Valvular Heart Diseases Flashcards
1
Q
Tx of MVP
A
Valve replacement
2
Q
Physical exam signs of pulmonary HTN related to MS and what does this mean in terms of severity?
A
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.
3
Q
What is an Austin flint murmur? When is it seen and how is it casued?
A
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.
4
Q
How is MR related to the Frank-Starling curve in compensated vs. decompensated phase?
A
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.
5
Q
A
Mitral regurg
6
Q
What are rare causes of mitral stenosis?
A
infective endocarditis with large vegetations that obstruct valve orifice, calcification of mitral annulus that extends onto leaflets
7
Q
When is S4 heard and what condition does this indicate?
A
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.
8
Q
What does this picture represent
A
MR
9
Q
LA and LV changes in AS
A
LV undergoes concentric hypertrophy due to pressure overload and decreased compliance.
LA also hypertrophies to fill noncompliant LV.
10
Q
What are complications of MVP?
A
Severe mitral regurgitation, infectious endocarditis, arrhythmias.
11
Q
A
Aortic regurg
12
Q
What type of factors bring on dyspnea of early/mild phase of mitral stenosis and why?
A
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.
13
Q
“Morphology” of presystolic/ late diastolic murmurs and examples that cause this
A
Flow occurs after S2, just before S1 during period of ventricular filling that follows atrial conrtaction.
Ex: MS, TS, left or right atrial myxoma
14
Q
What is Mitral valve prolapse?
A
Ballooning of mitral valve into left atrium during systole (w/ or w/o MR)
15
Q
What is a complication of chronic rheumatic herat disease?
A
Infectious endocarditis
16
Q
“Morphology” of mid-diastolic murmurs and examples that cause them
A
“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.
17
Q
Why does LV hypertrophy in aortic stenosis?
A
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.”
18
Q
Heart sounds in aortic regurgitation
A
Eary diastolic “Blowing” murmur at upper left stenral border.
19
Q
How does chronic valve disease manifest?
A
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.
20
Q
Pathophysiology of MR
A
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
21
Q
How is evidence of prior A beta-hemolytic strep infection in Jones criteria tested?
A
Elevated Antistreptolysin O antibodies (ASO) + Anti-DNase B titers
22
Q
Sounds heard in MS and why?
A
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.
23
Q
What is the most common cause of Mitral stenosis?
A
Rheumatic fever
24
Q
What are Aschoff bodies, what do they consist of, and when are they seen?
A
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.
25
Aortic regurg
26
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
27
Compensatory LV and LA changes in acute MR
There is no time for compensatory LV and LA dilitation.
28
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)
29
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.
30
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.
31
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
32
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
33
Most common cause of mitral stenosis
Rheumatic fever
34
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
35
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.
36
Aortc stenosis
37
What are the prognoses of acute rheumatic fever
Acute attack usually resolves but can progress into chronic rheumatic heart disease
38
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.
39
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.
40
Why does syncope with exertion occur in aortic stenosis?
Ventricle cannot increase cardiac output due to stenosis, decreasing flow to the brain.
41
"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
42
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.
43
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.
44
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
45
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.
46
Mitral regurg
47
Effect on EF, preload, SV, and starling curve during decompensated phase of chronic MR
Ejection fraction decreases. Volume overload causes too much dilitation of LV and now the heart is on the downward portion of Frank-Starling curve. As a result, although preload is increased, cardiac output/ stroke volume is decreased (decrease in ejection fraction). This results in heart failure and backing up of fluid into the lungs → pulmonary edema.
48
"Morphology" of mid to late systolic murmurs and examples of defects that cause them
High pitched murmurs that begin after S1 (e.g. middle of S1) and end before or at S2.
Ex:
MVP: Don't get regurgitation until mitral valve ballloons towards atrium at the middle of systole.
49
Jugular venous curve in tricuspid regurgitation
Prominent v waves (right atrial filling). More filling of right atrium during ventricular diastole due to regurgitation back to atrium → increased RAP.
50
What is acute rheumatic fever and what age group is most affected?
Systemic complication of pharyngitis due to group A beta-hemolytic streptococci
Affects children 2-3 weeks after episode of streptococcal pharyngitis ("strep throat")
51
What is the effect of LAP in mitral stenosis initially?
Initially, there is increased LAP due to decreased emptying from LA to LV. As a result, this increase in pressure is transmitted retrograde to the pulmonary circulation, resulting in pulmonary hypertension.
52
Tx of aortic stenosis
Valve replacement
53
What is the most common cause of aortic stenosis in young adults?
Congenital malformation (bicuspid aortic valve)
54
What is the Jones criteria and what are the main components?
Used to diagnose acute rheumatic fever. Consists of 3 main components:
1) Major criteria
2) Minor criteria
3) Evidence of group A streptococcal infection with presence of major and minor criteria.
55
how does CHF develop in aortic stenosis?
With progressive stenosis, left ventricle cannot handle the afterload, resulting in increased LV diastolic volume and pressure and herat failure. As a result, blood backs up into the LA → pulmonary system → etc.
56
When is S3 heard and at which age group is it normal/abnormal? What does it implicate in each group?
S3 is herad in early diastole following the opening of AV valves. It is a normal finding in children and young adults because it implies the presence of a flexible ventricle that can rapidly expand during early diastole, when atria is filling the ventricle. However, in middle-aged or older adults, S3 is a sign of disease resulting from dilated ventricle or transvalvular flow of AV valves.
57
What is the most common cause of death in acute rheumatic fever?
Myocarditis
58
What are some of the sx of minor criteria in the Jones criteria?
Nonspecific sx including fever, elevated ESR (erythrocyte sedimentation rate), arthralgias
59
Where is the apical impulse in MR and why?
Displaced to the axilla due to LV enlargement
60
What are innocent murmurs?
Systolic ejection murmurs that are present even though there is no stenosis.
61
What condition presents an S3 sound and why?
Chronic MR S3 due to dilation of LV and transvalvular flow through MV.
62
Jugular venous pressure curve for tricuspid stenosis
Large a wave (atrial contraction) bc it's right atrum is contracting against stenotic valve.
63
"Morphology" of early systolic murmurs and defects that can cause them
Constant volume murmur that begins with S1 and ends mid systole.
Ex:
Acute MR: LA has not had time to adjust to increasing pressures; open mitral valve causes pressures to equilibriate quickly so pressure gradient doesn't last all throughout systole.
64
Sx of decompensated phase of chronic MR
Heart failure sx:
1) Dyspnea (at rest), orthopnea, PND due to pulmonary edema
2) Peripheral edema
3) Fatigue and weakness
65
How does MS lead to right sided heart failure and what are the sx?
Increase in LAP is transmitted to the pulmonary system, resulting in pulmonary HTN. LV has to work against pulmonary HTN and eventually fails.
Sx: Hepatomegaly + ascites, increased JVP, peripheral edema
66
What is pulsus parvus et tardus
physical exam sign during aortic stenosis; when putting finger on carotid and listen to heart at the same time, towards end of systole is when you start feeling pulse in carotid (late + weak)
67
How is pulse pressure affected in AR?
Pulse pressure widens because diastolic pressure decreases while systemic pressure increases.
68
Effect on SV, preload, EF and Starlinv Curve during compensated phase of chronic MR
EF is maintained because preload increases as LV receives more volume and therefore SV is increasdd as well (on optimal length on Starling curve).
69
What are some sx of mitral stenosis at the severe/ late stages?
Dyspnea at rest, fatigue, more severe signs of pulmonary congestion (e.g. orthopnea, paraoxysmal nocturnal dyspnea), right sided heart failure sx (hepatomegaly, ascites, peripheral edema, jugular venous distension)
70
Mitral stenosis
71
"morphology" of holosystolic/ pansystolic murmurs and defects that have this murmur.
Sound is constant and lasts all throughout systole.
Ex: MR, TR, VSD
72
Murmur of acute MR
Early systolic, decrscendo murmur that begins with S1 but ends in midsystole. This is because as soon as ventricle contracts, MV opens up, and there is rapid equilibriation of LA and LV pressures.
73
What type of maneuvers intensify MS murmurs and why?
Hand grip (clenching fists), squatting, expiration.
Hand grip and squatting increases systemic vascular resistance and decfreases left ventricular emptying, so more blood regurgitates.
Expiration increases venous return to left atrium.
74
Etiology of acute severe MR
Abrupt rupture of papillary muscle (e.g. from MI). Infarction of papillary muscle leads to necrosis and tear, compromising the mitral valve.
75
Leaflet thickening and calcification, fusion of commissures, and thickening/shortening of chordae tendinae is seen with what?
Mitral stenosis (due to rheumatic fever) ⇒ "Fish-mouth" appearing stenosis
76
Etioloygies of aortic regurgitation (3)
1) Aortic root dilatation (due to syphilitic aneurysm and aortic dissection)
2) Valve damage (via infectious endocadtisi)
3) Bicuspid aortic valve
77
Murmur heard in MVP
Midsystolic click followed by regurgitation murmur (once there is mitral regurgitation). Midsystolic click due to tensing of chordae tendinae.
78
How is aortic pressure curve changed in AS?
During systole and beginning part of diastole, the aortic pressure should follow the left ventricular pressure until the aortic valve closes (at this time the aortic pressure should go up while ventricular pressure goes down). However, in aortic stenosis, during ventricular systole/ diastole, aortic pressure only goes up to about 90, while ventricular pressure goes up to 150 mmHg. After the aortic valve closes during diastole, the pressure (diastolic pressure) of aorta should level out at about 90 mmHg. In aortic stenosis, not as much blood goes through to the aorta from the ventricle due to the obstruction so during early part of diastole when aortic valve closes, the aortic pressure just drops.
79
How are systolic aortic blood pressure and diastolic aortic blood pressures affected in AR?
Diastolic pressure **decreases** due to regurgitation. For instance, when 100 mL of blood is in LV, it pumps out 100 mL and then relaxes. However, due to AR, 20 mL goes back into the LV. Thus, during diastole, aorta only sees 80 mL → reduced diastolic pressure.
Systolic pressure **increases** due to regurgitation. For instance, now that the LV sees an extra 20 mL of blood, it now has to pump out both the regurgitated volume and volume it receives from pulmonary veins and stroke volume increases.
80
Sx of acute AR and pathophsyiology.
Leads to dyspnea and pulmonary edema. This is because during acute AR, LV is normal size and **noncompliant,** as it is not used to seeing high pressures. As a result, regurgitant volume causes LV pressure during diastolic pressure to increase, increasing LVP. This increase in pressure is transmitted to LA → pulmoanry cirulcatoin → pulmonary edema.
81
What are the sx of early/mild MS and why?
Pts can be asymptomatic with dyspnea only with exertion.
82
What condition is associated with microangiopathic hemolytic anemia?
RBCs are damaged (ruptured) while crossing calcified aortic valve, producing schitocytes. Seen in aortic stenosis.
83
Why are one of early manifestations of mitral stenosis dyspnea (SOB)?
Due to increased LAP, pressure gets backed up into the pulmonary circulation → pulmonary HTN. Due to increased pulmonary venous/capillary pressures, hydrostatic pressures increase, causing plasma to leak into the lung interstitium and alveoli, causing dyspnea (+ heart failure sx).
84
What does squatting do to MVP sounds?
Click and murmur become softer with squatting. This is because increased systemic resistance decreases left ventricular emptying. (WHY?)
85
Mitral stenosis
86
What are the effects of mitral stenosis on the right side of the heart and how is this manifested?
Eventually, the pulmonary congestion that resulted from pulmonary HTN (from increased LAP) will back up from pulmonary veins → arterioles → RA. Over time, the right side of the heart has to work against this increased pulmonary pressure, and this results in right sided heart failure. This manifests as pulmonary edema, hepatomegaly, ascites, jugular venous distension, and other sx of right sided heart failure.
87
Sx and pathophysiology of chronic aortic regurgitation
HF sx including dyspnea, fatigue, decreased exercise tolerance. Also bounding pulse (water-hammer pulse), pulse nail bed (quincke pulse), head bobbing. These are all sensations of forceful heartbeat due to increased LV stroke volume, in which all the blood has to be forced out, some regurgitates back, builds up more volume, and forced out again.
88
What are Anitschkow cells?
Component of Aschoff body seen in myocarditis. Characterized by reactive histiocytes with slender, wavy nuclei
89
Sx of late/severe MS and why?
Dyspnea at rest, fatigue, pulmonary congestion (orthopnea, paroxsymal noctural dyspnea), right sided heart failure sx.
This occurs because CO becomes subnormal at rest and as LAP keeps increasing, blood continuously flows back to the pulmonary circulation, resulting in pulmonary HTN. Even at rest, there is lots of pulmonary congestion and pt will have dyspnea at rest.
90
EKG signs of mitral stenosis
Left atrial enlargement (prominent temrinal portion of P waves), RVH
91
EKG findings for MR
Left atrial enlargement, LVH
92
How is more severe AS sound regarding heart sounds?
The crescendo-decrescendo murmur is later peaking because LV has to squeeze harder and therefore gets to peak pressure later.
93
How is systolic and diastolic ventricular pressure affected in aortic stenosis?
Both left ventricular systolic and diastolic pressure increases due to hypertrophy and decreased complaince of the left ventricle.
94
CXR signs of MS
1) Left atrial enlargement
2) Prominent pulmonary arteries (Pulmoanry HTN)
3) Horizontal fissure- lines in between lung; evidence of pulmonary edema due to filling with fluid.
95
Heart sound associated with AS
Systolic ejection click followed by crescendo-decrescendo murmur.
96
What is chronic rheumatic heart disease?
Permanent valve scarring/deformity that arises as a consequence of acute rheumatic fever.
97
How is risk for chronic rheumatic heart disease increased?
By repeat exposure to group A beta-hemolytic streptococci. This results in relapse of acute phase and increases risk for chronic disease, which ultimatley results in mitral stenosis.
98
What occurs in the late/severe phase of mitral stenosis in regards the LA? What arrhythmia can this lead to?
Chronic pressure overload of LA leads to left atrial enlargement. This can disrupt the cardiac conduction system, resulting Atrial fibrillation.
99
Why angina occurs in AS
Due to imbalance between myocardial oxygen supply and demand.
Demand increased due to:
1) Increased muscle mass due to LVH → needs more oxygen
2) Wall stress increases over time bc LV compliance decreases, and therefore experiences elevated LVP during systole (increased systolic ventricular pressure).
Reduced myocardial oxygen supply due to:
Elevated left ventricular diastolic pressure (due to decreased compliance of LV along with increased volume) reduces coronary perfusion pressure gradient between aorta and myocardium (??)
100
"Morphology" of early diastolic murmurs and examples that cause this
High pitched and decrescendo murmur that begin with S2 and end before S1. Decrescendo due to ventricular relaxation that decreases pressure gradient between outflow tract and ventricle.
Ex: Aortic and pulmonic regurgitation
101
What LV and LA compensatory changes occur in chronic MR?
Dilitation of LV and LA due to extra volumes
102
Murmur for chronic MR
Holosystolic "blowing" murmur
103
Sx of MVP
Usually asymptomoatic; can have CP or palpitations
104
What does acute and recurrent inflammation seen in rheumatic fever result in?
Mitral stenosis
105
How does MVP lead to MR?
As valve keeps getting ballooned backward, gets stretched → regurgitation.
106
What does hemoptysis in the context of mitral stenosis indicate?
It indicates alveolar hemorrhage. As blood gets backed up into the lungs from the left ventricles, the capillaries can become engorged and rupture.
107
What factors can worsen sx of early/mild MS and why?
Symptoms that decrease diastolic filling time (increase HR) can worsen dyspnea. This is because during tachycardia, filling time for LV is low; as a result, there is not enough time to fill up the LV from the LA with the stenosis and therefore, more blood is in the LAP → more pressure backs up into pulmonary circulation.
Factors include: Exercise, emotional stress, infection/fever, Afib, anemia, hyperthyroidism.
108
Why are pts with mitral stenosis at risk for strokes?
They have an increased risk for mural thrombus formation due to Afib and left atrial enlargement. There is stasis of blood due to abnormal movement of the wall (Afib) which can form a thrombi and embolize → stroke.
109
General pathophysiology of aortic stenosis
LV squeezes but obstruction aorta → LVH → blood backs up into LA → increased LAP/ left atrial enlargement → Pulmonary HTN → Right sided heart failure.
110
What are the causes of aortic stenosis in adults, and what is the most common cause among them?
1) Fibrosis and calcification from "wear and tear" (most common)
2) Congenital malformation- bicuspid aortic valve increases risk and hastens disease onset.
3) Chronic rheumatic valve disease
111
When does aortic regurgitation occur?
Backflow of blood from aorta into LV occurs during diastole.
112
"Morphology" of continuous murmurs and examples of defects that produce them
Begin in systole (S1), peak near S2, and continuous into all or part of diastole.
Ex: PDA
113
3 common sx of aortic stenosis
1) Angina
2) CHF
3) Syncope (during exertion)
