Auscultation of the Heart Flashcards
S1
M1 and T1, best heart at lower left sternal border
when is normal splitting of s1 heard
complete RBBB
Describe s1 in mitral stenosis
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
S2
A1 and P1
physiologic splitting of S2
the A2 -P2 interval increases during inspiration and narrows in expiration
components are best heart at second left ICS in supine position
other causes of A2-P2 interval widening
complete RBBB - delayed pulmonic valve closure
Severe MR because of premature aortic valve closure
describe heartsound in pulmonary hpn
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
describe S2 in ostium secundum ASD
fixed splitting , the A2 P2 interval is wide and unchanged with respiration
Reverse or paradoxical splitting
consequence of a pathologic delay in aortic valve closure asmay occur with Complete LBBB, RV apical pacing,severe aortic stenosis,HOCM,MI
Nonejection clicks which occur after upstroke of carotid pulse
MVP
what happens in standing in MVP
ventricular preload AND afterload decrease and the click/murmur move closer to S1
what happens in squatting in MVP
ventricular preload and afterload increase - the prolapsing mitral valve tenses later in systole and the click and murmur move away from s1
Mitral stenosis
High-pitched opening snap (OS) a short distance after S2 (diastolic)
what is a pericardial knock
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
tumor plop
rarely heard with atrial myxoma
low-pitched sound from daistolic prolapse of tumor across the mitral valve, sometimes with diastolic murmur
S3
occurs at rapid filling phase of ventricular diastole
may be present in children/ adolescents
also systolic heart failure in older pxs
S4
occurs during atrial filling phase of ventricular diastole - presystolic ventricular expansion; common in pxs with accentuated atrial contribution to ventricular filling (LV hypertrophy)
palpable thrill is what grade
grade 4 or higher
acute severe MR
decrescendo, early systolic murmur (steep rise in pressure within the noncompliant atrium)
Severe MR
posterior mitral leaflet prolpase or flail radiates anteriorly and to the base
anterior leaflet involvement radiates posteriolry and to the axilla
acute TR with normal PA pressures
early systolic murmur increases with inspiration audible at lower left sternal border, with regurgitant CV waves
Aortic stenosis or sclerosis
causes most midsystolic murmurs in adults
midsystolic murmurs
AS, HOCM, pulmonic stenosis large ASD, left to right shunt
A late, apical systolic murmur indicates
MVP
explain the presence of apical systolic murmur in acute myocardial ischemia
MR is caused by apical tethering and mal-coaptation of leaflets due to structural and functional changes of the ventricle and mitral annulus
holosystolic murmurs found in
chronic MR, VSD
differentiate holosystolic murmurs in MR and VSD
MR best heard at cardiac apex; VSD best heard at mid-left sternal border with palpable thrill
Chronic AR
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
Murmur in pulmonic regurgitation
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
Classic cause of mid to late diastolic murmur
Mitral stenosis; may be silent in low CO and large habitus pxs
Murmur best heartd at apex, low pitched; with OS in early stage
low pitched mid to late apical diastolic murmur
associated with AR (Austin flint murmur)
how can AR be distinguished with MS
response to vasodilators and presence of associated findings
other causes of mid diastolic murmurs -
atrial myxoma, complete heart block, acute rheumatic mitral valvulitis (Carey Coombs murmur)
right sided events except pulmonic ejection sounds - increase in inspiration, decrease in expiration;
left sided events behave oppositely - 100% sensitivity, 88 % specificity
what murmurs will increase in response to increase LV afterload (handgrip, vasopressor administration) and decrease after exposure to vasodialting agents (amyl nitrite)
MR, VSD, AR
Describe murmur in HOCM
softer and shorter with squatting;
longer and louder on rapid standing
also increases in Valsalva maneuver
Aortic stenosis vs MR - regarding change in intensity of systolic murmur in the first beat after premature beat
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
Gallavardin effect
murmur in aortic stenosis is well transmitted to the apex
probability of HF was best predicted by
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
Dyspnea or discomfort in lateral decubitis
Trepopnea - accounts for right sided pleural effusions
Bendopnea
shortness of breath noticeable when bending forward; higher RA and PCWP
when is HF likely to be preserved
when pxs are female, older, increased BMI
Four signs used to predict elevated filling pressures
JV distension
AJR sign
S3/S4,rales
pedal edema
Provides the readiest bedside estimate of LV filling pressure
JVP
EStimated RA pressure higher than 12 and 2 pillow orthopnea provided prediction of PA wedge pressure >22mHg - compared favorably iwth BNP levels
ESCAPE trial
In pxs with chronic HF, how many will lack rales despite elevated PA wedge pressures
75-80%
Audible phases of Valsalva maneuver
Phase I and IV
Abnormal response to Valsalva in HF patients:
1) absence of phase IV overshoot - decreased systolic function
2) square-wave response -elevated filling pressures independed of EF
