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Managing acute pulmonary oedema

Megan Purvey
SUMMARY Advanced trainee1
George Allen
Acute pulmonary oedema has a high mortality. It requires emergency management and usually Staff specialist1
admission to hospital. Retrieval specialist2
The goals of therapy are to improve oxygenation, maintain an adequate blood pressure for perfusion 1
Emergency Medicine
of vital organs, and reduce excess extracellular fluid. The underlying cause must be addressed. Queen Elizabeth II Jubilee
There is a lack of high-quality evidence to guide the treatment of acute pulmonary oedema. The 2
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. Keywords
acute pulmonary oedema,
Routine use of morphine is not recommended because of its adverse effects. Oxygen should only
dobutamine, furosemide
be administered in cases of hypoxaemia. (frusemide), morphine,
Inotropic drugs should only be started when there is hypotension and evidence of reduced organ nitrates
perfusion. In these cases, dobutamine is usually first-line treatment.
Aust Prescr 2017;40:59–63

Introduction The drugs used in treatment include nitrates, diuretics,

Acute pulmonary oedema is a medical emergency morphine and inotropes. Some patients will require
which requires immediate management.1 It is ventilatory support. A working algorithm for the
characterised by dyspnoea and hypoxia secondary management of acute pulmonary oedema in the pre-
to fluid accumulation in the lungs which impairs gas hospital setting is outlined in the Figure.
exchange and lung compliance.2
The one-year mortality rate for patients admitted
Despite the widespread use of nitrates in acute
to hospital with acute pulmonary oedema is up to
pulmonary oedema, there is a lack of high-quality
40%.3 The most common causes of acute pulmonary
evidence to support this practice. When nitrates
oedema include myocardial ischaemia, arrhythmias
have been compared to furosemide (frusemide) and
(e.g. atrial fibrillation), acute valvular dysfunction
morphine, or furosemide alone, there has been no
and fluid overload. Other causes include pulmonary
difference in efficacy for outcomes such as the need
embolus, anaemia and renal artery stenosis.1,4 Non-
for mechanical ventilation, change in blood pressure
adherence to treatment and adverse drug effects can
or heart rate, and myocardial infarction.16
also precipitate pulmonary oedema.
The mechanism of nitrate action is smooth muscle
There are no current Australian data on the incidence
relaxation, causing venodilatation and consequent
of acute pulmonary oedema or heart failure. However,
preload reduction at low doses.13 Higher doses cause
self-reported data from 2011–12 estimated that 96 700
arteriolar dilatation, resulting in reduced afterload and
adults had heart failure, with two-thirds of these
being at least 65 years old.5 Most patients with chronic blood pressure. Specifically in the coronary arteries,
heart failure will have at least one episode of acute this dilatation results in increased coronary blood
pulmonary oedema that requires treatment in hospital.6 flow.9 These actions collectively improve oxygenation
and reduce the workload of the heart.13
There are several different clinical guidelines for
the management of acute pulmonary oedema.7-15 In general practice nitrates can be given sublingually.
However, these are based predominantly on low- Hospitals may use infusions as intravenous
quality evidence and expert opinion. The goals of administration is preferred due to the speed of onset
treatment are to provide symptomatic relief, improve and the ability to titrate the dose (Table 1).8,13
oxygenation, maintain cardiac output and perfusion Nitrates are associated with hypotension and
of vital organs, and reduce excess extracellular fluid. therefore blood pressure monitoring is essential to
Any underlying cause should be identified when ensure the systolic blood pressure is maintained
starting treatment. above 90 mmHg.8,13 They should not be given if the

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ARTICLE Managing acute pulmonary oedema

systolic blood pressure is less than 90 mmHg or the

Fig. Pre-hospital management of acute pulmonary oedema
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,
Clinical symptoms and signs of acute pulmonary oedema
nitrates are contraindicated. Nitrates are generally
well tolerated with the most common adverse effect
being headaches. Other adverse effects include
Arrange emergency transfer to hospital reflex tachycardia and paradoxical bradycardia.13
Position patient sitting up Nitrates are also associated with tachyphylaxis,
Monitor vital signs and cardiac rhythm with tolerance developing within 16–24 hours of
continuous administration.9

If systolic There is a lack of controlled studies showing that
Evidence of If oxygen saturation
blood pressure
fluid overload <92% diuretics are of benefit in acute pulmonary oedema.
>100 mmHg
However, diuretics are indicated for patients with
evidence of fluid overload.13 Loop diuretics such as
furosemide reduce preload and should be withheld
Glyceryl trinitrate Give 40 mg Provide or used judiciously in patients who may have
spray or furosemide supplemental oxygen intravascular volume depletion.9,13
sublingual tablet (frusemide) Target oxygen
intravenously Intravenous administration is preferred, with the
•• repeat every saturation 92–96%:
5 minutes dose of furosemide ranging from 40–80 mg
•• 4 L/min via nasal
(Table 2).1,2,8,13 The higher doses in the range are
used for patients already taking oral diuretics or with
•• 5–10 L/min via mask
chronic kidney disease. An initial bolus can be given
•• 15 L/min via a
non‑rebreather slowly intravenously and repeated 20 minutes later if
reservoir mask 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
If oxygen saturation is still
bolus and continuous infusion.18 Higher doses have
<92% commence:
been associated with greater improvement in
CPAP (10 cm water pressure) or
BiPAP (10/4 cm water pressure) 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
CPAP continuous positive airway pressure
catheter helps to monitor urine output.
BiPAP bi-level positive airway pressure
Source: References 1, 2, 8, 11 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
Table 1 Recommended nitrate dose regimens secondary to venodilatation, resulting in venous
pooling and preload reduction.1,7,19 However, this
Presentation and Dose Frequency Maximum dose
administration mechanism of action is now being questioned.19
Morphine also reduces sympathetic nervous activity
Glyceryl trinitrate spray 400 microgram repeat every 1200 microgram
and can reduce the anxiety and distress associated
(2 puffs) 5 min
with dyspnoea.1,18
Glyceryl trinitrate 300–600 microgram repeat every 1800 microgram
The adverse effects of morphine include respiratory
sublingual tablet 5 min
and central nervous system depression, reduced
Glyceryl trinitrate 5–10 microgram double every 200 microgram cardiac output and hypotension. Morphine used for
intravenous infusion* per min 5 min per min
acute pulmonary oedema has been associated with
adverse events such as significantly increased rates of
* first line in acute pulmonary oedema
Source: References 8 and 13 mechanical ventilation, intensive care admissions and
mortality.20 In the absence of high-quality randomised

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trial data, the best current evidence suggests that benefit of bi-level positive airway pressure ventilation
morphine may cause harm. Morphine is therefore (BiPAP) over continuous positive airway pressure
no longer recommended for routine use in acute ventilation (CPAP), so the modality chosen should
pulmonary oedema.19 It may be beneficial if there is be guided by local availability.22,23 Non-invasive
ongoing chest pain resistant to nitrates.20 Low doses ventilation should be commenced at 100% oxygen
of morphine (1–2.5 mg) can be useful to facilitate the with recommended initial settings of 10 cm of water
tolerance of non-invasive ventilation but the patient pressure for CPAP and 10/4 cm water pressure
needs to be monitored for sedation.8 (inspiratory positive airway pressure/expiratory
positive airway pressure) for BiPAP.8 Contraindications
Ventilatory support
to non-invasive ventilation include hypotension,
The first step in improving ventilation for patients with possible pneumothorax, vomiting, an altered level of
acute pulmonary oedema is to ensure that they are consciousness or non-compliance.7
positioned sitting up.1 This reduces the ventilation–
If, despite non-invasive ventilation, there is persistent
perfusion mismatch and assists with their work
hypercapnia, hypoxaemia or acidosis, then intubation
of breathing.
should be considered.7 Other indications for intubation
Oxygen is not routinely recommended for patients include signs of physical exhaustion, a decreasing
without hypoxaemia as hyperoxaemia may cause level of consciousness or cardiogenic shock.
vasoconstriction, reduce cardiac output and increase Endotracheal intubation is only indicated in a very
short-term mortality.21 There is a risk that prescribing limited number of cases and carries inherent risks
oxygen for a breathless patient in the absence of and challenges. The rapid sequence induction needs
hypoxaemia may mask clinical deterioration and to be modified to account for the haemodynamic
hence delay appropriate treatment.11 Supplemental compromise of the patient. After intubation constant
oxygen and assisted ventilation should only be used if suctioning is usually required and ventilation can be
the oxygen saturation is less than 92%.11 very challenging.7,19 Additionally, positive pressure
If required, oxygen should be administered to achieve ventilation is likely to potentiate any hypotension.
a target oxygen saturation of 92–96%. Depending on
the clinical scenario, oxygen titration can occur using a Inotropes
number of oxygen delivery devices. These include up Intravenous inotropic drugs are indicated in acute
to 4 L/minute via nasal cannulae, 5–10 L/minute via pulmonary oedema when there is hypotension and
mask, 15 L/minute via a non-rebreather reservoir mask evidence of reduced organ perfusion.12,14,15,19 Their use
or high-flow nasal cannulae with fraction of inspired is limited to this clinical situation in critically ill patients
oxygen greater than 35%. For patients with chronic as they are associated with a longer length of hospital
obstructive pulmonary disease, the target oxygen stay and increased mortality.19 In cases of impaired
saturation is 88–92% and the use of a Venturi mask left ventricular function and hypotension, first-line
with inspired oxygen set at 28% is recommended.11 therapy is an intravenous infusion of dobutamine.12,19,24
If the patient has respiratory distress, acidosis or As well as its positive inotropic actions, dobutamine
hypoxia, despite supplemental oxygen, non-invasive has peripheral vasodilatory effects that can result
ventilation is indicated.2 There is no significant clinical in worsening hypotension, which may require

Table 2 Recommended doses of furosemide (frusemide)

Presentation and administration Dose Frequency

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 continuous

* The oral bioavailability of furosemide (frusemide) is approximately half that of the intravenous formulation.
Source: References 1, 2, 8 and 13

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ARTICLE Managing acute pulmonary oedema

management with a vasopressor. Dobutamine can evidence of a reduced ejection fraction and chronic
cause arrhythmias and is contraindicated if the patient heart failure then an ACE inhibitor, beta blocker
has ventricular arrhythmias or rapid atrial fibrillation. and mineralocorticoid receptor antagonist should
Another inotrope that may increase cardiac output be considered.2
and improve peripheral perfusion is milrinone. It ACE inhibitors are best started at 24–48 hours after
should only be used for the short-term management admission, provided the patient is haemodynamically
of severe heart failure that has not responded to stable.2 They should be used cautiously in patients
other treatments. Milrinone may increase mortality in with hypotension or renal impairment, with close
acute exacerbations of chronic heart failure. It can be monitoring of blood pressure and renal function.7,9
considered in patients with chronic beta blockade.19 Beta blockers, such as bisoprolol, are commenced
at low dose once the patient is euvolaemic, before
discharge from hospital. Mineralocorticoid receptor
The underlying cause of the patient’s acute pulmonary antagonist drugs, such as spironolactone, are
oedema should be treated. This includes reviewing best started soon after discharge with careful
their medicines to see if any drugs, such as non- monitoring of blood pressure, serum potassium and
SELF-TEST steroidal anti-inflammatory drugs, verapamil or renal function.2
QUESTIONS diltiazem, could have contributed to the problem.
Additional monitoring including daily weights, and
True or false? Conclusion
1. Morphine reduces the measurements of serum electrolytes and renal
need for mechanical function is also recommended.15
ventilation in patients Guidelines have highlighted that there is a lack of
with acute pulmonary Once the patient with cardiogenic acute pulmonary evidence to support the currently used therapies.
oedema oedema has been stabilised the goal of therapy is to Additionally there are concerns regarding the efficacy
2. Nitrates should not improve long-term outcomes. If an echocardiogram and safety of these treatments for acute pulmonary
be given to patients shows a preserved left ventricular ejection fraction,
with acute pulmonary oedema. There has therefore been a shift over the
the focus is to treat any associated conditions. This last few years to favour nitrates and non-invasive
oedema if their systolic
blood pressure is below includes the management of hypertension with ventilation as first-line management. However, opioids
90 mmHg antihypertensive drugs, reduction of pulmonary and diuretics may have a role in some patients.
Answers on page 83 congestion and peripheral oedema with diuretics,
and rate control for atrial fibrillation. If there is Conflict of interest: none declared

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