Acute pulmonary oedema

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Chapter 9 Acute pulmonary oedema

Anthony F.T. Brown

Decompensated heart failure, or acute pulmonary oedema (APO), now accounts for 1% of emergency department visits, with a 16% in-hospital mortality for those admitted with frank pulmonary oedema and an overall 50% five-year mortality.

Although the typical frail, elderly patient may dominate the physician’s perspective, APO can present in the emergency department in a diverse group of patients, from those suffering from an underlying acute coronary syndrome (ACS), whether an ST-segment elevation myocardial infarct (STEMI), non-ST-segment elevation myocardial infarct (NSTEMI) or unstable angina (UA), to chronic decompensated heart failure to non-cardiogenic causes. All have often subtly different historical, examination and investigation findings, and may require a wide variety of urgent treatment modalities.

PATHOPHYSIOLOGY

Acute pulmonary oedema may be divided into cardiogenic and non-cardiogenic causes.

Acute cardiogenic pulmonary oedema

Acute cardiogenic pulmonary oedema is the most severe manifestation of congestive heart failure, and is associated with an increase in lung fluid secondary to hydrostatic leakage from pulmonary capillaries into the alveoli and interstitium of the lungs. Underlying this is a rise in left ventricular end-diastolic pressure and left atrial pressure related to left ventricular dysfunction.

The causative heart disease leading to left ventricular failure may be predominantly systolic failure with impaired cardiac contractility, i.e. an ejection fraction (EF) under 40%, diastolic failure with impaired myocardial relaxation and distensibility (but a normal or even supranormal EF), or a combination of both.

APO may develop out of the blue, or be precipitated in patients with existing heart disease as a result of an acute cause such as ischaemia, an arrhythmia or medication change. Table 9.1 gives the causes of cardiogenic pulmonary oedema.

Table 9.1 Causes of cardiogenic pulmonary oedema

Precipitating factors
• Myocardial ischaemia
• Cardiac arrhythmia

• tachycardia, including atrial fibrillation
• bradycardia, conduction abnormality

• Volume overload, including blood transfusion
• Hypertensive crisis
• Systemic infection, including septic shock
• Cardiac infection—myocarditis, endocarditis
• Pulmonary embolism
• Medication related

• inappropriate reduction of therapy
• drug non-compliance
• cardiac depressant (beta-blocker)
• salt-retaining (non-steroidal anti-inflammatory)

• High output state—anaemia, thyrotoxicosis, beriberi
• Alcohol excess or withdrawal

Predominant systolic heart failure
• Acute coronary syndrome
• Hypertension
• Cardiomyopathy
• Myocarditis
• Valvular disease, particularly acute aortic or mitral regurgitation

Predominant diastolic heart failure (one-third to one-half of all patients)
• Hypertension, including renovascular disease
• Aortic stenosis (indicates critical disease)
• Cardiomyopathy—hypertrophic (HCM), or restrictive
• Acute coronary syndrome

Non-cardiogenic pulmonary oedema

Non-cardiogenic pulmonary oedema occurs without a rise in pulmonary capillary wedge pressure. It may result from a wide variety of mechanisms, including:

• increased capillary permeability in acute respiratory distress syndrome (ARDS), septicaemia, aspiration of gastric contents, inhaled toxins, pancreatitis, uraemia or near drowning
• mixed or unknown causes such as neurogenic pulmonary oedema, high-altitude pulmonary oedema (HAPE), heroin overdose, smoking freebase cocaine, eclampsia, post lung re-expansion and post pulmonary embolism
• decreased oncotic pressure such as in hypoalbuminaemia, usually in combination with another cause.

Neurogenic pulmonary oedema

This is a relatively rare cause of APO, developing within a few hours of an acute neurologic insult, and is often associated with intracranial hypertension such as from prolonged seizures, a head injury or a subarachnoid or intracerebral haemorrhage.

It usually resolves over 48–72 hours, determined by the course of the underlying primary neurologic insult.

CLINICAL FEATURES

History

Patients may be too distressed to give a history until after aggressive medical management, but may report chest pain, a change in medication or recent fever (see Table 9.1) as a precipitating cause, or remember previous episodes of ‘fluid on the lung’.

Acute breathlessness is universal, and may occur precipitately or on a background of cough, exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea (PND) and dyspnoea at rest. Other non-specific features such as fatigue and nocturia may occur in compensated heart failure. Finally, confusion, coma and respiratory arrest may ensue.

Examination

Patients with APO are terrified, sweaty, unwilling to lie down, restless and may wheeze or froth pink sputum in extreme cases.

Tachypnoea, tachycardia, reduced oxygen saturation, hyper- or hypotension and cyanosis may all occur.

Inspiratory basal crackles, a raised jugular venous pressure (JVP) from secondary right-heart failure and a third heart sound S3 gallop are typical whereas, in non-cardiogenic pulmonary oedema, patients may have a warm periphery, bounding pulse, and usually absence of an S3 gallop or jugular venous distension.

A new systolic murmur may indicate an acute mechanical complication such as papillary muscle rupture or an acquired ventricular septal defect (VSD) in the setting of an acute myocardial infarction.

DIFFERENTIAL DIAGNOSIS

Pulmonary embolism (PE) and acute pneumonia must be excluded, although PE becomes more common in heart failure, and severe pneumonia may in itself lead to non-cardiogenic pulmonary oedema.

INVESTIGATIONS

Electrocardiogram (ECG)

This is essential to diagnose an acute myocardial infarction, arrhythmia or heart block and may determine the need for time-critical reperfusion therapy in the presence of chest pain (see Chapter 7, ‘Acute coronary syndromes’). It may also indicate underlying heart disease with left ventricular strain or hypertrophy, preexisting coronary artery disease or even an electrolyte disturbance.

Chest X-ray (CXR)

CXR can confirm the presence of APO, but due to its relatively poor sensitivity, it should not be used to rule out the diagnosis even when oedema fluid is not visible, or in the presence of technical issues particularly with a portable film. The CXR may help to differentiate APO from an exacerbation of chronic obstructive lung disease (COLD) or asthma.

1. Typical features of cardiogenic pulmonary oedema include cardiomegaly, pulmonary venous congestion with upper lobe diversion, perihilar ‘batswing’ infiltrates, Kerley B engorged subpleural lymphatics, interstitial oedema and small pleural effusions.
2. A normal heart size may occur in acute valvular rupture, diastolic dysfunction, myocarditis or non-cardiogenic causes of pulmonary oedema.
3. Non-cardiogenic pulmonary oedema will also show patchy or peripheral oedema, rather than even and central. Kerley B lines and pleural effusions are usually not present.

Laboratory tests

A full blood count, electrolyte and liver function tests, cardiac enzyme biomarkers including troponin, coagulation profile and thyroid function test should be sent, but usually add little to the immediate management.

Biomarkers

Troponin

An elevated troponin indicates myocardial damage from an ACS, particularly in the presence of ECG changes, but may also occur in the absence of ACS, for instance, in severe sepsis or from a pulmonary embolism.

B-type natriuretic polypeptide (BNP)

Other biomarkers such as BNP and N-terminal (NT) pro-BNP are of most value when the diagnosis is uncertain in a patient with acute dyspnoea. A BNP level under 100 pg/mL makes heart failure unlikely (approximate negative likelihood ratio (LR) = 0.1), and above 500 pg/mL makes heart failure likely (approximate positive LR = 6). However, both markers may be raised in the presence of pulmonary embolism or cor pulmonale, and conversely both may be low in confirmed heart failure. Thus their use and interpretation in the emergency department are still uncommon, and in the intensive care unit can be problematic.

Arterial blood gases

As with laboratory tests, arterial blood gases add nothing to the immediate management and serve only to delay therapy. They may be useful to monitor hypercapnoea in the non-responding patient.

MANAGEMENT OF APO

1. Sit the patient upright, apply high-flow oxygen via a non-rebreather mask and commence non-invasive monitoring in a resuscitation area.
2. Commence vasodilator therapy with nitrates to reduce preload.

a. Give glyceryl trinitrate (GTN) 150–300 μg sublingually. This dose may be repeated. Remove the tablet or cease if hypotension (systolic blood pressure (SBP) below 100 mmHg) occurs.
b. In resistant cases, particularly those associated with ischaemic chest pain, change to a glyceryl trinitrate (GTN) infusion. Add 200 mg GTN to 500 mL 5% dextrose (i.e. 400 μg/mL) in a glass bottle with low-absorption polyethylene infusion set. Commence at 1 mL/h (6.66 μg/min) and gradually increase to 20 mL/h or more, maintaining SBP above 100 mmHg.

3. Give frusemide 40 mg IV or twice the usual oral daily dose if already taking frusemide tablets, which may be repeated after 20–30 minutes. Avoid overdiuresis, as this may activate neurohormonal systems with a deterioration in renal function and a worsened outcome, particularly in those presenting hypertensive with predominant diastolic dysfunction. Interestingly, no randomised controlled trial has shown benefit for the use of frusemide alone in acute decompensated heart failure.
4. Give small increments of morphine if there is marked dyspnoea and agitation, starting at 0.5 mg IV in the elderly up to 2.5 mg in younger patients. Do not use morphine routinely, particularly if the patient is tired, may have COLD/asthma, or is becoming obtunded with a rising partial pressure of CO2 (PaCO2).
5. Commence non-invasive ventilatory assistance in those who do not respond to the above standard pharmacological therapy.

a. Use continuous positive airways pressure (CPAP) via a tight-fitting face mask, high-flow gas circuit and starting with 5–10 cm H2O. CPAP improves lung mechanics and enhances left ventricular performance, reducing the need for endotracheal intubation and the in-hospital mortality.
b. Consider bi-level positive airway pressure (BiPAP) non-invasive positive pressure ventilation (NIPPV) as an alternative. However, it is more complex to set up and costly, and does not appear to reduce the in-hospital mortality of cardiogenic pulmonary oedema, possibly relating to a negative association with an increased rate of acute myocardial infarction (AMI).

DISPOSAL

1. Patients who present hypotensive, or deteriorate and/or do not tolerate pharmacological vasodilation, have a poor prognosis, with mortality up to 80%.

a. Call for senior help if you have not already done so! Manage the patient as for cardiogenic shock with intubation and mechanical ventilation, applying 5–10 cmH2O positive end-expiratory pressure (PEEP).
b. Support the circulation with inotropes such as dopamine 2–20 μg/kg/min and dobutamine 2–30 μg/kg/min. Noradrenaline or adrenaline may be required for extreme hypotension, but the higher myocardial oxygen demand may ultimately be deleterious.
c. Look for a treatable mechanical cause with a transthoracic echocardiogram, such as an acute valvular rupture or VSD, and organise cardiac surgical care if one of these is found.
d. Admit the patient to intensive care. Consider an intra-aortic balloon pump as a temporising measure while reperfusion therapy—such as acute angioplasty or coronary revascularisation—is performed in the setting of an ST-elevation myocardial infarction, or while valvular or VSD repair is organised (see above).

2. The majority of patients respond to standard therapy. Arrange admission to a coronary care unit if there are ongoing cardiac issues such as pain, ischaemia, arrhythmias, or electrolyte disturbances, and close monitoring or respiratory support are necessary.

Otherwise, particularly in the elderly patient with brief decompensation of chronic heart failure, admit the patient to a non-monitored medical bed.

3. Non-cardiogenic pulmonary oedema is managed according to the underlying primary cause, with non-invasive or invasive respiratory support as necessary.

RESOURCES AND RECOMMENDED READING

Websites

UpToDate: http://www.uptodate.com/home/index.html. Multiple sites; May/June 2008.

Journal articles

Overview

Collins S., Storrow A.B., Kirk J.D., et al. Beyond pulmonary edema: Diagnostic, risk stratification, and treatment challenges of acute heart failure management in the emergency department. Ann Emerg Med. 2008;51:45-57.

Onwuanyi A., Taylor M. Acute decompensated heart failure: Pathophysiology and treatment. Am J Cardiol. 2007;99:25D-30D.

Ware L.B., Matthay M.A. Acute pulmonary edema. N Eng J Med. 2005;353:2788-2796.

Diastolic dysfunction

Kumar R., Gandhi S.K., Little W.C. Acute heart failure with preserved systolic function. Crit Care Med. 2008;36:S52-S56.

General management

Mebazza A., Gheorghiade M., Pina I.L., et al. Practical recommendations for prehospital and early in-hospital management of patients presenting with acute heart failure syndromes. Crit Care Med. 2008;36:S129-S139.

Silvers S.M., Howell J.M., Kosowsky J.M., et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes. Ann Emerg Med. 2007;49:627-669.

Medical management

Cotter G., Metzkor E., Kaluski E., et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet. 1998;351:389-393.

Noninvasive ventilation

Collins S.P., Mielniczuk L.M., Whittingham H.A., et al. The use of noninvasive ventilation in emergency department patients with acute cardiogenic pulmonary edema: a systematic review. Ann Emerg Med. 2006;48:260-269.

Ferrari G., Olliveri F., De Filippi G., et al. Noninvasive positive airway pressure and risk of myocardial infarction in acute cardiogenic pulmonary edema. Chest. 2007;132:1804-1809.

Peter J.V., Moran J.L., Phillips-Hughes J., et al. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet. 2006;367:1155-1163.

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