Aortic stenosis





A 65-year-old woman presented for aortic valve replacement. She had a history of congestive heart failure (CHF). Cardiac catheterization showed a peak systolic gradient of 90 mm Hg between the left ventricle and the aorta. During anesthetic induction with fentanyl and vecuronium, the patient developed a junctional rhythm and severe hypotension.





Describe the symptoms of and long-term prognosis for aortic stenosis.


The classic symptoms in patients with severe aortic stenosis (AS) are angina, syncope, and CHF. Life expectancy in untreated cases is approximately 5 years after developing angina, 3 years after developing syncope, and 2 years after developing CHF. Angina is present in approximately 66% of patients with critical AS, but only about 50% have clinically significant coronary artery disease (CAD). Patients without CAD develop angina because of inadequate oxygen delivery to hypertrophied myocardium. There is also evidence that patients with moderate to critical AS (i.e., aortic valve area 0.7-1.5 cm 2 ) are at increased risk for morbidity, which worsens with the onset of symptoms. Some clinicians recommend that aortic valve replacement should be performed promptly in symptomatic patients. However, percutaneous interventions, such as balloon valvuloplasty and percutaneous transcatheter aortic valve implantation (TAVI), may be indicated depending on the clinical situation.


Concentric left ventricular hypertrophy occurs in AS, as defined by increasing left ventricular wall thickness in a symmetric fashion without ventricular dilation. The advantage of a hypertrophied myocardium is the greater intraventricular pressure generated with a smaller increase in wall tension. The relationship between wall tension (T), intracavitary pressure (P), left ventricular radius (R), and wall thickness (h) is described by the law of Laplace: T = (P × R)/2h.


Tension generation in myocytes is the most inefficient way of performing cardiac work because it requires large amounts of oxygen. In patients with left ventricular hypertrophy, oxygen delivery is decreased because left ventricular end-diastolic pressure (LVEDP) is increased. Increased LVEDP decreases coronary perfusion pressure (CPP). CPP is defined as diastolic aortic pressure minus LVEDP.


As the severity of AS increases, a decrease in diastolic aortic pressure compromises CPP even more. The hypertrophied myocardium also results in decreased left ventricular compliance and higher left ventricular filling pressures, which leads to diastolic dysfunction and impaired cardiac filling. Neovascularization of the pressure-overloaded heart is inadequate for the degree of hypertrophy. Finally, the isovolumic phase of relaxation is inappropriately long, shortening the filling period of diastole, which diminishes the time for coronary perfusion. For all these reasons, patients with AS are prone to developing myocardial ischemia during anesthesia.


Syncope is the initial symptom of AS in 15%–30% of patients. It is usually exertional and is caused by exercise-induced vasodilation in the face of a fixed cardiac output. CHF portends the worst long-term prognosis. CHF occurs when the heart has exceeded its capacity to compensate for pressure work with myocardial hypertrophy. The heart progressively dilates, and symptoms of left ventricular failure appear.





Identify the etiology of aortic stenosis.


AS may be congenital or acquired. In adults, a congenitally bicuspid valve may become calcified and stenotic. Senile calcification of a trileaflet aortic valve is common in patients >70 years old. Rheumatic AS is almost always associated with rheumatic mitral valve disease. This etiology is becoming less common in developed countries because of the widespread use of antibiotic therapy.





What is the significance of aortic valve area and how is it calculated?


The normal aortic valve area is 2.5-3.5 cm 2 . According to the American College of Cardiology/American Heart Association (ACC/AHA) guidelines, valve area <1.0 cm 2 , peak transvalvular velocity >4.0 m/sec, and mean transvalvular gradient >40 mm Hg are considered to be parameters of hemodynamically severe AS ( Table 4-1 ).



TABLE 4-1

Aortic Valve Area






















Category Valve Area (cm 2 )
Normal 2.5–3.5
Mild stenosis 1.5–2.5
Moderate stenosis 1.0–1.5
Severe stenosis 0.7–1.0
Critical stenosis <0.7


In cardiac catheterization laboratories, aortic valve areas are calculated using the modified Gorlin equation, which in its simplified form states that the valve area is proportional to the flow across the valve divided by the square root of the mean pressure gradient. A variation of this formula is the Hakki equation: Valve area = cardiac output/√peak pressure gradient.


Using echocardiography, the aortic valve area can be calculated using the continuity equation, which is based on the principle that the stroke volume is equal in the left ventricular outflow tract (LVOT) and the aortic valve:


<SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='Velocity-time-integral(LVOT)× area(LVOT)= velocity-time-integral(aortic valve)× area(aortic valve)’>Velocity-time-integral(LVOT)× area(LVOT)= velocity-time-integral(aortic valve)× area(aortic valve)Velocity-time-integral(LVOT)× area(LVOT)= velocity-time-integral(aortic valve)× area(aortic valve)
Velocity-time-integral (LVOT) × area (LVOT) = velocity-time-integral (aortic valve) × area (aortic valve)

Only gold members can continue reading. Log In or Register to continue

Jul 14, 2019 | Posted by in ANESTHESIA | Comments Off on Aortic stenosis
Premium Wordpress Themes by UFO Themes