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5. Auscultation and physical diagnosis > Heart sounds > Flashcards

Heart sounds Flashcards

1
Q

Characteristics of S2

A
  • Higher pitched
  • Shorter duration
  • Louder at heart base
  • Mark the end of ventricular systole
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2
Q

Components of S2

A

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

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3
Q

Explain physiological split S2

A

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

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4
Q

Condition to hear splitting

A

Needs interval >20-30ms to hear a split

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5
Q

Types of pathologic split S2

A

Persistent
Fixed
Paradoxical

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6
Q

Persistent split S2

A

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

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7
Q

Fixed split S2

A

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

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8
Q

Paradoxical splitting

A

A2 delayed => AoV close after PV
o Split incr in expiration: P2 earlier (decr filling)
o Split decr in inspiration: P2 further delayed

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9
Q

Causes of spit S2

A

Delayed PV closure
Early AoV closure
Delayed AoV closure

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10
Q

Cause of delayed PV closure

A
  • 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
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11
Q

Causes of early AoV closure

A
  • Shorten LVET
    o MR
    o VSD
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12
Q

Causes of delayed AoV closure

A
  • LBBB
  • RV paced beats
  • PDA
  • AS
  • AI
  • Systemic hypertension
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13
Q

Accentuated S2 is secondary to

A

Accentuated P2 or A2

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14
Q

Causes of accentuated P2

A
  • PH 2nd to CHF
  • Congenital L to R shunt
    o PDA
    o VSD
    o ASD
  • Primary PH
  • PTE
  • PA dilation
  • Mild PS
  • HW dz
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15
Q

Causes of accentuated A2

A
  • Systemic hypertension
  • Ao dilation/aneurysm
  • Valvular Ao stenosis
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16
Q

S2 can be reduced 2nd to

A

Reduced S2
Reduced P2
Reduced A2

17
Q

Causes of reduced S2

A

Decr LV fct
* HypoT4
* Shock
* DCM

18
Q

Cause of decr P2

A

PS

19
Q

Cause of decr A2

A
  • Calcific valvular Ao stenosis
  • AI
20
Q

Characteristics S1

A
  • Higher frequency
  • Onset of ventricular systole
21
Q

Components of S1

A
  • 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
22
Q

Causes of S1 splitting

A

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

23
Q

Intensity of S1 determined by

A
  • 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
24
Q

Causes of accentuated S1

A
  • 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
25
Q

Causes of reduced S1

A
  • Prolonged P-R
  • Decr LV function
    o HypoT4
    o Severe CHF
    o Shock (hypovolemic)
  • LBBB
  • Negative inotropic agents
  • Abnormal IVCT
    o AI
    o MR
26
Q

Mid systolic click features

A

o Discrete high frequency sounds
o Mid to late ventricular systole
o Best heart over MV or TV area
 Can start a mid/late systolic murmur
 Be obscured by holosystolic murmur

27
Q

cause mid systolic click

A

Mitral valve prolapse
o Sudden tension of redundant chordae tendinae/MV leaflets
o Occasionaly heard w CVD

28
Q

Ejection click features

A

o Discrete high frequency sounds following S1
 High pitched, brief, clicky = ejection click
 Sounds heard best at L heart base
o At time of onset of ventricular ejection
 From Ao or PA
 Pulmonic ejection sounds best ausculted in pulmonic area
o Uncommon in dogs/cats

29
Q

Causes ejection click

A

o E release/vibrations from onset of ventricular ejection: LV => Ao
 Accentuation of normal second component of S1
 Increased/forceful flow in Ao: systemic hypertension
 Often associated w Ao root dilation
o Valvular Ao stenosis: fused AoV leaflets reach their opening limit after start of ejection

30
Q

DDX ejection click

A

Differentiate from S4-S1 or split S1

31
Q

Causes pulmonic ejection sounds

A
  • Dilated MPA (w or w/o PH)
    o Idiopathic PA dilation
  • Primary/secondary PH (HW, PTE)
  • ASD
  • Valvular PS
32
Q

Cause Ao ejection sounds

A
  • Forceful LV ejection
  • High output states
    o HyperT4
    o Exercise
    o Anemia
  • Dilation of ascending Ao (w or w/o systemic hypertension)
  • Valvular AS
33
Q

Horses atrial sounds

A

 S4, S3 and short diastolic murmurs may be audible in healthy horses
o Easier to detect on PCG because low frequency sounds
o S4: atrial contraction
 Even if present on phonocardiogram: not all audible
 Soft, low intensity
 Shortly before S1
 After P wave, before QRS
o S3: rapid filling
 Low intensity
 Shortly after S2

 AI: holodiastolic w decrescendo character
o ↑ intensity at end of diastole due to A kick → open MV → anterior septal leaflet hit AI jet
o Austin Flint murmur

5. Auscultation and physical diagnosis (8 decks)

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