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
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
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
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
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
- M1
- 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
- Degree of separation b/n AV valve leaflets at the beginning of ventricular systole
- 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
- Shrot PR interval
- 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
- Long PR interval
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
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
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
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
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
- Aortic & pulmonic stenosis
- Changes pulmonary impedance: “hangout interval”
- Atrial septal defects
- Pulmonary hypertension
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))
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
- General
- 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
- General
- 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
- General
- Pericardial knock
- Sharp early diastolic sound associatd w/ constrictive pericarditis
- Opening snaps
- In patients w/ rheumatic or congenital valvular disease
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
- Valvular clicks
- Intensity of valvular systolic ejection sounds
- Correlates w/ valve pliability, not severity of stenosis
- Increased calcification –> diminished/disappeared systolic ejection sounds
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
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
- Supine position