Complications
Pleural effusions are a common complication of chronic congestive HF.
A common reason for refractory symptoms is the cardiorenal syndrome, a spectrum of disorders involving the heart and kidneys in which acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ.[287] These patients show an impaired response to diuretics and ACE inhibitors and are at increased risk of adverse effects during treatment with digoxin.[247][288][289] Persistent or progressive renal functional impairment has been associated with a poor prognosis.[290][291] The symptoms of HF in patients with end-stage renal disease may be exacerbated by an increase in loading conditions produced both by anaemia and by fistulas implanted to permit dialysis.[292]
See Management approach for more information on chronic kidney disease and HF.
Patients with HF frequently have comorbid anaemia for a variety of reasons, which may worsen HF symptoms. Several studies have demonstrated worse outcomes in patients with HF and anaemia, such as a 1.027 higher risk for mortality associated with a 1% lower haematocrit, after adjustment for other factors.[293][294] It is unclear whether anaemia is the cause of decreased survival or a marker of more severe disease. Several small studies have suggested benefit from use of erythropoietin and iron for treatment of mild anaemia in HF, although at the cost of increased risk of thromboembolic events.[295][296][297] However, a larger study showed no clinical benefit of darbepoietin alfa treatment.[298]
Despite optimal treatment, many precipitating factors or even new events may cause acute decompensation of a previously stable patient, thus leading to pulmonary oedema (backward failure) or cardiogenic shock (forward failure). Common causes include myocardial infarction and its mechanical complications (papillary muscle rupture with new-onset acute mitral regurgitation, ventricular septal defect, and ventricular rupture), arrhythmias, pulmonary embolism, infection, anaemia, tamponade, myocarditis, acute renal failure or even increased salt intake, inappropriate drug therapy, or patient non-compliance.
Patients with acute decompensation require urgent haemodynamic stabilisation and diagnosis of the precipitating cause. Pharmacological therapy includes intravenous diuretics, intravenous positive inotropic agents, intravenous vasodilators, and intravenous vasopressors. Non-pharmacological treatment modalities will be necessary: these include oxygenation, balloon counterpulsation, pacing, urgent catheterisation or urgent cardiac surgery, or mechanical support with ventricular assist devices.
Patients have a high risk of developing acute renal insufficiency at any point of their clinical course as a result of either poor renal perfusion (low cardiac output state) or drug overuse to treat HF (diuretics, ACE inhibitors, aldosterone antagonists, angiotensin-II receptor antagonists). In addition, the use of carvedilol requires close monitoring of the renal function as it could contribute, with other agents, to the development of acute renal injury. Inability to maintain adequate renal perfusion on oral therapy may eventually necessitate intravenous inotropic infusion or urgent ultrafiltration and haemodialysis.
Sudden cardiac death is common in HF patients and accounts for approximately 30% to 40% of the deaths among these patients. It can be the consequence of both ventricular fibrillation and electromechanical dissociation, and can occur any time in the course of the disease, even in the asymptomatic patient.
In patients who survive an episode of cardiac arrest, prophylactic insertion of an implantable cardioverter defibrillator and initiation of appropriate anti-arrhythmic therapy is indicated.
Patients with heart failure have several factors that may put them at a high risk of hyperkalaemia; these include factors that are directly related to the condition (i.e., impaired delivery of sodium and water to the distal renal tubule), associated comorbidities (e.g., diabetes, CKD), and use of drugs that cause hyperkalaemia.[7]
Use of patiromer, a novel potassium-binder, to manage serum potassium levels and allow target doses of renin-angiotensin-aldosterone system inhibitor use (particularly aldosterone antagonists) in patients with HFrEF is being investigated.[299]
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