Valvular Heart Disease 2 Flashcards
1
Q
Aortic Stenosis causes in adults
A
congenital abnormality (less common)
rheumatic fever
age-related calcific AS (more common)
2
Q
Aortic stenosis evaluation with
A
echocardiogram
catheterization
3
Q
Aortic Stenosis - pathophysiology
A
blood flow across aortic valve is impeded in systole (i.e. valve stenotic –> doesn’t open well)
4
Q
response of LV in aortic stenosis
A
LV is able to compensate initially by undergoing CONCENTRIC hypertrophy in response to the higher systolic pressure it must generate
–> leads to reduced compliance of LV
5
Q
In aortic stenosis, the resulting elevation of diastolic LV pressure leads to
A
left atrial hypertrophy
6
Q
valve in aortic stenosis
A
calcified and stenotic
7
Q
Angina
A
substantial imbalance btw. myocardial oxygen supply and demand
8
Q
Clinical manifestations of AS
A
Angina
Exertional syncope
Dyspnea (heart failure)
Murmur
9
Q
In AS, myocardial oxygen demand is increased due to
A
- muscle mass of hypertrophied LV
- wall stress increased 2/2 elevated systolic ventricular pressure
10
Q
In AS, myocardial oxygen supply is decreased due to
A
-elevated LV diastolic pressure reduces coronary perfusion gradient
11
Q
Exertional syncope in AS
A
- ventricle cannot significantly increase its cardiac output during exercise because of fixed stenotic aortic orifice (“inability to augment cardiac output”)
- exercise leads to “vasodilation” of peripheral muscle beds
- this combination leads to “decreased cerebral perfusion pressure”
12
Q
Dyspnea (heart failure) in AS
A
LV develops “contractile dysfunction” due to the severely increased afterload –>
increased LV diastolic volume and pressure –>
marked elevation of LA and pulmonary venous pressures –>
pulmonary alveolar congestion/symptoms of HF
13
Q
AS murmur
A
crescendo-decrescendo systolic murmur
harsh, high-pitched (loudest at base of heart w diaphragm)
the more severe the AS, the later the peak of the murmur and the softer the A2 closure sound
carotid pulse is weal and delayed “parvus et tardus”
14
Q
Symptomatic aortic stenosis
A
life-threatening
15
Q
survival time in AS
A
5-year survival in severe inoperable AS
16
Q
natural history of severe symptomatic uncorrected AS
A
very poor
1 year survival rate in advanced disease is 57%
17
Q
In AS, when is aortic valve replacement indicated?
A
- development of symptoms
- evidence of progressive LV dysfunction
18
Q
effect of AVR (aortic valve replacement) in AS
A
dramatic
10 year survival rate rises to ~60%
19
Q
Aortic valve replacement in AS
A
greatly improves survival
- early and late outcomes similarily good in both symptomatic and asympotomatic patients
- omission of surgical treatment is most important risk factor for late mortality in asymptomatic patients with SAS
20
Q
AS treatment
A
valve replacement only effective treatment (open surgery or transcatheter percutaneous approach)
replace aortic valve when:
- AS is severe
- symptoms of AS
- reduced LV EF
21
Q
Percutaneous balloon valvuloplasty in AS
A
not a very effective treatment; can palliate symptoms
up to 50% patients develop “restenosis” w/in 6 months
option in patients who are poor surgical candidates or as a temporizing measure
22
Q
aortic regurgitation
A
failure of aortic valve to close tightly cuases backflow of blood into left ventricle
23
Q
Causes of Aortic Regurgitation (AR)
A
(1) Abnormalities of valve leaflets
(2) Abnormalities of aortic root
24
Q
Abnormalities of valve leaflets in AR
A
- congenital (bicuspid) valve
- endocarditis
- rheumatic
25
Abnormalities of aortic root in AR
- aortic aneurysm
- aortic dissection
- annuloaortic ectasia
- syphilis
26
AR - pathophysiology
abnormal regurgitation of blood from the aorta into the LV occurs during diastole
27
factors influencing severity of AR
- size of aortic refurfitant orifice
- pressure gradient across the aortic valve during diastole
- duration of diastole
28
hemodynamic abnormalities and symptoms in AR
differ in acute and chronic AR
29
in AR, slow heart rate is
harmful - don't want a lot of time in diastole
duration of diastole influences severeity of AR
30
Chronic AR - pathophysiology
AR subjects LV primarily to volume overload but also to an excessive pressure overload -->
ventricle compensates through chronic dilatation (eccentric hypertrophy) -->
increases compliance of LV -->
aortic diastolic pressure drops substantially
aortic systolic pressure raised 2/2 higher volume with each beat -->
WIDENED PULSE PRESSURE
31
type of hypertrophy in Chronic AR
eccentric hypertrophy (chronic dilatation)
32
Physical Exam findings in AR
```
Wide Pulse Pressure:
Corrigan pules
De Musset sign
Hill sign
Muller sign
Quincke sign
Traube sign
```
33
corrigan pulse
water-hammer pulses in carotids
34
de musset sign
head bobbing with each systole
35
hill sign
popliteal systolic pressure >40-60 mmHG greater than the brachial systolic pressure
36
muller sign
systolic pulsation of the uvula
37
quincke sign
capillary pulsations visible at the lip or proximal nail bed
38
traube sign
"pistol shot" sound heard over the femoral artery during systole
39
AR murmur
high-pitched, diastolic, decrescendo, heard best at 4th left intercostal space
increases with hand grip
* often also sytolic murmur (2/2 high flow during systole) headwith patient leaning forward after exhaling
* may be 2nd diastolic murmur at apex (Austin-Flint murmur) due to vibration of mitral leaflets and cho0rdae during diastole
40
Chronic AR - pathophysiology of angina
decreased aortic diastolic pressure -->
coronary artery perfusion pressure falls (angina) -->
reducing myocardial oxygen supply (anginga)
increased LV size
41
Chronic AR - pathophysiology of HF
gradually profressive remodeling of LV occurs -->
systolic dysfunction -->
increased left atrial and pulmonary vascular pressures -->
HEART FAILURE
42
Clinical progression from asymptomatic chronic AR and normal LV contractile function
very slow
43
Treatment for AR
differs in asymptomatic versus symptomatic patients
44
Treatment chronic AR - asymptomatic patients w normal LV function
Vasodilators (CCBs, ACE inhibitors) when HTN is present
45
Treatment chronic AR - symptomatic patients or severe AR and impaired LV contractile function (EF < 50%)
- AV replacement surgery
- replace valve when the AR is severe and the OV ejection fraction is under 50% or the LV end-diastolic dimension is > 50 mm, *even in the absence of symptoms*
46
How is valve replacement in chronic AR different from valve replacement in AS?
in AS, you can safely wait for symptoms before moving forward with AVR, so long as the LV function is normal
in chronic AR, even in the absence of symptoms, you replace valve if LV EF is less than 50%
47
Mitral stenosis
stenotic mitral valve; reduced blood flow into left ventricle
48
Mitral stenosis etiology
```
rheumatic fever
congenital
calcific/degenerative
endocarditis
tumors
```
49
cross-sectional area of a normal mitral valve
4-6 sq. cm
50
mitral stenosis (MS) valve size
valve area is reduced to less than 2 sq. cm
51
MS - pathophysiology
impaired filling of left ventricle across the narrowed mitral valve may
(1) reduce LV stroke volume and
(2) cardia output
52
Clinical symptoms in MS
```
dyspnea
hemoptysis
Right HF
Atrial fibrillation
stroke
```
53
MS - pathophys of dyspnea
High left atrial pressure is passively transmitted to pulmonary circulation -->
increased pulmonary venous and capillary pressures -->
transudation of plasma into lung interstitium and alveoli -->
DYSPNEA
54
MS - pathophys of hemoptysis
significant elevation of pulmonary venous pressure in severe MS -->
opening of collateral channels between pulmonary and bronchial veins -->
rupture of a bronchial vein into the lung parenchyma -->
HEMOPTYSIS
55
MS - Pulmonary HTN
The elevation of LA pressure in MS can result in two distinct forms of pulmonary HTN
- Passive pulmonary HTN
- Reactive pulmonary HTN
56
Passive pulmonary HTN
backward transmission of LA pressure into pulmonary vasculature
obligatory increase in pulmonary artery pressure
57
Reactive pulmonary HTN
medial hypertrophy and intimal fibrosis of the pumlonary arterioles --> "beneficial"
58
Right heart failure - MS
progressive elevation of right-sided heart pressures as the right ventricle pumps against the increased resistance -->
RVH and dilatation -->
Right heart failure
-JVD, Hepatomegaly, Ascites, Peripheral edema
59
Atrail Fibrillation - MS
chronic pressure overload of the LA -->
left atrial enlargement -->
stretch of the atrial conduction fibers may disrupt the integrity of the cardiac conduction system -->
A fibrillation
60
Stroke - MS
relative stagnation of blood flow in the filated LA (esp. when combined with a fib) -->
predispose to inta-atrial thrombus formation -->
thromboemboli to peripheral organs -->
STROKE
61
MS - Palpation on exam
right ventricular "Tap" - increased RV pressure
62
MS - Auscultation on exam
early stage Loud S1 - mitral leaflets are still wid eopen at the start of systole
late stage Soft S1 - leaflets are so severely restricted in their mobility due to severe scarrinf or calcification
Opening snap
Diastolic rumble
Presystolic accentuation
63
MS - hemodynamics
LA Pressure always higher than LV Pressure
64
survival in MS
10-year survival of untreated patients after symptom onset is 50-60%
survival exceeds 80% in asymptomatic or minimally symptomatic patients
mean survival <3 years for those who develop significant pulmonary HTN
65
MS - tretment
drugs
| mechanical correction of stenosis
66
MS - drug treatment
Vascular congestion --> diuretics
| Atrial fibrillation --> B-blockers, CCBs or digoxin; chronic anticoag therapy
67
MS - mechanical correction of stenosis (treatment)
Percutaneous balloon mitral valvuloplasty
-very effective for rheumatic MS (whih tears the commissurla fissure)
Surgery
- open mitral commissurotomy
- mitral valve replacement
68
Mitral regurgitation (MR)
mitral valve does not close properly when the heart pumps
abnormal leaking of blood backwards – regurgitation from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts
69
Causes of MR
Primary or Secondary
70
Primary causes of MR
"degenerative MR"
disorder of the VALVE
correct w surgical correction of valve
ex: mitralvalve prolapse
71
Secondary causes of MR
"functional MR"
MR is a result of an underlying problem of the myocardium
treat underlying cardiomyopathy
ex: dilated ischemic cardiomyopathy and HF leading to annular dilation and MR
72
MR - pathophys
a portion of the LV stroke volume is "ejected backward into the low pressure LA" during systole
LV stroke volume rises to meet the normal circulatory needs (accomplished via Frank-Sterliong mechanism)
73
Direct consequences of MR on heart
elevated LA volume and pressure
reduction of forward CO
volume-related stress on LV
74
Severity of MR and the ratio of forward CO to backward flow are dictated by:
size of mitral orifice during regurgitation
systolic pressure gradient between the LV and LA
SVR opposing forward LV flow
LA compliance
Duration of regurgitation with each systolic contraction
75
Regurgitant Fraction
Volume of MR / Total LV stroke volume
What proportion of blood is going through mitral valve as opposed to out the normal aortic valve
76
MR - murmur
high-pitched, blowing in nature
present in systole at apex
increases with hand grip
can hear S3
can radiate to axilla
canhear murmur on the back and spine
77
Acute MR - clinical presentation
Symptoms of Pulmonary Edema
| High LA Pressure
78
Chronic MR - clinical presentation
Low CO - fatigue, weakness (esp. exertion)
Low contractile dysfunction - dyspnea, orthopnea, paroxysmal noctural dyspnea
Right-sided HF - increase dabdominal girth, peripheral edema
79
the natural history of MR is related to
its underlying cause
ex:
Rheumatic MR - slow progression (15 year survival rate of 70%)
Rupture of chordae tendinae or endocarditis - result in immediate life-threatening situation
80
Acute MR w pulmonary edema - Treatment
IV diuretics - relieve pulmonary edema
Vasodilators - reduce resistance to forwrd flow and augment forward CO
Intra-aortic balloon pump - reduces afterload
81
Chronic MR - tretment
vasocilators - less useful!
treatment of accompanying HTN or LV systolic dysfunction
82
MR surgical options
Mitral valve repair - reconstruction of native valve
(mortality rate 2-4%)
Mitral valve replacement
(mortality rate 5-7%)
83
Valvular diseases of Tricuspid valve
Stenosis
| Regurgitation
84
Tricuspid stenosis
rare
usually 2/2 rheumatic fever
right heart failure predominate
large a wave seenin the JVP 2/2 high atrial pressre during atrial contraction
usually requires surgery
85
Tricuspid regurgitation
usually functional (secondary) to RV enlargement
carcinoid is another rare cause
large CV wave seen in the JVP
treat underlying cause
if severe, surgery may be required
86
Valvular diseases of Pulmonic Valve
Stenosis
| Regurgitation
87
Pulmonic Stenosis
rare
almost always congenital
carcinoid syndrome may be a cuase
only severe PS --> symptoms
transcatheter balloon valvuloplasty effective treatment
88
Pulmonic regurgitation
can be congenital
may be due to severe pulmonary HTN and dilation of the PA
other causes: infective endocarditis, carcinoid syndrome, tetralogy of fallot, chest trauma, rheumatic heart disease
surgical treatment if severe and leading to RV failure
