Heart sounds Flashcards
Characteristics of S2
- Higher pitched
- Shorter duration
- Louder at heart base
- Mark the end of ventricular systole
Components of S2
aortic (A2) & pulmonic (P2)
o May be audible in normal individuals: best at L heart base
o A2 normally louder: due to higher pressures in L heart
Explain physiological split S2
Incr split during inspi
decr intrathoracic pressures => incr venous return to RV + decr PVR => incr RVET => delay P2
Pooling of blood in pulmonary vasculature => decr LV venous return => decr LV ET => earlier A2 onset
Not detected in dogs/cats due to incr HR
Condition to hear splitting
Needs interval >20-30ms to hear a split
Types of pathologic split S2
Persistent
Fixed
Paradoxical
Persistent split S2
Widened
Incr A2-P2 interval throughout respiratory cycle
o Normal widening of split during inspiration, no fusion in expiration but narrowing of interval still occur
o Anomalous partial pulmonary venous return
incr RV venous return => incr RV ejection volume
* Systolic murmur at L base
Inspiration incr RV venous return further => wider splitting
Fixed split S2
Incr A2-P2 interval with minimal respiratory variation => constant
o ASD: P2 is delayed during expiration, unchanged in inspiration
Variations in systemic venous return counterbalanced by reciprocal changes in flow through the ASD => total RV flow constant
Paradoxical splitting
A2 delayed => AoV close after PV
o Split incr in expiration: P2 earlier (decr filling)
o Split decr in inspiration: P2 further delayed
Causes of spit S2
Delayed PV closure
Early AoV closure
Delayed AoV closure
Cause of delayed PV closure
- Delayed Rv activation
o RBBB
o LV paced beats/ectopy - Prolonged RV mechanical systole
o PS w intact IVS
o Acute PTE
o PH w R-CHF
o HW dz - decr impedance of pulmonary vascular bed
o ASD
o Idiopathic PA dilation
o Mild PS
Causes of early AoV closure
- Shorten LVET
o MR
o VSD
Causes of delayed AoV closure
- LBBB
- RV paced beats
- PDA
- AS
- AI
- Systemic hypertension
Accentuated S2 is secondary to
Accentuated P2 or A2
Causes of accentuated P2
- PH 2nd to CHF
- Congenital L to R shunt
o PDA
o VSD
o ASD - Primary PH
- PTE
- PA dilation
- Mild PS
- HW dz
Causes of accentuated A2
- Systemic hypertension
- Ao dilation/aneurysm
- Valvular Ao stenosis
S2 can be reduced 2nd to
Reduced S2
Reduced P2
Reduced A2
Causes of reduced S2
Decr LV fct
* HypoT4
* Shock
* DCM
Cause of decr P2
PS
Cause of decr A2
- Calcific valvular Ao stenosis
- AI
Characteristics S1
- Higher frequency
- Onset of ventricular systole
Components of S1
- Components: mitral (M1) & tricuspid (T1)
o M1: energy vibration from abrupt closing/tensing of MV apparatus early in systole
o T1: softer, idem but w TV
Causes of S1 splitting
Physiologic splitting is rarely appreciated
* Occasionnaly normal variant in large/giant breed dogs
* Best heard over TV area
* Should be differentiated from: S4, S1 ejection sound or S1 systolic click
Pathologic
* Ventricular conduction disturbances => delay electrical activation of 1 ventricle (BBB)
* Ventricular ectopic beat => asynchronous ventricular activation
Intensity of S1 determined by
- ½ to 2x S2 depending on listening location
- Depend on
o Force of MV closure => ventricular contraction
Contractile state: lV fct, IVCT
Ventricular volume
o Position of leaflets => determined by
Velocity of valve closure/normal position = P-R interval
* Short = atrial contraction just before valve closure => wide open => loud S1
Normal relationship btw atrial/ventricular depol
Integrity of valve closure/apparatus, leaflets mobility
o Thoracic cavity/chest wall
- Beat to beat variation:
o Varying P-R interval
o Marked R-R variation (Afib)
o Pronounced sinus arrhythmia
o Atrial/ventricular premature beats
o 2˚AVB Mobitz I
Causes of accentuated S1
- Short P-R
- Vigorous LV contraction
o Pregnancy
o HyperT4
o Exercise
o Fever
o Anemia
o Systemic hypertension
o Inotropic agents
o Excitement/fear - Arteriovenous fistula
