Pleural effusions are a common complication of chronic congestive heart failure.
chronic kidney disease
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. These patients show an impaired response to diuretics and ACE inhibitors and are at increased risk of adverse effects during treatment with digoxin. Persistent or progressive renal functional impairment has been associated with a poor prognosis. The symptoms of heart failure 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. Most patients will tolerate mild-to-moderate degrees of functional renal impairment without difficulty. However, if the serum creatinine increases to more than 265 micromols/L (>3 mg/dL), the renal insufficiency can severely limit the efficacy and enhance the toxicity of established treatments. Impaired renal function may exclude the therapeutic use of ACE inhibitors and angiotensin-II receptor antagonists. In patients with a serum creatinine greater than 442 micromols/L (>5 mg/dL), haemofiltration or dialysis may be needed to control fluid retention, minimise the risk of uraemia, and allow the patient to respond to and tolerate the drugs routinely used for the management of heart failure.
Patients with heart failure frequently have anaemia for a variety of reasons, which may worsen heart failure symptoms. Several studies have demonstrated worse outcomes in patients with heart failure and anaemia, such as a 1.027 higher risk for mortality associated with a 1% lower haematocrit, after adjustment for other factors. 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 heart failure, although at the cost of increased risk of thromboembolic events. However, a larger study showed no clinical benefit of darbepoietin alfa treatment.
acute decompensation of chronic heart failure
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.
acute kidney injury
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 heart failure (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 IV inotropic infusion or urgent ultrafiltration and haemodialysis.
sudden cardiac death
Sudden cardiac death is common in heart failure 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.
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