Pulmonary edema, or oedema, is fluid accumulation in the air spaces and parenchyma of the lungs.
It leads to impaired gas exchange and may cause respiratory failure.
It is due to either failure of the left ventricle of the heart to adequately remove blood from
the pulmonary circulation, or an injury to the lung parenchyma or vasculature of the
lung.
Treatment is focused on three aspects: firstly improving respiratory function, secondly,
treating the underlying cause, and thirdly avoiding further damage to the lung.
Pulmonary edema, especially in the acute setting, can lead to respiratory distress, cardiac
arrest due to hypoxia, and death.
Symptoms and signs The overwhelming symptom of pulmonary edema
is difficulty breathing, but may also include coughing up blood, excessive sweating, anxiety,
and pale skin.
Shortness of breath can manifest as orthopnea and/or paroxysmal nocturnal dyspnea.
These are common presenting symptoms of chronic pulmonary edema due to left ventricular development
of pulmonary edema may be associated with symptoms and signs of "fluid overload", this
is a non specific term to describe the manifestations of left ventricular failure on the rest of
the body and includes peripheral edema, raised jugular venous pressure and hepatomegaly,
where the liver is enlarged and may be tender or even pulsatile.
Other signs include end-inspiratory crackles on auscultation and the presence of a third
heart sound.
Causes
Pulmonary edema is an accumulation of fluid within the parenchyma and air spaces of the
lungs.
Classically it is cardiogenic but fluid may also accumulate due to damage to the lung.
This damage may be direct injury or injury mediated by high pressures within the pulmonary
circulation.
When directly or indirectly caused by increased left ventricular pressure pulmonary edema
may form when mean pulmonary pressure rises from the normal of 15 mmHg to above 25 mmHg.
Broadly, the causes of pulmonary edema can be divided into cardiogenic and non-cardiogenic.
By convention cardiogenic refers to left ventricular causes.
Cardiogenic Left ventricular failure may be due to a heart
attack leading to arrhythmias and fluid overload, e.g., from kidney failure or intravenous therapy
which may cause dilatation and failure of the left ventricle or may cause pulmonary
edema in the absence of heart failure.
Non-cardiogenic Hypertensive crisis.
The cause of pulmonary edema in the presence of a hypertensive crisis is probably due to
a combination of increased pressures in the right ventricle and pulmonary circulation
and also increased systemic vascular resistance and left ventricle contractility increasing
the hydrostatic pressure within the pulmonary capillaries leading to extravasation of fluid
and edema.
Upper airway obstruction Neurogenic causes.
Other/unknown Injury to the lung may also cause pulmonary
oedema through injury to the vasculature and parenchyma of the lung.
The acute lung injury-acute respiratory distress syndrome covers many of these causes, but
they may include: Inhalation of hot or toxic gases
Pulmonary contusion, i.e., high-energy trauma Aspiration, e.g., gastric fluid
Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post decortication,
removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema.
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
Immersion pulmonary edema Multiple blood transfusions
Severe infection or inflammation which may be local or systemic.
This is the classical form of ALI-ARDS.
There are also a range of causes of pulmonary edema which are less well characterised and
arguably represent specific instances of the broader classifications above.
Arteriovenous malformation Hantavirus pulmonary syndrome
High altitude pulmonary edema, probably a manifestation of neurogenic pulmonary edema
Envenomation, such as with the venom of Atrax robustus
Flash pulmonary edema Swimming induced pulmonary edema
Diagnosis
There is no one single test for confirming that breathlessness is caused by pulmonary
edema; indeed, in many cases, the cause of shortness of breath is probably multifactorial.
Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis
by suggesting a pulmonary shunt.
Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular
shadowing in a classical batwing peri-hilum pattern, upper lobe diversion, and possibly
pleural effusions.
In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic
edema Especially in the case of cardiogenic pulmonary
edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left
ventricular function, high central venous pressures and high pulmonary artery pressures.
Blood tests are performed for electrolytes and markers of renal function.
Liver enzymes, inflammatory markers and a complete blood count as well as coagulation
studies are also typically requested.
B-type natriuretic peptide is available in many hospitals, sometimes even as a point-of-care
test.
Low levels of BNP suggest a cardiac cause is unlikely.
Prevention In those with underlying heart disease, effective
control of congestive symptoms prevents pulmonary edema.
Dexamethasone is in widespread use for the prevention of high altitude pulmonary edema.
Sildenafil is used as a preventive treatment for altitude-induced pulmonary edema and pulmonary
hypertension, the mechanism of action is via phosphodiesterase inhibition which raises
cGMP, resulting in pulmonary arterial vasodilation and inhibition of smooth muscle cell proliferation.
While this effect has only recently been discovered, sildenafil is already becoming an accepted
treatment for this condition, in particular in situations where the standard treatment
of rapid descent has been delayed for some reason.
Management The initial management of pulmonary edema,
irrespective of the type or cause, is supporting vital functions.
Therefore, if the level of consciousness is decreased it may be required to proceed to
tracheal intubation and mechanical ventilation to prevent airway compromise.
Hypoxia may require supplementary oxygen, but if this is insufficient then again mechanical
ventilation may be required to prevent complications.
Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection,
for instance, would require the administration of appropriate antibiotics.
Cardiogenic pulmonary edema Acute cardiogenic pulmonary edema often responds
rapidly to medical treatment.
Positioning upright may relieve symptoms.
Loop diuretics such as furosemide or bumetanide are administered, often together with morphine
or diamorphine to reduce respiratory distress.
Both diuretics and morphine may have vasodilator effects, but specific vasodilators may be
used provided the blood pressure is adequate.
Continuous positive airway pressure and bilevel positive airway pressure has been demonstrated
to reduce the need of mechanical ventilation in people with severe cardiogenic pulmonary
edema, and may reduce mortality.
It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock,
in which the cardiac output is insufficient to sustain an adequate blood pressure.
This can be treated with inotropic agents or by intra-aortic balloon pump, but this
is regarded as temporary treatment while the underlying cause is addressed.
References
External links HeartFailureMatters.org Animation showing
How Heart Failure causes Fluid Accumulation - Created by the European Heart Failure Association