Thursday, March 18, 2021

Severe Aortic Stenosis in Non-Cardiac Surgery Case File

Posted By: Medical Group - 3/18/2021 Post Author : Medical Group Post Date : Thursday, March 18, 2021 Post Time : 3/18/2021
Severe Aortic Stenosis in Non-Cardiac Surgery Case File
Lydia Conlay, MD, PhD, MBA, Julia Pollock, MD, Mary Ann Vann, MD, Sheela Pai, MD, Eugene C. Toy, MD

Case 17
A 72-year-old woman presents with a long history of left shoulder pain recently increasing in intensity, and with a decreased range of motion over the past year. Her orthopedic surgeon has diagnosed a rotator cuff tear, and has scheduled her for an arthroscopic rotator cuff repair. The surgeon plans to perform this procedure in the “beach chair” position. The patient’s medical history is significant for severe aortic stenosis and moderate pulmonary hypertension. She experiences dyspnea after walking up one flight of stairs, which has been stable over a significant period of time. She can easily lay flat in bed at night, does not report paroxysmal nocturnal dyspnea, and has not had any recent episodes of syncope. The patient also has hypertension, well-controlled with metoprolol. She has no allergies to medications, and neither smokes nor consumes alcohol. Her review of symptoms is otherwise unremarkable.

The patient is 64 in tall and weights 65 kg. Her physical examination demonstrates a grade III/VI late-peaking systolic murmur, and lungs clear to auscultation. She has mild edema of her bilateral lower extremities. Her laboratory results are significant for a hematocrit of 32%, and are otherwise normal.

➤ What are the most important aspects of the evaluation prior to formation of the anesthetic plan for this patient?
➤ What are the goals for intraoperative hemodynamic management in patients with aortic stenosis?

Severe Aortic Stenosis in Non-Cardiac Surgery

Summary: A 72-year-old woman with severe aortic stenosis and pulmonary hypertension is scheduled for an arthroscopic rotator cuff repair to be performed in the beach chair position.

Preoperative evaluation: In patients with aortic stenosis, it is important to carefully probe for signs and symptoms of acute congestive heart failure, a history of syncope or near syncope, and functional exercise capacity prior to the development of an anesthetic plan. An ECG is useful to determine the presence or absence of sinus rhythm, and an echocardiogram unless the patient is currently followed and evaluated by a cardiologist.

Goals for intraoperative hemodynamic management: Patients with aortic stenosis include the avoidance of hypotension and tachycardia, and maintenance of a normal sinus rhythm and adequate preload.


1. Understand the etiology and pathophysiology of aortic stenosis.
2. Become familiar with the signs and symptoms of aortic stenosis, and recognize the importance of decompensated congestive heart failure and syncope in these patients.
3. List the intraoperative hemodynamic goals in patients with aortic stenosis, and the optimal ways of achieving them.
4. Be able to formulate an anesthetic plan for the patient with aortic stenosis presenting for non-cardiac surgery.

Since this patient is not symptomatic for her aortic stenosis, is in sinus rhythm and is closely followed by her cardiologist, she can safely proceed with the administration of anesthesia. Rotator cuffs are typically repaired under general anesthesia, with endotracheal intubation. The positioning of the patient in the “beach chair” position predisposes to venous pooling in the extremities resulting in hypotension, which is detrimental in the setting of aortic stenosis. Because of the significant possibility of hypotension following the induction of anesthesia and positioning in this 72-year-old patient, an arterial line for monitoring blood pressure is indicated. Since she is scheduled as the first case of the morning, insensible losses from her NPO status will be minimal, and since blood loss and fluid shifts are minimal for this type of surgery, no central line is indicated.

The optimal induction agent for this patient is etomidate, which causes less vasodilation and myocardial depression than the other anesthetic agents. Fentanyl is an opiate which reduces postoperative pain, and reduces heart rate, a desirable characteristic in patients with aortic stenosis. She will be paralyzed with vecuronium, and the relaxation reversed with neostigmine, and glycopyrrolate carefully titrated to minimize any changes in heart rate or blood pressure.

Severe Aortic Stenosis for Non-cardiac Surgery

As the average age of the American population increases, an ever-growing number of patients with heart disease will present for non-cardiac surgeries. Patients with aortic stenosis have significantly increased perioperative morbidity and mortality during non-cardiac surgery. An appropriate preoperative evaluation and risk-stratification, accompanied by a thorough understanding of hemodynamic variables is of paramount importance when anesthetizing these patients.


Aortic stenosis is the most common valvular lesion in the United States. It is either congenital, or acquired. Congenital aortic stenosis usually results from an incomplete development of the valve commissures, resulting in a unicuspid or bicuspid valve. A bicuspid aortic valve is the most common congenital valvular lesion, and is present in 1% to 2% of the population. This abnormal valve may present cause symptoms at birth, but more commonly, patients present with a murmur on examination in the fifth decade of life. The abnormal valve leaflets are more susceptible to hemodynamic stress which ultimately leads to valve thickening, calcification, and stenosis of the aortic orifice.

Acquired aortic stenosis is due to either calcific disease or rheumatic fever. Since the incidence of rheumatic valvular has declined dramatically over the past 50 years, aortic stenosis resulting from rheumatic fever is a rare occurrence. Calcific disease of a tri-leaflet valve accounts for the vast majority of aortic valve disease, and most likely reflects an inflammatory process with similarities to atherosclerosis. Calcific aortic stenosis occurs more often in males than in females, and symptoms are typically manifest in the seventh decade of life. Regardless of the etiology, the natural course of aortic stenosis is a long, asymptomatic latent period followed by the onset and rapid progression of symptoms.

Aortic stenosis is defined as a restriction in the opening of the aortic valve’s leaflets leading to an obstruction to flow during systole. This fixed obstruction produces a pressure gradient across the left ventricular outflow tract and aortic root, requiring the ventricle to generate an increased systolic pressure in order to produce flow across the valve. The normal aortic valve area is 2.5 to 3.5 cm2. Hemodynamic changes due to obstruction are generally not observed until the valve area is less than 1.0 cm2. Aortic stenosis is considered severe if the peak gradient across the valve is > 50 mm Hg, or if the valve area is < 0.8 cm2. The definition of the varying degrees of aortic stenosis is detailed in Table 17–1.

Over time, the increased pressures generated by the left ventricle lead to increases in ventricular wall tension in accordance with the law of Laplace:

Wall tension = [Pressure × Radius]/[Wall thickness × 2]

Concentric left ventricular hypertrophy also develops as a compensatory mechanism, to reduce wall tension while allowing the pressure overloaded ventricle to maintain stroke volume. As the walls of the left ventricle become thickened, they become less compliant. Thus filling during diastole is impaired (also known as diastolic dysfunction). Ventricular filling increasingly depends upon an adequate diastolic time, and upon the atrial contraction or “kick” during diastole. Thus, the maintenance of normal sinus rhythm in these patients is very important and tachycardia of any type is poorly tolerated. The maintenance of an adequate preload is also important for the optimal function of a stiff and noncompliant ventricle. However, as atrial pressures increase in response to the increasing left ventricular end diastolic pressures, pulmonary edema and pulmonary hypertension can result.

Signs and Symptoms
Patients with mild to moderate aortic stenosis are generally asymptomatic. Patients with severe aortic stenosis may present with angina, syncope, and/or shortness of breath. Angina can occur in the absence of coronary disease, due to the large, thick ventricle’s imbalance between myocardial oxygen supply








Peak gradient (mm Hg)


< 25


> 50

> 70

Aortic valve area (cm²)

> 2




< 0.7

and demand. An hypertrophic left ventricle has a greater oxygen demand due to its increased mass, and its generation of higher systolic pressures. The supply of oxygen to the hypertrophic ventricle is reduced by compression of the coronary arteries during systole. Dyspnea and orthopnea may reflect pulmonary edema associated with diastolic congestive heart failure. Syncope results from inadequate cerebral perfusion.

The onset of symptoms in patients with aortic stenosis has significant prognostic implications. Patients with angina have a 50% 5-year survival rate; patients with syncope or dyspnea have survival rates of 50% at 3 and 2 years, respectively. Consequently, the need for surgical intervention is based primarily upon the development of symptoms. Ironically, the aortic valvular area at which symptoms develop is variable.

Preoperative Evaluation
The preoperative evaluation of a patient with aortic stenosis presenting for non-cardiac surgery focuses on identifying patients at high risk. It is imperative that the severity of aortic stenosis be determined prior to any elective surgery. A careful history elicits any symptoms of aortic stenosis including angina, syncope, shortness of breath, and/or signs of heart failure such as peripheral edema, orthopnea, dyspnea on exertion, and paroxysmal nocturnal dyspnea. The patient’s general level of activity and exercise tolerance, and the New York Heart Association functional classification of heart disease are also useful tools for estimating the severity of heart disease and estimating prognosis (Table 17–2).

On physical examination a harsh, mid-systolic crescendo-decrescendo murmur heard best over the right sternal border at the second intercostal space is characteristic of aortic stenosis. This murmur may radiate upward toward the carotid arteries. The preoperative physical examination should focus on uncovering signs of heart failure. Thorough auscultation of the chest may reveal rales, wheezing or an S3 gallop, examination of the neck, jugular venous distension, and examination of the extremities and abdomen, pitting edema or ascites.








Asymptomatic except during severe exertion

Symptomatic with moderate activity

Symptomatic with minimal activity

Symptomatic at rest

An important tool in evaluating the severity of aortic stenosis is the Doppler and two-dimensional transthoracic echocardiography. If aortic stenosis is symptomatic, elective non-cardiac surgery should be canceled or postponed until after valve replacement surgery. If the patient refuses corrective valve surgery, non-cardiac surgery is accompanied by a mortality risk of approximately 10%. Elective surgery should be postponed or canceled for patients with severe asymptomatic aortic stenosis if the valve has not been evaluated within the past 12 months. Table 17–1 shows the valve areas and peak gradients associated with mild, moderate, and severe aortic stenosis.

Echocardiography will also detail other cardiac valve lesions. A current ECG should also be obtained, and may reveal left ventricular hypertrophy or myocardial ischemia. A chest radiograph may be warranted to rule out pulmonary edema if signs of congestive heart failure are present on examination.

Anesthetic Management
The intraoperative management of patients with aortic stenosis is based upon maintaining a normal sinus rhythm at a rate of 60 to 75 bpm, an adequate preload, and adequate systemic vascular resistance (SVR). In addition to the standard ASA monitors including the measurement of blood pressure and an ECG, invasive monitoring should be considered. Patients with severe aortic stenosis are often intolerant of even brief periods of hypotension. Given the expected hemodynamic perturbations associated with induction of anesthesia, intubation, and varying surgical stimulation, an arterial line is often indicated.

Monitoring of central venous and pulmonary artery pressures may be indicated if the surgical procedure will involve large fluid shifts or the use of vasodilators. As noted in the AHA Guidelines, the substantial risks of PA catheter placement must be weighed against the potential benefit of the data obtained in each individual patient. In this particular patient, the hemodynamic changes associated with reverse Trendelenburg or the “beach chair” position in combination with the severity of her aortic valve disease may warrant placement of a PA catheter.

Alternatively (or in combination with a PA catheter), transesophageal echocardiography may also be used to assess the effect of intraoperative therapeutic interventions. Alterations in cardiac filling and wall motion with therapeutic interventions and patient repositioning are quickly assessed using this relatively low-risk invasive monitor. However, neither the intraoperative use of a pulmonary artery catheter nor transesophageal echocardiography has been shown to change outcomes in patients with aortic stenosis presenting for non-cardiac surgery.

The anesthetic technique employed is of secondary importance as long as the hemodynamic goals of maintaining SVR, a slow heart rate, adequate preload, and normal sinus rhythm are met. Spinal and epidural anesthesia are typically well tolerated in patients with mild to moderate disease. These blocks have been relatively contraindicated in patients with severe disease, but with invasive monitoring and careful titration of agents, spinal and epidural anesthesia have been safely used in patients with severe aortic stenosis.

A balanced general anesthetic technique employing opiates, volatile anesthetics, and muscle relaxants is often employed. Since many agents typically used for the induction and maintenance of general anesthesia cause vasodilation and thus hypotension, careful titration of these agents is of critical importance. Alpha agonists such as phenylephrine treat hypotension, and maintain or increase SVR. Agents that increase inotropy are generally ineffective in patients with aortic stenosis, as the left ventricle is already in a highly contractile state, and the tachycardia often associated with these agents is undesirable. Hemodynamically-significant intraoperative arrhythmias should be promptly treated with synchronized cardioversion. In the event of cardiac arrest, restoring perfusion is important. However, chest compressions are generally ineffective given the extreme hypertrophy that often accompanies significant aortic stenosis. Nonetheless, in the event of an intraoperative arrest, the advanced cardiac life support (ACLS) algorithms should be applied.

Patients with severe aortic stenosis should be monitored closely for at least 24 hours after surgery including minor ambulatory procedures. For major surgeries involving large fluid shifts or patients with significant pulmonary hypertension, postoperative monitoring overnight in the intensive care unit should be strongly considered. In patients with severe aortic stenosis, the risk of cardiac death remains elevated in the immediate postoperative period.

Comprehension Questions

17.1. During your preoperative assessment, a 72-year-old man complains of dyspnea on exertion and intermittent chest pain. Upon auscultation of his heart, you notice a mid-systolic crescendo-decrescendo murmur that radiates to his carotid. This murmur is most characteristic of which valvular lesion?
A. Mitral stenosis
B. Mitral regurgitation
C. Aortic regurgitation
D. Aortic stenosis

17.2. What statement about the pathophysiology of aortic stenosis is most likely true?
A. Patients with aortic stenosis have decreased myocardial oxygen demand as the left ventricular hypertrophy offers a “protective” effect.
B. The increased pressure gradient between the left ventricle and aorta results in eccentric left ventricular hypertrophy.
C. Patients with aortic stenosis can develop impaired left ventricular filling because of diastolic dysfunction.
D. Myocardial ischemia in aortic stenosis is rare in the absence of coronary artery disease.

17.3. You will be taking care of a 72-year-old woman with a history of severe aortic stenosis (valve area 0.7 cm2) for a laparoscopic cholecystectomy. You are planning a general anesthetic with sevoflurane. What will be the hemodynamic goal for this patient?
A. Low systemic vascular resistance
B. Heart rate between 60 to 75 beats per minute
C. Low preload
D. Increased contractility

17.4. During insufflation of the peritoneum with carbon dioxide, the patient becomes hypotensive (blood pressure 60/48) while the heart rate remains unchanged at 84 beats per minute. You ask the surgeon to decrease the pneumoperitoneum; however, the blood pressure remains low. Which of the following would be the best course of action?
A. Administer an alpha-agonist drug such as phenylephrine.
B. Administer nitroglycerin.
C. Administer a beta agonist, such as dobutamine.
D. Administer an inotropic agent such as epinephrine.

17.1. D. The murmur described is characteristic of aortic stenosis. The murmur of mitral stenosis is a mid-diastolic rumbling murmur, best heard at the apex with the patient in the left lateral position. The murmur of mitral regurgitation is typically a holosystolic murmur that may radiate to the axilla. The murmur associated with aortic regurgitation is a mid-systolic ejection murmur generally heard best at the base of the heart and is transmitted to the jugular notch.

17.2. C. The pathophysiology of aortic stenosis involves left ventricular outflow obstruction with the subsequent development of a pressure gradient between the left ventricle and the aorta. This results in concentric left ventricle hypertrophy rather than an eccentric hypertrophy. As a result of left ventricular hypertrophy, myocardial oxygen consumption is increased and patients can develop myocardial ischemia as a result of increased myocardial oxygen consumption and decreased myocardial oxygen supply. Also as a result of left ventricular hypertrophy, ventricular relaxation and filling during diastole is impaired.

17.3. B. The hemodynamic goals for patients with aortic stenosis include maintenance of preload, systemic vascular resistance, contractility, and a sinus rhythm, as well as the avoidance of tachycardia. Because of their relatively fixed stroke volume, patients with aortic stenosis are dependent on adequate filling/preload. Tachycardia and rhythms other than sinus rhythm (ie, atrial fibrillation) are poorly tolerated and can be harmful. Patients with aortic stenosis have a fixed resistance at the level of the aortic valve; thus, maintenance of systemic vascular resistance is important to preserve diastolic coronary perfusion gradients. In patients with aortic stenosis, contractility should be preserved.

17.4. A. Hypotension is poorly tolerated in patients with severe aortic stenosis. Myocardial ischemia can develop rapidly; hence prompt recognition and treatment of hypotension is critical. In contrast to inotropic agents such as epinephrine or dobutamine, alpha agonists such as phenylephrine are generally regarded as the treatment of choice for hypotension, to restore coronary perfusion pressure. Vasodilators such as nitroglycerin can be harmful because of the potential for hypotension from decreased preload and afterload.

Clinical Pearls
➤ The hemodynamic goals for managing patients with aortic stenosis include maintaining sinus rhythm, a normal to high preload, normal to high SVR, and slow heart rate. As long as these goals are met, anesthesia can be maintained with many different techniques.
➤ Alpha agonists such as phenylephrine are the treatment of choice for hypotension.
➤ With severe aortic stenosis, ventricular relaxation and compliance are altered necessitating higher left ventricular filling pressures. Congestive failure and pulmonary edema may result.
➤ Arrhythmias are poorly tolerated in patients with severe aortic stenosis, and should be immediately treated with cardioversion.
➤ Elective (non-cardiac) surgery should be postponed or canceled for patients with symptomatic aortic stenosis, or for those with severe asymptomatic aortic stenosis if the valve has not been evaluated within the past 12 months.
➤ Cardiopulmonary resuscitation (CPR) is often unsuccessful in this setting.


ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: Executive Summary. Circulation. 2007;116:1971-1996. 

Cook D, Housmans P, Rehfeldt K. Valvular heart disease. In: Kaplan’s Cardiac Anesthesia. 5th ed. Saunders Elsevier; 2006: 645-690. 

Mends LA, Loscalzo J. Acquired Valvular heart disease. In: Andreoli, ed. Cecil Essentials of Medicine. 5th ed. Philadelphia, PA: W.B. Saunders Co; 2001: 69-70. 

Mittnacht Alexander JC, Fanshawe M, Konstadt S. Anesthetic considerations in the patient with valvular heart disease undergoing non-cardiac surgery. Semin Cardiothorac Vasc Anesth. 2008;12(33): 33-59.


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