mitral regurgitation hemodynamics. . (carpentier’s classification)

MITRAL REGURGITATION HEMODYNAMICS

(Carpentiers classification)

Carpentiers functional classification of MR

Clinical impact of MR Determined by the magnitude of the regurgitant leak Time course of development of the regurgitation Abrupt onset of severe MR markedly pul venous pr C/c MR exhibit prominent ventricular enlargement with chamber compliance & pulmonary venous pressure

Torricelli principle, states that flow through an orifice varies by the square root of the pressure gradient across the orifice, the duration of flow, and a discharge coefficient. The principal determinants of the RV are the regurgitant orifice area and the systolic pressure gradient between the ventricle and left atrium

Mitral regurgitation pathophysiology LV emptying LA pressure (if acute, pulmonary odema) LV filling LVedd LV stretch failure

NORMAL TO ACUTE MR

Two factors - maintenance of left ventricular performance a)increased diastolic volume b)reduction of afterload Primary response to acute volume overload is the Frank- Starling mechanism -end-diastolic fiber length- improving vent ejection by ing both the rate and force of contraction A 2 nd mechanism is the afterload afforded by the low- impedance pathway to ventricular ejection via the regurgitant leak

LV stress-volume loop in acute MR in EDV A systolic unloading that is characteristic of acute MR, A in ESV The Total Stroke Volume increases

Volume overload of a/cMR preload sarcomere length EDVfrom 150 to 170ml. Ejection of blood into LA afterload ( end-systolic stress ) End-systolic volume (ESV) 50 to 30 ml EF acutely 50% TSV is regurgitated into the left atrium-RF - 0.50 FSV 100 to 70 ml. volume in the LAraises pressure -normal to 25 mm Hg

Consequences of Acute severe MR Sudden volume overload of LA & LV PVH Pulmonary edema Low forward stroke volume, tachycardia Decreased cardiac output Hypotension/ cardiogenic shock flow work adds little to the energy requirements of the heart

Acute Severe Mitral Regurgitation Pathophysiology In acute severe MR, a sudden volume overload is imposed on the left atrium and left ventricle. Acute volume overload es LV preload, allowing for a modest in total LV stroke volume. Forward stroke volume and cardiac output are reduced due to the absence of compensatory eccentric hypertrophy. Unprepared LA and LV cannot accommodate the regurgitant volume large v waves in LA pulmonary congestion. The patient has both ed forward output (even shock) and pulmonary congestion. In severe MR, the hemodynamic overload often cannot be tolerated, and MV repair or replacement must often be performed urgently.

Large volume of regurgitant blood entering a relatively stiff and nondilated LA will result in a steep rise in the v wave The entry of a large volume of blood during diastole into a nondilated LV will raise the diastolic filling pressure in the LV. (The raised pre-a wave pressure may further add to the v wave height) High v wave buildup rapidly falling pressure difference between the LV and LA toward the later part of systole limit the regur flow during the later part of systole murmur decrescendo Excess flow more low and medium frequencies harsher

Continuing Medical Implementation ...bridging the care gap MR Pressure Tracing

V waves correspond to T waves on ECG The PA waveform appears falsely elevated large V wave reflected back from the LA through the compliant pulmonary vasculature The Y descent is quite rapid as the over distended LA quickly empties In C/C MR, an equivalent volume better tolerated by a markedly dilated LA Compared with a/c MR LA pr may be less and large V waves may be absent

ACUTE TO CHRONIC

Compensated Stage of MR Major adaptive change that occurs during the development of a c/c volume overload is LVE Large compliant ventricle that is well suited to deliver a large stroke volume Also seen during gradual progression of the severity of the regurgitation. Remodeling of the extramyocardial matrix rearrangement and slippage of myocardial fibers and chamber enlargement New sarcomeres are added in series, and at the ventricular level, eccentric hypertrophy develops

A/C MR C/C COMPENSATED MR

Dvpt of eccentric hypertrophy - EDV Now larger ventricle has an in afterload - Laplace eq = (P * R () / T ) ses ESV to normal Eccentric hypertrophy- in TSV & FSV LA enlargement accommodates vol overload at lower filling pr EF is supernormal

Cardiomyocytes exhibit an in length, but preload at the sarcomere level ( sarc length) does not increase progressively Sarcomere lengths tend to return toward normal despite progressive LV enlargement preload reserve is reestablished LV systolic unloading of a/c MR is gradually replaced by nl systolic wall stress TSV in c/c compensated MR mediated through a normal performance of each unit of an enlarged circumference. Compensated stage, preload (at the sarcomere level), afterload (at the ventricular level), and both contractility and EF are normal TSV is as a result of the large EDV

Volume overloads-the excess volume ejected into the aorta, where it widens PP SBP combined Pr and Vol overloads The extra volume from the LV in MR enters the LA and SBP is nl- PURE VOLUME OVERLOAD Preload in MR and AR but afterload greatly in AR comp to MR Unique loading conditions of MR - unique pattern of remodeling Largest radius-to-thickness ratio and the smallest mass-to-volume ratio of the 4 left-sided valve lesions Eccentric hypertrophy greater increase in volume than mass spheric MR- hypertrophy occur from a decrease in Myosin degradation

MYOSIN TURNOVER IN MR

LV volume allows TSV to - increasing FSV -compensating for the volume lost to regurgitation Relatively thin LV wall enhances diastolic filling MR is one of the very few cardiac diseases in which diastolic function is supernormal Increased radius to-thickness ratio Adaptive as well as Maladaptive

The loading conditions in MR are favorable to left ventricular ejection Preload is whereas afterload is nl or occasionally decreased- lesion itself facilitates left ventricular emptying Presence of normal muscle function- EF-supernormal in MR (Carabello BA. Mitral regurgitation: basic pathophysiologic principles;Mod Concepts Cardiovasc Dis 1988;57:53-8) Once the EF falls below 60 percent, the prognosis worsens (Wisenbaugh T. Does normal pump function belie muscle dysfunction in patients with chronic severe mitral regurgitation? Circulation 1988;77:515-25 )

Transitional Stage of MR Transition may occur as a consequence of:- a progressive increase in the RV a decrease in LV contractile function an increase in afterload OR combination of these factors. During this stage - EF declines to 50% to 59%. Structural and functional remodeling of the ventricle is largely reversible

Decompensated Stage of MR Substantial and progressive LV dilation LVEDP, systolic wall stress and - an EF of 50% The decline in EF is a consequence of depressed myocardial contractile state, LV afterload excess, or both

C/C COMPENSATED TO DECOMPENSATED

Contractility - ESV FSV Cardiac dilatation RF Favorable loading conditions permit the ejection fraction to remain normal

A decrease in myocardial contractile state or an increase in LV afterload cause a decrease in the EF

MR is often viewed as a lesion that unloads the LV by creating a second pathway for ejection A/c MR- ESV and afterload is low As the ventricle enlarges and adapts to the chronic volume overload afterload gradually increases Eventually in decompensated MR, afterload exceeds nl Such afterload excess contributes to a decline in EF Remodeling pattern-- increasing r/h- increase afterload Only in acute MR is afterload decreased C/c compensated MR afterload is normal C/c decompensated MR greater than normal

In MR, the volume-loaded LV faces relatively low impedance to outflow and nl or subnl afterload, even when myocardial dysfunction is established In MR- LVEF is higher relative to intrinsic LV contractility than in the normal LV or in AR A low or borderline EF (ie, 50% to 55%) indicate depressed LV function if afterload were low LV function- depressed if the EF were 55% to 60% in the presence of increased or even normal afterload

LVEF remains the best-validated predictor Prognostically important myocardial dysfunction exists when LVEF is 10% greater than the nominal lower normal limit(commonly 50% with echocardiography) LVEF = 60%, even among asympc/min symp patients FC I-II, long-term survival after MVR/MV repair worse than if LVEF is 60 %

Survival of patients with severe MR and EF

LV stress-volume loops in the 3 stages of chronic MR Progressive in LV EDV and systolicwall stress EF progressively from 65% in compensated MRto 55% during the transitional stage, and finally to 45% (or lower) in decompensated MR

Passive myocardial stiffness in those with systolic dysfunction LV dysfunction is associated with myocardial interstitial fibrosis, reduction in myofiber content, and decrease in myofiber contractility

Symptamatology and findings Anatomic malcoaptation ofmitral leaflets during systole ERO pressure gradient between LV and LA allows abnormal regurgitant flow into the LA Systolic pr gradient between the LV &LA begins with closure of the mitral valve (S1)and persists after closure of the aortic valve (S2) up to mitral opening Regurgitant flow lasts as long as the ERO and is holosystolic Determinants of R V are the area of ERO, the regurgitant gradient, and duration of regurgitation In both organic MR and functional MR ERO increases with afterload or ventricular volume and with decreased afterload or improved contractility, but is independent of changes in heart rate

Survival under medical management of patients with organic mitral regurgitation according to the effective regurgitant orifice area measurement

In the mitral regurgitant system energy produced by the LV remains constant Kinetic energy - Rvol and potential energy by LA, V-wave LA compliance is one of the major determinants of the V- wave and LA pressure. In a/cc severe MR- LA is smaller and less compliant compared - a similar RVol will result in higher V-wave and LA pressure. In c/c MR LA remodels and accommodates the RVol -normal or near normal LA pressure is maintained

LV end-diastolic volume and wall stress increase (29) and LV shape becomes more spherical. LV end-systolic volume is increased, but end-systolic wall stress is usually within normal limits LV dysfunction is associated with myocardial interstitial fibrosis, reduction in myofiber content, and decrease in myofiber contractility The RVol in ischemic MR is usually less than in organic MR (39) and the LV and LA dilatation are in excess to the degree of MR (22). Despite this appearance of low-volume regurgitation, MR is associated with elevated LA pressure (22) and poor clinical outcomewith reduced survival

S1 S1 intensity is usually normal, but may be decreased in chronic severeMR associated with defective leaflets or increased in rheumatic MR

S3 Presence of S3 is directly related to MR degree in organic MR In ischemic/functional MR, S3 reflects more restrictive LV filling than severity of MR Asso with a diastolic rumble which is low pitched and heard best in the left lateral decubitus position In AR signifies LV dysfunction

Murmers Systolic pr gradient between the LV &LA begins with closure of the mitral valve (S1)and persists after closure of the aortic valve (S2) up to mitral opening Excess flow more low and medium frequencies harsher A distinguishing feature is the lack of murmur intensity beat- to-beat variation with MR, such as with post extrasystolic beats or AF while marked murmur variation would be expected with aortic stenosis or dynamic left ventricular outflow tract obstruction Amyl nitrite MR murmur intensity and that of obstructive lesions. MR murmur with isometric exercise or phenylephrine, while these maneuvers obstructive murmurs

Hemodynamic characteristics Common Features of AR & MR: LV volume overload Progressive LV dilatation LV systolic dysfunction Clinical heart failure Differences in AR & MR: AR- High afterload, concentric & eccentric LVH MR- Low afterload, eccentric LVH

Large V waves in a case of mitral regurgitation. Simultaneous recording of ECG helps identify V waves in mitral valve regurgitation; V waves correspond to T waves on ECG. The PA waveform appears falsely elevated because of the large V wave reflected back from the LA through the compliant pulmonary vasculature. The Y descent is quite rapid as the overdistended LA quickly empties. Care must be exercised to distinguish a large V wave from a systolic PA waveform. Failure to recognize a large V wave may cause the PAC to be advanced further in an attempt to record a PCWP pressure, increasing the risk of perforation. In chronic mitral regurgitation, an equivalent volume of blood may regurgitate, but this volume is better tolerated by a markedly dilated LA. Compared with acute mitral regurgitation, LA pressure may be less and large V waves may be absent.

Two factors identified by this study which may account for the maintenance of left ventricular performance are increased diastolic volume andreduction of afterload. A primary compensatory response to acute volume overload is the Frank- Starling mechanism, augmented end-diastolic fiberlength- improving ventricular ejection by increasingboth the rate and force of contraction. A second potential compensatory mechanism is the reduced afterload afforded by the low-impedance pathway to ventricular ejection via the regurgitant leak although mean left atrial pressure was abnormally high (183 mm Hg), it nevertheless was considerably lower than mean systolic pressure (91 mm Hg) at any moment during ventricular contraction; hence, impedance to ventricular emptying was always lower than normal, and calculated myocardial wall tension, expressed as average stress per unit of myocardial wall thickness, did not rise to abnormal levels

Valvular regurgitation increases preload, reflected by greater left ventricular end- diastolic pressure, volume, circumferential length, and stress. To accommodatethe larger filling volume in acute volume overload, existing sarcomeres are stretched, thereby increasing ventricular volume and circumferential length.14 In chronic regurgitation, further augmentationof these dimensions is due to sarcomeres added in series and in parallel, and possibly to fiber slippage; not to extension of individual sarcomeres beyond their optimal contractile length.) The effect of the low pressure left atrium upon ejection and systolic afterload is manifested in several ways. Early regurgitation allows the ventricle to empty against a relatively low afterload. The consequently reduced dimensions and thickened wall act to decrease stress throughout ejection. Emptying into the low impedance left atrium occurs during the entire time that the aortic valve is open and it continues after aortic valve closure. Ventricular pressure is falling in this latter period. The net effect is to extend ejection time, enhance overall ventricular emptying, and diminish mean systolic afterload.

The short-term response to volume overload is an increase in left ventricular volume with a lengthening of sarcomeres along their normal length-tension curve.29 Progressive dilation of the ventricle leading to augmented volume in the chronic state is a result of the increased number of sarcomeres added in series and in parallel as the myocardium hypertrophies. Sarcomere length remains relatively constant during this period and the fiber is not extended beyond its optimal contractile length.14 301, 31 In both control and chronic volume overloaded ventricles, extension and recruitment of sarcomeres constitute the functional reserve of Starling's curve30; this reserve is used to an increasing extent as diastolic pressure and stress are elevated.

Pulmonary venous pulsed-wave Doppler in severe mitral regurgitation. Systolic flow reversal (ie, systolic flow into the pulmonary vein) is present (arrows).

Why do we need careful timing? Patients with pure regurgitant lesions may remain asymptomatic for long time. Some of them may develop LV dysfunction without warning symptoms. Onset of significant LV dysfunction increases the risk of surgery, and LV dysfunction may become irreversible. Valve replacement has important implications like risk of surgery, long term anticoagulation in mechanical valves, risk of valve failure in future for bioprosthetic valve and risk of endocarditis.

Load-Independent Measures of LV Function Complex measurements: LV dP/dT End-systolic stress-strain Myocardial Elastance Peak systolic pressure/end-systolic volume End-systolic diameter LVIDs >45 predicts poor outcome End-systolic volume index ESVI >50cc/m2 predicts poor outcome

Left ventricular performance can also be gauged in MR by assessing the diameter to which the LV can contract at the end of systole. End-systolic dimension is less dependent on preload than is ejection fraction When the end-systolic dimension exceeds 45 mm, the prognosis worsens

LV and LA pressures showing large V wave and persistent LALV gradient of mixed mitral regurgitation and stenosis

RV/EDV RATIO A high ratio indicates severe MR that is a potential target for corrective surgery. Alow ratio suggests severedecompensated MR or a cardiomyopathic process {If a patient end-diastolic diameter of 65 mm or end-diastolic volume of 130 mL/m, an EF of 30%, a regurgitant fraction of 50%, and a regurgitant volume of 20 mL/m2, the ratio of regurgitant volume to end-diastolic volume would be only 20/130, or 0.15. This should suggest severe, irreversible LV dysfunction. By contrast, a patient EDV 130 mL/m2, an EF of 50%, and a regurgitant fraction of 50% would have a ratio of regurgitant volume to end-diastolic volume of 33/130, or 0.25. The higher ratio of 0.25 indicates a potentially reversible phase of chronic MR}

Cardiac cycle-Systolic events EM delay-Q to LV pressure rise. ICT- LV pressure rise to LV-Ao pressure crossover. PEP- EM+ICT(QS2-LVET) LVET-Ao pre.rise & incisura.Duration of ejection. QS2- Q in ECG to first high frequency vibrations of A2 in ACG.

PEP/LVET- independent of heart rate PEP, LVET & PEP/LVET correlated significantly with angiographic EF &EDV. Closest correlation b/w EF& ratio. (Weissler et al Circulation 42 ;1970.) Echo FS of LV correlation with this ratio. ( McDonald &Hobson,1974) PEP-0.10-0.14 sec. PEP/LVET 0.34-0.42,children have shorter ratios than adults Adult value by 13 years

Pure MR- N PEP Pure MR- ET short PEP Prolongation>0.12 sec-LV dysfunction MR with N LV function- Ratio prolonged d/t short LVET, but ratio >0.5indicates LVD. PEP/LVET >0.5 indicates an EF

mitral regurgitation hemodynamics. . (carpentier’s classification)

Documents

acute mr slide

failure slide

heart slide

hg slide

left atrium slide

total lv stroke volume

regurgitant leak slide

large volume of blood