Cardiac valvular abnormalities Flashcards
Review, but systemic BP is directly related to the product of which two things, and how do those break down?
CO and SVR and CO is HR x SV.
In stenotic valvular lesions, there is a ___ overload state on which cardiac chamber?
pressure overload state on downstream cardiac chamber (LV in Aortic stenosis, LA in mitral stenosis)
IN regurgitant lesions, there is a ____ overload state on which chamber?
Volume overload state on downstream cardiac chamber. LA in Mitral regurg
Afterload: regurgitant vs stenotic lesions:
regurgitatnt: increases in afterload can lead to more regurgitation but a signifcant drop in afterload is awful for stenotic lesions.
Decreased afterload: good for regurgitant because it makes forward flow easier. Not good for stenotic
Aortic stenosis: presence and severity of symptoms are related to ?
related to prognosis of the disease
How is it that pts with AS end up having syncopal episodes?
Higher oxygen requirements during times of exertion lead to vasodilatation, but this decrease in SVR can NOT occur due to fixed output, so hypotension and decreased perfusion of the brain can happen=syncope
Normal aortic valve area:
1.6-2.5 cm^2
Vavle area and gradient in mild AS:
valve area: 1.5-1.0 resulting in minimal elevation in peak gradient to less than 20 mmHg
Valve area and gradient in moderate AS:
1.0-0.8 and peak gradient of greater than 50
Valve area and gradient in severe AS:
Valve area below 0.8 and peak gradients between 50-100 mmHg
What happens to the ventricle with aS:
myocardial hypertrophy leads to decrease in compliance of LV and thereby a decease in passive filling of LV during diastole.
Atrial systole and AS:
In a normal situation, atrial systole provides 20-30% of LV filling volume. these AS patients need this to maintain CO. If a fib develops-bad news
Goal HR of AS patients:
70-90-adequate cardiac output wile maintaining oxygen delivery and consumption
Preload in AS patients:
they need to be have adequate preload, being cautious as too much intravascular volume can tip the balance and place these patients in pulmonary edema
Contracitlity inAS:
Ventriclar performance decreases as a result of hypertrophy to overcome the narrowing of aortic valve
Aortic Insufficiency: optimal heart rate
slightly tachy 90-110
In AI, when does regurgitation occur, and how can you help?
It occurs during diastole, so limiting this period of the cardiac cycle can limit the amount of backward flow
As far as what happens to the ventricles in AS vs AI:
AS: hypertrophy
AI: dilation
Contractility in AI:
afterload in AI:
eventually dilation goes so far and myocardium becomes stretched and can result in myocardial failure
Afterload: slight, controlled drop in SVR can promote forward cardiac flow and a decrease in regurgitation
Mitral stenosis -how are you maintaining the HR? Why? What do many of these patients present with?
70-90 bpm. Too low-can’t get good CO due to fixed lesion. Too high, decreases time LV has to fill.
Most of these pts present with a fib due to a chronic increase in LAP and a resulting left atrial dilation to accommodate
Contractility in early vs late stages of Ms:
early: contractility is not impacted
late: LV function can be impacted
Mitral insufficiencY: what is your goal HR? and why? afterload?
Mitral insufficiency: HR of 90-110 brady is not tolerated because this can lead to LV fluid overload when a significant amount of cardiac output flows through incompetent mitral valve. Slight increase in HR leads to a decrease in diastolic time and therefore limits the amount of regurgitation that can occur.
Afterload: slight reduction in SVR leads to an increase in forward cO and is well tolerated
Contractility: Many pts with Mitral Insufficiency also have poor ventricular function-why?
Poorly functioning ventricle leads to hypertrophy and dilatlion of mitral annulus resulting in chronic mitral insufficiency
How can mitral valve repair actually end up being bad for a patient?
In patients with severely depressed LV function leading to significant Mit Regurg, the LV can decompensate. The lower pressured Left atrium serves as a pop off mechanism limiting strain on LV in times of increased aferload, but once mitral vlave is replaced, this increase in strain can go directly to LV and result in LV failure in the periop period if afterload is too great.
Severe AS patients: monitors:
Any deviation from baseline hemodynamics in these pts needs:
pre-induction a line
Any deviation needs to be treated slowly and carefully
