Acute Pulmonary Oedema

TAN PEI YE’

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 Introduction
• The immediate area outside of the small blood
vessels in the lungs is occupied by very tiny air
sacs called the alveoli, where oxygen from the air
is picked up by the blood passing by and carbon
dioxide in the blood is passed into the alveoli to
be exhaled out.
• Alveoli normally have a thin wall that allows air
exchange, and fluids are usually kept out of the
alveoli unless these walls lose their integrity.

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• Oedema, in general means swelling. This
typically occurs when fluid from inside blood
vessels seeps outside the blood vessel into the
surrounding tissues, causing swelling.
• This can happen either because of too much
pressure in the blood vessels or not enough
proteins in the bloodstream to hold on to the
fluid in the plasma.
• Pulmonary oedema is the term used when
oedema happens in the lungs.

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 Definition
• Acute pulmonary oedema is a
pathophysiological state characterized by
fluid-filled alveolar spaces and lung
interstitium, with impaired alveolar gas
exchange and reduced lung compliance.

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• APO occurs when
– increased pulmonary capillary pressure
– reduced plasma oncotic pressure
– pulmonary capillary permeability changes
– damage to the alveolar
– idiopathic (unknown) mechanism

• lead to plasma leaving the capillaries and building

up in the pulmonary interstitium. When this
occurs at such a rate that lymphatic drainage
from the lung cannot keep up (lymphatic
obstruction), flooding of the alveoli results.
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 Symptoms
• Shortness of breath
• Tachypnea and tachycardia
• Easy fatigue
• Dizziness
• Profuse diaphoresis
• Cough
• Pink, frothy sputum

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 Staging of Pulmonary Oedema
Three stages of PE can be distinguished based on the degree
of fluid accumulation:
• Stage 1 : all excess fluid can still be cleared by lymphatic
drainage.
• Stage 2 : characterized by the presence of interstitial
edema.
• Stage 3 : characterized by alveolar edema due to altered
alveolar-capillary permeability
• Mild: Only engorgement of pulmonary vasculature is seen.
• Moderate: There is extravasation of fluid into the interstitial
space due to changes in oncotic pressure.
• Severe: Alveolar filling occurs.

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 Types of pulmonary oedema
• Cardiogenic
• Non-cardiogenic

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 Cardiogenic
• Cardiogenic pulmonary edema (CPE) is
defined as pulmonary edema due to increased
capillary hydrostatic pressure secondary to
elevated pulmonary venous pressure. CPE
reflects the accumulation of fluid with a low-
protein content in the lung interstitium and
alveoli as a result of cardiac dysfunction.

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• In cardiogenic APO, an acute reduction in cardiac
output associated with an increase in systemic
vascular resistance (SVR) leads to back-pressure
on the pulmonary vasculature, with resultant
increased pulmonary capillary pressure. In most
cases, the patient has a maldistribution of fluid
rather than being fluid overloaded. They may, in
fact, have a whole-body fluid deficit.

 This understanding has led to a change in the management of this

condition, from the use of large doses of diuretics to a focus on
vasodilators and non-invasive ventilation that reduce SVR and
improve cardiac output.
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 Pathophysiology of Cardiogenic APO

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Examples included
• Left ventricular failure:
– Acute coronary syndromes
– Arrhythmias
– Pericarditis, myocarditis or endocarditis
– Valve dysfunctions (eg. Aortic stenosis, mitral
regurgitation)
• Increase intravascular volume:
– Fluid overload
– Non-compliance with fluid restriction or diuretics
– Renal failure
• Pulmonary venous outflow obstruction:
– Mitral valve stenosis
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 Non-cardiogenic
• In non-cardiogenic APO, pathological
processes acting either directly or indirectly
on the pulmonary vascular permeability. As a
result, proteins leak from the capillaries,
increase the interstitial oncotic pressure, so
that it exceeds that of the blood and fluid is
subsequently drawn from the capillaries.
Injury to alveolar cells will also reduce their
ability to clear this oedema fluid from the
alveolar space.
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Examples included
• High output states:
– Septicemia
– Anemia
– Thyrotoxicosis
• Systemic increase in vascular permeability:
– Pancreatitis
– Eclampsia
– Disseminated intravascular coagulation
– Burns
• Toxins / environmental:
– Immersion / submersion
– Toxic inhalation
– High altitude pulmonary oedema and decompression illness
• Others:
– Head injury or intracranial hemorrhage
– Drugs (eg. NSAIDs, calcium channel blocker)
– Pulmonary embolus Acute Pulmonary Oedema
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 Clinical assessment - History
• Usually a history of sudden-onset severe
dyspnoea.
• Recent occurrence of chest pain, a past history
of ischaemic heart disease or congestive heart
failure or an other causative factor is sought.
• Details of current medication and compliance
are also important.

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 Clinical assessment - Examination
• Vital sign:
– High respiratory rate
– Low oxygen saturation, reflecting hypoxia
– Most are hypertensive or normotensive. (Hypotension indicates cardiogenic
shock and a very poor prognosis).
• Inspection:
– Pale or cyanosed, sweaty (sometimes profusely) and frightened.
– Strive to maintain an upright position at all costs and may be unable to sit still.
– May cough up pink or white frothy sputum, adding to their feeling of
drowning.
– Use of the accessory muscles of respiration, and breathing is often noisy.
– Raised jugular venous pressure (JVP)
• Percussion
– Dull
• Auscultation
– Third heart sound or gallop.
– Signs of chronic heart failure should also be sought, as well as murmurs that
may hint at the cause.
– Fine crepitations, which are often extensive.
– Other adventitial lung sounds,
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Pulmonary Oedema
 Clinical investigations
 Electrocardiogram
 Imaging
– Chest X-ray
– Ultrasound
 Blood test
– Haemoglobin
– Electrolytes and ABG
– Cardiac biomarkers
• Brain or B-type natriuretic peptide (BNP)
• N-terminal pro-brain natriuretic peptide (NT-proBNP) levels
 Oximetry
 Echocardiography
 Special Investigations: Cardiac catheterization/coronary
angiography when acute intervention for acute myocardial
ischaemia or infarction/valvular disease is anticipated. Swan Ganz
catheter placement
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ECG
• looking for acute ischaemia, especially
evidence of ST-elevation myocardial infarction
(STEMI)

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Chest X-ray

Cardiogenic Non-cardiogenic

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Chest X-ray

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Echocardiogram
• to identify structural abnormalities and assess LV
systolic and diastolic dysfunction

Natriuretic peptides or their precursors (especially

BNP and NT-proBNP)
• If available, this investigation is useful in the
evaluation of patients presenting with acute
dyspnoea in the urgent care setting in whom the
clinical diagnosis of HF is uncertain. A low-normal
concentration of this marker in an untreated
patient makes the diagnosis of HF unlikely. Thus it
is a useful “rule–out” test in doubtful cases.

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 Management
• In all patients with APO, management strategies should
provide supportive care to maximize cardiac output and
oxygenation, followed by treatment of the underlying
cause.

• Treatment of the patient with non-cardiogenic pulmonary

oedema consists of
– removing the patient from the causative environment
– supportive therapies aimed at maintaining oxygenation,
including noninvasive and invasive ventilation in severe cases
– treating the underlying cause.

 These patients have lung injury and therefore low volume;

low pressure lung protective ventilation regimens should
be followed.
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• Treatment of the patient with cardiogenic pulmonary oedema

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The initial management includes a combination of the
following first line therapy:
• Oxygen: 5 to 6 liters/minute, by mask with the aim of
achieving oxygen
– saturation of more than 95% in order to maximize tissue
oxygenation and to prevent end organ dysfunction or multi
organ failure.
– Elective ventilation using non invasive positive pressure
ventilation (Continuous Positive Airway Pressure [CPAP] or
Bi-level Positive Airway Pressure [BiPAP]) should be
considered early if necessary.
– Should the oxygen saturation be inadequate or the patient
develop respiratory muscle fatigue, then endotracheal
intubation and mechanical ventilation is necessary.

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• Frusemide: (i.v.) 40 – 100mg. The dose should be
– individualized depending on the severity of the clinical
condition.
– Administration of a loading dose followed by a continuous
infusion has been shown to be more effective than
repeated bolus injections alone. The dose should be
titrated according to clinical response and renal function.
• Morphine sulphate: (i.v.) 3 – 5 mg bolus (repeated if
necessary, up to a total maximum of 10mg. It reduces
pulmonary venous congestion and sympathetic drive. It
is most useful in patients who are dyspnoeic and
restless. Intravenous anti-emetics (metoclopramide
10mg or prochlorperazine 12.5mg) should be
administered concomitantly. Care must be exercised in
patients with chronic respiratory diseases.
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• Nitrates: If the BP is adequate (SBP > 100
mmHg), nitrates are indicated
– as first line therapy in AHF51. It should be
administered sublingually or intravenously. The i.v.
route is more effective and preferable. Patients should
be closely monitored for hypotension. This commonly
occurs with concomitant diuretic therapy.
– Studies have shown that the combination of i.v.
nitrate and low dose frusemide is more efficacious
than high dose diuretic treatment alone .
– Extreme caution should be exercised in patients with
aortic and mitral stenosis.
– Nitrates are contraindicated in severe valvular stenosis

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