Differential diagnosis of causes of decompensated heart failure

Typical presentation

Although patients can present with asymptomatic ventricular dysfunction, most patients present with signs and symptoms of congestion and/or hypoperfusion. This includes worsening dyspnea on exertion, weight gain, and fatigue. The acuity of the presentation will depend on the mechanism of myocardial injury. For example, a patient with heart failure after an acute myocardial infarction may present with dyspnea increasing over hours or days without significant weight gain or edema. Evidence of hypoperfusion is less common, but is associated with a worse prognosis.

Clinical diagnosis

Laboratory diagnosis

Potential pitfalls/common errors made regarding diagnosis of disease

• The hemodynamic profile may be difficult to determine in many patients, particularly young patients. They can often present without lower extremity edema, normal lung auscultation, and lower NYHA class despite advanced underlying disease.
  
• BNP can be an inaccurate assessment of heart failure in several conditions. It can be elevated in patients with chronic renal disease. Conditions such as advanced age and obesity can lower the BNP level despite the presence of underlying heart failure.

Treatment rationale

• The aim of therapy is to quickly relieve symptoms, optimize the hemodynamic profile, manage reversible conditions which may be responsible for decompensation, and initiate long‐term medical therapy.
  
• Characterization of the patient into a particular hemodynamic profile helps guide initial therapy.
  
• Diuretics are the mainstay of medical therapy in patients with congestive symptoms. Dosing needs to be individualized. Initial high dose intravenous diuretics can generally be safely given to patients to rapidly improve symptoms in patients on chronic oral diuretic therapy.
  
• Vasodilator therapy is less frequently used in clinical practice, but can rapidly improve symptoms in patients without hypotension (‘warm and wet’). Vasodilators (nitroglycerin, nitroprusside, nesiritide) reduce the afterload on the heart with subsequent improvement in pulmonary congestion (Table 17.1).
  
• Supplemental oxygen and non‐invasive positive pressure ventilation can also be used to relieve dyspnea in conjunction with vasodilator and diuretic therapy. Non‐invasive positive pressure ventilation should be avoided in patients with hypotension, vomiting, pneumothorax, and poor mental status.

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Agent	Dose	Mechanism	Inotropy	CO	SVR	MAP
  Milrinone	0.375–0.75 μg/kg/min	PDE‐3 inhibitor	↑	↑↑	↓↓	↓
  Dobutamine	1–10 μg/kg/min	B‐1, B‐2, α‐1	↑↑	↑↑	↓	≈
  Dopamine	1–3 μg/kg/min	Dopamine‐1	≈	≈	↓	↓
  	3–10 μg/kg/min	B‐1 > α‐1	↑	↑	↑	↑
  	10–20 μg/kg/min	B‐1 < α‐1	↑	↑	↑↑	↑↑
  Epinephrine	2–10 μg/kg/min	B‐1, B‐2, α‐1	↑↑	↑↑	↑↑	↑↑
  Norepinephrine	2–10 μg/kg/min	B‐1, α‐1	↑↑	↑↑	↑↑	↑↑
  Nitroprusside	0.3–5 μg/kg/min	Nitric oxide	≈	↑	↓↓	↓
  Nitroglycerin	10–200 μg/kg/min	Nitric oxide	≈	↑	↓↓	↓
  Nesiritide	0.015–0.03 μg/kg/min	BNP	≈	↑	↓↓	↓
  α, alpha‐adrenergic agonist; B, beta‐adrenergic agonist; BNP, B‐type natriuretic peptide.

  
  
• Inotropic or mechanical support is used in patients with evidence of hypoperfusion with elevated filling pressure (‘cold and wet’) until the hemodynamic condition is corrected. There are several intravenous agents that can be used for inotropy. Except for cases of profound shock, dobutamine or milrinone are typical first line agents. These agents are continued until the hemodynamic profile is reversed. Mechanical support should be considered in refractory cases.
  
• Although less common, patients who are ‘cold and dry’ will require inotropic or mechanical support while a reversible cause is identified. If no reversible cause is noted, these patients need early consideration of mechanical support or cardiac transplantation evaluation.
  
• After stabilization of the patient’s hemodynamic profile and management of any precipitant of decompensation, patients with systolic heart failure should be initiated on chronic heart failure therapy prior to discharge. Neuro‐hormonal antagonists such as beta‐blockade, RAAS blockade, and aldosterone antagonists are essential to prevent further ventricular remodeling and decompensation. Treatment of diastolic heart failure largely focuses on management of associated hypertension and volume control with diuretic therapy.

When to refer

The acutely hospitalized patient provides an opportunity to assess their overall prognosis and determine if referral to an advanced heart failure specialist is indicated. The following patients are appropriate for referral:

• Patients with cardiogenic shock are appropriate for early referral, particularly prior to the development of irreversible multiorgan failure.
  
• Patients who require inotropic support and are unable to be weaned despite correction of the hemodynamic profile.
  
• Patients with intolerance to neurohormonal blockade, particularly due to hypotension or renal failure.
  
• Patients with recurrent hospitalizations for heart failure despite optimal medical therapy.

Prevention/management of complications

Diuretic dosing is often associated with or limited by worsening renal failure. If the patient is developing renal failure with diuresis, it is first important to confirm that the suspected hemodynamic profile is correct. If there is uncertainty, consider right heart catheterization. If there is evidence of hypoperfusion, empiric use of vasodilators or inotropic support can be considered.