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Potassium is one of the major intracellular cations, occupying a role that is parallel that of sodium in extracellular fluid. Physiological actions of potassium are related primary to concentration of cation in extra cellular fluid. Potassium is the essential mineral for maintaining intracellular osmotic pressure. It has major role in renal tubular function, cardiac rhythm, reproductive organs functions, bone hardness and homeostasis of PH. Potassium level inside cell will be reduced in acidosis. High level can inhibit muscular contraction. It is essential to promote nerve transmission, and it involves in ciliary movement. It may promote diastolic arrest in higher concentration. Normal level prevents hypertension, stone formation, edema and osteoporosis.
Normal intracellular K ion concentration is 150 meq/L. Normal extracellular concentration of K ion is about between 3.5 mmol/l to 5 mmol/L. Average ratio is about 30:1. K ion level more than 5.5 mmol/L - 7.0 mmol/L and less than 3 mmol/L may cause cardiac arrhythmia.
Extracellular sodium concentration is about 140 mmol/L and intracellular sodium level is 10 mmol/L. Extracellular chloride concentration is 100 mmol/L and intracellular chloride level is 10 mmol/L. Intracellular calcium level is very low.
Daily requirement
Adult 4000 mg /day.
Children 3500 mg/day.
Normal blood value 3.5 mEq /L - 4.5 mEq /L.
Hyperkalemia
Action potential in contractile cell
Resting membrane potential in contractile cell is about -90 mv. Resting potential is decreased to -70 mv due to impulse (pacemaker action potential) coming through adjacent cell (gap junction). Sodium ion enter into the cell in phase 0 by stimulation take place at one end. Polarity of cell changed -70 mv up to + 20 mv. Some calcium ion also enters inside in phase 0. The potential become more positive.
Sodium channel closed. K ion go out and its channel closed quickly. So potential become sharply lowered. This is phase 1 of repolerisation (Early repolerisation) Calcium channel open and more calcium influx take place. Potential mildly increased. Some calcium is released from calcium storage in sarcoplasmic reticulum. Chloride ion enter to cell. Some K ion go out from the cell.
Depolarization is maintained. It is called Plateau or phase 2. Calcium channel closed. K ion more go out the cell. Repolarization begins from opposite end of cell be stimulated. Cell potential become > -90 mv. This is phase 3. 3 sodium pumped out and 2 K ion enter inside the cell. 3 sodium ion enter the cell and exchanged with one calcium+++ to out slowly. Resting potential become negative near -90 mv due to entry of potassium and ready to be excited.
K ion in extra cellular become high in hyperkalemia above 5-7 meq/L. Potassium ion enter more inside in phase 4.so MRP is lowered <-70mv and thresh hold potential is increased. The cell become less excitable in phase 0. Less sodium enters into cell in phase. So, height of depolarization (R or S) wave become reduced.
If K ion channel is blocked by anti-cardio protein particle, the transfer of K ion will be interrupted. So, efflux of K + become less in phase1. So, the height of R wave may increase.
All living cells have resting membrane potential. Resting potential in non-pacemaker cell is in between -90 mv -80 mv. Threshold level of resting membrane of contractile cell is about -40 mv. Threshold potential is lowered from-40 mv to -30 mv due to increased intracellular Potassium due to entry of K ion in phase 4 by hyperkalemia or due to thickening of cell membrane. This affect excitability of cell and depolarization become slowed.The isoelectric line (ST segment) is looked as elevated. Thickness of membrane layer is due abnormal protein or increasing of fat as result of chronic degeneration. If extracellular Potassium level is very high the repolarization process in phase1 and phase 2 are deranged or failed more.
Ratio of extracellular and intracellular calcium ion is too high. So, more calcium ion enter into cell. in phase 2 If more calcium ion enters in and less K ion go out in phase 2 may make a wave form in plateau phase of repolarization. It causes ST-T junction elevation.
K ion efflux become more quickly and forcibly in hyperkalemia for repolarization process in phase 3. This make Tall repolarization wave. (Increased repolarization reserve). Tall T wave is developed. Potassium enter into cell more in phase 4 due to high Kion extra cellular fluid. So resting membrane potential become lowered from -95 mv to -70mv. thresh hold potential is increased. so excitability of cell is lowered. Entry of Sodium and some calcium into cell in phase 0 become weak. This cause formation of wide QRS interval in ECG.
Action potential in pacemaker cell
Pacemaker cells in Sinus node and AV node have no resting membrane potential. Potential become more negative when K ion goes out in phase 3. Sodium ion enter into cell automatically when potential reach at -70 mv. Calcium ion enter into cell when threshold level reach at - 40 mv. Threshold potential in pacemaker cell is decreased from - 40 mv to -30 mv due to increased K ion level. Intracelluar potential become less negative (decreased) due to efflux of K ion in phase 3 in hyperkalemia. So, excitability of nodal cell decreased. Action potential formation by calcium entry is interrupted in pacemaker cell (SA and AV node). Thus, height of P wave is reduced or origin of P wave is blocked in hyperkalemia.
Causes of hyperkalemia
Renal damage.
Cell necrosis.
Acidosis (K ion efflux from cell).
Steroid excess.
Less insulin.
Strophanthus is climbing vine. It is prime herbal medicine in dropsy with acidosis and hyperkalemia. It is cardiac stimulant in lower dose. Glycyrrhiza glabra is also hypokalemic agent. Ricinus communis is also medicine in hyperkalemia. Elimination of wastes is cure. Prefer diet with low potassium. Laxatives like terminalia chebula, Senna can control the potassium. Avoid potassium rich food items.Prefer potassium low food items.
Potassium -low items
Chicken.
Lychee.
Apple.
Cabbage.
Carrot.
Onion.
Eggplant.
Blueberries.
Alfalfa.
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Chronic hypokalemia
Action potential in contractile cell
Cells are more excitable due to increased resting potential as result of efflux of potassium in phase 3. Sodium ion enter into cell rapidly in zero phase on stimulation of action potential. Height of depolarization wave is increased. Some calcium also enters into cell. K ion going out sharply for brief period in phase 1 due to decreased gradient in extracellular space. This can cause a notch in height of R wave or height is lowered.
K ion efflux is more in phase1 and 2 if K ion channel become wide due to the deficiency of the cardio-protein that maintain the channel.
Threshold of resting membrane potential is increased from - 40 mv to -50 mv as less influx of K ion in phase 4 and more K ion going out in phase1. So isoelectric line at ST segment is looked as depressed. Calcium ion enter into cell more as more K ion going out in phase 2.
K ion efflux become slow in phase 3 as K ion concentration inside cell is also less, or because of more K efflux happened in phase 1 and 2. So T wave become low, flat and its duration is increased (decreased repolarization reserve)). QT interval also is increased. If sinus rate is very low, K ion efflux in bulk finally to reach and maintain negative resting potential. This late repolarization from basal part cause U wave formation. Potassium ion entry into cell in phase 4 become less due to decreased K level in extracellular fluid. so MRP is maintained in more negative than -90 mv. So, cell become more easily excitable.
Action potential in pacemaker cell
Entry of Sodium ion and Calcium ion into pacemaker cell become more efficient as increased negative resting membrane potential > –70 mv. So the action potential formation in pacemaker cell become sharp and quick.Thus sinus tachycardia will take place in hypokalemia.
Causes of hypokalemia
Diarrhea (K+ion loss).
Renal tubular acidosis.
Diabetes nephropathy.
Hyper insulin (Increased K+ ion entry into cell).
Digitalis, Ricinus communis, Boerhavia diffusa, Strophanthus, Glycyrrhiza glabra, Terminalia chebula,Cassia Alexandrina are potassium lowering herbs. These are remedies in chronic hypokalemic weakness. Taraxacum and Sinapis are also similar remedies in chronic hypokalemia due to chronic renal weakness. Prefer potassium rich food items and vegetables.
Potassium rich items
Buffalo milk (Reduces hypertension, may help to prevent arteriosclerosis).
Coconut water.
Spinach.
Avocado.
Sweet potatoes.
Potatoes.
Beetroot.
Kidney beans.
Dried apricot.
Banana.
Orange.
Tomato.
Lentil.
Melon.
Pomegranate.
Almond.
Green vegetable leaves.
Meat.
Seafood.
Egg.
Whey powder.
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