Cardiac - Specialized


    Based on:

    Chizner M. (2008) "Cardiac Auscultation: Rediscovering the Lost Art" Curr. Probl. Cardiol.  July 2008


    Key Principles

    • Low Frequency Sounds (use BELL)
      • S3, S4, diastolic rumbles
      • Do not push too hard with bell, otherwise stretches skin and turns bell into diaphragm.
    • High Frequency Sounds (use DIAPHRAGM)
      • Regurgitant murmers, S1, S2, pericardial friction rub
      • Press with diaphragm deeply enough to leave an imprint on chest wall.
    • One-Piece Stethoscope --> lets you pick up wide range of frequencies by varying pressure on chest wall.


    • Quiet room, ask conversations to stop
    • Warm the piece with your hand for patient comfort.
    • Change the position of the bed!  (CANNOT examine while uncomfortable)
    • Ask patient to move breast up and to the left (or use non-dominant hand to move it)
    • Selective Listening: Develop an approach to tune in and listen for one part at a time (i.e. first focus on S1, then S2, then systolic sounds, diastolic, etc...)

    Systematic Approach

    • Technique called "inching"
    • Place your non-dominant hand on the carotid, apex, or (preferrably) over subclavian to time cardiac cycle.
    • Start at RUSB (2nd intercostal) and inch slowly towards the LUSB (2nd intercostal)
    • Technique Listen For:
      1.  Set environment (quiet room, changed bed height, drapes, wash hands)  

      2.  Palpate the apex to know where the apex is supposed to be.


      3.  Use BELL and listen to APEX in patient left lateral decubitus position

         - Do not press too hard, or will convert bell into diaphragm

         - Press lightly..just enough to make a seal

      S3, S4, diastolic rumble of MS

      4.  Listen over left-sternal-border with patient sitting forward, during held

           deep expiration

          - With diaphragm press firmly enough to make an after-mark on skin

      Diastolic Murmur of AR

      Pulmonary HTN regurgitation

      Friction Rubs

      Splitting of the S2 (some only while sitting) 

      5.  Listen for S1 and S2..

           - Are both present? 

           - Is either loud/normal/faint? 

           - Does splitting of S2: widen? fixed? reverse with inspiration

      S1, S2, 

      S2 splitting

      6.  Listen for extra sounds in systole and diastole

      Systole (Mitral clics, pulmonic

           or aortic ejection sounds)

      Diastole (S4, S3, pericardial

           knock, mitral opening snap)

      7.  Listen for murmurs

           - Phase: Systolic? (early, mid, late, holosystolic)


           - Location & Radiation

           - Change with maneuvers (i.e. valsalva)

      8.  Pericardial Friction Rubs OR prosthetic valve sounds  


    I was taught opposite, which is nice because you know where to find the apex of the heart:

    • Palpate cardiac apex.
    • Place stethoscope there, this is where you hear the S1.
      • This is also where you hear S3 and S4, diastolic rumbles (USE THE BELL)
      • Inch slowy towards the lower left sternal border (LLSB)
      • Inch slowly along the left-border of the sternum towards the LUSB (2nd intercostal),
        • At some point S2 becomes louder than S1.
      • Inch slowly vertically towards the RUSB (2nd intercostal).


    S1 vs. S2

    • Several ways to tell them apart:
    1. S1 follows a longer pause, S2 follows a shorter pause (diastole is usually longer, but harder to notice with tachycardia).  ---longPause---S1 ---shortPause----S2
      • Problem: During faster rates diastole shortens more than systole.
    2. Palpate the subclavian, carotid, or cardiac apex.  S1 -->PULSE --> S2
    3. BEST Technique: "inching" technique:  place stethoscope over the LUSB (2nd intercostal), the louder sound is S2, inch towards the apex keeping in mind the S2 sound will get quieter, and S1 will get louder.  Helpful in tachycardias.


    • S1
      • --> closure of the tricuspid and bicuspid valves.
      • Two components M1 and T1
        • M1 --> mitral --> LV contracts first, M1 occurs earlier and louder).
        • T1 --> tricuspid --> Lower left sternal border.
      • S2 is louder than S1 in aortic area --> If S1 is louder considred "LOUD S1"
      • S1 is louder than S2 in apex  --> If S1 is quieter, considered "QUIET S1"
      • Intensity of S1 changed by: (usually mitral pathology)
        • PR interval, Mitral valve structure, ventricular contractility.
      • Increase in S1:
        • Heart is closer to chest wall (young, thin people)
        • Hypercontractile states (exercise, tachycardia, anemia, hyperthyroidism, fever, pregnancy, excitement).
        • Increased force of ventricular contraction or rate of pressure growth in systole.
        • High LA pressures !! (Rheumatic mitral disease)


    • Right-Upper Sternal Border 2nd intercostal space --> Aorta and Ao valve pathology. (aortic area)
    • Left-Upper Sternal Border 2nd intercostal space --> Pulmonic Area
    • Mid-Left sternal border --> AR murmurs. (blood rushing back into LV)
    • Lower-left sternal border --> RV/Tricuspid area:
      • S1, systolic clicks, R-sided S4/S3 gallops, Tricuspid sounds/murmurs.
      • TR murmur --> worse on inspiration ("Carvallo's Sign")
      • VSD (with thrill)
      • In general: murmurs on R-side of heart increase with inspiration.
    • Apex (Mitral Area)
      • L-sided S3, S4
      • Mitral Murmurs
      • Aortic ejection murmurs.


    Other locations:

    • Neck:
      • AS  --> quieter as inched up the neck.
      • Carotid occlussive disease.  --> quieter when inched down to chest.
    • Clavicle
      • Good bone sound transmission
      • Excellent for AS.
    • Subclavicular Fossa
      • Venous hum (children [normal], thyrotoxicosis, anemia, pregnancy, and any hyperkinetic state)
    • L-axillar + posterior lung base
      • Chronic MR (anterior mitral leaflet is involved).
    • R-sternal border
      • "Right-sided" diastolic murmurs of special type of AR (due to R-ward displacement of aorta) (dissection, aneurysm, Marfan's syndrome).
      • (NOTE: valvular AR best heard along the LUSB).
    • Abdomen:
      • Renal artery stenosis.

    Even More Special locations

    • Inferior edge of sternum (xiphoid area or epigastrium) in upright position --> Helpful especially in COPD/hyperinflation.




    • Position Changes:
      • Prompt Squatting --> compresses veins in legs and abdomen causing incr. preload and incr. afterload.
        • Physician seated comfortably, patient changes positions
          • 1.  Increased venous return to heart --> rises preload --> incr. LV volume, chamber size, stroke volume --> increases intensity of many murmurs.
          • 2.  Increased peripheral vascular resistance --> increases MR+AR murmurs.
          • Therebore:
            • Squatting increases all murmurs except: HOCM, MVP.
            • (Fills ventricles, delays MVP murmur+click later in cycle, and quiets it)
            • (In HOCM, ventricle fills removing the septal obstruction).
            • This is key, as it distinguishes AS from HOCM.
      • Prompt Standing --> Reverse of squatting (decreases all murmurs, except MVP and HOCM)
      • (NOTE: Physician seated, while patient stands/sits.  If patient cannot stand/sit, then can elevate legs or bend knees and compress kees into abdomen for a similar effect).
      • Valsalva Maneuver --> Decreases venous return to LV, following release increases venous return to the R-side.
        • Technique:
          • Physician asks the patient to "bear down" (i.e. strain as if having a baby or stool).
          • During the strain place hand on belly to ensure muscles tightening.
          • Alternatively "place finger in the mouth, seal with lips, and blow against it".
        • Once valsalva initated:
          • Increases intrathoracic pressure --> decreases venous return --> decreases LV volume.
          • Decreases length and intensity of murmurs EXCEPT HOCM and MVP.
            • Systolic click of MVP moves earlier in systole (closer to S1)
        • Once valsava is lifted:
          • Sudden increase in venous return
          • R-sided murmurs return to baseline earlier (one or two cardiac cycles)
          • L-sided murmurs return to baseline later (several cycles).
        • NOTE: transiently decreases coronary flow, avoid in recent MI or ischemia.
        • NOTE: DO NOT hold for >10s, decreases coronary flow, BP, can cause syncope.
      • Respiration
        • Generally murmurs originating from the R-side increase on inspiration (increase return to R-side)
          • Except pulmonic stenosis (overloaded RV thrusts leaflets open)
        • Generally L-sided murmurs/S3/4 decrease in intensity on inspiration (decr return to L-side)
        • Technique:
          • Can instruct to inspire/expire.
          • Can also move the hand up/down to signal inspiration, expiration.
        • Inspiration causes increased venous return to R-heart, causing delayed pulmonic valve closure (P2). (both earlier Aortic closure [less flow to LV] and delayed Pulmonic closure [higher RV volumes]). --> NORMAL
        • ABNORMAL --> Splitting of S2 on exp + insp while sitting (sometimes supine fixed split S2 can be normal)
        • RBBB and pulmonic stenosis widens S2 split to the point that it's heard on expiration. (slow RV contraction).
          • ASD --> (RA --> LA shunt) --> Fixed split S2 on insp + exp.  (to make ASD dx, increased pulmonary flow  (not through defect) causes systolic murmur; without murmur ASD is unlikely).
        • Wide split S2 in:
          • RBBB (late P2
          • PS (late P2)
          • MR (early A2)
          • VSD (early A2)
        • Paradoxical S2 splitting
          • --> Occurs in
            • LBBB    (longer LV contraction -- slow conduction)
            • AS  (if severe gradient) (longer LV contraction -- increased outflow resistance)
            • HOCM (if severe gradient)
            • HTN
            • RV Pacing
          • (All these delay LV contraction).
        • Pulmonary HTN --> Loud S2, narrow splitting.
        • Helps differentiate R or L-sided heart murmurs
          • All R-sided heart murmurs increase on INSPIRATION, except pulmonic ejection murmur of PS (can decrease or not change).
          • All L-sided heart murmurs DECREASE on INSPIRATION.
      • After a PVC or long-cycle length in AFib.
        • A pause after a premature beat or following long cycle length in AFib can change intensity of murmur and provide clues.
        • Mechanism:
          • Careful listen for a longest pause, and then hear if the murmur is louder in the following beat when the ventricle is more full and has a greater stroke volume. 
        • MR murmur remains unchanged after a long cycle (more filling -> LA and LV gradients both incr.)
        • AS murmur INCREASES after a longer cycle.
      • Isometric Handgrip Exercise and Transient Arterial Occlusion
        • Ask patient to make first with both hands (increases SVR + afterload)
        • Inflate BP cuff simultaneously on both upper arms to 20-40mmHg above peak sBP. (occlude)
        • Increases:
          • MR
          • AR
          • VSD
        • NO CHANGE in other murmurs
        • (don't do if recent MI, cerebrovascular disease, dissection, or hypertension)
      • Pharmacologic Maneuvers
        • Not done anymore due to 2D echo.
        • Essentially ask pt to inhale amyl nitrite (potent vasodilator, very transient effect)
          • Decreases systemic BP, followed by HR increase and contractility.
        • 1st phase (hypotension)
          • Increases: AS, PS, HOCM and innocent flow murmur
          • Decreases: MR, VSD, AR
        • Can distinguish "Austin Flint Murmur": AR will decrease, and MS will increase.

    More on S1

    • Aka "the lub"
    • Due to mitral (M1) and tricuspid (T1) valves closing during systole
    • M1 usually earlier because it's louder (but usually they occur simultaneously)
      • Listen to M1 with diaphragm at cardiac apex.
      • Listen to T1 with diaphgram at the LLSB (tricuspid area)
    • Intensity of S1 is most important (splitting not as important)
    • Intensity of S1 (loud, normal or faint) - intensity is most important. (splitting not important)
      • S1 should be louder than S2 (otherwise comment on "loud S1" or "soft S2").
      • Loud S1: (usually mitral origin, often due to wider opened leaflets)
        • Short PR Interval (valve opens wider early in diastole, closes more forcefully)
        • No MV calcification (i.e. candidate for commissurotomy or balloon valvuloplasty rather than replacement)
        • Ventricular contractility (strength of closure of MV) (i.e. exercise, tachycardia, anemia, hyperthyroidism, fever, pregnancy, excitement)
        • Mitral Stenosis (MV opens wider due to high LA pressure)
        • Mitral Valve Prolapse (LOUD S1 + MR murmur)
      • Faint S1
        • Heavy calcification of valve (immobilized by calcific deposits)
          • Often heard with calcific MR
        • Long PR (1st deg. AV block) (valve leaflets take longer, drift closer together before systole)
        • Systolic Dysfunction (Decreased contractility)
        • Acute AR (ventricle fills so fast that mitral valve leaflets never fully open)
        • Extracardiac Factors (obesity, heart position, pericardial effusion, chest wall width)
      • Variable Intensity S1
        • Varying PR intervals / AV dissociation (i.e. complete AV block and VT)
          • I.e. Find Variable S1 and slow rate ~40 = complete AV block
          • I.e. Find variable S1 with Wide-Complex Tachycardia = likely VT.
        • Atrial Fibrillation (variation in cycle length, varies position of leaflets.  Longer cycles = more time for leaflets to drift closer together = fainter S1)
    • S1 splitting - hard to comment on.  Wide splitting of S1 occurs with delay of RV contraction (RBBB, ASD)
      • I.e. Wide split S1 in addition to loud T1 = increased flow from RA to RV = ASD

    More on S2

    • Aka "the dub"
    • Clsoure of Aortic (A2) and pulmonic (P2) at start of ventricular diastole.
    • Normally higher pitch, sharper than s1
    • Pressure in Aorta is higher than PA, therefore Aortic Valve closes earlier.
      • A2 is louder and earlier than P2
    • Intensity and splitting are both important (unlike S1), Always comment on:.
      • Intensity of S2 (and A2/P2 components)
      • Splitting
      • Effect or respiration on splitting
    • On exam:
      • Intensity and Splitting of S2  (Listen at Upper + Mid Left Sternal Border, patient in sitting position)
        • Loud S2 (Elevation of pressure in great vessels forceful valve closure) 
          • Loud A2: Hypertension
          • Loud P2: Pulmonary HTN (L-HF, MS, etc.) - if hear S2 at apex = abnormal except rarely in kids.
        • Splitting of S2
          • Narrow Splitting: Pulm. HTN
          • Wide Splitting
            • P2 Delayed (RBBB, PS, etc.)
            • A2 Early (MR, VSD)
          • Pardoxical Splitting (A2 is delayed)
            • LBBB, RV pacing, AS [Severe!], HOCM [Severe!], HTN [Severe!]
          • Fixed (no resp variation)
            • ASD
        • Note: splitting less discernible in older pts (less pulmonary hang-out time) or those with high AP diameter.

    Extra Heart Sounds

    • Ejection Sounds
      • Normally opening aortic and pulmonic valves is silent.
      • Sometimes brief, sharp, high-pitched sounds in early systole heard just after S1 (Ao, Pulm opening/flow).
      • Use diaphragm
      • Loud = more mobile valve
      • Softer = more calcified/restricted valve
      • Often heard with mechanical valves
      • IF S1 seems louder in pulmonic or arotic area = suspect an ejetion sound
    • Systolic Click
      • Prolapse of mitral valve leaflets into LA during systole.

    Specific Conditions



    • Holosystolic murmur over the tricuspid area (LLSB)
    • Increases with inspiration (Carvallo's Sign)



    • Holosystolic murmur accompanied by palpable thrill.



    • Aortic Stenosis
    • If Severe:
      • Pradoxical Splitting of S2 (splits on expiration)
      • Faint or inaudible S2



    • Causes:
      • Acute
        • ***Infective Endocarditis (Destruction/Perforation of valve)
        • Chest Trauma (tears ascending aorta)
        • Post-TAVR
        • LVAD
        • Aortic Dissection
      • Chronic
        • Bicuspid Aortic Valve (usually AS, can cause aortopathy/AR)
        • Connective Tissue Disease
          • Marfan's Syndrome
          • Ehlers-Danlos
          • Floppy Aortic Valve, Aortic Valve prolapse, Sinus of valsalva aneurysm, aortic annular fistula
        • Medications (fenfluramine/dexfenfluramine [Phen-Fen] - weight loss pills)
        • Rheumatologic
          • Rheumatic Fever (fibrotic changes, thickening, retraction of leaflets, can fuse + cause AS)
          • Ankylosing Spondylitis (Aortitis)
          • Behcet Disease (5% - proximal aortitis +AR)
          • Giant Cell Arteritis (aortitis + AR)
          • RA (aortitis + AR)
          • SLE (valvular fibrosis + Libman-Sacks endocarditis)
          • Takayasu arteritis (aortic valvular + coronary involement, can cause aortitis)
        • Whipple Disease 
      • Another classification:
        • Congenital causes - Bicuspid aortic valve is the most common congenital cause
        • Acquired causes: Others (above)
        • ​Secondary to Aortic Dilatation (Marfan's, HTN, Takayasu arteritis, Giant Cell Arteritis, Syphilic Aortitis, Ank Spond, Whipple's Disease, Cystic Medial Necrosis, Idiopathic root dilatation)
    • Pathophysiology
      • Incompetence of the aortic valve = large diastolic volume/pressure, and increased stroke volume.
      • Eventually get pressure and volume overloaded ventricle
      • Acute:
        • LV has not dilated.  High pressure causes dilation of the mitral valve and pulmonary backflow, causing acute pulmonary edema and dyspnea.
        • Urgent surgery is indicated (esp if due to aortic dissection)
      • Chronic:
        • LV compensates--> enlargement, eccentric hypertrophy.  Cardiomyocytes  build sacromeres in series --> longer cardiomyocytes.
        • Early:
          • LV becomes larger, more compliant, better ability to deliver large stroke volume at higher preloads.
          • Increases EF (hyperdynamic) due to high preload volumes (Frank Starling)
        • Late:
          • LV enlargement surpasses preload reserve on the Frank-Starling curve, with the EF falling to normal and then subnormal levels.
          • The LV end-systolic volume rises and is a sensitive indicator of progressive myocardial dysfunction.
        • Very Late:
          • As LV dilates, LV dysfunction develops.
          • LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may worsen during exercise.
          • High  LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis. Grossly, the LV gradually transforms from an elliptical to a spherical configuration.
    • Symptoms:
      • Acute: Sudden severe dyspnea, heart failure, chest pain (low coronary perfusion or dissection)
      • Chronic:
        • Asymptomatic period x few years (only tachycardia) followed by:
        • Once LV dysfunction --> chance of symptoms 25%/year
        • Once symptoms develop --> mortality 10%/year
        • Palpitations
          • Uncomfortable awareness
          • Dyspnea
          • Chest Pain
    • Physical Exam:
      • Acute
        • Vitals: Tachycardia, arterial pulsus alternans (normal PMI pulse)
        • Peripheral: Peripheral Vasoconstriction, Cyanosis
        • Resp: Pulmonary edema
        • Auscultation:
          • Position: lean forward, full expiration.
          • Early Diastolic Murmur (lower pitched + shorter than chronic AR)
          • Austin-Flint Murmur (regurgitant flow vibrates mitral valve).
          • ***Faint S1 (valve leaflets never fully open) *** - early surgery can be lifesaving
      • Chronic
        • Wide Pulse Pressure (large stroke volume, low diastolic BP d/t regurg)
        • This causes following:
          • Becker Sign (systolic pulsations in retinal arterioles)
          • Müller sign - Uvula pulsations
          • de Musset sign - Bobbing of head with heartbeat
          • Corrigan Pulse ("water-hammer" pulse) - prominent peripheral pulse.
          • Quincke Sign - visible pulsations of nail bed with slight compression.
          • Hill Sign - popliteal sBP 40mmHg higher than brachial sBP
          • Duroziez Sign - Systolic murmur over femoral artery with proximal compression of artery + diastolic murmur with distal compression
          • Traube sign ("pistol-shot" pulse) - Ausc. booming systolic/diastolic sounds over femoral artery
        • Apex: displaced, hyperdynamic
        • S3 gallop if LV dysfunction present
        • High pitched diastolic murmur over LUSB (duration = severity of AR, NOT loudness)
      • Wide pulse pressure
      • Murmur
        • Diastolic murmur of the left-mid sternal border
        • Hear it on held deep expiration while patient sitting up + leaning forward.
        • Sometimes heard in mitral area.

    Pulmonary Hypertension

    • Loud palpable P2 with narrow inspiratory splitting of S2
      • If P2 is heard at apex (along with A2) consider pulmonary HTN (can be normal in young pts)



    • Pulmonic Stenosis
    • Faint P2
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