Emergency lowering of potassium levels is needed when new arrhythmias occur at any level of potassium in the blood, or when potassium levels exceed 6.5mmol/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 6.8mmol of calcium. A standard ampule of 10% calcium gluconate is also 10 mL but has only 2.26mmol of calcium. Clinical practice guidelines recommend giving 6.8mmol 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. 10–20mg). 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.
complications of Malignant hyperthermia
complications of Heat stroke
complications of Diabetic ketoacidosis
complications of Ventricular tachycardia
medical cause of Hyperthermia
complications of Rhabdomyolysis
complications of Carbon monoxide poisoning
complications of Myocardial stunning