Hyperkalemia - Wikipedia
Severe hyperkalemia may result from cell lysis when acute kidney injury develops in Severe metabolic acidosis, often with marked elevation in the anion-gap may . (A concise review summarizing the relationship between fluid balance and. Hyperkalemia, also spelled hyperkalaemia, is an elevated level of potassium (K+ ) in the blood This is especially pronounced in acute kidney injury where the glomerular Metabolic acidosis is a cause of hyperkalemia because increase in . There are important interactions between potassium and acid-base a plasma potassium concentration that is elevated in relation to total Changes in plasma potassium concentration during acute acid-base disturbances.
To the extent that water intake exceeds this decreased maximal free water excretion, hyponatremia will ensure. Treatment of hyponatremia is generally free-water restriction. In patients with severe AKI and more profound hyponatremia, renal replacement therapy may be necessary. In patients with severe hyponatremia dialysis may need to be performed, using a dialysate solution with a reduced sodium concentration in order to minimize the rate of correction of the serum sodium concentration.Respiratory Acidosis made easy in HD
Excessively rapid correction of hyponatremia can be associated with the development of central pontine myelinolysis. For this reason, the use of slower modalities of renal replacement therapy, such as continuous renal replacement therapy CRRT or sustained low efficiency dialysis SLEDmay be preferred over conventional intermittent hemodialysis.
- On the relationship between potassium and acid-base balance
- Acute Kidney Injury: Complications associated with Acute Kidney Injury
Hypernatremia is a less common complication of acute kidney injury, but may develop during the diuretic phase of recovering acute tubular necrosis ATN or in the setting of a post-obstructive diuresis, if water intake is inadequate to match free-water losses. Acid-Base Disturbances Metabolic acidosis is the most common acid-base disturbance associated with acute kidney injury, developing as the result of impaired excretion of the daily load of metabolic fixed acid.
Although initially a hyperchloremic metabolic acidosis develops, widening of the anion gap is often seen as the result of accumulation of phosphate, sulfate and small organic anions. Severe metabolic acidosis, often with marked elevation in the anion-gap may develop, as a result of underlying systemic disease, such as lactic acidosis due to tissue hypoperfusion, sepsis or advanced liver disease, diabetic ketoacidosis or toxic ingestions such as ethylene glycol.
Metabolic alkalosis is an infrequent finding in acute kidney injury, but may complicate overly aggressive treatment of acidemia with intravenous bicarbonate or loss of gastric acid due to vomiting or nasogastric drainage.
Complications of Mineral and Uric Acid Homeostasis Hyperphosphatemia is a common complication of acute kidney injury, developing as a direct consequence of decreased renal excretion. Hyperphosphatemia can usually be treated using oral phosphate binders; in severe hyperphosphatemia, dialysis may be necessary, however there is no specific threshold serum phosphate level as an indication for dialysis.
Hypocalcemia in AKI develops as a consequence of skeletal resistance to parathyroid hormone and reduced renal conversion of hydroxyvitamin D to the active 1,dihydroxyvitamin D by the kidney. In rhabdomyolysis, calcium sequestration in injured muscle may result in more profound degrees of hypocalcemia.
The hypocalcemia associated with AKI is usually asymptomatic and does not require specific treatment.
Symptomatic hypocalcemia requires treatment with intravenous calcium, however the aggressiveness of therapy may need to be tempered in the setting of concomitant severe hyperphosphatemia, as calcium infusion may result in metastatic calcium phosphate deposition.
It is unusual for hypercalcemia to develop as a consequence of AKI.
More commonly, when hypercalcemia is present in the setting of AKI, both are a consequence of an underlying disease, such as multiple myeloma, or the AKI is mediated in part by the hypercalcemia.
Hypercalcemia may develop during the recovery from myoglobinuric AKI in rhabdomyolysis as calcium deposited in injured muscle is mobilized. Mild asymptomatic hypermagnesemia is common in oliguric AKI as the result of impaired excretion of ingested magnesium.
More severe hypermagnesemia is usually iatrogenic, as the result of parenteral administration, as in the management of AKI associated with pre-eclampsia. This condition is usually suspected when patient is clinically well without any ECG changes. Mechanical trauma during blood drawing can cause potassium leakage out of the red blood cells due to haemolysed blood sample.
Since exercise can cause elevated potassium levels, repeated fist clenching can cause transient rise in potassium levels. Prolonged length of blood storage can also increase serum potassium levels. Potassium leaks out of platelets after clotting has occurred. On the other hand, processing of heparinised, unclot blood does not cause falsely elevated potassium.
This problem can be avoided by processing serum samples, because formation of clot protect the cells from haemolysis during processing. A familial form of pseudohyperkalemia may also be present, and is characterised by increased serum potassium in whole blood stored at or below room temperature, without additional hematological abnormalities.
This is due to increased potassium permeability in red blood cells. The potassium gradient is critically important for many physiological processes, including maintenance of cellular membrane potentialhomeostasis of cell volume, and transmission of action potentials in nerve cells. In the kidneys, elimination of potassium is passive through the glomeruliand reabsorption is active in the proximal tubule and the ascending limb of the loop of Henle.
There is active excretion of potassium in the distal tubule and the collecting duct ; both are controlled by aldosterone. In sweat glands potassium elimination is quite similar to the kidney, its excretion is also controlled by aldosterone. To compensate for this deficit in function, the colon increases its potassium secretion as part of an adaptive response. However, serum potassium remains elevated as the colonic compensating mechanism reaches its limits.
Ineffective elimination can be hormonal in aldosterone deficiency or due to causes in the kidney parenchyma that impair excretion.
On the relationship between potassium and acid-base balance
This depolarisation opens some voltage-gated sodium channelsbut also increases the inactivation at the same time. Since depolarisation due to concentration change is slow, it never generates an action potential by itself; instead, it results in accommodation.
Above a certain level of potassium the depolarisation inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiacand gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction, which can cause ventricular fibrillationabnormally slow heart rhythmsor asystole.
The normal serum level of potassium is 3. Generally, blood tests for kidney function creatinineblood urea nitrogenglucose and occasionally creatine kinase and cortisol are performed. Calculating the trans-tubular potassium gradient can sometimes help in distinguishing the cause of the hyperkalemia. Also, as noted abovehyperkalemia causes an overall membrane depolarisation 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.
As the extracellular potassium levels increase, potassium conductance is increased so that more potassium leaves the myocyte in any given time period. 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 electrolytesas well as levels of catecholamines, play a major role.
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. The choice depends on the degree and cause of the hyperkalemia, and other aspects of the person's condition. Myocardial excitability[ edit ] 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.
Clinical practice guidelines recommend giving 6.