Valvular Heart Diseases Flashcards
Tx of MVP
Valve replacement
Physical exam signs of pulmonary HTN related to MS and what does this mean in terms of severity?
1) RV heave: Can feel RV as it beats bc it is wrking hard against pulmonary HTN
2) Loud P2: Pulmonic pressure is so high that it closes pulmonic valve with more force.
Both these means that MS is severe.
What is an Austin flint murmur? When is it seen and how is it casued?
Seen in aortic regurgitation. Presents as a low frequency mid diastolic rumble. Due to retrograde force of aortic regurgitation blood that hits the mitral valve and causes a murmur.
How is MR related to the Frank-Starling curve in compensated vs. decompensated phase?
Compensated: due to increased volume in both LA and LV, they both dilate, going up the starling curve and optimizing tension. As a result, stroke volume increases.
Decompensated: After awhile, the volume increases too much for the LA and LV and it overdilates, falling off the starling curve, as the optimal length is surpassed. As a result, this results in a decrease in strove volume and ultimately heart failure.
Mitral regurg
What are rare causes of mitral stenosis?
infective endocarditis with large vegetations that obstruct valve orifice, calcification of mitral annulus that extends onto leaflets
When is S4 heard and what condition does this indicate?
S4 is heard in late diastole, coninciding with contractino of aorta. This is generated when atria are ejecting blood into a stiffened ventricle, seen in decrease in ventricular compliance (stiffness) due to hypertrophy. Most commonly seen in aortic stenosis.
What does this picture represent
MR
LA and LV changes in AS
LV undergoes concentric hypertrophy due to pressure overload and decreased compliance.
LA also hypertrophies to fill noncompliant LV.
What are complications of MVP?
Severe mitral regurgitation, infectious endocarditis, arrhythmias.
Aortic regurg
What type of factors bring on dyspnea of early/mild phase of mitral stenosis and why?
In mild MS, dyspnea may be absent at rest. However, factors that decrease diastolic filling time/ increase HR (e.g. exercise, emotional stress, infection/fever, anemia, hyperthyroidism, Afib) can bring on dyspnea. This is because with faster HR, diastolic filling time decreases and LA cannot push blood fast enough to the ventricle due to the stenosis. As a result, blood gets backed up causing pulmonary congestion and dyspnea.
“Morphology” of presystolic/ late diastolic murmurs and examples that cause this
Flow occurs after S2, just before S1 during period of ventricular filling that follows atrial conrtaction.
Ex: MS, TS, left or right atrial myxoma
What is Mitral valve prolapse?
Ballooning of mitral valve into left atrium during systole (w/ or w/o MR)
What is a complication of chronic rheumatic herat disease?
Infectious endocarditis
“Morphology” of mid-diastolic murmurs and examples that cause them
“Diastolic rumble”; occur after S2 when ventricle is filling and ends before S1, when ventricle is done filling. Rumbling due to disproportion between small valve orifice size and larger diastolic blood flow volume.
Ex: MS, TS.
Why does LV hypertrophy in aortic stenosis?
it initially reduces LV wall stress (Wall stress= Pxr/2h) by thickening. Over time, however, it reduces compliance of the ventricle, making it more “stiff.”
Heart sounds in aortic regurgitation
Eary diastolic “Blowing” murmur at upper left stenral border.
How does chronic valve disease manifest?
Results in stenosis with a classic “fish-mouth” appearance. It almost always affects the mitral valve, leading to thickening of chordae tendinae and cusps, leading to stenosis. Occsionally it involves the aortic valve, which leads to fusion of the commissures, which reduces orifice of the valve, causing stenosis.
Pathophysiology of MR
Reflux of blood from LV to LA during systole → decreased forward CO/ increased LA volume and pressure → increased volume load in LV due to regurgitant volume + pulmonary venous return → enlargement of ventricle (volume overload) → decreased ability to contract (Frank-Starling curve) / lower SV → left sided heart failure
How is evidence of prior A beta-hemolytic strep infection in Jones criteria tested?
Elevated Antistreptolysin O antibodies (ASO) + Anti-DNase B titers
Sounds heard in MS and why?
In both early and late type, there is an opening snap that occurs after S2 with diastolic decrescendo murmur (“diastolic rumble”) followed by a presystolic accentuation murmur that stops at S1. Opening snap occurs bc the mitral valve becomes so calcified that it takes a little pressrue to open and when it finally does, it makes an opening snap sound. The presystolic accentuation murmur is due to an “atrial kick” that occurs when the atria contracts right before the MV closes.
What is the most common cause of Mitral stenosis?
Rheumatic fever
What are Aschoff bodies, what do they consist of, and when are they seen?
Seen in myocarditis in acute rheumatic fever. They are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy neuclei (Anitschkow cells), giant cells, and fibrinoid material.
Aortic regurg
What is pancarditis in rheumatic fever? What parts of the heart does it involve and how are they affected?
Inflammation of each layer of the heart.
1) Endocarditis- involves Mitral valve > aortic valve. Characterized by small vegetations along lines of closure that lead to regurgitation.
2) Myocarditis- formation of Aschoff bodies
3) Pericarditis- leads to friction rub and chest pain
Compensatory LV and LA changes in acute MR
There is no time for compensatory LV and LA dilitation.
Two phases of chronic MR
1) Compensated phase- not many sx (e.g. dyspneic only during exertion)
2) Decompensated phase- more sx (left ventricular SV starts to decrease)
What aspect of the sounds heard in MS determines its severity?
Interval between S2 and opening snap is inversely related to its severity. For instance, short S2-OS interval means that there is a higher LAP so mitral valve opens faster.
Why is there sometimes an absent or reduced aortic component of second heart sound in AS?
Occurs during late in AS; valve becomes so stenotic that it doesn’t close well.
Causes of MR
1) Complication of Mitral valve prolapse
2) LV dilitation
3) Infective endocarditis
4) Acute rheumatic heart disease
5) Papillary muscle rupture after MI
Complications of MS and why? (6)
1) Left atrial enlargement/ dilitation (early): Due to volume overload from not being able to push all blood into LV
2) Pulmonary hypertension: High LAP transmitted to pulmonary circulation
3) Pulmonary congestion: blood backs up into pulmonary system → increased hydrostatic pressure → blood leakage → pulmonary edema
4) Right sided heart failure: RV has to pump against pulmonary HTN
5) Atrial fibrillation: dilitation of LA → abnormalities in conducting system → Afib
6) Thrombus/ embolization/ stroke: Abnormal movement of atrial wall from Afib causes stasis + atrial enlargement increases risk for thrombus formation
Most common cause of mitral stenosis
Rheumatic fever
How is pulmonary edema caused by MS and what are its symptoms?
Due to stenosis, there is more blood in the LA → increase in LAP → blood backs up into pulmonary capillaries → increased hydrostatic pressure → leakage of blood into lung interstitium
Sx of acute MR and why?
Acute pulmonary edema and dyspnea. Because there is no time for left atrium to adapt and dilate, regurgitant flow to LA results in rapid rise in LAP. As a result, blood quickly backs up into the lungs. Moreover, increased ventricular preload beyond optimal length leads to decreased SV and adds onto the regurgitation, leading to pulmonary congestion.
Aortc stenosis
What are the prognoses of acute rheumatic fever
Acute attack usually resolves but can progress into chronic rheumatic heart disease
Changes of LV in chronic AR
Over time, LV adjusts by dilating and undergoing eccentric hypertrophy (Volume overload). Compliance also increases, allowing LV to accommodate larger regurgitant volumes.
Jugular venous pulse pressure curve finding in MR
Tall V wave. This is because during systole, there is regurgitant backflow of blood from left ventricle to the left atrium. V wave represents atrial filling at the end of systole; however, it will be tall because during thsi time, left atrium is getting filled up even more.
Why does syncope with exertion occur in aortic stenosis?
Ventricle cannot increase cardiac output due to stenosis, decreasing flow to the brain.
“Morphology” of Midsystolic/ Systolic ejection murmurs and defects that produce this murmur
Starts shortly after S1 when ventricular pressure rises enough to open valve. Crescendo/Decrescendo murmur in which murmur increases when ejection increases and decreases when ejection decreases.
Ex: AS, PS, innocent murmurs
Difference between aortic stenosis from “wear and tear” and rheumatic AS
In rheumatic AS, there is usually coexisting MS. Moreover, there is fusion of aortic valve commissures due to scarring, which reduces orifice of the valve, leading to stenosis. In wear and tear, there is calcification/fibrosis of the valves, leading to stenosis; however, there is no fusion of aortic commissures.
How does systemic vascular resistance relate to the severity of MR?
If systemic resistance is lower when aortic valve is open, more blood will flow out from ventricles into aorta instead of regurgitating back into left atrium (target of therapy). However, increased systemic resistance will result in more backflow from ventricle to left atrium.
What are the components of major criteria in Jones Criteria?
J: Joint (migratory polyarthritis)- swelling and pain in large joint (e.g. wrist, knees, ankles) that resolves within days and “migrates” to involve another large joint.
O: Heart- Pancarditis
N: Nodules (subcutaneous)
E: Erythema marginatum- annular (ring shaped), nonpruritic rash with erythematous borders, commonly involving trunk and limbs
S: Sydenham chorea: rapid, involuntary muscle movements
What happens to S1 sound late in MS and why?
Later on, the loud S1 found in earlier stages of MS normalizes or becomes softer, because as valve leaflets thicken and calcify, they become less mobile.