HAEMODYNAMICS OF MITRAL STENOSIS

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HAEMODYNAMICS OF MITRAL STENOSIS. DR VINOD G V. Normal MVA 4-5 cm2 No pressure gradient across mitral valve during diastole Consequence of narrowed orifice 1.Development of pressure gradient across mitral valve 2.Progressive rise in LA pressure, pulmonary venous pressure - PowerPoint PPT Presentation

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HAEMODYNAMICS OF MITRAL STENOSIS

HAEMODYNAMICS OF MITRAL STENOSISDR VINOD G VNormal MVA 4-5 cm2No pressure gradient across mitral valve during diastole

Consequence of narrowed orifice

1.Development of pressure gradient across mitral valve2.Progressive rise in LA pressure, pulmonary venous pressure3.Dependence of LV filling on LA pressure4.Reduction of blood flow across mitral valve

Torricelli's 2

Torricelli's 1

F=CO/HR xDFPFactors affecting trans mitral gradient

Factors gradient COPExertion ,emotion,high output states DFPIncrease HR MVAProgression of diseaseFactors decreasing gradient COPSecond stenosisRV failure DFPSlow HR MVA

PAH in MSPassive -Obligatory increase in response to increased LA pressure to maintain gradient of 10 to 12 across pulmonary vascular bed(PA mean- LA mean)

ReactivePA mean pressure LA mean pressure >10 to 12Pulmonary vasoconstrictionObliterative changes in pulmonary arterioles Medial hypertrophy Intimal proliferation

Causes of reactive pulmonary HTN

Wood-pulmonary vasoconstrictionDoyle-pulmonary venous pressure prominent in the lower lobes, produce reflex arterial constrictionHeath &Harris- PA pressure causes reflex arteriolar constrictionJordan-pulmonary venous pressure-transudation of fluidcauses thickening and fibrosis of alveolar wallshypoventilation of lower lobes-hypoxemia in lower lobe vesselsSensed by chemoreceptors in pulmonary veinsPulmonary arteriolar vasoconstriction in regions supplying these alveoliLower lobe perfusion decreasesThis process eventually involve middle and upper lobe

Second Stenosis

Stage 1Asymptomatic at restStage 2Symptomatic due to elevated LA pressureNormal pulmonary vascular resistanceStage 3Increased pulmonary vascular resistancesymptoms of low COPStage 4Both stenosis severeExtreme elevation of PVR-RV failure

Consequence of PAH: RVH,TRReduced COElevated pre capillary resistance protects against development of pulmonary congestion at cost of a reduced COSevere pulmonary HTN leads to right sided failureEffect of AF HR,DFP-elevates trans mitral gradientCan result in acute pulmonary edema Loss of atrial contribution to LV fillingNormal contribution of LA contraction to LV filling 15%In MS, increases up to 25-30%Lost in AF

Calculation of MVA

Gorlins formulaFlow Total cardiac output divided by time in seconds during which flow occurs across the valve

F=COP/DFPXHR

Steps in calculating MVAAverage gradient=area(mm2)/length of diastole(mm)

Mean gradient=average gradient X scale factor

Average diastolic period=length of DFP(mm)/paper speed(mm/s)

HR(beat/min), COP(ml/min)

MVA=cardiac output/HR average diastolic periodperiod37.7mean gradient

Pitfalls in calculating MVAOverestimation of trans mitral gradient occurs when PCWP is not taken properly

Failure to wedge properly cause one to compare damped pulmonary artery pressure to LV pressureTo ensure proper wedging -mean wedge pressure is lower than mean PA pressure -Blood withdrawn from wedge catheter is >95% saturatedAlignment MismatchAlignment of the PCW and LV pressure tracings does not match alignment of simultaneous LA and LV tracings

There is a time delay of 50-70msec V wave in LA pressure tracing peaks immediately before LV pressure down stroke

Realign wedge tracing so that the V wave peak is bisected by or slightly to the left of the down stroke of LV pressure

CO determination

Simultaneous measurement with LA-LV pressure tracing

Under estimation of valve area in case of associated MR

Thermo dilution method inaccurate when associated TRDamped PCW-LV Vs LA-LV

Overestimation of MVG occur if damped PCW P is usedLA-LV gradient in AFWith long diastolic filling period ,progressive decrease in LA pressure

Increase with short diastole

Measure gradient in 3 to 4 diastolic complexes with nearly equal cycle length and measure the mean value

Symptoms and signs

Hemodynamic correlationAcute pulmonary edemaIncreased pulmonary venous pressure

Increased transudation of fluid

Decreased lymphatic clearance

Pulmonary capillary pressure exceeds tissue oncotic pressure of 25mm HgHemoptysisPulmonary apoplexy -rapture of bronchial vein -massive hemoptysis

Pink frothy sputum during pulmonary edema

Chronic bronchitis

Pulmonary infarctionLoud S1Rapidity with which LV pressure rises when mitral valve closes

Mitral valve closes at higher dp/dt of LV

Wide closing excursion of valve leaflets

A2-OS intervalOS occurs due to sudden tensing of valve leaflets after the valve cusps have completed their opening excursion

Follows A2 by 40-120msec

Interval varies inversely with LA pressure

Shorter A2-OS interval indicates severe MSDiastolic murmurMid diastolic component starts with OS

Holo diastolic in severe MS due to persistent gradient

Presystolic component: -Atrial contraction -Persistent LA-LV pressure gradient - can persists even in AFDoppler ECHORate of fall in flow velocity is slow No period of diastasis

Increased early diastolic peak velocity

Mitral Pressure Half TimeThe pressure halftime is defined as the time required for the pressure to decay to half its original value Mitral valve area (MVA) calculated as: MVA = 220/PHT

Not affected by CO,MRPHT =11 .6xCnx MPG/(CcxMVA) Cn-net compliance

Disadvantage

Poor ventricular compliance will increase the rate of pressure rise in diastole

Shorten PHT overestimate MVA

Significant AR, diastolic dysfunction alter PHT

Post BMV PHT is inaccurateQ1O2 consumption 180 ml/minA-V O2 difference 40 ml/LHR 76/min SRLV diastolic mean 6Diastolic filling period 0.42 sec/beatPCW mean 24PA 40/22 -mean 22

Q2Body surface area 1.4 m2O2 consumption 201ml/minA-V O2 difference 110 mL/LPR 92/minLV diastolic mean 10Diastolic filling period 0.36sec/beatPCW mean 33PA 125/65, mean 75