Venous air embolism

The sequelae of venous air emboli are variable. Air transported to the right ventricle and lungs may be completely asymptomatic owing to its rapid removal, or it can rapidly lead to cardiovascular collapse. Symptoms include cough, dyspnea, wheezing, chest pain, and hemoptysis. Often there is a feeling of impending death, confusion, and collapse as cardiovascular dysfunction worsens.

Significant emboli can result in tachypnea, tachycardia, and hypotension. A right ventricular heave may also be present. The classical mill-wheel (systolic-diastolic) murmur is rare and depends upon the presence of a very large amount of air in the right ventricle. A harsh systolic murmur or absence of a murmur is a more frequent occurrence.

Neurological sequelae with a depressed Glasgow Coma Scale and neurological dysfunction are probably the result of hypoxia and hypotension, although the possibility of paradoxical embolism should always be considered. The development of chest crepitations and wheeze are delayed signs which are due to the accumulation of extravascular fluid in the lungs.

Abnormalities found on investigation depend upon the severity of the embolism but may be normal. The electrocardiogram is non-specific with sinus tachycardia and evidence of right heart strain.

Chest radiography may demonstrate non-cardiogenic pulmonary edema or, more commonly, evidence of barotrauma (pneumothorax, pneumopericardium, interstitial emphysema, pneumomediastinum, or subcutaneous emphysema).

Arterial blood gases reveal hypoxemia, metabolic acidosis due to dependence upon anaerobic respiration, and a low, normal, or high CO 2 level depending on the severity of the insult.

Monitoring by oximetry and capnography can detect early falls in both oxygen saturation and end-tidal CO 2 concentration, and are reliable indicators of evolving venous gas embolism.

Invasive hemodynamic measurements and computed indices are diagnostic adjuncts in air embolism. Pulmonary arterial pressure can be normal or raised depending on whether the embolus is trapped low down in the pulmonary outflow tract or high in the pulmonary trunk. Central venous pressure may be elevated with a normal or low wedge pressure. The right ventricular stroke work is initially elevated in an attempt to compensate for the profound increase in afterload. Invasive lines can serve diagnostic and therapeutic purposes, as conduits for air aspiration. Ultrasonography, particularly in the form of transesophageal echocardiography, is of value in the diagnosis of venous air embolism and has the added advantage of detecting any paradoxical emboli ( Cucchiara,, eta[., 1984). Transesophageal echocardiography should be considered in any patient with cardiovascular instability and a history suspicious of air embolism.

Venous air embolism has a broad spectrum of presentation. The differential diagnosis often includes the numerous causes of acute cardiorespiratory collapse and neurological dysfunction. Pulmonary angiography and CT scan of the brain are used to exclude alternatives such as pulmonary thromboembolism and cerebrovascular accidents.

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