Which sign is a pansystolic mumur on deep inspiration ?
ANSWER: (A) Carvallo's signREF: Harrisons 18th Ed Ch: 237See APPENDIX- 79 below HEART MURMURSSee previous question APPENDIX- 79HEART MURMURSREF: Harrison 18th ed chapter 8Early diastolicTimeConditionDescriptionEarly diastolicAortic regurgitationThe murmur is low intensity, high-pitched, best heard over the left sternal border or over the right second intercostal space, especially if the patient leans forward and holds breath in full expiration. The radiation is typically toward the apex. The configuration is usually decrescendo and has a blowing character. The presence of this murmur is a good positive predictor for AR and the absence of this murmur strongly suggests the absence of AR. An Austin Flint murmur is usually associated with significant aortic regurgitation.Early diastolicPulmonaryregurgitationPulmonary regurgitation is most commonly due to pulmonaryhypertension (Graham-Steell murmur). It is a high-pitched and blowing murmur with a decrescendo configuration. It may increase in intensity during inspiration and best heard over left second and third intercostal spaces. The murmur usually does not extend to SI.Early diastolicLeft anterior descending artery stenosisThis murmur, also known as Dock s murmur, is similar to that of aortic regurgitation and is heard at the left second or third intercostal space. A Coronary artery bypass surgery can eliminate the murmur.Mid-diastolicTimeConditionDescriptionMid-diastolicMitral stenosisThe first heart sound (S,) is usually accentuated and slightly delayed. The pulmonic component of the second heart sound (P,,) also is often accentuated, and the two components of the second heart sound (S,,) are closely split. The opening snap(OS) of the mitral valve is most readily audible in expiration at, or just medial to the cardiac apex. This sound generally follows the sound of aortic valve closure (A2) by 0.05-0.12 s. The time interval between A2 and OS varies inversely with the severity of the MS. The OS is followed by a low-pitched, rumbling, diastolic murmur, heard best at the apex with the patient in the left lateral recumbent positionMid-diastolicTricuspid stenosisBest heard over the left sternal border with rumbling character and tricuspid opening snap with wide splitting SI. May increase in intensity with inspiration (Carvallos sign). Tricuspid stenosis often occurs in association with mitral stenosis. Isolated TS are often associated with carcinoid disease and right atrial myxoma.Mid-diastolicAtrial myxomaAtrial myxomas are benign tumors of the heart. Left myxomas are far more common than right myxomas and those may cause obstruction of the mitral valve producing a mid-diastolic murmur similar to that of mitral stenosis. An echocardiographic evaluation is necessary.Mid-diastolicIncreased flow across the atrioventricular valveThis can also produce a mid-diastolic murmur, such as in severe mitral regurgitation where a large regurgitant volume in the left atrium can lead to "functional mitral stenosis."Mid-diastolicAustin Flint murmurAn apical diastolic rumbling murmur in patients with pure aortic regurgitation. This can be mistaken with the murmur in mitral stenosis and should be noted by the fact that an Austin Flint murmur does not have an opening snap that is found in mitral stenosis.Mid-diastolicCarey-CoombsmurmurA mid-diastolic murmur over the left ventricular impulse due to mitral valvulitis from acute rheumatic fever.Late diastolicTimeConditionDescriptionLate diastolic (presystolic)Complete heart blockA short late diastolic murmur can occasionally be heard (Rytand's murmur).Mid-systolic ejectionTimeConditionDescriptionMid-systolicejectionAortic outflow obstruction (Aortic Stenosis)Can be due to aortic valve stenosis or hypertrophic cardiomyopathy (HCM), with a harsh and rough quality.**Valvular aortic stenosis can produce a harsh, or even a musical murmur over the right second intercostal space which radiates into the neck over the two carotid arteries. The most common cause of AS (Aortic Stenosis) is calcified valves due to aging. The second most common cause is congenital bicuspid aortic valves (normal valve is tricuspid). In aortic stenosis, heaving apical impulse is present. The distinguishing feature between these two causes is that bicuspid AS has little or no radiation. It can be confirmed if it also has an aortic ejection sound, a short early diastolic murmur, and normal carotid pulse. The murmur in valvular AS decreases with standing and straining with Valsalva maneuver.** Supravalvular aortic stenosis is loudest at a point slightly higher than in that of valvular AS and may radiate more to the right carotid artery **Subvalvular aortic stenosis is usually due to hypertrophic cardiomyopathy (HCM), with murmur loudest over the left sternal border or the apex. The murmur in HCM increases in intensity with a standing position as well as straining with Valsalva maneuver.Mid-systolic ejectionPulmonic outflow obstruction (Pulmonary Stenosis)A harsh murmur usually on left second intercostal space radiating to left neck and accompanied by palpable thrill. It can be distinguished from a VSD (Ventricular septal defect) by listening to the S2, which is normal in VSD but it is widely split in pulmonary stenosis. However, VSD is almost always pansystolic where the murmur of pulmonary stenosis is diamond-shaped and ends clearly before S2. Many innocent murmurs also arise from this location but SI and S2 must split normally.Mid-systolicejectionDilation of aortic root or pulmonary arteryProduces an ejection sound, with a short ejection systolic murmur and a relatively wide split S2. There is no hemodynamic abnormality. This is similar to pulmonary hypertension except the latter has hemodynamic instabilities.Mid-systolicejectionIncreased semilunar blood flowThis can occur in situations such as anemia, pregnancy, or hyperthyroidism.Mid-systolicejectionAortic valve sclerosisThis is due to degenerative thickening of the roots of the aortic cusps but produces no obstruction and no hemodynamic instability and thus should be differentiated from aortic stenosis. It is heard over right second intercostal space writh a normal carotid pulse and normal S2.Mid-systolicejectionInnocent midsystolic murmursThese murmurs are not accompanied by other abnormal findings. One example of a benign paediatric heart murmur is Still's murmur in children.Late systolicTimeConditionDescription This is the most common cause of late systolic murmurs. It can be heard best over the apex of the heart, usually preceded by clicks. The most common cause of mitral valve prolapse is "floppy" valve (Barlow's) syndrome. If the prolapse becomes severe enough, mitral regurgitation may occur. Any maneuver that decreases leftLate systolicMitral valve prolapseventricular volume -- such as standing, sitting, Valsalva maneuver, and amyl nitrate inhalation -- can produce earlier onset of dicks, longer murmur duration, and decreased murmur intensity'. Any maneuver that increases left ventricular volume -- such as squatting, elevation of legs, hand grip, and phenylephrine -- can delay the onset of clicks, shorten murmur duration, and increase murmur intensity.Late systolicTricuspid valve prolapseUncommon without concomitant mitral valve prolapse. Best heard over left lowrer sternal border.Late systolicPapillary muscle dysfunctionUsually due to acute myocardial infarction or ischemia, which causes mild mitral regurgitation.Holosystolic (pansystolic)TimeConditionDescriptionHolosystolic(pansystolic)TricuspidinsufficiencyIntensifies upon inspiration. Can be best heard over the fourth left sternal border. The intensity can be accentuated following inspiration (Carvallo's sign) due to increased regurgitant floiv in right ventricular volume. Tricuspid regurgitation is most often secondary to pulmonary hypertension. Primary tricuspid regurgitation is less common and can be due to bacterial endocarditis following IV drug use, Ebstein s anomaly, carcinoid disease, or prior right ventricular infarction.Holosystolic(pansystolic)Mitral regurgitationThe S1 is generally absent, soft, or buried in the holosystolic murmur of chronic MR. In patients with severe MR, the aortic valve may close prematurely, resulting in wide but physiologic splitting of S2. A lowT-pitched S.. occurring 0.12-0.17 s after the aortic valve closure sound. It may be followed by a short, rumbling, middiastolic murmur, even in the absence of MS. A fourth heart sound is often audible in patients with acute severe MR who are in sinus rhythm. A presystolic murmur is not ordinarily heard with isolated MR. A systolic murmur of at least grade III/VI intensity is the most characteristic auscultatory finding in chronic severe MR. It is usually holosystolic, but as previously noted it is decrescendo and ceases in mid- to late systole in patients with acute severe MR. The systolic murmur of chronic MR not due to MVP is intensified by isometric exercise (handgrip) but is reduced during the strain phase of the Valsalva maneuver.Holosystolic (pan systolic)Ventricular septal defectNo intensification upon inspiration. VSD is a defect in the ventricular wall, producing a shunt between the left and right ventricles. Since the L ventricle has a higher pressure than the R ventricle, flow during systole occurs from the L to R ventricle, producing the holosystolic murmur. It can be best heard over the left third and fourth intercostal spaces and along the sternal border. It is associated with normal pulmonary artery pressure and thus S2 is normal. This fact can be used to distinguish from pulmonary stenosis, which has a wide splitting S2. When the shunt becomes reversed ("Eisenmenger syndrome7'), the murmur may be absent and S2 can become markedly accentuated and single. Holosvstouc Murmur Differential Diagnosis Onset with S1 terminates at or beyond S2 | | | Maximum intercity over apexRadiation to axilla of bassA2 not Heard ever apexDecreased intensity with amyl nitrate Maximum intensity over left sternal borderRadiation to epigastrium and right sternal borderIncreased intensity during inspirationProminent c-v wave with sharp g descant in jugular venous pulse Maximum intensity over lower left third and lourith nterspareWildespreaed radiation, palpable thrillDecreased intensity with amyl nitrateNo change in intensity during inspirationWide splitting of S2 | | Mitral regurgitation Tricuspid regurgitation|||||Hyperdynamic left ventrioular impulse wide splitting of S2Suitatned left ventricular impulse Single S2 or narrow splitting of S2Prominent left parasternal - diastolic impulseNormal brilet left paraster - nal systolic impulseNormal P2 Rarely paradoxical S2Sustained systolic left parasternal impulseNarrow splitting of S2 wiin marked increase in intensity of P2Favors ventricular septal detect; often difficult todifferentiate from mitral regurgitant mumur |||| Primary mitral regurgitation (e.g,. rheumatic, naptuned chorclae)Secondary mitral regurgitation (dilated cardiomyopathy; papillary muscle dystunetion or late stage of primary mitral regurgitation)PrimarySecondary to pulmonary hypertension CMDT 2009 Table 10-1DIFFERENTIAL DIAGNOSIS OF VALVULAR HEART DISEASE MitralStenosisMitralRegurgitationAorticStenosisAorticRegurgitationTricuspidStenosisTricuspidRegurgitationInspectionMalar flush,precordialbulge, anddiffusepulsation inyoungpatients.Usually prominent and hyperdynamic apical impulse to left of MCL.Sustained PMI, prominent atrial filling wave.Hyperdynamic PMI to left of MCL and downward- Visible carotid pulsations. Pulsating nailbeds (Quincke), head bob (deMusset).Giant a wave in jugular pulse with sinus rhythm. Peripheral edema or ascites, or both.Large v wave in jugular pulse; time with carotid pulsation. Peripheral edema or ascites, or both.Palpation."Tapping" sensation over area of expected PMI. Right ventricular pulsation left third toForceful, brisk PMI; systolic thrill over PMI. Pulse normal, small, or slightly collapsing.Powerful, heaving PMI to left and slightly below MCL. Systolic thrill over aortic area, sternal notch, or carotid arteriesApical impulse forceful and displaced significantly to left and downward. Prominent carotid pulses. Rapidly rising and collapsing pulses (Corrigan pulse).Pulsating, enlarged liver in ventricular systole.Right ventricular pulsation. Systolic pulsation of liver. fifth ICSparasternallywhenpulmonary hypertension is present.P2. may be palpable. in severe disease. Small and slowly rising carotid pulse. If bicuspid AS check for delaj at femoral artery to exclude coarctation. Heart sounds, rhythm, and blood pressureS2 loud if valve mobile. Opening snap following S2. The worse the disease, the closer the S2-opening snap intervalS1 normal or buried in early part of murmur (exception is mitral prolapse where murmur may be late). Prominent third heart sound when severe MR.Atrial fibrillation common. Blood pressure normal. Midsystolic clicks may be present and may be multiple.A2 normal, soft, or absent. Prominem S4. Blood pressure normal, or systolic pressure normal with high diastolic pressure.S2 normal or reduced, A., loud. Wide pulse pressure with diastolic pressure < 60 mm Hg. When severe, gentle compression of femoral artery with diaphragm of stethoscope may reveal diastolic flow (Duroziez) and pressure in leg on palpation > 40 mm Hg than arm (Hill).S2 often loud.Atrial fibrillation may be present.MurmursLocationandtrans - missionLocalized at or near apex.Diastolicrumble bestheard inleft Lateralposition;may beaccentuatedby havingpatient dosit-ups.Rarely,shortdiastolicmurmuralonglower leftsternalborder(GrahamSteell) inseverepulmonaryhypertension.Loudest over PMI; posteriorly directed jets (ie, anterior mitral prolapse) transmitted to left axilla, left infrascapular area; anteriorly directed jets (ie, posterior mitral prolapse) heard over anterior precordium. Murmur unchanged after premature beat.Right second ICS parasternally or at apex, heard in carotid arteries and occasionally in upper interscapular area. May sound like MR at apex (Gallaverdin phenomenon), but murmur occurs after S1 and stops before S2. The later the peak in the murmur, the more severe the AS.Diastolic: louder along left sternal border in third to fourth interspace. Heard over aortic area and apex.May be associated with lowr-pitched middiastolic murmur at apex (Austin Flint) due to functional mitral stenosis.If due to an enlarged aorta, murmur may radiate to right sternal border.Third to fifth ICS along left sternal border out to apex. Murmur increases with inspiration.Third to fifth ICS along left sternal border. Murmur hard to hear but increases with inspiration. Sit- ups can increase cardiac output and accentuate.TimingRelation of opening snap to A2.important. The higherPansystolic: begins ivitb S1 and ends at or after A2. May be lateBegins after S1, ends before A2 The more severe the stenosis, the later the murmurBegins immediately after aortic second sound and ends before first sound (blurring both); helpsRumble often follows audible opening snap.At times, hard to hear. Begins with S1 and fills systole. Increases with inspiration. the LA pressure the earlier the opening snap. Presystolic accentuation before if in sinus rhythm. Graham Steel! begins with P2 (early diastole) if associated pulmonary hypertension.systolic in mitral valve prolapse.peaks.distinguish from MR. CharacterLow-pitched, rumbling; presystolic murmur merges with loud S1Blowing, high-pitched; occasionally harsh or musical.Harsh, rough.Blowing, often faint.As for mitral stenosis.Blowing, coarse, or musical.OptimumauscultatoryconditionsAfter exercise, left lateral recumbency. Bell chest piece lightly applied.After exercise; use diaphragm chest piece.In prolapse, findings may be more evident while standing.Use stethoscope diaphragm. Patient resting, leaning forward, breath held in full expiration.Use stethoscope expiration, diaphragm. Patient leaning forward, breath held inUse stethoscope bell. Murmur usually louder and at peak during inspiration. Patient recumbent.Use stethoscope diaphragm. Murmur usually becomes louder during inspiration.RadiographyStraight left heart border fromenlarged LA appendage. Elevation of left mainstem bronchus. Large right ventricle and pulmonary artery if pulmonary hypertension is present. Calcification in mitral valve in rheumatic mitral stenosis or in annulus in calcific mitral stenosis.Enlarged left ventricle and LA.Concentric left ventricular hypertrophy. Prominent ascending aorta. Calcified aortic valve common.Moderate to severe left ventricular enlargement. Aortic root often dilated.Enlarged right atrium with prominent SVC and azygous shadow.Enlarged right atrium and right ventricle.ECGBroad Pwaves in standard leads; broad negativeLeft axis deviation or frank left ventricular hypertrophy-Left ventricular hypertrophy.Left ventricular hypertrophy.Tall, peaked P waves. Possible right ventricular hypertrophy.Right axis usual. phase of diphasic P in V1 Ifpulmonary hypertension is present, tall peaked P waves, right axis deviation, or right ventricular hypertrophy appears.P waves broad, tall, or notched in standard leads. Broad negative phase of diphasic P in V1 EchocardiographyTwo - dimensional echocar - diographyThickened,immobilemitral valvewith anteriorand posteriorleafletsmovingtogether."Hockeystick" shapeto openedanteriorleaflet inrheumaticmitralstenosis.Annularcalciumwith thinleaflets incalcificmitralstenosis.LAenlargement, normal to small left ventricle. Orifice can be traced to approximate mitral valve orifice area.Thickened mitral valve in rheumatic disease; mitral valve prolapse; flail leaflet or vegetations may be seen. Dilated left ventricle in volume overload. Operate for left ventricular end- systolic dimension > 4.5 cm.Dense persistent echoes from the aortic valve with poor leaflet excursion. Left ventricular hypertrophy late in the disease. Bicuspid valve in younger patients.Abnormal aortic valve or dilated aortic root. Diastolic vibrations of the anterior leaflet of the mitral valve and septum. In acute aortic insufficiency, premature closure of the mitral valve before the QRS. When severe, dilated left ventricle with normal or decreased contractility. Operate when left ventricular end- systolic dimension > 5.0 cm.In rheumatic disease, tricuspid valve thickening, decreased early diastolic filling slope of the tricuspid valve. In carcinoid, leaflets fixed, but no significant thickening.Enlarged right ventricle with paradoxical septal motion. Tricuspid valve often pulled open by displaced chordae.Continuous and color flow Doppler and TEEProlongedpressurehalf-timeacross mitralvalve allowsestimationof gradient.MVAestimatedfrom pressurehalf-time.Regurgitant flow mapped into LA. Use of PISA helps assess MR severity. TEE important in prosthetic mitral valveregurgitation.Increased transvalvular flow velocity; severe AS when peak jet > 4 m/ sec (64 mm Hg}. Valve area estimate using continuity equation is poorly reproducible.Demonstrates regurgitation and qualitatively estimates severity based on percentage of left ventricular outflow filled with jet and distance jet penetrates into left ventricle.TEE important in aortic valveProlonged pressure half-time across tricuspid valve can be used to estimate mean gradient. Severe tricuspid stenosis present when mean gradient > 5 mm Hg.Regurgitant flow mapped into right atrium and venae cavae. Right ventricular systolic pressure estimated by tricuspid regurgitation jet velocity. Indirectevidence ofpulmonaryhypertensionby notingelevatedrightventricularsystolicpressuremeasuredfrom thetricuspidregurgitationjet. endocarditis to exclude abscess. Mitral inflow pattern describes diastolic dysfunction. MCL, midclavicular line; PMI, point of maximal impulse; ICS, intercostal space; P2, pulmonary second sound; AS, aortic stenosis; SI, first heart sound; S2, second heart sound; MR, mitral regurgitation; A2, aortic second sound; S4, fourth heart sound; LA, left atrial; SVC, superior vena cava; VI, chest ECG lead 1; TEE, transesophageal echocardiography; MVA, measured valve area; PISA, proximal isovelocity surface area.EFFECT OF RESPIRATION:Left-sided murmurs may be best heard at end expiration, when lung volumes are minimized and the heart and great vessels are brought closer to the chest wall. This phenomenon is characteristic of the murmur of AR. Murmurs of right-sided origin, such as tricuspid or pulmonic regurgitation, increase in intensity during inspiration. The intensity of left-sided murmurs either remains constant or decreases with inspiration. Normal Physiologic Splitting Wkide physiologic splittingPhysiologic but wide splitting diving the respiratory cycle implies either premature aortic valve closure, as can occur with severe MR, or delayed pulmonic valve closure due to PS or right bundle branch block.Reversed splittingReversed splitting can be a feature of severe AS, HOCM, left bundle branch block, right ventricular apical pacing, or acute myocardial ischemia.Narrow physiologic splitting (|P2)Narrow physiologic splitting occurs in pulmonary hypertension, and both A2 and P2 are heard during expiration at a narrow splitting interval because of the increased intensity and high - frequency composition of P2Mild Vs Severe MSMild MSIn mild MS, the dtastoiic gradient across the valve is limited to the phases of rapid ventneutar filling in early diastole and presystole. The rumble may occur during either or both periods.In severe MS, a large pressure gradient exists across the valve during the entire diastolic filling, and the rumble persists throughout diastole. As the left atrial pressure becomes greater, the Interval between A2 [or P2) and the opening snap (O.S.) shortens. Secondary pulmonary hypertension develops and results In a loud P? and the splitting Interval usually narrows.ECGSevere MS
Carvallo's sign
Muller's sign
Corrigan's sign
Duroziez sign
Valvular Heart Disease