Origin and path of gas emboli

GE is usually caused by the injection or penetration of gas through a vascular wall. An exception to this mechanism is decompression sickness, where gas bubbles may develop spontaneously within the circulation. The access route serves to distinguish GE into two types with very different specific manifestations:

• Arterial Gas Embolism where gas enters the vascular system beyond the pulmonary filter (i.e, at the point of the pulmonary veins, left heart or systemic arteries).

Even a small volume of gas can cause significant clinical manifestations, the degree of severity depending on the respective areas that may be obstructed (e.g., cerebral arteries or coronary arteries). Bubbles can also migrate upstream following the laws of buoyancy: In an experimental study in dogs involving 41 injections of air into the left ventricle, gas was later found in the mesenteric arteries in 17 animals; the cortical cerebral arteries of 16; the femoral arteries of 2; and the coronary arteries of one animal1. Although clinical manifestations can be immediately apparent, clinicians must be aware that bubble migration can stop temporarily and start up again with patient movements or coughing.

• Venous Gas Embolism where the gas enters the vascular system before the pulmonary filter.

When gas entry is sudden (bolus effect), the bubble is trapped in the ejection chamber of the right ventricle and the root of the pulmonary artery. Because of the gas compressibility, the bubble absorbs the mechanical energy produced by ventricular contraction and obstructs the pulmonary artery tract. This leads to a circulatory arrest2.

If gas enters more gradually, the gas entering the right ventricle is blended with the blood into a foamy mixture, which is propelled into the pulmonary bloodstream, obstructing it partially or completely. If the volume of gas is small, the obstruction is of no clinical consequence; the intra-vascular gas is eliminated by diffusion into the pulmonary alveoli3. However, if the volume is greater, the pulmonary arterial resistance is increased both because the pulmonary arterial tree is obstructed by the bubbles and because pulmonary artery vasoconstriction occurs due to the release of vasoconstrictive mediators (serotonin, histamine, thromboxane A2 and endotheline-1)4-6. This results in pulmonary arterial hypertension7-9, mismatch between ventilation and perfusion and subsequent hypoxemia10'11. The resulting clinical picture is an acute right ventricular failure 2.

Importantly, the increase of pulmonary arterial pressure may cause gas bubbles to pass through pulmonary capillaries into the venous pulmonary circulation and from there into the arterial circulation resulting in paradoxical embolism. Other mechanisms for this phenomenon include:

- bubbles passing through a patent foramen ovale (PFO) as a result of an elevation in right atrial pressure due to pulmonary hypertension12. Clinicians must remember that at least 20 to 25% of the population carries a patent foramen ovale13.

- the bubbles passing through arteriovenous shunts within the lungs that are not functional in normal conditions but are also recruited as a result of the increase of pulmonary arterial pressure14.

In a study on dogs, Butler et al. showed that quantities of air under 0.15 ml/kg/min do not cause an increase in Pulmonary Arterial Pressure (PAP) over 20 mmHg; quantities over 0.3 ml/kg/min increase PAP over 34 mmHg and leading to a passage of bubbles into arterial circulation15-17.

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