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Assessment and management of acute pulmonary oedema


Essentials

  • 1

    Severe acute pulmonary oedema (APO) is associated with high morbidity and mortality.

  • 2

    APO is a pathophysiological state characterized by a maldistribution of fluid; most patients do not have fluid overload.

  • 3

    Diagnosis relies on a thorough history, focused physical exam and investigations including ECG, lung ultrasound and chest x-ray.

  • 4

    Therapy is aimed at maintaining oxygenation and cardiac output and reversing the underlying pathophysiology. Reversible causes should be sought and corrected.

  • 5

    Hypotensive patients require ventilatory and inotropic support.

  • 6

    For most patients, the mainstays of therapy are oxygen; vasodilatation, usually with nitrates; and non-invasive ventilation (NIV).

  • 7

    NIV is safe and effective in APO. It has been shown to reduce rates of intubation, admission to an intensive care unit (ICU) and death.

Introduction

Acute pulmonary oedema (APO) occurs mainly in elderly patients; if severe, it is associated with a very poor long-term prognosis. It is a pathophysiological state characterized by fluid-filled alveolar spaces, with resulting impaired alveolar gas exchange and reduced lung compliance. Acute dyspnoea, hypoxia and increased work of breathing are the resultant symptoms and signs. APO occurs when increased pulmonary capillary pressure, reduced plasma oncotic pressure or changes in pulmonary capillary permeability cause plasma to leave the capillaries and build up in the pulmonary interstitium. When this occurs at such a rate that lymphatic drainage from the lung cannot keep up, flooding of the alveoli results.

Aetiology and pathophysiology

The causes of APO can be divided into two categories: cardiogenic (the commonest cause in emergency department [ED] patients) and non-cardiogenic. In cardiogenic APO, an acute reduction in cardiac output (left atrial outflow obstruction or left ventricular [LV] dysfunction) associated with an increase in systemic vascular resistance (SVR) leads to back pressure on the pulmonary vasculature, with a resultant increased pulmonary capillary pressure. Once established, APO can lead to a downward spiral where decreasing oxygenation and increasing pulmonary vascular resistance (with its resultant increased right ventricular end-diastolic pressure) worsens LV dysfunction as well as pulmonary oedema. In most cases the patient has a maldistribution of fluid rather than fluid overload. He or she may, in fact, have a whole-body fluid deficit. This understanding has led to a change in the management of this condition from the use of large doses of diuretics to a focus on vasodilators and NIV, which reduce SVR and improve cardiac output. Some of the causes of cardiogenic pulmonary oedema are listed in Box 5.3.1 .

Box 5.3.1
Causes of cardiogenic pulmonary oedema

  • Acute valvular dysfunction (e.g. rupture, endocarditis)

  • Anaemia

  • Arrhythmias (e.g. atrial fibrillation, ventricular tachycardia)

  • Dietary (including salt), physical or emotional excess

  • Fluid overload; may be iatrogenic

  • Medication adverse effect

  • Medication non-compliance

  • Myocardial ischaemia/infarction

  • Myocarditis

  • Post-cardioversion

  • Pulmonary embolus

  • Severe hypertension

  • Worsening congestive heart failure

In non-cardiogenic APO, the mechanism is thought to be increased pulmonary vascular permeability brought about by an insult and leading to alveolar flooding. Injury to alveolar cells will also reduce their ability to clear this oedema fluid from the alveolar space (which may also play some role in cardiogenic APO). Some of the causes of non-cardiogenic pulmonary oedema are listed in Box 5.3.2 .

Box 5.3.2
Causes of non-cardiogenic pulmonary oedema

  • Airway obstruction

  • Aspiration

  • Asthma

  • Disseminated intravascular coagulopathy (DIC)

  • Eclampsia

  • Head injury, intracerebral haemorrhage, hyperbaric oxygen treatment, inhalation injury

  • Lung re-expansion (e.g. after treatment of a pneumothorax)

  • Lung reperfusion

  • Near drowning/cold water immersion

  • Opiates and opiate antagonists (naloxone and naltrexone)

  • Pancreatitis

  • Pulmonary embolism (thrombus, fat, amniotic fluid, other)

  • Rapid ascent to high altitude

  • Renal/hepatic failure

  • Self-contained underwater breathing apparatus (SCUBA) diving

  • Sepsis

  • Shock

  • Toxins

  • Trauma

Clinical assessment

History

As with all emergencies, clinical assessment and management should take place in parallel. There is usually a history of sudden-onset severe dyspnoea that may be associated with a feeling of drowning. A focused history concentrating on the recent occurrence of chest pain, palpitations, a past history of ischaemic heart disease, worsening congestive heart failure or another causative factor (see Boxes 5.3.1 and 5.3.2 ) is sought. Details of current medications and compliance are also important.

Examination

Patients are usually pale or cyanosed, diaphoretic (sometimes profusely) and frightened. If hypoxic or hypercapnic, they may be confused. They strive to maintain an upright position at all costs and may be unable to sit still. They may cough up pink or white frothy sputum, adding to their feeling of drowning. They are almost always tachycardic. Their respiratory rate is high, with use of the accessory muscles of respiration, and their breathing is often noisy. They are hypoxic, with reduced oxygen saturations. Most patients are hypertensive or normotensive. Hypotension indicates cardiogenic shock and a very poor prognosis. Similarly, skin mottling or other signs of poor peripheral perfusion indicate worsening cardiac function and a poorer prognosis. There may be a raised jugular venous pressure (JVP), a third heart sound or gallop rhythm on cardiac auscultation and signs of right heart strain. (These features will not be present in cases of non-cardiogenic pulmonary oedema.) Signs of chronic heart failure should also be sought, as well as murmurs that may hint at the precipitant. The chest may be dull to percussion, and fine crepitations, which are often extensive, will be heard on auscultation. Initially these crepitations may be limited to the lung bases, but they can also be heard higher in the chest (right to the apices) as the oedema worsens. Importantly, there may be other adventitial lung sounds, including wheeze or ‘cardiac asthma’.

Clinical investigations

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