Cardiac Valve Stenosis Flashcards Preview

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Flashcards in Cardiac Valve Stenosis Deck (47):

The physiologic impact of a stenotic valve on the heart is determined by the _____ and the ______.

-valve position -obstruction severity (orifice size)


Stenotic valves effect on orifice size, flow velocity

-decrease orifice size which per the continuity equation requires increase in flow velocity to achieve physiologic flow rates--generates a clinically important pressure gradient


Pressure gradient due to a stenotic valve leads to a pressure load where?

-subjects the chamber UPSTREAM from the valve to a pressure load


Per Bernoulli, the relationship between the pressure gradient and flow velocity is _____.

-quadratic: ^2


How does blood acquire a velocity within the heart?

-transfer of blood across an orifice requires the blood have kinetic energy associated with the velocity it acquires -this is accomplished by transforming hydraulic potential (pressure) to haudric kinetic (velocity) energy -this causes a pressure decrease as the blood acquires velocity, thus generating a pressure gradient across the orifice


What does the continuity of flow state?

-fluid is incompressible -flow RATE in any section in a pipe is the same -flow rate=mean velocity X CSA -flow VELOCITY is inversely related to cross sectional area -if you decrease CSA of a pipe (say within stenosis), the blood must travel at a higher velocity. Per the Bernoulli equation, this means their must be a pressure gradient.


Given the Bernoulli theorem and continuity equation, how can one measure the degree of valve stenosis?

-measure the volume of blood and CSA at time 1, and the velocity outside of orifice. This will allow you to determine the CSA aka stenosis. The amount of velocity needed to cross a valve will determine the necessary pressure drop.


The pressure GRADIENT is related _______ to the flow VELOCITY.



Greatest magnitude of a pressure gradient between the LV and Aorta occurs when during systole?

-when peak flow velocity occurs into the aorta


Is there normally a big pressure gradient between the LV and aorta during peak systolic ejection velocity?

-no, at physiological flow rates, normal orifice sizes yield flow velocities that evoke small physiologically unimportant pressure gradients


Determinants of flow rate, flow velocity, and pressure gradients

1. flow rate (mL/sec) is determined by CO (linear, direct) and time available for flow (linear, inverse, time valves are open) 2. flow velocity: (cm/sec) is determined by flow rate (linear, direct) and valve orifice area (linear, inverse) 3. pressure gradient (mmHg): flow velocity (direct, QUADRATIC)


Gorlin Valve Area Equation

-allows us to measure CSA of orifice from pressure gradient and flow rate


Aortic stenosis can be viewed as a disorder of pure ___________.

-increased left ventricular afterload

-LV must generate a substantially greater pressure gradient to achieve the flow velocity needed to maintain flow rate across the stenotic valve= large aortic valve pressure gradient


Major differences comparing aortic and ventricular pressure waveforms in the setting of aortic stenosis.

-large aortic valve pressure gradient (necessary to achieve flow velocity across stenotic valve)

-aortic P does not rise with the ventricular pressure and it is very uneven--this is because it takes longer for the blood to reach aorta to generate pressure (usually 2/3 of flow occurs durign 1st 1/3 of systole) and it is very turbulent.

-LVEDP is also very elevated


Normal peak aortic valve flow velocity and pressure gradient

-80-100 cm/sec

-3-5 mmHg


4 things seen on echo of aortic stenosis and the LV

-heavily calcified poorly mobile aortic valve

-normal LV cavity size

-concentric LVH

-normal LV contractile function (recall HFpEF with concentric LVH)


How does Reynold's Law play into stenosis?

-decides velocity at which turbulent flow develops and in stenosis, glow across aortic valve into ascending aorta during systolic ejection is turbulent

-this turbulence= the murmur we hear

-can also see mild aortic regurgitation


Systolic flow velocity in normal vs AS

-normal: 80-100 cm/s (~1 m/sec); mostly uniform at this speed

-AS:~4m/sec and very turbulent and variable in speed distribution; rounded velocity envelope=uniform ejection rate



Mild, severe, and critial levels of valve orifice area in AS

-mild 1.5

-severe: 1.0

-critical: 0.8 cm2

-normal:3-4 cm2


Describe the effct of decreasing orifice surface area on flow rate and mean systolic P gradient.

-decreases in valve orifica area means that increasing larger pressure gradients are required for flow rates


Mean systolic pressure gradient able to be establish in AS

150 mmHg


So, does merely checking a patients pressure gradient and finding it to be low mean they are free of AS?

NO! the quadratic relationship between Pressure gradient, orifice area and flow rate means that at low flow rates, even with a small orifice area, the valve pressure gradient may be deceptively small. Therefore, the valve area must always be calculated using the pressure gradient and CO.



Why might AS limit ability to increase CO in response to demand?

-increasing blood flow across the valve requires a large increase in pressure gradient and thus, increased systolic pressure load on the LV..which will eventually max out

-limits ability to increase CO in response to demand


Consequences of severe AS

-at small valve orifice areas, small changes in orifice area or flow require large changes in the aortic valve pressure gradient

-this means that minor progressions in anatomic severity may cause large changes in LV afterload

-limited ability to increase CO in response to exercise-- must draw mostly on HR increase (long time spent in systole) which drastically raises myocardial metabolic requirements


Is AS acute or chronic?

it is a chronic disease that does not develop acutely


The heart can adapt to AS by developing ___________. What are the limitations of adaptive responses?

-concentric LVH to offset the increase in LV wall stress

limits: effect on LV diastolic compliance, limits of extent of hypertrophy due to coronary circulation and coexisting epicardial coronary disease, degradation of myocardial peformance due to fibrosis; can also have progression of stenosis severity


 3 mechanisms of decompensation due to AS

1. angina pectoris: limitation of coronary circulation's response to hypertrophy and increased wall stress

2. effort-related syncope or presyncope: inadequate CO response to exercise, arrhythmias provoked by exercise-induced hypotension or ischemia

3. CHF (systolic and/or diastolic): inadequacy of LVH to normalize wall stress leads to degradation of contractile performance and decrease in diastolic compliance; progression of obstruction severity


Implications of the presence or absence of symptoms in AS

-absence: compensatory mechanisms are working and patient is doing okay. Though not likely asymptomatic--will likely have reduced exercise capacity

-appearance of sxs: compensatory mechanisms are breaking down due to further progression of stenosis or degradation of LV performance=BIG TROUBLE


Natural history of aortic stenosis and sxs timing

-once sxs arise, you need to treat them ASAP!!! They will likely deteriorate SOON after sxs appear


With aortic stenosis, when sxs appear, its time to intervene with _______________. Symptoms include what 3 things?

-aortic valve replacement; some people believe that severely AS patients need intervention even if asxs.

1. AS severity has progressed

2.  compensatory mechanisms have reached their limit

3. LV function has deteriorated


How is it possible that aortic replacement can "cure" patients with such bad AS that they are in decompensated cardiogenic shock?

-bc their failure was due to the afterload rather than LV dysfunction itself


What does MS look like on echo?

-normal to small LV

-enlarged LA

-variably enlarged RV

-thickened mitral valve leaflets

-"smoke" in LA moving sluggishly into LV due to very slow stagnant flow


Mitral valve flow velocity: normal vs MS

-normal: max is 1 m/sec and more uniform flow velocity; see a rapid decline in mid diastole since most flow occurs during first 1/3 of diastole and a slight increase after this due to atrial systole

-MS: 1-2 msec, turbulent, and more sustained flow velocity due to pressure gradient.


Normal mitral valve peak velocity of flow and pressure gradient vs MS

-80-100 cm/sec with considerable variation during systole

-3 mmHg (small diastolic pressure across the mitral valve)

-in MS: attentuated Y wave seen and no transmission of LA A wave to LV; high initial inflow velocity of 160 cm/sec with a slow decay of inflow velocity during diastole--degree of decay decreases as duration of  diastole decreases



In mitral stenosis, there is a high initial inflow velocity of 160 cm/sec (vs 80-100 cm/sec in normal) that experiences a slow decay of inflow velocity during diastole. What happens to this degree of decay as the duration of diastole decreases (increased HR)?

-it decreases; this means there is progressive rise in LAP during short cardiac cycles


Mild, moderate, and critieral valve orifice area and upper level of diastolic pressure gradient

-mild: 2.0 cm2

-moderate: 1.5 cm2

-critical: 1.0 cm2

-upper level of diastolic  gradient is 35 here, vs 150 in AS due to pulmonary vasculature not being able to handle high P


Mechanisms available to the heart to adapt to MS



4 consequences of severe mitral stenosis

-LAP greater than 30 mmHg is poorly tolerated by pulmonary capillaries--limits max diastolic pressure gradient to 20 and chronic LA HTN causes dilation whicn impairs atrial transport function

-LV is inadequately preloaded

-normal circulatory reflexes in response to a demand for increased CO are detrimental: increased HR decreases available diastolic filling time

-progressive left atrial dilation can lead to chronic atrial fibrillation with loss of normal reflexes for appropriate regulation of HR and sluggish flow "smoke" capable for systemic embolization


A patient with long-standing MS that develops atrial fibrillation should be treated how?

-Warfarin: sluggish flow due to chaotic A-fib and MS has high clot risk


Long-term pulmonary vascular consequences of MS

-Pulmonary venous HTN and secondary PA HTN

-PV HTN: elevates capillary pressure and impairs gas exchange leading to dyspnea

-PA HTN: due to LA P provoking pulmonary arteriolar constriction which makes the PA pressure need to be even higher (reversible PVR increase). Sustained PA pressure elevation= obliteration of pulmonary arteriolar destruction which is irreversible PVR. This can all cause severe right ventricle afterload excess leading to dilation, tricuspid regurgitation and systemic venous HTN


Clinical course in Mitral stenosis

-due to lack of cardiac adaptive mechanisms, patients become symptomatic at mild-moderate severeities of MS: 1.8 cm2

-in contrast to AS, MS pts do not deteriorate rapidly after becoming symptomatic: gradual progression of sxs limitation over many years as the severity slowly increases

-predominant sxs: dyspnea on exertion due to LAP elevation; fatigue due to sustained low CO


Predominant sxs in MS

-dyspnea due to exertion due to LAP elevation

-fatigue due to sustained low CO


Why may a patient with severe MS not feel better after mitral valve replacement?

-they may have undergone obliterative pulmonary arteriolar disease which is irreversible


Valve stenosis causes a ______ load ont he cardiac chamber _____ from the stenotic valve. Differences in mechanisms between AS and MS

-pressure load on cardiac chamber upstream from the stenotic valve

-AS= concentric hypertrophy and is the reason patients may have long asxs period; appearance of symptoms has ominous implications

-MS: no effective adaptive mechanisms for MS; pulmonary congestion, HTN and low CO occur with progressive sxs correlated with progression of the stenosis severity


Which form of stenosis should be considered ominous to develop sxs during?

-AS-means they're deteriorating rapidly