Heart failure module 5: special cases in heart failure

Released1 November 2017     Expires: 01 November 2019      Programme:

Hyperkalaemia

Some 90% of potassium excretion is via the kidneys. Once filtered through the glomerulus, the majority is re-absorbed from the urine in the proximal convoluted tubule and loop of Henle. Excretion of excess potassium into the urine occurs in the principal cells of the collecting duct.37

Aldosterone stimulates potassium excretion in the collecting duct.38 Thus, a reduction in serum aldosterone levels or mineralocorticoid receptor antagonism reduces urinary excretion of potassium.

Renin-angiotensin-aldosterone system (RAAS) inhibitors are associated with higher serum potassium levels and increased risk of hyperkalaemia (figure 3).39,40 The rate of hyperkalaemia is higher with mineralocorticoid receptor antagonists (MRA) than with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) (table 2).41–4 Combination therapy can thus be dangerous, making close monitoring of potassium mandatory in patients receiving both an ACE inhibitor/ARB and an MRA.

Heart failure module 5 - Figure 3. RAAS inhibitors are associated with higher serum potassium levels
Figure 3. RAAS inhibitors are associated with higher serum potassium levels
Heart failure learning module 5: Table 2. Rates of hyperkalaemia in clinical trials of drugs that inhibit the RAAS in patients with heart failure
Table 2. Rates of hyperkalaemia in clinical trials of drugs that inhibit the RAAS in patients with heart failure.

Hyperkalaemia (>6.0 mmol/L) is associated with increased mortality in patients with heart failure,5 and discontinuation of drugs with proven prognostic benefit (such as MRAs) to avoid iatrogenic hyperkalaemia is common.45

In clinical trials, however, hyperkalaemia is also seen in the placebo groups, and thus hyperkalaemia is not solely due to heart failure treatment. Diabetes,46 and chronic kidney disease (CKD),47 are associated with hyperkalaemia (>5.5 mmol/L) independent of treatment with an MRA. Potentially as few as 54% of cases of hyperkalaemia among patients with heart failure who are taking an MRA are attributable to the drug itself.48

Figure 4. Electrocardiogram changes associated with hyperkalaemia
Figure 4. Electrocardiogram changes associated with hyperkalaemia
Hyperkalaemia and the ECG

Hyperkalaemia causes shortening of the action potential duration and slowed conduction velocity of the action potential across myocytes. The consequence is impaired AV node conduction and heart block which – in conjunction with suppression of infranodal pacemaking (the ability of ventricular myocardium to generate an ectopic beat) in hyperkalaemia – may cause asystole. Hyperkalaemia also predisposes to VT/VF through an incompletely understood mechanism.30

ECG changes associated with hyperkalaemia (figure 4) are:9

  • peaked T-waves (‘tall, tented T-waves’)
  • broad, small or absent P waves
  • broadened QRS
  • varying degrees of heart block
  • asystole
  • sine-wave pattern – T-waves fused with a broad QRS
  • idioventricular rhythm
  • ventricular tachycardia / fibrillation.
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