

Another quality measure is HAPI costs. While the AHRQ does not measure costs of HAPIs every single year, the most recent data is from 2017 [3].  

Deaths related to HAPIs 

Patient mortality rates related to HAPIs are a quality measure (calculated per 1,000 pressure injury cases). The most recent data is from 2017 [6]. 

Conclusion

 Pressure injuries are complex conditions that can lead to poor patient outcomes and a burdened healthcare system. The best strategy in the care of patients with pressure injuries or those at risk is prevention.  

However, preventing these injuries involves more than individual nurses taking specific steps. Prevention of pressure injuries involves a team effort from all members of the care team and a systemic plan for improvement.

Negative Pressure Wound Therapy (Wound Vac)

Introduction   

Negative pressure wound therapy (NPWT), also known as a wound vac, can be a powerful tool in combatting acute and chronic wounds. It relies on generating a negative pressure on the surface of a difficult wound to promote wound healing.

The goal of this course is to develop an understanding of mechanism of action of NPWT, discuss appropriate nursing assessment of these wounds, evaluate adjunct treatment options and troubleshooting support tips.

We will review basic concepts of the integumentary system and the normal wound healing process to support the rationale of NPWT.

Definition

Negative pressure wound therapy (NPWT) is the application of sub-atmospheric pressure to help reduce inflammatory exudate and promote granulation tissue in an effort to enhance wound healing (4). The idea of applying negative pressure therapy is that once the pressure is lower around the wound, the gentle vacuum suction can lift fluid and debris away and give the wound a fighting chance to heal naturally.

NPWT has a long and interesting history. The idea of suctioning fluid from wounds as therapy is not a new concept. The process was first called “cupping” and was described in Ebers Papyrus around 500 BC; historians tell us that a form of wound suction was used around 1000 BC in China, 600 BC in Babylon and Assyria, and in 400 BC by Greeks who heated copper bowls over wounds to remove blood and fluids (5).

Modern medicine has built upon a very old concept. Thankfully, nurses have a slightly easier tool in NPWT devices than heating copper bowls.

Indications for Use 

Negative pressure wound therapy is widely used for the management of both acute and chronic wounds. This therapy is helpful for a broad range of wounds, from pressure ulcers to closed surgical incisions.  

The system is now implemented routinely for open wounds, such as open fractures, fasciotomies, diabetic foot ulcers, and infected wounds. Delayed wound healing and difficult wounds are seen more commonly in elderly patients and those with comorbidities (1).  

It’s important to review the basic anatomy of our integumentary system, types of wounds, and barriers to healing to understand the usefulness of NPWT. 

Basic Anatomy of Integumentary System 

Our integumentary system is considered the body’s largest organ. Our skin acts as a shield against heat, light, bacteria, infection, and injury. Other functions include body temperature regulation, storage of water and fat, sensory function, prevention of water loss, and a basic storage compartment for the organs (6).  

The skin is made up of 3 layers. Each layer has unique functions: 

1. Epidermis 

1. Dermis 

1. Subcutaneous fat layer (hypodermis) 

The epidermis is the thin outer layer of our skin, it contains squamous cells, basal cells, and melanocytes (gives skin its color). The dermis is the middle layer of skin, it contains blood vessels, hair follicles, sweat glands, nerves, lymph vessels, fibroblasts, and sebaceous glands (6). It is important to remember that the dermis contains nerves and nerve receptors. 

The subcutaneous fat layer is the deepest layer of skin and is made up of a network of collagen and fat cells; this layer conserves the body's heat and protects the body from injury by acting as a shock absorber (6).

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Types of Wounds 

Negative pressure wound therapy is primarily used to treat complex wounds that are non-healing or at risk of non-healing. It is also indicated for acute wounds when the wound cannot be closed due to the risk of infection, active infection, skin tension, or swelling (7).  

Closure or skin grafting of acute wounds, such as open fractures or burns, are at high risk for infection due to microorganisms becoming trapped in the soft tissue leading to abscess development.  

Examples of possible wounds to apply NPWT (1):  

• Diabetic foot ulcers 
• Bed sores 
• Skin graft fixation  
• Burns 
• Crush injuries 
• Sternal/abdominal wound dehiscence  
• Fasciotomy wounds 
• Animal bites 

• Frostbite 

Barriers to Healing 

Age 

• Increased risk of tearing and shearing due to thinning of epidermis and decrease in elastin 
• Phases of healing are prolonged 
• Increased risk of dehiscence as the dermis has slower contractility 
• Skin more susceptible to bacterial growth and infections as pH becomes more neutral with age  

Co-morbidities 

• Cardiopulmonary Disease 

• Oxygen-transport pathways are affected 
• O2 necessary for wound healing 

• Diabetes Mellitus 

• High glycemic levels predispose patients to infection 
• Microvasculature and neuropathic components of DM increase the risk for impaired healing  
• Poor glycemic control can increase the risk of ulceration and delayed healing 

• Immune-suppressing conditions (Cancer, HIV, immunosuppressive therapy, immunosuppression syndrome) 

• Inflammatory phase (immunology) is impaired 
• Increased risk for infection 

Impaired Perfusion and Oxygenation 

• Peripheral Vascular Impairment 

• Proper perfusion is required for growth of new tissue and immunological responses of the tissue. 
• Arterial insufficiency (blood flow to extremities) leads to necrosis or lack of response to edema. 

Neurological Impairment  

• Peripheral neuropathy 

• Complication related to DM, alcoholism, chemotherapy 
• Loss of neuronal signaling and transmission 
• Loss of the sensory ability to recognize and react to sensations of touch, pressure, temperature, pain. Example: patient leaving foot on hot surface because there was no pain sensation, leading to burn wound. 

• Spinal cord injury 

Mechanism of Action 

The mechanism of action is dependent on applying negative pressure, which is below atmospheric pressure, to the wound. This pressure allows the gentle vacuum suction to lift fluid and exudate away from the wound to enhance healing (3).  

The vacuum is gentle because powerful suction would remove newly formed tissue as well. The mechanism of action is not only in removing fluid and debris from the tissue, but the pressure causes stimulation of the growth of granulation tissue at a macroscopic and microscopic level.  

The porous foam shrinks in size with the application of negative pressure and exerts strain on the wound bed, which leads to macro- and micro-deformation of the wound (3). Microdeformation is simply a term used to describe microscopic tissue cell reactions. This reaction can be compared to a battery jump-start of a car; the stimulation causes the battery to engage. 

NPWT systems consist of a sterile foam sponge, a semi-occlusive adhesive cover, a fluid collection system or canister, and a suction pump (1). The foam sponge is applied to the wound and covered. A fenestrated tube is embedded in the foam and the wound is sealed with adhesive tape to make it airtight, and the machine delivers continuous or intermittent suction, ranging from 50 to 125 mmHg (1). 

This design was created on Canva.com on October 1, 2023. It is copyrighted by Abbie Schmitt, RN, MSN and may not be reproduced without permission from Nursing CE Central. 

Proper application of the NPWT is important for the mechanism of action to be effective. Research supports that NPWT is effective at creating a stable wound environment, reduces inflammation and bacterial load, improves tissue perfusion, and stimulates granulation tissue and angiogenesis (1).  

Imagine you want to plant a garden in a swampy location, you would first need to divert the water and algae from the land, cover it with a greenhouse with consistent heat and pressure, and cultivate the soil for optimal growth. Similarly, NPWT creates the most ideal conditions possible for tissue regeneration.  

Contraindications 

NPWT would be contraindicated for the following: 

• Wounds involving untreated osteomyelitis. 
• Wounds that have exposed blood vessel 
• Wounds with exposed nerves, anastomotic sites, or organs 
• Wounds including open joint capsules 
• Malignant wounds 
• Wounds with necrotic tissue; it is recommended to excise first 

The following wounds could benefit from NPWT, but caution should be given (5): 

• Wounds with visible fistula 
• Wounds with exposed bone or tendon 

• The bone or tendon should be isolated from direct pressure  

• Patient with clotting disorders or that are taking anticoagulants, due to an increased risk of bleeding. 
• Compromised microvascular blood flow to the wound bed. 

Assessment 

A focused assessment should be done for patients with NPWT devices in place, both on the machine settings, the dressing, and the wound itself. Thorough documentation of the wound is essential to see the progression of wound healing. 

Suction Device Settings: 

• Continuous or intermittent 
• Pressure Setting: Range of pressure settings from -40mmHg to -200mmHg, which can be tailored for different types of wounds (7). This is set by the medical provider. 

Laboratory assessment is meaningful in wound care. Labs can be used to assess oxygenation or indicators of infection (6). 

Dressing Assessment 

The appearance of the NPWT and dressing should be clean, dry, intact, and sealed. The tubing should not be twisted or kinked, and the clear adhesive dressing should not be wrinkled or overlapping. Please see below an example of the appropriate appearance of a dressing. 

Wound Assessment: 

• Anatomic location 
• Type of wound  
• Degree of tissue damage 
• Description of wound bed 
• Wound size 
• Wound edges and surrounding skin 
• Signs of infection 
• Pain 

Anatomical Location  

Anatomical terms and numbering should be used to make sure the location of each wound is documented. Patients often have more than one wound, so the treatment needs to be specified for each wound.  

Wound Base 

Assess the color of the wound base. Healthy granulation tissue appears pink and moist due to the new capillary formation. The appearance of slough (yellow) or eschar (black) in the wound base should be documented and communicated to the health care provider (1).  

This tissue may need to be removed to optimize healing. If any discoloration or duskiness of the wound bed or wound edges are identified, the suction should initially be reduced or switched off (7).  

Type and Amount of Exudate 

Assess the color, thickness, and amount of exudate (drainage) The amount of drainage from wounds is categorized as scant, small/minimal, moderate, or large/copious.  

Terms are used when describing exudate: sanguineous, serous, serosanguinous, and purulent (6).  

• Sanguineous: fresh bleeding  
• Serous: Clear, thin, watery plasma 
• Serosanguinous: Serous drainage with small amounts of blood noted 
• Purulent: Thick and opaque. The color can be tan, yellow, green, or brown. This is an abnormal finding and should be reported to a physician or wound care provider. 

Wound Size  

Wounds should be measured on admission, wound vac dressing changes, or as needed for abnormal events. Many healthcare facilities use disposable, clear plastic measurement tools to measure the area of a wound.  

Consistent measurement is vital to the assessment of wound healing. 

• Measure the greatest length, width, and depth of the wound in centimeters 
• Examples of wound classification tools: 

• NPUAP staging system for pressure injuries 
• Payne-Martin classification system for skin tears 
• CEAP (clinical, etiologic, anatomic, and pathophysiology) system for venous ulcers 

Tunneling or Undermining 

Tunneling is when a wound has moved underneath the skin, making a “tunnel.” The depth of tunneling can be measured by gently inserting a sterile, cotton-tipped applicator into the tunnel and noting the length from the wound base to the end of the tract (7). Undermining occurs when the tissue under the wound edges becomes eroded, resulting in a pocket beneath the skin at the wound’s edge.  

Healing Process 

It is important to recognize the entire process of normal wound healing. There are four phases of wound healing: hemostasis, inflammatory, proliferative, and maturation (6).  

Hemostasis begins immediately after injury, involving platelet aggregation and activation of clotting factor (6). A platelet “plug” is formed as fibrinogen converts to fibrin and binds to itself. Vasoconstriction occurs at this time, decreasing blood loss and allowing clot formation.  

The inflammatory phase begins right after the injury and the injured blood vessels leak and cause localized swelling. The swelling, warmth, pain, and redness present during this stage of wound healing are related to the release of white blood cells, growth factors, nutrients, and enzymes to help control bleeding and prevent infection (6).  

The proliferative phase of wound healing involves “rebuilding” with new tissue made up of collagen and extracellular matrix; granulation tissue is built stronger with proper oxygen and nutrients.  

Key nursing knowledge: Dark granulation tissue can indicate infection, ischemia, or poor perfusion. The maturation phase of wound healing is when collagen is remodeled, aligns along tension lines, water is reabsorbed so the collagen fibers can lie closer together and cross-link, and the wound fully closes (1). 

There are three types of wound healing: primary intention, secondary intention, and tertiary intention.  

Primary intention means that the wound healing is supported by sutures, staples, glue, or otherwise closed so the wound heals beneath the closure (6).  

Secondary intention must happen when the edges of a wound cannot be approximated, or “brought together,” so the wound heals with the production of granulation tissue from the bottom up (6).  

Wounds that heal by secondary intention are at higher risk for infection, so contamination prevention is essential. Pressure ulcers are an example of wounds that heal by secondary intention.  

Tertiary intention refers to a wound that needs to remain open, often due to severe infection. Wounds with secondary and tertiary intention have longer healing times (2). 

Alternatives when NPWT fails 

• Hyperbaric Oxygen Therapy (HBOT): 

• HBOT is a treatment in which the wound is exposed to pure oxygen in a pressurized chamber to enhance wound healing (3). 

• Bioengineered Tissue:  

• Skin grafting or bioengineered tissue to promote tissue growth and healing.  
• Skin grafts are considered as a treatment option if a wound is so large that it can’t close on its own. In this procedure, skin is taken from another part of your body – usually your thigh – and transplanted onto the wound (2). 
• Some grafts are made from human cell products and synthetic materials. Studies have shown that these increase the chances of poorly healing venous leg ulcers closing faster. (2) 

• Electrical Stimulation Therapy:  

• Electrical stimulation therapy applies electrical currents to stimulate wound healing and tissue generation (4). It may be used to treat chronic wounds or pressure ulcers. 

Adjunct Treatment Options 

When selecting an adjunctive therapy for wound management, the patient's medical history, overall health, co-morbidities, ambulation status, psychosocial aspects, environmental factors, and the specific needs of the wound should all be considered. Each patient is unique, and an individualized care plan is the goal.  

Treatment of the underlying contributing disorder will be essential. For example, a patient with uncontrolled diabetes that has led to poor circulation can benefit from glycemic control.  

Take a look at the larger, holistic picture. It can be helpful for the healthcare team to create a concept map of problems that contribute to the wound. 

Topical Agents and Dressings 

Various creams, ointments, or dressings can promote wound healing and prevent infection. One example is silver-based products, which are commonly used in reducing bacterial burden and treating wound infection (4). 

Nutrition Therapy for Wound Healing 

Patients with wounds would benefit from nutrition consultation and ongoing support.  

Nutrients from foods help the body build and repair tissue and fight infection. An increase in calories and protein is important, as well as blood sugar control for diabetics.  

Vitamins C, D, B-6, B-12, folate, and others aid in repairing tissues (6). Minerals such as iron, magnesium, calcium, zinc, and others support the cardiovascular system making sure cells have enough oxygen, the nervous system, and immunological function (6). 

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Compression Therapy 

Compression therapy uses pressure to reduce swelling and improve blood flow to the wound. There are common compression devices or stockings available. It is frequently used to treat venous leg ulcers (6). 

Hyperbaric Oxygen Therapy (HBOT) 

HBOT can also be used as an adjunct treatment in which the patient breathes pure oxygen in a pressurized chamber to increase the amount of oxygen in the blood, which enhances wound healing (3). 

Troubleshooting Tips 

You may encounter complications with the wound dressing or the wound vac equipment. The most common complications associated with NPWT are pain, bleeding, and infection (7).  

The wound therapy relies on an adequate seal similar to a regular vacuum, so a loss of suction can result in ineffective treatment. If loss of seal occurs, the nurse should assess the seal around the wound dressing and note if the transparent adhesive sealant tape has either been misapplied or has come off due to poor contact with the underlying skin.  

A loss of suction could also result from incorrect placement of the suction drain tube, loss of battery power, blockage of the suction drain tube, or if the suction device is full of output (7). Sometimes the location of the wound leads to difficulty in keeping the dressing seal in place; for example, the abdomen or near joints, so movement can misplace the dressing and break the seal. Patient education is key to maintaining proper suction. 

Troubleshooting Tips: 

• Confirm the machine is on and set to the appropriate negative pressure. 
• Make sure the foam is collapsed and the NPWT device is maintaining the prescribed therapy and pressure. 
• Assess the negative pressure seal and check for leaks. 
• Check for kinks in the tubing and make sure all clamps are open. 
• Avoid getting the machine wet. 

• Assess the drainage chamber to make sure it is filling correctly and does not need changing. 
• Address alarm issues: 

• Canister may be full 
• Leak in the system  
• Low/dead Battery 

• The device should not be turned off for more than two hours without ordered discontinuation. 

• If the device is off, apply a moist dressing and notify the provider immediately. 

Case Study 

Mr. Smith is a 59-year-old male presented to his primary care provider and referred to general surgery; diagnosed with lymphedema and multiple, copiously draining ulcerations on the left lower extremity.  

The patient presented with lymphedema and multiple ulcerations on the left lower extremity with copious amounts of drainage. This is an ongoing, worsening issue for over 8 months and has failed to respond to compression, foam dressings, or hydrocolloid dressing.  

The hospitalist has ordered surgical consultation, who scheduled debridement of the wounds and application of a wound vac following the procedure; Negative pressure wound therapy (NPWT) orders in place.  

CHIEF COMPLAINT: "The sores on my feet are draining more and I can no longer go to work because my boots do not fit on my foot.” He also reports a loss of appetite, chills, and loss of sensation to his left lower extremity.  

HISTORY OF PRESENT ILLNESS: Patient is a 59-year-old truck driver who has previous medical history of DM Type II, hypertension requiring use of anti-hypertensive medication, and hyperlipidemia (non-compliant with medication regimen). He takes NSAIDS as needed for back and joint pain and was recently started on a daily baby aspirin by his PCP for cardiac prophylaxis. He denies alcohol intake. He reports smoking a pack of cigarettes per day. 

PHYSICAL EXAMINATION: Examination reveals an alert and oriented 59-YO male. He appears anxious and irritated. Vital sips are as follows. Blood Pressure 155/90 mmHg, Heart Rate 120/min - HR Thready - Respiratory Rate - 20 /minute; Temperature 98.0  

ENT/SKIN: Facial pallor and cool, moist skin are noted. No telangiectasia of the lips or oral cavity is noted. Wound: 3 cm x 2 cm x 1 cm wound to lateral LLE. Wound base is dark red with yellow-green drainage present. Removed 4 x 4 dressing has a 5 cm diameter ring of drainage present. The surrounding skin is red, warm, tender to palpation, and with a dusky appearance to the entire LLE.  

CHEST: Lungs are clear to auscultation and percussion. The cardiac exam reveals a regular rhythm with an S4. No murmur is appreciated. Peripheral pulses are present but are rapid and weak. A positive Stemmer sign was noted and palpable pedal pulses with mild symptoms of venous insufficiency were noted. 

ABDOMEN/RECTUM: The abdomen reveals a rounded abdomen. Bowel sounds are present.

Conclusion

Hopefully, upon completion of this course, you feel empowered and curious about the use of negative pressure wound therapy (NPWT). Wound vacs can be a powerful tool in combatting acute and chronic wounds, it is a well-documented concept throughout history.

The nurse should be knowledgeable on the integumentary system makeup and types of wounds this therapy is indicated for. The mechanism of action of NPWT is critical knowledge when assessing the healing of a wound. Adjunct treatment options and troubleshooting support tips are also meaningful in the care of patients with NPWT.

Nutritional Interventions to Promote Wound Healing

Introduction   

The medical field is an ever-evolving and constantly changing arena. Advances in technology and an increased understanding of how the body works have produced newer and better procedures and techniques in healing. These initiatives, as innovative as they may be, still depend on the body’s ability to heal itself as the foundation of the recovery process.  

In turn, the body needs proper nutrition to support the healing process within itself. Nutrition is often overlooked by nurses even though it is arguably the most critical aspect of physical healing. 

Factors That Impact Wound Healing 

Wound healing is a complex process. There are a myriad of factors that impact the body’s ability to heal and recover from an injury. Comorbidities, genetic disorders, medications, and, in some cases, disease treatments (chemotherapy, radiation, steroids, etc.) can all have the potential to slow, change, or interfere with normal wound healing (2). For this course, we will discuss a few of the more common factors that nurses will undoubtedly come across during their practice. 

Diabetes 

It is estimated that this growing, global disease will impact forty million people by the year 2030. It has been proven that diabetes is responsible for more than one hundred changes in wound healing.  

These alterations have been seen across all four phases of wound healing. Platelet activation, epithelialization, collagen deposition, and granulation tissue formation are among the alterations that take place with diabetes. Worsening renal function/failure and peripheral vascular disease as a result of diabetes also affect the wound-healing process (2). 

Renal Failure 

Though most patients who have chronic kidney disease or renal failure also have multiple comorbidities that cause the renal problem, renal failure does, independently, bring a risk of diminished wound healing. Tissue edema, delayed granulation, chronic inflammation, and decreased vessel formation are all ways that renal failure impacts wound healing.  

Hemodialysis, a life-sustaining treatment of chronic renal failure, adds fuel to the fire when it comes to risks of diminished wound healing. Protein and water-soluble vitamins and nutrients are lost through the dialysis process. This includes zinc and iron and will lead to deficiencies in these needed nutrients. Further, patients on hemodialysis and patients who receive a kidney transplant as treatment for renal failure are both at higher risk for developing infections (2).  

Smoking 

Smoking causes multiple alterations within the body at the molecular level that affect normal wound healing. Vasoconstriction caused by smoking worsens wound ischemia. The highly documented negative impact that smoking has on wound healing has led physicians to decline some elective surgeries due to the risk of poor wound healing (2). 

Infection 

It is not fully understood how infection alters wound healing. It is believed to be a multifactorial process that has a range of properties that can be progressive in nature; infection-necrosis-sepsis-death. The bacteria create an environment where the collagen that repairs the injured tissue is destroyed (2). 

Obesity 

Obesity complicates virtually every disease process including normal wound healing. Wound healing complications due to obesity include increased rates of infection, hematomas, and dehiscence. Local hypoxia is also a complication that impacts wound healing (2). 

Age 

Aging also has an impact on wound healing. During the aging process, the skin loses elasticity, thickness, and water content. There is also a decrease in the skin’s blood vessels as it ages, reducing the capacity for oxygenation and nutrients. Wound closure becomes slower with aging; by age forty, the amount of time for an identical wound to heal doubles from age twenty. After the age of fifty, dermal collagen decreases by one percent per year (2). 

Malnutrition 

Malnutrition or undernutrition has a variety of effects on wound healing. Good nutrition is essential for proper wound healing and the overall recovery of the body after an injury.  

Malnutrition can lead to the loss of immune function which will affect the body’s response to infection. With malnutrition, the skin becomes thin and frail thus more apt to develop wounds. Pressure wounds are also more likely as fat deposits over pressure points become depleted. The lack of energy during malnutrition leads to immobility, increasing the possibility of wounds. Collagen synthesis is also decreased (5).

Phases of Wound Healing 

Once again, wound healing is a complex process. From a simple pin prick to a stage-four decubitus ulcer, the wound healing process itself remains the same. The body will go through the four phases of wound healing to repair the damage.  

Hemostasis 

The first phase of wound healing is hemostasis. Whether by surgery or trauma, the body attempts to achieve hemostasis at the time of the injury. The intrinsic and extrinsic coagulation cascades are activated by the body.  

Vasoconstriction takes place while platelet aggregation occurs to form a fibrin clot. This is all in an effort of the body to stop the bleeding to bring about hemostasis. As the platelets arrive at the site of injury, cytokines and growth factors are released by the platelets to initiate the inflammation process (3) (4) (5). 

Inflammation 

Inflammation is the second phase of wound healing. It starts once hemostasis has been re-established. During this phase, the previous vasoconstriction reverses and the vessels dilate.  

This brings blood to the injury site along with neutrophils, macrophages, monocytes, and other inflammatory cells. Phagocytosis is initiated and the wound is cleansed by the removal of bacteria. The wound site will swell and there may be some restrictions in mobility to the affected area (3) (5). 

Proliferation 

Phase three is proliferation. In this phase, rebuilding of the wounded tissue begins. The number of fibroblasts increases and begins to build a collagen network and prepare the wound base for new granulation tissue.  

At the same time, new blood vessels are created; a highway for oxygen and nutrients to be supplied to the site. By the end of this phase, the foundation will have been laid for full epithelialization (3) (5). 

Remodeling 

The final phase of wound healing is remodeling. Epithelialization is in full swing once granulation tissue has filled the wound. This process stimulates skin integrity restoration.  

Scar tissue is formed as proteins such as collagen and elastin along with keratinocytes are produced. The wound closes and begins to strengthen and appear “normal”; it may take a couple of years for the site to return to its fully functional pre-injured status (3). 

How Does Nutrition Impact Healing? 

Nutrition is, perhaps, the most important underlying aspect of wound healing. The mechanism of wound healing and the role nutrition plays in that process is very complex.  

Adding nutritional interventions to the wound healing care plan is generally low cost and will increase the probability of a full recovery. Nutrition is essential for all phases of the healing process. It is the foundation of wound healing.  

The malnourished patient will have difficulty progressing through the wound healing phases. Proper nutrition will also help prevent wounds such as pressure ulcers from developing in the first place.  

Understanding which nutrients are needed through the phases of wound healing will help to devise a nutritional plan of care. Energy is required in all the phases of wound healing and is only made possible through proper nutrition (3). 

Common Deficiencies 

Nutrients and proteins are the building blocks of life. They are needed for growth, maintenance, and healing of the body. Many types of nutrient deficiencies greatly impact the healing process. Here, we will discuss some of the more common nutrient deficiencies. 

Iron 

Iron plays a key role in the synthesis of hemoglobin. Hemoglobin delivers oxygen throughout the body; oxygen is required through all phases of wound healing. Iron deficiencies can lead to anemia and decreased tissue perfusion. An iron deficiency will also affect protein synthesis, macrophage function, and overall wound strength (3) (6). 

Vitamin A 

When it comes to wound healing, vitamin A quickens collagen synthesis and the overall inflammatory phase. A deficiency in vitamin A decreases collagen production, epithelization, and tissue granulation (9). 

Vitamin B 

There are eight vitamins included in the vitamin B complex. Each of the eight vitamins has its own daily recommended intake. Vitamin B promotes cell proliferation and promotes normal metabolism. In the presence of a wound, some dietitians promote doubling the daily recommended intake of the B vitamins (3). 

Vitamin C 

Vitamin C (ascorbic acid) assists with iron absorption. It is also essential in the process of collagen formation. Without vitamin C, the immune response cannot take place as needed. There are many sources of vitamin C readily available for everyday consumption (6). 

Zinc 

Zinc is used through all phases of the wound-healing process. It is used to initiate and modulate enzyme function throughout the wound healing phases. It affects immunity and assists in fibroblast proliferation and collagen production. It is also needed for granulation tissue formation (5) (6). 

Amino Acids 

Protein and amino acids are another set of nutrients that are highly essential in wound healing. The blood’s most abundant amino acid, glutamine, provides the body’s preferred energy source, glucose. Increased levels of glutamine have been shown to help with wound strength and increase the levels of mature collagen.  

Generally, the body is able to produce enough glutamine for regular function. In times of stress on the body, such as a wound, glutamine is sought out in the diet. Arginine assists in modulating the collagen deposits, increases new vessel formation, and aids in wound contraction (3). 

Special Considerations 

Tube Feedings 

Patients who use tube feedings or enteral feedings are in a unique situation when it comes to wound healing and nutrition. Once a proper nutrition assessment has been performed, a tailor-made nutrition-rich diet can be formulated and administered directly into the gut.  

Studies have shown that different formulas with supplemental nutrients have increased the ability of the body to heal faster than those without supplements. With tube feedings, patients don’t need to prefer the taste of one formula over another as it is delivered through the tube.  

The amount of formula can also be adjusted as the patient’s needs change. Though some formulas may have side effects such as diarrhea, the overall benefits usually outweigh such side effects (8). 

Chronic and Terminal Illness 

Autoimmune, inflammatory, and cancers are among the chronic and terminal diseases that are under special consideration when it comes to wound healing. These types of diseases can interrupt the immune/inflammatory response of the body thus prolonging the phases of wound healing.  

When a wound develops on a patient who is immunocompromised, there is a higher incidence of wound infection which will delay wound healing. In many of these diseases, there may be circulatory issues that decrease the body’s ability to provide the affected area with nutrient-rich blood.  

Chronic illnesses often decrease the patient’s energy levels. This can lead to immobility and increases the risk of wounds developing.  

Further, for many of these types of issues, the treatment itself can have adverse effects on wound healing. Chemotherapy, radiation therapy, and immunosuppressants all decrease the body’s ability to heal and increase the rates of infection in wounds (2). 

Supplements 

Nutritional supplements have been shown to improve wound healing and recovery outcomes. It is important that the supplements are given under the supervision of a provider as too much of some nutrients can have a detrimental effect on wound healing.  

A proper nutrition screening should be performed on all patients with wounds so that the nutrition plan can be tailored to the individual patient. These improvements to wound healing with nutritional supplementation differ based on the type of wound and the overall health of the patient.  

The patient should be monitored and reassessed regularly by a dietitian. Again, there is no cookie-cutter supplement regimen.  

Another factor to consider with supplements is the ease of following the supplement regimen. Hard to swallow pills or foul-tasting food/liquids may have a negative impact on the patient’s ability to adhere to the supplement regimen.  

Allowing the patient to choose (with the input of the provider) the method of supplement delivery along with a choice of flavors will help increase compliance with the prescribed regimen (1). 

Patient Education 

Throughout the entire wound healing process, patient education is a must. Not only is it important so that the patient can make an informed decision about their care, but the patient should understand what is going on with their bodies.  

Education fuels compliance. A comprehensive nutrition assessment will not only provide a baseline of the patient’s nutritional status but will also help identify gaps in the patient’s understanding.  

This is where the education can be focused to best help the patient meet their wound healing goals. Education must include which foods contain which nutrients, the amount of these foods to eat, and which foods will interact with the absorption processes of the nutrients.  

Discussing normal daily requirements and the requirements needed during wound healing is also needed (1). 

Conclusion

Nutrition plays a key role in wound healing. There are many factors that affect the body’s ability to acquire and use the needed nutrients. One of the most important considerations that we as healthcare providers need to put into practice is determining a patient’s nutritional status.  

A nutritional assessment should be done on patients with wounds so that a proper plan of care can be developed. Often, nutrition is an afterthought when in reality it is the foundation on which other treatments should be built upon.  

Once this has been established, the patient’s plan of care can be implemented and must include nutritional education. Needed supplements to increase the patient’s ability to heal can be added or removed as necessary when the reassessments have been completed. 

Ostomy Management

Introduction   

Newton's law of gravity states: what goes up, must come down; similarly, the normal human gastrointestinal system has a law that what goes in, must come out. When disease inhibits the normal process, ostomy procedures are a life-saving intervention.

There are around one million people living with an ostomy or continent diversion in the US, and approximately 100,000 ostomy surgeries are performed annually in the US (1). We will build a stronger understanding of various types of ostomies, indication for the need, site selection, stoma care, complications, and patient education.

Types of Ostomies

An ostomy is a surgically created opening that reroutes stool or urine from the abdomen to the outside of the body through an opening called a stoma (9). The term stoma refers to the portion of the bowel that is sutured into the abdomen (9).

When you look at a stoma, you are looking at the lining (the mucosa) of the intestine. The color is similar to the mucosa inside your mouth and cheek. Throughout various healthcare environments, you may hear the terms ostomy or stoma interchangeably. The purpose of an ostomy is to bypass a diseased portion of the gastrointestinal tract that is not functioning properly or has been removed (2).

Ostomies are placed proximal to the diseased area, comparable to building a dam in a river to stop the flow of fluid and divert it somewhere else. An ostomy can be temporary or permanent.

There are three most common types of ostomies: ileostomy, colostomy, and urostomy (9). We will discuss these types, but it is important to recognize that gastrostomy, jejunostomy, duodenostomy, and cecostomy procedures are also done.

1. Ileostomy: A stoma is attached at the end of the small intestine (ileum) to bypass the colon, rectum, and anus.
2. Colostomy: A stoma is attached to a portion of the colon to bypass the rectum and anus.
3. Urostomy: A stoma is attached to the ureters (the tubes that carry urine from the kidney to the bladder) to bypass the bladder.

Ileostomy

The small intestine has three parts that are compact and folds over itself: the duodenum, jejunum, and the ileum. An ileostomy has a stoma attached and created from the ilium. The ileum is the final and longest segment of the small intestine (9).

The ileum terminates at the ileocecal valve, which controls the flow of digested material from the ileum into the large intestine and prevents the backup of bacteria into the small intestine (9). If a patient has this type of ostomy, the colon distal to the ostomy has a form of disease or disorder such as cancer. There are two main types of ileostomies, loop, and end ileostomy.

Loop ileostomy

In a loop ileostomy, a loop of the small bowel is lifted and held in place with a rod due to resection or repair to the distal bowel (Will). This ostomy is technically two stomas joined together (4). Loop ileostomies are typically temporary and will be closed or reversed through an operation in the future.

End ileostomy

In an end ileostomy, the ileum is surgically separated from the colon, the colon is removed or left to rest, and the end of the ileum is brought to the surface through the abdomen to form a stoma. Although end ileostomies are sometimes temporary and later rejoined, they are usually permanent (9).

Colostomy

A colostomy may be formed as an ascending, transverse, descending, or sigmoid colostomy (9). It is named according to the location of placement. An end colostomy is constructed from the ascending, transverse, descending, or sigmoid colon and has one opening for fecal elimination.

Loop Colostomy

The creation of a loop stoma takes a loop of the colon (usually the transverse colon) and pulls it to the outside of the abdominal wall (9). In this type of ostomy, the entire bowel is not dissected but left mostly intact.

End Colostomy

In end colostomies, the proximal end of the colon is dissected and pulled out of the abdominal cavity, which becomes the stoma (9). Additional procedures may involve repairing or removing portions of the distal colon or rectum.

Urostomy

Kidneys have an important job of filtering waste and excess fluid from your blood. This process creates urine, which then travels from the kidneys to the bladder through tubes called ureters (8). If the bladder is damaged or diseased, ostomies are a life-saving method of creating safe passage for the urine.

A urostomy is a surgical opening in the abdominal wall that redirects urine away from a bladder that’s diseased, has been injured, or isn't working properly (8). The bladder is either bypassed or removed (called a cystectomy) during surgery. Following the surgery, urine exits the body through a stoma.