Pulmonary Oedema: Pathophysiology, Clinical features, Preventive Measures & amp;Medical management


Pulmonary oedema is the abnormal accumulation of fluid in the interstitial spaces of the lungs that diffuses into the alveoli. The collection of fluid in the numerous air sacs in the lungs makes difficulty in breathing. Usually, the cardiac problems cause pulmonary oedema. However, other noncardiac reasons may be associated with accumulation of fluid such as pneumonia, renal failure, trauma to the chest, exposure to specific toxins and medications. Acute pulmonary oedema develops suddenly and is a medical emergency seeking immediate care.

Pathophysiology of Pulmonary Oedema

It is an acute event that results from left ventricular failure. It can occur suddenly (acutely) along with MI (myocardial infarction) or it can occur as an exacerbation of chronic heart failure. The left ventricle cannot handle the overload volume, blood volume, and pressure build-up in the left atrium. The rapid increase in atrial pressure results in an acute increase in pulmonary venous pressure, which produces an elevation in hydrostatic pressure that forces fluid out of the pulmonary capillaries into the interstitial spaces and alveoli. The fluid within the alveoli mixes with air, producing the classic symptoms of pulmonary oedema which is blood-tinged sputum. The fluid within the alveoli creates a diffusion block that severely impairs gas exchange, resulting in hypoxemia which is often severe condition. The onset may be preceded by premonitory symptoms of pulmonary congestion, but the condition also may develop quickly with a ventricle that has a little reserve to meet increased oxygen needs.


Clinical features of Pulmonary Oedema

  • Due to the decreased cerebral oxygenation, the patient becomes restless and anxious. Along with the sudden breathlessness and sense of suffocation the patient’s hands become cold and moist. The signs of cyanosis are seen as the fingernail beds become bluish and skin turns ashen. The pulse is weak, feeble, and rapid with distended veins of the neck. Coughing may occur producing quantities of foamy sputum. As pulmonary oedema progresses the patient becomes confused and stupor. The oxygen saturation is significantly decreased. and is nearly suffocated by the blood-tinged, frothy fluid filling the alveoli, is literally drowning in secretions. It is emergency situation demands emergent action.

Diagnostic findings of Pulmonary Oedema

  • The diagnosis is made by evaluating the clinical manifestation resulting from pulmonary congestion.
  • A chest X-ray is obtained to confirm the extent of a pulmonary vessel and tissue engorgement.
  • signs of left-sided heart failure (crackles on auscultation of the lung).
  • ABG (arterial blood gas) analysis demonstrates worsening hypoxemia.
  • Laboratory test including biochemistry, haematology, renal function test.
  • EEG and Echo

Preventive measures of Pulmonary Oedema

  • If recognised early, pulmonary oedema is easier to prevent than to treat. A patient in the hospital is assessed by a nurse and health care provider for the degree of dyspnoea, auscultation for the lung fields and heart sounds, and assess the degree of peripheral oedema, and decreased activity tolerance may be indicators of developing pulmonary oedema.

Medical management of Pulmonary Oedema

Pulmonary oedema is managed through different therapeutic measures.

Oxygen therapy

  • Oxygen is administered in a concentration adequate to relieve hypoxemia and dyspnoea through a face mask or nasal cannula. If respiratory failure is severe and prolonged, continuous positive airway pressure may be given. Sometimes endotracheal intubation and mechanical ventilation support are also needed.

Intravenous fluid infusion

  • A vasodilator such as IV nitroglycerin or nitroprusside may enhance symptom relief in pulmonary oedema. A continuous infusion of nesiritide may also be prescribed for the patient with acutely decompensated heart failure.

Administration of morphine

  • Morphine is administered intravenously in small doses to reduce peripheral resistance and venous return so that blood can be redistributed from the pulmonary circulation to other parts of the body. This decreases pressure in the pulmonary capillaries and diffusion of fluid into the lung tissue. Besides that morphine also reduces anxiety.


  • Diuretics help to increase the flow of urine which promotes the excretion of sodium and water by the kidneys. For instance, furosemide is administered by IV push or as a continuous infusion to produce a rapid diuretic effect. It can also cause vasodilation and pooling of the blood in peripheral blood vessels,  which reduces the amount of blood returned to the heart.

Supportive measures

  • proper positioning of the patient can help reduce venous return to the heart. The patient is positioned in an upright position with legs dangling over the side of the bed as a preference. This has an immediate effect of decrease venous return, decreasing the right ventricular stroke volume and decrease lung congestion.
  • Providing psychological support to the patient by reassuring the patient, providing care, providing accurate information regarding medications, dietary requirements, and maintaining hygiene.
  • The patient receiving continuous Iv infusions of vasoactive medications requires ECG monitoring and regular monitoring of vital signs.
  • Close observation of the side effects from the administration of morphine. Signs of hypotension due to an infusion of diuretics.
  • The patient receiving morphine is observed for respiratory depression, hypotension and vomiting; a morphine antagonist such as naloxone hydrochloride is kept available and given to the patient who exhibits serious respiratory depression.

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.