Until recently, the importance of hypochloraemia in heart failure has been overlooked. It is common and associated with a higher risk of mortality in patients with acute or chronic heart failure, independent of serum sodium levels.30,31
It is likely to develop through the same broad mechanisms that cause hyponatraemia but, unlike hyponatraemia, hypochloraemia may have a pathological effect – diuretic resistance.32,33 Whether or not low serum chloride is a therapeutic target in heart failure remains to be seen.
Hypokalaemia in patients with heart failure is a consequence of diuretic therapy.34 Hypomagnesaemia increases renal excretion of potassium and is often seen in conjunction with hypokalaemia. Hypokalaemia reduces action potential duration and reduces repolarisation reserve causing QT-interval prolongation, which can lead to ventricular tachycardia (VT).35 In animal studies, even a moderate hypokalaemia (2.5–3.0 mmol/L) can be highly arrhythmogenic; 50% of the rabbits tested had either VT or ventricular fibrillation (VF) after reducing serum potassium to 2.7 mmol/L.36
Electrocardiogram (ECG) changes associated with hypokalaemia (figure 2) are:
- U waves
- T-wave flattening
- ST-segment changes
- ventricular tachycardia
- pulseless electrical activity (PEA) or asystole.
Correction of hypokalaemia is indicated if ECG changes are present or if potassium is <2.5 mmol/L.9 Unless cardiac arrest is imminent, potassium replacement should be at a rate of 10–20 mmol/hr given intravenously with normal saline. Oral supplementation may be sufficient in mild cases. Correction of concurrent hypomagnesaemia is essential for effective potassium replacement.