Heart murmurs Flashcards
Cause of murmurs
- 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
Reynolds #
Reynold’s number = (radius x velocity x density)/viscosity
Description of HM
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
Systolic murmurs
Ejection
Regurgitant
Characteristics of ejection murmur
- 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
Causes of ejection murmur
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
Physiological ejection murmur: most commonly seen
young animals
o No structural dz
o Physiologic murmur: ↑CO, ↓ blood viscosity
o Typically disappear in early adults
Physiological ejection murmur: features
- 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
Physiological ejection murmur: common causes
o Anemia = most common cause
↓ blood viscosity tend to occur when Ht < 22-25%
o Hypertension
o Fever
o Pregnancy
o HyperT4
Regurgitant murmurs charateristics
- Longer duration (vs ejection murmurs): start with S1, end at or include S2
- Plateau configuration
- High frequencies with high pitched/blowing quality
Features of MR murmur
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
Regulation of blood flow across MV depend on
malfunction of any component can lead to MR
o MV annulus
o MV leaflets
o Chordae tendineae, papillary muscles
Causes of MR murmur
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
Causes of TR murmur
o PH: primary or secondary
o TVD
Type of HM: SAS
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
Type of HM: PS
- 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
Type of HM: HOCM
- Similar to SAS
- Can have concomitant MR
o Secondary to MV leaflet displacement w SAM
o Papillary muscle dysfct or distortion of MV annulus
Type of HM: VSD
- 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
Type of HM: ASD
- 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
Type of HM: TOF
- 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
Mechanism of diastolic murmurs
- 2 major mechanisms
o Regurgitant flow across incompetent Aov or PV
o Forward flow across stenosed MV or TV
Type of HM: MS
- 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
Type of HM: AI
- 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
Austin Flint murmur
Severe AI: presystolic murmur (Austin Flint)
o 2nd to premature MV closure → disturbed diastolic flow through M
Type of HM: PI
- 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
Continuous murmur: cause
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
Features of continuous HM
- 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
Features of To and Fro HM
- Systolic + diastolic murmur
- Often combination of congenital defects
Causes of To and Fro
- SAS + AI
- VSD + AI
- PS + PI
- Mitral atresia + ASD (Lutembacher syndrome)
Horses w/ AI also have
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
DDX ejection systolic click
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
DDX non ejection systolic click
Short, mid to high frequency sound
Mid to late systole
Causes:
o AV prolapse
o CVD
DDX protodiastolic transient sounds
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
What feature during physical examination can separate tricuspid from mitral valve regurgitation?
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
Dynamic auscultation
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
Effect of dynamic auscultation on HOCM
↓ intensity
* ↑LV volume → displace hypertrophied IVS → ↓ LVOTO
Effect of dynamic auscultation on MR
later systolic click
Dynamic auscultation: hand grip
↑BP → ↑ afterload
↑MR, AI intensity
No effect on AS
Dynamic auscultation: amyl nitrate
↓LV afterload
↓MR: ↓ resistance to blood flow → ↑SV and ↓ regurgitant volume
Valsalva maneuver
squat to stand => vasodilation
Effect of Valsalva maneuver on MR
↑ forward flow → shorter + softer
Effect of Valsalva maneuver on SAS
↑ intensity
Effect of Valsalva maneuver on HOCM
↓ intensity
↑LV volume → displace hypertrophied IVS → ↓ LVOTO
Effect of Valsalva maneuver on AI
↑ forward flow → ↓ murmur
Inspiration/hand grip: effect on MR
Inspiration/hand grip: effect on MR
