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5. Auscultation and physical diagnosis > Heart murmurs > Flashcards

Heart murmurs Flashcards

1
Q

Cause of murmurs

A
  • Arise from turbulent flow
    o Viscosity mostly determined by PCV
    o Turbulent flow can result from 2 main factors:
     High velocity → ↑ volume or narrow valve
  • Murmurs from increased blood flow are usually low intensity
     Low viscosity w normal velocity
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2
Q

Reynolds #

A

Reynold’s number = (radius x velocity x density)/viscosity

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3
Q

Description of HM

A

o Anatomic location: PMI
o Intensity, pitch
 High >300Hz
 Mid 100-300Hz
 Low <100Hz
o Timing: systolic, diastolic, continuous
o Duration w/i cardiac cycle: holo/pan, proto/meso/tele
o Quality: shape on phonocardiogram
 Plateau: equal intensity
 Decrescendo: gradually taper off from initial peak
 Crescendo-decrescendo (diamond-shaped): build to a peak and gradually diminish

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4
Q

Systolic murmurs

A

Ejection
Regurgitant

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5
Q

Characteristics of ejection murmur

A
  • Crescendo-decrescendo: ↑ intensity to peak in early-mid systole, then decreases and end before S2
  • ↑ severity of lesions: louder murmurs w delayed peak
    o If not associated w dynamic obstruction: shorter, softer, protosystolic
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6
Q

Causes of ejection murmur

A

o LVOTO (SAS, HCM)
o RVOTO (PS, TOF)
o Hyperkinetic/high flow states (anemia, hyperT4, fever)
o Functional/flow murmur:
 Young: size of Ao/PA vs high CO
 DRVOTO or DLVOTO
o Other:
 Ao/PA dilation distal to valve
 Degenerative changes to Ao w/o significant stenosis

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7
Q

Physiological ejection murmur: most commonly seen

A

young animals
o No structural dz
o Physiologic murmur: ↑CO, ↓ blood viscosity
o Typically disappear in early adults

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8
Q

Physiological ejection murmur: features

A
  • Usually soft (grade I or II/VI), early-mid systolic, high frequency
    o Character can change w body position, HR
    o DRVOTO common in cats = little clinical consequence
  • Basilar: loudest at AoV or PV
    o Do not radiate
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9
Q

Physiological ejection murmur: common causes

A

o Anemia = most common cause
 ↓ blood viscosity tend to occur when Ht < 22-25%
o Hypertension
o Fever
o Pregnancy
o HyperT4

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10
Q

Regurgitant murmurs charateristics

A
  • Longer duration (vs ejection murmurs): start with S1, end at or include S2
  • Plateau configuration
  • High frequencies with high pitched/blowing quality
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11
Q

Features of MR murmur

A

o Holosystolic, plateau shaped
 Frequent late systolic attenuation
o Soft: protosystolic
o Mixed frequency and harsh sounding
* Loudest at L cardiac apex
o Radiates dorsally and to R thorax
 If chordae tendineae rupture: radiation can vary according to which chordae
* Posterior: base of heart + 50% to neck and carotids
* Anterior: axilla and mid thoracic vertebrae, top of head
o Confounding reliable identification of TR)
* Common accentuation of P2

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12
Q

Regulation of blood flow across MV depend on

A

malfunction of any component can lead to MR
o MV annulus
o MV leaflets
o Chordae tendineae, papillary muscles

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13
Q

Causes of MR murmur

A

o CVD: clicks may be present if valve prolapse
 Loudness of murmur α severity
o DCM: annular dilation → mild to moderate loudness
 Arrhythmias often present
o Systemic hypertension

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14
Q
A
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15
Q

Causes of TR murmur

A

o PH: primary or secondary
o TVD

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16
Q

Type of HM: SAS

A

systolic crescendo-decrescendo murmur
o L heart base or R cranial thorax
o Intensity α severity
 Mild obstruction: mild murmur that ↑ w exercise (↑ SV)
 Moderate to severe: harsh murmur, mixed frequency, long
* Can radiate to thoracic inlet up to neck, along carotid arteries

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17
Q

Type of HM: PS

A
  • Murmur: harsh, med to high pitched, loud & long systolic
    o Loudest at L base, over PV
    o Opening snap: fused valve leaflet reach opening limit
    o Wide S2 split
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18
Q

Type of HM: HOCM

A
  • Similar to SAS
  • Can have concomitant MR
    o Secondary to MV leaflet displacement w SAM
    o Papillary muscle dysfct or distortion of MV annulus
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19
Q

Type of HM: VSD

A
  • Restrictive physiology of VSD
    o Determined by amount/velocity of shunt from L to R
     Size of VSD (larger = ↓ velocity of shunting)
     Pulmonary vascular resistance (PH = ↓ shunting)
  • Loud, harsh murmur
    o Holosystolic, medium to high pitched
     If PH, may be protosystolic
    o Plateau or mild crescendo-decrescendo
    o L cranial thorax
  • Can have soft ejection systolic murmur: functional/relative pulmonic stenosis 2nd to ↑ flow
20
Q

Type of HM: ASD

A
  • Systolic ejection murmur: medium pitched, short, soft
    o Loudest over PV area
    o Crescendo-decrescendo
    o Splitting of S2 → fixed respiratory splitting
  • Increased blood flow across PV → delayed closure
21
Q

Type of HM: TOF

A
  • VSD: R sternal border murmur
  • PS: L basilar ejection murmur
    o Tend to predominate
  • Nature/intensity of murmur → reflect
    o Severity of Ao override → degree of PS/hypoplasia
     More severe PS → ↑ RV pressure → ↑ R to L shunting → soft murmur
    o Degree of R to L shunting
22
Q

Mechanism of diastolic murmurs

A
  • 2 major mechanisms
    o Regurgitant flow across incompetent Aov or PV
    o Forward flow across stenosed MV or TV
23
Q

Type of HM: MS

A
  • Murmur: low pitched, low frequency, rumbling
    o Starts mid diastole after S2
  • In Hu: duration α to severity
  • Triscuspid stenosis: similar, best heart over Tv area, extremely rare
24
Q

Type of HM: AI

A
  • Most common diastolic murmur
    o Aortic endocarditis in adult dogs
    o Young dogs:
     Isolated congenital defects
     SAS
     Complication of VSD
  • Murmur: soft, blowing, high pitched
    o Crescendo-decrescendo
    o Start immediately after S2
    o Split S2 may be present
  • Disparity btwn loudness of murmur and degree of AI
    o Severe AI = soft, short
    o Moderate AI = no audible murmur
25
Q

Austin Flint murmur

A

Severe AI: presystolic murmur (Austin Flint)
o 2nd to premature MV closure → disturbed diastolic flow through M

26
Q

Type of HM: PI

A
  • Uncommon to have PI of sufficient magnitude to cause murmur
    o If 2nd to PH: usually louder, harsher, longer duration
  • Murmur: soft, high pitched, blowing
    o Early in diastole
    o Decrescendo
    o Best heard in PV area
    o Usually with an ejection systolic murmur
27
Q

Continuous murmur: cause

A

abnormal flow from arterial to venous circulation

  • Characteristic murmur of PDA
    o Blood flows from Ao (↑ pressure) to PA (↓ pressure) → turbulence
     Loudness/duration = pressure gradient btw Ao and PA
     If PH: ↓ intensity of diastolic component, ↑ S2 intensity
  • Reversed shunt: no murmur
    o Other differentials:
     Pulmonary arteriovenous fistula (AP window)
     Arteriovenous fistula
     Ruptured sinus aneurysm or CA communicate w RA
     Severe aortic coarctation
     PA branch stenosis
     Anomalous origin of LCA from PA
     Accessory CA
     Coronary stenosis
     Truncus/pseudotruncus arteriosus
     Total anomalous pulmonary venous connection
28
Q

Features of continuous HM

A
  • Continuous systolic and diastolic murmur
    o Best heard over AoV and PV
    o Start with S1, max intensity before S2, decrescendo toward next S1
    o Waxes and wanes → peak intensity = around S2
    o Systolic component often radiate extensively, diastolic localized
     Diastolic can be lost at end diastole
  • Systolic regurgitant murmur can be heard at L apex
29
Q

Features of To and Fro HM

A
  • Systolic + diastolic murmur
  • Often combination of congenital defects
30
Q

Causes of To and Fro

A
  • SAS + AI
  • VSD + AI
  • PS + PI
  • Mitral atresia + ASD (Lutembacher syndrome)
31
Q

Horses w/ AI also have

A

holodiastolic w decrescendo character
o Can ↑ intensity at end diastole w atrial contraction → opening of MV → anterior septal leaflet hit regurgitant flow
 Austin Flint murmur

32
Q

DDX ejection systolic click

A

 Early in systole
o Hypertension
o Dilation of great vessel
o Opening of abnormal but mobile semi lunar valve
 Causes:
o Systemic hypertension
o PA dilation: idiopathic, PH
o Tetralogy of Fallot
o AS/PS
o HW dz

33
Q

DDX non ejection systolic click

A

 Short, mid to high frequency sound
 Mid to late systole
 Causes:
o AV prolapse
o CVD

34
Q

DDX protodiastolic transient sounds

A

 Opening snaps
o Tricuspid or mitral stenosis

 Tumor
o Atrial tumor/myxoma

 Pericardial knock
o Constrictive pericarditis w abrupt termination of rapid ventricular filling

 S3 protodiastolic gallop
o LV or RV diastolic overload
o AI, PI, MR, TR
o L → R shunt
o High output states (anemia, hyperT4)
o ↓ ventricular compliance or ↑ diastolic pressures
o CM
o Ventricular failure
o Ischemic heart dz

35
Q

What feature during physical examination can separate tricuspid from mitral valve regurgitation?

A

Timing of murmur associated with respiration
* TR: ↑ murmur intensity with inspiration
o Carvallo’s sign
o Inspiration: ↓ intrathoracic pressure → ↑ venous return to R heart → ↑ regurgitant flow across the TV
* MR: murmur intensity is not affected by respiratory cycle

36
Q

Dynamic auscultation

A

 Clinical assessment → alter venous return or SV
o Rapid squat: blood volume stored in legs forced to return to heart
 ↑ venous return → ↑ preload → ↑ LV filling

37
Q

Effect of dynamic auscultation on HOCM

A

↓ intensity
* ↑LV volume → displace hypertrophied IVS → ↓ LVOTO

38
Q

Effect of dynamic auscultation on MR

A

later systolic click

39
Q

Dynamic auscultation: hand grip

A

↑BP → ↑ afterload
 ↑MR, AI intensity
 No effect on AS

40
Q

Dynamic auscultation: amyl nitrate

A

↓LV afterload
 ↓MR: ↓ resistance to blood flow → ↑SV and ↓ regurgitant volume

41
Q

Valsalva maneuver

A

squat to stand => vasodilation

42
Q

Effect of Valsalva maneuver on MR

A

↑ forward flow → shorter + softer

43
Q

Effect of Valsalva maneuver on SAS

A

↑ intensity

44
Q

Effect of Valsalva maneuver on HOCM

A

↓ intensity
 ↑LV volume → displace hypertrophied IVS → ↓ LVOTO

45
Q

Effect of Valsalva maneuver on AI

A

↑ forward flow → ↓ murmur

46
Q

Inspiration/hand grip: effect on MR

A

Inspiration/hand grip: effect on MR

5. Auscultation and physical diagnosis (8 decks)

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