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Cardiology > Cardiac Auscultation I: Heart Songs > Flashcards

Cardiac Auscultation I: Heart Songs Flashcards

1
Q

Origin of Heart Sounds

A
  • Abrupt “checking” of cardiac valves as they open and close
  • Vibrations are generated in response to th eabrupt deceleration fo blood flow as the AV & semilunar valve leaflets reach their elastic limits
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2
Q

High vs. Low Frequency Sounds

A
  • High
    • S1, S2, opening snaps, & systolic ejection clicks
    • Abrupt checking of heart valves as they open & close
    • Heard w/ diaphragm
  • Low
    • S3 & S4
    • Heard w/ bell
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3
Q

Location of Heart Sounds

  • Aortic valve
  • Pulmonic valve
  • Tricuspid valve
  • Mitral valve
  • Pneumonic
A
  • Aortic valve
    • 2nd or 3rd intercostal space at the right uppser sternal border
    • Can radiate to the suprasternal notch, left parasternal border, & apex
  • Pulmonic valve
    • 2nd or 3rd intercostal space at the left upper sternal border
  • Tricuspid valve
    • Left lower sternal border
  • Mitral valve
    • 5th intercostal space at the mid-clavicular line
    • Can radiate to the axilla, left sternal border, & posteriorly
  • Pneumonic
    • APT M
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4
Q

Relationship of Heart Sounds w/ Cardiac Cycle Events

  • P wave
  • PR interval
  • QRS complex
  • S1
  • Isovolumic contraction
  • LV relaxation
  • S2
  • Isovolumic relaxation
A
  • P wave
    • Atrial systole
  • PR interval
    • AV node delay
  • QRS complex
    • Beginning of ventricular systole & myocardial contraction
  • S1
    • As ventricular pressure > atrial pressure, AV valve closes
    • Rapid rise of ventricular pressure –> sudden retrograde surge of blood against the tensed closed AV valve
    • –> this high frequency sound
  • Isovolumic contraction
    • LV pressure rises until it > central aortic pressure
    • Aortic valve opens –> systolic ejection
  • LV relaxation
    • During the latter part of systole
    • LV presure < central aortic pressure
    • Forward flow in the aorta is maintained due to the momentum of the LV stroke volume
  • S2
    • Positive pressure gradient develops
    • Blood flow in the aorta reverses
    • Retrograde flow is checked by closure of the aortic valve
    • Generation of this high frquency high sound
    • Represented by the incisura ont he aortic pressure tracing
  • Isovolumic relaxation
    • LV pressure decreases w/ no change in LV volume until LA pressure > LV pressure
    • Mitral valve opens
    • Diastolic LV filling begins
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5
Q

Characteristics of S1

  • S1 sounds
    • M1
    • T1
    • Timing
  • Factors which influence the intensity (loudness) of S1
  • Conditions associated w/ a loud S1
  • Conditions associated w/ a soft S1
A
  • S1 sounds
    • M1
      • Louder (attenuated) mitral valve closure
      • Heard at apex
    • T1
      • Softer (diminished) tricuspid valve closure
      • Heard at LLSB
    • M1 occurs before T1
      • Separated by 20 ms
      • Appreciated as a single heart sound
  • Factors which influence the intensity (loudness) of S1
    • Degree of separation b/n AV valve leaflets at the beginning of ventricular systole
      • Greater separation –> louder sound
    • Pliability of valve leaflets
      • More calcified –> less pliable –> softer sound
    • Contractile state
      • Increase inotropic states –> increase ventricle contractility –> AV valves close more forcefully –> louder sound
  • Conditions associated w/ a loud S1
    • Shrot PR interval
      • WPW: early depolarization of the LV via an accessory bypass trac thta tinitiates ventricular contraction while the mitral valve is still open
    • Mitral stenosis
      • W/ a pliable valve
    • Hypercontractile state
      • Exercise, fever, hyperthyroidism
  • Conditions associated w/ a soft S1
    • Long PR interval
      • 1st degree AV block: atiogenic AV valve closure prior to the onset of ventricular systole
    • Mitral stenosis
      • W/ a calcified & restricted valve
    • Acute aortic regurgitation
      • Causes pre-closure of the mitral valve
    • Severe LV systolic dysfunction
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6
Q

S1 Splitting

A
  • Timing of M1 relative to T1 varies
    • Early closure of the mitral valve
    • Late closure of the tricuspid valve
  • May occur w/ RBBB & septal defects w/o Eisenmenger’s physiology (EP)
    • EP: pulmonary hypertension w/ near systemic pressures
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7
Q

Characteristics of S2

  • S2 sounds
  • Intensity of S2
  • Audible inspiratory splitting
A
  • S2 sounds
    • A2: closure of the aortic valve
    • P2: closure of the pulmonic valve
  • Intensity of S2
    • Correlates w/ rate of change of diastolic pressure gradient during valve closure
    • Greater deltaP / deltaT –> louder S2
  • Audible inspiratory splitting
    • A2 precedes P2
    • Present under normal physiological conditions
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8
Q

S2 Splitting

  • Best heard
  • Splitting interval
  • RV vs. LV systolic ejection timing
  • RV vs. LV ejection duration
  • A2 vs. P2
A
  • Best heard
    • At the left upper sternal border
    • More prominent in children, decreases w/ age
  • Splitting interval
    • Significant delay b/n A2 & P2
  • RV vs. LV systolic ejection timing
    • RV ejects into a high capacitance, low impedance pulmonary vascular bed
    • RV has a shorter isovolumic contraction time
    • RV ejection begins before LV ejection
  • RV vs. LV ejection duration
    • RV ejects into a low impedance vascular bed while LV ejects into a high pressure systemic circulation
    • RV ejection duration > LV ejection duration
  • A2 vs. P2
    • Hangout interval: prolonged interval b/n anacrotic notch & pulmonary incisura contributes to audible splitting of S2
    • A2 occurs before P2
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9
Q

Physiological S2 Splitting

  • Phonocardiogram & respirometer
  • Physiologic S2 splitting
  • Mechanism
  • Decreased intrathoracic pressure –>
  • S2 splitting vs. age
A
  • Phonocardiogram & respirometer
    • Phonocardiogram: records heart sounds
    • Respirometer: tracks timing of inspiration & expiration
  • Physiologic S2 splitting
    • S2 splitting interval varies w/ respiration
    • Expiration: shorter separation b/n A2 & P2 –> single heart sound
    • Inspiration: longer separation b/n A2 & P2 –> audible inspiratory splitting
  • Mechanism
    • Diaphragm & intercostal muscles –> negative pressure in the pleural cavity
  • Decreased intrathoracic pressure –>
    • Increased systemic venous return –> increased RV SV –> increased RV ejection time –> delayed P2 closure
    • Increased pulmonary vascular bed capacitance –> decreased pulmonary venous impedance –> longer hangout interval –> delayed P2 closure
    • Increased S2 splitting interval during inspiration
  • S2 splitting vs. age
    • S2 splitting decreases w/ age & should be absent in the elderly
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10
Q

Mechanism of Abnormal S2 Splitting

A
  • Abnormalities in conduction: electromechanical coupling
    • LBBB
    • RBBB
    • Ventricular paced beats
  • Changes in ventricular systole: isovolumetric contraction time (IVCT) + systolc ejection period (SEP) = “hangout interval”
    • Aortic & pulmonic stenosis
      • Abnormal calcification so door out of the ventricle doesn’t open well, increases sytolic ejection time
    • Mitral & tricuspid regurgitation
      • Backleaking of blood b/c doors don’t close properly
      • Opposite of stenosis
  • Changes pulmonary impedance: “hangout interval”
    • Atrial septal defects
    • Pulmonary hypertension
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11
Q

Causes of Abnormal Splitting of S2

  • Wide physiological splitting
  • Reversed (“paradoxical”) splitting
  • Narrow splitting
A
  • Wide physiological splitting
    • Audible splitting is present during expiration
    • Delayed pulmonic closure
      • RBBB
      • Pulmonic stenosis
      • Pulmonary hypertension
      • Atrial septal defects
    • Early aortic closure
      • Severe mitral regurgitation
      • Ventricular septal defects
  • Reversed (“paradoxical”) splitting
    • S2 split narrows during inspiration & widens during expiration
    • Early pulmonic closure
    • Delayed aortic closure
      • LBBB
      • Aortic stenosis
  • Narrow splitting
    • Can’t appreciate/hear inspiratory splitting
    • Early pulmonic closure
      • Severe tricuspid regurgitation
      • Pulmonary hypertension
    • Late aortic closure
      • Aortic stenosis
      • Decreased peripheral vascular resistance (peripheral vascular shutns, patent ductus arteriosus (PDA))
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12
Q

Diastolic Heart Sounds

  • S3
    • General
    • Physiological
    • Pathological
  • S4
    • General
    • Pathological
  • Generation of S3 & S4
  • Summation gallop
    • General
    • Left sided
    • Right sided
  • Pericardial knock
  • Opening snaps
A
  • S3
    • General
      • Low frequency early diastolic filling sound
      • Corresponds w/ rapid diastolic LV filling into an elastic/compliant ventricle
    • Phsyiological
      • In children and young adults
    • Pathological
      • Congestive heart failure w/ increased left heart pressures
      • Significant AV valve regurgitation
  • S4
    • General
      • Low frequency diastolic filling sound
      • Coincides w/ atrial contraction (atrial “kick”)
      • Corresponds w/ late diastolic flow into a stiff, noncompliant ventricle
    • Pathological
      • Hypertensive heart disease
      • Hypertrophic cardiomyopathy
      • Acute myocardial ischemia
  • Generation of S3 & S4
    • When the ventricla suddenly reaches its elastic limits w/ abrupt deceleration in blood flow –> vibrations
  • Summation gallop
    • General
      • When S3 & S4 occur in rapid succession
    • Left sided
      • Heard w/ bell at apex
    • Right sided
      • Heard w/ bell at left lower sternal border
      • May vary w/ respiration
  • Pericardial knock
    • Sharp early diastolic sound associatd w/ constrictive pericarditis
  • Opening snaps
    • In patients w/ rheumatic or congenital valvular disease
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13
Q

Systolic Ejection Sounds

  • General
  • 2 categories
    • Valvular clicks
    • Vascular / root sounds
  • Intensity of valvular systolic ejection sounds
A
  • General
    • High-frequency sound
    • Occurs simulatneously or shortly after onset of ventricular ejection
  • 2 categories
    • Valvular clicks
      • Associated w/ congenitally deformed A & P valves
      • Due to tensing of the deformed valve leaflets as they reach their elastic limits
      • Due to vibrations associated w/ rapid deceleration of the blood column during ventricular ejection
    • Vascular / root sounds
      • Due to the forceful ejection fo blood into tensed great vessels
      • Heard w/ significant systemic / pulmonary hypertension or w/ dilation of the great vessels
  • Intensity of valvular systolic ejection sounds
    • Correlates w/ valve pliability, not severity of stenosis
    • Increased calcification –> diminished/disappeared systolic ejection sounds
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14
Q

Systolic Ejection Sounds

  • Aortic systolic ejection sounds
    • Heard
    • Radiation
  • Pulmonic systolic ejection sounds
    • Heard
    • Inspiration
    • Expiration
A
  • Aortic systolic ejection sounds
    • Heard w/ diaphragm at base of heart
    • Can radiate to apex
  • Pulmonic systolic ejection sounds
    • Heard at left upper sternal border
    • Inspiration –> intensity decreases
      • Increased venous return to RV augments right atrial stroke
      • –> partial opening of the P2 valve prior to ventricular systole
      • Lack of a sharp opening movement of the P2 valve –> decreased intensity
    • Expiration –> intensity increases
      • P2 valve opens rapidly from fully closed position
      • “Halting” of this rapid opening movement –> max sound intensity
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15
Q

Mitral Valve Prolapse

  • General
  • Sound
  • Timing of the M1 click
    • Supine position
    • Upright / standing position
    • Squatting position
A
  • General
    • Mitral valve: abnormally thickened, redundant, & proportionally too long for the size of the mitral valve annulus
  • Sound
    • Click: ssociated high frequency non-ejection systolic sound
    • Associated w/ the sudden tensing of the mitral valve leaflets as the elastic limits of the valve are reached during ventricular contraction
    • Heard at the apex or left lower sternal border
      • Can radiate throughout the precordium
    • Occurs in mid to late systole
    • Associated w/ mitral regurgitant murmur
  • Timing of the M1 click
    • Supine position
      • Increase preload to LV –> increase LVEDV –> increase valve annular dimension –> increase redundancy of the abnormally long mitral valve leaflet –> delayed M1 click –> delayed regurgitant murmur
    • Upright / standing position
      • Decrease preload to LV –> decrease LVEDV –> increase valvular-annular mismatch –> increase M1 redundancy –> earlier M1 click –> earlier mitral regurgitant murmur
    • Squatting position
      • Preload & afterload increase –> increase LVEDV –> later M1 click –> later mitral regurgitant murmur
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Cardiology (40 decks)

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