Refractory Periods. Hyperkalemia is classified as mild when levels are in the range of 5. Hyperkalemia occurs when compensatory mechanisms are no longer able to cope with the imbalance, which is why it is usually multifactorial. Mild hyperkalemia is often asymptomatic, detected accidentally by laboratory tests, due to its vague symptoms such as malaise, muscle weakness and paraesthesia.
Severe hyperkalemia will affect the neuromuscular function in the form of skeletal muscle weakness and paralysis; however, this is not a frequent presentation as the cardiac toxicity dominates the picture and is the preliminary presentation.
Cardiac toxicity will usually present on the ECG in the following step-up escalating manner, although not necessarily so, depending on the etiology:. Hyperkalemia leads to hyperchloremic metabolic acidosis as the hyperkalemia promotes the intracellular uptake of potassium in exchange for hydrogen ions.
This creates intracellular alkalosis, suppressing kidney ammonia production in the proximal tubules, leading to a decrease in urinary ammonium and acid excretion and a type IV renal tubular acidosis [8].
The sodium potassium ATPase was discovered in by Skou, who was later awarded a share of the Nobel Prize in Chemistry for his discovery.
Skou was the first to discover the sodium potassium ATPase in the sarcolemma of the cardiac muscles' cell surface. Its presence was later detected in every eukaryotic single and multicellular organism. The sodium potassium pump functions by linking the hydrolysis of ATP to the cellular export of three sodium ions in exchange for two potassium ions against their electrochemical gradients. It is the molecular target for digitalis and digoxin, which have been in use since the 18th century as foxglove extracts.
The action of the sodium potassium pump is regulated by a phosphoprotein phospholemman, whose unphosphorylation leads to the inhibition of the pump and whose phosphorylation leads to an increase in the pump activity. It has three phosphorylation sites, two palmitoylation sites and one glutathionylation site, which explains the multitude of signals capable of stimulating and inhibiting the pump.
The sodium potassium pump itself is an enzyme composed of multiple subunits with multiple isoforms. The presence of the alpha and beta subunits mainly B1 in the heart is essential for its function.
Recently, a third protein gamma subunit has been identified in the kidneys, but to date its function remains unknown. The alpha subunit is the catalytic core of the sodium potassium pump enzyme. It is approximately kDa and contains the binding sites for sodium, potassium, ATP, and cardiotonic steroids such as ouabain. Only alpha 1 and alpha 2 display a significant presence in a normal cardiac myocyte and are functionally linked to the sodium calcium exchanger NCX. Alpha 3 has been reported to replace alpha 2 in experimental heart failure models [2].
Data from recent experiments favor the involvement of both alpha 1 alpha 2 subunits of the pump in the regulation of the excitation-contraction E-C coupling. The alpha 1, which was found to be more evenly distributed across the sarcolemma, is thought to play more of a "housekeeping" role, controlling both contractility and the bulk intracellular sodium, while the alpha 2 whose expression is concentrated in the T-tubules along with other key components of E-C coupling is thought to focus mainly on contractility [2,9].
Its end result is life-threatening. As all of the cells in the body are ultimately affected by the sodium potassium pump, and ischemic cardiac muscles are known to extrude their potassium extracellularly leading to a reduction in the arrhythmia threshold with the possibility of ventricular arrhythmias that aggravate the hypopolarization and lower the threshold even more, more studies need to be focused on the manipulation of the sodium potassium enzyme, as its control could favorably alter the outcomes of cardiac arrests and rewrite the current CPR guidelines.
Our mission: To reduce the burden of cardiovascular disease. Help centre. All rights reserved. Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more. Show navigation Hide navigation. Sub menu. First in a series on hyperkalemia: hyperkalemia, the sodium potassium pump and the heart Vol. Topic s : Epidemiology. Background Potassium is a soft, silvery-white highly reactive cation belonging to the alkali metal group family in the periodic table.
Action potential of a non-pacemaker cardiomyocyte There are five phases to an action potential, which begin and end at phase 4. Phase 4. The resting phase: this has a resting potential of mV as a result of the constant outward movement of potassium via the inward rectifier channels.
During this phase, both the sodium and calcium channels are closed. Phase 0. The depolarization phase: the firing of a pacemaker cell or its conduction through a neighboring cell triggers the rise of TMP to above mV. Phase 1. Phase 2. The plateau phase: here the two counter currents are electrically balanced and result in the maintenance of the TMP balanced at just below 0 mV. The delayed rectifier potassium channel allows the passage of potassium to the outside of the cell down its concentration gradient.
Phase 3. The repolarization phase: during this phase, the calcium channels are gradually inactivated and the persistent flow of potassium to the outside of the cell thus exceeds the inward calcium flow, returning the potassium to the intracellular space and the sodium and calcium to the outside of the cell.
Action potential of a cardiac pacemaker cell The cardiac pacemaker cells have an innate automaticity, allowing their depolarization in rhythmic cycles. Current conduction All the cardiomyocytes are electrically coupled through the gap junction, including the pacemaker cell. Refractory period The longer refractory period during the long plateau in phase 2 due to the slow calcium channels provides the time needed for the complete emptying of the ventricles before the next contraction.
Causes Hyperkalemia occurs when compensatory mechanisms are no longer able to cope with the imbalance, which is why it is usually multifactorial. Increase in the intake of potassium via any route, e. Retention by the kidneys: since potassium excretion depends on aldosterone and the delivery of a sufficient distal amount of sodium and water within the nephrons, conditions such as renal failure, adrenal insufficiency Addison's disease , hyporeninemic hypoaldosteronism type IV, renal tubular acidosis, especially in patients with diabetic nephropathy as well as any condition that promotes hypoperfusion as in volume depletion and congestive heart failure, will affect the intricate balance of potassium in the body and predispose to hyperkalemia.
Adrenal insufficiency: this must be excluded in hyperkalemic patients, particularly in the presence of hyponatremia and muscle weakness. To screen for primary adrenal Insufficiency, a standard cosyntropin stimulation test is performed in which 0.
Drugs that retain potassium: prescription medication drugs which reduce sodium potassium ATPase activity such as beta-adrenergic receptor blockers, and drugs that reduce aldosterone secretion such as ACE and ARB inhibitors, non-steroidal anti-inflammatory drugs, and potassium-sparing diuretics, need close follow-up to avoid iatrogenic hyperkalemia, especially in the geriatric age group with their progressive decline in renal function as part of the aging process.
Perturbations in the transcellular shift of potassium: this may occur with conditions of acidosis, hyperglycemia, hyperosmolality, severe exercise, tissue breakdown, hyperkalemic periodic paralysis, and with beta-adrenergic blockers.
For every 0. Pseudo-hypoaldosteronism is a congenital autosomal recessive disease in which the kidneys are resistant to the actions of aldosterone. Pseudo-hyperkalemia must also not be overlooked: as the name implies, this occurs when there is elevated serum potassium in the presence of normal plasma potassium.
It may be seen in hemolyzed blood, prolonged tight tourniquet during a blood sampling procedure, causing the extracellular release of potassium, with repeated clenching of the fist during phlebotomy, traumatic venepuncture, with leukocytosis and thrombocytosis, and in some uncommon genetic syndromes such as familial pseudo-hyperkalemia and hereditary spherocytosis. However, it could simply just be a result of a simple laboratory error.
Effects of hyperkalemia Mild hyperkalemia is often asymptomatic, detected accidentally by laboratory tests, due to its vague symptoms such as malaise, muscle weakness and paraesthesia. Cardiac toxicity will usually present on the ECG in the following step-up escalating manner, although not necessarily so, depending on the etiology: At levels greater than 5.
These T waves can be differentiated from those of myocardial infarction and CVA by their short duration ranging from msec. At potassium levels greater than 6. Caution must be taken when replacing potassium in renal disease. If replacement is needed, consideration should be given to administering a smaller replacement 0. Intravenous replacement should be given through a central venous catheter or multiple peripheral intravenous catheters since potassium infusions greater than 0.
Repeat serum potassium levels should be evaluated after each replacement initially every 2 to 4hrs. If there is not a significant response to the initial replacements, a magnesium level should be evaluated as hypomagnesemia may be contributing to an intractable hypokalemic state. If the patient is not critically ill, does not have symptoms of hypokalemia, and has no reason for ongoing potassium losses, mild hypokalemia is likely to self-resolve simply by ensuring adequate potassium intake in diet.
Enteral replacement is less likely to lead to overtreatment and resultant hyperkalemia, and should always be considered if there is no urgency for treating mild hypokalemia. It is generally not necessary to exceed these concentrations under normal circumstances for mild hypokalemia. If there are ongoing losses, scheduled enteral KCl replacement may need to be continued at a dose that is based on calculated losses estimated.
Some circumstances may need consideration for ongoing potassium losses. These situations include: treatment of diabetic ketoacidosis, polyuric states such as diabetes insipidus, or severe diarrhea. Diabetic Ketoacidosis: In diabetic ketoacidosis, total body potassium levels are depleted due to extracellular movement of serum potassium levels, and resultant increased renal excretion of potassium. Initially, serum potassium levels will be elevated on presentation.
But once treatment with an insulin infusion is initiated, serum potassium levels will fall, and potassium replacement will often be necessary. Serum potassium levels should be monitored every 2 to 4 hours at the onset of treatment.
Once serum potassium levels fall below 4. Potassium levels are continued to be monitored every 4 to 6 hrs depending on the response. Once the insulin infusion is complete, and the patient is stabilized out of diabetic ketoacidosis, further potassium replacement is not necessary provided the serum potassium level is normalized.
This may lead to clinically significant potassium loss with high levels of urine output. Most of the time, close monitoring with potassium replacements as needed is sufficient. Including potassium in IVF replacement should be considered if above IV replacement strategies are unable to keep up with potassium losses.
If there are no EKG changes, eliminate all potassium from diet and intravenous fluid replacement. If there are no risk factors for potassium levels to continue increasing e. The patient should be followed on cardiorespiratory monitoring to watch for rhythm changes or changes in T waves.
Repeat potassium levels should be performed at least every 12 to 24 hours to ensure resolution of hyperkalemia. If there are risk factors for potassium levels to continue increasing, such as in renal failure, additional measures should be taken to eliminate potassium.
Recheck serum potassium levels every 6 hrs or sooner if there signs of EKG changes on cardiorespiratory monitoring. If the serum potassium level is greater than 6. If EKG changes improve, but do not normalize, may repeat calcium infusion in 10 minutes. Expect that EKG changes will return in 15 to 30 minutes if other measures are not taken to reduce serum potassium levels quickly.
Do not administer with calcium gluconate as is not compatible. Flush IV well between infusions. Administer insulin 0. May repeat dose 30 to 60 minutes after first dose. Monitor glucose hourly. May also consider infusion of insulin at 0. The most important adverse effect for the management of hypokalemia is overtreatment and iatrogenic hyperkalemia. To avoid this, one must carefully consider the urgency of treating hypokalemia, risk factors for an overresponse to intravenous replacement e.
Calcium chloride or Calcium gluconate: Can cause ventricular arrhythmia and cardiac arrest if given too fast. Calcium solutions must be given slowly over 3 to 5 minutes. Calcium chloride replacement is contraindicated in ventricular fibrillation. Both calcium solutions can cause significant tissue necrosis if extravasated.
Do not use Calcium chloride peripherally. Ensure the peripheral IV is working properly and is not infiltrated prior to administration. Sodium bicarbonate: Can cause hypernatremia, hypokalemia, hypocalcemia, and hypomagnesemia. Can also cause tissue necrosis with extravasation. In infants and neonates, use 4.
Insulin and glucose: Can cause hypoglycemia or hyperglycemia. Blood sugars should be checked after each dose, or hourly if on infusion. Sodium polystyrene: Can cause iatrogenic hypokalemia requiring potassium replacements if too much is given. Can also cause hypernatremia, hypocalcemia, and hypomagnesemia. There have been reports of colonic necrosis, gastrointestinal bleeding, colitis and perforation when used with sorbitol in patients with underlying gastrointestinal risk factors.
Use with caution in patients with prematurity or evidence of gastrointestinal compromise. Hemodialysis: Carries substantial risks from both the procedure of intermittent hemodialysis as well as the procedure of catheter placement necessary for performing dialysis.
Should be used as last resort if above treatments fail. If left untreated, both severe hypokalemia and severe hyperkalemia can lead to paralysis, cardiac arrhythmias, and cardiac arrest. Hyperkalemia, generally carries a higher risk of morbidity and mortality if left untreated.
Severe hypokalemia may also cause respiratory failure, constipation and ileus. The most important aspect of prevention is consideration of comorbidities or medical therapies that may increase or decrease serum potassium levels, and then adjusting potassium intake as necessary. To prevent hypokalemia, consider adding enteral potassium replacement to patients on a substantial amount of diuretics, patients with diarrhea or polyuria, or patients who may have heightened mineralocorticoid activity.
Also consider replacement of magnesium sulfate in conditions that can cause depletion of magnesium. To prevent hyperkalemia, consider restricting potassium replacement or eliminating potassium from intake in patients with renal disease, anuria, on ACE inhibitors, or with conditions with increased tissue breakdown such as rhabdomyolysis, burn injuries or crush injuries.
Aune, GJ, Custer, Rau. A practical outline for managing fluid and electrolye disorders in children. A general review of fluid and electrolyte physiology, derangements and management. All rights reserved. No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC.
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