Auscultation of the Heart Flashcards

1
Q

S1

A

M1 and T1, best heart at lower left sternal border

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2
Q

when is normal splitting of s1 heard

A

complete RBBB

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3
Q

Describe s1 in mitral stenosis

A

at early stage, s1 intensity is increased when valve leaflets are still pliable in hyperkinetic states and with short PR intervals
in late stages - s1 becomes softer - leaflets are rigid and calcified with contractile dysfunction, b adrenergic receptor blockers and long PR intervals

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4
Q

S2

A

A1 and P1

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5
Q

physiologic splitting of S2

A

the A2 -P2 interval increases during inspiration and narrows in expiration
components are best heart at second left ICS in supine position

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6
Q

other causes of A2-P2 interval widening

A

complete RBBB - delayed pulmonic valve closure

Severe MR because of premature aortic valve closure

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7
Q

describe heartsound in pulmonary hpn

A

unusually narrow but physiologic splitting of s2 with increased intensity of P2 comparedto A2 indicates PA hpn

P2 can be heartd at most sites across the pericardium

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8
Q

describe S2 in ostium secundum ASD

A

fixed splitting , the A2 P2 interval is wide and unchanged with respiration

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9
Q

Reverse or paradoxical splitting

A

consequence of a pathologic delay in aortic valve closure asmay occur with Complete LBBB, RV apical pacing,severe aortic stenosis,HOCM,MI

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10
Q

Nonejection clicks which occur after upstroke of carotid pulse

A

MVP

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11
Q

what happens in standing in MVP

A

ventricular preload AND afterload decrease and the click/murmur move closer to S1

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12
Q

what happens in squatting in MVP

A

ventricular preload and afterload increase - the prolapsing mitral valve tenses later in systole and the click and murmur move away from s1

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13
Q

Mitral stenosis

A

High-pitched opening snap (OS) a short distance after S2 (diastolic)

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14
Q

what is a pericardial knock

A

high pitched early diastolic sound that corresponds in timing to abrupt cessation of ventricular expansion after AV valve opening and to the prominent y descent in JV waveform in pxs with constrictive pericarditis

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15
Q

tumor plop

A

rarely heard with atrial myxoma

low-pitched sound from daistolic prolapse of tumor across the mitral valve, sometimes with diastolic murmur

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16
Q

S3

A

occurs at rapid filling phase of ventricular diastole
may be present in children/ adolescents
also systolic heart failure in older pxs

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17
Q

S4

A

occurs during atrial filling phase of ventricular diastole - presystolic ventricular expansion; common in pxs with accentuated atrial contribution to ventricular filling (LV hypertrophy)

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18
Q

palpable thrill is what grade

A

grade 4 or higher

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19
Q

acute severe MR

A

decrescendo, early systolic murmur (steep rise in pressure within the noncompliant atrium)

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20
Q

Severe MR

A

posterior mitral leaflet prolpase or flail radiates anteriorly and to the base

anterior leaflet involvement radiates posteriolry and to the axilla

21
Q

acute TR with normal PA pressures

A

early systolic murmur increases with inspiration audible at lower left sternal border, with regurgitant CV waves

22
Q

Aortic stenosis or sclerosis

A

causes most midsystolic murmurs in adults

23
Q

midsystolic murmurs

A

AS, HOCM, pulmonic stenosis large ASD, left to right shunt

24
Q

A late, apical systolic murmur indicates

A

MVP

25
Q

explain the presence of apical systolic murmur in acute myocardial ischemia

A

MR is caused by apical tethering and mal-coaptation of leaflets due to structural and functional changes of the ventricle and mitral annulus

26
Q

holosystolic murmurs found in

A

chronic MR, VSD

27
Q

differentiate holosystolic murmurs in MR and VSD

A

MR best heard at cardiac apex; VSD best heard at mid-left sternal border with palpable thrill

28
Q

Chronic AR

A

Diastolic murmur - highpitched descrescendo, early to mid diastolic murmur

Murmur is softer and shorter in acute AR - includes tachycardia, soft s1, absence of peripheral findings of diastolic runoff

29
Q

Murmur in pulmonic regurgitation

A

heard at left sternal border; associated with annular enlargement from chronic PA hpn (Graham steell murmur)
signs of RV overload present
invariably present after TOF repair

30
Q

Classic cause of mid to late diastolic murmur

A

Mitral stenosis; may be silent in low CO and large habitus pxs

Murmur best heartd at apex, low pitched; with OS in early stage

31
Q

low pitched mid to late apical diastolic murmur

A

associated with AR (Austin flint murmur)

32
Q

how can AR be distinguished with MS

A

response to vasodilators and presence of associated findings

33
Q

other causes of mid diastolic murmurs -

A

atrial myxoma, complete heart block, acute rheumatic mitral valvulitis (Carey Coombs murmur)

34
Q

right sided events except pulmonic ejection sounds - increase in inspiration, decrease in expiration;

A

left sided events behave oppositely - 100% sensitivity, 88 % specificity

35
Q

what murmurs will increase in response to increase LV afterload (handgrip, vasopressor administration) and decrease after exposure to vasodialting agents (amyl nitrite)

A

MR, VSD, AR

36
Q

Describe murmur in HOCM

A

softer and shorter with squatting;
longer and louder on rapid standing
also increases in Valsalva maneuver

37
Q

Aortic stenosis vs MR - regarding change in intensity of systolic murmur in the first beat after premature beat

A

if there is change in intensity of systolic murmur after a premtaure beat - more likely to be AS because of enhanced LV filling / forward flow acceleration hence increase in gradient and louder murmur vs in MR - there is minimal further increase in mitral valve flow or change in gradient

38
Q

Gallavardin effect

A

murmur in aortic stenosis is well transmitted to the apex

39
Q

probability of HF was best predicted by

A

past history of HF (LR 5.8)
PND ( LR 2.6)
s3 (LR 11)
AF (LR 3.8)

Except PND - same features predicted HF in concomitant pulmonary dse

40
Q

Dyspnea or discomfort in lateral decubitis

A

Trepopnea - accounts for right sided pleural effusions

41
Q

Bendopnea

A

shortness of breath noticeable when bending forward; higher RA and PCWP

42
Q

when is HF likely to be preserved

A

when pxs are female, older, increased BMI

43
Q

Four signs used to predict elevated filling pressures

A

JV distension
AJR sign
S3/S4,rales
pedal edema

44
Q

Provides the readiest bedside estimate of LV filling pressure

A

JVP

45
Q

EStimated RA pressure higher than 12 and 2 pillow orthopnea provided prediction of PA wedge pressure >22mHg - compared favorably iwth BNP levels

A

ESCAPE trial

46
Q

In pxs with chronic HF, how many will lack rales despite elevated PA wedge pressures

A

75-80%

47
Q

Audible phases of Valsalva maneuver

A

Phase I and IV

48
Q

Abnormal response to Valsalva in HF patients:

A

1) absence of phase IV overshoot - decreased systolic function
2) square-wave response -elevated filling pressures independed of EF