Heart failure resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahmoud Sakr, M.D. [2]

Definition

Heart failure is a complex syndrome whereby there is inadequate output of the heart to meet the metabolic demands of the body. Abnormal function of different anatomic parts of the heart cause heart failure including the pericardium, the myocardium, the endocardium, the heart valves and the great vessels. Symptoms of heart failure are due to a lack of both forward blood flow to the body, and backward flow into the lungs. Heart failure is a clinical syndrome characterized by symptoms of dyspnea, edema and fatigue and signs such as rales on physical examination.

Causes

Life Threatening Causes

Acute decompensated heart failure is a life-threatening condition and must be treated as such irrespective of the causes. Life-threatening conditions can result in death or permanent disability within 24 hours if left untreated.

• Accelerated hypertension
• Acute kidney injury
• Acute myocardial ischemia
• Acute or progressive valvular disease (e.g. acute mitral regurgitation)
• Acute or subacute valve disease endocarditis
• Aortic dissection
• Cardiac arrhythmias, specially ventricular arrhythmias
• Cardiotoxic agents (e.g. alcohol, cocaine, and certain chemotherapy drugs)
• Diabetic emergencies (e.g. ketoacidosis)
• Myopericarditis
• Pulmonary embolus
• Severe anemia (e.g. acute hemolysis or blood loss)
• Systemic Inflammatory response syndrome
• Thyrotoxicosis

Common Causes

• Accelerated hypertension
• Acute kidney injury
• Acute myocardial ischemia
• Acute or progressive valvular disease (e.g. acute mitral regurgitation)
• Cardiac arrhythmias
• Excessive alcohol or illicit drug use (e.g. cocaine)
• Myocardial ischemia (e.g. AF)
• Pulmonary embolus
• Systemic Inflammatory response syndrome

Management

• Figure 1: Approach to patients presenting with acutely decompensated HF.

* Focused history (e.g. dyspnea, orthopnea, edema, Hx of HF, Hx of drug abuse) * Vital signs * Physical exam (e.g. assess volume status and perfusion) * Initial labs to include BNP and troponins * EKG *Chest X-ray

Patient is in shock or respiratory failure; Address emergently (e.g. intubate, IV inotropes (e.g.dobutamine 2-20mcg/kg/min IV), ICU)

Hemodynamically stable acute HF

Accelerated HTN; IV vasodilators (e.g. Enalaprilat 0.625-1.25mg IV ) loop diuretics (e.g. Furosemide 0.1mg/kg IV once, then double dose Q2h as needed)

Acute myocardial ischemia

Atrial fibrillation

No precipitating factors identified

Renal injury

Other etiologies

Nitrates, Beta blockers,anticoagulation, antiplatelets Urgent revascularization

Beta blockers (e.g. carvedilol); Anticoagulation (e.g. enoxaparin 1mg/kg sc stat)

Hydral-nitrates Avoid combining ACEI, ARB, Aldosterone blockers

Treat accordingly

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• Acute decompensated HF patient will most likely fall in the stage C or stage D of the ACC/AHA HF classification. see figure 2

Figure 2: Stages in the development of HF:

Determine ACC/AHA stage of HF

STAGE A At high risk for HF but without structural heart disease or symptoms of HF

STAGE B Structural heart disease but without signs or symptoms of HF

STAGE C Structural heart disease with prior or current symptoms of HF

STAGE D Refractory HF

*

Do's

• Make sure your patient is on DVT prophylaxis unless contraindicated.
• Make use of aldosterone receptor antagonists [or mineralocorticoid receptor antagonists] in patients with NYHA class II-IV and who have LVEF of 35% or less, unless contraindicated, to reduce morbidity and mortality. Patients with NYHA class II should have a history of prior cardiovascular hospitalization or elevated plasma natriuretic peptide levels to be considered for aldosterone receptor antagonists. Creatinine should be 2.5 mg/dL or less in men or 2.0 mg/dL or less in women (or estimated glomerular filtration rate >30 mL/min/1.73 m2), and potassium should be less than 5.0 mEq/L. Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation and closely followed thereafter to minimize risk of hyperkalemia and renal insufficiency.
• Start hydralazine and isosorbide dinitrate to reduce morbidity or mortality in patients with current or prior symptomatic HFrEF who cannot be given an ACE inhibitor or ARB because of drug intolerance, hypotension, or renal insufficiency, unless contraindicated. This combination has proven beneficial in African American population as well.
• Consider adding thiazides for worsening congestion despite high doses of loop diuretics.
• Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of IV diuretics or active titration of heart failure medications.
• Use a combination of hydralazine and isosorbide dinitrate. They have been proven to reduce morbidity or mortality in patients with current or prior symptomatic HFrEF who cannot be given an ACE inhibitor or ARB because of drug intolerance, hypotension, or renal insufficiency, unless contraindicated.
• Schedule an early follow-up visit (within 7 to 14 days) and early telephone follow-up (within 3 days) of hospital discharge .

• Refer your HF patients to the local Multidisciplinary HF disease-management programs for those with high risk for hospital readmission, to facilitate the implementation of GDMT, to address different barriers to behavioral change, and to reduce the risk of subsequent rehospitalization for HF

Don'ts

• Don't Use parenteral inotropes in normotensive patients with acute decompensated HF without evidence of decreased organ perfusion.
• Don't combine an ACEI, ARB, and aldosterone antagonist in patients with HFrEF unless otherwise indicated as this combination carries a risk of renal functions worsening and hyperkalemia.
• Don't use aldosterone receptor antagonists in patients with hyperkalemia or renal insufficiency when serum creatinine is more than 2.5 mg/dL in men or more than 2.0 mg/dL in women (or estimated glomerular filtration rate <30 mL/min/1.73 m2), and/or potassium more than 5.0 mEq/L.
• Don't continue nutritional supplements with no proven benefit.

References

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