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Commercial air travel and in-flight pulmonary hypertension.
BACKGROUND: It has recently been shown that commercial air travel triggers hypoxic pulmonary vasoconstriction and modestly increases pulmonary artery pressure in healthy passengers. There is large interindividual variation in hypoxic pulmonary vasoreactivity, and some passengers may be at risk of developing flight-induced pulmonary hypertension, with potentially dangerous consequences. This study sought to determine whether it is possible for a susceptible passenger to develop pulmonary hypertension in response to a routine commercial flight. CASE REPORT: Using in-flight echocardiography, a passenger was studied during a 6-h commercial flight from London to Dubai. The passenger was generally well and frequently traveled by air, but had been diagnosed with Chuvash polycythemia, a genetic condition that is associated with increased hypoxic pulmonary vasoreactivity. Hematocrit had been normalized with regular venesection. During the flight, arterial oxygen saturation fell to a minimum of 96% and systolic pulmonary artery pressure (sPAP) rapidly increased into the pulmonary hypertensive range. The in-flight increase in sPAP was 50%, reaching a peak of 45 mmHg. DISCUSSION: This study has established that an asymptomatic but susceptible passenger can rapidly develop in-flight pulmonary hypertension even during a medium-haul flight. Prospective passengers at risk from such responses, including those who have cardiopulmonary disease or increased hypoxic pulmonary vasoreactivity, could benefit from preflight evaluation with a hypoxia altitude simulation test combined with simultaneous echocardiography (HAST-echo). The use of in-flight supplementary oxygen should be considered for susceptible individuals, including all patients diagnosed with Chuvash polycythemia.
Effects of dopamine and domperidone on ventilatory sensitivity to hypoxia after 8 h of isocapnic hypoxia.
Acclimatization to altitude involves an increase in the acute hypoxic ventilatory response (AHVR). Because low-dose dopamine decreases AHVR and domperidone increases AHVR, the increase in AHVR at altitude may be generated by a decrease in peripheral dopaminergic activity. The AHVR of nine subjects was determined with and without a prior period of 8 h of isocapnic hypoxia under each of three pharmacological conditions: 1) control, with no drug administered; 2) dopamine (3 microg. min-1. kg-1); and 3) domperidone (Motilin, 40 mg). AHVR increased after hypoxia (P = 0. 001). Dopamine decreased (P = 0.01), and domperidone increased (P = 0.005) AHVR. The effect of both drugs on AHVR appeared larger after hypoxia, an observation supported by a significant interaction between prior hypoxia and drug in the analysis of variance (P = 0. 05). Although the increased effect of domperidone after hypoxia of 0. 40 l. min-1. %saturation-1 [95% confidence interval (CI) -0.11 to 0. 92 l. min-1. %-1] did not reach significance, the lower limit for this confidence interval suggests that little of the increase in AHVR after sustained hypoxia was brought about by a decrease in peripheral dopaminergic inhibition.
Effect of a single inflation of the lungs on oxygenation during total extracorporeal carbon dioxide removal in experimental respiratory distress syndrome.
Respiratory distress syndrome (RDS) was modelled in rabbits using pulmonary lavage to remove surfactant. The stability of the resulting pressure-volume hysteresis of the lungs in vivo was studied with the aid of whole-body plethysmography during apnoeic oxygenation made possible by total extracorporeal carbon dioxide removal. Systemic oxygen delivery was measured as a function of the constant airway pressure during apnoea. In 6 subjects a single brief inflation of the lungs to 3.5 kPa resulted in a doubling of both expired lung volume (volume above functional residual capacity) and arterial oxygen partial pressure at an airway pressure of 0.65 kPa. These rises were well maintained for 40 min following the inflation. In a further 6 subjects with RDS single inflations permitted optimum systemic oxygen transport to occur at the low airway pressure of 0.3 kPa, similar to the optimum airway pressure in 6 healthy control subjects. Where pressure-volume hysteresis is present in RDS it can be exploited during apnoeic oxygenation, and probably during high frequency ventilation, to improve oxygenation by the use of infrequent single inflations of the lungs.
A randomized comparison of total extracorporeal CO2 removal with conventional mechanical ventilation in experimental hyaline membrane disease.
Apnoeic oxygenation (AO) combined with extracorporeal CO2 removal (ECCO2R), using venovenous perfusion across a membrane area of 0.1 m2 has been shown to be feasible in six healthy anaesthetized rabbits. In a further twelve rabbits, ECCO2R has been randomly compared with conventional mechanical ventilation (CMV) following saline lavage to induce respiratory failure. Blood gases were maintained for up to 6 h within the same range (PaO2 = 8-20 kPa, PaCO2 = 4-6 kPa) in two groups of six by varying airway pressures and the oxygen fraction delivered either to the membrane lung (ECCO2R group) or to the ventilator (CMV group). The influence of single hourly sustained inflations (SI) on oxygenation was studied. ECCO2R subjects remained stable and survived. CMV subjects deteriorated and had 80% mortality. Hyaline membranes were absent from ECCO2R subjects and present in all CMV subjects. The response to SI suggests that a lung volume recruitment is maintained during AO for up to 1 h but is ineffective during CMV.
Inhibition of active sodium absorption leads to a net liquid secretion into in vivo rabbit lung at two levels of alveolar hypoxia.
Active sodium transport across alveolar epithelium is known to contribute to the resolution of pulmonary oedema. We have attempted to assess whether sodium transport is essential to prevent liquid accumulation in healthy pulmonary alveoli exposed to mild hypoxia, and whether its contribution to liquid absorption differs between mild and moderate levels of hypoxia. In twenty-four anaesthetized adult rabbits we used direct bronchial cannulation to measure liquid movement from the liquid-filled left lung over 3.5 h. Half of the rabbits were studied at a level of mixed venous (and alveolar) oxygen partial pressure, PVO2, of 6.5 kPa and half at 4.5 kPa. PVO2 was altered by changing the inspired oxygen fraction in the ventilated right lung. Alveolar hydrostatic pressure was 0.3 kPa. In each group of 12, six animals with inhibitors of sodium transport in the isosmotic instillate were compared with six controls. We have shown an alveolar liquid secretion (approximately 0.6 microl min(-1) (kg body weight)(-1)) in the presence of inhibitors of active transport and an absorption (approximately 4 microl min(-1) (kg body weight)(-1)) in controls. Changing PVO2 had no influence on these movements. We conclude that, in this model of pulmonary oedema, active sodium transport appears to be essential for prevention of alveolar liquid accumulation via secretion. Furthermore, the contribution of active sodium transport to liquid absorption remains constant at oxygen tensions between 4.5 and 6.5 kPa.