Valve Abnormality Concept

7/30/2019 Valve Abnormality Concept

1/7

AR causes a volume load of the left ventricle (LV); in diastole, the LV fills antegrade from the

left atrium and retrograde from the aorta through the leaky aortic valve. The pathophysiologydepends upon whether the AR is acute or chronic. In acute AR, the LV does not have time to

dilate in response to the volume load, whereas in chronic AR, the LV may undergo a series of

adaptive (and maladaptive) changes.

Acute aortic regurgitation

Acute AR of significant severity leads to increased blood volume in the LV during diastole.

The LV does not have sufficient time to dilate in response to the sudden increase in volume.

As a result, LV end-diastolic pressure increases rapidly, causing an increase in pulmonary

venous pressure. As pressure increases throughout the pulmonary circuit, the patient

develops dyspnea and pulmonary edema

Chronic aortic regurgitation

Chronic AR causes gradual left ventricular (LV) volume overload that leads to a series ofcompensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs

through addition of sarcomeres in series (resulting in longer myocardial fibers) as well asrearrangement of myocardial fibers. As a result, the LV becomes larger and more compliant,

with greater capacity to deliver a large stroke volume that can compensate for the regurgitant

volume. The resulting hypertrophy is necessary to accommodate the increased wall tension andstress that results from LV dilation (Laplace law).

During the early phases of chronic AR, the LV ejection fraction (EF) is normal or even increased

(due to the increased preload and the Frank-Starling mechanism). Patients may remain

asymptomatic during this period. As AR progresses, LV enlargement surpasses preload reserve

on the Frank-Starling curve with the EF falling to normal and then subnormal levels. The LVend-systolic volume rises and is a sensitive indicator of progressive myocardial dysfunction.

Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting

in symptoms (dyspnea) that may be worse during exercise. Increasing LV end-diastolic pressure

may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia,necrosis, and apoptosis. Grossly, the LV gradually transforms from an elliptical to a spherical

configuration

Worldwide, rheumatic heart disease is the most common cause of AR In

United States, congenital and degenerative valve abnormalities are most common, with the age

of detection peaking at 40-60 years

The typical presentation of acute severe aortic regurgitation (AR) includes sudden, severe

shortness of breath, rapidly developing heart failure, and chest pain if myocardial perfusionpressure is decreased or an aortic dissection is present. Because the LV is non-compliant in acute

cases, the LV end-diastolic pressure is high resulting in a smaller diastolic gradient across the

aortic valve and, in some cases, a short or minimal diastolic murmur on examination

Patients with chronic AR often have a long-standing asymptomatic period that may last forseveral years. A compensatory tachycardia may develop to maintain a large forward stroke


2/7

volume, resulting in a decreased diastolic filling period. As a result, patients may be

asymptomatic even with exercise. Over time, chronic volume overload eventually leads to LVdysfunction as the LV dilates.

Symptoms of chronic severe AR include the following:

Palpitations, often described as the sensation of having forceful heart beats, due towidened pulse pressure with hyperdynamic circulation

Shortness of breath, which may not worsen with exertion in the early stages due tocompensatory tachycardia with shortened diastole

Chest pain, if LV end-diastolic pressure compromises coronary perfusion pressuregradients

Sudden cardiac death, although this is uncommon (< 0.2%/y) in asymptomatic patientswith preserved LV function

Manifestations of chronic severe AR are often the result of widened pulse pressure (ie, an

exaggerated difference between systolic and diastolic blood pressure) because (1) of elevated

stroke volume during systole and (2) the incompetent aortic valve allows the diastolic pressurewithin the aorta to fall significantly. Diastolic pressures are often lower than 60 mm Hg with

pulse pressures (ie, the difference between the systolic and diastolic pressure) often exceeding100 mm Hg, although younger patients with more compliant vessels may have a less widened

pulse pressure. Many physical examination findings have associated eponyms.

Becker sign - Visible systolic pulsations of the retinal arterioles Corrigan pulse ("water-hammer" pulse) - Abrupt distention and quick collapse on

palpation of the peripheral arterial pulse

de Musset sign - Bobbing motion of the patient's head with each heartbeat Hill sign - Popliteal cuff systolic blood pressure 40 mm Hg higher than brachial cuff

systolic blood pressure Duroziez sign - Systolic murmur over the femoral artery with proximal compression of

the artery, and diastolic murmur over the femoral artery with distal compression of the

artery

Mller sign - Visible systolic pulsations of the uvula Quincke sign - Visible pulsations of the fingernail bed with light compression of the

fingernail

Traube sign ("pistol-shot" pulse) - Booming systolic and diastolic sounds auscultatedover the femoral artery

On palpation, the point of maximal impulse may be diffuse or hyperdynamic but is often

displaced inferiorly and toward the axilla. Peripheral pulses are prominent or bounding.Auscultation may reveal an S3 gallop if LV dysfunction is present. The murmur of AR occurs in

diastole, usually as a high-pitched sound that is loudest at the left sternal border. The duration of

the murmur correlates better with the severity of AR than the loudness of the murmur. Afunctional systolic flow murmur may also be present because of increased stroke volume,

although concurrent aortic stenosis may also be present. An Austin Flint murmur may be present

at the cardiac apex in severe AR and is a low-pitched, mid-diastolic rumbling murmur due to


3/7

blood jets from the AR striking the anterior leaflet of the mitral valve, which results in premature

closure of the mitral leaflets.

Certain weight loss medications, such as fenfluramine and dexfenfluramine (commonly referredto as Phen-Fen), may induce degenerative valvular changes that result in chronic AR

beta-blocker therapy has been discouraged in patients with severe AR because heart ratereduction could prolong diastole, thus worsening AR.

Acute aortic insufficiency

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

will be a sudden increase in the volume of blood in theleft ventricle. The ventricle is unable todeal with the sudden change in volume. In terms of theFrank-Starling curve, the end-diastolic

volume will be very high, such that further increases in volume result in less and less efficient

contraction. The filling pressure of the left ventricle will increase. This causes pressure in theleft

atriumto rise, and the individual will developpulmonary edema.

Severe acute aortic insufficiency is considered amedical emergency. There is a highmortalityrate if the individual does not undergo immediate surgery foraortic valve replacement. If the

acute AI is due to aortic valveendocarditis, there is a risk that the new valve may become seeded

withbacteria. However, this risk is small.]

Acute AI usually presents as floridcongestive heart failure, and will not have any of the signsassociated with chronic AI since the left ventricle had not yet developed the eccentric

hypertrophy and dilatation that allow an increased stroke volume, which in turn cause bounding

peripheral pulses. Onauscultation, there may be a shortdiastolicmurmur and a soft S1. S1 is soft

because the elevated filling pressures close the mitral valve indiastole(rather than the mitralvalve being closed at the beginning ofsystole).

Chronic aortic insufficiency

If the individual survives the initial hemodynamic derailment that acute AI presents as, the left

ventricle adapts by eccentrichypertrophyanddilatationof the left ventricle, and the volumeoverload is compensated for. The left ventricular filling pressures will revert to normal and the

individual will no longer have overt heart failure.

In this compensated phase, the individual may be totally asymptomatic and may have normal

exercise tolerance

Thephysical examinationof an individual with aortic insufficiency involvesauscultationof theheart to listen for the murmur of aortic insufficiency and theS3 heart sound(S3 gallop correlates

with development of LV dysfunction).[2]

The murmur of chronic aortic insufficiency is typicallydescribed as early diastolic and decrescendo, which is best heard at aortic area when the patient

is seated and leans forward with breath held in expiration. The murmur is usually soft and

seldom causes thrill. there is radiation to the right parasternal region, ascending aortic aneurysmhas to be excluded. Theapex beatis typically displaced down and to the left[2]
http://en.wikipedia.org/wiki/Endocarditishttp://en.wikipedia.org/wiki/Endocarditishttp://en.wikipedia.org/wiki/Endocarditishttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/w/index.php?title=Frank-Starling_curve&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Frank-Starling_curve&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Frank-Starling_curve&action=edit&redlink=1http://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Medical_emergencyhttp://en.wikipedia.org/wiki/Medical_emergencyhttp://en.wikipedia.org/wiki/Medical_emergencyhttp://en.wikipedia.org/wiki/Deathhttp://en.wikipedia.org/wiki/Deathhttp://en.wikipedia.org/wiki/Deathhttp://en.wikipedia.org/wiki/Aortic_valve_replacementhttp://en.wikipedia.org/wiki/Aortic_valve_replacementhttp://en.wikipedia.org/wiki/Aortic_valve_replacementhttp://en.wikipedia.org/wiki/Endocarditishttp://en.wikipedia.org/wiki/Endocarditishttp://en.wikipedia.org/wiki/Endocarditishttp://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Congestive_heart_failurehttp://en.wikipedia.org/wiki/Congestive_heart_failurehttp://en.wikipedia.org/wiki/Congestive_heart_failurehttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Left_ventricular_hypertrophyhttp://en.wikipedia.org/wiki/Left_ventricular_hypertrophyhttp://en.wikipedia.org/wiki/Left_ventricular_hypertrophyhttp://en.wikipedia.org/wiki/Dilatationhttp://en.wikipedia.org/wiki/Dilatationhttp://en.wikipedia.org/wiki/Dilatationhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Third_heart_soundhttp://en.wikipedia.org/wiki/Third_heart_soundhttp://en.wikipedia.org/wiki/Third_heart_soundhttp://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Apex_beathttp://en.wikipedia.org/wiki/Apex_beathttp://en.wikipedia.org/wiki/Apex_beathttp://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Apex_beathttp://en.wikipedia.org/wiki/Aortic_insufficiency#cite_note-agabegi2nd-ch1-1http://en.wikipedia.org/wiki/Third_heart_soundhttp://en.wikipedia.org/wiki/Auscultationhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Dilatationhttp://en.wikipedia.org/wiki/Left_ventricular_hypertrophyhttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Congestive_heart_failurehttp://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Endocarditishttp://en.wikipedia.org/wiki/Aortic_valve_replacementhttp://en.wikipedia.org/wiki/Deathhttp://en.wikipedia.org/wiki/Medical_emergencyhttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/w/index.php?title=Frank-Starling_curve&action=edit&redlink=1http://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Endocarditis


4/7

If there is increased stroke volume of the left ventricle due to volume overload, an ejection

systolic 'flow' murmur may also be present when auscultating the same aortic area. Unless thereis concomitantaortic valve stenosis, the murmur should not start with an ejection click.

There may also be anAustin Flint murmur, a soft mid-diastolic rumble heard at the apical area. It

appears when regurgitant jet from the severe aortic insufficiency renders partial closure of theanterior mitral leaflet.

Mitral valve prolapse (MVP), the most common anomaly of the mitral valve apparatus, occurs when one

or both mitral valve leaflets excessively billows into the left atrium toward the end of systole.Mitral

regurgitation(MR) develops in some patients with mitral valve prolapse, particularly those with more

significant prolapse, when the valve edges fail to coapt. An extreme form of prolapse could include

chordal rupture, in which the prolapsed mitral valve is flail. Electron microscopy of the affected valve

leaflets shows a haphazard arrangement, disruption, and fragmentation of collagen fibrils. Myxomatous

proliferation of the mitral valve, in which the middle spongiosa layer is predominantly involved, leads to

the presence of unusually large amounts of myxomatous material and acid mucopolysaccharide.

Degeneration of collagen within the central core of the chordae tendineae may lead to chordal rupture.

Mitral valve prolapse can also follow rheumatic fever and myocardial infarction, in which case the

prolapse is secondary to inflammatory or ischemic chordal rupture, respectively.

o Chest pain may be caused by any of the following factors: Excessive stretching of the chordae tendineae, leading to traction on

papillary muscles

Coronary microembolism from platelet aggregates and fibrin deposits inthe angle between the left atrium and the posterior mitral leaflet

Inappropriate tachycardia and excessive postural changes and physical andemotional stresses

Hyperadrenergic state, which increases myocardial oxygen demandDynamic auscultatory changes reflect alterations in the timing of the mitral valve prolapse, the timing

and extent of the MR, the expected changes in left ventricular volume, myocardial contractility, and

heart rate. In the upright posture, venous return decreases, as does the left ventricular volume. The

reflex tachycardia that occurs in the upright position further reduces left ventricular volume. Timing and

degree of the prolapse are determined by the position of the mitral leaflets at end diastole, which, in

turn, is dependent on the distance from the mitral valve annulus to the attachment of the chordae to

papillary muscles. Low left ventricular end-diastolic volume shortens the mitral annular papillary muscle

distance, allowing the leaflets to prolapse earlier in systole.

Prompt squatting from standing position increases venous return and left ventricular volume; thus, the

systolic click and murmur may become late systolic. Squatting, however, may also be associated with anincrease in peripheral vascular resistance, which, in turn, increases the tension on the mitral valve

apparatus, preferentially directing blood flow into the left atrium, rather than to the peripheral

circulation. The late systolic click and murmur then become accentuated in the squatting position

The most specific, fundamental, and characteristic histologic changes are (1) collagen dissolutionand disruption in the pars fibrosa of the mitral valve leaflet and (2) replacement of the dense
http://en.wikipedia.org/wiki/Aortic_valve_stenosishttp://en.wikipedia.org/wiki/Aortic_valve_stenosishttp://en.wikipedia.org/wiki/Aortic_valve_stenosishttp://en.wikipedia.org/wiki/Austin_Flint_murmurhttp://en.wikipedia.org/wiki/Austin_Flint_murmurhttp://en.wikipedia.org/wiki/Austin_Flint_murmurhttp://emedicine.medscape.com/article/758816-overviewhttp://emedicine.medscape.com/article/758816-overviewhttp://emedicine.medscape.com/article/758816-overviewhttp://emedicine.medscape.com/article/758816-overviewhttp://emedicine.medscape.com/article/758816-overviewhttp://emedicine.medscape.com/article/758816-overviewhttp://en.wikipedia.org/wiki/Austin_Flint_murmurhttp://en.wikipedia.org/wiki/Aortic_valve_stenosis


5/7

collagenous fibrosa by loose myxomatous connective tissue with high acid mucopolysaccharide

content. Similar histologic abnormalities are observed in chordae tendineae.

Scanning electron photomicrographs demonstrate surface folds and focal loss of endothelial cellson mitral valve leaflets obtained from patients with severe mitral valve prolapse and significant

MR. These surface abnormalities may predispose to thromboembolic complications and/or

infectious endocarditis.

Continuous pressure and stress on the leaflets and chordae tendineae during left ventricular

systole contribute to gradual progression of these histologic changes.

Themitral valve, so named because of its resemblance to abishop'smitre, is theheart valvethatprevents the backflow ofbloodfrom theleft ventricleinto theleft atriumof the heart. It is

composed of two leaflets, one anterior and one posterior, that close when the left ventricle

contracts.

Each leaflet is composed of three layers oftissue: the atrialis,fibrosa, and spongiosa. Patients

with classic mitral valve prolapse have excessconnective tissuethat thickens the spongiosa and

separatescollagenbundles in the fibrosa. This is due to an excess ofdermatan sulfate, aglycosaminoglycan. This weakens the leaflets and adjacent tissue, resulting in increased leaflet

area and elongation of thechordae tendineae. Elongation of the chordae tendineae often causesrupture, commonly to the chordae attached to the posterior leaflet. Advanced lesionsalso

commonly involving the posterior leafletlead to leaflet folding, inversion, and displacement

toward the left atrium

Subtypes

Diagnosis of mitral valve prolapse is based on modernechocardiographictechniques which can pinpoint

abnormal leaflet thickening and other related pathology.

Prolapsed mitral valves are classified into several subtypes, based on leaflet thickness, concavity,

and type of connection to the mitral annulus. Subtypes can be described as classic, nonclassic,

symmetric, asymmetric, flail, or non-flail.[4]

All measurements below refer to adult patients; applying them to children may be misleading.
http://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Bishophttp://en.wikipedia.org/wiki/Bishophttp://en.wikipedia.org/wiki/Bishophttp://en.wikipedia.org/wiki/Mitrehttp://en.wikipedia.org/wiki/Mitrehttp://en.wikipedia.org/wiki/Mitrehttp://en.wikipedia.org/wiki/Heart_valvehttp://en.wikipedia.org/wiki/Heart_valvehttp://en.wikipedia.org/wiki/Heart_valvehttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Ventricle_(heart)http://en.wikipedia.org/wiki/Ventricle_(heart)http://en.wikipedia.org/wiki/Ventricle_(heart)http://en.wikipedia.org/wiki/Atria_of_the_hearthttp://en.wikipedia.org/wiki/Atria_of_the_hearthttp://en.wikipedia.org/wiki/Atria_of_the_hearthttp://en.wikipedia.org/wiki/Biological_tissuehttp://en.wikipedia.org/wiki/Biological_tissuehttp://en.wikipedia.org/wiki/Biological_tissuehttp://en.wikipedia.org/wiki/Connective_tissuehttp://en.wikipedia.org/wiki/Connective_tissuehttp://en.wikipedia.org/wiki/Connective_tissuehttp://en.wikipedia.org/wiki/Collagenhttp://en.wikipedia.org/wiki/Collagenhttp://en.wikipedia.org/wiki/Collagenhttp://en.wikipedia.org/wiki/Dermatan_sulfatehttp://en.wikipedia.org/wiki/Dermatan_sulfatehttp://en.wikipedia.org/wiki/Dermatan_sulfatehttp://en.wikipedia.org/wiki/Glycosaminoglycanhttp://en.wikipedia.org/wiki/Glycosaminoglycanhttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Echocardiographyhttp://en.wikipedia.org/wiki/Echocardiographyhttp://en.wikipedia.org/wiki/Echocardiographyhttp://en.wikipedia.org/wiki/Mitral_valve_prolapse#cite_note-freshlook-3http://en.wikipedia.org/wiki/Mitral_valve_prolapse#cite_note-freshlook-3http://en.wikipedia.org/wiki/Mitral_valve_prolapse#cite_note-freshlook-3http://en.wikipedia.org/wiki/File:MVP_subtypes.pnghttp://en.wikipedia.org/wiki/Mitral_valve_prolapse#cite_note-freshlook-3http://en.wikipedia.org/wiki/Echocardiographyhttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Glycosaminoglycanhttp://en.wikipedia.org/wiki/Dermatan_sulfatehttp://en.wikipedia.org/wiki/Collagenhttp://en.wikipedia.org/wiki/Connective_tissuehttp://en.wikipedia.org/wiki/Biological_tissuehttp://en.wikipedia.org/wiki/Atria_of_the_hearthttp://en.wikipedia.org/wiki/Ventricle_(heart)http://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Heart_valvehttp://en.wikipedia.org/wiki/Mitrehttp://en.wikipedia.org/wiki/Bishophttp://en.wikipedia.org/wiki/Mitral_valve


6/7

Classic versus nonclassic

Prolapse occurs when the mitral valve leaflets are displaced more than 2mmabove themitral

annulushigh points. The condition can be further divided into classic and nonclassic subtypesbased on the thickness of the mitral valve leaflets: up to 5 mm is considered nonclassic, while

anything beyond 5 mm is considered classic MVP

Symmetric versus asymmetric

Classical prolapse may be subdivided into symmetric and asymmetric, referring to the point atwhich leaflet tips join the mitral annulus. In symmetric coaptation, leaflet tips meet at a common

point on the annulus. Asymmetric coaptation is marked by one leaflet displaced toward the

atrium with respect to the other. Patients with asymmetric prolapse are susceptible to severe

deterioration of the mitral valve, with the possible rupture of the chordae tendineae and thedevelopment of a flail leaflet

Flail versus non-flail

Asymmetric prolapse is further subdivided into flail and non-flail. Flail prolapse occurs when a

leaflet tip turns outward, becoming concave toward the left atrium, causing the deterioration of

the mitral valve. The severity of flail leaflet varies, ranging from tip eversion to chordal rupture.Dissociation of leaflet and chordae tendineae provides for unrestricted motion of the leaflet

(hence "flail leaflet"). Thus patients with flail leaflets have a higher prevalence ofmitral

regurgitationthan those with the non-flail subtype

Both valsalva maneuver and standing decrease venous return to the heart thereby decreasing left

ventricular diastolic filling (preload) and causing more laxity on thechordae tendineae. Thisallows the mitral valve to prolapse earlier insystole, leading to an earlier systolic click (i.e.

closer toS1), and a longer murmur. Hand grip maneuver increasestotal peripheral resistance(afterload) and therefore increases back pressure on the mitral valve resulting in a more intensemurmur without changing the timing of the systolic click
http://en.wikipedia.org/wiki/Millimetrehttp://en.wikipedia.org/wiki/Millimetrehttp://en.wikipedia.org/wiki/Millimetrehttp://en.wikipedia.org/wiki/Mitral_annulushttp://en.wikipedia.org/wiki/Mitral_annulushttp://en.wikipedia.org/wiki/Mitral_annulushttp://en.wikipedia.org/wiki/Mitral_annulushttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Preload_(cardiology)http://en.wikipedia.org/wiki/Preload_(cardiology)http://en.wikipedia.org/wiki/Preload_(cardiology)http://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Total_peripheral_resistancehttp://en.wikipedia.org/wiki/Total_peripheral_resistancehttp://en.wikipedia.org/wiki/Total_peripheral_resistancehttp://en.wikipedia.org/wiki/Afterloadhttp://en.wikipedia.org/wiki/Afterloadhttp://en.wikipedia.org/wiki/Afterloadhttp://en.wikipedia.org/wiki/Afterloadhttp://en.wikipedia.org/wiki/Total_peripheral_resistancehttp://en.wikipedia.org/wiki/Heart_soundshttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Preload_(cardiology)http://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Mitral_regurgitationhttp://en.wikipedia.org/wiki/Mitral_annulushttp://en.wikipedia.org/wiki/Mitral_annulushttp://en.wikipedia.org/wiki/Millimetre


7/7
http://rds.yahoo.com/_ylt=A0PDoS.A6YZOREMArN2jzbkF;_ylu=X3oDMTBpcGszamw0BHNlYwNmcC1pbWcEc2xrA2ltZw--/SIG=13gibbhsf/EXP=1317493248/**http:/www.e-heart.org/Pages/06_Valvular_Disease/06_Valvular_Disease_MV_Acquired_MVP_003.htmhttp://rds.yahoo.com/_ylt=A0PDoS.A6YZOREMArN2jzbkF;_ylu=X3oDMTBpcGszamw0BHNlYwNmcC1pbWcEc2xrA2ltZw--/SIG=13gibbhsf/EXP=1317493248/**http:/www.e-heart.org/Pages/06_Valvular_Disease/06_Valvular_Disease_MV_Acquired_MVP_003.htm

Valve Abnormality Concept

Documents

Transcript of Valve Abnormality Concept