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Description : Check out this medical presentation on Heart Murmur, which is titled "Murmur and Dynamic Auscultation of Cardiovascular System", to know about heart murmurs, and its classification, i.e., organic, functional and innocent.

Tags : Heart Murmur, Dynamic Auscultation, Cardiovascular System, organic, functional, innocent

Published on : Jul 01, 2021 | Views : 2679 | Downloads : 10

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MURMUR AND Dynamic Auscultation OF Cardiovascular System ANKUR KAMRA
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Defining a heart murmur A cardiac murmur is defined as a relatively prolonged series of auditory vibrations of Varying intensity(loudness), frequency (pitch), quality, configuration, and duration
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How is a murmur produced? Sound is produced by vibration Vibration is generated by turbulence Turbulence generated in the blood column set up vibrations in the vessel wall & cardiac structures causes murmurs
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Leatham has attributed the production of murmurs or turbulence to three main factors: (1) high flow rate through normal or abnormal orifices, (2) forward flow through a constricted or irregular orifice or into a dilated vessel or chamber, and (3) backward or regurgitant flow through an incompetent valve, septal defect, or patent ductus arteriosus. Frequently, a combination of these factors is operative
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CLASSIFICATION Can be classified into organic, functional and innocent. Organic refer to structural defect responsible for murmur Important is that the term innocent and functional are not interchangeable. Functional murmur should subserve a function like increased flow across aortic valve as in severe AR. While innocent occur in absence of abnormalities of heart and circulation, more common in children and on right side.
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Description of a Murmur Position in the cardiac cycle Site of murmur ] Shape of murmur Intensity Quality & Pitch Conduction Dynamic changes
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Dynamic Auscultation Listening to the change in character, behaviour and the intensity of the heart sounds and murmurs to physiological and pharmacological maneuvers……. “AUSCULTATE WITH ALTERED HEMODYNAMICS”
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Conditions and interventions Respiration Postural Change Valsalva maneuver Exercise Change in Cardiac Cycle length Pharmacological agents.
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What happen during respiration Normal inspiration → ↑ venous return to right side of the heart due to fall in intra thoracic pressure → ↑ stroke volume of right side Dilatation of pulmonary vascular system causing decrease in pulmonary impedance there by increasing pulmonary hang out interval(>80 ms) So leads to accentuation of R side murmur
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RESPIRATION CONTINUE Normal expiration → ↓ lung volume → ↑ pulmonary venous flow Therefore, left sided murmurs are loudest during expiration except MR which remain unchanged. While no change is seen When complicated by RVF as due to high RVEDP no increase in venous return. Aortic valvular ES do not vary with respiration MR murmur do not vary with respiration
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RESPIRATION CONTINUE Assess changes during normal respiration Patient should be in semiupright or sitting posture In RV failure and PHT, no increase in venous return with inspiration, hence no inspiratory augmentation of right sided murmurs and gallops Absence of respiratory influence is of no particular diagnostic value. Effects of inspiration may be accentuated by Muller maneuver.
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STANDING Auscultation is carried out immediately before and after the change in posture since effects may be quite transient persisting for only 10 – 15 heart beats If patient is unable to sit upright or stand, rapid application of tourniquets at upper thigh level may reduce venous return reproducing similar response
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STANDING Rapid standing or sitting up from lying position or rapid standing from squatting posture results in decreased venous return due to venous pooling in legs and splanchnic vessels leads to- decreased stroke volume decreased mean arterial pressure decrease in heart size followed by reflex increase in heart rate & systemic resistance
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standing All murmurs decrease except- ESM of HOCM becomes louder and longer Click occurs earlier, murmur becomes longer in MVP while loudness shows variable response
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Sudden assumption of LYING DOWN POSITION PASSIVE ELEVATION OF LEGS Increase in venous return → increase R.V. stroke volume → later after several cardic cycles left ventricle volume also increase . So Systolic murmur of AS,PS,MR, TR & VSD increase. MVP & HOCM murmurs decrease due to increase in LVEDV and LV size.
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Squatting Sudden change from standing to squatting leads to- Increases venous return & Stroke Volume Increase of systemic vascular resistance due to kinking of iliac artery and reduction of pressure of gravity Increase of systemic Arterial pressure with transient bradycardia
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Squatting Increased venous return and CO - augments most murmurs (AS,PS,MR,AR,VSD) Right heart murmurs do so earlier Increased left ventricular volume - decreases murmur of HOCM and delayed murmur and click of MVP Ejection murmur of TOF↑ due to increase pulmonary blood flow and decrease in right to left shunt
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Other postural changes Assumption of L Lateral Position Causes closeness of heart to chest wall and transient rise of HR. So leads to – Increased murmur of MS, MR and austin flint murmur of AR Early appearance of click and systolic murmur of MVP due to increasec HR.
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Sitting up and leaning forward causes more closeness of base of heart to chest wall so AR and PR murmurs more readly audible PRONE POSITION & KNEE CHEST POSITION Bring heart close to chest wall making pericardial rub more prominent
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Valsalva Maneuver Relatively deep inspiration followed by forced exhalation against a closed glottis for 10 to 20 seconds Physician has to keep flat of the hand on the abdomen to provide the patient a force to breathe against
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VALSALVA MANEUVER Forced expiration against closed glottis Manometer method: Patient blows into the mercury manometer and maintains 40 mmHg for 15 seconds Valsalva equivalent: Patient pushes back against examiner’s hand which is pressed downward on mid abdomen. The maneuver is demonstrated and patient practices the maneuver before assessment of murmur Caution : Not to be performed in IHD as it will reduce Coronary Blood Flow.
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PHASES OF VALSALVA PHASE 1-due to increase in intra thoracic pressure there is transient rise in LV output and systemic arterial pressure but there occurs fall in HR phase 2(stain phase)- decrease in venous return first to right then to left leads to decrease in systolic, diastolic and pulse pressure and reflex tachycardia
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PHASE 3- cessation of staining result in- sudden increase in systemic venous return but transient decrease in arterial pressure due to fall in intra-thoracic pressure PHASE 4- return to pre valsalva a transient overshoot of systemic arterial pressure Reflex bradycardia
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EFFECTS ON MURMUR PHASE1 –as stroke volume fall there is decrease in – systolic murmur of AS, PS, MR, TR diastolic murmur of AR PR MS TS PHASE2- reduction in LV volume and size leads to- increase in systolic murmur of HOCM increase in degree of MVP prolapse
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PHASE 3- sudden increase in SVR leads to increase in right side murmurs PHASE 4-left side murmur comes to control levels and may transiently increase. ASD, MS and CHF – Phase 1 and 3 are normal but there is absence of decrease in arterial pressure tracing during phase 2 and overshoot of BP does not occur in phase 4 that leads to SQUARE WAVE RESPONSE ie. Instead of four phases there is only two phase.
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The Muller Maneuver Converse of Valsalva Maneuver Less frequently employed Forcibly inspires while the nose is held closed and mouth is firmly sealed for about 10 sec. Augments murmur and filling sound originating in right side of the heart.
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ISOMETRIC EXERCISE Use calibrated handgrip device or tennis ball or rolled up BP cuff. Measure the maximum effort. Patient exerts 70 – 100% of this maximum for about 30 seconds Simultaneous handgrip using both hands Valsalva maneuver during handgrip should be avoided
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ISOMETRIC EXERCISE Hemodynamic changes: Significant increase in Arterial pressure Heart rate Cardiac output LV filling pressure LV size
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Isometric Exercise Systolic Murmur of AS reduced due to reduced gradient across aortic valve AR , MR , VSD – increased due to increase systemic vascular resistance MDM of MS – increased due to Increased CO Syst Murmur of HOCM reduced MVP murmur + click delayed
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ISOMETRIC EXERCISE Avoid in those with ventricular arrhythmias and myocardial ischemia Contraindicated in recent myocardial infarction, uncontrolled hypertension, cerebrovascular disease, suspected aortic dissection
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Cardiac cycle length changes post PVC and AF ↑ preload will increases ventricular filling and size Also in addition there is secondry increase in ventricular contractibilty of new beat and transient increase in arterial pressure.
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Cardiac cycle length changes Increased ( L or R vent ejection murmurs ) AS PS HOCM(there is inc in SM but also decrese volume of pulse known as BROCKENBROUGH PHENOMENA) No change for MR , TR DM of AR increases due to transient rise in arterial pressure
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Amylnitrite Inhalation Inhalation of Amyl Nitrate Crush ampoule in towel take 3-4 deep breaths over 10 – 15 secs Changes observed- < 30 secs : Systemic vasodilatation 30 – 60 secs : increase HR & CO However majority of auscultaory changes are observed in first 30 sec
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Due to increse in CO- SM of AS and PS SM of TR All functional SM DM of MS and TS DM of PR
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Due to decrease in SVR following murmur are decreased- SM of MR DM and austin flint murmur of AR SM of TOF Due to decrease LV volume and size – SM of HCM increases early appearance of MVP click and murmur but softening of murmur occur due to decrease resistance to LV resistance
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Amyl Nitrite Inhalation Augments Diminishes Aortic stenosis Mitral regurgitation Pulmonary stenosis TOF Tricuspid regurgitation Mitral regurgitation Mitral stenosis Austin Flint Pulmonary regurgitation Aortic Regurgitation
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Phenylephrine ↑ BP & SVR ↓ CO & HR – last for 3-5mts Reduces intensity of S1, A2-OS may widen Augments the murmurs of VSD, PDA, MR, AR, TOF, Systemic AVF Diminishes AS, MS & functional murmurs ESM of HOCM diminishes Click & murmur of MVP get delayed
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Methoxamine & Phenylephrine Opposite effect of Amyl Nitrate Phenylephrine - due to short duration of action Systolic pressure elevated by 30 mm Hg for 3 to 5 mts EFFECT Increases systemic arterial pressure Reflex Bradycardia , decrease CO, decrease Contractility Caution : Not to be used in patients with CHF or Systemic hypertension.
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Methoxamine & Phenylephrine AR , MR , VSD , TOF – Louder SM OF AS, PS and DM of PR and TS -show no changes LV size increases HOCM – Softer Click and Murmur of MVP - Delayed
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Some general points about murmur before discussing individual murmurs
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Timing
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Sometime it is difficult to identify the timing of murmur Murmur can be timed by simultaneous palpation of the carotid arterial pulse or by identifying S2 at base Inching technique of Harvey and Levine In tachycardia carotid sinus massage can slow down heart rate In case of extra systole indentify the beat that follows pause and then first sound after pause will be S1
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LENGTH It generally reflect the pressure difference b/w two sites and this is true for all stenotic lesions like MS, AS, PS or TS In regurgitant lesion length has no correlation with severity. In AR length of murmur correlates better then MR but still not as reliable as stenotic lesions
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CHARACTER High frequency murmur occur when pressure difference b/w two chambers are high and low pressure difference has low frequency and pitch. As a general rule regurgitant lesions are high frequency and stenotic are rough or low frequency. Murmur of AV stenosis are of low frequency while semilunar are of mixed frequency High frequency or soft component of murmur is more widely audible this is reason why AS soft component is audible at apex and mistaken for MR While low frequency or rough component is audible at site of best audibility of murmur.
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Systolic Murmurs
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Early Systolic murmurs Early systolic murmurs begin with S1 and extend for a variable period of time, ending well before S2 1. Acute severe mitral regurgitation Regurgitation occurs into a normal-sized, relatively noncompliant left atrium and as LV-LA pressure gradient is abolished during late systole, termination of retrograde flow occurs well before S2. best heard at apical impulse Caused by: i. Papillary muscle rupture due to ishemia ii. Infective endocarditis -destruction of leaflet tissue, chordal rupture, or both
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iii. Rupture of the chordae tendineae in myxomatous mitral valve disease iv. Blunt chest wall trauma-papillary muscle contusion and rupture, chordal detachment, or leaflet avulsion. 2.Congenital, small ventricular septal defect- ventricular size decrease and septum thickness increases which seals off defect 3. VSD with high PA pressure- high pulmonary resistance will decrease the late shunting Tricuspid regurgitation with normal PA pressures- The murmur is soft (grade 1 or 2), best heard at the lower left sternal border, and may increase in intensity with inspiration (Carvallo's sign). Regurgitant "c-v" waves may be visible in the jugular venous pulse.
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Midsystolic (ejection) murmurs Mid-systolic murmurs begin at a short interval following S1, end before S2 Murmur is due to flow across LV or RV outflow tract when flow proceeds , murmur increase in in crescendo and when it decrease murmur decrease in decrescendo. Intensity of murmur depend on cardic output. So when flow and cardic output changes like in various maneuver murmur changes. Causes are: 1. Innocent: due to flow across normal ventricular outflow tract 2. Functional: dilation of aortic root, pulmonary trunk increase flow into aorta and pulmoary artery 3. Pathologic are secondary to structural CV abnormalities e.g. Aortic stenosis, Hypertrophic cardiomyopathy, Pulmonic stenosis
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Aortic stenosis Harsh, medium pitch, loudest in aortic area; radiates along the carotid arteries and apex. Intensity varies directly with CO Severity varies with murmur may have an early peaking and short duration or late peaking and prolonged duration. A/W parvus et tardus Other conditions which may mimic the murmur of aortic stenosis w/o obstructing flow: 1. Aortic sclerosis 2. Bicuspid aortic valve 3. Dilated aorta 4. Increased flow across the valve during systole
Slide 54-

Hypertrophic cardiomyopathy Loudest b/t left sternal edge and apex; Grade 2-3/6 Does NOT radiate into neck; carotid upstrokes are brisk and may be bifid The murmur will classically increase in intensity with maneuvers that result in increasing degrees of outflow tract obstruction, such as a reduction in preload or afterload (Valsalva, standing, vasodilators) or to an augmentation of contractility (inotropic stimulation). Maneuvers that increase preload (squatting, passive leg raising, volume administration) or afterload (squatting, vasopressors) or that reduce contractility (-adrenoreceptor blockers) decrease the intensity of the murmur
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Pansystolic (Holosystolic) Murmurs Are pathologic Murmur begins immediately with S1 and continues up to S2 1. Mitral valve regurgitation Loudest at the left ventricular apex Radiation reflects the direction of the regurgitant jet i. To the base of the heart = anterosuperior jet (flail posterior leaflet) ii. To the axilla and back = posterior jet (flail anterior leaflet Also usually associated with a systolic thrill, a soft S3, and a short diastolic rumbling (best heard in left lateral decubitus 2. Tricuspid valve regurgitation 3. Ventricular septal defect
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Early diastolic murmur AR murmur -Soft high frequency early diastolic murmur with pt sitting & leaning forward in full held expiration -3 LICS [ 2 & 3 RICS in root dil] -musical quality -Austin Flint murmur
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AR Difference between acute and chronic AR Austin Flint Murmur to be discussed
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High Pressure PR High pitched soft blowing decrescendo murmur usually lasts throughout diastole heard in the left upper sternal border Associated with loud P2 and other features of PAH PR vs. AR Loud P2, murmur begins after P2 Normal pulse pressure Clinical setting Squatting and sustained hand grip increases AR
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High Pressure vs. Normal Pressure
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Mid Diastolic Murmur RV - TS LV - MS Austin Flint murmur - Carey-Comb's OTHERS -Atrial Myxoma - TR - ASD - VSD - PDA - MR
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MS Low pitch rough rumbling [sound of distant thunder] MDM Localized to apex, better heard in left lateral position with bell Length a severity Long murmurs up to S1 even in long cycles of AF- severe MS Late diastolic or Pre systolic accentuation usually seen in pliable valves and in NSR [ sometimes in AF]
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TS Similar to MS Murmur usually seen associated with AF Diff. from MS Increases during inspiration [Augmentation of RV volume, RV Diastolic Pr., Flow rate and gradient across valve] LLSB
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Austin Flint Murmur Severe AR regurgitant jet directed toward the AML prevent the latter from opening well during diastole generating turbulent flow Low pitch MDM or late diastolic, best heard at the apex. To differentiate from MS No OS Amyl nitrate inhalation
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Late Diastolic/ Pre-systolic Murmurs MS Higher frequency than MDM Sometimes only PSA heard- mild MS Generally absent in calcified valves and most of AF [ may be present during short cycle lengths in AF] Cause- Increased flow during atrial contraction in late systole
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Valsalva Maneuver
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DYNAMIC AUSCULTATION Proper assessment requires Good stethoscope Quiet room Cooperative patient Bare chest Intact autonomic function and normovolemia Knowledge about the maneuver and the changes expected
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THE CAVEATS ARE……… Avoid dynamic auscultation in sick patients When postures are changed, transition should be abrupt Continuous auscultation is required, when maneuvres are being elicited Concentrate on the first few cycles after maneuvres Realize that each maneuvre induces more than one alterations in hemodynamics
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early systolic mid systolic Systolic murmur late systolic pan/holo systolic early diastolic Diastolic murmur mid diastolic pre systolic
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Other diastolic murmurs Cabot– Locke Murmur- [Diastolic Flow murmur] The Cabot–Locke murmur is a diastolic murmur that sounds similar to aortic insufficiency but does not have a decrescendo; it is heard best at the left sternal border. [High flow thru coronary vessels, LMCA, LAD] The murmur resolves with treatment of anaemia. Dock’s murmur diastolic crescendo-decrescendo, with late accentuation, [consistent with blood flow through the coronary] in a sharply localized area, 4 cm left of the sternum in the 3LICS, detectable only when the patient was sitting upright. Due to stenosis of LAD
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Other Mid Diastolic Murmur Carey Coomb’s murmurs Acute rheumatic fever, mitral valve structures acutely inflamed with some thickening and edema turbulence of flow during the rapid filling phase. + moderate MR [increased mitral inflow in diastole] Low pitched short MDM. good evidence of active carditis
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Other diastolic murmurs Key–Hodgkin murmur EDM of AR; it has a raspy quality, [sound of a saw cutting through wood]. Hodgkin correlated the murmur with retroversion of the aortic valve leaflets in syphilitic disease. Rytand’s murmur in complete heart block MDM or Late diastolic murmur Atrial contraction coincides with the phase of rapid diastolic filling increased flow short MDM [intermittent]. Another theory- Delayed V. contraction following A. contraction may lead to diastolic MR & TR, because AV valve closure does not occur [unless V. systole supervenes]. When higher V than A pressure during atrial relaxation, an incompletely closed AV valve may lead to a reverse gradient with a considerable regurgitation volume.
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SHAPE crescendo, decrescendo, crescendo-decrescendo, plateau The crescendo (grows louder) Configuration of the murmur of chronic AS can be understood in terms of the progressive increase in the systolic pressure gradient between the left ventricle and aorta. Decrescendo Configuration(decreasing) of the murmur of chronic AR can be understood in terms of the progressive decline in the diastolic pressure gradient between the aorta and the left ventricle. The crescendo-decrescendo(increasing-decreasing or diamond shape) configuration of the murmur of AS reflects the changes in the systolic pressure gradient between the left ventricle and the aorta as ejection occurs, The plateau(even or unchanged) configuration of the murmur of chronic rheumatic MR is consistent with the large and nearly constant pressure difference between the left ventricle and the left atrium.