Acute decompensated heart failure

Acute decompensated heart failure (ADHF), also called acute-on-chronic heart failure, heart failure exacerbation or simply acute heart failure, refers to the heart failure which develops or worsens acutely. They may occur in a patient with chronic heart failure who has decompensated for any reason, or it may occur de novo (without preexisting chronic heart failure, rare). It's a severe condition, usually requiring hospitalisation. Many conditions can cause acute decompensated heart failure.

ADHF is a common cause of hospitalisation in elderly and has relatively high mortality. Cardiogenic shock is the most severe type of ADHF.

Types

We can distinguish four main different clinical "types" or presentations of ADHF, which are not necessarily mutually exclusive:

Acute decompensated heart failure without pulmonary oedema, where a person with chronic heart failure is fluid overloaded
Acute decompensated heart failure with pulmonary oedema, where a person with chronic heart failure develops pulmonary oedema
Right ventricular failure, where mainly the right ventricle fails (rather than the left)
Cardiogenic shock, where myocardial function is decreased to the point where systemic or cerebral hypoperfusion occurs

Cardiogenic shock is defined as a sustained hypoperfusion (SBT < 90 mmHg) secondary to myocardial dysfunction that persists despite volume therapy.

Etiology

The mnemonic CHAMP is used to remember the main causes of ADHF:

acute Coronary syndrome (including myocardial infarction) (most common cause)
Hypertensive crisis
Arrhythmia (usually tachyarrhythmia, for example atrial fibrillation with rapid ventricular rate)
Mechanical cause (acute valvular disease, myocarditis, Takotsubo cardiomyopathy)
Pulmonary embolism

Other less common causes are tamponade, papillary muscle rupture, aortic dissection, peripartum cardiomyopathy, etc.

Cardiogenic shock typically develops secondary to a large myocardial infarction, or due to a smaller myocardial infarction which affects the papillary muscles, causing severe acute mitral regurgitation. It may also develop in case of arrhythmia (like atrial fibrillation with rapid ventricular rate) in a patient with chronic heart failure.

Clinical features

It's helpful to determine the patient's pulmonary congestion status (present or not) as well as whether there are signs of systemic hypoperfusion. We usually nickname pulmonary congestion or oedema "wet" and the absence of them "dry". We also nickname presence of systemic hypoperfusion "cold" and the absence "warm", which comes from the temperature of the skin in shock.

"Warm and dry" patients have the best prognosis, as they have neither pulmonary congestion nor systemic hypoperfusion. They usually have significant pitting leg oedema or ascites.

"Warm and wet" patients usually have signs of pulmonary oedema or congestion like dyspnoea, tachypnoea, cough, foamy sputum. They are often hypertensive.

"Cold and dry" patients usually have signs of shock like confusion, hypotension, have cold extremities, and elevated lactate levels. The right ventricular failure group usually belongs here.

"Cold and wet" patients (cardiogenic shock) have it the worst. There are signs of pulmonary oedema or congestion as well as signs of shock.

Diagnosis and evaluation

These patients may be critically ill so rapid evaluation is necessary. Initial stabilisation with the ABC approach may be necessary. Chest radiography may show signs of pulmonary congestion or oedema. Troponin to rule out acute infarction is recommended. Echocardiography to evaluate ventricular function, look for regional hypokinesia (as sign of myocardial infarction), rule out pericardial effusion and valvular disease. Echocardiography can also evaluate the patient's fluid status by examining the inferior vena cava (IVC). If the IVC is dilated or its diameter does not decrease by more than 50% during inspiration, this can be interpreted as a sign of fluid overload. ECG must be taken to look for any arrhythmia which may cause the ADHF.

Ultrasonography of the lungs may show B-lines (sign of congestion), pleural effusion. Lactate and organ function tests should be measured to rule out shock. Measuring urine output allows for monitoring for acute kidney injury and hypotension.

Management

Many of these patients require intensive care, especially those in shock. The initial mangement should aim to stabilise the patient, after which the underlying cause should be sought and treated.

General supportive therapy

Non-invasive ventilation (CPAP or BiPAP) may be used if there is pulmonary oedema, as the expiratory pressure helps "push" fluid out of the lungs. However, too much post end-expiratory pressure (PEEP) may impair the cardiac function if the patient is dependent on preload, as more PEEP decreases the preload.

Give oxygen to maintain an oxygen saturation above 90%. If there are signs of fluid overload, IV loop diuretic should be given. In hypotension, IV fluids should be given rapidly, but one must monitor closely, as too much fluid can be detrimental. Overhydration is especially detrimental in right ventricular failure and should be avoided in these cases. Acute kidney failure may necessitate renal replacement therapy.

Inotropic drugs or vasopressors are indicated for severe hypotension and hypoperfusion. Norepinephrine is the preferred vasopressor, while dobutamine or levosimendan may be used for inotropy. In the most severe cases, mechanical circulatory support (MCS) may be necessary. These may involve an intraaortic balloon pump, Impella, or extracorporeal membrane oxygenation (ECMO).

Management of any underlying cause

If acute coronary syndrome is suspected, the patient should be taken for percutaneous coronary intervention. Tachyarrhythmias may require cardioversion. Bradyarrhythmias may require temporary pacing or atropine. In case of atrial fibrillation with rapid ventricular rate, digoxin or amiodarone can be given. Specific treatment for any pulmonary embolism should be given.

"Warm and dry" patients

These patients usually do not need more than a few days of intensive diuretic therapy, either IV or an increase in their usual PO loop diuretic dose.

"Warm and wet" patients

The patient should remain in a half-seated position (as a supine position worsens the pulmonary oedema). CPAP or BiPAP is indicated to remove fluid. In case of hypertension, give intravenous infusion of nitroglycerine or nitroprusside, which gives vasodilation and effectively reduces afterload.

If there are signs of hypervolaemia, IV loop diuretic should be given. However, some of the "warm and wet" patients are not hypervolaemic, and for these patients diuretics may make things worse. If patients are already on a beta blocker, the dose should be temporarily reduced (to reduce inotropy) but stopping the drug altogether is unneccesary.

"Cold and dry" patients

For this group, careful rehydration with IV fluid is necessary. They are not overhydrated and so diuresis is contraindicated. Any habitual diuretics, mineralocorticoid receptor antagonists, and antihypertensives should be temporarily discontinued until clinical improvement. If patients are already on a beta blocker, the dose should be temporarily reduced (to reduce inotropy) but stopping the drug altogether is unneccesary. If the hypoperfusion is refractory to fluids, consider using an inotropic agent or mechanical support like an intraaortic balloon pump (IABP) or Impella.

Nitrates must be avoided for those with right ventricular failure because they may decrease right ventricular preload, which may worsen the heart failure.

"Cold and wet" patients/cardiogenic shock

These patients require intensive care. Careful IV hydration is indicated. Vasopressor or inotropic may be necessary, as may be mechanical circulatory support.