Definition

There is no universal definition. We have defined hyperkalaemia as a serum potassium concentration higher than 5.5 mmol l⁻¹; in practice, hyperkalaemia is a continuum. As the potassium concentration increases above this value the risk of adverse events increases and the need for urgent treatment increases. Severe hyperkalaemia has been defined as a serum potassium concentration higher than 6.5 mmol l⁻¹.

Causes

There are several potential causes of hyperkalaemia, including renal failure, drugs (angiotensin converting enzyme inhibitors (ACE-I), angiotensin II receptor antagonists, potassium sparing diuretics, non-steroidal anti-inflammatory drugs (NSAIDs), beta-blockers, trimethoprim), tissue breakdown (rhabdomyolysis, tumour lysis, haemolysis), metabolic acidosis, endocrine disorders (Addison's disease), hyperkalaemic periodic paralysis, or diet (may be sole cause in patients with advanced chronic kidney disease). Abnormal erythrocytes or thrombocytosis may cause a spuriously high potassium concentration. ² x W.S. Smellie. Spurious hyperkalaemia. BMJ 334 (2007) (693 - 695) The risk of hyperkalaemia is even greater when there is a combination of factors such as the concomitant use of ACE-I and NSAIDs or potassium sparing diuretics.

Recognition of hyperkalaemia

Exclude hyperkalaemia in patients with an arrhythmia or cardiac arrest. ³ x J.T. Niemann, C.B. Cairns. Hyperkalemia and ionized hypocalcemia during cardiac arrest and resuscitation: possible culprits for postcountershock arrhythmias?. Ann Emerg Med 34 (1999) (1 - 7) Patients may present with weakness progressing to flaccid paralysis, paraesthesia, or depressed deep tendon reflexes. Alternatively, the clinical picture can be overshadowed by the primary illness causing hyperkalaemia. The first indicator of hyperkalaemia may also be the presence of ECG abnormalities, arrhythmias, cardiopulmonary arrest or sudden death. The effect of hyperkalaemia on the ECG depends on the absolute serum potassium as well as the rate of increase. Most patients will have ECG abnormalities at a serum potassium concentration higher than 6.7 mmol l⁻¹. ⁴ x J. Ahmed, L.S. Weisberg. Hyperkalemia in dialysis patients. Semin Dial 14 (2001) (348 - 356) The use of a blood gas analyser that measures potassium can reduce delay in recognition.

The ECG changes associated with hyperkalaemia are usually progressive and include:

• first degree heart block (prolonged PR interval) [>0.2 s];
• flattened or absent P waves;
• tall, peaked (tented) T waves [T wave larger than R wave in more than 1 lead];
• ST-segment depression;
• S and T wave merging (sine wave pattern);
• widened QRS [>0.12 s];
• ventricular tachycardia;
• bradycardia;
• cardiac arrest (pulseless electrical activity [PEA], ventricular fibrillation/pulseless ventricular tachycardia [VF/VT], asystole).

Treatment of hyperkalaemia

There are three key treatments for hyperkalaemia ⁵ x A.V. Alfonzo, C. Isles, C. Geddes, C. Deighan. Potassium disorders – clinical spectrum and emergency management. Resuscitation 70 (2006) (10 - 25) :

• 1. cardiac protection;
• 2. shifting potassium into cells;
• 3. removing potassium from the body.

Intravenous calcium salts are not generally indicated in the absence of ECG changes. Monitor effectiveness of treatment, be alert to rebound hyperkalaemia and take steps to prevent recurrence of hyperkalaemia. When hyperkalaemia is strongly suspected, e.g., in the presence of ECG changes, start life-saving treatment even before laboratory results are available. The treatment of hyperkalaemia has been the subject of a Cochrane review. ⁶ x B. Mahoney, W. Smith, D. Lo, K. Tsoi, M. Tonelli, C. Clase. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev (2005) (CD003235)

Indications for dialysis

Haemodialysis (HD) is the most effective method for removal of potassium from the body. The principle mechanism of action is the diffusion of potassium ions across the membrane down the potassium ion gradient. The typical decline in serum potassium is 1 mmol l⁻¹ in the first 60 min, followed by 1 mmol l⁻¹ over the next 2 h. The efficacy of HD in decreasing serum potassium concentration can be improved by performing dialysis with a low potassium concentration in the dialysate, ⁹ x C. Zehnder, J.P. Gutzwiller, A. Huber, C. Schindler, D. Schneditz. Low-potassium and glucose-free dialysis maintains urea but enhances potassium removal. Nephrol Dial Transplant 16 (2001) (78 - 84) a high blood flow rate ¹⁰ x J.P. Gutzwiller, D. Schneditz, A.R. Huber, C. Schindler, E. Garbani, C.E. Zehnder. Increasing blood flow increases kt/V(urea) and potassium removal but fails to improve phosphate removal. Clin Nephrol 59 (2003) (130 - 136) or a high dialysate bicarbonate concentration. ¹¹ x R.M. Heguilen, C. Sciurano, A.D. Bellusci, et al.. The faster potassium-lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients. Nephrol Dial Transplant 20 (2005) (591 - 597)

Consider haemodialysis early for hyperkalaemia associated with established renal failure, oliguric acute kidney injury (<400 ml day⁻¹ urine output) or when there is marked tissue breakdown. Dialysis is also indicated when hyperkalaemia is resistant to medical treatment. Serum potassium frequently rebounds after initial treatment. In unstable patients continuous renal replacement therapy (CRRT) (e.g., continuous veno-veno haemofiltration) is less likely to compromise cardiac output than intermittent haemodialysis. CRRT is now widely available in many intensive care units.

Cardiac arrest in haemodialysis patients

Cardiac arrest is the most common cause of death in haemodialysis patients. ¹² x P.H. Pun, R.W. Lehrich, S.R. Smith, J.P. Middleton. Predictors of survival after cardiac arrest in outpatient hemodialysis clinics. Clin J Am Soc Nephrol 2 (2007) (491 - 500) Events occurring particularly during haemodialysis treatment, pose several novel considerations.

Definition

Hypokalaemia is defined as a serum potassium < 3.5 mmol l⁻¹. Severe hypokalaemia is defined as a K⁺ < 2.5 mmol l⁻¹ and may be associated with symptoms.

Causes

Causes of hypokalaemia include gastrointestinal loss (diarrhoea), drugs (diuretics, laxatives, steroids), renal losses (renal tubular disorders, diabetes insipidus, dialysis), endocrine disorders (Cushing's Syndrome, hyperaldosteronism), metabolic alkalosis, magnesium depletion, and poor dietary intake. Treatment strategies used for hyperkalaemia may also induce hypokalaemia.

Recognition of hypokalaemia

Exclude hypokalaemia in every patient with an arrhythmia or cardiac arrest. In dialysis patients, hypokalaemia occurs commonly at the end of a haemodialysis session or during treatment with peritoneal dialysis.

As serum potassium concentration decreases, the nerves and muscles are predominantly affected causing fatigue, weakness, leg cramps, constipation. In severe cases (K⁺ < 2.5 mmol l⁻¹), rhabdomyolysis, ascending paralysis and respiratory difficulties may occur.

ECG features of hypokalaemia are:

• U waves;
• T wave flattening;
• ST-segment changes;
• arrhythmias, especially if patient is taking digoxin;
• cardiopulmonary arrest (PEA, pulseless VT/VF, asystole).

Treatment

This depends on the severity of hypokalaemia and the presence of symptoms and ECG abnormalities. Gradual replacement of potassium is preferable, but in an emergency, intravenous potassium is required. The maximum recommended IV dose of potassium is 20 mmol h⁻¹, but more rapid infusion (e.g., 2 mmol min⁻¹ for 10 min, followed by 10 mmol over 5–10 min) is indicated for unstable arrhythmias when cardiac arrest is imminent. Continuous ECG monitoring is essential during IV infusion and the dose should be titrated after repeated sampling of serum potassium levels.

Many patients who are potassium deficient are also deficient in magnesium. Magnesium is important for potassium uptake and for the maintenance of intracellular potassium levels, particularly in the myocardium. Repletion of magnesium stores will facilitate more rapid correction of hypokalaemia and is recommended in severe cases of hypokalaemia. ²¹ x J.N. Cohn, P.R. Kowey, P.K. Whelton, L.M. Prisant. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med 160 (2000) (2429 - 2436)

Calcium and magnesium disorders

The recognition and management of calcium and magnesium disorders is summarised in Table 8.1 .