Heart failure is typically an acute on chronic condition. Treatment of the exacerbations should aim both to stabilize clinical and hemodynamic status, and to identify the precipitating factors and determine whether they are preventable and reversible. Although in most cases the specific cardiac disease responsible for the heart failure has already been diagnosed, the precipitating factors (Table) can usually be pinpointed by history, physical examination, electrocardiogram, echocardiogram, chest x-ray, and appropriate blood workup.
Tachyarrhythmia (atrial fibrillation/flutter, ventricular tachycardia)
Bradycardia (sinus dysfunction, high-degree atrioventricular block)
Onset or aggravation of valvular regurgitation (mitral or tricuspid)
Myocardial ischemia/infarction (often asymptomatic)
Patient noncompliance (medication/lifestyle)
Recent change in treatment strategy (antiarrhythmic drugs, P-blockers, verapamil, diltiazem, nonsteroidal anti-inflammatory drugs)
Tolerance (nitrates, hydralazine, a-blockers)
Toxicity (substance abuse, alcoholism)
Renal dysfunction (excessive diuretics)
Acute infections (bacterial, viral)
Embolism (pulmonary, systemic)
Thyroid dysfunction (amiodarone)
Anemia (occult bleeding)
Decompensated diabetes mellitus
Poor compliance with lifestyle advice and medication inadequate fluid intake, excessive physical activity, stress, and failure to take medication at the correct time, in the correct dose, or at all is the most frequent and predictable precipitant of exacerbation (observed in over 60% of heart failure patients). It will usually be identified in an accurate history.
Examples of inappropriate prescribing include excessive doses of diuretics, inadequate doses of angiotensin-converting enzyme inhibitors, and the use of class I antiarrhythmic drugs (verapamil, diltiazem) or first-generation dihydropyridines. Nonsteroidal anti-inflam-matory drugs, tricyclic antidepressants, and steroids are examples of noncardiovascular malprescribing. A drug history and laboratory tests are useful for identifying such factors. Drug effects that can precipitate destabilization include thyroid dysfunction due to amiodarone (periodic thyroid function tests are a useful preventive), renal dysfunction due to excessive use of diuretics (suspect hypovolemia if the increase in azotemia exceeds that expected from the increase in creatinine, or if the hematocrit is elevated), and electrolyte abnormalities. Failure of a drug to achieve its desired effect, such as to control hypertension, can also be clinically destabilizing. Patients with more severe disease are more prone to destabilization because their compensatory resources are that much more limited. Compliance with guidelines and cooperative follow-up between primary care physician and cardiologist are important factors in preventing iatrogenic decompensation.
Infection can be both a concomitant and precipitating factor. Usually respiratory, it accompanies destabilization in one quarter of cases. It is more frequent in the
Symptoms and diagnosis
elderly and those who are hemodynamically unstable. In addition, many heart failure patients are immunocompromised, malnourished, or affected by concomitant disease (hyperglycemia, hyperuricemia), and are thus infection-prone. They are also frequently exposed to sources of infection from repeated hospitalization, placement of venous lines, and treatment with blood derivatives. A further factor is the depression often associated with heart failure, which may impair activities of daily living, including compliance with basic lifestyle advice. Prevention lies in augmenting compliance. Advise patients to avoid overcrowded, unhealthy public places, abrupt temperature changes, etc. Identify and treat potential sources of infection (eg, dental caries), and maintain anti-flu and anti-hepatitis B vaccination.
Tolerance attenuates the desired effects of several drugs (eg, nitrates and hydralazine). In the case of nitrates, it can be largely prevented by leaving a window of 6 to 8 hours between doses. Choose a window appropriate to the patient’s needs. For a patient with dyspnea on exertion, choose a nocturnal window; for a patient whose chief complaint is paroxysmal nocturnal dyspnea, choose a daytime window. Another technique is to use incremental dosing, which overcomes tolerance by doubling the previous dose: begin with 20 mg, proceed to 40 mg, then to 80 mg, followed by a window.
Atrial arrhythmia (usually fibrillation) is a common precipitant, together with sustained ventricular arrhythmia. Destabilizing bradyarrhythmias include iatrogenic arrhythmia (eg, pacemaker malfunction, iatrogenic atrioventricular block) and spontaneous arrhythmias. Many patients improve with cardioversion to sinus rhythm or better control of the ventricular response, either with drugs (eg, amiodarone, (i-blockers) or, if unsuccessful or contraindicated, electrical methods (eg, atrioventricular node ablation, pacemaker implantation). Holter electrocardiography is useful for diagnostic purposes.
Ischemic heart disease
Myocardial ischemia, which may often be silent, can precipitate decompensation or sudden death. Always suspect ischemia if a patient with known or suspected heart disease suddenly develops pulmonary edema or severe dyspnea on exertion, especially if their basal clinical and hemodynamic status was not severe. To prevent such episodes, remember the importance of screening heart failure patients for ischemia and myocardial viability using such investigations as dobu-tamine stress echocardiography or perfusion scintigraphy, followed as appropriate by coronary angioplasty. It is also important to identify and correct other risk factors and coach the patient in sublingual nitrate therapy (not only for angina, but also for dyspnea and predictable responses to unavoidable exertion).
Thromboembolism is more frequent in patients with major cardiac dilatation, severe systolic dysfunction, atrial fibrillation, and low cardiac output. There is no current consensus on the indications for anticoagulant therapy, but several trials on the efficacy of oral anticoagulation in chronic heart failure are ongoing.
Aggravated mitral insufficiency can precipitate destabilization and make decompensation refractory to medical treatment. In the presence of regurgitation, consider surgical repair or more aggressive medical therapy (eg, high-dose nitrates, or cyclical unloading therapy with nitroprusside or intravenous nitroglycerin).
symptom; diagnosis; destabilizing factor; compliance; iatrogenic factor; infection; drug tolerance; arrhythmia; ischemic heart disease
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