Approach to Cardiac Auscultation Mehul Bhatt, MD Interventional Cardiology/Vascular Medicine Heart and Vascular Care 3rd Cherokee Cardiovascular Summit October 4, 2014

Approach to Cardiac Auscultation Physiology Sounds Maneuvers Pathology Valvular Disease Differentiating disease Live Auscultation Cases Aortic stenosis versus Hypertrophic cardiomyopathy

Physiology Human ear: Cardiac sounds: Stethoscope 20 - 20,000 Hz Best 1,000 – 5,000 Hz Cardiac sounds: 30 – 1,000 Hz Stethoscope Bell – low frequency sounds Diaphragm – 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 sound Normal 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: Maneuvers Position 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 stenosis Mid-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: HOCM Hypertrophic cardiomyopathy Harsh systolic murmur with varying frequencies Murmur 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: HOCM Hypertrophic cardiomyopathy Maneuvers: 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: Mitral Mitral 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 Maneuvers: 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: Mitral Mitral 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

Effect of Physiological Maneuvers on Murmur LIVE Physical Examination: Maneuvers Differentiate aortic stenosis (AS) and hypertrophic cardiomyopathy (HOCM) Effect of Physiological Maneuvers on Murmur MANEUVER Supine Standing Valsalva Deep Inspiration Deep Expiration AORTIC STENOSIS   HOCM

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/