Acute pulmonary oedema has a high mortality. It requires emergency management and usually admission to hospital.

The goals of therapy are to improve oxygenation, maintain an adequate blood pressure for perfusion of vital organs, and reduce excess extracellular fluid. The underlying cause must be addressed.

There is a lack of high-quality evidence to guide the treatment of acute pulmonary oedema. The strongest evidence is for nitrates and non-invasive ventilation.

Diuretics are indicated for patients with fluid overload. Furosemide (frusemide) should be given by slow intravenous injection.

Routine use of morphine is not recommended because of its adverse effects. Oxygen should only be administered in cases of hypoxaemia.

Inotropic drugs should only be started when there is hypotension and evidence of reduced organ perfusion. In these cases, dobutamine is usually first-line treatment.


Acute pulmonary oedema is a medical emergency which requires immediate management.1 It is characterised by dyspnoea and hypoxia secondary to fluid accumulation in the lungs which impairs gas exchange and lung compliance.2

The one-year mortality rate for patients admitted to hospital with acute pulmonary oedema is up to 40%.3 The most common causes of acute pulmonary oedema include myocardial ischaemia, arrhythmias (e.g. atrial fibrillation), acute valvular dysfunction and fluid overload. Other causes include pulmonary embolus, anaemia and renal artery stenosis.1,4 Non-adherence to treatment and adverse drug effects can also precipitate pulmonary oedema.

There are no current Australian data on the incidence of acute pulmonary oedema or heart failure. However, self-reported data from 2011–12 estimated that 96 700 adults had heart failure, with two-thirds of these being at least 65 years old.5 Most patients with chronic heart failure will have at least one episode of acute pulmonary oedema that requires treatment in hospital.6

There are several different clinical guidelines for the management of acute pulmonary oedema.7-15 However, these are based predominantly on low-quality evidence and expert opinion. The goals of treatment are to provide symptomatic relief, improve oxygenation, maintain cardiac output and perfusion of vital organs, and reduce excess extracellular fluid. Any underlying cause should be identified when starting treatment.

The drugs used in treatment include nitrates, diuretics, morphine and inotropes. Some patients will require ventilatory support. A working algorithm for the management of acute pulmonary oedema in the pre-hospital setting is outlined in the Figure

Fig. Pre-hospital management of acute pulmonary oedema

CPAP    continuous positive airway pressure

BiPAP   bi-level positive airway pressure

Source: References 1, 2, 8, 11 and 13


Despite the widespread use of nitrates in acute pulmonary oedema, there is a lack of high-quality evidence to support this practice. When nitrates have been compared to furosemide (frusemide) and morphine, or furosemide alone, there has been no difference in efficacy for outcomes such as the need for mechanical ventilation, change in blood pressure or heart rate, and myocardial infarction.16

The mechanism of nitrate action is smooth muscle relaxation, causing venodilatation and consequent preload reduction at low doses.13 Higher doses cause arteriolar dilatation, resulting in reduced afterload and blood pressure. Specifically in the coronary arteries, this dilatation results in increased coronary blood flow.9 These actions collectively improve oxygenation and reduce the workload of the heart.13

In general practice nitrates can be given sublingually. Hospitals may use infusions as intravenous administration is preferred due to the speed of onset and the ability to titrate the dose (Table 1).8,13

Table 1 - Recommended nitrate dose regimens


Presentation and administration



Maximum dose

Glyceryl trinitrate spray

400 microgram
(2 puffs)

repeat every 5 min

1200 microgram

Glyceryl trinitrate sublingual tablet

300–600 microgram

repeat every 5 min

1800 microgram

Glyceryl trinitrate intravenous infusion*

5–10 microgram
per min

double every 5 min

200 microgram
per min

* first line in acute pulmonary oedema

Source: References 8 and 13

Nitrates are associated with hypotension and therefore blood pressure monitoring is essential to ensure the systolic blood pressure is maintained above 90 mmHg.8,13 They should not be given if the systolic blood pressure is less than 90 mmHg or the patient has severe aortic stenosis, as these patients are preload dependent.2,8,17 If the patient has recently taken a phosphodiesterase inhibitor, such as sildenafil, nitrates are contraindicated. Nitrates are generally well tolerated with the most common adverse effect being headaches. Other adverse effects include reflex tachycardia and paradoxical bradycardia.13 Nitrates are also associated with tachyphylaxis, with tolerance developing within 16–24 hours of continuous administration.9


There is a lack of controlled studies showing that diuretics are of benefit in acute pulmonary oedema. However, diuretics are indicated for patients with evidence of fluid overload.13 Loop diuretics such as furosemide reduce preload and should be withheld or used judiciously in patients who may have intravascular volume depletion.9,13

Intravenous administration is preferred, with the dose of furosemide ranging from 40–80 mg (Table 2).1,2,8,13 The higher doses in the range are used for patients already taking oral diuretics or with chronic kidney disease. An initial bolus can be given slowly intravenously and repeated 20 minutes later if required.8 After the bolus, a continuous intravenous infusion may be considered, commencing at a rate of 5–10 mg per hour.1 A small randomised controlled trial did not find any difference in outcomes between bolus and continuous infusion.18 Higher doses have been associated with greater improvement in dyspnoea. They are also associated with worsening of renal function and increased admissions to intensive care, but this association is likely to reflect more severe disease.18 In hospital, insertion of an indwelling catheter helps to monitor urine output.

Table 2 - Recommended doses of furosemide (frusemide)


Presentation and



Slow intravenous bolus

4 mg/min

repeat after 20 min if necessary

- normal renal function

40–80 mg

- renal insufficiency or severe
  heart failure

up to 160–200 mg

- chronic loop diuretic users initial intravenous dose equal
to maintenance oral dose,*
titrate to response

Intravenous infusion

5–10 mg per hour


* The oral bioavailability of furosemide (frusemide) is approximately half that of the intravenous formulation.

Source: References 1, 2, 8 and 13


Morphine has been part of the traditional treatment for acute pulmonary oedema as it can reduce dyspnoea.1,19 This effect was presumed to be secondary to venodilatation, resulting in venous pooling and preload reduction.1,7,19 However, this mechanism of action is now being questioned.19 Morphine also reduces sympathetic nervous activity and can reduce the anxiety and distress associated with dyspnoea.1,18

The adverse effects of morphine include respiratory and central nervous system depression, reduced cardiac output and hypotension. Morphine used for acute pulmonary oedema has been associated with adverse events such as significantly increased rates of mechanical ventilation, intensive care admissions and mortality.20 In the absence of high-quality randomised trial data, the best current evidence suggests that morphine may cause harm. Morphine is therefore no longer recommended for routine use in acute pulmonary oedema.19 It may be beneficial if there is ongoing chest pain resistant to nitrates.20 Low doses of morphine (1–2.5 mg) can be useful to facilitate the tolerance of non-invasive ventilation but the patient needs to be monitored for sedation.8

Ventilatory support

The first step in improving ventilation for patients with acute pulmonary oedema is to ensure that they are positioned sitting up.1 This reduces the ventilation–perfusion mismatch and assists with their work of breathing.

Oxygen is not routinely recommended for patients without hypoxaemia as hyperoxaemia may cause vasoconstriction, reduce cardiac output and increase short-term mortality.21 There is a risk that prescribing oxygen for a breathless patient in the absence of hypoxaemia may mask clinical deterioration and hence delay appropriate treatment.11 Supplemental oxygen and assisted ventilation should only be used if the oxygen saturation is less than 92%.11

If required, oxygen should be administered to achieve a target oxygen saturation of 92–96%. Depending on the clinical scenario, oxygen titration can occur using a number of oxygen delivery devices. These include up to 4 L/minute via nasal cannulae, 5–10 L/minute via mask, 15 L/minute via a non-rebreather reservoir mask or high-flow nasal cannulae with fraction of inspired oxygen greater than 35%. For patients with chronic obstructive pulmonary disease, the target oxygen saturation is 88–92% and the use of a Venturi mask with inspired oxygen set at 28% is recommended.11

If the patient has respiratory distress, acidosis or hypoxia, despite supplemental oxygen, non-invasive ventilation is indicated.2 There is no significant clinical benefit of bi-level positive airway pressure ventilation (BiPAP) over continuous positive airway pressure ventilation (CPAP), so the modality chosen should be guided by local availability.22,23 Non-invasive ventilation should be commenced at 100% oxygen with recommended initial settings of 10 cm of water pressure for CPAP and 10/4 cm water pressure (inspiratory positive airway pressure/expiratory positive airway pressure) for BiPAP.8 Contraindications to non-invasive ventilation include hypotension, possible pneumothorax, vomiting, an altered level of consciousness or non-compliance.7

If, despite non-invasive ventilation, there is persistent hypercapnia, hypoxaemia or acidosis, then intubation should be considered.7 Other indications for intubation include signs of physical exhaustion, a decreasing level of consciousness or cardiogenic shock. Endotracheal intubation is only indicated in a very limited number of cases and carries inherent risks and challenges. The rapid sequence induction needs to be modified to account for the haemodynamic compromise of the patient. After intubation constant suctioning is usually required and ventilation can be very challenging.7,19 Additionally, positive pressure ventilation is likely to potentiate any hypotension.


Intravenous inotropic drugs are indicated in acute pulmonary oedema when there is hypotension and evidence of reduced organ perfusion.12,14,15,19 Their use is limited to this clinical situation in critically ill patients as they are associated with a longer length of hospital stay and increased mortality.19 In cases of impaired left ventricular function and hypotension, first-line therapy is an intravenous infusion of dobutamine.12,19,24 As well as its positive inotropic actions, dobutamine has peripheral vasodilatory effects that can result in worsening hypotension, which may require management with a vasopressor. Dobutamine can cause arrhythmias and is contraindicated if the patient has ventricular arrhythmias or rapid atrial fibrillation.

Another inotrope that may increase cardiac output and improve peripheral perfusion is milrinone. It should only be used for the short-term management of severe heart failure that has not responded to other treatments. Milrinone may increase mortality in acute exacerbations of chronic heart failure. It can be considered in patients with chronic beta blockade.19


The underlying cause of the patient’s acute pulmonary oedema should be treated. This includes reviewing their medicines to see if any drugs, such as non-steroidal anti-inflammatory drugs, verapamil or diltiazem, could have contributed to the problem. Additional monitoring including daily weights, and measurements of serum electrolytes and renal function is also recommended.15

Once the patient with cardiogenic acute pulmonary oedema has been stabilised the goal of therapy is to improve long-term outcomes. If an echocardiogram shows a preserved left ventricular ejection fraction, the focus is to treat any associated conditions. This includes the management of hypertension with antihypertensive drugs, reduction of pulmonary congestion and peripheral oedema with diuretics, and rate control for atrial fibrillation. If there is evidence of a reduced ejection fraction and chronic heart failure then an ACE inhibitor, beta blocker and mineralocorticoid receptor antagonist should be considered.2

ACE inhibitors are best started at 24–48 hours after admission, provided the patient is haemodynamically stable.2 They should be used cautiously in patients with hypotension or renal impairment, with close monitoring of blood pressure and renal function.7,9 Beta blockers, such as bisoprolol, are commenced at low dose once the patient is euvolaemic, before discharge from hospital. Mineralocorticoid receptor antagonist drugs, such as spironolactone, are best started soon after discharge with careful monitoring of blood pressure, serum potassium and renal function.2


Guidelines have highlighted that there is a lack of evidence to support the currently used therapies. Additionally there are concerns regarding the efficacy and safety of these treatments for acute pulmonary oedema. There has therefore been a shift over the last few years to favour nitrates and non-invasive ventilation as first-line management. However, opioids and diuretics may have a role in some patients.

Conflict of interest: none declared

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