HEART
FAILURE
Clinical Overview
Evaluation
Initial Evaluation
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In a patient presenting with symptoms of heart failure, the initial evaluation is the first step towards the rational management of that patient. A physical exam and initial testing is followed by a decision whether the patients requires hospital management. If outpatient management will be adequate, a measurement of left-ventricular function should follow, to determine ejection fraction and thus determine whether the heart failure is due to diastolic or systolic dysfunction. From this determination, proper treatment may then be determined.1
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Signs1 |
Symptoms1 |
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While many patients with severely impaired left-ventricular function may not have any symptoms of heart failure, when clinical heart failure develops, dyspnea on exertion appears to be the earliest symptom.2 As recommended by the AHCPR Guidelines for heart failure, all patients who complain of paroxysmal nocturnal dyspnea (awakening from sleep with shortness of breath), or new-onset dyspnea on exertion should undergo evaluation for heart failure unless history and physical examination clearly indicate a noncardiac cause for their symptoms, such as severe pulmonary disease.1 The presence of any one of the above symptoms is sufficient to consider heart failure as an underlying cause, but orthopnea, dyspnea on exertion, and paroxysmal nocturnal dyspnea are the greatest concern.
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Nonspecific symptoms of heart failure1 |
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severity |
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Electrocardiogram Electrolytes, serum creatinine Complete blood count Urinalysis T4 and TSH Liver function tests Assessment of LV function |
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A search for precipitating, complicating, or primary causative factors should
be undertaken in every patient with suspected new onset heart failure.1
A chest x-ray should be obtained as an early diagnostic test. Cardiomegaly
in symptomatic patients is highly suggestive of heart failure, although a normal
chest x-ray does not rule it out. An electrocardiogram (ECG) should be
performed to assess evidence of acute ischemia, arrhythmias, prior myocardial
infarction (MI), and left ventricular hypertrophy, however it is usually nonspecific
in heart failure patients. Routine chemistry profiles including serum
electrolytes, blood urea nitrogen (BUN), and liver function tests should be
obtained for all patients to establish baseline levels and assist in decisions
on treatment.1Low
hematocrits of 25-35% may aggravate underlying heart failure and therefore a
complete blood count (CBC) is recommended. A urinalysis to rule out renal
complications, such as the nephrotic syndrome should also be performed.
Radionuclide ventriculography
Echocardiography (Echo)
Measurement of ventricular performance can help to avoid inappropriate pharmacologic treatment, for example, the use of digoxin in a patient with diastolic dysfunction and normal sinus rhythm.
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Negative Inotropes |
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One of the mechanisms for drug-induced heart failure is inhibition of myocardial contractility which is caused by the negative inotropic agents.6 Antiarrhythmics, including disopyramide and flecainide, decrease myocardial contractility through a negative inotropic action.
Beta blockers as a class, are the most recognized agents contributing to heart failure. Less negative inotropic action may be seen with those having intrinsic sympathomimetic activity (ISA) such as pindolol, and acebutolol. Beta blocking eye drops (timolol) may also cause a negative inotropic effect, therefore, patients with both heart failure and glaucoma should be monitored.
On the other hand, specific beta-blockers, such as carvedilol, are being studied for the management of heart failure based on their mechanism of blunting the sympathetic nervous system activity. These benefits are discussed in the pharmacotherapy section of the clinical overview on this site.
Calcium channel antagonists are also implicated as having negative inotropic effects, the most negative inotropic agent being verapamil followed by diltiazem. The dihydropyridines (nifedipine, felodipine) have the least, if any, negative inotropic effect but caution should be exercised. While calcium channel blockers may be beneficial in patients with diastolic dysfunction, these agents worsen heart failure and increase the risk of death in patients with systolic dysfunction. An exception to this may be amlodipine, which did not increase cardiovascular mortality and morbidity in severe heart failure in the recent PRAISE trial.7
Medications with Cardiotoxic Properties
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Chemotherapeutic agents such as doxorubicin, daunorubicin, have direct dose-related
cardiotoxic effects on the heart muscle.6 It is not always possible
to avoid these drugs when a diagnosis of cancer is made, when these are the
best agents to treat the disease, but care can be taken not to exceed the total
cumulative doses. Cocaine and amphetamines with long-term use and overdoses
are also implicated in exacerbation of heart failure because of cardiotoxic
effects.
6
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Agents Causing Sodium and Water Retention
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Another common drug-induced mechanism causing exacerbation of heart failure is expansion of blood volume. Drugs that act primarily on the kidneys to either alter renal blood flow or increase sodium retention can affect heart failure.6 Vasodilators, including hydralazine and minoxidil, decrease renal blood flow which activates the renin-angiotensin system and causes increased sodium and water retention. Nonsteroidal anti-inflammatory agents (NSAIDs), glucocorticoids, and estrogen can cause sodium retention. Drugs that contain a high sodium content such as ticarcillin (an intravenous antibiotic), can increase total body sodium and water, thereby expanding blood volume resulting in worsening heart failure.
1
Konstam M, Dracup K, Baker D et al. Heart Failure: Evaluation and Care
of Patients with Left-Ventricular Systolic Dysfunction. Clinical Practice Guideline
No. 11. AHCPR Publication No. 94-0612. Rockville, MD: Agency for Health Care Policy
and Research, Public Health Service, U.S. Department of Health and Human Services.
June 1994.
2 Marantz PR, Tobin JN, Wassertheil-Smoller S et al. The relationship between left-ventricular systolic function and congestive heart failure diagnosed by clinical criteria. Circulation 1988;77:607-12.
3 Patterson JH, Adams KF. Pathophysiology of heart failure: Changing perceptions. Pharmacotherapy 1996;16(2 Pt 2):27S-
4 Gaasch WH. Diagnosis and treatment of heart failure based on left ventricular systolic or diastolic dysfunction. JAMA 1994;271:1276-80.
5 Beier MT, Lawhorne LW, Phillips NG. The utilization of echocardiography for community nursing facility residents with congestive heart failure. Annals of Long-Term Care. 1998; 6(12):376-381.
6 Kradjan WA. Congestive heart failure. In: Koda-Kimble MA, Young LY, eds. Applied Therapeutics. The clinical use of drugs, 5th ed. Vancouver, WA: Edward's Brothers;1992:9-2-9-12.
7 Packer M, O'Connor CM, Ghali JK et al. Effect of amlodipine on morbidity and mortality in severe chronic heart failure (PRAISE trial). N Engl J Med. 1996;335:1107-14.
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