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Chapter: Medicine and surgery: Cardiovascular system

Acute pulmonary oedema - Cardiac failure

Fluid accumulation within the interstitial lung tissue and alveoli. Pulmonary oedema may be a sign of chronic heart failure (also termed pulmonary venous conges-tion) or may occur acutely. - Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Acute pulmonary oedema

 

Definition

 

Fluid accumulation within the interstitial lung tissue and alveoli. Pulmonary oedema may be a sign of chronic heart failure (also termed pulmonary venous conges-tion) or may occur acutely.

 

Aetiology/pathophysiology

 

Acute pulmonary oedema is usually an acute deterioration in patients with cardiac failure who have chronic pulmonary oedema. There may be a provoking factor such as excessive fluid intake/administration, arrhythmias, negative inotropic drugs, angina, myocardial infarct or infection. There is an acute accumulation of fluid in the alveoli. Other causes include inhalation of toxic gases, drowning and renal failure.

 

Clinical features

 

Patients develop acute severe dysnoea at rest, hypoxaemia and distress. There may be wheeze and cough productive of frothy pink sputum. On examination there may be poor peripheral perfusion resulting in moist, cold cyanosed skin. On auscultation crepitations may be heard throughout the lung fields.

 

Investigations

 

Chest X-Ray: There may be signs of chronic pulmonary oedema such as upper lobe vein diversion, pleural effusions and Kerley B lines. In acute pulmonary oedema there may be ‘bat wing’ or ground glass pulmonary shadowing.

 

Blood gases: There is an initial fall in arterial pO2 and pCO2 due to hyperventilation. As the patient tires or in severe cases the pCO2 rises.

 

Other investigations include ECG and an echocardio-gram to look for the underlying cause.

 

Management

 

The patient is placed in the sitting position and should be given high flow oxygen. Careful fluid balance is essential and may include urinary catheterisation.

 

Additional ventilatory support may be required including continuous positive airway pressure.

 

Intravenous diuretic gives immediate venodilatation and later increased renal fluid excretion.

 

Intravenous diamorphine (with an antiemetic) reduces distress, venodilates and relieves dyspnoea.

 

Intravenous glyceryl trinitrate is used to venodilate and thus reduce the cardiac preload.

 

Aminophylline infusion can be considered if there is bronchoconstriction. It also increases vasodilatation and increases cardiac contractility.

 

If patient is hypertensive hydralazine or diazoxide (arterial dilators) can be used to reduce cardiac afterload and hence increase stroke volume.

 

Any underlying problem such as arrhythmia should be corrected.

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Medicine and surgery: Cardiovascular system : Acute pulmonary oedema - Cardiac failure |


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