afrocaribb
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hi, can anyone pls explain why we see a prolonged QT interval in pts who have hypocalcemia. thank u.
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| silver
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i'm just taking a stab at this. Normally, sodium voltage gated channels are guarded by calcium in order to repel sodium so that there isn't too much influx of sodium. However, in hypocalcemia, calcium levels decrease in interstitial fluid and blood, so the calcium guarding the sodium voltage gated channels compensate the decreased levels, thereby rendering these sodium volt. gated channels 'unguarded', so there's excessive influx of sodium. action potential is easily produced, because RMP reaches threshold and tissue becomes hyperexcitable....takes longer time to relax, so QT int. prolonged.
Not too sure if this is right. 
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| afrocaribb
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tks for trying though i didnt think of it that way, but your explantion makes more sense than mine in a way, i was thinking of it based on the action potential curve and if ca is absent it means there would be more efflux of potassium and so will lead to rapid repolarization ......but i dont think thats right either
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| silver
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as far as i remember, and again i'm open to anyone who knows better...but potassium only effluxes when there is calcium influx (this will happen only when electrolyte levels are normal)...this is what creates the plateau of the action potential curve for atrial cells. the calcium that comes in stimulates sacroplasmic reticulum to release more intracellular calcium leading to contraction. but if there's hypocalcemia, none of this is going to take place. it will take longer for the cells to repolarize.
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| afrocaribb
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Tks! that makes more sense. 
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| new_n_lost
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The series of events in Hypocalcemia
THe ICF concerntration Falls below n then is replaces by ECF conc. therefore we have hypo presentation of any electrolyte
Normal Phases of Action Potential in Cardiac Muscle.
Phase 1: During initial upstroke of action potential in a normal cardiac cell, a rapid net influx of positive ions (Na+ and Ca++) occurs, which results in the depolarization of the cell membrane. This is followed by a rapid transient outward potassium current (Ito), while the influx rate of positive ions (Na+, Ca++) declines. This represents the initial part of the repolarization, or phase 1.
Phase 2 is characterized by the plateau, the distinctive feature of which is the cardiac repolarization. The positive currents flowing inward and outward become almost equal during this stage.
Phase 3 of the repolarization is mediated by activation of the delayed rectifier potassium current (IK) moving outward while the inward positive current decays. If a slow inactivation of the Ca++ and Na+ currents occurs, this inward “window” current can cause single or repetitive depolarization during phases 2 and 3 (ie, EADs). These EADs appear as pathologic U waves on a surface ECG, and, when they reach a threshold, they may trigger ventricular tachyarrhythmias.
Now in Hypocalcemia we have low calcium levels Calcium contiues to be the factor which goes in the cell late n due imbalance of Electrolytes the normal tendencies r interupted so the replorization of the individual myocardial fibers begins to vary and thus we have a Prolong QT interval.
I hope i have go it right.
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| afrocaribb
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Thanks Nnl,ur right abt the phases and it makes more sense,thank u.
Edited by afrocaribb on 04/21/07 - 07:18 PM
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| verapamil
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for those who need simpler terms like me, simply put;
since "T" in the ecg tracing is the ventricular repolarization of the heart; and Ca is responsible for the plateau,
we can therefore say that a decrease in Ca would mean a slower influx, delaying the plateau formation, and thus prolonging the action potential, delaying the repolarization of the heart!
just to add some more info; calcium ch blockers block the L-type, which is responsible for this plateau in the AV and SA nodes.
anyway i hope that helped
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| Medusin
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Nice explanation verapamil
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| Mikeland
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good explanations, everones
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