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Systolic murmer
- 1.
- 2. HEART MURMURS ARECAUSED 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. • THEY TRADITIONALLY ARE DEFINED IN TERMS OF THEIR TIMING WITHIN THE CARDIAC CYCLE
- 3. • SYSTOLIC MURMURSBEGIN WITH OR AFTER THE FIRST HEART SOUND(S1) AND TERMINATE AT OR BEFORE THE COMPONENT (A2 OR P2) OF THE SECOND HEART SOUND (S2) THAT CORRESPONDS TO THEIR SITE OF ORIGIN (LEFT OR RIGHT RESPECTIVELY). • DIASTOLIC MURMURS BEGIN WITH OR AFTER THE ASSOCIATED COMPONENT OF S2 AND END AT OR BEFORE THE SUBSEQUENT S1. • CONTINUOUS MURMURS ARE NOT CONFINED TO EITHER PHASE OF THE CARDIAC CYCLE BUT INSTEAD BEGIN IN EARLY SYSTOLE AND PROCEED THROUGH S2 INTO ALL OR PART OF DIASTOLE.
- 4. • THE ACCURATETIMING OF HEART MURMURS IS THE FIRST STEP IN THEIR IDENTIFICATION. THE DISTINCTION BETWEEN S1 AND S2 AND, THEREFORE, SYSTOLE AND DIASTOLE IS USUALLY A STRAIGHTFORWARD PROCESS BUT CAN BE DIFFICULT IN THE SETTING OF A TACHYARRHYTHMIA, IN WHICH CASE THE HEART SOUNDS CAN BE DISTINGUISHED BY SIMULTANEOUS PALPATION OF THE CAROTID UPSTROKE, WHICH SHOULD CLOSELY FOLLOW S1.
- 5. • DURATION ANDCHARACTER • THE DURATION OF A HEART MURMUR DEPENDS ON THE LENGTH OF TIME OVER WHICH A PRESSURE DIFFERENCE EXISTS BETWEEN TWO CARDIAC CHAMBERS, THE LEFT VENTRICLE AND THE AORTA, THE RIGHT VENTRICLE AND THE PULMONARY ARTERY, OR THE GREAT VESSELS. • THE MAGNITUDE AND VARIABILITY OF THIS PRESSURE DIFFERENCE, COUPLED WITH THE GEOMETRY AND COMPLIANCE OF THE INVOLVED CHAMBERS OR VESSELS, DICTATE THE VELOCITY OF FLOW; THE DEGREE OF TURBULENCE; AND THE RESULTING FREQUENCY, CONFIGURATION , AND INTENSITY OF THE MURMUR.
- 6. • THE DIASTOLICMURMUR OF CHRONIC AORTIC REGURGITATION (AR) IS A BLOWING, HIGH-FREQUENCY EVENT, WHEREAS THE MURMUR OF MITRAL STENOSIS (MS), INDICATIVE OF THE LEFT ATRIAL–LEFT VENTRICULAR DIASTOLIC PRESSURE GRADIENT, IS A LOW-FREQUENCY EVENT, HEARD AS A RUMBLING SOUND WITH THE BELL OF THE STETHOSCOPE. THE FREQUENCY COMPONENTS OF A HEART MURMUR MAY VARY AT DIFFERENT SITES OF AUSCULTATION • THE COARSE SYSTOLIC MURMUR OF AORTIC STENOSIS (AS) MAY SOUND HIGHER PITCHED AND MORE ACOUSTICALLY PURE AT THE APEX, A PHENOMENON
- 7. • SOME MURMURSMAY HAVE A DISTINCT OR UNUSUAL QUALITY, SUCH AS THE “HONKING” SOUND APPRECIATED IN SOME PATIENTS WITH MITRAL REGURGITATION (MR) DUE TO MITRAL VALVE PROLAPSE (MVP).
- 8. THE CONFIGURATION OFA HEART MURMUR • CRESCENDO, DECRESCENDO, CRESCENDO-DECRESCENDO, OR PLATEAU. • THE DECRESCENDO CONFIGURATION 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 CRESCENDODECRESCENDO CONFIGURATION OF THE MURMUR OF AS REFLECTS THE CHANGES IN THE SYSTOLIC PRESSURE GRADIENT BETWEEN THE LEFT VENTRICLE AND THE AORTA AS EJECTION OCCURS. • WHEREAS THE PLATEAU CONFIGURATION OF THE MURMUR OF CHRONIC MR IS CONSISTENT WITH THE LARGE AND NEARLY CONSTANT PRESSURE DIFFERENCE BETWEEN THE LEFT VENTRICLE AND THE LEFT ATRIUM.
- 9. INTENSITY OF MURUMUR •THE INTENSITY OF A HEART MURMUR IS GRADED ON A SCALE OF 1–6(OR I–VI). • A GRADE 1; MURMUR IS VERY SOFT AND IS HEARD ONLY WITH GREAT EFFORT. • A GRADE 2 ;MURMUR IS EASILY HEARD BUT NOT PARTICULARLY LOUD. • A GRADE 3; MURMUR IS LOUD BUT IS NOT ACCOMPANIED BY A PALPABLE THRILL OVER THE SITE OF MAXIMAL INTENSITY. • A GRADE 4 ;MURMUR IS VERY LOUD AND IS ACCOMPANIED BY A THRILL. • A GRADE 5; MURMUR IS LOUD ENOUGH TO BE HEARD WITH ONLY THE EDGE OF THE STETHOSCOPE TOUCHING THE CHEST, • A GRADE 6 ;MURMUR IS LOUD ENOUGH TO BE HEARD WITH THE STETHOSCOPE SLIGHTLY OFF THE CHEST.
- 10. • MURMURS OFGRADE 3 OR GREATER INTENSITY USUALLY SIGNIFY IMPORTANT STRUCTURAL HEART DISEASE AND INDICATE HIGH BLOOD FLOW VELOCITY AT THE SITE OF MURMUR PRODUCTION. • SMALL VENTRICULAR SEPTAL DEFECTS (VSDS) ARE ACCOMPANIED BY LOUD, USUALLY GRADE 4 OR GREATER, SYSTOLIC MURMURS AS BLOOD IS EJECTED AT HIGH VELOCITY FROM THE LEFT VENTRICLE TO THE RIGHT VENTRICLE. • LOW-VELOCITY EVENTS, SUCH AS LEFT-TO-RIGHT SHUNTING ACROSS AN ATRIAL SEPTAL DEFECT (ASD), ARE USUALLY SILENT. • THE INTENSITY OF A HEART MURMUR MAY BE DIMINISHED BY ANY PROCESS THAT INCREASES THE DISTANCE BETWEEN THE INTRACARDIAC SOURCE AND THE STETHOSCOPE ON THE CHEST WALL, SUCH AS OBESITY, OBSTRUCTIVE LUNG DISEASE,AND A LARGE
- 11. LOCATION AND RADIATION .RECOGNITIONOF THE LOCATION AND RADIATION OF THE MURMUR HELPS FACILITATE ITS ACCURATE IDENTIFICATION ADVENTITIOUS SOUNDS, SUCH AS A SYSTOLIC CLICK OR DIASTOLIC SNAP, OR ABNORMALITIES OF S1 OR S2 MAY PROVIDE ADDITIONAL CLUES. CAREFUL ATTENTION TO THE CHARACTERISTICS OF THE MURMUR AND OTHER HEART SOUNDS DURING THE RESPIRATORY CYCLE AND THE PERFORMANCE OF SIMPLE BEDSIDE MANEUVERS COMPLETE THE AUSCULTATORY EXAMINATION
- 14. SYSTOLIC HEART MURMURS •EARLYSYSTOLIC MURMURS • EARLY SYSTOLIC MURMURS BEGIN WITH S1 AND EXTEND FOR A VARIABLE PERIOD, ENDING WELL BEFORE S2. • ACUTE, SEVERE MR INTO A NORMAL-SIZED, RELATIVELY NONCOMPLIANT LEFT ATRIUM RESULTS IN AN EARLY, DECRESCENDO SYSTOLIC MURMUR BEST HEARD AT OR JUST MEDIAL TO THE APICAL IMPULSE.
- 15. CLINICAL SETTINGS INWHICH ACUTE, SEVERE MR OCCUR INCLUDE (1) PAPILLARY MUSCLE RUPTURE COMPLICATING ACUTE MYOCARDIAL INFARCTION (MI) (2) RUPTURE OF CHORDAE TENDINAE IN THE SETTING OF MYXOMATOUS MITRAL VALVE DISEASE (3) INFECTIVE ENDOCARDITIS (4)BLUNT CHEST WALL TRAUMA
- 16. • ACUTE, SEVEREMR FROM PAPILLARY MUSCLE RUPTURE USUALLY ACCOMPANIES AN INFERIOR, POSTERIOR, OR LATERAL MI AND OCCURS 2–7 DAYS AFTER PRESENTATION. • IT OFTEN IS SIGNALED BY CHEST PAIN, HYPOTENSION, AND PULMONARY EDEMA, BUT A MURMUR MAY BE ABSENT IN UP TO 50% OF CASES. • THE POSTEROMEDIAL PAPILLARY MUSCLE IS INVOLVED 6 TO 10 TIMES MORE FREQUENTLY THAN THE ANTEROLATERAL PAPILLARY MUSCLE.
- 17. • THE MURMURIS TO BE DISTINGUISHED FROM THAT ASSOCIATED WITH POST-MI VENTRICULAR SEPTAL RUPTURE, WHICH IS ACCOMPANIED BY A SYSTOLIC THRILL AT THE LEFT STERNAL BORDER IN NEARLY ALL PATIENTS AND IS HOLOSYSTOLIC IN DURATION. • THE DISTINCTION BETWEEN ACUTE MR AND VENTRICULAR SEPTAL RUPTURE ALSO CAN BE ACHIEVED WITH RIGHT HEART CATHETERIZATION, SEQUENTIAL DETERMINATION OF OXYGEN SATURATIONS AND ANALYSIS OF THE PRESSURE WAVEFORMS (TALL V WAVE IN THE PULMONARY ARTERY WEDGE PRESSURE IN MR)
- 18. CONGENITAL, SMALL MUSCULARVSD MAY BE ASSOCIATED WITH AN EARLY SYSTOLIC MURMUR. THE DEFECT CLOSES PROGRESSIVELY DURING SEPTAL CONTRACTION, AND THUS, THE MURMUR IS CONFINED TO EARLY SYSTOLE. IT IS LOCALIZED TO THE LEFT STERNAL BORDER AND IS USUALLY OF GRADE 4 OR 5 INTENSITY. SIGNS OF PULMONARY HYPERTENSION OR LEFT VENTRICULAR VOLUME OVERLOAD ARE ABSENT. ANATOMICALLY LARGE AND UNCORRECTED VSDS, WHICH USUALLY INVOLVE THE MEMBRANOUS PORTION OF THE SEPTUM,MAY LEAD TO PULMONARY HYPERTENSION.
- 19. • THE MURMURASSOCIATED WITH THE LEFT-TO-RIGHT SHUNT, WHICH EARLIER MAY HAVE BEEN HOLOSYSTOLIC, BECOMES LIMITED TO THE FIRST PORTION OF SYSTOLE. • AS THE ELEVATED PULMONARY VASCULAR RESISTANCE LEADS TO AN ABRUPT RISE IN RIGHT VENTRICULAR PRESSURE AND AN ATTENUATION OF THE INTERVENTRICULAR PRESSURE GRADIENT DURING THE REMAINDER OF THE CARDIAC CYCLE. • IN SUCH INSTANCES, SIGNS OF PULMONARY HYPERTENSION (RIGHT VENTRICULAR LIFT, LOUD AND SINGLE OR CLOSELY SPLIT S2) MAY PREDOMINATE.
- 20. •TRICUSPID REGURGITATION (TR)WITH NORMAL PULMONARY ARTERY PRESSURES, AS MAY OCCUR WITH INFECTIVE ENDOCARDITIS, MAY PRODUCE AN EARLY SYSTOLIC MURMUR. • THE MURMUR IS SOFT (GRADE 1 OR 2), IS 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. TR IN THIS SETTING IS NOT ASSOCIATED WITH SIGNS OF • RIGHT HEART FAILURE. • MID-SYSTOLIC MURMURS MID-SYSTOLIC MURMURS BEGIN
- 21. MID-SYSTOLIC MURMURS • • MID-SYSTOLICMURMURS BEGIN AT A SHORT INTERVAL AFTER S1, END BEFORE S2 AND ARE USUALLY CRESCENDO-DECRESCENDO IN CONFIGURATION. • AORTIC STENOSIS IS THE MOST COMMON CAUSE OF A MID SYSTOLIC MURMUR IN AN ADULT. • THE MURMUR OF AS IS USUALLY LOUDEST TO THE RIGHT OF THE STERNUM IN THE SECOND INTERCOSTAL SPACE (AORTIC AREA) AND RADIATES INTO THE CAROTIDS. • TRANSMISSION OF THE MIDSYSTOLIC MURMUR TO THE APEX, WHERE IT BECOMES HIGHER- PITCHED, IS COMMON (GALLAVARDIN EFFECT). • DIFFERENTIATION OF THIS APICAL SYSTOLIC MURMUR FROM MR CAN BE DIFFICULT. • THE MURMUR OF AS WILL INCREASE IN INTENSITY, OR BECOME LOUDER, IN THE BEAT AFTER A PREMATURE BEAT, • WHEREAS THE MURMUR OF MR WILL HAVE CONSTANT INTENSITY FROM BEAT TO BEAT.
- 22. • THE INTENSITYOF THE AS MURMUR ALSO VARIES DIRECTLY WITH THE CARDIAC OUTPUT. • WITH NORMAL CARDIAC OUTPUT, A SYSTOLIC THRILL AND A GRADE 4 OR HIGHER MURMUR SUGGEST SEVERE AS. • THE MURMUR IS SOFTER IN THE SETTING OF HEART FAILURE AND LOW CARDIAC OUTPUT. • OTHER AUSCULTATORY FINDINGS OF SEVERE AS INCLUDE A SOFT OR ABSENT A2, PARADOXICAL SPLITTING OF S2, AN APICAL S4, AND A LATE-PEAKING SYSTOLIC MURMUR.
- 23. • IN CHILDREN,ADOLESCENTS, AND YOUNG ADULTS WITH CONGENITAL VALVULAR AS, AN EARLY EJECTION SOUND (CLICK) IS USUALLY AUDIBLE, MORE OFTEN ALONG THE LEFT STERNAL BORDER THAN AT THE BASE. • ITS PRESENCE SIGNIFIES A FLEXIBLE, NON CALCIFIED BICUSPID VALVE (OR ONE OF ITS VARIANTS)LOCALIZES THE LEFT VENTRICULAR OUTFLOW OBSTRUCTION TO THE VALVULAR (RATHER THAN SUB- OR SUPRA VALVULAR) LEVEL.
- 24. • ASSESSMENT OFTHE VOLUME AND RATE OF RISE OF THE CAROTID PULSE CAN PROVIDE ADDITIONAL INFORMATION. A SMALL AND DELAYED UPSTROKE (PARVUSET TARDUS) IS CONSISTENT WITH SEVERE AS. • ELECTROCARDIOGRAM (ECG) SHOWS SIGNS OF LEFT VENTRICULAR HYPERTROPHY (LVH) AS THE SEVERITY OF THE STENOSIS INCREASES.
- 25. OBSTRUCTIVE FORM OFHYPERTROPHIC CARDIOMYOPATHY (HOCM) • IS ASSOCIATED WITH A MID-SYSTOLIC MURMUR THAT IS USUALLY LOUDEST ALONG THE LEFT STERNAL BORDER OR BETWEEN THE LEFT LOWER STERNAL BORDER AND THE APEX. • THE MURMUR IS PRODUCED BY BOTH DYNAMIC LEFT VENTRICULAR OUTFLOW TRACT OBSTRUCTION AND MR, AND THUS, ITS CONFIGURATION IS A HYBRID BETWEEN EJECTION AND REGURGITANT PHENOMENA. • THE INTENSITY OF THE MURMUR MAY VARY FROM BEAT TO BEAT AND AFTER PROVOCATIVE MANEUVERS BUT USUALLY DOES NOT EXCEED GRADE 3.
- 26. • THE MURMURCLASSICALLY WILL 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 WITH AN AUGMENTATION OF CONTRACTILITY (INOTROPIC STIMULATION). • MANEUVERS THAT INCREASE PRELOAD (SQUATTING, PASSIVE LEG RAISING, VOLUME ADMINISTRATION) OR AFTERLOAD (SQUATTING, VASOPRESSORS) OR THAT REDUCE CONTRACTILITY(Β-ADRENORECEPTOR BLOCKERS) DECREASE THE INTENSITY OF THE MURMUR. IN RARE PATIENTS, THERE MAY BE REVERSED SPLITTING OF S2. A SUSTAINED LEFT VENTRICULAR APICAL IMPULSE AND AN S4 MAY BE APPRECIATED.
- 27. IN CONTRAST TOAS, THE CAROTID UPSTROKE IS RAPID AND OF NORMAL VOLUME. • RARELY, IT IS BISFERIENS OR BIFID IN CONTOUR DUE TO MID-SYSTOLIC CLOSURE OF THE AORTIC VALVE. • ALTHOUGH THE SYSTOLIC MURMUR ASSOCIATED WITH MVP BEHAVES SIMILARLY TO THAT DUE TO HOCM IN RESPONSE TO THE VALSALVA MANEUVER AND TO STANDING/SQUATTING. • THESE TWO LESIONS CAN BE DISTINGUISHED ON THE BASIS OF THEIR ASSOCIATED FINDINGS, SUCH AS THE PRESENCE OF LVH IN HOCM OR A NON EJECTION CLICK IN MVP.
- 28. CONGENITAL PULMONARY STENOSIS• •THE MID-SYSTOLIC, CRESCENDO-DECRESCENDO MURMUR IS BEST APPRECIATED IN THE SECOND AND THIRD LEFT INTERCOSTAL SPACES (PULMONIC AREA) • THE DURATION OF THE MURMUR LENGTHENS AND THE INTENSITY OF P2 DIMINISHES WITH INCREASING DEGREES OF VALVULAR STENOSIS. • AN EARLY EJECTION SOUND, THE INTENSITY OF WHICH DECREASES WITH INSPIRATION, IS HEARD IN YOUNGER PATIENTS. A PARASTERNAL LIFT AND ECG EVIDENCE OF RIGHT VENTRICULAR HYPERTROPHY INDICATE SEVERE PRESSURE OVERLOAD. • IF OBTAINED, THE CHEST X-RAY MAY SHOW POST STENOTIC DILATION OF THE MAIN PULMONARY ARTERY.
- 29. • SIGNIFICANT LEFT-TO-RIGHTINTRACARDIAC SHUNTING DUE TO AN ASD LEADS TO AN INCREASE IN PULMONARY BLOOD FLOW AND A GRADE 2–3 MID-SYSTOLIC MURMUR AT THE MIDDLE TO UPPER LEFT STERNAL BORDER ATTRIBUTED TO INCREASED FLOW RATES ACROSS THE PULMONIC VALVE WITH FIXED SPLITTING OF S2. • OSTIUM SECUNDUM ASDS ARE THE MOST COMMON CAUSE OF • THESE SHUNTS IN ADULTS.
- 30. • FEATURES SUGGESTIVEOF A PRIMUM ASD INCLUDE • THE COEXISTENCE OF MR DUE TO A CLEFT ANTERIOR MITRAL VALVE LEAFLET AND • LEFT AXIS DEVIATION OF THE QRS COMPLEX ON THE ECG • WITH SINUS VENOSUS ASDS, THE LEFT-TO-RIGHT SHUNT IS USUALLY NOT LARGE ENOUGH TO RESULT IN A SYSTOLIC MURMUR, ALTHOUGH THE ECG MAY SHOW ABNORMALITIES OF SINUS NODE FUNCTION.
- 31. • A GRADE1 OR2 MID-SYSTOLIC MURMUR OFTEN CAN BE HEARD AT THE LEFT STERNAL BORDER WITH PREGNANCY, HYPERTHYROIDISM, OR ANEMIA, PHYSIOLOGIC STATES THAT ARE ASSOCIATED WITH ACCELERATED BLOOD FLOW. •STILL’S MURMUR REFERS TO A BENIGN GRADE 2, VIBRATORY OR MUSICAL MID-SYSTOLIC MURMUR AT THE MID OR LOWER LEFT STERNAL BORDER IN NORMAL CHILDREN AND ADOLESCENTS, BEST HEARD IN THE SUPINE POSITION.
- 32. • LATE SYSTOLICMURMUR • LATE SYSTOLIC MURMURS A LATE SYSTOLIC MURMUR THAT IS BEST HEARD AT THE LEFT VENTRICULAR APEX IS USUALLY DUE TO MVP. • OFTEN, THIS MURMUR IS INTRODUCED BY ONE OR MORE NON EJECTION CLICKS. • THE RADIATION OF THE MURMUR CAN HELP IDENTIFY THE SPECIFIC MITRAL LEAFLET INVOLVED IN THE PROCESS OF PROLAPSE OR FLAIL. • THE TERM FLAIL REFERS TO THE MOVEMENT MADE BY AN UNSUPPORTED PORTION OF THE LEAFLET AFTER LOSS OF ITS CHORDAL ATTACHMENT(S).
- 33. •IN POSTERIOR LEAFLETPROLAPSE OR FLAIL, THE RESULTANT JET OF MR IS DIRECTED ANTERIORLY AND MEDIALLY, AS A RESULT OF WHICH THE MURMUR RADIATES TO THE BASE OF THE HEART AND MASQUERADES AS AS. •ANTERIOR LEAFLET PROLAPSE OR FLAIL RESULTS IN A POSTERIORLY DIRECTED MR JET THAT RADIATES TO THE AXILLA OR LEFT INFRASCAPULAR REGION. • LEAFLET FLAIL IS ASSOCIATED WITH A MURMUR OF GRADE 3 OR 4 INTENSITY THAT CAN BE HEARD THROUGHOUT THE PRECORDIUM IN THIN-CHESTED PATIENTS. • THE PRESENCE OF AN S3 OR A SHORT, RUMBLING MID-DIASTOLIC MURMUR DUE TO ENHANCED FLOW SIGNIFIES SEVERE MR.
- 34. • A LATE,APICAL SYSTOLIC MURMUR INDICATIVE OF MR MAY BE HEARD TRANSIENTLY IN THE SETTING OF ACUTE MYOCARDIAL ISCHEMIA. • IT IS DUE TO APICAL TETHERING AND MALCOAPTATION OF THE LEAFLETS IN RESPONSE TO STRUCTURAL AND FUNCTIONAL CHANGES OF THE VENTRICLE AND MITRAL ANNULUS. • THE INTENSITY OF THE MURMUR VARIES AS A FUNCTION OF LEFT VENTRICULAR AFTERLOAD AND WILL INCREASE IN THE SETTING OF HYPERTENSION. • TTE IS RECOMMENDED FOR ASSESSMENT OF LATE SYSTOLIC MURMURS.
- 35. HOLOSYSTOLIC MURMUR • HOLOSYSTOLICMURMURS BEGIN WITH S1 AND CONTINUE THROUGH SYSTOLE TO S2. • THEY ARE USUALLY INDICATIVE OF CHRONIC MITRAL OR TRICUSPID VALVE REGURGITATION OR A VSD AND WARRANT TTE FOR FURTHER CHARACTERIZATION. • THE HOLOSYSTOLIC MURMUR OF CHRONIC MR IS BEST HEARD AT THE LEFT VENTRICULAR APEX AND RADIATES TO THE AXILLA IT IS USUALLY HIGH-PITCHED AND PLATEAU IN CONFIGURATION, BECAUSE OF THE WIDE DIFFERENCE BETWEEN LEFT VENTRICULAR AND LEFT ATRIAL PRESSURE THROUGHOUT SYSTOLE.
- 36. • IN CONTRASTTO ACUTE MR, LEFT ATRIAL COMPLIANCE IS NORMAL OR EVEN INCREASED IN CHRONIC MR. • AS A RESULT, THERE IS ONLY A SMALL INCREASE IN LEFT ATRIAL PRESSURE FOR ANY • INCREASE IN REGURGITANT VOLUME • SEVERAL CONDITIONS ARE ASSOCIATED WITH CHRONIC MR AND AN APICAL HOLOSYSTOLIC MURMUR, -RHEUMATIC SCARRING OF THE LEAFLETS, -MITRAL ANNULAR CALCIFICATION, - POST INFARCTION LEFT VENTRICULAR REMODELLING, • -SEVERE LEFT VENTRICULAR CHAMBER ENLARGEMENT.
- 37. • THE CIRCUMFERENCEOF THE MITRAL ANNULUS INCREASES AS THE LEFT VENTRICLE ENLARGES AND LEADS TO FAILURE OF LEAFLET COAPTATION WITH CENTRAL MR IN PATIENTS WITH DILATED CARDIOMYOPATHY . • THE SEVERITY OF THE MR IS WORSENED BY ANY CONTRIBUTION FROM APICAL DISPLACEMENT OF THE PAPILLARY MUSCLES AND LEAFLET TETHERING (REMODELLING). • BECAUSE THE MITRAL ANNULUS IS CONTIGUOUS WITH THE LEFT ATRIAL ENDOCARDIUM, GRADUAL ENLARGEMENT OF THE LEFT ATRIUM FROM CHRONIC MR WILL RESULT IN FURTHER STRETCHING OF THE ANNULUS AND MORE MR; THUS, “MR BEGETS MR.”
- 38. • THE HOLOSYSTOLICMURMUR OF CHRONIC TR IS GENERALLY SOFTER THAN THAT OF MR, IS LOUDEST AT THE LEFT LOWER STERNAL BORDER, AND USUALLY INCREASES IN INTENSITY WITH INSPIRATION (CARVALLO’S SIGN). • ASSOCIATED SIGNS INCLUDE C-V WAVES IN THE JUGULAR VENOUS PULSE, AN ENLARGED AND PULSATILE LIVER, ASCITES, AND PERIPHERAL EDEMA • THE ABNORMAL JUGULAR VENOUS WAVEFORMS ARE THE PREDOMINANT FINDING AND ARE SEEN VERY OFTEN IN THE ABSENCE OF AN AUDIBLE MURMUR DESPITE DOPPLER ECHOCARDIOGRAPHIC VERIFICATION OF TR.
- 39. • CAUSES OFPRIMARY TR - MYXOMATOUS DISEASE(PROLAPSE), - ENDOCARDITIS, - RHEUMATIC DISEASE, - RADIATION, CARCINOID, -EBSTEIN’S ANOMALY, - CHORDAL DETACHMENT AS A COMPLICATION OF RIGHT VENTRICULAR ENDOMYOCARDIAL BIOPSY. • TR IS MORE COMMONLY A PASSIVE PROCESS THAT RESULTS SECONDARILY FROM ANNULAR ENLARGEMENT DUE TO RIGHTVENTRICULAR DILATATION IN THE FACE OF
- 40. THE HOLOSYSTOLIC MURMUROF A VSD IS LOUDEST AT THE MID- TO LOWER LEFT STERNAL BORDER AND RADIATES WIDELY • A THRILL IS PRESENT AT THE SITE OF MAXIMAL INTENSITY IN THE MAJORITY OF PATIENTS. • THERE IS NO CHANGE IN THE INTENSITY OF THE MURMUR WITH INSPIRATION. • THE INTENSITY OF THE MURMUR VARIES AS A FUNCTION OF THE ANATOMIC SIZE OF THE DEFECT. •SMALL, RESTRICTIVE VSDS, AS EXEMPLIFIED BY THE MALADIE DE ROGER, CREATE A VERY LOUD MURMUR DUE TO THE SIGNIFICANT AND SUSTAINED SYSTOLIC PRESSURE GRADIENT BETWEEN THE LEFT AND RIGHT VENTRICLES. •WITH LARGE DEFECTS,THE VENTRICULAR PRESSURES TEND TO EQUALIZE, SHUNT FLOW IS BALANCED, AND A MURMUR IS NOT APPRECIATED.
- 43.