and 5.3 mmol/l. levels above 5.5 mmol/l generally indicate hyperkalemia, and those below 3.5 mmol/l indicate hypokalemia. ecg findings with mild to moderate hyperkalemia, there is prolongation of the pr interval and development of peaked t waves. severe hyperkalemia results in a widening of the qrs complex, and the ecg complex can evolve to a sinusoidal shape. there appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarisation. also, (as noted above), hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. the faster repolarisation of the cardiac action potential causes the tenting of the t waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller p waves and widening of the qrs complex. some of potassium currents are sensitive to extracellular potassium levels, for reasons that are not well understood. as the extracellular potassium levels increase, potassium conductance is increased so that more potassium leaves the myocyte in any given time period. to summarize, classic ecg changes associated with hyperkalemia are seen in the following progression: peaked t wave, shortened qt interval, lengthened pr interval, increased qrs duration, and eventually absence of the p wave with the qrs complex becoming a sine wave. bradycardia, junctional rhythms and qrs widening are particularly associated with increased risk of adverse outcomes the serum potassium concentration at which electrocardiographic changes develop is somewhat variable. although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other electrolytes, as well as levels of catecholamines, play a major role. ecg findings are not a reliable finding in hyperkalemia. in a retrospective review, blinded cardiologists documented peaked t-waves in only 3 of 90 ecgs with hyperkalemia. sensitivity of peaked-ts for hyperkalemia ranged from 0.18 to 0.52 depending on the criteria for peak-t waves. prevention preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of a diuretic (such as furosemide or hydrochlorothiazide). sodium polystyrene sulfonate and sorbitol (combined as kayexalate) are occasionally used on an ongoing basis to maintain lower serum levels of potassium though the safety of long-term use of sodium polystyrene sulfonate for this purpose is not well understood. high dietary sources include vegetables such as avocados, tomatoes and potatoes, fruits such as bananas, oranges and nuts. treatment emergency lowering of potassium levels is needed when new arrhythmias occur at any level of potassium in the blood, or when potassium levels exceed 6.5 mmol/l. several agents are used to temporarily lower k+ levels. the choice depends on the degree and cause of the hyperkalemia, and other aspects of the person's condition. myocardial excitability calcium (calcium chloride or calcium gluconate) increases threshold potential through a mechanism that is still unclear, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. a standard ampule of 10% calcium chloride is 10 ml and contains 6.8 mmol of calcium. a standard ampule of 10% calcium gluconate is also 10 ml but has only 2.26 mmol of calcium. clinical practice guidelines recommend giving 6.8 mmol for typical ekg findings of hyperkalemia. this is 10 ml of 10% calcium chloride or 30 ml of 10% calcium gluconate. though calcium chloride is more concentrated, it is caustic to the veins and should only be given through a central line. onset of action is less than one to three minutes and lasts about 30–60 minutes. the goal of treatment is to normalise the ekg and doses can be repeated if the ekg does not improve within a few minutes. some textbooks suggest that calcium should not be given in digoxin toxicity as it has been linked to cardiovascular collapse in humans and increased digoxin toxicity in animal models. recent literature questions the validity of this concern. temporary measures several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. the effect of these measures tends to be short-lived, but may temporise the problem until potassium can be removed from the body. insulin (e.g. intravenous injection of 10 units of regular insulin along with 50 ml of 50% dextrose to prevent the blood sugar from dropping too low) leads to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium atpase. its effects last a few hours, so it sometimes must be repeated while other measures are taken to suppress potassium levels more permanently. the insulin is usually given with an appropriate amount of glucose to help prevent hypoglycemia following the insulin administration, though hypoglycaemia remains common especially in the context of acute or chronic renal impairment and capillary blood glucose measurements should be taken regularly after administration to identify this. salbutamol (albuterol), a β2-selective catecholamine, is administered by nebuliser (e.g. 10–20 mg). this medication also lowers blood levels of k+ by promoting its movement into cells, and will work within 30 minutes. it is recommended to use 20 mg for maximum potassium lowering effect, but to use lower doses if the patient is tachycardic or has ischaemic heart disease. note that 12-40% of patients do not respond to salbutamol therapy for reasons unknown, especially if on beta-blockers, so it should not be used as monotherapy sodium bicarbonate may be used with the above measures if it is believed the person has metabolic acidosis, though time to effectiveness is longer and its use is controversial. elimination severe cases require hemodialysis, which are the most rapid methods of removing potassium from the body. these are typically used if the underlying cause cannot be corrected swiftly while temporising measures are instituted or there is no response to these measures. loop diuretics (furosemide, bumetanide, torasemide) and thiazide diuretics (e.g., chlortalidone, hydrochlorothiazide, or chlorothiazide) can increase kidney potassium excretion in people with intact kidney function. potassium can bind to a number of agents in the gastrointestinal tract. sodium polystyrene sulfonate with sorbitol (kayexalate) has been approved for this use and can be given by mouth or rectally. however, high quality evidence to demonstrate the effectiveness of sodium polystyrene are lacking, and use of sodium polystyrene sulfonate, particularly with high sorbitol content, is uncommonly but convincingly associated with colonic necrosis. there are no systematic studies (>6 months) looking at the long-term safety of this medication. patiromer is taken by mouth and works by binding free potassium ions in the gastrointestinal tract and releasing calcium ions for exchange, thus lowering the amount of potassium available for absorption into the bloodstream and increasing the amount lost via the feces. the net effect is a reduction of potassium levels in the blood serum. sodium zirconium cyclosilicate is a medication that binds potassium in the gastrointestinal tract in exchange for sodium and hydrogen ions. onset of effects occurs in one to six hours. it is taken by mouth. epidemiology hyperkalemia is rare among those who are otherwise healthy. among those who are in hospital, rates are between 1% and 2.5%. society and culture in the united states, hyperkalemia is induced by lethal injection in capital punishment cases. potassium chloride is the last of the three drugs administered and actually causes death. injecting potassium chloride into the heart muscle disrupts the signal that causes the heart to beat. this same amount of potassium chloride would do no harm if taken orally and not injected directly into the blood.