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Alain Boussuges

Publications and source records attributed to Alain Boussuges.

6 recordsLinked to original sources

Hyperoxia-induced arterial compliance decrease in healthy man.

INTRODUCTION: Oxygen therapy is commonly used in emergency department and intensive care units without careful evaluation of its effects, especially on the haemodynamics and artery characteristics. MATERIALS AND METHODS: A prospective laboratory study evaluated brachial circulatory effects of normobaric hyperoxia using ultrasonography-Doppler. The study was set in a hospital research laboratory. The subjects were thirteen healthy volunteers. Investigations were performed under normal air ventilation and after 20 min of hyperoxic mixture ventilation using a high concentration mask. Two dimensional images and brachial blood flow velocities were recorded using ultrasonography and pulsed Doppler to study changes in cross sectional area, blood flow, resistance index, and cross-sectional compliance coefficient. RESULTS: During hyperoxic exposure, mean PaO2 was 372 +/- 21 mmHg. A significant decrease of heart rate was observed. Arterial pressures (systolic and diastolic arterial pressures) were not modified. A decrease of cross sectional areas at end diastole and end systole was observed. Pulsed Doppler study showed a decrease of brachial artery blood flow and an increase of the resistance index. Furthermore, a decrease of the cross-sectional compliance coefficient was observed during hyperoxic exposure in all subjects. CONCLUSION: This study using two-dimensional ultrasonography and pulsed Doppler could demonstrate an increase in brachial arterial tone and a decrease in brachial blood flow under normobaric hyperoxia.

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Haemodynamic effects of hyperbaric hyperoxia in healthy volunteers: an echocardiographic and Doppler study.

In the present study, we observed the haemodynamic changes, using echocardiography and Doppler, in ten healthy volunteers during 6 h of compression in a hyperbaric chamber with a protocol designed to reproduce the conditions as near as possible to a real dive. Ambient pressure varied from 1.6 to 3 atm (1 atm=101.325 kPa) and partial pressure of inspired O2 from 1.2 to 2.8 atm. Subjects performed periods of exercise with breathing through a closed-circuit self-contained underwater breathing apparatus (SCUBA). Subjects did not eat or drink during the study. Examinations were performed after 15 min and 5 h. After 15 min, stroke volume (SV), left atrial (LA) diameter and left ventricular (LV) end-diastolic diameter (LVEDD) decreased. Heart rate (HR) and cardiac output (CO) did not vary, but indices of the LV systolic performance decreased by 10% and the LV meridional wall stress increased by 17%. After 5 h, although weight decreased, the serum protein concentration increased. Compared with values obtained after 15 min, SV and CO decreased, but LV systolic performance, LA diameter, LVEDD and LV meridional wall stress remained unchanged. Compared with the reference values obtained at sea level, total arterial compliance decreased, HR remained unchanged and CO decreased. In conclusion, hyperbaric hyperoxia results in significant haemodynamic changes. Initially, hyperoxia and the SCUBA system are responsible for reducing LV preload, increasing LV afterload and decreasing LV systolic performance, although CO did not change. Prolonged exposure resulted in a further decrease in LV preload, because of dehydration, and in a further increase in LV afterload, due to systemic vasoconstriction, with the consequence of decreasing CO.

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Evaluation of left ventricular filling pressure by transthoracic Doppler echocardiography in the intensive care unit.

OBJECTIVE: To determine whether Doppler transmitral and pulmonary venous flow pattern is related to left ventricular filling pressures in critically ill patients. DESIGN: Prospective clinical investigation. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Fifty-four mechanically ventilated patients (age, 63 +/- 16 yrs) were investigated via transthoracic echocardiography and Doppler. Main diagnoses were pneumonia (31%), acute exacerbation of chronic obstructive pulmonary disease (24%), congestive heart failure (11%), and poisoning (11%). INTERVENTIONS: Doppler examinations were performed simultaneously with measurements of pulmonary artery occlusion pressure via a right heart catheter. MEASUREMENTS AND MAIN RESULTS: Pulmonary artery occlusion pressure correlated with transmitral peak E-wave velocity (r =.46) and E/A ratio (r =.55). Pulmonary artery occlusion pressure inversely correlated with deceleration time of the transmitral E-wave (r = -.52), pulmonary venous peak S-wave velocity (r = -.37), and systolic fraction of the pulmonary forward flow (r = -.56). An E/A ratio >2 predicted a pulmonary artery occlusion pressure >18 mm Hg with a positive predictive value of 100%. A duration of pulmonary venous A-wave reversal flow exceeding the duration of the transmitral A-wave forward flow predicted a pulmonary artery occlusion pressure >15 mm Hg with a positive predictive value of 83%. A systolic fraction of the pulmonary venous forward flow <0.4 predicted a pulmonary artery occlusion pressure >12 mm Hg with a positive predictive value of 100%. CONCLUSION: Transmitral and pulmonary venous flow patterns measured by transthoracic Doppler echocardiography can be used to estimate the left ventricular filling pressure in critically ill patients.

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Operation Everest III (Comex'97): altitude-induced decompression sickness during a hypobaric chamber experiment: necessity for circulating venous gas emboli monitoring for the investigators.

INTRODUCTION: Acute exposure to altitude changes increases the risk of decompression sickness (DCS). Altitude-induced DCS incidence is from 15 to 20% and > 30% above 8,000 m. A particular risk occurs for scientific investigators during hypobaric chamber experiments. OBJECTIVE: In the present study, we assess whether the detection of nitrogen venous gas emboli (VGE) could help to screen the investigators at risk for altitude-induced DCS. MATERIAL AND METHODS: During a 32-day hypobaric chamber experiment, we collected clinical episodes of DCS symptoms in the investigators, and performed detection of VGE using two-dimensional (2D) echocardiography and pulsed Doppler ultrasonography guided by 2D images, graded from 0 to 5. RESULTS: Eight investigators made a total of 32 flights, including 8 flights above 8,000 m, with a 15.6% overall incidence of DCS symptoms and a 50% incidence above 8,000 m. VGE detections were systematically performed at or above 8,000 m (eight detections), and some detections were performed at 5,000 m, 6,000 m, and 7,000 m. VGE grades 3 and 4 were present in all but one subject with DCS symptoms and preceded the "bends" in all cases. VGE detection thus confirmed, in a more sensitive way compared to clinical examination, that our precautionary measures for DCS were not optimized. CONCLUSION: VGE monitoring for investigators during hypobaric chamber experiments increased the sensitivity for the detection of subjects at risk for DCS.

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Transient neurological disorders during a simulated ascent of Mount Everest.

BACKGROUND: Transient neurological disorders are often observed at high altitude but are poorly documented under field conditions. The mechanism usually invoked is a hypocapnic vasoconstriction due to severe hypoxic hyperventilation. During a simulated ascent of Mount Everest in a hypobaric chamber by eight volunteer alpinists (Operation Everest III, Comex '97), three subjects presented neurological symptoms. We report here on the clinical observations and testing to detect mechanisms in addition to hypocapnic vasoconstriction. METHODS: The experiment was designed to investigate factors limiting physiological performance at altitude and the pathophysiology of acute mountain sickness. A retrospective analysis was made comparing the three cases of transient neurological disorder at high altitude (TNDHA) with the five subjects who had no neurological symptoms. RESULTS: Analysis of clinical and blood parameters showed no difference between cases and controls. The cases showed no neurological sequelae following the experiment and were normal on cardiac imaging. However, one case had a history of migraine in his youth, leading us to hypothesize that segmental vasoconstriction was a factor. In another case, gas bubbles were detected in the pulmonary artery by transthoracic echocardiography when he was symptomatic, suggesting that gas emboli may have played a role. All three cases shared a possible triggering factor in that each experienced hyperventilation alternating with straining against a closed glottis shortly before the onset of symptoms. CONCLUSION: Mechanisms other than hypocapnic vasoconstriction in hypoxia may be causal factors of TNDHA. The existence of triggering factors and evidence of a possible embolic mechanism should be further explored.

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