Acute pulmonary oedema

Published on 14/03/2015 by admin

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Chapter 9 Acute pulmonary oedema

Anthony F.T. Brown

Decompensated heart failure, or acute pulmonary oedema (APO), now accounts for 1% of emergency department visits, with a 16% in-hospital mortality for those admitted with frank pulmonary oedema and an overall 50% five-year mortality.

Although the typical frail, elderly patient may dominate the physician’s perspective, APO can present in the emergency department in a diverse group of patients, from those suffering from an underlying acute coronary syndrome (ACS), whether an ST-segment elevation myocardial infarct (STEMI), non-ST-segment elevation myocardial infarct (NSTEMI) or unstable angina (UA), to chronic decompensated heart failure to non-cardiogenic causes. All have often subtly different historical, examination and investigation findings, and may require a wide variety of urgent treatment modalities.

PATHOPHYSIOLOGY

Acute pulmonary oedema may be divided into cardiogenic and non-cardiogenic causes.

Acute cardiogenic pulmonary oedema

Acute cardiogenic pulmonary oedema is the most severe manifestation of congestive heart failure, and is associated with an increase in lung fluid secondary to hydrostatic leakage from pulmonary capillaries into the alveoli and interstitium of the lungs. Underlying this is a rise in left ventricular end-diastolic pressure and left atrial pressure related to left ventricular dysfunction.

The causative heart disease leading to left ventricular failure may be predominantly systolic failure with impaired cardiac contractility, i.e. an ejection fraction (EF) under 40%, diastolic failure with impaired myocardial relaxation and distensibility (but a normal or even supranormal EF), or a combination of both.

APO may develop out of the blue, or be precipitated in patients with existing heart disease as a result of an acute cause such as ischaemia, an arrhythmia or medication change. Table 9.1 gives the causes of cardiogenic pulmonary oedema.

Table 9.1 Causes of cardiogenic pulmonary oedema

Predominant systolic heart failure

• Acute coronary syndrome

• Hypertension

• Cardiomyopathy

• Myocarditis

• Valvular disease, particularly acute aortic or mitral regurgitation

Predominant diastolic heart failure (one-third to one-half of all patients)

• Hypertension, including renovascular disease

• Aortic stenosis (indicates critical disease)

• Cardiomyopathy—hypertrophic (HCM), or restrictive

• Acute coronary syndrome

Non-cardiogenic pulmonary oedema

Non-cardiogenic pulmonary oedema occurs without a rise in pulmonary capillary wedge pressure. It may result from a wide variety of mechanisms, including:

• increased capillary permeability in acute respiratory distress syndrome (ARDS), septicaemia, aspiration of gastric contents, inhaled toxins, pancreatitis, uraemia or near drowning

• mixed or unknown causes such as neurogenic pulmonary oedema, high-altitude pulmonary oedema (HAPE), heroin overdose, smoking freebase cocaine, eclampsia, post lung re-expansion and post pulmonary embolism

• decreased oncotic pressure such as in hypoalbuminaemia, usually in combination with another cause.

Neurogenic pulmonary oedema

This is a relatively rare cause of APO, developing within a few hours of an acute neurologic insult, and is often associated with intracranial hypertension such as from prolonged seizures, a head injury or a subarachnoid or intracerebral haemorrhage.

It usually resolves over 48–72 hours, determined by the course of the underlying primary neurologic insult.

CLINICAL FEATURES

History

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