Please note: this guideline has exceeded its review date and is currently under review by specialists. Exercise caution in the use of the clinical guideline.

Management of Acute Pulmonary Oedema / Heart Failure

Introduction

Acute pulmonary oedema may be the first presentation of heart failure or an exacerbation of existing known heart failure. It also may be secondary to another cause e.g. atrial fibrillation (AF), other tachycardias or bradycardia, critical cardiac ischaemia, valvular disease or renal artery stenosis.

Assessment

If critical cardiac ischaemia / infarction, see Initial management of STEMI presenting to A&E
Measure blood gases, record ECG and CXR and pulse oximetry.
If in fast AF / flutter, see Atrial fibrillation or flutter- recent onset

General management / drug treatment

Sit patient upright and give 100% oxygen via facemask unless CO₂ retention (see Guidelines for blood gas analysis for interpretation of blood gases).
Consider slow titrated small increments of intravenous diamorphine or morphine if associated chest pain or severe distress. Also consider antiemetic. Do not give opiate if patient is drowsy, exhausted or hypotensive. Give: furosemide IV 50mg (or in patients already receiving oral diuretics, give, intravenously, double the patient's normal oral dose). Repeat bolus at 30 mins to 1 hour. Double dose at first repeat. If further diuretic required - refer immediately to senior medical staff.
Glyceryl trinitrate IV. Commence at 0.5 mg/hour. Titrate according to BP but only if systolic BP >90mmHg (see local dosing charts for details).
Consider continuous positive airway pressure (CPAP - see protocol below) or NIV if acidotic or poor response to furosemide and nitrates.
Refer to senior medical staff and intensive care for consideration of intravenous inotropes or invasive ventilation.

N.B. Once the acute episode is resolved and the patient is more stable consider long-term management.

CPAP in cardiogenic pulmonary oedema

CPAP can be considered in patients who have not responded to medical treatment. However, discuss this option with a senior.
CPAP increases intrathoracic pressure, which reduces preload by decreasing venous return.
CPAP lowers afterload by increasing the pressure gradient between the left ventricle and the extrathoracic arteries, which may contribute to the associated increase in stroke volume.
Intubation should be considered in patients with persistent hypoxaemia on CPAP or persistent hypercapnia despite the administration of oxygen, morphine, diuretics, and vasodilators. In addition, intubation is required in the setting of apnoea or profound respiratory depression (respiratory rate <10bpm).

Contraindications to CPAP:

Reduced conscious level (not responding to pain or unconscious on the AVPU scale: unable to protect airway therefore consider invasive ventilation)
Dementia resulting in intolerance of therapy
Systolic blood pressure <90mmHg
Pneumothorax
Facial trauma / base of skull fracture
Type II respiratory failure / severe emphysema

Complications of CPAP:

Hypotension - CPAP increases mean intrathoracic pressure, reducing systemic venous return and cardiac output
Aspiration - gastric contents may be aspirated due to large volumes of air being blown into the stomach
Gastric distension - large volumes of air swallowed can overcome resistance of lower oesophageal sphincter
Anxiety - hypoxia and tight fitting mask can induce anxiety and panic

When to stop CPAP:

Continue CPAP until chest clear of rales and haemodynamically stable. Initially wean airway pressure then wean supplemental oxygen and change to standard facemask. If there has been no clinical improvement after 30 minutes, CPAP should be stopped.