Comparison of haemodynamic effects during venous air infusion and after decompression in pigs

Abstract

We have compared haemodynamic effects of venous gas emboli during continuous air infusion into the right atrium and after rapid decompression in pigs. Eight anaesthetized and spontaneously breathing pigs received continuous air infusion at a rate of either 0.05 ml.kg-1.min-1 (six pigs, air infusion group) or 0.10 ml.kg-1.min-1 (two pigs). Another eight pigs (decompression group) underwent a 30-min compression to 5 bar (500 kPa, absolute pressure), followed by a rapid decompression (2 bar.min-1). Haemodynamic variables were measured or calculated, and bubbles in the pulmonary artery were monitored using transoesophageal echocardiography. The results showed less variation in the maximal increase in mean pulmonary arterial pressure (BPa,pulm) during air infusion (0.05 ml.kg-1.min-1) than after decompression, although the mean maximal increase did not differ between the two groups [28.0 mmHg (3.73 kPa), 95% confidence interval (CI) 23.5-32.5, vs 32.0 mmHg (4.27 kPa), 95% CI 25.3-38.7, P = 0.3]. The BPa,pulm stabilized or decreased very slowly after peak values were reached in the air infusion group, whereas the BPa,pulm decreased rapidly during the same period in the decompression group. No significant changes in mean arterial pressure were observed during air infusion (0.05 ml.kg-1.min-1), in contrast to the rapid increase and the subsequent decrease, that appeared after decompression. Finally, the maximal bubble count was much lower in the air infusion group than in most of the pigs in the decompression group. The two pigs that received 0.10 ml.kg-1.min-1 stopped breathing after 5-min infusion, developed arterial hypotension and died.

Increased expired NO and roles of CO2 and endogenous NO after venous gas embolism in rabbits

“…To our knowledge, this is the Wrst study showing a clear FeNO increase following embolization with gas in amounts comparable with that seen in models of decompression sickness (Vik et al 1994). Two prior studies have measured NO in association with gas infusions.…”

“…See also less than that liberated in decompression sickness. For example, Vik et al (1994) found that a continuous infusion of 50 l kg ¡1 min ¡1 elicited a similar response in pulmonary artery pressure (PAP) as animals underwent a 30-min compression to 5 bar followed by a rapid decompression (2 bar min ¡1 ), although the bubble count was much lower in the decompression group.…”

Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles

“…As the VGE get trapped however in the pulmonary microcirculation, they provoke a gradual increase in pulmonary artery pressure (PAP). PAP may rise by 15-20% after 20-30 min; this depends on the severity of the pulmonary embolization [36]. As a consequence of this rise in PAP, after a short time also the right atrial pressure will increase, allowing a more frequent or more abundant shunting into the left atrium [37].…”

Cardiopulmonary responses to intravenous infusion of soluble and relatively insoluble gases

“…Paradoxical arterial embolism may occur, due to intracardiac shunts or transpulmonary passage of the bubbles [15,20]. Subsequent compromise of the coronary blood flow is presumed to be the cause of death, either from intracardiac gas or from pulmonary vascular obstruction leading to reduced blood flow from the right to the left heart [5,21]. In addition to their mechanical effects, gas bubbles can also cause biophysical effects at the bloodbubble interface.…”

“…Gases were infused through a 0.062-inch internal diameter femoral venous catheter. Bubble size was not measured since any bubbles which remained undissolved upon reaching the heart would coalesce and then be fractured into bubbles of different sizes by the pumping of the ventricle [21]. Mean pulmonary arterial pressure (MPAP) was used as a clinical measure of the degree of pulmonary embolism.…”