Cardiovascular and blood gas responses to hyperbaric oxygenation

Whalen, Robert E.; Saltzman, Herbert A.; Holloway, David H.; McIntosh, Henry D.; Sieker, Herbert O.; Brown, Ivan W.

doi:10.1016/0002-9149(65)90350-4

Cited by 100 publications

(50 citation statements)

References 15 publications

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“…Forty years ago, investigators reported that this reduction in HR was associated with decreased cardiac output (Q ) (48), an observation supported by subsequent research (Table 1) (21,24,27,29,48). Generally accepted hemodynamic effects of HBO 2 now "include mild bradycardia, leading to a proportional decline in Q and a small increase in systemic vascular resistance" (28).…”

mentioning

confidence: 94%

Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen

Weaver¹,

Howe²,

Snow³

et al. 2009

Journal of Applied Physiology

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Weaver LK, Howe S, Snow GL, Deru K. Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen. J Appl Physiol 107: 336-345, 2009. First published April 30, 2009 doi:10.1152/japplphysiol.91012.2008.-Divers and hyperbaric chamber attendants breathe hyperbaric air routinely. Hyperbaric oxygen (HBO2) is used therapeutically frequently. Although much is understood about the hemodynamic physiology and gas exchange effects during hyperbaric air and HBO2 exposure, arterial and pulmonary arterial (PA) catheter data, including blood gas values during hyperbaric air and HBO2 exposure of normal humans, have not been reported. We exposed 10 healthy volunteers instrumented with arterial and PA catheters to air at 0.85, 3.0, 2.5, 2.0, 1.3 (decompression stop), 1.12 (decompression stop), and 0.85 atm abs (our altitude) and then at identical pressures breathing O2 followed by atmospheric pressure air while we measured arterial and PA pressures (PAP), cardiac output (Q ), and blood gas measurements from both arterial and PA catheters. Although hemodynamic changes occurred during exposure to both hyperbaric air and HBO2, we observed a greater magnitude of change under HBO2 conditions: heart rate changes ranged from Ϫ9 to Ϫ19% (air to O2), respiratory rate from Ϫ12 to Ϫ17%, Q from Ϫ7 to Ϫ18%, PAP from Ϫ18 to Ϫ19%, pulmonary vascular resistance from Ϫ38 to Ϫ48%, and right-to-left shunt fraction from Ϫ87 to Ϫ107%. Mixed venous CO2 fell 8% from baseline during HBO2 despite mixed venous O2 tensions of several hundred Torr. The stroke volume, O2 delivery, and O2 consumption did not change across exposures. The arterial and mixed venous partial pressures of O2 and contents were elevated, as predicted. O2 extraction increased 37% during HBO2. hyperbaric oxygen; pulmonary arterial catheter; cardiac output; oxygen extraction THOUSANDS OF PATIENTS have been treated with hyperbaric oxygen (HBO 2 ); however, the precise arterial and pulmonary arterial (PA) hemodynamic and gas exchange responses that occur during HBO 2 are not clearly known. Determining precise hemodynamic and gas exchange information requires the subject or patient to be instrumented with arterial and PA (SwanGanz) catheters, permitting measurement of intravascular pressures and blood gases, and PA catheter data collected in normal humans exposed to HBO 2 has been reported only once (24).It has long been established that heart rate (HR) falls during HBO 2 (3). Forty years ago, investigators reported that this reduction in HR was associated with decreased cardiac output (Q ) (48), an observation supported by subsequent research (Table 1) (21,24,27,29,48). Generally accepted hemodynamic effects of HBO 2 now "include mild bradycardia, leading to a proportional decline in Q and a small increase in systemic vascular resistance" (28).As (43), possibly due to high O 2 concentrations reducing myocardial relaxation factor (nitric oxide), thereby making the heart stiffer (23), or by an increase in afterload from i...

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confidence: 94%

Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen

Weaver¹,

Howe²,

Snow³

et al. 2009

Journal of Applied Physiology

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“…The effect of arterial hyperoxia, on the other hand, is less well understood (Daly and Bondurant 1962; Whalen et al 1965; Ishikawa et al 1974b). Oxygen inhalation has been applied to patients with acute myocardial infarction in hope that this might increase oxygen delivery to the ischemic myocardium (Weglicki et al 1969).…”

mentioning

confidence: 99%

Reduction of left ventricular epicardial segment length by 100% oxygen breathing in open-chest dogs.

Ishikawa

Kanamasa

Yamakado

et al. 1982

Tohoku J. Exp. Med.

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We conducted this study in order to learn whether or not oxygen inhalation reduces left ventricular size, one of the major determinants of myocardial oxygen demand. In 11 open-chest dogs, a Mercury-in-Silastic gauge was applied to measure left ventricular circumferential length while the dogs were being ventilated with either room air or 100% oxygen. Four characteristic notches were identified on the resulting length curve : L1, length at the beginning of ejection; L2, length at the end of ejection; L3, length in early diastole; and L4, length at end diastole, L1 was shortened from 24.9+10.5 to 24.4+9.9 mm (a decrease of 1.4+2.1%) by oxygen breathing, L2 was also shortened from 26.8+11.5 to 26.2+10.7 mm (a decrease of 1.5+2.9%), L3 from 17.5+4.4 to 17.4±4.3 mm (a decrease of 0.7+ 2.7%) and L4 from 17.7±4.8 to 17.5±4.7 mm (a decrease of 1.3±2.4%). These changes all disappeared when the inspiratory gas was changed from oxygen back to air. Heart rate and left ventricular end-diastolic pressure showed no significant changes but were accompanied by a slight reduction in aortic pressure and myocardial contractile force. This study demonstrated a small but consistent reduction in left ventricular circumferential length by oxygen breathing. This reduction in left ventricular size will reduce left ventricular tension and thus result in reduction of left ventricular myocardial oxygen demand when oxygen inhalation is applied to patients with ischemic heart disease.--oxygen inhalation therapy; myocardium; myocardial ischemia; left ventricle

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“…The lack of change in V̇E with depth is somewhat puzzling as most other studies have found differences [7,25,26]. Some studies have found increased ⩒ E as a function of depth, which has historically been attributed to the Haldane effect [27], whereby the high PO 2 at depth inhibits O 2 unloading from hemoglobin and impairs CO 2 transport. More recently, hyperoxic hyperventilation [28], which may occur when the high PO 2 blunts peripheral chemosensitivity but an accumulation of free radicals stimulates central chemoreceptors, has been suggested as an alternative explanation.…”

Section: ⩒ Ementioning

confidence: 98%

Rest and exercise work of breathing calculated from alveolar pressure-volume loops, submersed and at depth

Pendergast¹,

Wach²,

Held³

2017

Lung Breath J

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Exercise capacity is decreased in submersion and depth. A possible explanation for this is an increase in the work of breathing (WOB) due to increased effort to move the chest, increased breathing resistance, and increased gas density. WOB has been measured by the esophageal balloon technique, although this method does not measure alveolar pressure. One purpose of the present study was to test a modification of the P .1 interrupter technique that measures alveolar pressure (P A ) based on mouth pressure after a rapid interruption of flow by insertion of a wedge in the air supply as an alternative method of quantifying WOB and WOB per minute (POB) in the diving environment. A second purpose was to use this method to determine WOB submersed and at pressure. It was hypothesized that both submersion and depth would increase the WOB and POB. P A -volume loops were generated based on the P .1 method and WOB and POB calculated for both rest and exercise in 10 healthy male subjects during submersion and at depth. These results were compared to control conditions. Ventilation was increased in submersion, but was not significantly affected by depth. POB was found to be significantly increased in submersion, and further increased as a function of depth. The increased POB in these conditions were observed both at rest and during exercise, both during inspiration and expiration. The POB determined by the P .1 interrupter technique confirmed previous studies that used the esophageal balloon technique, with accurate determination of alveolar pressure and pressure-volume loops.

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Cardiovascular and blood gas responses to hyperbaric oxygenation

Cited by 100 publications

References 15 publications

Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen

Arterial and pulmonary arterial hemodynamics and oxygen delivery/extraction in normal humans exposed to hyperbaric air and oxygen

Reduction of left ventricular epicardial segment length by 100% oxygen breathing in open-chest dogs.

Rest and exercise work of breathing calculated from alveolar pressure-volume loops, submersed and at depth

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