CHAPTER 47

Acute pulmonary oedema

DAVID SPRIGINGS AND JOHN B. CHAMBERS

Figure 47.1 Approach to the patient with suspected pulmonary oedema.

Acute Medicine: A Practical Guide to the Management of Medical Emergencies, Fifth Edition. Edited by
David Sprigings and John B. Chambers.
© 2018 John Wiley & Sons Ltd. Published 2018 by John Wiley & Sons Ltd.

305
306 Acute Medicine

Figure 47.1 (Continued)

 Acute pulmonary oedema 307

Table 47.1 Causes of acute pulmonary oedema.

Causes due to elevated pressure in the pulmonary capillaries

Cardiac disease, new presentation:
• Acute myocardial infarction or severe myocardial ischaemia
• Acute myocarditis
• Severe aortic or mitral stenosis
• Acute aortic regurgitation (aortic dissection, infective endocarditis, chest trauma)
• Acute mitral regurgitation (infective endocarditis, ruptured chordae or papillary muscle, chest trauma)
• Ventricular septal rupture after myocardial infarction
• Left atrial myxoma
Precipitants of pulmonary oedema in patients with previously stable valve or left ventricular disease:
• Acute myocardial infarction or myocardial ischaemia
• Arrhythmia
• Poor compliance with diuretic therapy
• Drugs causing fluid retention (e.g. NSAIDs, steroids)
• Iatrogenic fluid overload
• Infective endocarditis
• Progression of disease
• Intercurrent illness (e.g. pneumonia, anaemia)
Renal disease:
• Acute kidney injury or advanced chronic kidney disease
• Renal artery stenosis
Iatrogenic fluid overload
Subarachnoid haemorrhage
Negative-pressure pulmonary oedema (Table 47.8)

Causes due to increased pulmonary capillary permeability

(acute lung injury/ARDS); for management see Table 47.7

Direct lung injury Indirect lung injury

Common causes
Pneumonia (viral or bacterial) Sepsis
Aspiration of gastric contents Severe trauma with shock and multiple
transfusions
Less common causes
Pulmonary contusion Cardiopulmonary by-pass
Fat emboli Drug overdose
Drowning Acute pancreatitis
Inhalational injury Transfusions of blood
Reperfusion pulmonary oedema after lung transplantation or pulmonary products
embolectomy

ARDS, acute respiratory distress syndrome; NSAIDs, non-steroidal anti- inflammatory drugs.

Table 47.2 Focused assessment in acute pulmonary oedema.

What is the cause of the pulmonary oedema?

• Usually cardiac disease (Table 47.1), less often acute kidney injury
• Pulmonary oedema developing in hospital is often due to fluid overload in patients with pre-existing cardiac or renal
disease
• Consider acute respiratory distress syndrome in patients without evidence of cardiac disease (Table 47.1)
• In post-operative patients, negative-pressure pulmonary oedema is occasionally seen (Table 47.8)
• Neurogenic pulmonary oedema may complicate subarachnoid haemorrhage (Chapter 67)
308 Acute Medicine

Table 47.3 Initial drug therapy in acute pulmonary oedema.

Drug Comment

Oxygen Give oxygen 60–100%.

Pulse oximetry may be unreliable due to peripheral vasoconstriction.
Check arterial blood gases if the patient is hypotensive or there is no improvement within 30 min.
Target oxygen saturation >92%, PaO2 >8 kPa.
Furosemide Give furosemide 40 mg IV if plasma creatinine is <150 μmol/L and 80 mg if 150–200 μmol/L.
In patients with plasma creatinine >200 μmol/L, standard doses of furosemide are often ineffective. Try a
furosemide infusion (100 mg IV over 60 min by syringe pump).
Nitrate Give nitrate (sublingual, buccal or IV infusion).

Table 47.4 Urgent investigation in acute pulmonary oedema.

• ECG Arrhythmia? Evidence of acute myocardial infarction or ischaemia? Evidence of other cardiac disease, e.g. left
ventricular hypertrophy, left bundle branch block?
• Chest X-ray (to confirm the clinical diagnosis and exclude other causes of breathlessness). With non-cardiogenic
pulmonary oedema, the heart size is usually normal; septal lines and pleural effusions are usually absent; and air
bronchograms are usually present.
• Arterial blood gases and pH.
• Blood glucose.
• Creatinine, sodium and potassium.
• Full blood count.
• Erythrocyte sedimentation rate (ESR) or C-reactive protein.
• Transthoracic echocardiography, in all newly diagnosed cases especially if acute valve lesion or ventricular septal
rupture is suspected, or distinction between cardiogenic/non-cardiogenic pulmonary oedema is uncertain (in other
patients, echocardiography should be done within 24 h).
• Cardiac biomarkers: plasma troponin and brain natriuretic peptide.

Table 47.5 Further drug therapy of acute cardiogenic pulmonary oedema.

Systolic blood pressure Action

>110 mmHg Give another dose of furosemide 40–80 mg IV

Start a nitrate infusion
90–110 mmHg Start a dobutamine infusion at 5 μgm/kg/min; this can be given via a peripheral line
Increase the dose by 2.5 μgm/kg/min every 10 min until systolic BP is >110 mmHg or a
maximum dose of 20 μgm/kg/min has been reached
A nitrate infusion can be added if systolic BP is maintained at >110 mmHg
80–90 mmHg Start a dopamine infusion at 10 μgm/kg/min; this must be given via a central line
Increase the dose by 5 μgm/kg/min every 10 min until systolic BP is >110 mmHg
If systolic BP remains <90 mmHg despite dopamine 20 μgm/kg/min, use norepinephrine
instead
A nitrate infusion can be added if systolic BP is maintained at >110 mmHg
<80 mmHg Start a norepinephrine infusion at 2.5 μgm/kg/min; this must be given via a central line
Increase the dose by 2.5 μgm/kg/min every 10 min until systolic BP is >110 mmHg
A nitrate infusion can be added if systolic BP is maintained at >110 mmHg
 Acute pulmonary oedema 309

Table 47.6 Ventilatory support for respiratory failure due to cardiogenic pulmonary oedema.

Mode of ventilation Indications Contraindications Disadvantages and

complications

Non-invasive ventilatory
support with continuous
positive airways pressure
(CPAP)
Endotracheal intubation and
mechanical ventilation
Oxygenation failure: oxygen
saturation
<92% despite
FiO2 >40%
Ventilatory failure: mild to
moderate respiratory
acidosis, arterial pH
7.25–7.35
Upper airway obstruction
Impending respiratory arrest
Airway at risk because of
neurological disease or
coma (GCS 8 or lower)
Oxygenation failure:
PaO2 <7.5–8 kPa despite
supplemental oxygen/NIV
Ventilatory failure:
moderate to severe
respiratory acidosis, arterial
pH <7.25
Recent facial, upper airway
or upper gastrointestinal
tract surgery
Vomiting or bowel
obstruction
Copious secretions
Haemodynamic instability
Impaired consciousness,
confusion or agitation
Severely impaired
functional capacity and/or
severe comorbidity
Cardiac disorder not
remediable
Patient has expressed wish
not to be ventilated
Discomfort from tightly
fitting facemask
Discourages coughing
and clearing of
secretions
Adverse
haemodynamic effects
Pharyngeal, laryngeal
and tracheal injury
Pneumonia
Ventilator-induced
lung injury (e.g.
pneumothorax)
Complications of
sedation and
neuromuscular
blockade

GCS, Glasgow Coma Scale score.

Table 47.7 Management of acute respiratory distress syndrome (ARDS).

Element Comment

Transfer to ICU ARDS is usually part of multiorgan failure

Oxygenation Increase inspired oxygen, target PaO2 >8 kPa
Ventilation will be needed if PaO2 is <8 kPa despite FiO2 60%
Ventilation in the prone position improves oxygenation
Haemoglobin should be kept around 10 g/dl (to give the optimum balance
between oxygen-carrying capacity and blood viscosity)
Fluid balance Acute kidney injury is commonly associated with ARDS
Consider early haemofiltration
Prevention and treatment of sepsis Sepsis is a common cause and complication of ARDS
Culture blood, tracheobronchial aspirate and urine daily
Treat presumed infection with broad-spectrum antibiotic therapy
Nutrition Enteral feeding if possible, via nasogastric tube if ventilation needed
DVT prophylaxis Give DVT prophylaxis with stockings and LMW heparin
Prophylaxis against gastric stress Give proton pump inhibitor
ulceration

DVT, deep vein thrombosis; ICU, intensive care unit; LMW, low molecular weight.
310 Acute Medicine

Table 47.8 Negative-pressure pulmonary oedema.

• Seen in the early postoperative period

• Due to forced inspiration in the presence of upper airway obstruction (e.g. from laryngospasm after extubation)
• After relief of laryngospasm, patients develop clinical and radiological features of pulmonary oedema
• Typically resolves over the course of a few hours with supportive care
• Cardiogenic pulmonary oedema should be excluded by clinical assessment, ECG and echocardiography

Further reading

Busl KM, Bleck TP. (2015) Concise definitive review: Neurogenic pulmonary edema. Critical Care Medicine 43,
1710–1715. DOI: 10.1097/CCM.0000000000001101.
Mac Sweeney R, McAuley DF. (2016) Acute respiratory distress syndrome. Lancet 388, 2416–2430.
The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of
Cardiology (ESC) (2016) 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart
failure. European Heart Journal 37, 2129–2200. http://eurheartj.oxfordjournals.org/content/ehj/early/2016/
05/19/eurheartj.ehw128.full.pdf.