Pathophysiology

The most common scenario for venous gas embolism is insidious, where there is continuous entry of small gas bubbles into the venous system. With rapid entry or larger volumes of gas, increasing strain on the right ventricle follows because of the migration of the emboli to the pulmonary circulation. Pulmonary arterial pressure increases, while increased resistance to right ventricle outflow causes diminished pulmonary venous return. This is reflected in decreased left ventricular preload, resulting in diminished cardiac output and, ultimately, systemic cardiovascular collapse.⁶ Quite often, tachyarrhythmias develop, but bradycardias are possible as well. When large quantities of gas/air (over 50 mL) are injected abruptly, acute cor pulmonale and/or asystole can occur.³ These alterations of lung vessel resistance and ventilation/perfusion mismatch in the lung cause intrapulmonary right-to-left shunt with increased alveolar dead space, leading to arterial hypoxia and hypercapnia.

Diagnosis

The so-called mill-wheel cardiac murmur, a continuous churning murmur, is relatively typical of venous gas embolism and can be auscultated by a precordial or esophageal stethoscope. A capnometric decrease of end-tidal carbon dioxide suggests ventilation/perfusion mismatching resulting from obstruction of the pulmonary arteries.⁷ Precordial Doppler ultrasonography is a sensitive and practical monitor to detect intracardiac air,^1,8 but an even more sensitive and specific monitor in procedures with a high risk for gas embolism is transesophageal echocardiography (TEE). TEE is the current gold standard for detecting intracardiac gas; however, this technique requires significant training in application and interpretation to be effective.^1,9

Treatment

When a diagnosis of venous gas embolism is considered (Table 63-2), further entry of gas into the venous circulation must be avoided. Catecholamine therapy and cardiopulmonary resuscitation should be initiated for cardiovascular collapse. Adequate oxygenation is often only possible with a significant increase in the oxygen concentration of the inspired gas (i.e., 100% oxygen); 100% oxygen also reduces the size of the gas embolism by increasing the gradient for nitrogen egress from the bubble.¹⁰ Rapid-volume resuscitation is recommended to elevate venous pressure, thus decreasing the continued entry of gas into the venous circulation. Some authors recommend attempting to evacuate air from the right ventricle by a central venous catheter (multi-orifice catheters may be more effective than a single lumen) or a pulmonary arterial catheter.¹¹ A left-lateral decubitus position had been recommended in the past but has largely been abandoned because recent hemodynamic studies showed no benefit. Hyperbaric oxygen therapy is not a first-line treatment but may be a useful adjunct in severe cases and should certainly be considered if there are neurologic findings. If central nervous system symptoms are present, a paradoxical embolism should be presumed.

TABLE 63-2 Treatment of Gas Embolism

Treatment

Therapy of paradoxical embolism is identical to that of a primary arterial gas embolism (see Table 63-2). It should be stressed that every venous gas embolism has the potential to evolve into an arterial gas embolism.

Pathophysiology

Entry of gas into the aorta causes distribution of gas bubbles into nearly all organs. Small emboli in the vessels of the skeletal muscles or viscera are well tolerated, although organ dysfunction such as rhabdomyolysis and/or renal insufficiency may occur.¹⁵ Embolization to the cerebral or coronary circulation may result in severe morbidity or death. Embolization into the coronary arteries can induce electrocardiographic changes typical of ischemia and infarction, with arrhythmias, myocardial depression, cardiac failure, and cardiac arrest. Circulatory responses may also be seen with embolization to the cerebral vessels.¹⁶ Cerebral arterial gas embolization typically involves migration of gas to small arteries of the brain. The emboli generate pathology by two broad mechanisms: reduced perfusion distal to the obstruction and an inflammatory response to the bubble.¹

Clinical Features

The signs and symptoms associated with cerebral arterial gas embolism can develop suddenly. The clinical presentation is determined by the absolute quantity of gas and the areas of the brain affected. Thus, the clinical picture can vary from minor motor weakness, headache, or moderate confusion to complete disorientation, hemiparesis, convulsions, loss of consciousness, and coma. Additionally, asymmetry of pupils, hemianopsia, and impairment of respiratory and circulatory centers (bradypnea, Cheyne-Stokes breathing, cardiac arrhythmias, and circulatory failure) are all well-known complications. After surgical procedures with risks for the development of gas embolism, a delayed recovery from general anesthesia or a transitional stage of impaired consciousness can be a clue to a cerebral arterial gas embolism. The diagnosis in these cases is not easy because anesthesia complications, such as central anticholinergic syndrome or residual anesthetic effects, can mimic a mild cerebral arterial gas embolism.

Diagnosis

The most important criterion is the patient’s history, because the clinical suspicion of embolism is based on the initial neurologic symptoms and the direct temporal relation with an invasive procedure. The greatest risks for venous or arterial gas embolism are present in craniotomies performed in the sitting position, cesarean sections, hip replacements, and cardiac surgery using cardiopulmonary bypass. All of these procedures have in common an open vascular bed and a hydrostatic gradient favoring the intravascular entry of gas.