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/