| Systolic dysfunction | Diastolic dysfunction |
|---|---|
| Impaired contractility | Structural abnormality |
| Myocardial infarction Dilated cardiomyopathy, including peripartum cardiomyopathy Myocarditis Alcohol abuse Papillary muscle rupture | Ventricular hypertrophy (often related to hypertension) Hypertrophic or constrictive cardiomyopathy Constrictive pericarditis Infiltrative disease such as sarcoidosis |
| Increased afterload | Impaired myocyte relaxation |
| Systemic hypertension, including hypertensive crisis caused by underlying disease (e.g., pregnancy or thyrotoxicosis) | Myocardial ischemia or hypoxia Medications (e.g., digitalis) Hypercalcemia |
| Pulmonary hypertension, including pulmonary embolism | |
| Aortic stenosis | |
| Cocaine abuse | |
| Medication noncompliance | |
| Dietary intake |
Presentation
Classic presentation
- Left-sided heart failure classically presents with dyspnea, usually related to pulmonary vascular congestion.
- The symptoms may be acute or subacute in onset.
- The duration of symptoms may be helpful in identifying the etiology of the decompensation.
- The symptoms may be acute or subacute in onset.
- Orthopnea and paroxysmal nocturnal dyspnea may be noted in the history.
- On examination, the lungs may reveal crackles or wheezing.
- Right-sided heart failure presents with jugular venous distension (JVD), hepatic congestion, and dependent edema.
- Patients may report significant weight gain due to increased fluid retention.
- Many cases of ADHF will present with a mixed clinical picture that includes signs and symptoms of both left- and right-sided heart failure.
- The differential diagnosis of ADHF includes other etiologies of poor cardiac output and dyspnea such as
- Acute coronary syndromes (ACS)
- Chronic obstructive pulmonary disease (COPD) exacerbation
- Pulmonary embolism
- Pneumonia (including severe sepsis and septic shock)
- Pneumothorax
- Pericardial tamponade
- Hypertensive crisis
- Noncardiogenic pulmonary edema (including acute respiratory distress syndrome)
- Papillary muscle rupture.
- Acute coronary syndromes (ACS)
Critical presentation
- Patients with severe ADHF will present with respiratory distress and impending respiratory failure.
- Associated symptoms may include frothy oral secretions, diaphoresis, and hypoxia.
- Patients may also have other symptoms related to poor cardiac output and poor perfusion such as chest pain and altered mental status.
- Patients may be hypertensive or hypotensive depending on the etiology of symptoms.
- Hypotension can be indicative of cardiogenic shock and is particularly concerning.
Diagnosis and evaluation
- History
- Important elements of history will include past history of cardiac dysfunction and potential causes of new cardiac dysfunction:
- Prior history of heart disease
- Recent weight gain or increasing edema
- Dietary or medication noncompliance
- Alcohol or cocaine abuse
- Recent use of negative inotropic agents (e.g., calcium channel blockers)
- Medication changes
- Duration of symptoms.
- Prior history of heart disease
- Important elements of history will include past history of cardiac dysfunction and potential causes of new cardiac dysfunction:
- Physical examination
- Vital signs:
- Typically, patients with ADHF have abnormal vital signs. Tachypnea, hypertension, and tachycardia are common given the pathophysiology of the disease.
- Hypoxia is also possible, and may indicate impending respiratory failure.
- Hypotension is particularly concerning, and may indicate that the patient is in cardiogenic shock.
- Hypotension should prompt further evaluation into other etiologies of shock that may have exacerbated any underlying cardiac pathology.
- These patients will usually be euthermic.
- Typically, patients with ADHF have abnormal vital signs. Tachypnea, hypertension, and tachycardia are common given the pathophysiology of the disease.
- On examination, patients will exhibit signs of poor cardiac output and pulmonary congestion:
- General: respiratory distress, diaphoresis
- HEENT: cyanosis, frothy oral secretions
- Cardiac: S3, murmurs corresponding to valvular lesions, JVD
- Pulmonary: crackles in lower lung fields, wheezing, diminished breath sounds
- Extremities: edema, cyanosis, mottled or diaphoretic skin. Patients in cardiogenic shock will have cool and clammy extremities because of the increased systemic vascular resistance.
- General: respiratory distress, diaphoresis
- Vital signs:
- Laboratory tests
- A complete blood count with differential is obtained to assess for anemia or elevated white count.
- Electrolytes are useful to evaluate for any disturbances associated with ADHF or cardiac rhythm (e.g., hyponatremia, hypokalemia, hyperkalemia, or hypomagnesemia).
- An elevated troponin level may reflect a recent myocardial infarction (MI) causing acute heart failure, or may be caused by myocardial ischemia from ventricular strain.
- Brain (or B-type) natriuretic peptide (BNP) can aid clinical decision-making in patients with undifferentiated dyspnea and an intermediate risk of heart failure. A BNP >500 pg/mL suggests heart failure while levels <100 pg/mL decrease the likelihood of heart failure. BNP levels may be difficult to interpret in the setting of atrial fibrillation or renal failure.
- An alcohol level or urine toxicology panel for common drugs of abuse (e.g., cocaine, amphetamines) can be sent based on clinical suspicion.
- A TSH level can be requested to rule out thyrotoxicosis.
- Blood cultures, urine cultures, and lactic acid should be ordered if sepsis is suspected.
- A complete blood count with differential is obtained to assess for anemia or elevated white count.
- Imaging and ancillary tests
- Chest radiography:
- Look for signs of pulmonary edema (increased interstitial markings, Kerley B lines, widened pulmonary fissures, cephalization of pulmonary vessels).
- Rule out other causes of respiratory distress (e.g., pneumothorax).
- Evaluate for focal infiltrate suggestive of pneumonia.
- Look for signs of pulmonary edema (increased interstitial markings, Kerley B lines, widened pulmonary fissures, cephalization of pulmonary vessels).
- ECG:
- Evaluate for ischemia, dysrhythmias, or signs of pericardial effusion (e.g., electrical alternans).
- The ECG can also be useful to evaluate underlying cardiac disease or electrolyte abnormalities.
- Evaluate for ischemia, dysrhythmias, or signs of pericardial effusion (e.g., electrical alternans).
- Echocardiography:
- Should be obtained emergently in an unstable patient if there is a concern for cardiac tamponade physiology. It can also detect wall motion abnormalities if there is a concern for ischemia.
- Chest radiography:
Critical management
- When approaching a patient with ADHF, one must be sure to address any underlying cause while simultaneously managing the physiological derangements.
- Optimize oxygenation:
- Sitting patients upright will improve oxygenation. Avoid recumbent or supine positioning as this will exacerbate respiratory distress.
- Provide suctioning for frothy oral secretions.
- Supplement oxygen as needed to maintain a saturation of
90%.
- Sitting patients upright will improve oxygenation. Avoid recumbent or supine positioning as this will exacerbate respiratory distress.
- Consider supportive respiratory adjuncts and prepare for potential respiratory deterioration:
- For patients with moderate to severe respiratory distress who are able to maintain their airway, consider immediate noninvasive positive-pressure ventilation (NPPV).
- NPPV reduces both preload and afterload, thereby relieving heart failure symptoms. Anticipate and prepare for relative hypotension after starting NPPV.
- Both continuous positive airway pressure (CPAP) and bi-level positive airway pressure (Bi-PAP) have demonstrated efficacy in patients with ADHF, particularly if initiated early.
- Begin with a PEEP of 5 cmH2O and increase incrementally until an improvement in oxygenation is seen.
- If Bi-PAP is used, the initial inspiratory pressure can be set at 10–12 cmH2O and incrementally increased. The inspiratory pressure should not exceed 20 cmH2O.
- Begin with a PEEP of 5 cmH2O and increase incrementally until an improvement in oxygenation is seen.
- For patients with moderate to severe respiratory distress who are able to maintain their airway, consider immediate noninvasive positive-pressure ventilation (NPPV).
- Modulation of preload and afterload are the primary components of therapy for ADHF.
- Nitrate therapy is among the mainstays of treatment for ADHF.
- Glyceryl trinitrate causes venodilation, thereby decreasing preload.
- It can be administered as sublingual tablets (0.4 mg/tablet) while intravenous (IV) access is obtained.
- Nitrate therapy can also be given as a continuous infusion.
- Start with 20–50 micrograms/minute and titrate by 20 micrograms/minute every 3–5 minutes until a maximum of 200 micrograms/minute or a MAP
65 mmHg.
- Start with 20–50 micrograms/minute and titrate by 20 micrograms/minute every 3–5 minutes until a maximum of 200 micrograms/minute or a MAP
- Glyceryl trinitrate causes venodilation, thereby decreasing preload.
- Nitrate therapy is among the mainstays of treatment for ADHF.
- Angiotensin-converting enzyme (ACE) inhibitors work by decreasing afterload and, in the long term, preventing ventricular remodeling.
- Though not always given during initial assessment and stabilization, captopril can be used sublingually for immediate afterload reduction.
- IV enalaprilat (5–10 mg) can also be used as primary or adjunctive therapy.
- Avoid giving these drugs to patients with potential hyperkalemia, or during pregnancy.
- Though not always given during initial assessment and stabilization, captopril can be used sublingually for immediate afterload reduction.
- Diuretics, and particularly loop diuretics, can be used to combat the renin-angiotensin mediated increases in circulating blood volume.
- It is important to realize that not all patients with pulmonary edema are volume overloaded.
- In the absence of evidence of chronic volume overload, diuresis should only be initiated after other modalities of treatment including NPPV and nitrate therapy have been attempted. Inappropriate diuresis can lead to hypotension and acute kidney injury.
- Furosemide (40–80 mg IV), torsemide (10–20 mg IV), or bumetanide (0.5–1 mg IV) can be used as initial therapy.
- If the patient is on home diuretics, give a bolus dose equal to 100–200% of the home dose.
- Diuretics can be used as a continuous infusion, but this will likely not be required in the immediate stabilization.
- It is important to realize that not all patients with pulmonary edema are volume overloaded.
- Hypotension will limit the use of any of the above therapies and should prompt consideration for vasopressors or inotropes (see below).
Sudden deterioration
- Patients who become hypoxic, lethargic, or more confused despite NPPV should be intubated.
- Patients who are hypotensive, especially those requiring intubation, may require cautious use of inotropes or vasopressors to enhance cardiac output and maintain their coronary filling pressure. Titrate these agents to a MAP >60 mmHg, or less if limited by signs or symptoms of cardiac ischemia.
- Dobutamine: start IV infusion at 5–10 micrograms/kg/minute.
- Milrinone: load 50 micrograms/kg IV over 10 minutes, then infuse 0.375– 0.75 micrograms/kg/minute.
- Dopamine: start IV infusion at 5–10 micrograms/kg/minute.
- Dobutamine: start IV infusion at 5–10 micrograms/kg/minute.
- Some patients may need specialized interventions based on their underlying disease:
- Cardiac catheterization for ongoing ischemia.
- Intra-arterial balloon pump for cases of severe cardiogenic shock.
- Implantable cardioverter-defibrillators (ICDs) may be indicated for patients with ischemic or dilated cardiomyopathy and impaired systolic function (left ventricular ejection fraction <30%).
- Cardiac resynchronization therapy (CRT) may be appropriate for patients with severe systolic heart failure and QRS interval prolongation (>120 milliseconds).
- Patients with severe end-stage systolic heart failure may be considered for a left ventricular assist device (LVAD) as a bridge to heart transplant.
- Cardiac catheterization for ongoing ischemia.
Vasopressor of choice: Patients with ADHF who are hypotensive can be suffering from low-output heart failure or cardiogenic shock. Inotropes and/or vasopressors should be used judiciously in order to avoid exacerbating the condition:
- SBP
80 mmHg: dobutamine
- SBP <80 mmHg: dopamine
- SBP <70 mmHg: norepinephrine.
References
Heart Failure Society of America, Lindenfeld J, Albert NM, Boehmer JP, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010; 16: e1–194.
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