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Cardio Final > Valvular Heart Disease 2 > Flashcards

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)

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2
Q

Aortic stenosis evaluation with

A

echocardiogram

catheterization

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3
Q

Aortic Stenosis - pathophysiology

A

blood flow across aortic valve is impeded in systole (i.e. valve stenotic –> doesn’t open well)

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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

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5
Q

In aortic stenosis, the resulting elevation of diastolic LV pressure leads to

A

left atrial hypertrophy

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6
Q

valve in aortic stenosis

A

calcified and stenotic

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7
Q

Angina

A

substantial imbalance btw. myocardial oxygen supply and demand

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8
Q

Clinical manifestations of AS

A

Angina
Exertional syncope
Dyspnea (heart failure)
Murmur

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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

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10
Q

In AS, myocardial oxygen supply is decreased due to

A

-elevated LV diastolic pressure reduces coronary perfusion gradient

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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”
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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

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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”

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14
Q

Symptomatic aortic stenosis

A

life-threatening

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15
Q

survival time in AS

A

5-year survival in severe inoperable AS

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16
Q

natural history of severe symptomatic uncorrected AS

A

very poor

1 year survival rate in advanced disease is 57%

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17
Q

In AS, when is aortic valve replacement indicated?

A
  • development of symptoms

- evidence of progressive LV dysfunction

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18
Q

effect of AVR (aortic valve replacement) in AS

A

dramatic

10 year survival rate rises to ~60%

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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
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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
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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

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22
Q

aortic regurgitation

A

failure of aortic valve to close tightly cuases backflow of blood into left ventricle

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23
Q

Causes of Aortic Regurgitation (AR)

A

(1) Abnormalities of valve leaflets

(2) Abnormalities of aortic root

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24
Q

Abnormalities of valve leaflets in AR

A
  • congenital (bicuspid) valve
  • endocarditis
  • rheumatic
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25
Q

Abnormalities of aortic root in AR

A
  • aortic aneurysm
  • aortic dissection
  • annuloaortic ectasia
  • syphilis
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26
Q

AR - pathophysiology

A

abnormal regurgitation of blood from the aorta into the LV occurs during diastole

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27
Q

factors influencing severity of AR

A
  • size of aortic refurfitant orifice
  • pressure gradient across the aortic valve during diastole
  • duration of diastole
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28
Q

hemodynamic abnormalities and symptoms in AR

A

differ in acute and chronic AR

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29
Q

in AR, slow heart rate is

A

harmful - don’t want a lot of time in diastole

duration of diastole influences severeity of AR

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30
Q

Chronic AR - pathophysiology

A

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

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31
Q

type of hypertrophy in Chronic AR

A

eccentric hypertrophy (chronic dilatation)

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32
Q

Physical Exam findings in AR

A 
Wide Pulse Pressure: 
Corrigan pules
De Musset sign 
Hill sign 
Muller sign
Quincke sign
Traube sign
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33
Q

corrigan pulse

A

water-hammer pulses in carotids

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34
Q

de musset sign

A

head bobbing with each systole

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35
Q

hill sign

A

popliteal systolic pressure >40-60 mmHG greater than the brachial systolic pressure

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36
Q

muller sign

A

systolic pulsation of the uvula

37
Q

quincke sign

A

capillary pulsations visible at the lip or proximal nail bed

38
Q

traube sign

A

“pistol shot” sound heard over the femoral artery during systole

39
Q

AR murmur

A

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
Q

Chronic AR - pathophysiology of angina

A

decreased aortic diastolic pressure –>

coronary artery perfusion pressure falls (angina) –>

reducing myocardial oxygen supply (anginga)

increased LV size

41
Q

Chronic AR - pathophysiology of HF

A

gradually profressive remodeling of LV occurs –>

systolic dysfunction –>

increased left atrial and pulmonary vascular pressures –>

HEART FAILURE

42
Q

Clinical progression from asymptomatic chronic AR and normal LV contractile function

A

very slow

43
Q

Treatment for AR

A

differs in asymptomatic versus symptomatic patients

44
Q

Treatment chronic AR - asymptomatic patients w normal LV function

A

Vasodilators (CCBs, ACE inhibitors) when HTN is present

45
Q

Treatment chronic AR - symptomatic patients or severe AR and impaired LV contractile function (EF < 50%)

A
  • 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
Q

How is valve replacement in chronic AR different from valve replacement in AS?

A

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
Q

Mitral stenosis

A

stenotic mitral valve; reduced blood flow into left ventricle

48
Q

Mitral stenosis etiology

A 
rheumatic fever
congenital
calcific/degenerative
endocarditis
tumors
49
Q

cross-sectional area of a normal mitral valve

A

4-6 sq. cm

50
Q

mitral stenosis (MS) valve size

A

valve area is reduced to less than 2 sq. cm

51
Q

MS - pathophysiology

A

impaired filling of left ventricle across the narrowed mitral valve may

(1) reduce LV stroke volume and
(2) cardia output

52
Q

Clinical symptoms in MS

A 
dyspnea
hemoptysis
Right HF 
Atrial fibrillation 
stroke
53
Q

MS - pathophys of dyspnea

A

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
Q

MS - pathophys of hemoptysis

A

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
Q

MS - Pulmonary HTN

A

The elevation of LA pressure in MS can result in two distinct forms of pulmonary HTN

  • Passive pulmonary HTN
  • Reactive pulmonary HTN
56
Q

Passive pulmonary HTN

A

backward transmission of LA pressure into pulmonary vasculature

obligatory increase in pulmonary artery pressure

57
Q

Reactive pulmonary HTN

A

medial hypertrophy and intimal fibrosis of the pumlonary arterioles –> “beneficial”

58
Q

Right heart failure - MS

A

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
Q

Atrail Fibrillation - MS

A

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
Q

Stroke - MS

A

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
Q

MS - Palpation on exam

A

right ventricular “Tap” - increased RV pressure

62
Q

MS - Auscultation on exam

A

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
Q

MS - hemodynamics

A

LA Pressure always higher than LV Pressure

64
Q

survival in MS

A

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
Q

MS - tretment

A

drugs

mechanical correction of stenosis

66
Q

MS - drug treatment

A

Vascular congestion –> diuretics

Atrial fibrillation –> B-blockers, CCBs or digoxin; chronic anticoag therapy

67
Q

MS - mechanical correction of stenosis (treatment)

A

Percutaneous balloon mitral valvuloplasty
-very effective for rheumatic MS (whih tears the commissurla fissure)

Surgery

  • open mitral commissurotomy
  • mitral valve replacement
68
Q

Mitral regurgitation (MR)

A

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
Q

Causes of MR

A

Primary or Secondary

70
Q

Primary causes of MR

A

“degenerative MR”

disorder of the VALVE

correct w surgical correction of valve

ex: mitralvalve prolapse

71
Q

Secondary causes of MR

A

“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
Q

MR - pathophys

A

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
Q

Direct consequences of MR on heart

A

elevated LA volume and pressure
reduction of forward CO
volume-related stress on LV

74
Q

Severity of MR and the ratio of forward CO to backward flow are dictated by:

A

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
Q

Regurgitant Fraction

A

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
Q

MR - murmur

A

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
Q

Acute MR - clinical presentation

A

Symptoms of Pulmonary Edema

High LA Pressure

78
Q

Chronic MR - clinical presentation

A

Low CO - fatigue, weakness (esp. exertion)

Low contractile dysfunction - dyspnea, orthopnea, paroxysmal noctural dyspnea

Right-sided HF - increase dabdominal girth, peripheral edema

79
Q

the natural history of MR is related to

A

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
Q

Acute MR w pulmonary edema - Treatment

A

IV diuretics - relieve pulmonary edema
Vasodilators - reduce resistance to forwrd flow and augment forward CO
Intra-aortic balloon pump - reduces afterload

81
Q

Chronic MR - tretment

A

vasocilators - less useful!

treatment of accompanying HTN or LV systolic dysfunction

82
Q

MR surgical options

A

Mitral valve repair - reconstruction of native valve
(mortality rate 2-4%)

Mitral valve replacement
(mortality rate 5-7%)

83
Q

Valvular diseases of Tricuspid valve

A

Stenosis

Regurgitation

84
Q

Tricuspid stenosis

A

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
Q

Tricuspid regurgitation

A

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
Q

Valvular diseases of Pulmonic Valve

A

Stenosis

Regurgitation

87
Q

Pulmonic Stenosis

A

rare
almost always congenital
carcinoid syndrome may be a cuase
only severe PS –> symptoms

transcatheter balloon valvuloplasty effective treatment

88
Q

Pulmonic regurgitation

A

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

Cardio Final (6 decks)

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