Anesthetic management of patients with aortic stenosis

Anesthetic management of patients with aortic stenosis 

Preoperative consideration 

Etiology: 

Valvular aortic stenosis is nearly always congenital, rheumatic or degenerative. 

Congenitally bicuspid valves are prone to calcification with eventual stenosis. 

Rheumatic stenosis is rarely isolated; it is more commonly associated with AR or mitral valve diseases. 

Clinical picture: 

Classically patients with advanced AS HAVE THE TRIAD OF  

• DYSPNEA ON EXERTION 
• ANGINA 
• SYNCOPE(EXERTIONAL) 

Angina caused by increased o2 demand due to lt ventricular hypertrophy and decreased o2 supply due to compression of intramyocardial  vessels by high LV pressure. 

Pathophysiology and hemodynamic consequences 

• Obstruction of LV outflow caused by AS is almost always gradual allowing the lv to initially compensate and maintain stroke volume. 
• Concentric ventricular hypertrophy enable LV to maintain SV by generating a significant transvalvular pressure gradient   and reduce  ventricular wall stress. 
• With long standing AS, myocardial contractility deteriorates and further compromise LV function. 
• A prominent feature of AS is a decrease in LV compliance as a result of hypertrophy. 
• Diastolic dysfunction  result from an increase in ventricular mass, fibrosis, or ischemia. 
• The decreased diastolic pressure gradient between LA and LV impairs ventricular filling which become quite dependent on normal atrial contraction. 
• Loss of atrial contraction can precipitate CHF or hypotension in patients with AS.  

TEE severity scale: 

Normal aortic valve area 2.5 – 3.5 cm2  

Normal pressure gradient less than 10 mmhg 

Aortic stenosis 

Indicator	Mild	Moderate	severe
Valve area cm2	2-1.2	1.1-.8
Pressure gradient mmhg	20-30	30-50	>50

Doppler Echo and cardiac cauterization data 

Using Gorlin equation 

[Equation] 

K= 44 

Aortic valve area[Equation] 

The pressure gradient can be determined by using continuous wave Doppler Echo: 

Δp= 4V2 

Δp= peak pressure gradient 

V= peak blood flow 

Aortic valve area(V2) =[Equation] 

A1 cross sectional area of LVOT 

V1 maximum blood flow velocity in LVOT 

V2 maximum blood flow velocity through aortic valve 

 

 The hallmark of Pressure-volume loop of AS are high left ventricular systolic pressure and upward and counterwise rotation AB segment indicative of decreased LV compliance. 

Treatment of AS: 

• Percutaneous balloon valvuplasty is generally indicated for younger patients or elderly who are poor candidate for valve replacement. 
• Valve replacement. 
• Medical treatment for CHF: digoxin, Na restriction, and small dose of diuretics. 

Preoperative evaluation: 

These patients need to be evaluated for CHF and angina: 

ECG: look for any arrhythmia or evidence of LV hypertrophy or MI. 

Exercise tests: exercise tolerance test or cardiopulmonary exercise test for patients with disabilities. 

Echo: to assess ventricular and valvular function 

Coronary angiography 

Dobutamine stress echo 

Anesthetic management: 

Hemodynamic objectives or goals: 

The important considerations are  

• To maintain SVR and DBP. This is essential to maintain coronary perfusion. 
• To maintain the preload at the upper end of the normal by giving fluids and avoiding excessive VD. 
• To avoid tachycardia or bradycardia,  and maintain sinus rhythm if present preoperatively and treat AF aggressively. 
• Aim of HR between 60-70\min. 
• To maintain myocardial contractility 

Premedication: 

Patients with AS may benefit from premedication by preventing unnecessary increase of HR. 

Concerns must be taken to ensure adequate venous return and preservation of sinus rhythm. 

Monitoring: 

In addition to the standard monitors, intraarterial pressure monitoring is desirable in severe AS. 

Pulmonary artery pressure monitoring is useful and a prominent ‘a’ wave is often seen on PCWP waveform. 

Close monitoring of ECG for signs of myocardial ischemia. 

TEE can be useful for monitoring ischemia, preload, valvular function, and the effect of therapeutic interventions. 

Anesthetic technique: 

The selection of general anesthetic agents is most critical in patients with symptomatic (moderate tosevere) aortic stenosis. In these patients, a primarily opioid-based anesthetic technique generally results inminimal cardiac depression.

suitable nonopioid induction agents include etomidate and the combination of ketamine and abenzodiazepine.

If a volatile agent is used, the concentration should be carefully controlled to avoid excessive myocardialdepression, vasodilation, or loss of normal atrial systole.

Tachycardia and hypertension, which can precipitate ischemia, should be treated by increasing anestheticdepth. If a -adrenergic blocking agent is used, esmolol may be preferable because of its short half-life.Most patients with aortic stenosis are extremely sensitive to vasodilators. Moreover, because of an alreadyprecarious myocardial oxygen demand–supply balance, they tolerate even mild degrees of hypotensionpoorly.

Hypotension should generally be treated with small doses (25–50 g) of phenylephrine. Intraoperativesupraventricular tachycardias with hemodynamic compromise should be treated with immediatesynchronized cardioversion. Frequent ventricular ectopy (which often reflects ischemia) is usually poorlytolerated hemodynamically and should be treated with intravenous lidocaine. Amiodarone is generallyeffective for both supraventricular and ventricular arrhythmias.