As well as dealing with disease modifying therapies, heart failure specialists also manage the complications of heart failure. This module will familiarise the reader with the clinical significance and treatment of the more commonly encountered problems; electrolyte disturbances, anaemia and iron deficiency.
Electrolyte abnormalities in patients with heart failure
Electrolyte disturbances are a common complication of heart failure, which affect treatment decisions and outcome (table 1).1–7 Hyponatraemia, both hypo- and hyper- kalaemia and, more recently, hypochloraemia are the best defined. However, abnormalities in calcium, phosphate, bicarbonate and magnesium may also be common in patients with heart failure,8 and can be life threatening if severe, requiring urgent treatment.9
Hyponatraemia is the most common electrolyte abnormality seen in patients admitted with acute heart failure. Hyponatraemia is strongly associated with an adverse outcome in acute and chronic heart failure and is a marker of severe chronic heart failure that might prompt consideration for transplant.11 It arises through two mechanisms:12
Reduced effective circulating volume in heart failure stimulates baroreceptors in the atria, aorta and peripheral arteries thus increasing the activity of the renin-angiotensin-aldosterone (RAAS) and sympathetic nervous systems. It also causes increased secretion of anti-diuretic hormone (ADH; also known as arginine vasopressin). ADH is normally secreted in response to increasing plasma osmolality, and so in patients with heart failure, there must be a non-osmolar stimulus to its release. The net result is water retention in excess of sodium retention (figure 1).13
Additionally, reduced renal blood flow reduces glomerular filtration rate thus limiting the rate at which the kidneys can excrete free water.14 Increased water retention leads to a relative sodium reduction; the serum is diluted although the body has an absolute excess of sodium.
The first-line treatment of venous congestion in heart failure is loop diuretics which act by inhibition of the sodium potassium chloride (Na2+-K+-2Cl–) symporter in the ascending limb of the loop Henle. The resulting increase in urine sodium, potassium and chloride causes increased free water excretion alongside electrolyte loss.15
However, in the context of a significant reduction in effective circulating volume (and thus, renal blood flow), the ability of the kidneys to produce dilute urine is reduced. Under such circumstances, loop diuretics cause urinary electrolyte loss without significant free water excretion.14–6
Approximately 90% of patients admitted with acute HF are treated with loop diuretics and a similar proportion remains on them one year from discharge.17