Aortic Stenosis

 

1. Role of physical exam in diagnosis of AS:

a) Unlike some of the other conditions we have discussed, the physical exam is quite good in ruling in/out AS.

b) Delayed carotid upstrokes (remember pulses tardus et parvus from med school) and a late peaking systolic murmur have positive LRs in the 100 range.

c) Absence of radiation of the murmur to the R carotid has a negative LR of 0.1.

 

 

2. Pathophysiology of AS:

a) In the US, calcific valvular degeneration is the most common cause, followed by bicuspic aortic valve. Worldwide, rheumatic disease is most common.

b) Recall LaPlace's law: wall stress (afterload) = pressure / radius x wall thickness.

c) In response to systolic pressure overload, the LV hypertrophies in order to maintain normal wall stress.

d) LVH --> impaired diastolic relaxation --> increased LVEDP --> increased LAP --> LAE

e) After prolonged loading of the LV, its compensatory hypertrophy is no longer able to keep up --> increased wall stress (afterload) --> LV begins to fail.

 

 

3. Symptoms of AS:

a) Because of the above compensatory mechanisms, there is a prolonged latent period in AS before sx arise.

b) Once they do, there is a marked increase in mortality (avg survival 2-3 years), and thus that is when referral for therapy should be made

c) Classic sx: angina (due to increased myocardial O2 demand from LVH), syncope (due to arrhythmias and decreased CO), dyspnea (due to diastolic and systolic dysfunction).

 

 

4. How to determine severity of AS:

a) As in this patient, when there is LV dysfunction, the gradient may be underestimated secondary to a low flow state.

b) In these cases, one must differentiate between true symptomatic aortic stenosis and pseudostenosis, in which the symptoms are secondary to LV dysfunction and not the AS - these patients will not benefit from AVR.

c) One way to do this is to subject the patient to a dobutamine stress echo - in patients with contractile reserve, the stroke volume will increase (see attached JACC paper).

d) In true AS, the valve area will be fixed, and thus the gradient will increase.

e) In pseudostenosis, the valve area will actually increase, resulting in a decreased gradient.

 

 

5. Management of ADHF secondary to AS:

a) Given the tenuous hemodynamics that result from AS, management of HF sx (as in this pt) can be challenging.

b) Ohm's law (V = IR) translated into hemodynamics: MAP = CO x SVR.

c) In AS, there is a fixed outflow obstruction, so unlike in pure systolic dysfunction, the LV cannot increase CO in response to afterload reduction. Thus, vasodilators result in a decrease in SVR without a concomitant increase in CO, leading to potential hypotension (decreased MAP).

d) Because of this, the classic teaching is to avoid vasodilators in severe AS, but interestingly, one study showed that nitroprusside improved hemodyanamics in patients with AS, suggesting that even in AS, SVR may actually contribute to some of the afterload that the LV experiences (see attahced NEJM paper).

d) Similarly, overly aggressive diuresis can lead to a reduction in CO (CO = SVR x HR) by decreasing stroke volume.

 

 

 

(Christopher Woo MD, 6/18/10)