Normal Heart
Refer to Reference Ranges Page

For details on the disease click here.
Laboratory Findings

Right to Left Shunt:

• Decreased arterial pO2
  Decreased pO2 is seen with ventilation-perfusion mismatch, alveolar-capilliary block, right to left shunts and hypoventilation.
  Reference Interval: 11.0-13.5 kPa Method: Oxygen specific electrode
• Increased Red Blood Count, Haematocrit Haemoglobin: This is a secondary erythrocytosis which results from arterial hypoxia and tissue hypoxia.
  This stimulates erythropoietin formation and erythropoiesis.


• Caution: Iodine which is present in some X-ray contrast material may cause alteration of some tests of thyroid function


• Complications
  
• Secondary Hypertension
  <
• Myocardial Infarction
  
• Cor Pulmonale
  
• Pericarditis
  
• Infective endocarditis
  
• Congestive heart failure

Rheumatic Fever and Rheumatic Heart Disease

For details on the disease click here.
Rheumatic Fever
There are no specific tests for Rheumatic fever. Some tests are useful in confirming the presence of inflammation and the recent occurrence of streptococcal infection.

Nonspecific tests indicating inflammation:

• Increased ESR (Erythrocyte Sedimentation Rate)


• Increased C-reactive protein


• Leukocytosis

These are used to follow disease activity and response to therapy




• Mild normocytic anaemia - haemoglobin (8 g/dl - 12 g/dl) with an occasional microcyte


• Increased fibrinogen


• Increased alpha2 globulin

These are acute phase reactants indicating acute inflammation.
• Decreased albumin due to haemodilution


Tests indicating current infection

• Throat culture showing Group A streptococci


Tests Indicating Prior Recent Infection

• Elevated serum anti-streptolysin O (ASO) titre

This occurs in 80% of patients convalescing from Streptococcal sore throat. It appears two weeks after infection and peaks at 4-6 weeks - may remain elevated for months. Titre is not related to the severity of th edisease and the rate of fall is not related to the course of the disease.
• Increased anti-deoxyribonuclease (DNase) B titre


• Increased "streptozyme" titre. This measures several streptococcal antibodies


• Synovial fluid analysis may demonstrate an elevated white blood cell count with no crystals or organisms.



Rheumatic Heart Disease


Laboratory Findings of complications:

• Active Rheumatic Fever


• Infective endocarditis


• Congestive heart failure


• PR interval prolongation is present in approximately 25% of all cases and is neither specific to nor diagnostic of ARF.

Useful Links
• Virtual Hospital: Cardiology: Rheumatic Fever and Rheumatic Carditis


• Rheumatic Fever This document contains a good discussion of treatment Regimes (Medication)

Echocardiography may be helpful in establishing carditis. Synovial fluid analysis may demonstrate an elevated white blood cell count with no crystals or organisms.

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Coronary Artery Disease and Myocardial Infarction

LABORATORY FINDINGS

Cardiac Enzymes

• When heart-muscle fibers die, their intracellular enzymes are released from the cells into the surrounding tissue and ultimately appear in the circulating bloodstream. Different enzymes reach peak blood levels at different times following a myocardial infarction (Fig. 1-5). The enzymes of greatest diagnostic value for myocardial infarction are creatine phosphokinase (CPK) and lactate dehydrogenase (LDH).5

• CPK is found primarily in skeletal and myocardial muscle and also in the brain and intestines. There is little or no CPK activity in the lungs, liver, kidneys pancreas, or RBC. CPK activity in the blood begins to rise about 4 hours to 8 hours after myocardial infarction, reaching levels of five times to ten times the upper limit of normal, depending on the size of the infarct. Peak activity usually occurs 18 hours to 24 hours after infarction, and CPK activity returns to normal by the fifth day. CPK activity provides a highly sensitive test, but its low specificity is a drawback to its usefulness as the sole diagnostic laboratory test for myocardial infarction.

• LDH activity is found in almost all human tissues. The liver and skeletal muscle have the greatest concentrations, followed by the heart. LDH is also found in RBC, the kidneys, the lungs, the pancreas, and the brain. LDH activity in the blood starts to rise about 12 hours to 24 hours after myocardial infarction, often reaching levels of two to three times the upper limit of normal. Peak activity usually occurs on the third day following infarction, and activity may remain raised for as long as 10 days postinfarction. This is a sensitive test; however its wide tissue distribution decreases its specificity.

  
  Fig. 1-4. Myocardial infarction caused by blockage of a branch of the anterior descending coronary artery. (Modified)(DeBakey M, Gotto A: The Living Heart, p 123. New York, Raven Press, 1977)
  
  

• The specificity of both CPK and LDH may be greatly increased by electrophoretically separating and quantitating their isoenzymes. An isoenzyme is a varied molecular form of an enzyme. All of the isoenzymes of a particular enzyme have similar catalytic effects on substrates but differ in their physical characteristics.
  
  
• LDH may be electrophoretically separated into five isoenzymes; these are designated as LDHI (fastest migration), LDH2. LDHa. LDH4, and LDHs (slowest migration) (Table 1-1).
  
  

Distribution of LDH Isoenzymes in Normal Tissues

• Release of increased LDHI isoenzyme from the myocardium into the bloodstream following a myocardial infarction results in the preponderant isoenzyme changing from LDH2 (in normal serum) to LDHI. This reversal of isoenzyme predominance is referred to as a "flipped-LDH" pattern.
  This is seen following acute myocardial or renal infarction and in hemolysis associated with prosthetic heart valves, hemolytic anemia, or pernicious anemia. Elevation and predominance of LDHI show far greater specificity for infarction than does elevation of the total LDH enzyme.
  The flipped pattern occurs within 12 hours to 24 hours of the infarction; by 48 hours after infarction, 80% of patients show this pattern. Fewer than 50% of these patients still have flipped patterns after 7 days. CPK may also be electrophoretically separated into isoenzymes: CPK1 (BB), CPK2 (MB), CPK3 (MM) (Table 1-2). Each CPK isoenzyme is made up of a combination of Band/or M subunits. The B polypeptide chain is so called because it has been isolated from the brain, and the M chain is found in skeletal muscle.
  The isoenzyme found in the brain consists of two similar units, termed BB.
  The isoenzyme found in the skeletal muscle consists of two other identical subunits and is termed the MM isoenzyme. Heart tissue has a virtually specific isoenzyme, which is a hybrid of both subunits and is termed MB.
  
  
• CPK-BB, occurring predominantly in brain tissue, is rarely seen in serum even after cerebral infarction because the enzyme does not usually cross the blood-brain barrier. CPK-BB has been found in serum in patients who have had neurosurgery, in patients with certain tumors, and in some patients with bowel infarction. CPK-MM, found predominantly in skeletal muscle, increases in the serum in cases of muscle trauma, in muscular dystrophy, following intramuscular injections, in shock, after major surgical procedures, and following acute myocardial infarction.
  
  
• CPK-MB, found almost exclusively in heart muscle, is usually indicative of an acute myocardial infarction when it is found in serum.
  This is more specific for myocardial damage than is LDH1' Following acute myocardial infarction, CPK-MB appears in 4 hours to 8 hours, reaches peak activity at 18 hours to 24 hours, and may last for another 2 days. CPK-MB always precedes the appearance of a flipped-LDH pattern. CPK-MM, which also occurs in heart muscle, remains elevated 4 days to 5 days following myocardial infarction.
  Myocardial injury other than infarction may also result in serum elevation of CPK-MB. Examples of conditions that injure heart muscle include myocarditis, heart trauma, open heart surgery, coronary angiography, cardiomyopathy, cardiac resuscitation, and electrical cardioversion. CPK-MB may also be present, usually in small amounts, in the following neuromuscular disorders: muscular dystrophies, polymyositis, dermatomyositis, viral myositis, malignant hyperpyrexia, severe skeletal-muscle trauma, and Reye's syndrome.
  The highest sensitivity and specificity in diagnosing acute myocardial infarction are obtained by testing for both LDH and CPK enzymes and isoenzymes on admission, after 24 hours, and again at 48 hours after the onset of symptoms; some suggest testing at 12 hours and 24 hours. The presence of CPK-MB and flipped LDH within 48 hours of the onset of symptoms offers laboratory confirmation of acute myocardial infarction. The presence of CPK-MB alone is insufficient evidence for diagnosing acute myocardial infarction. If CPK-MB does not appear within 48 hours of the onset of chest pain, acute myocardial infarction may be ruled out. CPK-MB occurs in some cases of myocardial infarction in the absence of abnormally elevated total CPK activity.

• Leukocytosis-12,000/,u1 to 20,000/,u1 with 75% to 90% neutrophils
  Increased sedimentation rate starts after 2 days, peaks after 4 days to 5 days, and persists for 2 months to 6 months. The degree of increase does not correlate with the severity of the infarction or with prognosis.
  
• Increased serum glucose and urine glucose, attributed to adrenal cortical stimulation secondary to stress or to shock
  
• Decreased arterial PO2 and oxygen saturation-frequent occurrence, 2 days to 3 days following infarction; especially abnormal in the presence of shock, left ventricular failure, or pulmonary edema; this reflects impaired arterial oxygenation in the lungs
  
• Metabolic acidosis (decreased pH, decreased HCOi, increased lactic acid) due to impaired circulation and consequent tissue hypoxia
  

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Pulmonary Heart Disease

LABORATORY FINDINGS


• Decreased arterial PO2 and oxygen saturation due to underlying lung disease
  
• Increased RBC, hemoglobin, hematocrit, blood volume, and red cell mass, all reflecting erythrocytosis secondary to tissue hypoxia

• Laboratory Findings of Underlying Lung Disease.

• Chronic bronchitis
  
• Pulmonary emphysema ---
  
• Pulmonary embolism and infarction
  

Pericarditis

LABORATORY FINDINGS

Acute Pericarditis
Table 1.0 Pericardial Fluid: Transudate Vs Exudate
Pericardial fluid (Table 1-3)

• WBC-elevated in bacterial pericarditis, normal or low in viral or tuberculous pericarditis
• Positive pericardial culture for bacteria, mycobacteria and viruses

• Fourfold rise in viral antibody titers from acute to convalescent sera

  Constrictive Pericarditis

• Increased LDH (especially LDH3) and decreased albumin, due to hepatic congestion

• Laboratory Findings of Congestive heart failure

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LABORATORY FINDINGS

• Positive blood culture is essential to establishing the diagnosis and is positive in 80%-90% of patients. Streptococcus viridans, group D streptococci and Staphylococcus aureus cause more than 75% of cases of endocarditis. Other bacteria, fungi, or rickettsiae are responsible for the remaining cases. The diagnosis should be based on two or more cultures that are positive for the same organism. Three separate blood cultures should be collected as quickly as possible for severe, life-threatening septicemia. For suspected SBE, the three blood cultures should be taken within the first 24 hours, at intervals no shorter than 1 hour. In patients already on antibiotic therapy, four to six separate blood cultures should be collected within the first 48 hours. Positive blood cultures are difficult to obtain in patients already on antibiotics and in patients whose endocarditis is due to unusual or fastidious organisms.

• Normocytic anemia-the degree of anemia is related to the duration of illness, rather than to the virulence of the organism

• WBC-normal or elevated to 15,OOO/,u1 with 65%-85% neutrophils

• Increased sedimentation rate indicates active inflammation

• Increased y-globulins reflect chronic inflammation

• Albuminuria and hematuria-the former occurs even without renal involvement

LABORATORY FINDINGS

• Increased serum CPK, CPK-MB, LDH, and LDHI are the result of severe myocardial damage; levels do not approach those encountered in myocardial infarction

• Increased blood eosinophils suggest trichinosis, polyarteritis, or allergic endomyocarditis.

• Fourfold rise in coxsackie virus or echovirus antibody titer from acute-phase to convalescent-phase sera

  Laboratory Findings of Complications

• Congestive heart failure
  
• Systemic or pulmonary emboli
  
• Pericardial effusion
  

LABORATORY FINDINGS

Renal Functions

• Urine specific gravity <1.020 as a result of diminished renal-concentrating ability Decreased urine sodium and urine volume due to the effects of increased renin and aldosterone formation
  
• Slight albuminuria «1 g/day)
  
• Occasional urine RBC, WBC, casts
  
Decreased creatinine clearance and increased serum BUN (usually <60 mg/dl); this occurs in severe heart failure

• Decreased serum sodium, chloride, protein, and albumin due to dilution by increased blood volume and edema fluid; the increased blood volume is due to increased renin and aldosterone formation
• Metabolic acidosis (decreased pH and decreased HCOi) due to superimposed chronic renal failure.
  
Liver Functions
• Increased serum bilirubin (1 mg/dl-5 mg/dl), urine bilirubin, and urobilinogen; reflects severity of the heart failure and hepatic congestion
  
• Decreased erythrocyte sedimentation rate due to decreased fibrinogen synthesis by the liver
  
Increased LDH, especially LDHs, due to severe heart failure and congestive hepatocellular necrosis
• Mild to moderate increase in alkaline phosphatase due to hepatic congestion and impaired enzyme excretion by the liver
  
• Slight increase in prothrombin time due to decreased fibrinogen synthesis by the liver
  
Pulmonary Functions
• Decreased arterial PO2 due to impaired gas exchange in congested lungs Respiratory alkalosis (increased pH and decreased PCO2) due to hyperventilation in response to hypoxemia
  
• Respiratory acidosis (decreased pH and increased PCO2); acute pulmonary edema impairs ventilation and blood flow resulting in CO2 retention.
  
• Table 1-4 shows the characteristics of pleural and peritoneal effusions that occur in congestive heart failure.
  

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LABORATORY FINDINGS

A statistical analysis of the roles of various lipids in predicting the risk of CHD showed a significant inverse relationship between HDL cholesterol and myocardial infarction.ll HDL cholesterol was shown to be the most sensitive single predictor of a patient's risk of developing CHD by the age of 50; the HDL measurement is eight times more sensitive than measurement of the total cholesterol level. Various combinations of lipid measurements as ratios further increased the predictability of CHD. Probably the best predictor is the LDL-HDL ratio; the tests for this ratio require that the patient be fasting. The total cholesterol-HDL cholesterol ratio is almost as good a predictor.2o The tests for this ratio may be done in a nonfasting patient. HDL cholesterol is determined by first separating HDL from the other plasma lipids, through precipitation or electrophoresis, and then measuring the cholesterol content of the separated HDL.
The total cholesterol-HDL cholesterol ratio in various populations is shown in Table 1-5.

Table 1-5

POPULATION	RATIO
Vegetarians	2.8
Eskimos	3.2
Those with ½ average risk of CHD	3.4
Marathon Runner	3.4
Female, Normal	4.5
Male, Normal	5.0
Those with CHD	5.3 - 5.7
Those with 2x average risk of CHD	7 - 10
Those with 3x average risk of CHD	11 - 23

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Aneurysm

Laboratory Findings

Rupture of Aneursym


• Leukocytosis
  
• Increased ESR
  
• Findings associated with shock
  Interference With Blood Supply to the Following
  
• Heart see (Myocardial Infarction and Congestive Heart Failure)
  
• Brain (Cerebral Infarction)
  
• Kidney (Renal Infarction)
  
• Intestines (Mesenteric Infarction)
  

For details on the disease click here.

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Heart Valve Disease

(Data yet to be entered here!) Link to excellent reference
http://my.clevelandclinic.org/heart/disorders/valve/sbe.aspx

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Syphilitic Cardiovascular Diseases

LABORATORY FINDINGS

• Positive serum FTA-ABS test (95% of patients) and VORL (77% of patients) Laboratory findings of congestive heart failure due to aortic-valve insufficiency Laboratory findings of myocardial infarction due to narrowing of coronary-artery openings Laboratory findings of aneurysm

  
  For details on the disease click here.
  

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  Reynauds Disease

  LABORATORY FINDINGS

• Cold agglutinins are occasionally present.
• Cryoglobulins may be present in multiple myeloma or leukemia.
• Laboratory findings of scleroderma, systemic lupus erythematosus, rheumatoid arthritis

  
  For details on the disease click here.
  

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  Shock

  LABORATORY FINDINGS - Shock

• WBC: Increased with hemorrhage; decreased when shock is severe, as in gram-negative septicemia; increased neutrophils, decreased lymphocytes and eosinophils
• Increased hematocrit, hemoglobin, BUN, and albumin due to hemoconcentration, which occurs in dehydration and burns
• Decreased hematocrit and hemoglobin due to hemodilution, which occurs in hemorrhage, crush injury, and skeletal trauma
• Early increase in blood glucose due to increased epinephrine formation in response to stress
• Metabolic acidosis (low pH, low CO2 content, increased lactic acid) due to tissue hypoxia when shock is severe
• Decreased urine volume, low urine specific gravity, proteinuria; increased serum creatinine, BUN, and potassium; all due to decreased renal circulation
• Increased LDH, proportionate in all five isoenzymes; if shock is due to myocardial infarction or cardiogenic shock, LDH1 will be predominant; if there is severe hepatic congestion and necrosis, LDHs will be increased

For details on the disease click here.
Peripheral Venous Disease LABORATORY FINDINGS. Peripheral Venous Disease

• Laboratory findings of underlying disease (e.g., carcinoma of the pancreas, polycythemia)
• Leukocytosis with increased bands and positive blood culture often occurs in septic phlebitis.
• Laboratory findings of pulmonary infarction
• ..If a patient is maintained on anticoagulant therapy, the effect of Coumadin or heparin should be monitored in the laboratory.
  

For details on the disease click here.

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Temporal Arteritis

LABORATORY FINDINGS - Temporal Arteritis

• Marked increase in sedimentation rate (5Omm/hr-132 mm/hr, Westergren method) is a characteristic finding.
• Moderate normocytic anemia (mean hemoglobin = 11.4 g/dl)
• Slight increase in WBC (up to 20,OOOIILI)
• Increased fibrinogen and a2-globulin parallel the sedimentation rate. These are indicators of inflammation.
• Biopsy of the temporal artery is required for definitive diagnosis.
  
  

For details on the disease click here.

Polyarteritis Nodosa LABORATORY FINDINGS - Polyarteritis Nodosa

• Indicators of Inflammation
• Increased leukocytes and neutrophils; eosinophilia suggests pulmonary involvement
• Marked increase in sedimentation rate
• Increased complement
• Increased a2-globulin and )i-globulin
• Indicators of Renal Involvement
• Increased urine protein, ABC, and granular casts
• Decreased serum albumin is the result of marked proteinuria, which occurs in nephrosis
• Microcytic anemia due to blood loss and renal failure
  Other Findings
• Increased platelets
  

For details on the disease click here.

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Arterial Thrombosis and Embolism

Laboratory Findings of Underlying Disorders

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