ivms- basic medical science of valvular heart disease

7/22/2019 IVMS- Basic Medical Science of Valvular Heart Disease

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Tutorial Notes Marc Imhotep Cray,M.D.

BASIC MEDICAL SCIENCE OF VALVULAR HEART DISEASE

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Cardiac cycle

(From USMLE First Aid 2008 pg. 192)

Phasesleft ventricle:1. Isovolumetriccontractionperiod betweenmitral valve closure and aortic

valve opening; period ofhighest O2 consumption2. Systolic ejectionperiodbetween aortic valve opening

and closing3. Isovolumetric relaxationperiod between aortic valve

closing and mitral valveopening4. Rapid fillingperiod justafter mitral valve opening

5. Reduced filling

periodjust before mitral valveclosure


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Phasesleft ventricle:1. Isovolumetric contractionperiod between mitralvalve closure and aortic valve opening; period ofhighest O2 consumption

2. Systolic ejection

period between aortic valveopening and closing3. Isovolumetric relaxationperiod between aorticvalve closing and mitral valve opening4. Rapid fillingperiod just after mitral valveopening5. Reduced fillingperiod just before mitral valveclosure

Ventricular Pressure-VolumeLoop Changes in Valve

Disease

Cardiac valve diseasesignificantly alters ventricular

pressure and volumerelationships during thecardiaccycle. A convenient way toanalyze cardiac pressure and

volume changes is by usingventricularpressure-volumeloops. The links below will

illustrate the pressure-volumechanges that occur with thefollowing valve defects:

Mitral stenosis Aortic stenosis Mitral regurgitation

Aortic regurgitation
http://www.cvphysiology.com/Heart%20Disease/HD002.htmhttp://www.cvphysiology.com/Heart%20Disease/HD002.htmhttp://www.cvphysiology.com/Heart%20Disease/HD002.htmhttp://www.cvphysiology.com/Heart%20Disease/HD002.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009a.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009a.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009b.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009b.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009c.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009c.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009d.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009d.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009d.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009c.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009b.htmhttp://www.cvphysiology.com/Heart%20Disease/HD009a.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Cardiac%20Function/CF024.htmhttp://www.cvphysiology.com/Heart%20Disease/HD002.htmhttp://www.cvphysiology.com/Heart%20Disease/HD002.htm


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Cardiac Valve Disease Tutorial

Aortic valve stenosis

http://en.wikipedia.org/wiki/Aortic_valve_stenosis Aortic valve stenosis (AS) is a valvular heart disease caused by the incomplete opening of theaortic valve.

The aortic valve controls the direction of blood flow from the left ventricle to the aorta. When ingood working order, the aortic valve does not impede the flow of blood between these twospaces. Under some circumstances, the aortic valve becomes narrower than normal, impedingthe flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as

AS.

An aortic valve that, due to rheumatic heart disease, has a severe stenosis (centre of image).The pulmonary trunk is seen at the lower right (of the image). The proximal portion of rightcoronary artery and its ostium can be seen at the lower left (of the image). The proximal left

main coronary artery and its ostium are seen on the right (of the image). Autopsy specimen.
http://en.wikipedia.org/wiki/Aortic_valve_stenosishttp://en.wikipedia.org/wiki/Aortic_valve_stenosishttp://upload.wikimedia.org/wikipedia/commons/b/b4/Aortic_stenosis_rheumatic,_gross_pathology_20G0014_lores.jpghttp://en.wikipedia.org/wiki/Aortic_valve_stenosis


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Simultaneous left ventricular and aortic pressure tracings demonstrate a pressure gradient

between the left ventricle and aorta, suggesting aortic stenosis. The left ventricle generateshigher pressures than what is transmitted to the aorta. The pressure gradient, caused by aorticstenosis, is represented by the green shaded area. (AO = ascending aorta; LV = left ventricle;ECG = electrocardiogram.)

Symptoms of aortic stenosis

Congestive heart failure

Syncope

Angina

BMS TUTORIAL/ Cardiovascular Physiology Concepts

Cardiovascular Physiology ConceptsCardiac Valve DiseasePathophysiology of valve disease

CLINICAL READ/ EmedicineAortic Stenosis
http://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://emedicine.medscape.com/article/150638-overviewhttp://emedicine.medscape.com/article/150638-overviewhttp://upload.wikimedia.org/wikipedia/commons/8/83/Aortic_Stenosis_-_Hemodynamic_Pressure_Tracing.svghttp://emedicine.medscape.com/article/150638-overviewhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htm


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Aortic insufficiency

http://en.wikipedia.org/wiki/Aortic_insufficiency

Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valveof the heart that causes blood to flow in the reverse direction during ventricular diastole, fromthe aorta into the left ventricle.

Aortic insufficiency can be due to abnormalities of either the aortic valve or the aortic root (thebeginning of the aorta).

BEFORE SURGICAL REPAIR AFTER SURGICAL REPAIR

Pathophysiology

In aortic insufficiency, when the pressure in the left ventricle falls below the pressure in theaorta, the aortic valve is not able to completely close. This causes a leaking of blood from theaorta into the left ventricle. This means that some of the blood that was already ejected from theheart is regurgitating back into the heart. The percentage of blood that regurgitates backthrough the aortic valve due to AI is known as the regurgitant fraction.

For instance, if an individual with AI has a stroke volume of 100 ml and during ventricular

diastole 25 ml regurgitates back through the aortic valve, the regurgitant fraction is 25%. Thisregurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore anincrease in the pulse pressure (systolic pressure - diastolic pressure).

Since some of the blood that is ejected during systole regurgitates back into the left ventricleduring diastole, there is decreased effective forward flow in AI.
http://en.wikipedia.org/wiki/Aortic_insufficiencyhttp://en.wikipedia.org/wiki/Aortic_insufficiencyhttp://en.wikipedia.org/wiki/Aortic_insufficiency


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Note that while diastolic blood pressure is diminished and the pulse pressure widens, systolicblood pressure generally remains normal or can even be slightly elevated. This is becausesympathetic nervous system and the renin-angiotensin-aldosterone axis of the kidneyscompensate for the decreased cardiac output. Catecholamines will increase the heart rate andincrease the strength of ventricular contraction, directly increasing cardiac output.

Catecholamines will also cause peripheral vasoconstriction, which causes increased systemicvascular resistance and ensures that core organs are adequately perfused. Renin, a proteolyticenzyme, cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II, which isalso a potent vasoconstrictor. In the case of chronic aortic insufficiency with resultant cardiacremodeling, heart failure will develop, and it is possible to see systolic pressures diminish.

Aortic insufficiency causes both volume overload (elevated preload) and pressureoverload (elevated afterload) of the heart.

The pressure overload (due to elevated pulse pressure and the systemic effects ofneuroendocrine hormones) causes left ventricular hypertrophy (LVH). There is both concentrichypertrophy and excentric hypertrophy in AI. The concentric hypertrophy is due to the increased

left ventricular systolic pressures associated with AI, while the excentric hypertrophy is due tovolume overload caused by the regurgitant fraction.

Hemodynamics

The hemodynamic sequelae of AI are dependent on the rate of onset of AI. Acute AI andchronic AI will have different hemodynamics and individuals will have different signs andsymptoms.

Acute aortic insufficiency

In acute AI, as may be seen with acute perforation of the aortic valve due to endocarditis, there

will be a sudden increase in the volume of blood in the left ventricle. The ventricle is unable todeal with the sudden change in volume. In terms of the Frank-Starling curve, the end-diastolicvolume will be very high, such that further increases in volume result in less and less efficientcontraction. The filling pressure of the left ventricle will increase. This causes pressure in the leftatrium to rise, and the individual will develop pulmonary edema.

Severe acute aortic insufficiency is considered a medical emergency. There is a high mortalityrate if the individual does not undergo immediate surgery for aortic valve replacement. If theacute AI is due to aortic valve endocarditis, there is a risk that the new valve may becomeseeded with bacteria. However, this risk is small.

Acute AI usually presents as florid congestive heart failure, and will not have any of the signs

associated with chronic AI since the left ventricle had not yet developed the eccentrichypertrophy and dilatation that allow an increased stroke volume, which in turn cause boundingperipheral pulses. On auscultation, there may be a short diastolic murmur and a soft S1. S1 issoft because the elevated filling pressures close the mitral valve in diastole (rather than themitral valve being closed at the beginning of systole).


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Chronic aortic insufficiency

If the individual survives the initial hemodynamic derailment that acute AI presents as, the leftventricle adapts by eccentric hypertrophy and dilatation of the left ventricle, and the volume

overload is compensated for. The left ventricular filling pressures will revert to normal and theindividual will no longer have overt heart failure.

In this compensated phase, the individual may be totally asymptomatic and may have normalexercise tolerance.

Eventually (typically after a latency period) the left ventricle will become decompensated, andfilling pressures will increase. While most individuals would complain of symptoms of congestiveheart failure to their physicians, some enter this decompensated phase asymptomatically.Proper treatment for AI involves aortic valve replacement prior to this decompensation phase.


Cardiac Valve DiseasePathophysiology of valve disease

CLINICAL READ/eMEDICINEAortic Regurgitation

Mitral stenosis

http://en.wikipedia.org/wiki/Mitral_valve_stenosis Mitral stenosis is a valvular heart disease characterized by the narrowing of the orifice of themitral valve of the heart.
http://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://emedicine.medscape.com/article/150490-overviewhttp://emedicine.medscape.com/article/150490-overviewhttp://en.wikipedia.org/wiki/Mitral_valve_stenosishttp://en.wikipedia.org/wiki/Mitral_valve_stenosishttp://upload.wikimedia.org/wikipedia/commons/2/2f/Mitral_stenosis,_gross_pathology_20G0015_lores.jpghttp://en.wikipedia.org/wiki/Mitral_valve_stenosishttp://emedicine.medscape.com/article/150490-overviewhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htm


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Mitral stenosis with marked thickening of the leaflets and left atrial hypertrophy. Superior view.Autopsy preparation.

Rheumatic heart disease at autopsy with characteristic findings (thickened mitral valve,thickened chordae tendineae, hypertrophied left ventricular myocardium).
http://upload.wikimedia.org/wikipedia/en/7/79/Mitral_stenosis_pressure_tracings.pnghttp://upload.wikimedia.org/wikipedia/commons/9/97/Rheumatic_heart_disease,_gross_pathology_20G0013_lores.jpghttp://upload.wikimedia.org/wikipedia/en/7/79/Mitral_stenosis_pressure_tracings.pnghttp://upload.wikimedia.org/wikipedia/commons/9/97/Rheumatic_heart_disease,_gross_pathology_20G0013_lores.jpg


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Intracardiac pressure measurements in an individual with severe mitral stenosis. Pressuretracings in the left atrium (LA) and the left ventricle (LV) in an individual with severe mitralstenosis. Blue areas represent the diastolic pressure gradient due to the stenotic valve.

Pathophysiology

The normal area of the mitral valve orifice is about 4 to 6 cm2. Under normal conditions, anormal mitral valve will not impede the flow of blood from the left atrium to the left ventricleduring (ventricular) diastole, and the pressures in the left atrium and the left ventricle duringventricular diastole will be equal. The result is that the left ventricle gets filled with blood duringearly ventricular diastole, with only a small portion of extra blood contributed by contraction ofthe left atrium (the "atrial kick") during late ventricular diastole.

When the mitral valve area goes below 2 cm2, the valve causes an impediment to the flow ofblood into the left ventricle, creating a pressure gradient across the mitral valve. This gradientmay be increased by increases in the heart rate or cardiac output. As the gradient across themitral valve increases, the amount of time necessary to fill the left ventricle with blood increases.Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases,

the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolicfilling period) decreases. When the heart rate goes above a certain point, the diastolic fillingperiod is insufficient to fill the ventricle with blood and pressure builds up in the left atrium,leading to pulmonary congestion.

When the mitral valve area goes less than 1 cm2, there will be an increase in the left atrialpressures (required to push blood through the stenotic valve). Since the normal left ventriculardiastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHgdue to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrialpressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension.Pulmonary capillary pressures in this level cause an imbalance between the hydrostaticpressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and

pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).

The constant pressure overload of the left atrium will cause the left atrium to increase in size. Asthe left atrium increases in size, it becomes more prone to develop atrial fibrillation. When atrialfibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).

In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrialkick. The loss of the atrial kick due to atrial fibrillation can cause a precipitous decrease incardiac output and sudden congestive heart failure.

Patients with mitral stenosis prompts a series of hemodynamic changes that frequently causedeterioration of the patient's clinical status. A reduction in cardiac output, associated with

acceleration of heart rate and shortening of the diastolic time, frequently leads to congestiveheart failure. In addition, when AF sets in, systemic embolization becomes a real danger.


Cardiac Valve DiseasePathophysiology of valve disease

CLINICAL READ/ eMEDICINE
http://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htmhttp://www.cvphysiology.com/Tutorials/Tutorial%20-%20cardiac%20valve%20disease.htm


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Mitral Stenosis

Mitral regurgitation

http://en.wikipedia.org/wiki/Mitral_insufficiency

Mitral regurgitation (MR), mitral insufficiency or mitral incompetence is a disorder of the heart inwhich the mitral valve does not close properly when the heart pumps out blood. It is theabnormal leaking of blood from the left ventricle, through the mitral valve, and into the leftatrium, when the left ventricle contracts, i.e. there is regurgitation of blood back into the leftatrium. MR is the most common form of valvular heart disease.

An illustration of mitral annular calcification, an aging phenomenon which can cause mitral regurgitation. Itcan also be associatedwith calcifications of aortic cusps causing stenosis and extension of calcificationinto cardiac skeleton causing heart block.

Acute phase

Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae tendineae orpapillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle.The left ventricle develops volume overload because with every contraction it now has to pumpout not only the volume of blood that goes into the aorta (the forward cardiac output or forwardstroke volume), but also the blood that regurgitates into the left atrium (the regurgitant volume).The combination of the forward stroke volume and the regurgitant volume is known as the totalstroke volume of the left ventricle.
http://emedicine.medscape.com/article/155724-overviewhttp://emedicine.medscape.com/article/155724-overviewhttp://en.wikipedia.org/wiki/Mitral_insufficiencyhttp://en.wikipedia.org/wiki/Mitral_insufficiencyhttp://www.brown.edu/Courses/Digital_Path/systemic_path/cardio/mv-annularcalcification.htmlhttp://en.wikipedia.org/wiki/Mitral_insufficiencyhttp://emedicine.medscape.com/article/155724-overview


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In the acute setting, the stroke volume of the left ventricle is increased (increased ejectionfraction), this happens because of more complete emptying of heart. However, as it progressesthe LV volume increases and the contractile function deteriorates and thus leading todysfunctional LV and a decrease in ejection fraction.The mechanism by which the total strokevolume is increased is known as the Frank-Starling mechanism.

The regurgitant volume causes a volume overload and a pressure overload of the left atrium.The increased pressures in the left atrium inhibit drainage of blood from the lungs via thepulmonary veins. This causes pulmonary congestion.

Chronic phase

Compensated

If the mitral regurgitation develops slowly over months to years or if the acute phase can bemanaged with medical therapy, the individual will enter the chronic compensated phase of thedisease. In this phase, the left ventricle develops eccentric hypertrophy in order to bettermanage the larger than normal stroke volume. The eccentric hypertrophy and the increaseddiastolic volume combine to increase the stroke volume (to levels well above normal) so that theforward stroke volume (forward cardiac output) approaches the normal levels.

In the left atrium, the volume overload causes enlargement of the chamber of the left atrium,allowing the filling pressure in the left atrium to decrease. This improves the drainage from thepulmonary veins, and signs and symptoms of pulmonary congestion will decrease.

These changes in the left ventricle and left atrium improve the low forward cardiac output stateand the pulmonary congestion that occur in the acute phase of the disease. Individuals in thechronic compensated phase may be asymptomatic and have normal exercise tolerances.

Decompensated

An individual may be in the compensated phase of mitral regurgitation for years, but willeventually develop left ventricular dysfunction, the hallmark for the chronic decompensatedphase of mitral regurgitation. It is currently unclear what causes an individual to enter thedecompensated phase of this disease. However, the decompensated phase is characterized bycalcium overload within the cardiac myocytes.

In this phase, the ventricular myocardium is no longer able to contract adequately tocompensate for the volume overload of mitral regurgitation, and the stroke volume of the leftventricle will decrease. The decreased stroke volume causes a decreased forward cardiacoutput and an increase in the end-systolic volume. The increased end-systolic volume translatesto increased filling pressures of the ventricular and increased pulmonary venous congestion.The individual may again have symptoms of congestive heart failure.

The left ventricle begins to dilate during this phase. This causes a dilatation of the mitral valveannulus, which may worsen the degree of mitral regurgitation. The dilated left ventricle causesan increase in the wall stress of the cardiac chamber as well.


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While the ejection fraction is less in the chronic decompensated phasethan in the acute phase or the chronic compensated phase of mitralregurgitation, it may still be in the normal range (ie: > 50 percent), andmay not decrease until late in the disease course. A decreased ejectionfraction in an individual with mitral regurgitation and no other cardiacabnormality should alert the physician that the disease may be in its

decompensated phase.

Demonstrations: HeartSounds & Murmurs

ttp://depts.washington.edu/p

hysdx/heart/demo.html

escription Sounds

ormal

eart sounds

urmurs Audio examples

ortic

enosis (

arly)

AS- late

itral

gurgitation

ulmonic

enosis

ortic

sufficiency

itral

enosis

enign

urmur

trial septal

efect

entricular

ptal defect

atent

uctus

teriosus

xtra heartunds

Audio examples

plit S2
http://depts.washington.edu/physdx/heart/demo.htmlhttp://depts.washington.edu/physdx/heart/demo.htmlhttp://depts.washington.edu/physdx/heart/demo.htmlhttp://depts.washington.edu/physdx/audio/s31.mp3http://depts.washington.edu/physdx/audio/splits21.mp3http://depts.washington.edu/physdx/audio/pda.mp3http://depts.washington.edu/physdx/audio/vsd.mp3http://depts.washington.edu/physdx/audio/asd.mp3http://depts.washington.edu/physdx/audio/innocent.mp3http://depts.washington.edu/physdx/audio/ms.mp3http://depts.washington.edu/physdx/audio/ar.mp3http://depts.washington.edu/physdx/audio/ps.mp3http://depts.washington.edu/physdx/audio/mr.mp3http://depts.washington.edu/physdx/audio/lateas.mp3http://depts.washington.edu/physdx/audio/as-early.mp3http://depts.washington.edu/physdx/audio/normal.mp3http://depts.washington.edu/physdx/heart/demo.htmlhttp://depts.washington.edu/physdx/heart/demo.html

ivms- basic medical science of valvular heart disease

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