Cardiac Murmur & Dynamic Auscultation Dr Awadhesh Kr Sharma Professor Cardiology,LPS Institute of Cardiology,Kanpur
UNDERSTANDING STETHOSCOPE Size of Tubing=10-12 inches Ear-tips should point forward and fit properly Chest piece should be held between straightened index and middle fingers Don’t touch the tube or rub it against the patient’s skin Tube should be relatively straight Bell for low frequency & diaphagm for higher frequencies
HOLD IT THE RIGHT WAY Like this – the thumb under the tube keeps it from rubbing the skin, which causes extra noise Not like this – it’s harder to control and harder to hold gently.
DEFINITION OF MURMUR Heart murmur results from auditory vibrations caused by increased turbulence and are defined by their timing with in the cardiac cycle ( Braunwald 11ed) Heart murmurs are caused by audible vibrations that are due to increased turbulence from accelerated blood flow through normal or abnormal orifices, flow through a narrowed or irregular orifice into a dilated vessel or chamber, or backward flow through an incompetent valve, ventricular septal defect, or patent ductus arteriosus (Harrison 20 ed.)
PHYSIOLOGY OF MURMUR PRODUCTION
Description of a Murmur Timing in the cardiac cycle Site of murmur Shape of murmur Intensity/ Loudness Quality & Pitch Conduction/ Radiation Dynamic changes
TIMING OF MURMURS SYSTOLIC Early systolic i.e Acute severe MR, Acute TR Ejection(mid)-systolic i.e. AS, PS, HCMP ➜Late systolic i.e. MVP Pansystolic i.e. MR, TR, VSD DIASTOLIC Early diastolic i.e. AR, PR, Dock’s murmur Mid-diastolic i.e. MS, TS, Austin Flint, Carey-coombs, LA myxoma Late diastolic / pre-systolic i.e. MS CONTINUOUS PDA, severe COA, Severe AS with AR
TIMING OF COMMON MURMURS A – Normal, no murmur B – Mid-systolic murmur of AS C – Pansystolic murmur of MR D – Early diastolic murmur of AR E – Mid-diastolic murmur of MS F – Continuous murmur of PDA
SHAPE OF MURMUR CRESCENDO Grow louder mid-systolic murmur of MVP DECRESCENDO Grow softer early diastolic murmur of AR CRESCENDO-DECRESCENDO Grow louder than softer mid-systolic murmur of AS PLATEAU Remains uniform throughout pan-systolic murmur of MR JONAS TEXTBOOK OF CARDIOLOGY
PITCH & QUALITY OF MURMUR PITCH Hz Pr Gr QUALITY E.g.: LOW 25-125 Less Rumbling, rough MDM-MS MEDIUM 125-300 mix Harsh, rough AS HIGH >300 high Blowing, soft, musical MR,AR
LOCATION OF MURMURS AREA LOCATION SYSTOLIC DIASTOLIC AORTIC Right 2 nd ICS AS, flow murmur AR PULMONIC Left 2 nd ICS PS, flow murmur PR ERB’S Left 3 rd ICS AR, PR, ASD, Dock’s murmur TRICUSPID LLSB TR, VSD, HCM TS, ASD MITRAL Left 5 th ICS medial to MCL MR MS, Austin Flint, Carey Coombs Left infra-clavicular area : PDA, CoA
RADIATION OF MURMURS
Freeman and Levine Grading of Heart Murmur
Murmurs accentuated during Inspiration TS TR ( Carvallo's sign) PR Mild or moderate PS Severe PS (no further increase in gradient) No change of murmur on deep inspiration in RV failure and severe PAH Expiration MS MR AS AR VSD Pericardial rub VARIATION WITH RESPIRATION
VARIATION WITH MANEUVRES STANDING, VALSALVA Decreases venous return and ventricular filling Decreases intensity of all murmurs except MVP Since outflow obstruction is increased by decreasing preload, it increases the intensity of HOCM murmur as well SQUATTING, LAYING DOWN and LEG RAISING Increases venous return and ventricular filling (preload), Hence, increases cardiac output It increases the murmurs of AS, AR, MR and VSD It decreases the murmurs of HOCM and MVP
VARIATION WITH MANEUVRES HAND-GRIP and PHENYLEPHRINE Increases total peripheral resistance (afterload) Increases murmurs of AR, MR, VSD and MS Decreases murmurs of AS, MVP and HOCM INHALED AMYL NITRATE Vasodilation causes decreased TPR and afterload Increases murmurs of AS, MS, PS, MVP and HOCM Decreases murmurs of AR, MR and VSD SITTING UP and LEANING FORWARD Accentuates S2 and increases the murmur of AR LEFT LATERAL DECUBITUS POSITION Accentuates the murmur of MS
AORTIC STENOSIS An ejection click (EC) followed by a crescendo-decrescendo ejection systolic murmur at the aortic area. Heard best with breath held in expiration in a leaning forward. Sometimes radiates to the carotid arteries In mild AS, the diamond-shaped murmur has an early peak whereas In severe AS, the murmur has a late peak Gallavardin phenomenon? It is the systolic murmur of fibrocalcific AS seen with aging. It has a harsh and noisy quality in aortic area but is musical over the apex area .
PULMONIC STENOSIS An ejection click (EC) followed by a crescendo-decrescendo ejection systolic murmur at the pulmonic area, EC may be absent Murmur becomes louder with inspiration unlike ESM of AS which becomes softer May radiate towards the left clavicle
PS with or without VSD If IVS is intact, as obstruction becomes more severe: The murmur lengthens Peak of murmur moves closer to S2 P2 becomes softer If VSD is present (e.g. tetralogy of Fallot / TOF) as obstruction becomes more severe: The murmur becomes shorter Peak becomes more closer to S1 P2 is very soft or absent
TRICUSPID REGURGITATION A holosystolic murmur (HSM) at LLSB (tricuspid area) that may obscure S1 Heard best with diaphragm with breath held in inspiration Murmur becomes louder with inspiration ( Carvallo sign ) unlike murmur of MR Murmur may radiate upwards to upper left sternal border Acute severe TR may present as an early systolic murmur
MITRAL REGURGITATION A holosystolic murmur (HSM) at apex area that may obscure S1 Heard best with diaphragm Murmur may radiate into the precordium or axilla , due to intra-atrial backflow jet Murmur becomes softer with inspiration unlike murmur of TR (turns loud) Murmur of MR is ‘ rumbling ’ as opposed to musical quality of fibro-calcific AS
VARIANTS OF MR Acute severe MR may present as an early systolic murmur as left atrium has a normal size with limited distensibility. Papillary muscle dysfunction (PMD) seen in acute MI may present as an late systolic murmur without a preceding click. Also called ischemic MR
MVP A mid-systolic click (MSC) followed by a mid-to-late diastolic murmur at the apex area. It has a “whooping” musical quality. Maneuvers that preload (standing, Valsalva) or afterload (amyl nitrate): earlier onset of click (closer to S1) longer murmur duration decreased murmur intensity Maneuvers that preload (leg elevation, squatting) or afterload (hand grip) : Delayed onset of click (closer to S2), Shorten murmur duration Increase murmur intensity.
HOCM A crescendo-decrescendo systolic murmur at the left sternal border Best heard with diaphragm in standing position. Like in AS, there is LVOT* obstruction but at a sub-valvular level, due to ASH** Aortic valve is not involved so there is no ejection click, as heard with AS
VSD A pansystolic murmur (PSM) at the left sternal border, with a harsh blowing character, becomes louder with expiration There may be an associated systolic thrill, louder the murmur, smaller the defect Roger’s murmur – the loud PSM of small VSD Murmur of supra- cristal type of VSD is heard in the pulmonic area If pulmonary hypertension is present, there will be a loud P2 and a right ventricular heave. But if there is an associated severe pulmonic stenosis (TOF), P2 will be soft/absent
ASD A ejection systolic murmur (ESM) without a preceding click is heard at the upper sternal border. It is due to the excessive flow across the pulmonary valve. It is soft and heard best with a bell . Louder the murmur, smaller the defect Wide fixed splitting of S2 at pulmonic area is the most important feature A diastolic murmur may be heard at the LLSB due to increased flow across tricuspid valve
AORTIC REGURGITATION In chronic AR, a decrescendo type EDM of “ blowing ” quality and high pitch is heard after S2 (or A2) at the left 3rd ICS- Erb’s area It is heard best with a diaphragm with breath held in expiration in a patient leaning forward If the AR is due to aortic root dilatation , diastolic murmur will radiate into the aortic area Any maneuver that increases the afterload will increase the murmur of AR, as it will tend to favor backflow into the ventricle. i.e. handgrip
Aortic regurgitation cont … There can also be a mid-systolic murmur with AR, due to the increased flow across the aortic valve during systole In AR, a third murmur may be heard, called Austin-Flint murmur, which is a soft mid-to-late diastolic murmur of low pitch and “rumbling” quality. It is heard at the apex, best with a bell during expiration It is thought to be due to functional mitral valve stenosis , as backflow jet from aorta presses on the anterior mitral leaflet to slightly occlude the blood flow from LA into LV during diastole Rarely, an early diastolic murmur, called Cole-Cecil murmur , may be heard in axilla
PULMONARY REGURITATION In chronic PR, a decrescendo type early EDM of “ blowing ” quality and high pitch is heard after S2 (or P2) at the pulmonic area (left 2nd ICS) Heard best with a diaphragm with breath held in inspiration in a supine patient. Unlike AR, it is not increased by handgrip maneuver It is called Graham Steel murmur. If PR is with PAH (pulmonary artery HTN), murmur will have a low pitch, heard with a bell
MITRAL STENOSIS Preceded by a high pitch opening snap (OS), then by a low pitch mid-diastolic murmur that becomes augmented (high-pitched) before loud S1 (late diastolic or pre-systolic component) MDM is best heard with bell placed lightly over the apex in left decubitus position There may be a diastolic thrill Why is there an Opening Snap? There is a pressure gradient across the mitral valve (MV), which causes sharp movement of the tethered anterior cusp of MV at the time when the flow commences, resulting in OS.
AUSTIN FLINT VS MDM OF MS
TRICUSPID STENOSIS A Mid diastolic rumble of more high pitch than mitral rumble It is best heard with the diaphragm placed over the tricuspid area with breath held in inspiration while lying supine Murmur becomes louder with inspiration ( Carvallo sign) unlike MDM of MS (softer) Tricuspid component (T1) of S1 is loud. There may be an opening snap. There may be a diastolic thrill.
CAREY COOMB MURMUR Feature of mitral valvulitis in acute rheumatic fever , commonly heard in children who also have fever and anemia A short mid-diastolic rumble at the apex Usually preceded by an S3 gallop S3 gallop is distinguished from the opening snap of MS by the frequency.
CABOT-LOCKE MURMUR Feature of severe anemia An early diastolic murmur, resembling the murmur of AR, can be heard at the Erb’s area Unlike murmur of AR, it does not have a decrescendo It is an innocent murmur that resolves with treatment of anemia It is due to the increased flow from aorta to coronary arteries that arise from the aortic root
DOCK’S MURMUR Feature of severe stenosis of left anterior descending coronary artery (LAD) A crescendo-decrescendo type diastolic murmur with late accentuation In a sharply localized area: 4 cm left of sternal border in left 4th ICS It is detected only if the patient is sitting upright
RYTAND MURMUR Feature of chronic complete heart block A mid-to-late diastolic murmur at the apex It is thought that murmur is due to increased flow across AV valves due to a slow heart rate It may also be due to antegrade flow across the closing mitral valve (when LA is contracting but LV also contracts before it is full)
KEY HODGKIN MURMUR Feature of syphilitic aortitis An early diastolic murmur, resembling the murmur of AR, but heard only at the aortic area instead of Erb’s area It has a “raspy” quality (saw cutting through wood) It is due to the retroversion of aortic valve leaflets during diastole due to inflammation
“Innocent murmur” AKA “functional murmur or flow murmur” Doesn’t radiate Underlying cardiovascular system is entirely normal and murmur is audible at rest Resuts from normal tubulence occurring during ejection of blood from heart Typical innocent flow murmur arises in pulmonary artery
INNOCENT MURMUR CHARACTERSTICS
Physiologic murmurs Caused by transient increase in blood volume and/or velocity of ejection Common causes-Anemia, anxiety, fever, thyrotoxicosis, pregnancy Murmur will no longer audible or become faint (grade 1-2/6) innocent murmur after correction of increase blood flow or augmented cardiac contractility
EJECTION CLICK (EC) Results from sudden opening of a stenotic valve AORTIC EJECTION CLICK High-pitched, best heard at the aortic area, but widely audible. Occurs earlier as severity of stenosis increases ➜Followed by a systolic murmur and not seen in calcific AS as the cusps are rigid PULMONARY EJECTION CLICK High-pitched, best heard at the pulmonic area with a diaphragm, softens with inspiration. ➜Coincides with a wave of JVP.
MID-SYSTOLIC CLICK (MSC) Mitral valve prolapse (MVP) Usually followed by a late systolic murmur Results from abrupt halting of prolapsing mitral valve leaflets into the atrium by the chordae High-pitched, best heard at apex with diaphragm Moves closer to S1 with valsalva and standing.
OPENING SNAP (OS) Mitral stenosis (MS), rarely in tricuspid stenosis Occur early in diastole after S2 but before S3 May be followed by apical diastolic rumble in MS Results from sudden opening of a stenotic valve High-pitched, best heard at apex by diaphragm in left decubitus position “Softer and closer to S2 in severe MS”
PERICARDIAL KNOCK (PK) Constrictive pericarditis Occur early in diastole, after S2 but before S3 Sharper, higher pitch than S3 and OS Heard widely but best at apex with diaphragm Knock coincides with rapid Y descent of JVP JVP increases with inspiration ( Kussmaul’s sign)
TUMOR PLOP Myxoma or vegetation in left atrium Causing ventricular in-flow obstruction Occurs in early diastole, after S2 Low pitch, heard best at apex with bell A diastolic murmur may also be appreciated
PERICARDIAL FRICTION RUB A coarse scratching or leathery sound (acute viral pericarditis and Dressler’s syndrome 24-72 hours after MI) Best heard over the bare area of heart with diaphragm with the breath held in expiration. Vary in intensity over time, and with position of patient (louder when leaning forward and over) No change with respiration. In contrast, pleural rub disappears when breath is held 3 components : presystolic rub during atrial filling ventricular systolic rub (loudest) ventricular diastolic rub (after a2p2)
HAMMAN’S CRUNCH A series of precordial crackles that correlate with the heartbeat and not with respiration “Crunching” sounds are produced by the heart beating against air-filled tissues. A finding heard in pneumo-pericardium: Following heart surgery Vigorous resuscitation Iatrogenic i.e. pericardiocentesis, bronchoscopy Also in pneumo-mediastinum, spontaneous mediastinal emphysema, Boerhaave syndrome
Physiological maneuver Valsalva Muller Passive leg elevation Sudden standing from squatting or lying down Sudden squatting Isometric exercise Respiration Dynamic Auscultation
Physiological maneuver Valsalva Muller Passive leg elevation Sudden standing from squatting or lying down Sudden squatting Isometric exercise Pharmacological Amyl Nitrate inhalation Methoxamine/phenylephrine
Physiological maneuver Valsalva Muller Passive leg elevation Sudden standing from squatting or lying down Sudden squatting Isometric exercise Respiration Pharmacological Amyl Nitrate inhalation Methoxamine/phenylephrine Other postural changes Left lateral- MS Sitting up and lying forward- AR Stretching of neck- venous hum
1.Valsalva maneuver Exhale forcefully in to a mercury manometer to generate pressure of 40 mm Hg for 20 sec Deep inspiration followed forced expiration against a closed glottis for 20 seconds
Stages Onset of straining Continued straining (Strain phase) End of expiration (Release phase) Recovery (5-10 sec after end of expiration) (Overshoot phase)
Stages Onset of straining Continued straining End of expiration Recovery (5-10 sec after end of expiration) VALSALVA PHASE I increased intrathoracic pressure-> pulmonary circulation is squeezed, so blood is pushed to left heart and there is increase in BP and LV output
Stages Onset of straining Continued straining End of expiration Recovery(5-10 sec after end of expir ) VALSALVA PHASE I increased intrathoracic pressure-> pulmonary circulation is squeezed, so blood is pushed to left heart and there is increase in BP and LV output VALSALVA PHASE II d/t increase intrathoracic pressure, systemic venous return decrease Filling of right and then left side chamber reduced Stroke volume reduced Mean arterial and pulse pressures falls Reflex tachycardia
Stages Onset of straining Continued straining End of expiration Recovery(5-10 sec after end of expir ) VALSALVA PHASE I increased intrathoracic pressure-> pulmonary circulation is squeezed, so blood is pushed to left heart and there is increase in BP and LV output VALSALVA PHASE II d/t increase intrathoracic pressure, systemic venous return decrease Filling of right and then left side reduced Stroke volume reduced Mean arterial and pulse pressures falls Reflex tachycardia PHASE III VALSALVA RELEASE As the pressure on chest is released, allowing pulmonary vessels and aorta to re-expand causing a further initial slight fall in SV due to decrease LA return and increase aortic volume Venous blood can once more enter chest and heart, CO begins to increase
Stages Onset of straining Continued straining End of expiration Recovery(5-10 sec after end of expir ) VALSALVA PHASE I increased intrathoracic pressure-> pulmonary circulation is squeezed, so blood is pushed to left heart and there is increase in BP and LV output VALSALVA PHASE II d/t inc intrathoracic pressure, systemic venous return decrease Filling of right and then left side reduced Stroke volume reduced Mean arterial and pulse pressures falls Reflex tachycardia PHASE III VALSALVA (RELEASE PHASE) As the pressure on chest is released, allowing pulmonary vessels and aorta to re-expand causing a further initial slight fall in SV due to decr LA return and incr aortic volume Venous blood can once more enter chest and heart, CO begins to incr PHASE IV (OVERSHOOT PHASE) Blood pressure over shoots increased Vagal stimulation in carotids heart rate decrease (bradycardia)
Importance of Valsalva The Valsalva maneuver is helpful in differentiating right-sided systolic murmurs from those originating from the left heart Most useful in identifying the systolic murmurs of HOCM and MVP Upon release of the Valsalva maneuver, murmurs from the right heart generally return to baseline intensity within 2-3 cardiac cycles whereas left sided murmurs generally takes 5-10 cycles Not useful in heart failure, ASD and MS
2.Muller’s maneuver Nares held closed, patient has to suck forcibly into a manometer to generate a negative pressure of 40-50 mm Hg for 10 seconds and see for changes in intensity of murmur at end of 10 sec Nares pinched, mouth firmly sealed, and asked patient to inspire for 10 sec
Historically used to accentuate right sided murmur Objective studies has found not useful Infrequently performed
Dynamic auscultation helpful in • AS vs HOCM : Squatting ( A /v)/ Post VPCS Valsalva/Standing (v/a) • AS x MR : Handgrip (v/a) Phenyl ephrine (v/a) Post PVC (a/v) Amyl nitrate (a/v) MS X Austin Flint murmur: Amyl nitrate( A /v) PR X AR : Squatting (_/a) S ustained handgrip (-/a) PS X Small VSD : Amyl nitrate (a/v) Respiration