Severe acute heart failure

Aetiology

Acute on chronic heart failure

Common precipitants

• Myocardial ischaemia or infarction
• Infection
• Arrhythmias

Acute heart failure

• Myocardial ischaemia or infarction (by far the most common)
• Acute mitral regurgitation due to ruptured papillary muscle or chordae
• Acute aortic regurgitation due to bacterial endocarditis
• Acute ventricular septal defect

Pathophysiology

Approximately 50% of patients presenting with acute heart failure present with diastolic heart failure as a result of impaired relaxation of the heart. This results in a fall in cardiac compliance with a resultant increase in left ventricular end diastolic, left atrial and pulmonary capillary pressures (figure 1). The rise in pulmonary capillary pressure results in an increase flux of fluid out of capillaries into the interstitial space and hence pulmonary oedema. These patients are generally not significantly fluid overloaded.

Clinical features

• Sudden onset or exacerbation of shortness of breath. Classically occurs over a few minutes but may come on over hours
• ± Chest pain
• ± Palpitations
• Bilateral crackles
• Marked hypertension with peripheral vasoconstriction is common but hypotension may occur

Investigations

• Chest X-ray: signs of pulmonary oedema. May be cardiomegaly in acute on chronic cases
• Raised brain natriuretic peptide
• Investigations to determine the cause: ECG, troponin, creatine phosphokinase, echo
• Arterial blood gases
  • Metabolic acidosis is common
  • Normocapnic respiratory failure is usual but hypercapnia may occur

Treatment

In pathophysiological terms the aims of treatment are to decrease preload, decrease afterload and to increase contractility.
High flow oxygen is vital to correct hypoxia and to help break the vicious cycle of impaired LV function → pulmonary oedema → hypoxia → further impairment of LV function → worsening pulmonary oedema.
Intravenous glyceryl trinitrate infusion to reduce preload and reduce myocardial ischaemia (thus improving contractility). Titrate the dose against the blood pressure remembering that the dose can be rapidly escalated (or reduced) due to the short half life of the drug
Diuretics are traditionally given for acute heart failure to reduce preload although there are doubts about the pathophysiological rationale. A bolus of frusemide causes transient vasoconstriction before vasodilatation, fluid overload is not a significant feature in many patients and there are more easily titrated vasodilators.
Most patients respond to nitrates. Patients with more severe respiratory failure may require non-invasive ventilation. Use continuous positive airway pressure (CPAP) initially and reserve bilevel positive airway pressure (BiPAP) for patients in whom CPAP is unsuccessful. Invasive mechanical ventilation may be required for patients with severe disease (figure 2).

After the hyperacute stage consider treatment with angiotension converting enzyme inhibitors, spironolactone and β blockers.

It is, of course, vital to treat the cause. Given the limited time frame for re-perfusion therapy for myocardial infarction, it is particularly important to consider this at an early stage. Patients with STEMI and severe heart failure should be referred urgently for percutaneous coronary intervention.