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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
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.
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.
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
ISOENZYME
NORMAL SERUM (%)
HEART MUSCLE (%)
LIVER (%)
SKELETAL MUSCLE (%)
LDH1
25
40
0
0
LDH2
35
35
5
0
LDH3
20
20
10
10
LDH4
10
5
15
30
LDH5
10
0
70
60
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.
Table 1-2. Distribution of CPK Isoenzymes in Normal Tissues
ISOENZYME
NORMAL SERUM (%)
SKELETAL MUSCLE (%)
HEART (%)
BRAIN (%)
CPK1 (BB)
0
0
0
90
CPK2 (BB)
0
0
40
0
CPK3 (BB)
100
100
60
10
Other Laboratory Findings
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
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 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
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.
Until recently, the major laboratory test used to classify the risk of developing coronary heart disease (CHD) has been a total cholesterol assay. However, only when the serum cholesterol is above 350 mg/dl (which occurs in less than 1 % of the population) is there a significantly increased risk of CHD.
Most patients have cholesterol values between 150 mg/dl and 300 mg/dl, whether or not they have CHD. The Framingham Heart Institute Study has shown that if the HDL cholesterol value is less than 45 mg/dl, the rate of CHD is very high.7,lO On the other hand, when the HDL cholesterol exceeds 55 mg/dl, the rate of CHD is very low. HDL appears to have a salutary effect on CHD. It functions to remove cholesterol from atherosclerotic vessels and from other tissues and returns the cholesterol to the liver for excretion in bile. The higher the levels of HDL, the greater the degree of lipid excretion.
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.
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
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
Increased C-reactive protein and sedimentation rate; the former usually
precedes the latter
Leukocytosis
If there is extensive tissue necrosis, there will be increased LDH (es;pecially
LDH1), CPK (especially CPK-MM), and serum glutamic-oxaloacetic
transaminase (SGOT).
Skin biopsy showing characteristic necrotizing vasculitis; lesions less than 24
hours to 36 hours old may show immunofluorescent deposits of immunoglobulins and complement
Presence of circulating immune complexes
Decreased serum complement
Detection of specific infectious agents, such as streptococci or HB,Ag
Positive ASO test indicating prior streptococcal infection
Findings of connective-tissue disease, indicated by presence of rheumatoid
factor, antinuclear antibody, anti-DNA.
Findings of renal involvement, such as proteinuria or decreased creatinine
clearance
Presence of occult blood in stool, indicating gastrointestinal involvement
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