Aortic Stenosis in Noncardiac Surgery Patients

Key action points in the management of aortic stenosis (AS) in noncardiac surgery patients include the following:

• AS results in changes to the left ventricular (LV) myocardium (eg, hypertrophy, reduced compliance, and increased end-diastolic pressures), and these changes make the patient more sensitive to increases in myocardial oxygen demand and decreases in systemic vascular resistance (SVR), coronary perfusion pressure (CPP), or preload; in severe AS, the LV cannot increase cardiac output by increasing stroke volume
• Patients with AS are at risk for increased complications after noncardiac surgery, including hypotension, myocardial ischemia or infarction, arrhythmias, heart failure, stroke, and death
• Proper triaging of AS patients for noncardiac surgery depends on identifying the urgency and risk of surgery, the degree of stenosis, the presence of symptoms related to valve pathology, the systolic function of the LV, and the presence of other valvular lesions
• Maintaining CPP, sinus rhythm, and adequate preload is important for anesthetic management of AS patients
• Appropriate hemodynamic monitoring for AS patients includes continuous arterial blood pressure (BP) monitoring and American Society of Anesthesiologists (ASA) standard monitors, and it may include monitoring with echocardiography or pulmonary artery catheterization (as dictated by the clinical scenario)
• Phenylephrine is the agent of choice for treatment of hypotension in AS patients; through its effect on alpha receptors, it increases systemic vascular resistance and maintains CPP without increasing chronotropy

AS is one of the most common valvular abnormalities. Severe AS has a prevalence of 1-2% in individuals aged 65-75 years and 3-5% in those older than 75 years. ^{[1, 2, 3, 4]} Several studies suggest that severe AS is associated with increased morbidity and mortality after noncardiac surgery. ^{[5, 6, 7]}  Perioperative complications in noncardiac surgery patients with AS include the following:

• Myocardial infarction (MI)
• Hypotension
• Arrhythmias
• Heart failure
• Stroke
• Death

Etiology and pathophysiology

Progressive calcific degeneration of the trileaflet aortic valve is the most common cause of AS, especially in the elderly population. Beyond advanced age, clinical risk factors for the development of AS include the following:

• Hypertension
• Hyperlipidemia
• Smoking
• Diabetes

Over time, inflammation, atherosclerosis and calcification thicken the aortic valve leaflets and restrict mobility. In patients with a bicuspid aortic valve (BAV), these degenerative changes occur at an earlier age as a consequence of the abnormal hemodynamics across the valve leaflets. Rheumatic heart disease, infection, and systemic lupus erythematosus (SLE) are other, albeit rare, causes of AS.

Regardless of the etiology, calcification of the aortic valve leads to stenosis, inevitably resulting in a fixed obstruction to LV emptying. In response to the progressive narrowing of the aortic valve opening, the LV myocardium becomes hypertrophic in order to generate increased pressure during systole and thus force blood past the obstruction.

Initially, these compensatory changes allow the LV to maintain cardiac output, and patients are asymptomatic. Over time, chronic pressure overload and compensatory LV hypertrophy result in reduced compliance of the LV, with the subsequent development of diastolic dysfunction and increased LV end-diastolic pressure (LVEDP). Additionally, myocardial hypertrophy results in increased wall tension and myocardial oxygen consumption.

If the ventricular wall hypertrophy is not able to compensate for the increase in afterload, LV systolic function may decrease, and heart failure can ensue. As the stenosis progresses, patients are unable to increase stroke volume, and as a result, they are unable to increase cardiac output so as to compensate for increases in myocardial oxygen demand.

Furthermore, the hypertrophic LV requires a higher CPP to maintain myocardial oxygen supply in the setting of increased end-diastolic pressure. Thus, decreases in SVR, such as occur during general anesthesia, can result in decreased CPP; patients become particularly susceptible to myocardial ischemia and are at risk for subsequent hemodynamic deterioration. Late in the disease course, patients develop a triad of AS symptoms, as follows:

• Angina - This occurs when oxygen demand exceeds oxygen supply to the myocardium
• Syncope - Usually exertional, this may occur as a consequence of the heart's inability to increase stroke volume in response to increased exertion or decreased peripheral vascular resistance (PVR); it may also be due to arrhythmias resulting from the imbalances in myocardial oxygen supply and demand
• Dyspnea - Generally a late symptom of AS, this is related to congestive heart failure (CHF), both systolic and diastolic, that develops as a result of the stenotic valve and changes to the myocardium

Staging

The severity of AS determines the appropriate course of therapy (ie, medical management or surgical intervention) for these patients. AS severity is staged on the basis of the following factors ^[8] :

• Degree of stenosis/valve hemodynamics
• LV ejection fraction (LVEF)
• Absence or presence of symptoms

Stages are defined as follows (see Table 1 below):

• Stage A - Patients at risk for AS
• Stage B - Patients with progressive hemodynamic obstruction
• Stage C - Patients with severe but asymptomatic disease
• Stage D - Patients with severe symptomatic AS 

Table 1. Stages of Aortic Stenosis ^[8] (Open Table in a new window)

Two subsets of severe AS (stages D2 and D3) are defined by low-flow and low-gradient valvular hemodynamics. In these subsets, AS is defined by an aortic valve area (AVA) of 1.0 cm² or less but a maximum aortic jet velocity (Vmax) of less than 4.0 m/s and a mean pressure gradient of 40 mm Hg or lower. The low velocity and low gradient are a result of a low flow rate across the valve that is due to either (1) poor LV systolic function (reduced LVEF) secondary to the valvular pathology or (2) LV hypertrophy with small ventricular volumes and resultant small stroke volumes despite a normal LVEF.

Some patients with a primary cardiomyopathy may have a low valvular gradient as a result of the reduced forward flow, which results in limited valve opening and a misleadingly low calculated valve area. These patients are considered to have so-called pseudostenosis because their symptoms are due to poor LV systolic function rather than valvular pathology.

A dobutamine stress echocardiogram can differentiate between patients with pseudostenosis and those with true AS by augmenting cardiac output. Patients with true AS will have an increase in the mean pressure gradient but no increase in the AVA, whereas patients with pseudostenosis will have an increase in the AVA but no increase in the mean pressure gradient.

Surgical interventions to relieve obstruction

Once symptoms are present, outcomes are extremely poor unless an intervention to relieve obstruction occurs. Accordingly, the 2014 American Heart Association (AHA)/American College of Cardiology (ACC) guideline for the management of patients with valvular heart disease made the following recommendations ^[8] :

• Aortic valve replacement (AVR) is recommended in patients with symptomatic severe AS (stage D) promptly after the onset of symptoms unless significant comorbid conditions exist that would prevent intervention (class I recommendation; level of evidence, B)
• AVR is also recommended for asymptomatic patients with severe AS and an LVEF of less than 50% (stage C2); in these patients, survival is better for those who undergo AVR than for those treated medically (class I recommendation; level of evidence, B)

Valve replacement may be performed via surgical or transcather approaches. Transcather aortic valve replacement (TAVR) has emerged as a valuable alternative to surgical AVR (SAVR) in the last decade. Studies have shown that TAVR is superior to medical management in patients ineligible for SAVR ^[9] and noninferior to SAVR in high-surgical-risk patients. ^{[10, 11]} The use of TAVR has also expanded to include intermediate-surgical-risk patients, with studies showing noninferiority to SAVR in this population. ^{[12, 13]}  

The 5-year follow-up for the PARTNER 2 trial, published in 2020, reported that the incidences of the composite end point of death or disabling stroke at 5 years were similar between surgical and transcatheter aortic valve patients, as were improvements in functioning status and quality-of-life measures. ^[14] TAVR was associated with higher incidences of paravalvular regurgitation, need for reintervention, and rehospitalization.

In view of these findings, the US Food and Drug Administration (FDA) has approved several ballon-expandable and self-expanding valves for use in intermediate-surgical-risk patients. The results of two large multicenter randomized controlled trials evaluating the role of TAVR (both balloon-expandable and self-expanding valves) in low-surgical-risk patients have been published. ^{[15, 16]} These trials both showed an advantage of TAVR over SAVR in the short term. 

In the PARTNER 3 trials, the rate of the composite end point of death, stroke, or rehospitalization at 1 year was significantly lower with TAVR than with SAVR, and TAVR was also associated with a significantly lower rate of new-onset atrial fibrillation (AF) and a shorter period of hospitalization. ^[15]

In the Evolut Low Risk Trial, TAVR was noninferior to surgery with respect to the composite end point of death or disabling stroke at 24 months, and it was associated with a lower incidence of bleeding complications, acute kidney injury, and AF. ^[16] However, TAVR was associated with a high incidence of moderate-to-severe aortic regurgitation and pacemaker implantation.

The data on long-term outcomes, including structural valve deterioration, in this patient population are still lacking. These trials also excluded patients with BAVs. Studies on this patient population are ongoing. A study by Yoon et al suggested that outcomes may vary according to valve morphology. ^[17] Randomized controlled trials are lacking at this time.

In 2017, the ACC partnered with several other societies to develop Appropriate Use Criteria for the treatment of patients with severe AS. ^[18] These guidelines were intended to help further identify and evaluate treatment options, including the appropriateness of TAVR versus SAVR, for a variety of clinical scenarios.

Current guidelines do not recommend AVR in patients with moderate AS unless cardiac surgery is required for other reasons. However, the presence of moderate AS in patients with heart failure who have a reduced ejection fraction remains challenging, in that the goal of pharmacologically reducing afterload to improve ejection fraction is hindered by presence of AS. The TAVR UNLOAD trial (NCT02661451), a multicenter randomized controlled trial, is under way to address whether reducing the transaortic gradient with TAVR will improve clinical outcomes in these patients. ^[19]

Addressing the problem; evidence-based recommendations

A detailed preoperative assessment and risk stratification are essential to deciding which AS patients should undergo noncardiac surgery. If the decision is made to proceed with surgery, careful consideration should be given to intraoperative monitoring and anesthetic approach.

Preoperative assessment

Evaluation of AS should begin with a thorough history and physical examination to assess for symptoms related to AS, as well as other cardiac risk factors. Physical examination may reveal the presence of a systolic ejection murmur with the following qualities:

• Middle to late peak intensity
• Loudest at the second right intercostal space
• Radiating to the carotids

Other associated clinical examination findings include the following:

• Slow rise and reduced peak in the carotid pulse
• Reduced intensity of the second heart sound (S2)

Although the physical examination can help detect the presence of aortic pathology, determining the severity of such pathology requires further investigation with echocardiography or cardiac catheterization. Because of its noninvasive approach, its good safety profile, and its ability to obtain diagnostic images in nearly all patients, echocardiography is the most commonly used means of diagnosing and quantifying aortic valve pathology.

On transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE), the severity of AS can be assessed by using Doppler measurements of Vmax, mean pressure gradient, and estimated AVA as determined by the continuity equation. During cardiac catheterization, transaortic pressures are directly measured, and AVAs are derived by using Gorlin’s equation. (See Table 2 below.)

Table 2. Classification of Aortic Stenosis Severity (Open Table in a new window)

Hemodynamically, severe AS is defined as follows:

• Vmax of 4.0 m/s or greater
• Mean transvalvular pressure gradient of 40 mm Hg or greater
• AVA of 1.0 cm ² or less, or AVA indexed for body surface area (BSA) of 0.6 cm ²/m ² or less (as estimated by the continuity equation)

The 2014 AHA/ACC guideline for the management of patients with valvular heart disease stated that “TTE is indicated in patients with signs or symptoms of AS or a bicuspid aortic valve for accurate diagnosis of the cause of AS, hemodynamic severity, LV size and systolic function, and for determining prognosis and timing of valve intervention.” ^[8]  Cardiac catheterization for assessment of AS was recommended only if noninvasive data are nondiagnostic or if there is a discrepancy between clinical and echocardiographic evaluation.

Similarly, the 2014 AHA/ACC guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery recommended that “patients with clinically suspected moderate or greater degrees of valvular stenosis or regurgitation should undergo preoperative echocardiography if there has been either 1) no prior echocardiography within one year or 2) a significant change in clinical status or physical examination since the last evaluation.” ^[20]

Preoperative risk stratification

Frequently used preoperative risk models for noncardiac surgery, including the American College of Surgeons (ACS) National Surgical Quality Improvement Program (NSQIP) Risk Calculator and the Revised Cardiac Risk Index (RCRI), do not include AS in their calculations of risk assessment. However, several studies suggest that severe AS is associated with increased morbidity and mortality after noncardiac surgery. ^{[5, 6, 7]}

Although many earlier studies did not differentiate between symptomatic and asymptomatic severe AS, emerging data suggest that during intermediate- to high-risk noncardiac surgery, patients with asymptomatic AS may have morbidity and mortality outcomes similar to those of patients without AS. ^{[7, 21, 22]} In a study by Agarwal, significant predictors of 30-day mortality and postoperative MI after noncardiac surgery were as follows ^[7] :

• High-risk surgery
• Symptomatic severe AS
• Coexisting mitral regurgitation
• Preexisting coronary artery disease (CAD)

Thus, these factors should be taken into account in assessing a patient’s suitability for noncardiac surgery.

Guidelines regarding noncardiac surgery in patients with severe AS have been published by the AHA/ACC ^[20] and by the European Society of Cardiology (ESC)/European Society of Anaesthesiology (ESA). ^[23] The AHA/ACC guidelines provide the following statements and recommendations ^[20] :

• Emergency noncardiac surgery may occur in the presence of severe AS
• For adults who meet indications for valvular intervention on the basis of symptoms and severity of stenosis, SAVR is recommended before elective noncardiac surgery to reduce perioperative risk (class I recommendation; level of evidence, C)
• Elevated-risk elective noncardiac surgery with appropriate intraoperative and postoperative hemodynamic monitoring is reasonable to perform in patients with asymptomatic severe AS (class IIa recommendation; level of evidence, B)

The recommendations of the ESC/ESA guideline are similar to those of the AHA/ACC guideline, as follows ^[23] :

• In patients with symptomatic severe AS, elective noncardiac surgery should be postponed, and valve replacement should be considered first
• In patients with asymptomatic severe AS, the risk of surgery should be taken into consideration; low- to moderate-risk noncardiac surgery may be safe, but high-risk surgery may pose an increased risk, and elective surgery should be performed only if strictly necessary; otherwise, patients should first be evaluated for possible SAVR or TAVR

In view of the morbidity and mortality associated with AVR procedures, replacing the valve may not be a viable option in every patient. Each patient must be evaluated carefully before the decision is made to proceed with either AVR or noncardiac surgery. The risks and benefits of both AVR and noncardiac surgery, as well as the patient’s preferences, should be considered.

Proper triaging of AS patients before noncardiac surgery is dependent on the urgency of surgery, the degree of stenosis, the presence of symptoms related to valve pathology, and LV function.

Intraoperative management

The perioperative risks associated with noncardiac surgery in the AS patient can be mitigated with careful preoperative planning and vigilant intraoperative management. Using the severity of stenosis and the risk of surgery as bases, the anesthesiologist must choose a suitable anesthetic approach and consider the appropriate level of intraoperative monitoring needed to provide optimal care.

Safe anesthetic management of these patients involves maintaining CPP, sinus rhythm, and adequate preload while avoiding tachycardia. General anesthesia or neuraxial (ie, spinal or epidural) anesthesia can be employed, depending on other anesthetic and surgical considerations, provided that any adverse hemodynamic effects are minimized.

The greatest concern with neuraxial anesthesia is the subsequent decrease in SVR associated with local anesthetic medications. The resulting hypotension can decrease CPP and precipitate cardiovascular collapse. However, the effects of neuraxial anesthesia on SVR can be mitigated with careful monitoring, meticulous fluid management, and appropriate medication administration.

In patients with mild-to-moderate AS who are undergoing low-risk surgical procedures, standard ASA monitors, including noninvasive BP monitoring, may be adequate; however, in patients with severe AS and those undergoing moderate- to high-risk procedures, more advanced monitoring is warranted. Invasive arterial catheterization allows continuous BP monitoring, enabling the anesthesiologist to react quickly to changes in afterload and optimize CPP. Placement of an arterial line before induction of anesthesia is often warranted to minimize the hemodynamic affects associated with induction agents.

With impaired LV compliance, maintaining preload is important. If large shifts in intravascular volume are expected, pulmonary artery catheterization may be helpful in assessing ventricular filling pressures and cardiac output; it may also be beneficial in patients with reduced LV systolic function as a means of tracking trends in mixed venous oxygen saturation and cardiac output. In addition, central venous access enables the administration of vasopressors and inotropic agents that may be needed to support hemodynamics.

Intraoperative echocardiography can provide real-time monitoring of ventricular systolic and diastolic function and assessment of wall motion and ventricular filling. TTE can be performed if optimal windows can be accessed during the case and are not limited by the surgical field. TEE offers the ability to carry out continuous monitoring in almost any clinical situation.

Maintaining sinus rhythm is vital in the setting of AS. In patients with reduced ventricular compliance and diastolic dysfunction, the atrial component of diastole may provide as much as 40% of ventricular filling. Arrhythmias are poorly tolerated by these patients. Additionally, tachycardia limits the time in systole and diastole, which may limit the heart's ability to increase stroke volume in response to increases in oxygen demand and decrease the diastolic coronary artery perfusion time. Significant bradycardia may also reduce the heart's ability to provide enough cardiac output in times of stress.

Electrocardiographic (ECG) monitoring is routinely performed as part of the ASA standard monitors and can help detect myocardial ischemia and identify arrhythmias that occur during anesthesia. TEE can also show signs of myocardial ischemia, with regional wall-motion abnormalities or changes in LVEF.

Phenylephrine is the preferred agent for treating hypotension. Through its alpha-agonist properties, phenylephrine increases SVR and maintains CPP without increasing chronotropy or inducing tachycardia. In patients with a reduced LVEF, inotropic agents (eg, norepinephrine or epinephrine) may be considered. However, these medications should be administered with caution and under advanced hemodynamic monitoring. Avoiding tachycardia and arrhythmias is of the utmost importance.

With close intraoperative monitoring and careful anesthetic planning, emergency and elective noncardiac surgical procedures can be performed safely and with an acceptable risk profile. Making the surgical team aware of the patient’s cardiac risk factors further conduces to safe surgery. Collaboration between the anesthesia and surgical teams permits the identification of appropriate intraoperative hemodynamic goals and fluid resuscitation strategies, as well as allows for changes in surgical techniques that may be warranted to minimize the risk of adverse outcomes.

Postoperative monitoring

For AS patients undergoing noncardiac surgery, it is also important to determine the optimal location for postoperative recovery. Depending on the patient’s comorbidities, intraoperative course, and expected postoperative hemodynamic changes, it may be necessary to arrange for postoperative recovery in a location that permits more intensive hemodynamic monitoring (eg, an intensive care unit [ICU] or a stepdown unit with telemetry). Again, maintaining adequate BP and preload and avoiding tachycardia and arrhythmias are crucial.

Inadequately treated pain may result in tachycardia; therefore, appropriate pain control with medications or regional anesthetic techniques should be encouraged.

Clinical scenario

A 67-year-old man presents to the anesthesia preoperative clinic before undergoing elective total knee replacement. His past medical history includes hypertension, diabetes, and hyperlipidemia. He denies any history of angina or heart attacks. He denies experiencing shortness of breath or chest pain with exertion, though he reports that his exercise tolerance is limited by severe knee pain. On examination, the presence of a loud, late-peaking systolic murmur is noted.

Resolution

This patient has several risk factors for CAD and AS. In addition, he has physical examination findings suggestive of a pathologic murmur. In patients with severe pain that limits mobility, it can be difficult to assess functional capacity or exercise tolerance. Often, patients with AS are diagnosed when cardiac auscultation reveals a systolic murmur. In this case, the elective procedure should be delayed to allow further cardiac workup.

Per the AHA/ACC guideline, when there is an unexplained systolic murmur or symptoms that might be due to AS, TTE is indicated as part of the initial evaluation “to confirm the diagnosis, establish etiology, determine severity, assess hemodynamic consequences” and determine risk stratification prior to noncardiac surgery. ^[8]  

Clinical scenario

A 54-year-old man with a history of BAV and mild AS presents for multilevel laminectomy and decompression for spinal stenosis. The patient reports that he last underwent TTE 5 years ago but states that he has not experienced any symptoms such as dyspnea, chest pain, or angina. The degree of his back pain is such that he is unable to walk up more than one flight of stairs. 

Resolution

This patient has known asymptomatic valvular heart disease and is scheduled to undergo an elective but nonetheless high-risk surgical procedure. Per AHA/ACC guidelines, he should have a preoperative TTE evaluation because his last echocardiogram was more than 1 year ago. ^[20] If the results of TTE show moderate or severe AS, proceeding with surgery may still be reasonable if advanced hemodynamic monitoring is provided, per the guidelines.

If the patient's AS is severe, consideration can be given to delaying his spine surgery and proceeding with AVR first. This discussion should occur during a consultation with a cardiothoracic surgeon. The patient's age makes him a likely candidate for a mechanical valve; however, this would require lifelong anticoagulation, which might complicate future spine surgery. The risks of AVR should be weighed against the risks of proceeding with this noncardiac surgical procedure.

If the patient proceeds with noncardiac surgery, intraoperative monitoring with a preinduction arterial line should be employed. When he is in the prone position, the ability to perform echocardiography will be limited. Thus, if a decreased ejection fraction or other concerning echocardiographic findings are noted, further advanced monitoring with a pulmonary artery catheter may be considered. This patient is likely to have significant blood loss and postoperative pain. Postoperative monitoring in an ICU or a stepdown unit with telemetry should be considered. 

Clinical scenario

A 72-year-old woman with known severe AS and normal LV systolic function presents with a femoral neck fracture after a fall down a flight of stairs at home. She reports occasional shortness of breath and lightheadedness when doing light housework.

Resolution

The surgical treatment this patient requires is an emergency and therefore should proceed. If the patient’s last echocardiogram was more than 1 year ago, preoperative TTE to assess for disease progression or a worsening ejection fraction is reasonable for guiding intraoperative management.

Either general or neuraxial anesthesia can be considered for this case, depending on the comorbid conditions present, the surgical plan, and the patient's preference. If a neuraxial technique is chosen, care should be taken to avoid hypotension, with fluid boluses and administration of phenylephrine to counteract the decrease in SVR caused by the local anesthetics. As in case example 2, a preinduction arterial line should be placed for BP monitoring.

It is also reasonable to perform TTE or TEE during the procedure to provide continuous monitoring or to aid in diagnosis should hemodynamic instability arise. Finally, it is important to discuss the patient’s valvular pathology with the surgical team so that intraoperative hemodynamic goals can be appropriately addressed. 

Clinical scenario

A 65-year-old man with symptomatic severe AS is scheduled to undergo a Whipple procedure for pancreatic adenocarcinoma. In view of the urgency of his medical condition, the decision is made to proceed with the Whipple procedure and defer SAVR. TTE done 5 months previously confirmed the patient's severe AS and showing moderately decreased LV systolic function, with an LVEF of 37%.

The patient undergoes general anesthesia after placement of a preinduction arterial line and epidural catheter. During the procedure, the anesthesiologist injects 5 mL of bupivacaine 0.125% into the epidural catheter. Five minutes later, the patient becomes hypotensive. 

Resolution

The severe AS, the presence of symptoms, and the reduced LV systolic function place this patient is at increased risk for adverse outcomes in the perioperative period. Accordingly, the intraoperative hypotension that develops in this case mandates immediate intervention and evaluation.

While IV fluids and phenylephrine are being administered, the anesthesiologist should seek the cause of the hemodynamic deterioration. The hypotension could be due to decreased SVR resulting from the recent administration of the bupivacaine bolus. General anesthetics can cause a decrease in SVR as well.

In addition, the surgical field should be assessed for recent blood loss; large decreases in preload will result in decreased ventricular filling and cardiac output. A survey of other hemodynamic parameters (eg, HR and cardiac rhythm) should be quickly carried out to assess for tachycardia or arrhythmia as a cause of hypotension.

If the patient does not respond to the interventions administered or if hypotension continues, myocardial ischemia and acute heart failure should be considered as possible causes. The anesthesiologist can consider obtaining TTE or TEE imaging to evaluate for new wall-motion abnormalities or signs of decreased cardiac output. If the LVEF has decreased, inotropic support may be required, but it must be judiciously administered.