Approach to Cardiac Auscultation
Mehul Bhatt, MDInterventional Cardiology/Vascular Medicine
Heart and Vascular Care 3rd Cherokee Cardiovascular Summit
October 4, 2014
Approach to Cardiac Auscultation
PhysiologySoundsManeuvers
PathologyValvular DiseaseDifferentiating disease
Live Auscultation CasesAortic stenosis versus Hypertrophic
cardiomyopathy
Physiology
Human ear: 20 - 20,000 HzBest 1,000 – 5,000
Hz
Cardiac sounds:30 – 1,000 Hz
StethoscopeBell – low
frequency soundsDiaphragm – high
frequency sounds
Bell
Diaphragm
Physiology: Sounds
S1: S1 = M1T1: comprised of mitral valve closure
(M1) then tricuspid valve closure (T1)Hear high-frequency vibrations from
deceleration of blood after valve closure (not clapping of valve leaflets together)
Usually heard as one sound
Physiology: Sounds
S2:
S2 = A2P2: comprised of aortic closure (A2) then pulmonary closure (P2)
Hear high-frequency vibrations from deceleration of blood after valve closure (not clapping of valve leaflets together)
Often heard as split soundNormal split: increases with inspiration as P2 delayed
with increased RV volume and pulmonary vascular capacitance; typically hear single S2 with expiration
Physiology: Sounds
Murmurs: Cause: Turbulence / Non-laminar flow
Reynold’s number = inertial force / viscous force
= (length X velocity X density) / (viscosity)
= length X velocity X constant Reynold’s number > 30: turbulent or non-laminar flow
When: High flow rate through normal or abnormal orifice Flow through constricted or irregular orifice into dilated area Backwards or regurgitant flow
Physiology: ManeuversPosition
Supine: Increase preload:
increased blood volume in heart
Rapid standing: Decrease preload:
decreased blood volume in heart
Valsalva (bear down) Decrease venous return
(preload)
Breathing Deep breath in: Increased
preload Deep breath out: Decrease
preload
Pathology: Aortic Valve Stenosis
Bicuspid AV stenosis: Occurs in ages 40s-50s
Senile AV stenosis: Occurs in aged 70s-80s
Progressive obstruction
Severity determined by exam, echo, and cardiac cath
Normal AV
Stenotic AV
Pathology: Aortic Valve Regurgitation
Incompetent aortic valve
Maybe in conjunction with aortic stenosis
Maybe associated with dilated aorta root
Pathology: Aortic Valve Stenosis
Aortic stenosisMid-systolic high-
frequency cresendo-descrendo
May have ejection sound and soft S2 based on calcification (valve motion)
Pathology: Aortic Valve
Manuevers: Decrease afterload or
increase preload: Lying down, Deep breath in accentuate murmur;
Increase afterload or decrease preload: Standing, Deep breath out attenuate murmur
Pathology: Aortic Valve
Aortic Regurgitation Early diastolic descrendo
high-frequency murmur Maneuvers:
Increase afterload: squatting, isometric exercise (sustained handgrip) accentuate murmur
Pathology: HOCM
Hypertrophic cardiomyopathy:Dynamic
restriction of LVOT due to thickening of ventricular septal muscle
Genetic and environmental components
Cause of sudden cardiac death Often in young athletes
Pathology: HOCMHypertrophic
cardiomyopathyHarsh systolic murmur
with varying frequenciesMurmur combination of
mid-systolic ejection from obstruction and holosystolic from MR and TR
S2 is intact as aortic valve in normal
Suspect when heart harsh systolic murmur in young person (although maybe bicuspid aortic valve)
Murmur more dyanamic with maneuvers than aortic stenosis murmur
Pathology: HOCMHypertrophic
cardiomyopathyManeuvers:
Decrease gradient: Increase preload or Increase afterload will decrease murmur: Standing to Supine
(increase preload), squatting (increase preload + afterload), inspiration (increase preload)
Pathology: HOCM
Hypertrophic cardiomyopathy:
Manuevers: Increase
gradient: Decrease preload or Decrease afterload will increase murmur:
Supine to standing, Valsalva (decrease preload)
Pathololgy: Aortic stenosis versus Hypertrophic cardiomyopathy
MANEUVER
Supine
Standing
Valsalva
Deep Inspiration
Deep Expiration
AORTIC STENOSIS
HOCM
Pathology: MitralMitral stenosis
Mid-diastolic and pre-systolic low frequency“rumble” Murmur after mitral opening snap Opening snap: depend on calcification α 1/valve mobility Often difficult to hear as soft and low frequency Aerobic exercise and left lateral decubitus position accentuate
Pathology: Mitral
Mitral regurgitation Holosystolic constant
high-frequency
Maneuvers: Typical MR and
Rheumatic MR: Increase with increase
afterload Not effected much by
respiration Mitral valve prolapse:
Significant changes with respiration
Pathology: Mitral Valve Prolapse
Mitral valve prolapse “floppy valve syndrome”
Incompetent mitral valve that allows blood to leak back into left atrium during left ventricular systole
Can be seen in Marfan’s syndrome, Ehlers-Danlos syndrome
Murmurs very sensitive to breathing manuevers
Pathology: MitralMitral valve prolapse
Redundant mitral valve tissue “Too much tissue for size
ventricle” Mid- to late-systolic click
intoduces regurgitant murmur
Maneuvers: Increase size of ventricle:
delay click and murmur; murmur softer Deep inspiration,
supine Decrease size of
ventricle: earlier click and murmur; murmur louder Valsalva, standing
LIVE Physical Examination:Maneuvers
Differentiate aortic stenosis (AS) and hypertrophic cardiomyopathy (HOCM)
MANEUVER
Supine
Standing
Valsalva
Deep Inspiration
Deep Expiration
AORTIC STENOSIS
HOCM
Effect of Physiological Maneuvers on Murmur
Approach to Cardiac Auscultation: References
Dr. Joseph Esterson, MD
Director, Cardiology Training
Center for Research and Medical Education
University of Miami School of Medicine
Braunwald E et al. Heart Disease. W.B. Saunders Co. Philidelphia, PA. 2001.
Alexander RW et al. The Heart. McGraw-Hill. New York, NY. 1998
http://depts.washington.edu/~physdx/heart/demo.html
http://egeneralmedical.com/egeneralmedical/listohearmur.html
http://home.cwru.edu/~dck3/heart/listen.html
http://www.auscultation.com/