Pulmonary valve stenosis

Pulmonary valve stenosis is a medical condition in which outflow of blood from the right ventricle of the heart is obstructed at the level of the pulmonic valve. This results in the reduction of flow of blood to the lungs. Symptoms include jugular venous distention, cyanosis (usually visible in the nailbeds), and general symptoms of lowered oxygenation of the blood. When the stenosis is mild, it can go unnoticed for many years. If stenosis is severe, you may see sudden fainting or dizziness if exercised too much. Valve replacement or surgical repair (depending upon whether the stenosis is in the valve or vessel) may be indicated. Stenosis can occur in dogs as well as in humans.
Contents

1 Causes
2 See also


Causes
The most common cause is congenital. If severe, it can lead to blue baby syndrome. It can also be secondary to other conditions such as endocarditis.
See also
Aortic valve stenosis Mitral regurgitation
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,

Mitral valve prolapse

From Wikipedia, the free encyclopedia
Mitral valve prolapse (MVP) is a heart valve condition marked by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. In its nonclassic form, MVP carries a low risk of complications. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, and — in rare circumstances — cardiac arrest usually resulting in sudden death.
see also: Mitral valve prolapse dysautonomia
Contents

1 Overview
2 History
3 Subtypes
3.1 Classic versus nonclassic
3.2 Symmetric versus asymmetric
3.3 Flail versus non-flail
4 Signs and symptoms
4.1 Auscultation
5 Complications
5.1 Mitral regurgitation
5.2 Sudden death
6 Prognosis
7 Diagnosis
8 Treatment
8.1 IE prevention
9 Prevalence
10 References

//
Overview
The mitral valve, so named because of its resemblance to a bishop's miter, is the heart valve that prevents the backflow of blood from the left ventricle into the left atrium. It is composed of two leaflets (one anterior, one posterior) that close when the left ventricle contracts.
Each leaflet is composed of three layers of tissue: the atrialis, fibrosa, and spongiosa. Patients with classic mitral valve prolapse have excess connective tissue that thickens the spongiosa and separates collagen bundles in the fibrosa. This is due to an excess of dermatan sulfate, a glycosaminoglycan. This weakens the leaflets and adjacent tissue, resulting in increased leaflet area and elongation of the chordae tendineae. Elongation of the chordae often causes rupture, and is commonly found in the chordae tendineae attached to the posterior leaflet. Advanced lesions — also commonly involving the posterior leaflet — lead to leaflet folding, inversion, and displacement toward the left atrium.
History
The term mitral valve prolapse was coined by J. Michael Criley in 1966 and gained acceptance over the other descriptor of "billowing" of the mitral valve (as described by Dr. Barlow).
For many years, mitral valve prolapse was a poorly understood anomaly associated with a wide variety of both related and seemingly unrelated signs and symptoms, including late systolic murmurs, inexplicable panic attacks, and polythelia (extra nipples). Recent studies suggest that these symptoms were incorrectly linked to MVP because the disorder was simply over-diagnosed at the time. Continuously-evolving criteria for diagnosis of MVP with echocardiography made proper diagnosis difficult, and hence many subjects without MVP were included in studies of the disorder and its prevalence. In fact, some modern studies report that as many as 55% of the population would be diagnosed with MVP if older, less reliable methods of MVP diagnosis—notably M-mode echocardiography—were used today.
In recent years, new criteria have been proposed as an objective measure for diagnosis of MVP using more reliable two- and three-dimensional echocardiography. The disorder has also been classified into a number of subtypes with respect to these criteria.
Subtypes

Diagnosis of mitral valve prolapse is based on modern echocardiographic techniques 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.
Note: all measurements below refer to adult patients and applying them to children may be misleading.
Classic versus nonclassic
Prolapse occurs when the mitral valve leaflets are displaced more than 2 mm above the mitral annulus high points. The condition can be further divided into classic and nonclassic subtypes based 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 at which 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 prone to severe deterioration of the mitral valve, with the possible rupture of the chordae tendineae and the development 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 of mitral regurgitation than those with the non-flail subtype.
] Signs and symptoms
Some patients with MVP experience heart palpitations, atrial fibrillation, or syncope, though the prevalence of these symptoms does not differ significantly from the general population. Between 11 and 15% of patients experience moderate chest pain and shortness of breath. These symptoms are most likely not caused directly by the prolapsing mitral valve, but rather by the mitral regurgitation that often results from prolapse.
For unknown reasons, MVP patients tend to have a low body mass index (BMI) and are typically leaner than individuals without MVP. Other features associated with MVP include Pectus excavatum, scoliosis, greater armspan than height, fatigue, and unusual joint flexibility.[1]
Auscultation
Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late systolic murmur heard best at the apex is common.
Complications
Mitral regurgitation
Most cases of mitral valve prolapse are associated with mild mitral regurgitation, where blood aberrantly flows from the left ventricle into the left atrium during systole. Approximately 7% of classic MVP patients experience severe regurgitation, often due to chordae tendineae rupture.
Sudden death
Severe mitral valve prolapse is associated with arrhythmias and atrial fibrillation that may progress and lead to sudden death. As there is no evidence that a prolapsed valve itself contributes to such arrythmias, these complications are more likely due to mitral regurgitation and congestive heart failure.
] Prognosis
The major predictors of mortality are the severity of mitral regurgitation and the ejection fraction. Patients with moderate to severe mitral regurgitation have a relative risk for mortality that is three times that of the general population. Similarly, a left ventricular ejection fraction at or below 50% carries a relative risk of 3.8.


Transthoracic and transesophageal echocardiograms of mitral valve prolapseLeft. A transthoracic echocardiogram displaying prolapse of both the anterior leaflet (AL) and posterior leaflet (PL) of the mitral valve. Right. A transesophageal echocardiogram displaying the heart in the same individual as in the figure to the left. Both figures are during ventricular systole, with the mitral valve closed. AL=Anterior leaflet; PL=Posterior leaflet; LA=Left atrium; LV=Left ventricle; AO=Aorta; Blue line represents the plane of the mitral valve annulus.




DiagnosisEchocardiography, a noninvasive method of visualizing the heart, is the most useful method of diagnosing a prolapsed mitral valve. Two- and three-dimensional echocardiography are particularly valuable as they allow visualization of the mitral leaflets relative to the mitral annulus. This allows measurement of the leaflet thickness and their displacement relative to the annulus. Thickening of the mitral leaflets >5 mm and leaflet displacement >2 mm indicates classic mitral valve prolapse.
Treatment
Mitral valve prolapse can be treated with surgical replacement of the mitral valve. This may be necessary in as many as 11% of patients with classic MVP, and is indicated for patients with an ejection fraction below 60% and progressive left ventricular dysfunction.
IE prevention
People with mitral valve prolapse are at higher risk of infective endocarditis (that is, bacterial infection of the heart tissue), as a result of surgical operations. Therefore they need preventive antibiotic treatment, before any operation that involves massive bleeding. Minor skin wounds (and plastic surgeries, etc), are not a problem, but dental operations such as pulpectomy ("root canal") are. Thus, as a risk lowering measure, people with Mitral valve prolapse should take extra care of their dental hygiene.
Prevalence
Figures vary widely, but most recent studies of mitral valve prolapse indicate a prevalence of 1.3% for classic and 1.1% for nonclassic MVP. MVP occurs less frequently in children, and does not vary significantly with sex. Though the reasons are not understood, patients with mitral valve prolapse tend to be leaner with a relatively low body mass index.
References
^ http://www.nursing.wright.edu/practice/mvp/, Understanding the Mitral Valve Prolapse Syndrome
Playford D, Weyman AE (2001). "Mitral valve prolapse: time for a fresh look". Rev Cardiovasc Med 2 (2): 73-81. PMID 12439384.

Mitral stenosis

From Wikipedia, the free encyclopedia
Mitral stenosis is a narrowing of the orifice of the mitral valve of the heart.
Contents
1 Overview
2 Etiology
3 Pathophysiology
4 Physical examination
5 Diagnosis
6 Natural history
7 Treatment
8 See also
9 External links
10 References

Overview
Mitral stenosis with marked thickening of the leaflets and left atrial hypertrophy. Superior view. Autopsy preparation.
In normal cardiac physiology, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. The reason the blood flows in the proper direction is that, during this phase of the cardiac cycle, the pressure in the left ventricle is less than the pressure in the left atrium, and the blood flows down the pressure gradient. In the case of mitral stenosis, the valve does not open completely, so the left atrium has to have a higher pressure than normal to have the blood overcome the increased gradient caused by the mitral valve stenosis.
Etiology
Most cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Less common causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease.
Pathophysiology
The normal area of the mitral valve orifice is about 4 to 6 cm2. Under normal conditions, a normal mitral valve will not impede the flow of blood from the left atrium to the left ventricle during (ventricular) diastole, and the pressures in the left atrium and the left ventricle during diastole will be equal. The result is that the left ventricle gets filled with blood during early diastole, with only a small portion of extra blood contributed by contraction of the 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 of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral 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 diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period 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 atrial pressures (required to push blood through the stenotic valve). Since the normal left ventricular diastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHg due to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure 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).
Increases in the heart rate will allow less time for the left ventricle to fill, also causing an increase in left atrial pressure and pulmonary congestion.
The constant pressure overload of the left atrium will cause the left atrium to increase in size. As the left atrium increases in size, it becomes more prone to develop atrial fibrillation. When atrial fibrillation 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 atrial kick. The loss of the atrial kick due to atrial fibrillation can cause a precipitous decrease in cardiac output and sudden congestive heart failure.
Physical examination
Upon auscultation of an individual with mitral stenosis, the first heart sound is unusually loud and may be palpable (tapping apex beat) because of increased force in closing the mitral valve.
If pulmonary hypertension secondary to mitral stenosis is severe, the P2 (pulmonic) component of the second heart sound (S2) will become loud.
An opening snap maybe heard after the A2 (aortic) component of the second heart sound (S2), which correlates to the forceful opening of the mitral valve. The mitral valve opens when the pressure in the left atrium is greater than the pressure in the left ventricle. This happens in ventricular diastole (after closure of the aortic valve), when the pressure in the ventricle precipitously drops. In individuals with mitral stenosis, the pressure in the left atrium correlates with the severity of the mitral stenosis. As the severity of the mitral stenosis increases, the pressure in the left atrium increases, and the mitral valve opens earlier in ventricular diastole.
A mid-diastolic rumbling murmur will be heard after the opening snap. The murmur is best heard at the apical region and is not radiated. Since it is low-pitched it should be picked up by the bell of the stethoscope. Rolling the patient towards left, as well as isometric exercise will accentuate the murmur. A thrill might be present when palpating at the apical region of the praecordium.
Peripheral signs include:
Malar flush - pulmonary hypertension is prominent in patients with mitral stenosis
Ankle/sacral oedema when there is right heart failure
Atrial fibrillation - irregularly irregular pulse and loss of 'a' wave in jugular venous pressure
Left parasternal heave - presence of right ventricular hypertrophy due to pulmonary hypertension
Tapping apex beat which is not displaced
Diagnosis
Severity of mitral stenosis
Degree of mitral stenosis
Mean gradient
Mitral valve area
Mild mitral stenosis
<5>1.5 cm2
Moderate mitral stenosis
5 - 10
1.0 - 1.5 cm2
Severe mitral stenosis
> 10
< title="Echocardiography" href="http://en.wikipedia.org/wiki/Echocardiography">echocardiography, which shows decreased opening of the mitral valve leaflets, and blunted flow of blood in early diastole.
The trans-mitral gradient as measured by doppler echocardiography is the gold standard in the evaluation of the severity of mitral stenosis.
Another method of measuring the severity of mitral stenosis is the simultaneous left heart catheterization and right heart catheterization. The right heart catheterization (commonly known as Swan-Ganz catheterization) gives the physician the mean pulmonary capillary wedge pressure, which is a reflection of the left atrial pressure. The left heart catheterization, on the other hand, gives the pressure in the left ventricle. By simultaneously taking these pressures, it is possible to determine the gradient between the left atrium and right atrium during ventricular diastole, which is a marker for the severity of mitral stenosis. This method of evaluating mitral stenosis tend to over-estimate the degree of mitral stenosis, however, because of the time lag in the pressure tracings seen on the right heart catheterization and the slow Y descent seen on the wedge tracings. If a trans-septal puncture is made during right heart catheterization, however, the pressure gradient can accurately quantify the severity of mitral stenosis.
Natural history
The natural history of mitral stenosis secondary to rheumatic fever (the most common cause) is an asymptomatic latent phase following the initial episode of rheumatic fever. This latent period lasts an average of 16.3 ± 5.2 years. Once symptoms of mitral stenosis begin to develop, progression to severe disability takes 9.2 ± 4.3 years.
In individuals who were offered mitral valve surgery but refused, survival with medical therapy alone was 44 ± 6% at 5 years, and 32 ± 8% at 10 years after they were offered correction.
Treatment
The treatment options for mitral stenosis include medical management, surgical replacement of the valve, and percutaneous balloon valvuloplasty.
Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to NYHA functional class II symptoms to the development of atrial fibrillation to the development of NYHA functional class III or IV symptoms. Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates.
The indication for invasive treatment with either a mitral valve replacement or valvuloplasty is NYHA functional class III or IV symptoms.
To determine which patients would benefit from percutaneous balloon mitral valvuloplasty, a scoring system has been developed.2 Scoring is based on 4 echocardiographic criteria: leaflet mobility, leaflet thickening, subvalvar thickening, and calcification. Individuals with a score of ≥ 8 tended to have suboptimal results.3 Superb results with valvotomy are seen in individuals with a crisp opening snap, score < title="Echocardiography" href="http://en.wikipedia.org/wiki/Echocardiography">Echocardiography
Mitral valve
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,
Health disesae,Health disesae,Health disesae,

Mitral regurgitation

From Wikipedia, the free encyclopedia
Mitral regurgitation (MR), also known as mitral insufficiency, is the abnormal leaking of blood through the mitral valve, from the left ventricle into the left atrium of the heart.
Contents

1 Etiology
2 Pathophysiology
2.1 Acute phase
2.2 Chronic compensated phase
2.3 Chronic decompensated phase
3 Symptoms
4 Diagnostic studies
4.1 Chest x-ray
4.2 Echocardiography
5 Quantification of mitral regurgitation
6 Treatment
6.1 Indication for surgery
7 References
8 See also

Etiology
The mitral valve is composed of the valve leaflets, the mitral valve annulus (which forms a ring around the valve leaflets), the papillary muscles (which tether the valve leaflets to the left ventricle, preventing them from prolapsing into the left atrium), and the chordae tendineae (which connect the valve leaflets to the papillary muscles). A dysfunction of any of these portions of the mitral valve apparatus can cause mitral regurgitation.
Primary mitral regurgitation is due to any disease process that affects the mitral valve apparatus itself. The causes of primary mitral regurgitation include:
Myxomatous degeneration of the mitral valve
Ischemic heart disease / Coronary artery disease
Infective endocarditis
Collagen vascular diseases (ie: SLE, Marfan's syndrome)
Rheumatic heart disease
Trauma
Balloon valvulotomy of the mitral valve
Certain forms of medication (e.g. fenfluramine)
The most common cause of primary mitral regurgitation in the United States (causing about 50% of primary mitral regurgitation) is myxomatous degeneration of the valve. Myxomatous degeneration of the mitral valve is more common in males, and is more common in advancing age. It is due to a genetic abnormality that results in a defect in the collagen that makes up the mitral valve. This causes a stretching out of the leaflets of the valve and the chordae tendineae. The elongation of the valve leaflets and the chordae tendineae prevent the valve leaflets from fully coapting when the valve is closed, causing the valve leaflets to prolapse into the left atrium, thereby causing mitral regurgitation.
Ischemic heart disease causes mitral regurgitation by the combination of ischemic dysfunction of the papillary muscles, and the dilatation of the left ventricle that is present in ischemic heart disease, with the subsequent displacement of the papillary muscles and the dilatation of the mitral valve annulus.
Secondary mitral regurgitation is due to the dilatation of the left ventricle, causing stretching of the mitral valve annulus and displacement of the papillary muscles. This dilatation of the left ventricle can be due to any cause of dilated cardiomyopathy, including aortic insufficiency and nonischemic dilated cardiomyopathy.
Pathophysiology
Comparison of acute and chronic mitral regurgitation

Acute mitral regurgitation
Chronic mitral regurgitation
Electrocardiogram
Normal
P mitrale, atrial fibrillation, left ventricular hypertrophy
Heart size
Normal
Cardiomegaly, left atrial enlargement
Systolic murmur
Heard at the base, radiates to the neck, spine, or top of head
Heard at the apex, radiates to the axilla
Apical thrill
May be absent
Present
Jugular venous distension
Present
Absent
The pathophysiology of mitral regurgitation can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase.
Acute phase
Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae tendineae or papillary 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 pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke 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 total stroke volume of the left ventricle.
In the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction), but the forward cardiac output is decreased. The mechanism by which the total stroke volume 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 the pulmonary veins. This causes pulmonary congestion.
Chronic compensated phase
If the mitral regurgitation develops slowly over months to years or if the acute phase can be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. In this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. The eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume (to levels well above normal) so that the forward 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 the pulmonary 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 state and the pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances.
Chronic decompensated phase
An individual may be in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. It is currently unclear what causes an individual to enter the decompensated phase of this disease. However, the decompensated phase is characterized by calcium overload within the cardiac myocytes.
In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the stroke volume of the left ventricle will decrease. The decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume. The increased end-systolic volume translates to 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 valve annulus, which may worsen the degree of mitral regurgitation. The dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well.
While the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase of mitral regurgitation, it may still be in the normal range (ie: > 50 percent), and may not decrease until late in the disease course. A decreased ejection fraction in an individual with mitral regurgitation and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
Symptoms
The symptoms associated with mitral regurgitation are dependent on which phase of the disease process the individual is in. Individuals with acute mitral regurgitation will have the signs and symptoms of decompensated congestive heart failure (ie: shortness of breath, pulmonary edema, orthopnea, paroxysmal nocturnal dyspnea), as well as symptoms suggestive of a low cardiac output state (ie: decreased exercise tolerance). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute mitral regurgitation due to papillary muscle rupture or rupture of a chordae tendineae.
Individuals with chronic compensated mitral regurgitation may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure. These individuals may be sensitive to small shifts in their intravascular volume status, and are prone to develop volume overload (congestive heart failure).
Diagnostic studies
There are many diagnostic tests that have abnormal results in the presence of mitral regurgitation. These tests suggest the diagnosis of mitral regurgitation and may indicate to the physician that further testing is warranted. For instance, the electrocardiogram (ECG) in long standing mitral regurgitation may show evidence of left atrial enlargement and left ventricular hypertrophy. Atrial fibrillation may also be noted on the ECG in individuals with chronic mitral regurgitation. The ECG may not show any of these finding in the setting of acute mitral regurgitation.
The quantification of mitral regurgitation usually employs imaging studies such as echocardiography or magnetic resonance angiography of the heart.
Chest x-ray
The chest x-ray in individuals with chronic mitral regurgitation is characterized by enlargement of the left atrium and the left ventricle. The pulmonary vascular markings are typically normal, since pulmonary venous pressures are usually not significantly elevated.


Echocardiography


transesophageal echocardiogram of mitral valve prolapse
The echocardiogram is commonly used to confirm the diagnosis of mitral regurgitation. Color doppler flow on the transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole.
Because of the inability in getting accurate images of the left atrium and the pulmonary veins on the transthoracic echocardiogram, a transesophageal echocardiogram may be necessary to determine the severity of the mitral regurgitation in some cases.
Factors that suggest severe mitral regurgitation on echocardiography include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.
Quantification of mitral regurgitation

Determination of the degree of mitral regurgitation
Degree of mitral regurgitation
Regurgitant fraction
Regurgitant Orifice area
Mild mitral regurgitation
<> 60 percent
> 0.3 cm2






The degree of severity of mitral regurgitation can be quantified by the percentage of the left ventricular stroke volume that regurgitates into the left atrium (the regurgitant fraction).
Methods that have been used to assess the regurgitant fraction in mitral regurgitation include echocardiography, cardiac catheterization, fast CT scan, and cardiac MRI.
The echocardiographic technique to measure the regurgitant fraction is to determine the forward flow through the mitral valve (from the left atrium to the left ventricle) during ventricular diastole, and comparing it with the flow out of the left ventricle through the aortic valve in ventricular systole. This method assumes that the aortic valve does not suffer from aortic insufficiency. The regurgitant fraction would be described as:
Another way to quantify the degree of mitral regurgitation is to determine the area of the regurgitant flow at the level of the valve. This is known as the regurgitant orifice area, and correlates with the size of the defect in the mitral valve. One particular echocardiographic technique used to measure the orifice area is measurement of the proximal isovelocity surface area (PISA). The flaw of using PISA to determine the mitral valve regurgitant orifice area is that it measures the flow at one moment in time in the cardiac cycle, which may not reflect the average performance of the regurgitant jet.
Treatment
The treatment of mitral regurgitation depends on the acuteness of the disease and whether there are associated signs of hemodynamic compromise.
In acute mitral regurgitation secondary to a mechanical defect in the heart (ie: rupture of a papillary muscle or chrordae tendineae), the treatment of choice is urgent mitral valve replacement. If the patient is hypotensive prior to the surgical procedure, an intra-aortic balloon pump may be placed in order to improve perfusion of the organs and to decrease the degree of mitral regurgitation.
If the individual with acute mitral regurgitation is normotensive, vasodilators may be of use to decrease the afterload seen by the left ventricle and thereby decrease the regurgitant fraction. The vasodilator most commonly used is nitroprusside.
Individuals with chronic mitral regurgitation can be treated with vasodilators as well. In the chronic state, the most commonly used agents are ACE inhibitors and hydralazine. Studies have shown that the use of ACE inhibitors and hydralazine can delay surgical treatment of mitral regurgitation1,2. The current guidelines for treatment of mitral regurgitation limit the use of vasodilators to individuals with hypertension, however.
There are two surgical options for the treatment of mitral regurgitation: mitral valve replacement and mitral valve repair.
Indication for surgery
Indications for surgery for chronic mitral regurgitation3
Symptoms
LV EF
LVESD
NYHA II - IV
> 60 percent
< title="Pulmonary artery" href="http://en.wikipedia.org/wiki/Pulmonary_artery">Pulmonary artery systolic pressure ≥ 50 mmHg
Indications for surgery for chronic mitral regurgitation include signs of left ventricular dysfunction. These include an ejection fraction of less than 60 percent and a left ventricular end systolic dimension (LVESD) of greater than 45 mm.
References
1. Greenberg BH, Massie BM, Brundage BH, Botvinick EH, Parmley WW, Chatterjee K. Beneficial effects of hydralazine in severe mitral regurgitation. Circulation. 1978 Aug;58(2):273-9. (Medline abstract)
2. Hoit BD. Medical treatment of valvular heart disease. Curr Opin Cardiol. 1991 Apr;6(2):207-11. (Medline abstract)
3. Bono w et al. ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. ACC/AHA Task Force Report. JACC Vol. 32, No. 5, November 1998:1486-1588 (Full article)
See also
Mitral valve
Left ventricle
Left atrium
Systole (medicine)
Diastole
Cardiac output
Mitral valve prolapse

Libman-Sacks endocarditis

From Wikipedia, the free encyclopedia
Libman-Sacks endocarditis is a form of nonbacterial endocarditis that is seen in systemic lupus erythematosus. It was named after American physicians Emanuel Libman and Benjamin Sacks. It is the most common cardiac manifestation of lupus. The vegetations are formed from strands of fibrin, neutrophils, lymphocytes, and histiocytes. The mitral valve is typically affected, and the vegetations occur on the ventricular surface of the valve. Libman-Sacks lesions rarely produce significant valve dysfunction and the lesions only rarely embolize. The pathology is the same as nonbacterial thrombotic endocarditis except focal necrosis (hematoxylin bodies) can be found only in Libman-sacks endocarditis.
Retrieved from "http://en.wikipedia.org/wiki/Libman-Sacks_endocarditis"

Heart valve dysplasia

Heart valve dysplasia is a congenital heart defect which in dogs and cats affects the aortic, pulmonary, mitral, and tricuspid heart valves. Pulmonary valve stenosis and aortic valve stenosis are discussed separately. Dysplasia of the mitral and tricuspid valves can cause leakage of blood or stenosis.
Dysplasia of the mitral and tricuspid valves - also known as the atrioventricular (AV) valves - can appear as thickened, shortened, or notched valves. The chordae tendinae can be fused or thickened. The papillary muscles can be enlarged or atrophied. The cause is unknown, but genetics play a large role. Dogs and cats with tricuspid valve dysplasia often also have an open foramen ovale, an atrial septal defect, or inflammation of the right atrial epicardium.[1] In dogs, tricuspid valve dysplasia can be similar to Ebstein's anomaly in humans.[2]
Mitral valve stenosis is one of the most common congenital heart defects in cats. In dogs, it is most commonly found in Great Danes, German Shepherd Dogs, Bull Terriers, Golden Retrievers, Newfoundlands, and Mastiffs. Tricuspid valve dysplasia is most common in the Old English Sheepdog, German Shepherd Dog, Weimaraner, Labrador Retriever, and Great Pyrenees.[1] It is inherited in the Labrador Retriever.[3]
The disease and symptoms are similar to progression of acquired valve disease in older dogs. Valve leakage leads to heart enlargement, arrhythmias, and congestive heart failure. Heart valve dysplasia can be tolerated for years or progress to heart failure in the first year of life. Diagnosis is with an echocardiogram. There is a poor prognosis with significant heart enlargement.
References
a b Ettinger, Stephen J.;Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine, 4th ed., W.B. Saunders Company. ISBN 0-7216-6795-3.
Abbott, Jonathan A. (2000). Small Animal Cardiology Secrets, 1st ed., Hanley & Belfus, Inc.. ISBN 1-56053-352-8.
Famula, Thomas R.; Siemens, Lori M.; Davidson, Autumn P.; Packard, Martin (2002). "Evaluation of the genetic basis of tricuspid valve dysplasia in Labrador Retrievers". American Journal of Veterinary Research 63 (6): 816-820. Retrieved on 2006-08-26.

Endocarditis

Endocarditis

EndocarditisClassifications and external resources

Bartonella henselae bacilli in cardiac valve of a patient with blood culture-negative endocarditis. The bacilli appear as black granulations.

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves.
Endocarditis can be classified by etiology as either infective or non-infective, depending on whether a microorganism is the source of the problem.
Contents

1 Infective endocarditis
1.1 Classification
1.2 Etiology and pathogenesis
1.3 Clinical and pathological features
1.4 Diagnosis
1.5 Micro-organisms responsible
1.6 Treatment
2 Non-infective endocarditis
3 References
4 External links
//
] Infective endocarditis
As the valves of the heart do not actually receive any blood supply of their own, which may be surprising given their location, defense mechanisms (such as white blood cells) cannot enter. So if an organism (such as bacteria) establish hold on the valves, the body cannot get rid of them.
Normally, blood flows smoothly through these valves. If they have been damaged (for instance in rheumatic fever) bacteria have a chance to take hold.
Classification
Traditionally, infective endocarditis has been clinically divided into acute and subacute (between acute and chronic) endocarditis. This classifies both the tempo of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.
This terminology is now discouraged. The terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred despite the lack of advantage in meaning.
Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be fastidious because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.
Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important.
The Russian classification includes "endocarditis in narcotic abusers" in addition to above given classification, as this disease is very common in narcotic drug users who inject with non-sterile injections/syringes.
Etiology and pathogenesis
As previously mentioned, altered blood flow around the valves is a risk factor in obtaining endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged part of a heart valve becomes covered with a blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE).
In a healthy individual, a bacteraemia (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with a piece of a blood clot, the valve provides a place for the bacteria to attach themselves and an infection can be established.
The bacteraemia is often caused by minor dental procedures, such as a tooth removal. It is important that a dentist is told of any heart problems before commencing.
Another group of causes result from a high number of bacteria getting into the bloodstream. Colorectal cancer, serious urinary tract infections, and IV drug use can all introduce large numbers of bacteria. With a large number of bacteria, even a normal heart valve may be infected. A more virulent organism (such as Staphylococcus aureus) is usually responsible for infecting a normal valve.
Intravenous drug users tend to get their right heart valves infected because the veins that are injected enter the right side of the heart. The injured valve is most commonly affected when there is a pre-existing disease. (In rheumatic heart disease this is the aortic and the mitral valves, on the left side of the heart.)
Clinical and pathological features
Fever (often spiking)
Continuous presence of micro-organisms in the bloodstream determined by serial collection of blood cultures
Vegetations on valves on echocardiography
Septic emboli, causing circulatory problems (stroke, gangrene of fingers)
Chronic renal failure
Osler's nodes (painful subcutaneous lesions in the distal fingers)
Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)
Roth spots on the retina
Conjunctival petechiae
A new or changing heart murmur, particularly murmurs suggestive of valvular incompetence
Splinter hemorrhages
Diagnosis
In general, a patient should fulfill the Duke Criteria[1] in order to establish the diagnosis of endocarditis.
As the Duke Criteria relies heavily on the results of echocardiography, research has addressed when to order an echocardiogram by using signs and symptoms to predict occult endocarditis among patients with intravenous drug abuse[2][3][4] and among non drug abusing patients [5][6]. Unfortunately, this research is over 20 years old and it is possible that changes in the epidemiology of endocarditis and bacteria such as staphylococcus make the following estimates incorrectly low.
Among patients who do not use illicit drugs and have a fever in the emergency room, there is a less than 5% chance of occult endocarditis. Mellors [6] in 1987 found no cases of endocarditis nor of staphylococcal bacteremia among 135 febrile patients in the emergency room. The upper confidence interval for 0% of 135 is 5%, so for statistical reasons alone, there is up to a 5% chance of endocarditis among these patients. In contrast, Leibovici [5] found that among 113 non-selected adults admitted to the hospital because of fever there were two cases (1.8% with 95%CI: 0% to 7%) of endocarditis.
Among patients who do use illicit drugs and have a fever in the emergency room, there is about a 10% to 15% prevalence of endocarditis. This estimate is not substantially changed by whether the doctor believes the patient has a trivial explanation for their fever[4]. Weisse[2] found that 13% of 121 patients had endocarditis. Marantz [4] also found a prevalence of endocarditis of 13% among such patients in the emergency room with fever. Samet [3] found a 6% incidence among 283 such patients, but after excluding patients with initially apparent major illness to explain the fever (including 11 cases of manifest endocarditis), there was a 7% prevalence of endocarditis.
Among patients with staphylococcal bacteremia (SAB), one study found a prevalence of 29% in community-acquired SAB versus 5% in nosocomial SAB[7]. However, only 2% of strains were resistant to methicillen and so these numbers may be low in areas of higher resistance.
EchocardiographyThe transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probabable' or 'almost certain' evidence of endocarditis[8][9].
[Discussion is needed here, including transthoracic versus transesophageal]
Micro-organisms responsible
Many types of organism can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is removed, and any growth is noted and identified.
Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia.
If the bacteraemia was introduced through the skin, such as contamination in surgery, during catheterisation, or in an IV drug user, Staphylococcus aureus is common.
A third important cause of endocarditis is Enterococci. These bacteria enter the bloodstream as a consequence of abnormalities in the gastrointestinal or urinary tracts. Enterococci are increasingly recognized as causes of nosocomial or hospital-acquired endocarditis. This contrasts with alpha-haemolytic streptococci and Staphylococcus aureus which are causes of community-acquired endocarditis.
Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific.
Candida albicans, a yeast, is associated with IV drug users and the immunocompromised.
Pseudomonas species, which are very resilient organisms that thrive in water, may contaminate street drugs that have been contaminated with drinking water.
Streptococcus bovis, which is part of the natural flora of the bowel, tends to present when the patient has bowel cancer.
HACEK organisms are a group of bacteria that live on the dental gums, and are associated with IV drug users who contaminate their needles with saliva.
Treatment
High dose antibiotics are administered by the intravenous route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adherent to them are supplied by blood vessels. Antibiotics are continued for a long time, typically two to six weeks. Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed bioprosthetic valves. Infective endocarditis is associated with a 25% mortality.
Non-infective endocarditis
Non-infective or marantic endocarditis is rare. A form of sterile endocarditis is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and the antiphospholipid syndrome. Non-infective endocarditis may also occur in patients with cancers, particularly mucinous adenocarcinoma.
References
^ Durack D, Lukes A, Bright D (1994). "New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service.". Am J Med 96 (3): 200-9. PMID 8154507.
^ a b Weisse A, Heller D, Schimenti R, Montgomery R, Kapila R (1993). "The febrile parenteral drug user: a prospective study in 121 patients.". Am J Med 94 (3): 274-80. PMID 8452151.
^ a b Samet J, Shevitz A, Fowle J, Singer D (1990). "Hospitalization decision in febrile intravenous drug users.". Am J Med 89 (1): 53-7. PMID 2368794.
^ a b c Marantz P, Linzer M, Feiner C, Feinstein S, Kozin A, Friedland G (1987). "Inability to predict diagnosis in febrile intravenous drug abusers.". Ann Intern Med 106 (6): 823-8. PMID 3579068.
^ a b Leibovici L, Cohen O, Wysenbeek A (1990). "Occult bacterial infection in adults with unexplained fever. Validation of a diagnostic index.". Arch Intern Med 150 (6): 1270-2. PMID 2353860.
^ a b Mellors J, Horwitz R, Harvey M, Horwitz S (1987). "A simple index to identify occult bacterial infection in adults with acute unexplained fever.". Arch Intern Med 147 (4): 666-71. PMID 3827454.
^ Kaech C, Elzi L, Sendi P, Frei R, Laifer G, Bassetti S, Fluckiger U (2006). "Course and outcome of Staphylococcus aureus bacteraemia: a retrospective analysis of 308 episodes in a Swiss tertiary-care centre.". Clin Microbiol Infect 12 (4): 345-52. PMID 16524411.
^ Shively B, Gurule F, Roldan C, Leggett J, Schiller N (1991). "Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis.". J Am Coll Cardiol 18 (2): 391-7. PMID 1856406. ^ Erbel R, Rohmann S, Drexler M, Mohr-Kahaly S, Gerharz C, Iversen S, Oelert H, Meyer J (1988). "Improved diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approach. A prospective study.". Eur Heart J 9 (1): 43-53. PMID 3345769

Aortic valve stenosis

Aortic valve stenosis
Aortic valve stenosis (AS) is a heart condition caused by the incomplete opening of the aortic valve.
The aortic valve controls the direction of blood flow from the left ventricle to the aorta. When in good working order, the aortic valve does not impede the flow of blood between these two spaces. Under some circumstances, the aortic valve becomes narrower than normal, impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS.
Contents

1 Pathophysiology
2 Etiology
3 Prevalence
4 Physical examination
5 The electrocardiogram (ECG) in aortic stenosis
6 Major complications of aortic stenosis
6.1 Congestive heart failure
6.2 Syncope
6.3 Angina
7 Associated symptoms
8 Cautions
9 Calculation of valve area
9.1 Planimetry
9.2 The continuity equation
9.3 The Gorlin equation
9.4 The Hakki equation
10 References

Frank-Starling law of the heart

Frank-Starling law of the heart
The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
Effectively, this means that the force of contraction will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fibre. The force that any single muscle fibre generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibres is related to the end-diastolic volume of the ventricle. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometres, a length which is rarely exceeded in the normal heart.
This can be seen most dramatically in the case of a premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end diastolic volume. Because of the Frank-Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.
For example, during venoconstriction the end diastolic volume increases, increasing preload, this will increase stroke volume. The heart will pump what it receives.
The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.
History
The law is named after the two physiologists, Otto Frank and Ernest Starling who first described it.
Long before the development of the sliding filament hypothesis and our understanding that active tension depends on the sarcomere's length, in 1914 Ernest Starling hypothesized that "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." Therefore, the initial length of myocardial fibers determines the work done during the cardiac cycle.
See also
Starling equation

Cardiac output

Cardiac output
From Wikipedia, the free encyclopedia
Cardiac output is the volume of blood being pumped by the heart, in particular a ventricle in a minute. It is equal to the heart rate multiplied by the stroke volume.
Therefore, if there are 70 beats per minute, and 70 ml blood is ejected with each beat of the heart, the cardiac output is 4900 ml/minute. This value is typical for an average adult at rest, although cardiac output may reach up to 30 liters/minute during extreme exercise.
When cardiac output increases in a healthy but untrained individual, most of the increase can be attributed to increase in heart rate. Change of posture, increased sympathetic nervous system activity, and decreased parasympathetic nervous system activity can also increase cardiac output. Heart rate can vary by a factor of approximately 3, between 60 and 180 beats per minute, whilst stroke volume can vary between 70 and 120 ml, a factor of only 1.7.
Contents

1 Measuring Cardiac Output
1.1 The Fick Principle
1.2 Dilution methods
1.3 Doppler method
1.4 Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
1.5 PulseCO and PiCCO Technology
1.6 FloTrac technology
1.7 Impedance plethysmography
2 Equations

//
Measuring Cardiac Output
There are many invasive and several non-invasive methods for measuring cardiac output in mammals.
A non-invasive method, often used in teaching students of physiology, reasons as follows:
The pressure in the heart rises as blood is forced into the aorta
The more stretched the aorta, the greater the pulse pressure
In healthy young subjects, each additional 2ml of blood results in a 1 mmHg rise in pressure
Therefore Stroke volume = 2ml x Pulse pressure
Cardiac Output is therefore 2ml x Pulse Pressure x Heart Rate
The Fick Principle
Fick principle involves measuring:
VO2 consumption per minute using a spirometer (with the subject re-breathing air) and a CO2 absorber
the oxygen content of blood taken from the pulmonary artery (representing venous blood)
the oxygen content of blood from a cannula in a peripheral artery (representing arterial blood)
From these values, we know that:
where CO = Cardiac Output, CA = Oxygen concentration of arterial blood and CV = Oxygen concentration of venous blood.
This allows us to say
and therefore calculate cardiac output.
Dilution methods
This method measures how fast flowing blood can dilute an indicator substance introduced to the circulatory system, usually using a pulmonary artery catheter. Early methods used a dye, the cardiac output being inversely proportional to the concentration of dye sampled downstream. More specifically, the cardiac output is equal to the quantity of indicator dye injected divided by the area under the dilution curve measured downstream (the Stewart-Hamilton equation):
The trapezoid rule is often used as an approximation of this integral. A more modern technique is to use cold saline as the indicator, and then measure the change in temperature downstream. Cardiac output can be affected by the phase of respiration, especially under mechanical ventilation, and should therefore be measured at a defined phase of the respiratory cycle (typically end-expiratory).
Doppler method
This technique uses ultrasound and the Doppler effect to measure cardiac output. The blood velocity through the aorta cause a 'Doppler shift' in the frequency of the returning ultrasound waves. Echocardiographic measurement of the aortic root cross-sectional area (or, alternatively, the descending aorta area) multiplied by the measured velocity time integral of flow through that area and heart rate, yields the cardiac output.
Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
The pulmonary artery catheter (PAC) also known as the Swan-Ganz thermodilution catheter provides right heart blood pressures. Using the PAC thermodilution cardiac output can be measured. Modern catheters are fitted with a distal heated filament, which allows automatic thermodilution measurement via heating the blood and measuring the resultant thermodilution trace. This provides near continuous cardiac output monitoring. The PAC is used in assessment of haemodynamic status and direct intracardiac and pulmonary artery pressures. The distal (pulmonary artery) port allows sampling of mixed venous blood for the assessment of oxygen transport and the calculation of derived parameters such as oxygen consumption, oxygen utilization coefficient, and intrapulmonary shunt fraction.
The PAC is balloon tipped which can be inflated to occlude the pulmonary artery, the subsequence back pressure is a reflection of the left atrial filling pressure and until recently was considered a good indicator of preload.
The pulmonary artery wedge pressure (PAWP) has been superseded by more reliable techniques such as intrathoracic blood volume or stroke volume variation as indicators of volume status. The PAC also allows sampling of mixed venous blood, the oxygen content of which can be used to indicate the adequacy of overall oxygen delivery. The PAC has fallen out of common use as clinicians favour less invasive, less hazardous technologies for monitoring haemodynamic status. Considerable controversy exists over whether the PAC increases mortality; recent studies suggest it neither increases nor improves mortality. Complications such as cardiac tamponade, pulmonary artery rupture and air emboli are a danger.
PulseCO and PiCCO Technology
PiCCO (PULSION Medical Systems AG, Munich, Germany) and PulseCO (LiDCO Ltd, London, England) generate continuous cardiac output by analysis of the arterial blood pressure waveform. In both cases, an independent technique is required to provide initial calibration of the continuous cardiac output analysis, as arterial waveform analysis cannot account for unmeasured variables such as compliance of the vascular tree.
In the case of PiCCO, transpulmonary thermodilution is used as the independent technique. This uses the Stewart-Hamilton principle outlined above, but measured from central venous line to a central (i.e. femoral or axillary) arterial line. The cardiac output derived from this cold-saline thermodilution is used to calibrate the arterial pulse contour analysis, which can then provide continuous cardiac output monitoring. The PiCCO algorithm is dependent on blood pressure waveform morphology (i.e. mathematical analysis of the pulse contour waveform) and calculates continuous cardiac output as described by Wesseling and co-workers. Transpulmonary thermodilution spans right heart, pulmonary circulation and left heart; this allows further mathematical analysis of the thermodilution curve, giving measurements of cardiac filling volumes (GEDV), intrathoracic blood volume, and extravascular lung water.
In the case of LiDCO, the independent calibration technique is lithium dilution, again using the Stewart-Hamilton principle. Lithium dilution has the advantage of being usable from a peripheral vein to a peripheral arterial line; however, it does not provide information on cardiac filling volumes and extravascular lung water. Dilution measurements cannot be performed too frequently, and can be subject to error in the presence of certain muscle relaxants. The PulseCO algorithm used by LiDCO is based on pulse power derivation and is not dependent on waveform morphology.
FloTrac technology
A more recent development is the FloTrac system which can derive cardiac output from the arterial waveform without the need for an independent method of calibration. Hence continuous cardiac output can be measured directly from a conventional arterial line. This method has yet to be extensively evaluated, but early studies suggest that it is accurate. Another similar system that uses the arterial pulse is the pressure recording analytical method (PRAM). Neither the FloTrac nor the PRAM require external calibration.
Impedance plethysmography
This advanced technique was developed by NASA, it measures changing impedance in the chest as the heart beats to calculate cardiac output. This technique has progressed clinically (often called BioZ, i.e. biologic impedance, as promoted by the leading manufacturer in the US) and allows low cost, non-invasive estimations of cardiac output and total peripheral resistance, using only 4 skin electrodes, with minimal removal of clothing in physician offices having the needed equipment.
Equations
By simplifying D'arcy's Law, we get the equation that
When applied to the circulatory system, we get:
Where ABP = Aortic (or Arterial) Blood Pressure, RAP = Right Atrial Pressure and TPR = Total Peripheral Resistance.
However, as ABP>>RAP, and RAP is approximately 0, this can be simplified to:
Physiologists will often re-arrange this equation, making ABP the subject, to study the body's responses.
As has already been stated, Cardiac Output is also the product of the heart rate and the stroke volume, which allows us to say: