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Aortic stenosis is the second most common valvular heart disease in the Western world, and it is usually diagnosed after the age of sixty-five. With a burgeoning elderly population in the U.S., it is estimated that the number of Americans over the age of sixty-five will double by the year 2060 (2). Therefore, having a full understanding of TAVR nursing care, aortic stenosis, and its effects on the body is essential to provide care for patients undergoing a transaortic valve replacement (TAVR) procedure.

In this course we will discuss the relevant anatomy pertaining to TAVR nursing care and procedure, indications and contra-indications, and the post-operative care of patients undergoing TAVR nursing care and procedure.

Introduction to TAVR Nursing Care

Aortic stenosis is the second most common valvular heart disease in the Western world, and it is usually diagnosed in patients over the age of sixty-five. (1) With a burgeoning elderly population, it is estimated that the number of Americans over the age of sixty-five will double by the year 2060 (2). Consequently, many more patients with aortic stenosis will be encountered in the clinical context.

Intervention to replace the aortic valve in these patients is crucial because once diagnosed with critical stenosis patients have a mortality rate of 75% within three years. (1) Aortic stenosis is the second most common valvular heart disease in the Western world, and it is usually diagnosed in patients over the age of sixty-five. (1) With a burgeoning elderly population, it is estimated that the number of Americans over the age of sixty-five will double by the year 2060 (2).

The number of TAVR nursing care procedures is likely to increase as the procedure matures and the elderly population continues to grow.

The rate of aortic stenosis in the elderly population is estimated to be between 3.4-12% depending on severity. A recent metanalysis compiled data from seven studies and observed a total of 9,723 patients aged seventy-five years or older. The study showed the prevalence of aortic stenosis to be approximately 12%. The estimated rate of severe aortic stenosis, in the same study, was estimated at 3.4%.

Figure 1: Valves of the heart

This image depicts the left and right coronary arteries as they branch off the aortic valve. The left coronary artery sits behind the left coronary cusp and the right coronary artery sits behind the right coronary cusp. The remaining cusp is termed the non-coronary cusp as there is no coronary artery associated.

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Given the prevalence of aortic stenosis in the sample population, researchers estimate that approximately 27,000 patients will become eligible for trans-aortic valve replacement each year. (6) Therefore, having a full understanding of aortic stenosis and its effects on the body is essential to provide care for patients undergoing TAVR nursing care and procedure.

Normal Anatomy and Function of the Aortic Valve

The aortic valve works in conjunction with the other three valves of the heart to keep blood moving forward. A brief review of a normally functioning aortic valve helps us understand how the pathology of aortic stenosis causes such profound effects on the rest of the body systems.

The aortic valve is situated between the left ventricle and the aorta. This area is also called the left ventricular outflow tract or LVOT, which simply means the track that flows out of the left ventricle. The opening of the aortic valve, known as the valve area, normally measures 2.6-3.5 cm2. (7)

The aortic valve is referred to as a semilunar valve because when closed it looks like three semilunar structures coming together to form a Y-shape (Figure 1). The aortic valve can be divided into four elements (8) and they are as follows:

1. One annulus
2. Three cusps (leaflets) with four layers
3. Three sinuses
4. Three commissures

The three semilunar shaped pockets, known as cusps (or leaflets), attach to a fibrous ring known as the annulus. The annulus is a part of the cardiac skeleton, a dense network of connective tissue that lies between the atria and ventricle reinforcing the structure of the heart (9). The annulus also acts as a shock absorber by transferring the force of the high-pressure circulatory system into the framework of the cardiac skeleton causing less wear and tear on the leaflets.

The cusps are named as the right coronary cusp, the left coronary cusp, and the non-coronary cusp. They are named this way because just behind the cusps, on the ventricle side of the outflow tract, lie three nodules, known as the sinus of Valsalva. The sinus is the area where the left and right main coronaries attach to the aorta (Figure 1). During diastole, the sinuses fill with blood that was just pushed out of the ventricles. As the ventricle begins to relax, the coronary sinuses drain blood into the coronary vessel system, preparing for the next contraction by providing oxygen and nutrients to the heart muscle.

The cusps are pearlescent in appearance and have four layers all less than 1mm thick; each layer has a distinct function (Table 1) (10). The names of the layers are as follows:

1. Endothelium

2. Fibrosa

3. Spongiosa

4. Ventricularius

The layers are connected in the following arrangement starting from the aortic endothelium and working toward the ventricular endothelium:

Aortic Endothelium > Fibrosa > Spongiosa > Ventricularis > Ventricle Endothelium

Figure 2. Aortic Valve Histology – Microscopic view of the aortic valve leaflet layers.

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Table 1. Layers and Function of the Aortic Valve Leaflets

Aortic Valve’s Role in the Cardiac Cycle

We have looked at the composition of the aortic valve now let’s look at its role in the cardiac cycle, starting with the venous circulation. (Figure 32) Deoxygenated blood from the body travels to the heart through the superior and inferior vena cava:

1. The superior and inferior vena cava empty into the right atrium of the heart. The atrium contracts, the tricuspid valve opens, and the blood flows into the right ventricle. As the right atrium relaxes, the tricuspid valve closes.
2. The right ventricle contracts and opens the pulmonic valve. Blood travels into the pulmonary circulation to eliminate waste and reoxygenate. The oxygen rich blood then travels from the pulmonary circulation into the left atrium of the heart.
3. The left atrium contracts, opening the mitral valve and blood flows into the left ventricle. The atrium relaxes and the mitral valve closes. The left ventricle contracts, sending blood out of the aortic valve and to the body through the aorta and carotid arteries. The valve will close when the pressure in the aorta is higher than the pressure in the ventricle.

Closure of the aortic valve is part of the second heart sound, S2, and is heard as the “dub” part of “lub-dub.” Originally, the S1 and S2 heart sounds were thought to be the sounds of the valves snapping shut. However, we now know that the heart sounds occur because of vibrations that happen just after the valve has shut (11).

As the aortic and pulmonic valves initially close some blood flows back and hits against the valves. The blood hitting against the valves causes vibrations that travel along the corresponding chamber producing the “lub” or “dub” sound as it travels.

Figure 3: Blood Flow Through the Heart

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Pathophysiology and Assessment

In aortic stenosis, the leaflets of the aortic valve become calcified, scarred, and stiff. The calcifications narrow the valve opening from the normal 2.6-3.5 cm2 to ˂1 cm2. The narrow valve obstructs the left ventricular outflow tract (LVOT), increasing the work the heart must do to overcome the obstruction or the afterload. To compensate for this obstruction and increased afterload, the heart begins to squeeze harder, increasing pressure in the left ventricle.

Left ventricle pressures have been reported as high as 300 mmHg in some cases (11). The constant exposure to high pressure causes the left ventricle to fibrose, thicken, and remodel. The increased muscle mass also demands more oxygen which causes stress on the microvasculature of the heart and contributes to the symptom of angina (12).

Typically, the left ventricle can relax and to allow for passive filling from the left atrium. The passive filling of the ventricle makes up the 80-85% of the end-diastolic volume, and the remaining 15-20% is provided by the “atrial kick” at the end of diastole. However, aortic stenosis patients have stiff, non-compliant ventricles that do not relax enough for proper filling during diastole; these patients depend on the atrial kick for 40% of their blood volume (7).

Therefore, abnormal rhythms such as atrial fibrillation or tachycardia cause patients with aortic stenosis to lose the benefits of the atrial kick, which causes a subsequent decrease in cardiac output to the body which leads to syncope and in some cases sudden cardiac death.

Ultimately, in the course of aortic stenosis, the left ventricle will dilate, fail, lead to pulmonary congestion, shortness of breath, and chest pain, which are the hallmark symptoms of aortic stenosis. Patients presenting with the classical triad of aortic stenosis have a 2-5 year prognosis if untreated (7).

Hallmark Symptoms: Syncope Angina Dyspnea

In severe aortic stenosis, blood from the left ventricle is being pushed out of a tiny calcified and critically stenosed opening at tremendous pressures creating what is called a “nozzle effect”. It is termed the “nozzle effect” because blood is spraying out of the aortic valve like water out of a fire hose (11).

As the blood hits the sides of the aorta, it causes vibrations that are heard, sometimes even without a stethoscope, and are felt like the thrill of a fistula. The murmur of aortic stenosis is heard and felt loudest in the 2nd intercostal space on the right side (Figure 5) this is the area directly over the aorta (13). The murmur can be heard best during systole since this is when blood is spraying out of the ventricle and creating turbulence in the aortic arch.

Figure 4: Left Ventricular Remodeling

Left ventricular hypertrophy (LVH) develops in response to elevated pressures in the ventricle. Patients who develop LVH are 4.5 times more likely to experience adverse events. Sustained exposure to increased afterload causes apoptosis, or cellular death, in the ventricles which leads to dilation and heart failure. Heart failure contributes to the hallmark symptoms of syncope, angina, and dyspnea.

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It is important to be able to identify the murmur of aortic stenosis given that many patients can go decades without any symptoms, and earlier detections can lead to earlier treatment and fewer long-term complications and morbidity. The murmur of aortic stenosis is considered a mid-systolic murmur described as a harsh crescendo-decrescendo murmur. Initially, as blood is pushed out of the ventricle, there is no sound, but as the ventricle squeezes harder the turbulence of the blood flow causes the crescendo and gradually as the ventricle begins to relax the decrescendo ensues.

In the late stages of the disease, S2 may be obscured by the murmur or even lost as the aortic valve becomes less compliant; this is an abnormal finding. The presence of S4 is indicative of left ventricular hypertrophy that develops over time in aortic stenosis (13). The S4 rhythm is called a gallop rhythm because it sounds like the hoof-beats of a horse (13).

When listening to a normal heartbeat, during S2 with inspiration, you may be able to distinguish two heart sounds; this is a normal finding called physiological splitting, and it only indicates that the pulmonic valve is taking a bit longer to close due to the inspiration. However, in aortic stenosis, it takes the aortic valve longer to close due to delayed emptying and the ventricles inability to relax. This abnormal finding is called paradoxical splitting, and it is heard during expiration rather than inspiration. (7)

Pulsus Tardus is a weakening of the carotid pulse that can be felt with light palpitation of the carotid artery. Pulsus parvus et tardus is when the carotid upstroke is delayed (7, 13). The carotid upstroke can be assessed by listening to the heart for systole and noting by palpation how long it takes to travel to the carotid artery.

Figure 5. The Murmur of Aortic Stenosis

The murmur of aortic stenosis is best heard over the second intercostal space at the sternal border and may radiate toward the carotids. Also, depending on the turbulence of blood flow the murmur may be palpable as a thrill

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Etiology and Risk Factors of TAVR Nursing Care

There are a few ways in which aortic stenosis can occur. These causes are listed below from most to least common.

1. Idiopathic calcification
2. Congenital bicuspid valve
3. Rheumatic heart disease
4. Radiation or Endocarditis
5. Genetic elevation of lipoprotein (a) (13)

Idiopathic calcification occurs mostly in patients over the age of sixty-five; this by far is the most common cause of aortic stenosis and is found in 3 to 5% of the general population (14). Risk factors for patients in this class to develop aortic stenosis include smoking, male gender, hypertension, hyperlipidemia, and diabetes. They are mostly the same risk factors associated with atherosclerosis (1).

Bicuspid aortic valve disease, a congenital condition, is a condition where a person is born with only two cusps on the aortic valve. Bicuspid valve disease is the most common congenital heart disease and is found in 1 to 2% of the population (15). Symptoms usually show up in this group around 40-50 years of age as age-related changes begin to affect the bicuspid aortic valve. Nearly 40% of these patients also have aortic dilatation which can lead to rupture, a medical emergency (15).

Rheumatic aortic disease, now a rare cause of aortic stenosis, is caused by an autoimmune response to group A streptococci, which leads to scarring along the commissure of the valve leaflets lessening their pliancy and causing an obstruction to the outflow tract of the left ventricle (14). Rheumatic aortic stenosis can easily be remedied with antibiotics and with the combination of rapid strep testing and access to antibiotics this is very rarely encountered in the clinical area.

Some cases of aortic stenosis are believed to be caused by a genetic variation in the genes that express lipoprotein (a). The elevation of lipoprotein (a) along with low-density-lipids are thought to induce inflammatory changes on the layers of the valve leaflets leading to valve calcification and stenosis (16, 17). Other rare causes of aortic stenosis include; endocarditis, radiation therapy, Paget disease, Fabry disease, ochronosis, and end-stage renal disease (14).

Natural History of Aortic Stenosis

In aortic stenosis the aortic valve causes an obstruction of the left ventricular outflow tract. The heart attempts to overcome this obstruction by pushing harder. This causes a tremendous difference in pressure between the left ventricle and the aorta. This difference is measured and termed the transvalvular gradient. Transvalvular gradients higher than 50 mm Hg with a small valve area such as 0.8 cm2 is considered “severe aortic stenosis”.

In severe aortic stenosis the left ventricle compensates in two ways:

1. Remodeling
2. Thickening

Remodeling happens on a cellular level and is caused by changes to the cellular matrix in response to elevated pressure. Thickening of the heart muscle occurs because of how hard the heart must push against the transvalvular gradient (Fig. 4.). The more the heart muscle is worked the larger it becomes, just like any other muscle of the body. The thickening, however, has consequences.

The first being that the muscle of the left ventricle has thickened, but the excess tissue leaves no room for blood in the ventricle. Less blood in the ventricle leads to less blood being pushed out to the body. This leads to diastolic heart failure. These patients can appear to have a normal Ejection Fraction (EF), but this can be deceiving. Let’s look at normal ejection fraction vs. the ejection fraction of a patient with diastolic dysfunction.

The Normal Ejection Fraction
A. The heart fills will 100 ml
B. The heart ejects 60 ml
B/A=0.60 or 60%

The Ejection Fraction of Diastolic Dysfunction
A. The heart can only fill 50 ml
B. The heart ejects 30 ml
B/A=0.60 or 60%

The ejection fractions are identical, but the patient with diastolic dysfunction is filling up with half the blood and pumping out half the blood of the normal patient. The deficit leads to under perfusion to the body, which leads to exertional chest pain. On the other hand, because the ventricle cannot fill up enough or pump out enough blood begins to backup from the left ventricle to the left atrium and finally all the way back to the vasculature of the lungs.

The vessels of the lungs begin to leak excess fluid causing pulmonary edema and dyspnea. This dyspnea is especially increased during exertion, because on top of the fact that the heart cannot push out enough blood, now there is tachycardia which decreases the amount of time the heart has to fill up. Patients with aortic stenosis often adjust their activity level over time so that they do not over exert themselves which leads to the chest pain and shortness of breath.

Now let’s look at the other scenario. Aortic stenosis patients with systolic dysfunction usually have an ejection fraction that is lower than normal. In this scenario the left ventricle has become worn out and is unable to pump blood to the rest of the body. The ventricle dilates and thins causing it to lose its ability to pump effectively (fig. 4). Let’s compare the ejection fraction to that of a normal patient.

The Normal Ejection Fraction
A. The heart fills with 100 ml
B. The heart ejects 60 ml
B/A=0.6 or 60%

The Ejection Fraction of Systolic Dysfunction
A. The heart fills with 100 ml
B. The heart ejects 30 ml
B/A=0.30 or 30%

In this case the ventricle has enough room for the normal amount of blood, but the muscle of the ventricle is only able to squeeze out 30 ml to the body. If you notice in both scenarios the patient is only pushing 30 ml of blood out of the ventricles; so regardless of whether the patient has systolic or diastolic heart failure they end up with the same consequences of chest pain from under-perfusion and shortness of breath from blood backing up into the pulmonary vasculature.

As patients with aortic stenosis progress slight changes in heart rate, afterload, and vascular resistance mean wide swings in symptoms and if not corrected can lead to sudden death. With excessive fluid volume aortic stenosis patients will develop dyspnea while dehydration will not allow the ventricle to fill adequately.

Tachycardia does not allow the ventricles to fill while bradycardia will decrease the cardiac output further. Patients with aortic stenosis are best kept close to their baseline vital signs while preparing for TVAR nursing care and procedure.

Overview of TAVR Nursing Care and Procedure

Perhaps the most essential element of TAVR nursing care is the actual transcatheter aortic valve replacement, or TAVR procedure.  This procedure is approved for patients who have severe symptomatic aortic stenosis and who are at high risk for surgical valve replacement.

Sheaths are used to make a conduit for the valve deployment device. The valve is round and made of a metal mesh network to which bovine leaflets attached.

The TAVR nursing care procedure does not require that the heart is stopped to perform the valve replacement, though the heart is usually paced at a high rate during deployment.

Diagnostic Imaging in TAVR Nursing Care

Diagnostic imaging is crucial if TAVR nursing care is to be planned. Solid imaging of the aortic valve decreases the risk of sub-optimal valve deployment during procedure, which can result in paravalvular regurgitation, aortic injury, heart block, or embolization of the valve prosthesis (18).

The gold standard of evaluation of aortic stenosis is the transthoracic echocardiogram (TTE). In this section we will look at what a diagnostic TTE assesses. Performing a TTE helps to (19):

• Confirm the diagnosis of AS
• Identify the cause of AS
• Assess valve morphology
• Identify the severity of the valve lesion
• Note left ventricular remodeling
• Estimate functional capacity of the left ventricle
• Assess for the presence of mitral valve regurgitation
• Assess for concomitant pulmonary hypertension

Morphology

Echocardiography can be used to determine the number of leaflets that are present and if the valve is tricuspid or bicuspid. This is of importance since the bicuspid valve is not yet approved for replacement via TAVR.

Another morphological notation on echocardiography is the presence of calcification on the valves. The ultrasound can quantify the amount, location, and severity of the calcium deposits (20).

Rheumatic valve disease is usually differentiated by the pattern of calcification. While rheumatic heart disease usually shows calcification at the commissure line, aortic stenosis usually affects the base of the leaflet and works in an outward pattern (14).

Severity

Echocardiographic parameters classify the severity of the valve lesion into mild, moderate, and severe stenosis. The severity of the disease is determined by the valve area, valve gradients, and peak velocity.

Table 2. Measure of Severity in Aortic Stenosis

Based on information from Mixon & Dehmer

Aortic Valve Area

The aortic valve area (AVA) is a calculation that measures the obstruction of the left ventricular outflow tract, by the stenosed valve. The normal aortic valve area is 2.5-3.5 cm2. The more stenosed the valve, the smaller the aortic valve area.

Figure 6. Peak Velocity Illustration

The narrowed opening in aortic stenosis causes a “nozzle” effect as the force from the ventricle ejects blood across the valve at a high speed, known as peak velocity. (figure B) The normal peak velocity shown in (figure A) is smooth with laminar flow

Le, K. (2019) Peak Velocity Illustration. BA.

Valve Gradient

The valve gradient is another calculation that measures the difference in flow across the valve. The gradient can be calculated on echocardiography or performed directly in the cath lab. In the cath lab, the pressure in the left ventricle and the pressure in the aorta are measured simultaneously. The difference between the two numbers is the gradient. High pressures in the ventricle with low pressures in the aorta is indicative of aortic stenosis. The normal mean gradient is ˂20 mmHg.

Peak Velocity

The peak velocity is a calculation that estimates how fast the blood is traveling across the valve and is measured in meters/second. The standard peak velocity is 2.0-2.9 m/sec. Peak velocity is related to the “nozzle effect,” where the ventricle is trying to push blood out of a narrowed opening. The enormous pressure generated translates into a higher peak velocity.

Left Ventricular Hypertrophy

Left ventricular hypertrophy (LVH) is abnormal thickening and reshaping of the left ventricle in response to the extreme pressures generated in the ventricle as it pushes against the stenotic valve. LVH is present in approximately 67% of patients diagnosed with asymptomatic severe aortic stenosis (12). The onset insidious and can develop long before the onset of symptoms. LVH increases the risk of adverse cardiovascular outcomes up to 4.5-fold (12). Therefore, echocardiographic evaluation of the left ventricle is useful to estimate the functional capacity and determine the severity of LVH before the TAVR procedure.

Mitral Regurgitation

The echocardiography is also able to detect concomitant Mitral Regurgitation (MR). MR is when the blood flows backward from the left ventricle into the atrium. This process can either be acute or chronic. Acute cases of MR usually occur in the setting of myocardial infarction, infective endocarditis, rupture of a chordae tendineae, or malpositioning of the aortic valve during TAVR (18).

In acute cases, there is an overwhelming back up of blood from the left ventricle to the left atrium and back to the pulmonary circulation. The rapid onset does not allow time for compensation, and it can easily lead to pulmonary congestion, hypoxia, reduced cardiac output, hypotension or even shock (18).

Non-acute cases of MR can occur when the left ventricle becomes hypertrophic, and subsequently the annulus of the mitral valve becomes dilated, which is common in aortic stenosis (18).

Regurgitation can lead to pulmonary congestion and edema. The mitral valve can be repaired along with the aortic valve in patients undergoing SAVR, but it is not yet performed in conjunction with TVAR. Ultimately, the decision to perform TAVR vs. SAVR in these patients is based on the heart valve team and the patient.

Other Imaging Modalities

Other imaging modalities include computed tomography (CT) or cardiac magnetic resonance (CMR). Cardiac catheterization is recommended in all patients since concomitant coronary artery disease is found in 50% of patients with aortic stenosis (7).

Many modalities are used so that a complete picture of the valve can be obtained before the procedure.

Decision to Intervene in TAVR Nursing Care

The heart valve team is tasked with deciding the best pathway for the patient based on current evidence and guidelines. The team typically consists of cardiologists, structural interventional cardiologists, imaging specialists, cardiovascular surgeons, a cardiovascular anesthesiologist, and cardiovascular nursing professionals (18).

The patient and family are involved in each step of the process, and they may be assigned a heart valve coordinator that works closely with them ensuring high-quality education and information for the decision-making process.

The decision to proceed to intervention is based on several factors (18):

1. The patients goals and beliefs
2. The presence or absence of symptoms
3. The severity of the lesion
4. Remodeling of the ventricles
5. Pulmonary or systemic congestion
6. A change from baseline heart rhythm
7. Risk/benefit based on age
8. Co-morbidities and life expectancy

Evaluation of Risk

The Society of Thoracic Surgery Predicted Risk of Mortality (STS-PROM) is a scoring system that is based on years of data collected by the Society of Thoracic Surgery. The heart valve team takes the STS score and classifies the patient into low, intermediate and high risk for surgical intervention.

Before surgery other factors are also measured such as the frailty index which takes into consideration the patients ability to perform activities of daily living, assesses any weight loss in the previous year, and tests the patient’s ability to rise from a chair. The patient may also be asked to perform a six-minute walk test or pass the Mini-Mental State Exam that assesses cognitive function.

Patients are further classified into stages A-D3 (Table 4.). These stages describe the severity of stenosis, characteristics of the stenosis, and presences or absences of symptoms.

The AHA/ACC guidelines are made to go along with the STS-PROM assessment. For example, a patient at high surgical risk, with symptomatic severe aortic stenosis would fall into the TAVR category, while a patient at intermediate risk with severe symptomatic stenosis would be recommended for SAVR. Intervention recommendations for stage A-D3 can be found in Table 4., while absolute contraindications for TAVR are listed below:

Contraindications for TAVRc
Based off information from Nitya & Kumar

• Bicuspid or non-calcified aortic valve
• Peripheral vascular or aortic disease
• Coronary artery disease requiring revascularization within 30 days
• End stage renal disease
• Severe left ventricular hypertrophy
• LVEF<20%, severe mitral regurgitation
• Significant neurological disease
• Life expectancy <1 year

Ultimately, Surgical Aortic Valve Replacement (SAVR) is preferred in patients with low to intermediate surgical risk. However, for patients at high surgical risk measured by STS score>10% TAVR is the preferred intervention (7).

Table 4. Staging and Timing of Intervention
Based on information from Kanwar, A., Thaden J.J., and Nkomo, V.

Pre-Planning Stage

Choice of Valve

Multi-detector computed tomography (MDCT), is the preferred imaging method to determine the annular size of the aortic valve, and it facilitates the decision of what valve should be chosen (18). The 3D data set that MDCT provides produces a more tangible image by which to choose valve size; and it is also able to measure the annulus of the aortic valve during systole when the valve is usually wider and fully open. 

The MDCT scan measures the aortic root which produces an anatomical image of the sinus of Valsalva, the coronary ostia, and the size of the aorta and sinotubular junction (18). These views can be used to seat the valve properly since any obstruction to the coronary ostia can lead to ischemia and possible cardiovascular arrest. 

MDCT imaging can help determine whether a balloon-expandable, self- expanding, or mechanical deploying valve should be chosen. The balloon-expandable valve fits over a balloon and when the balloon expands it pushes the valve onto the annulus of the aortic valve.

Figure 7. Common TAVR Nursing Care Access Sites

A self-expanding valve expands in a spring-like manner without the need for a balloon. The mechanical valves have a seal to reduce paravalvular leak and can be expanded by the cardiologist in a controlled manner. However, the Lotus valve was the only mechanical valve on the market and has been pulled temporarily due to issues with its locking mechanism (21).

Regarding preference, Otto et. Al states that a self-expanding valve is a gentler option and may be preferred in patients with “severe calcification of the valve and outflow tract with a risk of rupture, patients with an extremely oval-shaped annulus, or for small transfemoral access” (18).

If a patient requires the transapical approach, as in the case of severe atherosclerosis of the vasculature, the only valve approved for use is the balloon-expandable version (18). Many versions on the market today can be repositioned if malpositioned (18). Often, however, the choice of valve is merely physician preference.

Choice of Access

The outer diameter (OD) of the sheaths used for valve deployment range anywhere from 6.9 cm to 8.68 cm depending on the intended valve. Access sites are thoroughly imaged to ensure an entry point that is non-tortuous and mostly free of atherosclerosis which can put the patient at risk for cerebral embolization (18). If entry through the femoral artery is not feasible, other options include transaxillary, transapical, direct aortic, carotid, or transvenous approach (Figure 7).

Procedure Considerations

Hybrid Operating Room

Facilities, where TAVR procedures are performed, have a dedicated hybrid operating room that is a mix between a cath lab and a standard operating room. There is a cardiopulmonary bypass machine available if the procedure is converted to open-chest. Coronary occlusion wires are on hand if coronary embolization occurs intra-procedure, and anesthesia is equipped with advanced airway supplies if necessary. A crash cart and defibrillator are nearby, and defibrillator pads are placed on the patient per routine.

Anesthetic Considerations

Many of these patients have both cardiovascular and non-cardiovascular risk factors. Cardiovascular collapse is a real concern and proper anesthetic management can decrease this risk. Optimal hemodynamics should be maintained through the case, and attention should especially be paid to hypotension. Prompt administration of vasoactive medications aids in the avoidance of hypoperfusion.

While general anesthesia with endotracheal tube is the most common delivery method of anesthesia in TAVR patients, studies have shown that moderate sedation decreases the need for vasoactive medications (18, 22). However, an endotracheal tube should be considered if imaging by TEE is expected due to patient comfort.

If moderate sedation is to be utilized, the practitioner must be certain that airway securement can be done quickly in the event of respiratory or circulatory collapse. Due to the amount of equipment surrounding the patients head, attention should be paid to the environment and maneuverability in the event of emergent intubation (18).

Intra-Operative Complications

This procedure is performed on a high-risk population; therefore, complications are not uncommon. There are many different types of complications; however, if recognized promptly most can be managed or reversed.

Some complications are caused by improper placement of the new valve; these complications look different based on whether the valve is deployed too high or too low. Valve placement on the aortic side can cause a blockage of the aorta, injury to the aortic intima, or blockage of the coronary arteries. Valve placement too far into the ventricle can interfere with the mitral valve, causing mitral regurgitation, and subsequent pulmonary edema.

Also, pressure on the atrioventricular node can lead to conduction abnormalities and possible heart block (20). In these cases, the valve is retrieved and repositioned if possible. A transvenous pacer is inserted at the start of the procedure, which is used if the patient experiences complete heart block or any other non-perfusing rhythm.

If the surgical valve fails to cover the entire annulus, a paravalvular leak may occur. The leak can usually be corrected by inflating a balloon inside the valve, effectively pushing it outward to create a better seal, if this fails the valve may need to be recaptured and repositioned or replaced with a larger size.

Some complications are systemic such as cardiovascular collapse, shock, stroke, and myocardial infarction. Shock or hemodynamic collapse is always a risk in unrepaired aortic stenosis patients. The best management is to keep the patient within tight hemodynamic parameters, however, if cardiovascular failure ensues, and is irreversible the patient should be placed on coronary bypass.

If the ventricle or annulus is ruptured the procedure should be converted to an open heart. Also, if coronary occlusion and subsequent ischemia ensues the procedure should be converted to an open CABG. In the event of an embolic stroke catheter-based retrieval should be attempted.

In the event of a hemorrhagic stroke anti-coagulation should be reversed and treatment with this type of stroke is conservative. Access site complications such as dissection of the artery may require endovascular or surgical repair. Lastly, bleeding complications can be related to systemic heparinization that may need to be reversed.

Post-Procedure Complications

Post-procedure Monitoring

When obtaining report some items to note are; size and type of valve placed, concern of mal-placement or leak, the type of sheath that was used, and the number of vascular access sites the patient has.  

• Was the repair transapical and if so were any drains placed?  
• Were any irregular arrhythmias noted post-deployment?  
• Does the patient have a transvenous pacer still in place?  
• Is the patient pacer dependent, if so what are the settings, and where is the sheath and control box?  
• What type of closure device was used?  
• Were there any bleeding incidences in the surgery suite? When and what was the last ACT?  
• Does the patient have any risk factors for bleeding; such as von Willebrand factor deficiency?  
• Are any hematomas noted?  

If there are hematomas what size and how firm are they? If the patient has a femoral access as they are at risk for retroperitoneal hematomas- this may manifest as back pain, hemodynamic instability, and bruising along the flank. It is also advisable to mark the borders of the hematoma as a reference since patients can bleed insidiously.  

• Is the patient having any pain?  
• What type of anesthetic was used local, monitored anesthesia care, or general? 
• If it was general anesthesia, what type of airway was used?  
• Time and dose of last known pain medication and was local anesthetic used at the access site?  
• How much vasoactive medication was necessary during the procedure?  
• How much fluid was administered intraoperatively?  
• Is there a urinary catheter and how much was the urine output during the procedure? 
• How much contrast dye was utilized for the procedure? 

TAVR Nursing Care Complications Ordered Most to Least Common
Based off information from Nitya & Kumar (7)

1. Bleeding (15%)
2. Vascular site complications (10-15%)
3. Need for permanent pacemaker (5-15%)
4. Significant perivalvular leak (10%)
5. Stroke (2-5%)
6. Death (2-5%)
7. Acute kidney injury (1-2%)
8. Coronary Occlusion (0.6%)
9. Valve embolization (0.3%)

If there are hematomas what size and how firm are they? If the patient has a femoral access as they are at risk for retroperitoneal hematomas- this may manifest as back pain, hemodynamic instability, and bruising along the flank. It is also advisable to mark the borders of the hematoma as a reference since patients can bleed insidiously. Is the patient having any pain?

What type of anesthetic was used local, monitored anesthesia care, or general? If it was general anesthesia, what type of airway was used? Time and dose of last known pain medication and was local anesthetic used at the access site? How much vasoactive medication was necessary during the procedure? How much fluid was administered intraoperatively? Is there a urinary catheter and how much was the urine output during the procedure? How much contrast dye was utilized for the procedure?

These questions take into consideration some of the most common complications such as; bleeding, vascular site complications, need for permanent pacemaker, significant perivalvular leak, stroke, and acute kidney injury. Occurrence rate on each complication can be found above (TAVR Complications Ordered Most to Least Common).

Bleeding and Vascular Site Complications in TAVR Nursing Care

Before the procedure, patients undergo a series of imaging scans to identify potential vascular access sites. The scans included are a left and right heart catheterization and aortography, transthoracic and transesophageal echocardiography, computed tomography and angiography of the chest, and computed tomography of the abdomen and pelvis (23).

However, it is still estimated that about 15% of patients experience periprocedural bleeds which outranks all other complications (7). Many of these bleeds are related to the vascular entry site which carries a complication rate of 10-15%.

Proper monitoring of the access site, and the 5 P’s pain, pallor, pulse, paresthesia, and paralysis helps to identify any occlusion of the artery which is considered a surgical emergency. Most bleeding can be resolved by proper monitoring and intervention by manual pressure applied to the site. However, for continuous uncontrolled bleeding manual pressure should be applied, an ACT should be assessed, and if manual pressure is not adequate, the patient will require surgical stenting of the vessel (24).

Acquired Von Willebrand Syndrome

Aortic stenosis patients are also at high risk to acquire von Willebrand syndrome. (25) This happens because the stenosed aortic valve causes shearing forces and as blood crosses the valve clotting factors are destroyed; which in some cases this can lead to an induced VonWillebrand syndrome.

This condition can subsequently cause Heyde’s syndrome which is a gastrointestinal bleed caused in the setting of absent or defective von Willebrand factor. Replacing the valve may decrease the shearing effect, but it takes time for clotting factors to stabilize. The adenosine diphosphate closure time (CT-ADP) is a bedside test that is run much like an activated clotting time which may be useful in helping to identify paravalvular leaks and patients at risk for bleeding complications (25).

Atrioventricular Blockage

Complete heart block is a condition where the electrical signal of the heart is blocked and cannot travel through the atrioventricular (AV) node. This is characterized by a complete dissociation of p-waves and QRS complexes. Patients can also experience different degrees of AV dissociation which may lead to 1° AVB and 2nd° AVB.

While it is known that AV blockage can occur after TVAR, it is not well understood why this happens. Some studies have attempted to predict which patients are at risk for AV blockage post-TAVR. Studies have shown that larger valve sizes and the Edwards Sapien 3 Valve in particular have a higher rate of AV block. (27)

In another interesting study, patients with a QRS >120s were found to have a 38% rate of permanent pacemaker placement after TVAR, while none of the patients with a QRS ≤120s had any semblance of heart block. (28) In yet another study they found that longer P-R intervals, QRS duration, history of Right Bundle Branch Block (RBBB) and pre-existing 1°/2° block were more common in patients that required permanent pacemakers post procedure.

(29) Most incidences of heart block occur immediately after the procedure (30) while the patient is in the critical care unit. A thorough look at the patients pre-operative EKG and cardiac history may reveal patients at risk of needing a pacer post-operatively, allowing the nurse to prepare for placement of a transvenous pacer or utilization of one that is already in place.

Stroke

The mechanism by which stroke occurs after procedure is debatable, but both embolic and hemorrhagic strokes may occur after TAVR. However, more advanced catheters and valves lessen the risk of stroke. (31) The risk of stroke does appear to be the same as patients undergoing surgical aortic valve placement (SAVR), however, one study found that TVAR patients who experienced a TIA post-procedure had a lower 1-year survival rate (31).

Patients who are immediately post-op and in the ICU are at the most risk of experiencing a stroke or transient ischemic attack (TIA). However, after the immediate preoperative period, the risk of stroke/TIA decreases dramatically (31). Since it is postulated that debris from the valve is the cause of many neurological events studies are examining the use of cerebral protective devices such as a filter to decrease the incidence of embolic stroke. (32) Additionally, the use of antiplatelet therapy does seem to minimize the risk of embolic type strokes. (31) A full neurological exam should be performed upon admission per standard practice.

Patients may still be sleepy from procedure at this time, but it is important to assess for a proper baseline since TVAR patients are at high risk for stroke especially within the first twenty-four hours. Full neuro assessments that include a pupillary check should be performed every four hours at minimum or per hospital policy. Abbreviated neuro assessments may be performed in between full assessments and they should include at minimum an assessment of balance, dizziness, headache, blurred vision, facial drooping, and speech difficulty. Performing regular neurological checks will aid in early identification and treatment for TAVR patients Policies will vary by institute but a sample schedule may be as follows:

• Full neurological exam x1 then q 4hrs
• Abbreviated exam q 15 min x 8
• Abbreviated exam q 30 x4
• Abbreviated exam q hr

Acute Kidney Injury, Pain Management and Early Mobilization

Acute Kidney Injury During TAVR Nursing Care

The development of acute kidney injury after TAVR is associated with a four-fold increase in mortality. (33, 34) Risk factors for AKI after TVAR are hypertension, COPD, pulmonary disease, and blood transfusions (33-35). Some hospitals employ a preoperative infusion of acetylcysteine and IV bicarbonate as a protective measure against the contrast dye, but there is conflicting evidence as to whether this actually decreases risk.

Measuring intake and output for patients at risk for AKI are nursing measures that may help with early diagnosis and treatment. Proper fluid management and avoidance of hypovolemia may reduce the risk of AKI.

Pain Management and Early Mobilization

Pain management should be titrated to the patient’s needs. Ideally, pain medication should be adjusted so that the patient is comfortable during early ambulation and remains alert and oriented. Early mobilization is linked to shorter hospital stays and a decreased risk of venous thrombus. (36) Patients with femoral access sites will usually need to lie with the head of the bed in ≤15° for a minimum of six hours to ensure hemostasis, then they may resume sitting and walking activities.

Patients with other access sites may be able to ambulate sooner dependent upon hospital policy. Patients should make a goal of walking the unit at least 3-4 times a day if possible.

TAVR Nursing Care – Discharge Planning

Respiratory problems, infections, and bleeding events are the main reasons that TVAR nursing care patients are readmitted (18). Proper education throughout the hospital stay may help decrease the incidence of these events.

Most patients will be sent home on a regimen of aspirin and clopidogrel for at least six months to prevent thrombus formation of the newly placed valve. TAVR nursing care education should be provided for the patient on how to monitor their access site for any signs of bleeding and they should be aware that the clopidogrel will put them at greater risk for bleeding.

The patient should be instructed on how to keep the incision site clean and how to apply any dressings if necessary. Educate the patient undergoing TAVR nursing care, making them aware that ambulation along with coughing and deep breathing will decrease the chance of pneumonia and respiratory infections.

Any medication changes should be discussed, and the patient should go home with a medication reconciliation form stating what dose should be taken and at what time when discharged from TAVR nursing care.

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