Aortic Stenosis

Description

The aortic valve normally consists of 3 leaflets which open during ventricular systole with an area of >2.5 cm² and close during diastole. Since the aortic valve is the smallest area through which blood leaves the heart, its diameter determines maximum blood flow.
Aortic valve stenosis is a narrowing of this area at the valve itself. New recommendations classify severe aortic stenosis (AS) as an area <1.0 cm² with a transvalvular mean gradient >40 mm Hg, although symptoms may begin at much earlier stages. It is the most common valvular lesion in the US.

Epidemiology

Incidence

Congenital AS occurs in 4–8 per 1,000 live births.
Congenitally bicuspid aortic valves occur in 1–2% of the US population and later in life accounts for 30–40% of AS.
>50% of AS is acquired.

Prevalence

Present in 2–4% of adults aged 65 years and older (1) [B].

Morbidity

Risk for acute myocardial infarction, syncope, congestive heart failure (CHF), and endocarditis
Low-grade severe stenosis with preserved ejection fraction has similar outcomes to those with moderate stenosis (2) [B].
Asymptomatic very severe AS (area <0.75 cm²) has a very poor prognosis and rapid deterioration; elective valve surgery should be considered (3) [A].

Mortality

9% mortality per year
Symptomatic AS sudden death risk is 15–20% with a 3-year mortality of 75%.
When symptoms of angina, syncope, or CHF are present, 50% mortality is seen at approximately 5, 3, and 2 years, respectively.

Etiology/Risk Factors

Age <70 years: The etiology of AS is more commonly rheumatic or bicuspid aortic valve disease.
Age >70 years: The etiology of AS is more commonly calcific AS.
Risk factors are similar to vascular disease and may include hyperlipidemia, hypertension, and diabetes.

Physiology/Pathophysiology

The basic pathophysiology of AS stems from obstruction of cardiac output with a highly resistant valve opening. As the stenosis becomes more severe, the left ventricle (LV) compensates with concentric hypertrophy to overcome the increasing afterload/tension; stroke volume is maintained. Additionally, cardiac output becomes fixed and highly dependent upon heart rate and filling (diastolic dysfunction).
Myocardial oxygen supply and demand
- Supply decreases from: A thickened myocardium (coronary blood flow must perfuse/penetrate), increased left ventricular end diastolic pressure (decreased coronary diastolic perfusion pressure), and limited cardiac output.
- Demand increases from: A thickened myocardium (more muscle equals increased energy consumption) and increased afterload.
Over time, systolic function can decrease as the LV decompensates and dilates or becomes ischemic. Ventricular systolic and diastolic dysfunction can lead to pulmonary congestion and CHF. Additionally, sympathetic tone increases and may contribute to symptoms.
A slow heart rate is desired to allow time for forward flow after an adequate LV pressure has been attained. Maintaining a sinus rhythm is necessary, as LV hypertrophy impairs filling and the atrial kick is needed to maintain adequate LV end diastolic volume (preload).
Both normal and congenitally bicuspid valves undergo degeneration through which scarring, calcification, and sclerosis become the most common cause of acquired AS.

Anesthetic GOALS/GUIDING Principles

Maintenance of cardiac output, coronary perfusion (diastolic perfusion pressure), normal sinus rhythm, volume status, and prevention of cardiac decompensation are the primary goals.
Inotropic support may be necessary to prevent cardiovascular overload or collapse.

Symptoms

Severity of symptoms may be classified by NYHA I–IV. Early symptoms often include exertional shortness of breath.
- Anginal pain may be an early symptom and may occur in the absence of coronary occlusion.
- Syncope may occur due to a decrease in cardiac output and exertional systemic vasodilation.
- CHF is often a late sign that signifies severe valve stenosis or cardiomyopathy.

History

Commonly diagnosed after symptomatic exercising or during workup for diastolic or systolic CHF
May be discovered early after detailed physical exam and heart auscultation

Signs/Physical Exam

Crescendo–decrescendo systolic murmur and decreased S2 sound
Pulsus parvus et tardus with narrow pulse pressure
Signs of CHF and increased sympathetic tone

Treatment History

Previous history of balloon aortic valvuloplasty or valve replacement

Medications

Antihypertensives including beta-blockers and calcium channel blockers
Anti-anginals including nitrovasodilators
Heart failure treatments including digoxin, ACEI/ARB, and diuretics
Statin therapy

Diagnostic Tests & Interpretation

Labs/Studies

Basic metabolic profile to monitor electrolytes and kidney function; aids with perioperative management
CBC: WBC to monitor for infection; Hct and platelet counts should be adequate for surgery.
CXR to assess cardiopulmonary status
Echocardiogram for diagnosis and classification of disease severity (valve area, transvalvular gradient) and ventricular function
Basic coagulation studies to evaluate liver function

CONCOMITANT ORGAN DYSFUNCTION

Cardiac: LV hypertrophy, diastolic dysfunction, hypertension, aortic regurgitation (due to poor valve closure), mitral stenosis, or regurgitation in rheumatic heart disease
Pulmonary: Hypertension, congestion, and pleural effusion
Renal insufficiency

Circumstances to delay/Conditions

Decompensated CHF
Sepsis or infection
Unrelated end-organ failure
Recent myocardial infarction or stroke

Classifications

AS severity by valve area:
- >2.5 cm²: Normal
- 1.5–2.0 cm²: Mild stenosis
- 1.0–1.5 cm²: Moderate stenosis
- <1.0 cm²: Severe stenosis
AS severity by mean pressure gradient:
- <25 mm Hg: Mild stenosis
- 25–40 mm Hg: Moderate stenosis
- >40 mm Hg: Severe stenosis

PREOPERATIVE PREPARATION

Premedications

Benzodiazepines may be useful to prevent anxiety and tachycardia; however, they should be titrated cautiously to avoid sympatholysis.

INTRAOPERATIVE CARE

Choice of Anesthesia

Depends on the procedure: Sedation, general (endotracheal tube or laryngeal mask airway) and peripheral nerve blocks may be utilized.
Neuraxial techniques can result in a sympathectomy and decreased systemic vascular resistance (SVR) that can impair coronary perfusion. This technique may be considered in mild or moderate AS. Epidurals can allow for slower bolusing, time for fluid loading, and treatment of hypotension with vasopressors (phenylephrine).

Monitors

Standard ASA monitors
5-lead EKG for arrhythmia and ischemia
Arterial line for beat-to-beat BP monitoring
Invasive monitors may be chosen based upon the severity of AS and the surgical procedure.

Induction/Airway Management

A smooth, controlled induction should be performed to maintain vital signs within normal limits (heart rate and SVR) and allow time for treatment.

Maintenance

Volatile anesthetics, intravenous, or a combination may be utilized. The goal should be to maintain normal sinus rhythm and SVR.
- Total intravenous anesthesia with propofol and high-dose narcotics can result in bradycardia and hypotension; consider concurrent phenylephrine, ephedrine, or an anticholinergic.
- Volatile agents can decrease SVR and myocardial contractility; consider concurrent phenylephrine.
Preload. Because stroke volume is fixed, adequate filling volumes are essential in maintaining a stable cardiac output. for patients at risk for ischemic events, hematocrit values may also be of concern.
Rhythm, rate, blood pressure
- Normal sinus rhythm may be maintained by minimizing cardiac stress and avoiding pro-arrhythmic drugs
- Slight bradycardia may improve coronary perfusion time and LV filling but may decrease total cardiac output (stroke volume is fixed). Conversely, tachycardia increases myocardial oxygen consumption along with decreases in LV filling time and diastolic coronary perfusion time. Caution should be exercised when using powerful chronotropes or anticholinergics.
- Hypotension and hypertension should be managed with rate and rhythm in mind. All inotropes and vasopressors may be used with caution.
Ischemia usually occurs with arrhythmia, tachycardia, or hypotension, and the treatment usually lies in the reversal of those conditions.

Extubation/Emergence

Avoid tachycardia and hypotension
Use standard extubation criteria

Bed Acuity

Depends on surgical procedure, severity of underlying disease, and intraoperative events

Medications/Lab Studies/Consults

Cardiology consult may be considered in severe disease if ischemic events occurred intraoperatively.

Complications

Perioperative arrhythmia
Mental status changes and stroke
Myocardial infarction

Freeman RV , Otto CM. Spectrum of calcific aortic valve disease: Pathogenesis, disease progression, and treatment strategies. Circulation. 2005;111(24):3316–3326.
Jander N , Minners J , Holme I , et al. Outcome of patients with low gradient "severe" aortic stenosis and preserved ejection fraction. Circulation. 2011;123(8):887–895.
Rosenhek R , Zilberszac R , Schemper M , et al. Natural history of very severe aortic stenosis. Circulation. 2010;121(1):151–156.

andritsos M , Singh N , Patel P , et al. The year in cardiothoracic and vascular anesthesia: Selected highlights from 2010. J Cardiothorac Vasc Anesth. 2011;25(1):6–15.

See Also (Topic, Algorithm, Electronic Media Element)

ICD9

395.0 Rheumatic aortic stenosis
424.1 Aortic valve disorders
746.3 Congenital stenosis of aortic valve

ICD10

I35.0 Nonrheumatic aortic (valve) stenosis
Q23.0 Congenital stenosis of aortic valve
I06.0 Rheumatic aortic stenosis

Severity is classified by valve area and transvalvular gradients; values <1.0 cm² and a mean pressure gradient of 40 mm Hg indicate severe AS.
Maintenance of general anesthesia includes supporting cardiac systolic function, optimizing fluid management, sustaining normal sinus rhythm, and monitoring for ischemia.

Brian L. Marasigan , MD

section name header

Basics ⬇

Incidence

Prevalence

Morbidity

Mortality

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆

section name header

Basics ⬇

Incidence

Prevalence

Morbidity

Mortality

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Special Concerns for Informed Consent

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆