Chapter 6. Aortic Valve Disease

• The aortic valve (AV) is the gateway through which the stroke volume is ejected from the left ventricle (LV) into the systemic circulation. When the AV is normal, systolic and diastolic pressures are maintained and the delivery of oxygenated blood to the tissues unencumbered. Should the gateway be narrowed as in aortic stenosis (AS), the LV hypertrophies concentrically to generate increased pressure to push the blood through the reduced aortic valve orifice. The thickened heart muscle and the increased work of ventricular ejection augments the oxygen demand of the ventricle, which if not met, can result in the development of myocardial ischemia. On the other hand, if the valve is incompetent resulting in aortic insufficiency or regurgitation (AR), the left ventricle will dilate and hypertrophy eccentrically to accommodate the increased volume filling the LV cavity during diastole. Diastolic pressure falls, and coronary perfusion pressure (CPP) decreases, increasing the risk of ischemia. Providing anesthesia for patients with AV disease undergoing aortic valve surgery or noncardiac procedures can be challenging.

The American Heart Association Task Force on Practice Guidelines reports the current recommendations for the management of patients with AV disease.1 Although in the past valvular diseases were most likely the consequence of rheumatic heart disease, currently, in an increasingly aging population, degenerative diseases of the valves are most frequently diagnosed.2 More than one in eight individuals older than 75 years of age have moderate or severe valvular heart disease of one type or another.2 Life span is reduced in patients with severe valvular disease (Figures 6–1 and 6–2). Additionally, elderly women may have underdiagnosed valvular heart diseases.2 Consequently, it is likely that as the population ages, AV disease will become ever more prevalent in cardiac surgical and noncardiac surgical patients alike. Sometimes, anesthesiologists are the first to diagnose a heart murmur during preoperative assessment.3 Van Klei et al in a study from the Netherlands found during routine preoperative examination a prevalence of 2.4% for AS in patients greater than 60 years of age scheduled for noncardiac surgery.3

The aortic valve is normally tricuspid, with semilunar cusps and an aortic valve area (AVA) of 2.5 to 3.5 cm2. The most common causes of AS are degenerative changes of a normal trileaflet valve (Figure 6–3) or of a congenital bicuspid valve (Figure 6–4 and Videos 6–1 and 6–2).4 Other congenital malformations of the AV, such as unicuspid and quadricuspid valves, although uncommon, can lead to aortic stenosis even in the adolescent population. However, the majority of patients will develop AS as a consequence of inflammation, lipid accumulation, and calcification of normal trileaflet valves associated with aging.5 Degenerative processes also contribute to the development of AR.

Aortic Stenosis

Severe AS is associated with an aortic valve area of less than 1.0 cm2. Calcification of the AV progresses with time which leads to the presentation of clinical symptoms including: angina, syncope, and dyspnea. With progressive stenosis, a pressure gradient develops across the valve and a systolic murmur results from the turbulent ejection of blood through the narrowed orifice. Over time, ventricular function can become impaired reducing the force of left ventricular ejection and surprisingly reducing the intensity of the murmur even as the stenosis itself remains unchanged or progresses. Patient survival following the onset of symptoms is fairly limited (2-5 y).6

Chronic Aortic Regurgitation

AR (Video 6–3) may occur as a consequence of any number of etiologies including: infectious endocarditis, rheumatic heart disease, connective tissue diseases producing aortic root dilatation, Marfan syndrome, vasculitis, and syphilis.1 Irrespective of the cause of AR the end result is the same. Namely, the leaflets of the aortic valve fail to coapt, allowing the retrograde flow of blood from the aorta into the left ventricular outflow track (LVOT) during diastole. The heart becomes volume overloaded from the incompetent valve, and develops eccentric hypertrophy and increased end-diastolic pressure.7 Patients frequently develop diastolic hypotension and a widened pulse pressure secondary to the run off of blood through the AV into the heart during diastole and the augmented ejection of blood volume during ventricular systole. Clinically, the patient with chronic AR frequently becomes dyspneic. Over time, the volume overloaded LV fails and heart failure ensues.

Acute Aortic Regurgitation

Unlike the patient with chronic AR, the acute AR patient often presents with pulmonary edema in the setting of acute congestive heart failure. The heart of the patient with chronic AR generally adapts to volume overload with time. The heart of the patient with acute AR is presented with a large, regurgitant volume challenge at the time of disease onset and does not have the opportunity to compensate. Such patients often present in cardiogenic shock. Conditions leading to acute AR include: aortic dissection, traumatic aortic injury, and endocarditis.

Combined Aortic Stenosis and Regurgitation

At times patients will manifest both AS and AR. Echocardiography can frequently help to discern the dominant physiologic derangement.

The heart of the patient with AV disease attempts to compensate for the additional pressure and/or volume work challenges presented to it by either an incompetent or a stenotic aortic valve.8

The LV of the patient with worsening AS attempts to produce ever-increasing ventricular systolic pressures in order to force blood through the narrowed aortic valve. Increased ventricular wall tension develops leading to an increased myocardial oxygen demand. Recall, LaPlace law:

Wall tension = (Ventricular pressure × Ventricular radius)/2 × Myocardial wall thickness

By increasing LV wall thickness, the heart compensates for the increased pressure necessary to overcome obstruction to systolic ejection. Increased wall thickness decreases wall tension. Although LV hypertrophy can over time compensate for worsening AS, compensatory adaptations have limits. Myocardial ischemia may develop secondary to inadequate blood supply to the thickened myocardium. The AS patient may also have coronary artery disease. Moreover, as wall tension increases and the heart becomes unable to compensate by increasing wall thickness myocardial oxygen demands increase even more. The thickened ventricle is also at risk for diastolic dysfunction because the hypertrophied LV is relatively noncompliant.9 Often the noncompliant ventricle tolerates volume challenges poorly and is heavily dependent upon atrial contraction to effectively load the LV during diastole. Particularly, the loss of the "atrial kick" through the development of atrial fibrillation greatly reduces the CO.

AR challenges the heart by overwhelming it with volume. Compensation in this instance is directed at increasing the heart's ability to push an increased blood volume out of the LV.10 The heart attempts to dilate in order to accommodate ever greater amounts of diastolic volume. By dilating, over time, the heart can increase its diastolic capacity with minimal change in left ventricular end-diastolic pressure (LVEDP). Whereas the AS ventricle becomes noncompliant, the AR ventricle becomes increasingly compliant.1 The LV hypertrophies eccentrically to respond to both volume and pressure work challenges. The increased volume load of the LV produces an increase in stroke volume (SV) and can contribute to an increase in systolic pressure. Over time the LV can no longer dilate sufficiently to remain highly compliant. As LV compliance becomes impaired, the heart is no longer able to accommodate increased diastolic volume with a minimal increase in diastolic pressure. Intraventricular pressures increase leading to reduced CPP and increased wall tension. Heart failure ensues. As time passes, the heart no longer compensates for the challenges presented to it, resulting in subclinical ischemia, myocyte cell death, LV fibrosis, and ventricular dysfunction.8

The patient with acute AR lacks the time for any compensatory remodeling of the heart's structure. In such instances, a rapid increase in left ventricular end-diastolic volume produces a dramatic rise in left ventricular end-diastolic pressure (LVEDP). The elevated LVEDP can result in myocardial ischemia and cardiogenic shock with systemic hypoperfusion and pulmonary edema. The anesthetic management of these patients can be very challenging as they frequently present to the operating room in cardiogenic shock.

Basic views and diagnostic approaches to the AV were presented in the introduction to echocardiography at the start of this text and should be briefly reviewed before proceeding with this section. The role of echocardiography in the management of these patients cannot be underestimated.1

Aortic Stenosis

The aortic valve can be examined in the midesophageal short-axis (MESAX) and long-axis views (MELAX) of the aortic valve. The MESAX provides an ideal opportunity to examine the three leaflets of the valve. By using color flow Doppler turbulent flow across the AV can be seen. Planimetry (Figure 6–5) of the stenotic valve permits a rough estimate of the valve area. Planimetry of the AV is performed by obtaining the midesophageal short-axis view. Once the leaflets are imaged, the freeze button is pressed. Using the trace function the valvular orifice is highlighted. Estimates of AV orifice area by planimetry are at times unreliable secondary to poor visualization of the valve or secondary to leaflet thickening and calcification.11

Stenotic orifice area can be calculated using the "continuity equation" which follows the conservation of flow or mass. As water flows down a river its velocity is slow where the river is wide and its velocity is fast where it is narrow—the rapids!!! The flow of blood thorough the LVOT and the aortic valve follows the same conservation law.

The aortic valve area can be calculated using either the conservation of flow or the conservation of mass.

According to the conservation of flow:

LVOT flow = AV flow

LVOT flow = LVOT CSA × LVOT Vmax

AV flow = AV CSA × AV Vmax

Therefore,

AV CSA = (LVOT CSA × LVOT Vmax)/AV Vmax

CSA = cross-sectional area

Vmax = maximal velocity

So if the velocity of blood in the LVOT is known and the cross-sectional area of the LVOT is also known, then the flow through the LVOT can be calculated. Obtaining the velocity of flow through the stenotic AV permits calculation of the stenotic valve area.

According to the conservation of mass, the same volume of blood that goes through the LVOT will traverse the AV:

LVOT volume = AV volume

LVOT volume = LVOT CSA × LVOT TVI

Recall that the TVI (time-velocity integral) represents the distance that the blood travels during systole as the result of the machine integrating the velocities with the systolic ejection time. The LVOT TVI is measured in the deep transgastric long-axis view, by placing the pulsed wave sample gate in the LVOT and tracing the spectral envelope obtained (Figure 6–6). The TVI is expressed in centimeters.

CSA is estimated by approximating the LVOT with a cylinder. CSA in this setting is estimated for that of a circle or πr2, where r is the radius of the circle. By measuring the LVOT diameter (d) (Figure 6–7), the CSA of the LVOT can be calculated:

LVOT CSA = 0.785 × d2 (cm2)

Knowing both the CSA and the TVI of the LVOT permits calculation of the volume of blood going across the LVOT during systole.

Next, using the deep transgastric long-axis view, the Doppler beam is aligned in parallel with flow across the stenotic aortic valve and continuous wave Doppler is used to obtain the maximal velocity and the TVI across the AV (Figure 6–8).

With these three elements it is possible to calculate the orifice area of the AV valve.

LVOT volume = AV volume

LVOT volume = LVOT CSA × LVOT TVI

AV volume = AV CSA × LVOT TVI

Therefore,

AV CSA = LVOT CSA × LVOT TVI/AV TVI

Pressure gradients across a narrowed aortic valve are also used as an estimate of the severity of AS. Here, too, echocardiography is essential in determining the maximal and mean pressure gradients across a narrowed orifice.

Recall from the introductory chapter the Bernoulli equation:

Pressure gradient = 4V2

where V is the maximal velocity.

Generally flow within the heart proceeds at a velocity < 1.2 m/s. In areas of narrowing, velocity can increase to upward of 5 to 6 m/s. Using Bernoulli equation it is clear that a 5 m/s velocity would be associated with a 100 mm Hg pressure gradient.

It must be remembered that a low-pressure gradient does not exclude a narrowed aortic valve. The ventricle must be capable of doing sufficient pressure work to generate pressures of this degree. As heart failure ensues the gradient can fall simply because the LV can no longer generate such dramatic intracavitary pressures.

Aortic Regurgitation

Echocardiography is likewise essential in the evaluation of AR.12,13 There are a number of approaches available to determine just how leaky the AV is. Anesthesiologists use everything from visual estimates of the regurgitant jet to more quantitative approaches.

AR can be evaluated in both MESAX and MELAX views of the aortic valve. Application of color flow Doppler in both views provides an image of the regurgitant flow during diastole. Both qualitative and quantitative methods are used to assess the severity of chronic AR.

One of the quantitative parameters is the width of the regurgitant jet relative to the width of the LVOT. Severe AR is associated with jets which occupy greater than 65% of the LVOT width.11 Unfortunately, the AR regurgitant jet can be subject to many factors unrelated to the severity of AR making it a less reliable estimate for AR severity.

Another quantitative parameter is the "vena contracta." Figure 6–9 demonstrates the vena contracta of a regurgitant jet. The vena contracta is the smallest diameter of the regurgitant jet measured at the level of the aortic valve. The size of the vena contracta should correspond to the area of the effective regurgitant orifice (EROA). Simply, vena contracta permits an estimation of how big is the leak through the aortic valve. A vena contracta greater than 6 mm is considered indicative of severe AR. An EROA greater than 0.30 cm2 is considered severe.

Most patients encountered by the cardiac anesthesiologist will already have their diagnosis and a surgical plan at the time of surgery and determination of the severity of AV disease is usually unnecessary perioperatively (Figure 6–10). Occasionally, moderate aortic stenosis or aortic regurgitation is detected during the course of surgery, which necessitates a discussion between the anesthesiologist and surgeon regarding course of action. The recent guidelines of the American Heart Association1 provide definitions for mild, moderate, and severe AV disease.1 Moreover, they provide guidelines for indications for AV replacement (AVR). While incidentally discovered severe AS will generally be addressed by the surgeon, the risks and benefits of surgical intervention in the setting of incidentally discovered moderate disease should be considered by the surgeon in consultation with the patient's cardiologist.

Once it has been determined that the AV requires replacement, the type of intervention must be determined. Bioprosthetic and mechanical valves are both employed in AVR. It is a surgical/patient decision as to the type of valve that is placed. The patient's tolerance for anticoagulation influences the choice of a mechanical or bioprosthetic valve. Ultimately the choice of valve and method of placement are not the considerations of the anesthesiologist. There is some evidence that in patients aged 50 to 70 years, a mechanical valve may offer advantages.14 Even patients with significantly reduced left ventricular ejection fractions are increasingly seen as candidates for valve replacement.15 Likewise, in patients with severe, asymptomatic AS, AVR has long-term benefit.16 Elderly patients too are increasingly seen as acceptable candidates for AVR.17 Consequently, it is likely that cardiac anesthesiologists will encounter patients for AVR who are older and have reduced ventricular function.

Various catheter-delivered aortic valves have also recently been employed in the management of elderly patients with severe aortic valvular disease and significant comorbidities18 (Figure 6–11). These are referred to as "minimally invasive" procedures and are either percutaneous or involve a small thoracic incision. Percutaneous aortic valve implantation techniques take many different forms. A femoral transarterial approach has been successfully employed to position a prosthetic valve.19 Likewise, a catheter can be introduced through a small incision into the apex of the left ventricle and a valve positioned within the aortic annulus. Risks of catheter-mediated valve placement include perivalvular leaks and stroke from embolic material as the native valve is pressed by expansion of the catheter-delivered prosthetic valve. During deployment of the valve, rapid ventricular pacing can be used to reduce cardiac output to permit correct seating of the valve in the aortic annulus. Valve migration and occlusion of coronary artery ostia can also complicate the procedure. It is likely that the use of catheter-mediated valves in elderly patients will increase with the aging population as the procedure is refined.

Traditional AV valve surgery is accomplished by the surgeon correctly sizing the valve and sewing it into position in the aortic annulus.20 Placement of too small a valve can lead to elevated transvalvular pressure gradients even in the setting with a perfectly working prosthetic valve. In such instances, ventricular dysfunction can progress in spite of surgery. At times surgeons will enlarge the aortic root to permit the placement of a larger valve. AVR surgery can be done through a full sternotomy, a partial sternotomy, or a mini thoracotomy.

The cardiac anesthesiologist must be familiar with the surgery as well as the valve placed and most importantly with its echo patterns. Video 6–4 demonstrates a bileaflet mechanical aortic valve. Video 6–5 shows a bioprosthetic valve in the aortic position. Perivalvular leaks, aorto-atrial fistulas, and aortic ruptures and dissections can occur and complicate AV replacement. TEE is useful in detecting these developments during the perioperative period. Oversewing of a coronary artery or coronary ostium, a rare complication, can likewise present during AV replacement resulting in ischemia and infarction. TEE can often be employed to demonstrate continuation of blood flow through the left main coronary artery (and occasionally the right coronary artery) following AVR (Video 6–6). Occlusion of a coronary artery should be suspected whenever there is new, unexpected ventricular wall motion abnormality following AVR. Although other etiologies can similarly impair ventricular function attempts to visualize flow in the coronary arteries by TEE can be helpful.

Anesthetic management of the AV surgery patient is formulated based upon the answers to the following questions:

• What is the dominant valvular pathology: AS or AR?
• What other cardiac pathologies are manifest?
• How well compensated is the patient?
• How are those compensatory mechanisms likely to be affected following the induction of anesthesia?

The patient with critical AS is at significant risk during anesthesia induction. The hypertrophied LV is in need of sufficient coronary blood flow to prevent myocardial ischemia. Moreover, the LV of the patient with AS is often noncompliant leading to an increase in LVEDP. Induction of anesthesia can reduce CPP producing myocardial ischemia. Maintenance of vascular tone with phenylephrine administration at the time of induction can reduce the development of perioperative hypotension associated with anesthesia induction. The fixed obstruction through the stenotic valve prevent the AS patient from augmenting CO should systemic vascular tone decrease at the time of induction. Consequently, patients can very quickly deteriorate and become profoundly hypotensive. Maintenance of sinus rhythm is essential as the atrial contraction contributes as much as 40% to the LV filling in the context of LV hypertrophy and diastolic dysfunction. Should the patient have coexisting coronary artery disease (and most patients probably do) the possibility of peri-induction hemodynamic collapse increases.

The choice of particular anesthetic agents for the AS patient matters less than managing the consequences of the loss of vascular tone or sinus rhythm. Should the patient experience hemodynamic collapse, various vasoconstrictors can be employed including phenylephrine, norepinephrine, and vasopressin. Vasopressin can restore vascular tone until the patient is placed on cardiopulmonary bypass. At times patients with severe AS can arrest during anesthetic induction simply because their cardiac reserve is such that loss of vascular tone leaves them too hypotensive to generate an effective CPP. In this instance, resuscitative measures are taken but efforts should be directed toward the rapid institution of cardiopulmonary bypass. Consequently, it is prudent to have both the surgeon and perfusionist readily available at the time of anesthetic induction in patients with limited cardiac reserve and severe aortic stenosis.

Anesthetic management of the AR patient is often dependent upon the degree of compensation and the time course of the patient's disease. The chronic AR patient often has had adequate time to develop compensatory mechanisms to maintain an adequate cardiac output. The dilated heart of the AR patient can generate a sufficient stroke volume in spite of a relatively low ejection fraction simply because of the size of the LV cavity. Moreover, the vasodilation and mild tachycardia, which often accompany anesthesia induction and maintenance, promote forward blood flow and reduce diastolic time—thereby reducing the degree of AR.

On the other hand, in those patients with long-standing AR and a noncompliant LV, the induction of anesthesia can produce problems similar to those encountered in the AS patient. In AR patients with poor ventricular compliance, LVEDP is increased. Anesthesia induction reduces the already low diastolic blood pressure producing dramatic reductions in CPP with resultant ischemia and hemodynamic collapse.

The acute AR patient will likely be in or close to cardiogenic shock. Such patients can present with acidosis, tissue ischemia, low cardiac output, and pulmonary edema. Frequently they will be on many vasoactive agents and will arrive intubated emergently to the operating room for an attempt at salvage. Anesthetic management may center solely upon administration of amnestics and muscle relaxants until the patient can be placed on CPB.

Following valve replacement, separation of the AV patient from bypass can be rather challenging. The thickened myocardium of the AS patient may have been underprotected with cardioplegia during CPB resulting in dysfunction and difficulty weaning from CPB. Likewise, the patient with a newly competent AV following long-standing AR can have a profoundly dysfunctional left ventricle. Intra-coronary air can also complicate the weaning process leading to ischemia and at times fibrillation in the immediate post bypass or postoperative period. Patients can experience both systolic and diastolic dysfunction. Strategies to weaning patients with poor LV function from CPB are discussed in Chapter 5.

The Patient with Mixed as/AR and the Emergency Institution of CPB

A 55-year-old man presents to the hospital following a syncopal episode. He is found to have aortic stenosis with an area of 0.7 cm2 and 50% occlusion of the left main coronary artery. Additionally he reports that following surgery for an appendix 3 years earlier he required admission to the ICU secondary to traumatic intubation. He reports that he was told never to have anesthesia without warning the staff that it is impossible to place a breathing tube in him!!

Case Questions

What are the anesthesia issues at play here? What other information would be helpful?

The patient has tight AS and is at great risk for myocardial ischemia during anesthesia induction. The AS and 50% left main occlusion place him at great jeopardy for hemodynamic collapse at the time of anesthesia induction. However, the airway issue has to be the first concern. Awake fiberoptic or video-assisted intubation can be performed in the patient at risk for cardiac collapse. Frequently it is useful to assign one anesthesiologist to monitor and manage the patient's hemodynamics while another focuses on securing the airway. Since tachycardia associated with awake intubation could exacerbate myocardial ischemia some degree of sedation and analgesia should be considered. It is important to understand that during the performance of an awake intubation the patient could arrest and collapse hemodynamically. Consequently, hemodynamic management is directed at avoiding tachycardia and maintaining systemic pressure.

The anesthesiologist also learns that the patient has a decreased ejection fraction of 25%. Following successful awake intubation, anesthesia is induced. How should one proceed?

Again, the choice of anesthetic agents is secondary to maintaining vascular tone and providing for a sufficiently long diastolic time to load the noncompliant heart of the AS patient. It may be safe to place a intraaortic balloon pump prior to induction in the effort to maintain adequate coronary perfusion pressure.

Bypass proceeds uneventfully and the surgeon places the valve seen on TEE in Video 6–6. What type of valve is this?

A tissue prosthetic valve has been placed.

Bubbles are seen on the TEE examination and the patient experiences VF arrest. What should be done?

If the patient remains connected to the CPB machine and no protamine has been given, the patient can be placed back on bypass. Additionally, the surgeon can attempt to defibrillate using internal paddles. Should the patient have already been given protamine, an additional full dose of heparin is required before returning to bypass should the VF be refractory to multiple shocks. Surgeons initiate open chest massage while they attempt to replace the CPB cannula. Once back on CPB, vasoconstrictors are used to increase mean arterial pressure to eliminate any trapped air from the coronary vasculature. Additionally, the surgeons will attempt to further remove air from the heart.