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CARDIAC ENZYME

Enzymes

Are special proteins that catalyzechemical reactions in living cells.

Cardiac enzymes are present in high

concentrations in myocardial tissue.

Tissue damage causes release ofenzyme from their intracellular

storage areas. For example,

myocardial infarction causes cellular

anoxia, which alters membrane

permeability and causes spillage of

enzymes into the surroundingtissue.

Tissue damage causes release ofenzyme 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 myocardialnectosis that is rapidly released

from the circulation within 1 to 2

hours of infarction.

Its release allows very earlydetection, 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 commonenzyme to detect myocardialdamage.

Serum elevation of these twoenzymes occurs in sequence after

myocardial insult.

This enzyme are also found in otherorgans (skeletal muscle and liver)

Cardiac specificity must bedetermined by measuring

isoenzyme activity.

ISOENZYMES are various forms ofCK 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 indicatesmyocardial damage.

Plasma MB is significantly elevatedwithin 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 takenimmediately on admission and

every 6-8 hours for the first 24

hours.

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Diagnosis of injury requires nofewer 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 thedetection 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 ofmyocardial injury, troponins can be

used to exclude myocardial

infarction when CK-MB may be

falsely positive.

FUNCTIONS OF THE

HEARTHEXITABILITY

The ability of cardiac musclecells to depolarize in

response to stimulus.

Excitability is influence byhormones, electrolytes,

nutrition, oxygen supply,

medication, infection and

autonomic nerve activity.

AUTOMATICITY

The ability of cardiac pacemakercells to initiate an impulse

spontaneously and repetitive,

without external neurohormonal

control; known as automacity or

rhythmicity.

SA node has the highest automacityor rhythmicity.

SA node automacity is due tochanges in ionic permeability ( forNa+ and Ca+ ions) move the cell

membrane potential more positively

toward threshold voltage.

Norepinephrine and acetylcholinecause heart rate to increase and

decrease respectively.

The rate of spontaneousdepolarization can also be affected

by other hormones, bodytemperature, drug and disease.

CONTRACTILITY

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 samesliding filament of mechanism

described for skeletal muscle.

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The action potential initiates themuscle contraction by releasing

calcium through the

One important difference betweencardiac and skeletal muscle is thatcardiac muscle needs extracellular

calcium.

T tubules of all cell membraneREFRACTORINESS

Refractoriness is the hearts inabilityto respond to a new stimulus while

still in state of depolarization from

an earlier stimulus.

It is develops when the sodiumchannels of the cardiac cell

membrane become inactivated and

unexcitable during an action

potential.

Refractoriness occur in two periodsa.The absolute refractory period

Occurs during depolarization and thefirst part of repolarization .

During this period, cardiac cells canagain conduct action potentials.

b.The relative refractory period

Occurs in the final stages ofrepolarization; refractoriness

diminishes and a stronger-than-normal

stimulus can excite the heart muscle to

contract.

At the end of refractory period, there isa transient hyperexcitability (ulnerable

period).

The sodium channels are reset and thecardiac cells can again conduct action

potentials.

Normally the ventricles had therefractory period of 0.25 to 0.3 seconds,

which approximates the duration action

potentials.

The relative refractory period for theventricles last about 0.5 seconds.

The atria have a refractory period ofabout 0.15 seconds, and they can

therefore contract rhythmically much

more quickly than the ventricles.

The refractory duration of the actionpotential is not fixed, however; both

can shorten as a heart rate increases.

CONDUCTIVITY

Conductivity is the ability of heartmuscle fibers to propagate electrical

impulses along and across cell

membranes.

The conduction system consist of the

following parts:

1. Sinoatrial (SA) node2. AV node3. Bundle of His and bundle

branches

4. Purkinje fibers.