Intrapulmonary shunting and pulmonary gas exchange during normoxic and hypoxic exercise in healthy humans

Abstract

Exercise-induced intrapulmonary arteriovenous shunting, as detected by saline contrast echocardiography, has been demonstrated in healthy humans. We have previously suggested that increases in both pulmonary pressures and blood flow associated with exercise are responsible for opening these intrapulmonary arteriovenous pathways. In the present study, we hypothesized that, although cardiac output and pulmonary pressures would be higher in hypoxia, the potent pulmonary vasoconstrictor effect of hypoxia would actually attenuate exercise-induced intrapulmonary shunting. Using saline contrast echocardiography, we examined nine healthy men during incremental (65 W + 30 W/2 min) cycle exercise to exhaustion in normoxia and hypoxia (fraction of inspired O(2) = 0.12). Contrast injections were made into a peripheral vein at rest and during exercise and recovery (3-5 min postexercise) with pulmonary gas exchange measured simultaneously. At rest, no subject demonstrated intrapulmonary shunting in normoxia [arterial Po(2) (Pa(O(2))) = 98 +/- 10 Torr], whereas in hypoxia (Pa(O(2)) = 47 +/- 5 Torr), intrapulmonary shunting developed in 3/9 subjects. During exercise, approximately 90% (8/9) of the subjects shunted during normoxia, whereas all subjects shunted during hypoxia. Four of the nine subjects shunted at a lower workload in hypoxia. Furthermore, all subjects continued to shunt at 3 min, and five subjects shunted at 5 min postexercise in hypoxia. Hypoxia has acute effects by inducing intrapulmonary arteriovenous shunt pathways at rest and during exercise and has long-term effects by maintaining patency of these vessels during recovery. Whether oxygen tension specifically regulates these novel pathways or opens them indirectly via effects on the conventional pulmonary vasculature remains unclear.

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

“…Hypoxia directly stimulates the endothelial and smooth muscle cells in pulmonary blood vessels, causing vasoconstriction throughout the lungs and an increase in pulmonary blood pressure that can persist for prolonged durations at high altitude (Reeves and Grover, 1975;Gurney, 2002). This global vasoconstriction impairs O 2 diffusion because it can divert blood flow away from the gas exchange surface to pulmonary shunt vessels (Lovering et al, 2008), and the resultant pulmonary hypertension can cause fluid leakage into the air spaces, which in turn causes a thickening of the O 2 diffusion barrier (Maggiorini et al, 2001;Eldridge et al, 2006). Hypoxic pulmonary hypertension can also overburden the right ventricle of the heart and can contribute to pathophysiological conditions, such as chronic mountain sickness (Monge and León-Velarde, 1991;León-Velarde et al, 2010).…”

A case of intrapulmonary transmission of air while transitioning a patient from a sitting to a supine position after venous air embolism during a craniotomy

“…With deteriorating gas exchange, as reflected by an increased difference between EtCO 2 and PaCO 2 and impaired oxygenation, pulmonary vasoconstriction may have been present in some pulmonary regions in this patient. This concept is supported by evidence from a study by Lovering et al 9 which showed that, during exercise, 90% (8/9) of subjects recruited intrapulmonary shunt pathways during normoxia, whereas all subjects shunted during hypoxia. If patency of intrapulmonary anastomoses can possibly be modified through adjustment of the F I O 2 , then this should be taken into account.…”

“…[4][5][6][7] While these physiological transpulmonary arteriovenous pathways are subclinical in most instances, they have potential to open in up to 90% of individuals during hyperdynamic situations such as exercise. [8][9][10] A recent review of pulmonary pathways and mechanisms pertaining to their autoregulation highlights the interest and importance of this subject. 11 Neuroanesthesiologists are well aware of the multiple pathways for paradoxical air embolism (PAE) to occur.…”

VESTPD as a measure of ventilatory acclimatization to hypobaric hypoxia

“…The HCO 3 − was obtained from an equation derived with data from two studies. In one study, VO 2 max was measured at sea level and on the first day at altitude (406 mmHg) in 10 subjects (19). Another study included an incremental exercise study in 10 subjects breathing 12% O 2 , where VO 2 , arterial lactate (LA), and HCO 3 − were serially obtained (10).…”