new_n_lost
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I dont think so it doesnt increase in Cardiac Contractility rather it causes the cardiac muscle to go into hyperrepolarization and the cell response to a Action potential becomes less sensitive and therefore it leads to Bradycardia.
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| Luckyall
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hypo K-emia---> DOES lead to Ventricular arrhythmias and also Atrial arrthythmias through cells HyperPOLARIZATION
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| redpriest
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true, it does lead to bradycardia due to hyperpolarisation of the SAN cells, however i've now figured out my question. due to the decreased extracellular [K+] the 3Na+/2K+ATPase pump works slower, leading to a higher intracellular [Na+]. this slows down the 3Na+/Ca2+ATPase exchanger by reducing the Na+ concentration gradient, so Ca2+ remains in the cell longer and attains a higher concentration after an action potential, leading to a slight increase in contractility
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| new_n_lost
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Was this a Trick Questions Y do ppl act like REally Smart Asses as if their asses can tell the flavor fo the icecream just by sitting on it
God this is so High School !!!!!!!!!!!
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| Luckyall
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| redpriest
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ha! someone doesn't like being wrong...it wasn't a trick question rather, as noone knew on here, i went away and asked one of our tutors who happens to be a muscle physiologist at oxford university (hence probably knows what he's on about!) and that's what he told me so i thought i'd share it...and what kind of an insult involves sitting on ice cream?! 
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| silver
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didn't know oxford univ. professors had so much time on their hands
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| Luckyall
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Actually, interesting point, redpriest... i'll recheck on that soon !
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| new_n_lost
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Dude I have One Question U Really At Oxford then Plz Work Over Ur English
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| RayBerg
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The stress of USMLE prep getting onto you nnl? Take a day off bud.
Redpriest, that's a very good explanation btw.
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| silver
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i would really like to know what book/source this oxford univ. professor is using. do let us know redpriest
hypokalemia will cause hyperpolarization of the cells. cells will be difficult to stimulate because they have become more electronegative. bringing them to threshold will be more difficult because cells have become more negative inside.
in your explanation redpriest, if calcium has accumalated within the cell then contractility won't be increased rather cationic loading of cells brings resting membrane potential near threshold and the cells are over-excitable leading to premature beats-->arrythmias
this is especially the case if what you're saying is that sodium AND calcium BOTH have accumulated within the cells then, such excessive loading of cells with cations will bring RMP closer to threshold and the cells will over-fire.
Ganong is a very authentic source...and nowhere is it written that hypokalemia would lead to increased contractility of the myocardium.
like i said, i'd be interested in seeing the references this professor is teaching from.
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| new_n_lost
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Rayberg........ I think u guys r confusing the simple concept of Maintance of RMP and AP in Cardiac Muscle If u r having Hypokalemia there will be a shift of K from the intracellular compartment to Extracellular compartment. The Na/K ATP works against the concerntration of the Ions and is the resetter of the Original Concerntrations. Since the most of the K ion is extracelluar the resetting takes time cos the most of the Cells need to reach the RMP of -90mV before they can depolarize again. the Calcium Channels remain open n there is increased presence of Ca thus cardiac muscle has different potentials and the Summation of the Contraction is lost cos the RMP is now resetting itself closer to the K potential.
Remember the RMP is determined by the K ions and the Na determines the Magnitude of the AP if the Na and Ca r in the Cell the cell hasnt repolarized completely and there fore u will have premature beats
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| RayBerg
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Can someone remind me about the directionality of ion flow in Na/Ca pump. Pls...
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| redpriest
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Well i certainly know there is a slight increase in contractility as I've seen it on the animal hearts...i presume that explanation is just the current theory! as with all these things i doubt it is that simple! being that half of these professors write the textbooks i guess they come up with their own theories from their lab work! i think most of the textbooks don't mention it because it's not particularly large or important...if someone is hypokalaemic then the benefits of increased contractility are not going to a) outweigh the bradycardia to increase cardiac output or b) the chances of dying from an arrhythmia!
the Na/Ca (NCX) pump pumps calcium out of the cell in exchange for sodium into the cell, using the Na+ gradient for energy. SERCA pumps Ca2+ into the sarcoplasmic reticulum so both pumps are extruding calcium from the contact of the muscle filaments
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| ssrpk
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Well first of all hypokalemia woudn't cause that much of an increase in contractility, although as the oxford professor explains its plausible but that would require huge electrolyte shifts which will not be the case with hypokalemia as potassium is maintained within a very narrow range in the ECF.
The ratio of ICF and ECF K+ is the principal determinant of membrane excitability and the RMP is dependent on K+ more than other ions, more importantly it depends on membrane equilibration potential of K+.
Lowering ECF K+ won't effect K+ in terms of concentration so as to bring more K+ outwards however it has two major effects on the maintenance of RMP: 1) it increases the membrane equillibrium potential (will make it more negative) and its not the same as to say tht RMP will become more negative 2) it will also decrease the permeability of K+ through various channels.
Now during phase three of action potential due to rapid efflux of K+ because of huge concentration gradient will bring the cell close to its RMP and will decrease the effective refractory period which will make the cells more excitable especially of non-conducting cardiac muscles.
Secondly, due to decreased permeability of K+ across the cell membrane there will be lesser efflux of K+ during phase four of the action potential in the cells which have an intrinsic firing rate. This efflux of K+ is important because it counteracts the influx of other cations viz. Na+ and Ca++, thus as more K+ stays in this makes the membrane potential unstable and will bring the RMP to the threshold sooner, this accounts for the hyperexcitability.
Opposite effect is seen when there is hyperkalemia --> K+ membrane permeability increases --> more K+ efflux duering phase 4 which will effectively counter incoming cations and the RMP will be stabilized for a longer duration, thus loweruing the excitability.....that is the reason why dangerous hyperkalemia or rapidly rising hyperkalemia gives ASYSTOLE.
To summarize, hypokalemia destabilize the RMP while hyperkalemia stabilize the RMP.
I had an extensive discussion on this topic with my peers here and they have taught me well, our resources were Katzung, Ganong as well as other web based materials.
Edited by ssrpk on 06/03/07 - 11:15 AM
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| ssrpk
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to silver,
if Ca++ accumulates inside the cell it will definitely increase the permeability and that can be very well understood by reviewing the mechanism of action of digitalis.
Digitalis inhibits Na+/K+ exchanger and this inhibition over time will result in serious electrolyte shifts across the cell membrane. As the Na+ stays in it reverses the Na+/Ca++ exchanger [as explained by the professor] and brings more Ca++ inside the cell which causes more pumping of Ca++ inside the cell's SER, Now overtime as the action potential is reached more Ca++ will be released by the SER and this accounts for the increase in contractility. Also as the Ca++ gets saturated it brings us different kinds of conduction problems a) resting depolarization (high Na+ and Ca++) - causes conduction block. b) oscillatory afterdepolarizations - high Ca++, increased automaticity
Also remember that with digitalis toxicity whenever RMP is just below threshold, it interferes with conduction as Na+ gates are in their inactivated state while when RMP reaches above threshold it can cause ectopic beats.
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| silver
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ssrpk wrote:
to silver,
if Ca++ accumulates inside the cell it will definitely increase the permeability and that can be very well understood by reviewing the mechanism of action of digitalis.
Digitalis inhibits Na+/K+ exchanger and this inhibition over time will result in serious electrolyte shifts across the cell membrane. As the Na+ stays in it reverses the Na+/Ca++ exchanger [as explained by the professor] and brings more Ca++ inside the cell which causes more pumping of Ca++ inside the cell's SER, Now overtime as the action potential is reached more Ca++ will be released by the SER and this accounts for the increase in contractility. Also as the Ca++ gets saturated it brings us different kinds of conduction problems a) resting depolarization (high Na+ and Ca++) - causes conduction block. b) oscillatory afterdepolarizations - high Ca++, increased automaticity
Also remember that with digitalis toxicity whenever RMP is just below threshold, it interferes with conduction as Na+ gates are in their inactivated state while when RMP reaches above threshold it can cause ectopic beats.
Agreed, digitalis does have the ability to inhibit Na+/K+ ATPase pump thereby causing an increase in intracellular sodium concentration and a slight decrease in intracellular K+ conc.
But, there's one part about the mechanism of action of digitalis that you're not understanding. As digitalis inhibits the Na+/K+ ATPase pump resulting in increase in intracell. levels of sodium and decreasing the sodium gradient across the membrane--->this will result in decrease Na+ influx and calcium efflux (the sodium/calcium antiport gets deranged as well), so this will cause increase in Ca++ conc. inside the cell. You wrote that this will result in "bringing more calcium in"--you're wrong, calcium isn't brought in when the antiport gets deranged, rather the calcium just gets retained inside the cell thereby increasing the Ca++ conc. and ultimately leading to increased contractility. (Ganong p. 81).
I'm not refuting that Ca++ doesn't increase contractility--I agree with that concept in and of itself, but not in the context of a situation where hypokalemia is occurring.
The point I'm trying to make is that when talking about hypokalemia, you can't say that the slight increase in contractility is a major and foremost manifestation, rather the first thing that occurs and also the main manifestation of hypokalemia is the arrythmias.
The increase in contractility that eventually might occur in hypokalemia is minor and slight, and is mainly overlooked, because the arrythmias that are occurring in hypokalemia are the major manifestations of low potassium levels and warrant immediate attention.
Edited by silver on 06/03/07 - 04:26 PM
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| ssrpk
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hey buddy, thanks for correcting me on this part, Ca++ do indeed gets retained because of decreased expulsion via Na+/Ca++ exchanger, but there are mechanisms thru which Ca++ gains increased entry into cells as mentioned in Katzung....but anyway who cares, Ca++ is increased because it is increased...
and yeah as i mentioned that too that hypokalemia does'nt hv much to do with increase in contractility...so i guess we are even with that
right bro 
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