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CARDIAC ENZYME

Enzymes Are special proteins that catalyze chemical reactions in living cells. Cardiac enzymes are present in high concentrations in myocardial tissue. Tissue damage causes release of enzyme from their intracellular storage areas. For example, myocardial infarction causes cellular anoxia, which alters membrane permeability and causes spillage of enzymes into the surrounding tissue. Tissue damage causes release of enzyme from their intracellular storage areas. For example, myocardial infarction causes cellular anoxia, which alters membrane permeability and causes spillage of enzymes into the surrounding tissue. MYOGLOBIN Is useful marker of myocardial nectosis that is rapidly released from the circulation within 1 to 2 hours of infarction. Its release allows very early detection, but its short half-life makes it less useful in clients who presents several hours after onset. Measurement of myoglobin levels is not recommended if there is evidence of muscle damage, trauma, or renal failure because of greater potential of false-positive test results in this circumstance.

2. CREATINE KINASE (CK) 3. LACTIC ACID AND DEHYDROGENASE (LDH) CK AND LDH , the most common enzyme to detect myocardial damage. Serum elevation of these two enzymes occurs in sequence after myocardial insult. This enzyme are also found in other organs (skeletal muscle and liver) Cardiac specificity must be determined by measuring isoenzyme activity. ISOENZYMES are various forms of CK and LDH, identified by a process known as electrophoresis. THREE ISOENZYME OF CK CK-MM (skeletal muscle) CK-MB (myocardial muscle) CK-BB (brain)

Elevated CK-MB indicates myocardial damage. Plasma MB is significantly elevated within 6-8 hours of the onset of manifestations of myocardial infarction, maximal levels are reached between 14 and 36 hours, and levels return to a normal after 48-72 hours. Samples should be taken immediately on admission and every 6-8 hours for the first 24 hours.

Diagnosis of injury requires no fewer than two samples separated by at least 4 hours. LDH1 and LDH2 Are the only cardiac-specific. If the serum concentration of LDH1 is higher than the concentration of LDH2, the pattern is said to have flipped, signifying myocardial necrosis TROPONIN Has led to increase specificity in the detection of myocardial infarction. Has three components; I, C, and T. Troponin I modulates the contractile state. Troponin C binds calcium. Troponin C binds I and C. Elevated levels of troponin I are as sensitive as CK-MB for the detection of the myocardial injury. Because of their higher specificity of myocardial injury, troponins can be used to exclude myocardial infarction when CK-MB may be falsely positive.

medication, infection and autonomic nerve activity. AUTOMATICITY The ability of cardiac pacemaker cells to initiate an impulse spontaneously and repetitive, without external neurohormonal control; known as automacity or rhythmicity. SA node has the highest automacity or rhythmicity. SA node automacity is due to changes in ionic permeability ( for Na+ and Ca+ ions) move the cell membrane potential more positively toward threshold voltage. Norepinephrine and acetylcholine cause heart rate to increase and decrease respectively. The rate of spontaneous depolarization can also be affected by other hormones, body temperature, drug and disease.

CONTRACTILITY

FUNCTIONS OF THE HEARTH


EXITABILITY The ability of cardiac muscle cells to depolarize in response to stimulus. Excitability is influence by hormones, electrolytes, nutrition, oxygen supply,

The heart muscle is composed of long, narrow cells or fibers. Cardiac muscle fibers , like striated skeletal muscle, contain myofibrils, Z bands, sarcomeres, sarcolemas, sarcoplasm, and sarcoplasmic reticulum.

Contraction results from the same sliding filament of mechanism described for skeletal muscle.

The action potential initiates the muscle contraction by releasing calcium through the One important difference between cardiac and skeletal muscle is that cardiac muscle needs extracellular calcium. T tubules of all cell membrane REFRACTORINESS Refractoriness is the hearts inability to respond to a new stimulus while still in state of depolarization from an earlier stimulus. It is develops when the sodium channels of the cardiac cell membrane become inactivated and unexcitable during an action potential. Refractoriness occur in two periods
a.The absolute refractory period Occurs during depolarization and the first part of repolarization . During this period, cardiac cells can again conduct action potentials. b.The relative refractory period Occurs in the final stages of repolarization; refractoriness diminishes and a stronger-than-normal stimulus can excite the heart muscle to contract. At the end of refractory period, there is a transient hyperexcitability (ulnerable period). The sodium channels are reset and the cardiac cells can again conduct action potentials. Normally the ventricles had the refractory period of 0.25 to 0.3 seconds, which approximates the duration action potentials.

The relative refractory period for the ventricles last about 0.5 seconds. The atria have a refractory period of about 0.15 seconds, and they can therefore contract rhythmically much more quickly than the ventricles. The refractory duration of the action potential is not fixed, however; both can shorten as a heart rate increases. CONDUCTIVITY Conductivity is the ability of heart muscle fibers to propagate electrical impulses along and across cell membranes. The conduction system consist of the following parts: 1. Sinoatrial (SA) node 2. AV node 3. Bundle of His and bundle branches 4. Purkinje fibers.