Congenital heart disease is a relatively common problem with approximately one baby in 100 births having some abnormality of the cardiovascular system. 97% of these events cannot be ascribed to a particular cause. Of the remaining 3% the common causes are maternal rubella (german measles) which has occurred in the first two months of pregnancy. Down's syndrome may result in congenital abnormalities (Chromosome abnormality).
Most abnormalities are the result of an abnormal routing of the blood or obstruction of the blood flow. Re-routing indicates the presence of a shunt which is an abnormal passage of blood from one side to the other. In right to left shunt some poorly oxygenated venous blood bypasses the lungs and appears in the left ventricle., in the aorta and throughout the body. These babies is often referred to as "blue babies" due to the poorly oxygenated blood imparting a bluish tint to the lips skin and nail beds. In left to right shunting arterial blood which is fully oxygenated passes to the right side of the heart. This does not impart cyanosis. No cyanosis occurs when malformations in which there are obstructions, but not re-routing are present.

Diagnostic tools for congenital heart disease are physical examination, medical ghistory, ECG, echocardiography and chest X-ray. Where surgical intervention is required or further diagnostic confirmation is needed, cardiac catherisation and angiocardiography are performed. During catherisation an intra cardiac catheter may be used to measure pressure and blood oxygenation in various parts of the heart.
Laboratory Diagnosis of Congenital Heart Disease:

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Rheumatic Fever: Group A streptococci amy cause infection of the throat and tonsils which if untreated may cause an immunologic reaction. This occurs in about 0.3% of those infected. The major symptoms of rheumatic fever are: carditis, polyarthritis, chorea, subcutaneous nodules, and a rash called erythema marginatum. This may take 2 to 3 weeks to develop. This is known as acute rheumatic fever Inflammation of the large joints of the body, known as polyarthritis, occurs in about 85% of cases. Polyarthritis is arthritis in a number of joints at a time. Chorea is a neurologic syndrome that may appear after a latent period of several months. Chorea is seen as rapid, purposeless, involuntary movements in the extremities and the face. Subcutaneous nodules are firm, painless lesions that occur over bony surfaces just under the skin. Erythema marginatum is a rash that appears mostly on the trunk and extremities.
Carditis is the most significant manifestation of rheumatic fever because it may cause permanent organ damage or death. Carditis is frequently mild or asymptomatic and therefore difficult to detect. Although not fully understood, a person's immune system response to a streptococcal infection appears to be the result of autoimmunity induced by streptococcal antigens that cross react with the heart muscle.This can lead to tissue degeneration, most frequently heart valve tissue, and subsequently, cardiac disability or death.
Damage to the heart valves interferes with their normal opening and closing and may result in heart failure. Rheumatic valvulitis also increases to suspectibility to infective endocarditis. Thrombi may form on the injured endocardial lining of the valves. atrium, or atrial appendage. These may fragment and circulate as emboli, occludig arteries and causing brain, kidney, intestine, spleen or limb infarction.
In approximately 65% of cases inflammation occurs. The myocardial lesions are probably
The average duration of an attack of acute rheumatic fever is 3 months or longer. After the acute attack has subsided, many people are left with damaged heart valves (rheumatic heart disease). Some people will have recurrent acute attacks of rheumatic fever, frequently causing more damage to the heart valves.

How is it diagnosed?
May be difficult to diagnose. There are no specific laboratory tests to diagnose acute rheumatic fever. In general, rheumatic fever can be diagnosed with documentation of a recent infection with group A streptococcal infection and observation of one or more of the major symptoms (described above).
Laboratory Findings in Rheumatic Heart Disease:

Cor pulmonale is heart disease that occurs secondary to lung disease.It is defined as a complication of disorders that slow or block blood flow in the lungs, resulting from raised blood pressure in the lungs. A deadly form of Congestive Heart Failure, it creates enlargement or hypertrophy of the right ventricle in response to increased right ventricular afterload. Cor Pulmonale presents as right heart failure, which is defined by a sustained increase in right ventricular pressures combined with an inability to balance the cardiac output in response to exercise or other stimuli.
Cor pul- monale may be a consequence of any of the following long-standing pulmonary disorders: advanced emphysema, chronic bronchitis, pulmonary fibrosis, and cystic fibrosis. Both sexes and all ages are effected by this devistating illness, but it is most common in men over 40.
These disorders all cause a decreased cross-sectional area of the pulmonary vascular bed and hypoxemia, resulting in pulmonary arterial hyper- tension. Increased pulmopary vascular resistance causes the right ventricle of the heart to enlarge and fail, resulting in right-sided congestive heart failure. Arterial hypoxemia and tissue hypoxia stimulate erythropoietin formation. This might result in secondary erythrocytosis and hypervolemia, which further aggravate congestive failure.

SYMPTOMS
There are generally no symptoms in the early stages.
The most common presenting complaints of patients with cor pulmonale are:
dyspnea on exertion
fatigue
Syncope and near syncope
chest pain
palpitations
leg edema
Distended neck veins
Bluish skin
Enlarged liver and swollen abdomen

DIAGNOSIS Physical findings may be subtle early. Jugular venous pressures are always increased. Cardiac palpation may reveal a right ventricular heave. P2 is increased and moves closer to A2 as the pulmonary pressures increase. Eventually S2 may be fixed and paradoxically split. Increased right atrial pressures may lead to dependent edema, hepatojugular reflux, and ascites.
The chest x-ray may reveal right ventricular hypertrophy, manifest as filling of the retrocardiac space on the lateral film, and increased PA size.
The ECG may be normal or show right atrial and ventricular enlargement as well as an R axis deviation. Supraventricular tachycardias are common.
Diagnosis is often expected based on clinical examination although findings may be subtle. Increasingly, the diagnosis of pulmonary hypertension is made with echocardiagraphy which demonstrates increased right ventricular size and wall thickness as well as evidence of ventricular interdependence (i.e. the septum moves with the right ventricle instead of the left). In the presence of tricuspid regurgitation (which is almost invariably present in right heart failure), pulmonary artery pressures can be estimated based on the velocity of the regurgitant jet. The diagnosis is confirmed with right heart catheterization which demonstrates elevated right atrial, ventricular and pulmonary artery pressures. Left atrial pressure is normal unless there is mitral stenosis or left ventricular failure. In addition, measurement of chamber oxygen saturations during right heart catheterization can be diagnostic for left to right shunts.


Laboratory Findings in Pulmonary Heart Disease:

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Myocardial ischaemia is the most common cause of death in the western world, and encompasses the range of conditions in which the myocardium, or heart muscle, is deprived of oxygen to some extent, and, as a result, becomes damaged (ischaemic). The most common ischaemic heart disease is angina and it is caused by narrowing of the arteries (atherosclerosis).

Despite the relatively small size of the heart, about 20% of the total cardiac output is needed to provide nourishment for the heart itself. The cardiac blood supply is carried by the coronary arteries, which are so named because they encircle the heart like a crown. Approximately 15 gallons of blood are pumped through these arteries each hour. The heart muscle extracts more oxygen from the blood than does any other tissue in the body. A cross-sectional reduction of 60% to 70% in the arterial lumen is usually required before clinical symptoms of reduced coronary blood flow appear. The major underlying cause of coronary-artery obstruction is the develop- ment of atherosclerotic plaques. Recent studies have demonstrated that in- creased platelet aggregation and coronary-arterial spasm may contribute to the formation of thrombi or blood clots in the coronary arteries.12 A thrombus may partially or completely occlude a coronary artery. When the vessel lumen is partially obstructed, inadequate amounts of blood and oxygen are available to support the needs of the heart muscle. This condition is known as myocardial ischemia. If the blood and oxygen supplies to a portion of heart muscle become severely or totally reduced, death of heart cells results. This is called a myocardial infarction or heart attack (Fig. 1-4). If collateral blood vessels have formed, as occurs when vessel narrowing is gradual, coronary-artery occlusion might not result in infarction. An infarct is diagnosed by clinical signs and symptoms, electrocardiogram (ECG), and the finding of an elevation of certain enzymes in the blood. In approximately 30% of patients with myocardial infarction, the ECG shows no evidence of an infarct. This is most frequently the case postopera- tively, in diabetics, in hypertensives, in patients with electrical cardiac conduc- tion defects, or in those with previous myocardial infarctions. In these situa- tions, findings of elevated cardiac enzymes in the circulation are essential for establishing the diagnosis.

Laboratory Findings in Coronary Heart Disease:

Please note in this EKG strip the fast regular Atrial rhythm, the P-R interval is normal or increased in length. Also note that the QRS Complex can be normal or prolonged due to abnormal condition patterns, also wide QRS complexes can be caused by Bundle Branch Blocks.

Clinical Terms:

Atrial Tachycardia may be seen as Uniform or Multiform. Multiform Atrial Tachycardia is seen most often in patients with respiratory failure, or severe respiratory complications.

Two of the most common forms of Uniform Atrial Tachycardia are:

(a.) Paroxysmal Supra ventricular Tachycardia, (PSVT).

(b.) Non paroxysmal Atrial Tachycardia.

Other forms of Uniform Supra Ventricular Tachycardia:

Junctional Tachycardia

Atrial Flutter

Multi-focal Atrial Tachycardia

Paroxysmal Supra Ventricular Tachycardia:

Paroxysmal Supra Ventricular Tachycardia is a repeating clinical syndrome that is characterized by sudden onsets of Tachycardia, that can last a from few seconds to hours in duration.

Paroxysmal Supra Ventricular Tachycardia occurs due to a reentry mechanism, usually involving the AV-Node, or an extra AV-Node bypass tract such as Wolf-Parkinson syndrome.

Onset can be initiated by closely coupled, Pre-Atrial Contractions ( PAC) with a prolonged P-R interval. This syndrome can last for a number of years in patients.

Commonly associated causes: Irritability of of Atrial or AV Junctional tissues, (Supra ventricular).

Treatment: The syndrome can be quickly terminated by initiating a Vagal maneuver in these patients or treated with Adenosine, Verapamil, Beta Blockers or Synchronized Cardiac Conversion . .

Prognosis: Young individuals usually tolerate this condition well if no underlying pathology exists. In elderly patients and individuals with underlying clinical cardiac pathology, this condition can lead to cardiac ischemia, infarction, or possible pulmonary edema. The prognosis for individuals with cardiac pathology is guarded.

EKG ANALYSIS of PSVT:

The SA node or the Junctional tissues are acting as the pacemaker.

The heart rate is greater then 150 beats a minute.

The Atrial Rhythm is regular.

The P-wave is very hard to measure due to the rapid heart rate.

The P-R interval may not be accurately measured. Depending on the conduction pattern the P-R interval may be prolonged due to blocks, or vary as seen in Atrial Flutter, Premature Junctional Complexes

The QRS Complex appears normal, but very narrow, or wide due to blocked conduction paths.

Example of an Extra AV-Node bypass mechanism PSVT:

Laboratory Findings in Paroxysmal Supra Ventricular Tachardia:

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Inflammation of the lining of the heart or heart valves is called endocarditis. This is most frequently caused by bacteria, but it may also result from fungal or rickettsial infection. Altered or abnormal endocardial surfaces are particularly susceptible to the deposition and aggregation of circulating bacteria. Altered endocardial surfaces occur on a valve that has been previously damaged by rheumatic fever or syphilis. These are less common today than heretofore. Certain congenital malformations of the heart, or the presence of an artificial heart valve or graft, also predispose a patient to the development of endocarditis.

Endocarditis usually involves the mitral and aortic valves, producing small, wartlike growths or vegetations (Fig. 1-7). The growths, which usually contain a mixture of bacteria, blood cells, and fibrin, may deform or even destroy heart valves. Vegetations may break off, seed the bloodstream with bacteria, and enter the circulation as emboli. Emboli block peripheral arteries, forming small abscesses and infected foci of tissue necrosis known as septic infarcts. These may occur in the brain, kidneys, spleen, or heart.

Acute bacterial endocarditis results from circulating virulent bacteria, such Staphylococcus aureus and gram-negative cocci. These bacteria are deposited on intact heart valves and cause their destruction. The severe damage to heart valves usually results in heart failure. More frequently, the process of infection is slow and is referred to as subacute bacterial endocarditis (SBE). SBE is caused by organisms of low virulence that occur normally in the upper-respiratory and gastrointestinal tracts. Such transient bacteremia may occur following dental traction, tonsillectomy, endoscopic examination, barium enema, or even vigorous chewing. Streptococcus viridans and group D streptococci are the most frequent causes of SBE. These bacteria are deposited on previously damaged heart valves and produce smaller vegetations than those occurring in acute bacterial endocarditis. In SBE, the valves are not usually destroyed. Bacteria multiply and are discharged from endocardial vegetations into the circulation at a relatively constant rate. They are frequently sources of embolization, characteristically producing capillary thrombi and petechiae.

Hospital-acquired infections and septicemia in addicts using intravenous drugs have resulted in an increased incidence of infections with Staphylococcus epidermidis, gram-negative bacilli, Candida, and "opportunistic" microorganisms. The increased incidence of hospital-acquired infections is associated with greater use of intravascular prostheses, including prosthetic cardiac valves, and with the use of invasive mechanical life-support and monitoring systems. Death may occur as a result of congestive heart failure, neurologic involvement, or overwhelming infection.

Laboratory Findings in :Infective Endocarditis

Definition

Description

Causes & symptoms

Diagnosis

Treatment

Prognosis

Prevention

Inflammation of the pericardial sac around the heart is called pericarditis. Acute pericarditis is associated with the accumulation of fluid in the pericardial cavity (Fig. 1-6). When the fluid causes pressure on the heart, interfering with blood flow into the heart's chambers, this compression is called cardiac tamponade. If the inflammation persists, chronic pericarditis results; the formation of fibrous tissue in the pericardium is referred to as constrictive pericarditis.

Acute pericarditis is usually caused by infection with coxsackie B virus, echovirus, or influenza virus. Viruses are assumed to be bloodbome, but they may originate from viral myocarditis. Pyogenic bacteria usually invade the pericardium from an adjacent infected site such as the lung, pleura, or medias- tinum. Pericarditis may also be due to rheumatic fever, bacterial infection, uremia, surgery, radiation, metastatic malignant tumors, or myocardial infarction.

Chronic pericarditis is usually due to tuberculosis, hypothyroidism, metastatic tumor, or lupus erythematosus. Chronic constrictive pericarditis, especially following tuberculosis, may result in congestive heart failure and marked hepatic congestion.

Laboratory Findings in : Pericarditis

CARDIOMYOPATHIES Disease of the heart muscle that is not due to impaired coronary circulation and ischemia is called cardiomyopathy. This may be either primary or secondary to a specific disease, which often also involves other organs.
Factors that have been suggested as possible causes of primary card iomyopathy include viral infections, hyperimmune responses, genetic abnormlality of the heart muscle, nutritional deficiency, lack of oxygen, toxins, and drugs.
Secondary cardiomyopathy occurs associated with many disorders. A recent classification follows;
Infective Cardiomyopathies
Viral-coxsackie B virus and echovirus are the most frequent causes of myocarditis
Rickettsial, fungal, parasitologic
Metabolic Cardiomyopathies
Endocrine-thyrotoxicosis, hypothyroidism, adrenal cortical insufficiency, pheochromocytoma, acromegaly
Familial storage disease-hemochromatosis, glycogen storage disease eficiency-potassium-metabolism disturbances, magnesium deficiency, and nutritional disorders
Amyloidosis
General System Diseases
Connective tissue disorders-systemic lupus erythematosus, polyarteritis nodosa, rheumatoid arthritis, scleroderma, dermatomyositis
Infiltrations and granulomas-sarcoidosis, leukemia
Heredofamilial Cardiomyopathies
Muscular dystrophies
Friedreich's ataxia
Sensitivity and Toxic Reactions
Sulfonamides
Penicillin
Alcohol
Two principal functional types of cardiomyopathy are described: hyper trophic and dilated. The former results in an increased muscle mass, usually of the left ventricle. This diminishes the volumes of the left ventricular chamber and the blood flowing through it. In dilated cardiomyopathy, the volumes of one or both ventricular chambers increase. This impairs normal cardiac pumping function. Dilated cardiomyopathy is also termed congestive cardiomyopathy, because the impaired circulation results in the vascular congestion of most organs.
Laboratory Findings in :Cardiomyopathies

CONGESTIVE HEART FAILURE

Congestive heart failure is a symptom complex that is a consequence of impaired cardiac pumping ability and fluid retention. Impaired cardiac pumping ability may be due to hypertension or to diseases of heart valves, heart muscle, or coronary arteries.

When there is a decrease in cardiac output, increased backward pressure on the venous circulation causes the volume of blood within the cardiovascular system to become abnormally expanded. This diminishes blood flow in all organs and tissues. There is also an excessive accumulation of fluid in the lungs, legs, and other body tissues. This fluid accumulation is known as edema. Renal retention of salt and water further increases edema.

In congestive heart failure, diminished blood flow and vascular engorgement result in impairment of function of the liver, kidneys, and lungs.

Laboratory Findings in :Congestive Heart failure

Arteriosclerosis refers to the process of thickening and loss of elasticity of the arterial wall in any artery. Atherosclerosis is the most common type of arteriosclerosis and is characterized by complex degenerative changes involving predominantly the inner, or intimal, layer of medium to large arteries. Atherosclerosis is regarded as a pathologic response of the vessel wall to chronic multifactorial injury. Endothelial damage, platelet aggregation, and smooth- muscle proliferation are important early events in the development of an atherosclerotic lesion. Platelets contribute to the development of atherosclerosis in at least two different ways: by the release from activated platelets of chemical mediators that damage the vessel wall or alter its metabolism and by repeated microthrombus and microembolus formation, which augment occlusion of already damaged arteries. The evolution of an atherosclerotic lesion from childhood includes the following stages:i5 (Fig. 1-8)

1. Damage to the endothelial lining
2. Focal accumulation of intimal lipids (fatty streak)
3. Proliferation of smooth-muscle cells (fibrous plaque)
4. Cell death and injury
5. Formation of a necrotic, lipid-rich, complicated lesion

It is generally accepted that the cholesterol of the atheromatous plaque is derived chiefly from plasma cholesterol. When an atheromatous plaque develops, it interferes with the normal oxygenation and nourishment of the arterial wall, producing further damage. Bleeding may occur into a plaque, or the plaque surface may ulcerate. These events stimulate formation of an overlying blood clot or thrombus, which results in partial or complete obstruction of the arterial lumen, bringing about impairment or complete interruption of circulation. The latter causes death of tissue, known as infarction or gangrene.

The consequences of impaired blood flow depend on which organ or tissue is affected and on the rapidity of the process. Gradual vascular occlusion results in the formation of many new small collateral vessels, which can maintain tissue viability with diminished function. Involvement of the aorta or coronary, cere-' bral, or peripheral vessels is quite variable, and many patients may have more than one area affected. Coronary arteries tend to be involved earlier than are cerebral or peripheral arteries.

Atherosclerosis may not produce occlusive disease but, in some patients, it leads to a "ballooning out" of the arterial wall; this is called an aneurysm. The consequences of atherosclerotic occlusion of different vessels include the following:

• Coronary artery-myocardial infarct (heart attack)
• Cerebral artery-cerebral infarct (stroke)
• Peripheral artery-gangrene
• Renal artery-renal infarct
• Mesenteric artery-gangrene of the intestines

Hyperlipidemia is an elevation of plasma cholesterol or triglyceride. Water insoluble cholesterol and other plasma lipids are carried in the bloodstream by emulsified water-soluble compounds called lipoproteins. Plasma lipoproteins may be separated and classified by means of ultracentrifugation and electrophoresis. Through ultracentrifugation, several types of lipoproteins have been identified based on their different densities:

1. Chylomicrons
2. Very low-density lipoproteins (VLDL)
3. Low-density lipoproteins (LDL)
4. High-density lipoproteins (HDL).

Through electrophoresis, the lipoproteins are classified on the basis of their migration:

1. Chylomicrons do not leave their points of origin.
2. VLDL (prebetalipoproteins) migrate near the ß-globulins
3. LDL ({3-lipoproteins) migrate with the ß-globulins.
4. HDL (a-lipoproteins) migrate with the a-globulins.
Using electrophoresis of the plasma lipoproteins, measurement of plasma cholesterol and triglyceride, and observation of plasma clarity or opacity, Fredrickson, Levy, and Lees of the National Heart Institute proposed a system for classifying the hyperlipoproteinemias into several types. It has en observed that patients with Type II hyperlipoproteinemia, which has the highest ß fraction (LDL), have the greatest incidence of coronary heart disease. LDL is found to be associated with cholesterol in atherosclerotic plaques; LDL thus appears to be the most atherogenic of all lipoproteins.

Laboratory Findings in : Athersclerosis

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The word aneurysm is from the Greek, meaning a widening. An aneurysm is a localized abnormal dilatation or ballooning of an artery. It is the result of weakening of the wall of an artery, which is usually secondary to atherosclerosis; may also be caused by syphilis or aging. Due to the combined effects of the pulsatile nature of blood flow and its pressure, the affected artery tends to become progressively larger and frequently ruptures (Fig. 1-10). An aneurysm either dilates throughout its entire circumference, giving a fusiform appearance, or balloons out like a large bubble at only one area on the artery wall. The latter is known as a sacciform or saccular aneurysm (Fig. 1-11). Although an aneurysm may develop in any artery, the abdominal aorta below the origin of the renal arteries is the most common site.

A dissecting aneurysm occurs when a tear in the inner lining of the artery wall allows blood to enter the middle layer, creating a new channel within the arterial wall and blocking the arterial branches from the aorta. The tear is usually located in the ascending aorta. The cause of spontaneous aortic dissection is usually unknown, and intrinsic abnormality in the wall of the aorta is usually not identified. About 70% of patients with aortic dissection have, or have had, systemic hypertension. The most frequent mechanism of death is rupture of the aorta. Diagnosis is usually based on the clinical signs and symptoms that occur when the aneurysm ruptures or occludes various aortic branches.

Laboratory Findings in :Aneursym

Syphilitic Heart Disease

SYPHILITIC CARDIOVASCULAR DISEASES

Syphilis is generalized infection caused by the spirochete Treponema pallidum. Syphilis is acquired through sexual contact. Multiple serious effects on the cardiovascular system appear many years after a patient contracts the original infection. There is damage to the aortic valve ring, resulting in dilatation and backward leakage of blood from the aorta, through the dilated aortic valve, into the left ventricle during each diastole. This backward leakage through the aortic valve is known as insufficiency. The additional workload placed on the left ven- tricle causes enlargement of the heart and often results in congestive heart failure.

Another late cardiovascular complication of syphilis is damage to the me- dial layer of the ascending or thoracic aorta. This results in an aneurysm, which may cause pressure on adjacent thoracic structures and nerves.

Laboratory Findings in :Syphilitic Heart Disease

Raynaud's phenomenon is a condition in which the smallest arteries supplying the fingers or toes go into spasm on exposure to cold or as a result of emotional stresses. Because the small veins remain open, the blood drains out of the capillaries and the fingers or toes become pale, cold, and numb. This may result in ulcers, or even gangrene, of the affected tissues. The condition may be pri- mary or secondary to another disease. The secondary form of Raynaud's phe- nomenon is associated with one of the connective-tissue diseases, such as scleroderma, rheumatoid arthritis, or systemic lupus erythematosus.

Laboratory Findings in :Reynauds Phenomenon ARTERIAL THROMBOSIS AND EMBOLISM

In arterial thrombosis, the initiating features are vascular injury and platelet aggregation. In contrast to its primary occurrence in venous thrombosis, activa- tion of the clotting mechanism is a secondary occurrence in arterial thrombosis. Sudden occlusion of an artery may occur if a thrombus forms at the site of an atherosclerotic plaque or if a thrombus that has formed in the heart or aorta is carried by the bloodstream as an embolus to a peripheral artery. When an artery is blocked suddenly, time is not allowed lor collateral circulation to develop. Tissues supplied by the occluded vessel consequently have diminished blood supplies. Such diminished blood supply is known as ischemia. Other arteries in the affected region undergo secondary spasm, further reducing the blood sup- ply. This may result in tissue death, known as ischemic necrosis, or gangrene. Gangrene is ischemic necrosis plus suppurative inflammation. A segmental i zone of necrosis involving only the region supplied by the occluded vessel is I called an infarct. An infarct secondary to thrombotic or embolic arterial occlu- sion may involve the extremities, heart muscle, kidney, brain, or intestines. Arterial emboli may originate from thrombi in the left heart chambers, from the lining of an atherosclerotic artery, or from ~n aneurysm of the aorta or any of its branches. Cardiac thrombi may form in the left atrium or its appendage in patients with rheumatic heart disease, with narrowing (stenosis) of the mitral valve, or with an irregular heart rhythm, such as atrial fibrillation. A thrombus may also form on the endothelial lining of the heart following a myocardial infarction. This type is known as a mural thrombus. Large emboli may block large arteries, whereas small emboli usually occlude small arteries. In bacterial or infective endocarditis, emboli consisting of bacteria, fibrin, , and blood cells from involved heart valves are usually disseminated throughout the systemic circulation, causing petechiae, small abscesses, and septic infarcts.


Laboratory Findings in :ARTERIAL THROMBOSIS AND EMBOLISM

The most frequent cause of arterial occlusion is atherosclerosis. As occlusion progresses and the blood supply diminishes, the organ or tissue supplied by that artery becomes ischemic, infarcted, and then (possibly) gangrenous. Gan- grene is ischemic necrosis, or death of tissue, with superimposed infection. This most frequently affects the extremities or the intestines when the arterial blood flow is interrupted. When venous occlusion also occurs this is referred to as "wet" gangrene because fluid is retained in the tissues.

Laboratory Findings in :Gangrene

The necrotizing vasculitides are a group of inflammatory diseases of the blood vessels in which there is destruction of the vessel wall. The most common form of necrotizing vasculitis is allergic, or hypersensitivity, vasculitis.16 This in- volves small blood vessels, is manifested by palpable small hemorrhages (pur- pura) of the skin, and appears to be due to immune-complex deposition in the involved vessels. In addition to cutaneous involvement, there may also be involvement of small vessels of the kidneys, joints, gastrointestinal tract, lungs, or central ner- vous system. The most common causes include streptococcal infection and drug inges- tion. Other causes include hepatitis antigen, foreign proteins, and exposure to insecticides or petroleum products. Immunofluorescent studies of biopsy specimens from active lesions dem- onstrate immunoglobulins and complement distributed in a granular pattern within the vessel walls. This finding is presumptive evidence that the disease is due to immune complexes. An immune complex is a substance composed of antigen (i.e., streptococcal protein or hepatitis B surface antigen [HBsAg]) that is combined with an antibody. If relatively small, this complex remains soluble within the circulation and causes no problems. If large, it is usually cleared by phagocytes. In some patients, however, this complex may deposit within vessel walls, bind and activate complement, and attract leukocytes. Neutrophils re- lease enzymes that damage vessel walls, allowing red cells to leak into the surrounding tissue. This results in the formation of palpable purpura.
Laboratory Findings in :Hypersensitivity Vasculitis

Peripheral venous disease refers to any interference with venous return of deoxygenated blood from the tissues to the heart and lungs. Veins that carry blood from regions of the body below the heart must work in opposition to the force of gravity. The direction of flow is aided by skeletal-muscle contractions and by venous valves, which prevent blood from flowing backward (Fig. 1-12). The most common problem affecting the venous system is that of varicosity; this dilatation occurs most often in the superficial veins of the legs. The actual cause is uncertain, although heredity may playa role. Varicosities may develop because the valves fail to function properly. This results in backward blood flow, increased venous resistance, venous stagnation, pooling, venous dilata- tion, and possibly thrombus formation. A thrombus or clot in a vein may partly or completely stop the flow of blood.

In the presence of diminished blood flow, the fluidity of blood is main- tained by an intact endothelium, abundant plasma coagulation inhibitors, and vigorous fibrinolysis. When the last two mechanisms fail, a thrombus may be formed, even over an intact endothelium. Activation of the coagulation system is primarily responsible for the formation of venous thrombi. Platelet aggrega- tion, vascular stasis, and endothelial damage play secondary roles. This process is in contrast to that in arterial thrombosis, in which vascular injury and platelet aggregation are of primary importance.

Venous thrombosis is a serious medical disorder because of its possible complication: pulmonary embolism. If a portion of a venous thrombus breaks off, it is called an embolus. Major emboli are more likely to come from thrombi proximal to the knee, which usually have extended from the calf. An embolus is carried in the venous circulation into the right side of the heart and, through the pulmonary arteries, into the lungs. This results in decreased circulation to the affected portion of the lung and may cause localized death of tissue or infarction.

Venous thromboembolism may occur in an apparently healthy person, but it is more likely to strike the elderly, those who are immobilized for a long time (e.g., stroke and arthritis victims and patients in plaster casts), those who have stasis of blood due to varicosities, and those who have recently undergone surgery, childbirth, heart failure, or shock. It may also occur after certain infec- tions and malignant tumors or with the use of oral contraceptives. It is one of the most common causes of death following major orthopedic surgery and is a contributing factor in deaths among patients with chronic cardiac and pulmo- nary diseases.


Laboratory Findings in :Peripheral Venous Disease

Shock is the state of circulatory collapse that is frequently associated with insuf- .I ficient return of blood to the heart and manifested by persisting deficiency of blood flow to peripheral tissues. Any condition that causes deficient blood vol- ume, peripheral vasodilatation, cardiac insufficiency, or combinations of these factors may initiate a series of functional alterations and compensatory re- sponses that constitute the clinical syndrome of shock. Shock may follow severe trauma, major surgery, massive hemorrhage, dehydration, myocardial infarc- tion, overwhelming infection, poisoning, or a drug reaction. Circulatory collapse is manifested by a fall in cardiac output, a decrease in blood volume, a fall in blood pressure, and a rapid pulse rate. The diagnosis is based primarily on the patient's history and clinical findings. The laboratory findings are secondary.


Laboratory Findings in :Shock

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