Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution. II: Pathophysiology (original) (raw)
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Intensive Care Medicine, 1994
The regulation of the distribution of ventilation/perfusion ratios by hypoxic pulmonary vasoconstriction contributes to both the efficiency of gas exchange and to pulmonary hemodynamics. In this review, the first of a two part series, are summarized the physiologic principles on which the analysis of ventilation/perfusion ratios and of pressure-flow relationships are based. A new combined analysis is introduced that permits the important contributions of hypoxic pulmonary vasoconstriction to overall gas exchange to be demonstrated in the circumstances of clinical complexity.
Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution
Intensive Care Medicine, 1994
The regulation of the distribution of ventilation/perfusion ratios by hypoxic pulmonary vasoconstriction contributes to both the efficiency of gas exchange and to pulmonary hemodynamics. In this review, the first of a two part series, are summarized the physiologic principles on which the analysis of ventilation/perfusion ratios and of pressure-flow relationships are based. A new combined analysis is introduced that permits the important contributions of hypoxic pulmonary vasoconstriction to overall gas exchange to be demonstrated in the circumstances of clinical complexity.
Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man
Respiration Physiology, 1987
Blood gases, hemodynamics and ventilation were measured in 7 healthy volunteers at baseline while breathing room air (FIo2 0.21), during hypoxia (Fio2 0.125, 15 min) and after nifedipine 20 mg sublingually at FIo2 0.21 (45 min) and at Fro2 0.125 (15 min). Distributions of ventilation-perfusion ratios (VA/t)) were determined, using the multiple inert gas elimination technique, at baseline, during hypoxia, and again during hypoxia after nifedipine intake. Hypoxia was associated with an average increase in pulmonary vascular resistances by 1049/o,which was partially inhibited by nifedipine. The inert gas data showed a mild deterioration in the distribution of ~rA/(~ ratios during hypoxia. However, when blood flow and ventilation were constrained to the baseline normoxic values in the distributions recovered during hypoxia ('normalization procedure') a slight improvement in ~rA/(~ matching could be evidenced, which was blunted during hypoxia after nifedipine. This was interpreted as the functional effect of hypoxic pulmonary vasoconstriction (HPV). Using the 'normalized' distributions, we computed the relationship between the decrease in compartmental blood flow that occurred during hypoxia and the corresponding alveolar Po2, and calculated the gain due to HPV feedback using equations of the control theory. The contribution of HPV to the stability of compartmental VA/t~ was greatest for alveolar Po2 values around 60 mm Hg, but at best the feedback had only a moderate efficiency.
The dose-response relationship for hypoxic pulmonary vasoconstriction
Respiration physiology, 1994
In 12 pentobarbital anesthetized dogs the lungs were independently ventilated with a double piston ventilator. The right lung was ventilated throughout with 100% oxygen. Blood was drawn from the right atrium and pumped through a bubble oxygenator to a cannula in the ligated left main pulmonary artery. The pressures in the left main pulmonary artery and the left atrium were recorded during constant flow while the oxygen tension in the left lung alveolar gas and the perfusate were varied either to match each other (Protocol 1) or differ (Protocol 2) over the range from "zero" to "100%" oxygen. From the combined data a three dimensional response surface for hypoxic pulmonary vasoconstriction was derived. The maximum increase of pulmonary vascular resistance (r%PVRmax) was defined at a stimulus oxygen tension (PSO2) of 10 mmHg amounting to a 3.15 +/- (0.18)-fold increase of the vascular resistance on "100%" oxygen. The stimulus oxygen tension was shown to b...
Journal of clinical monitoring and computing, 2015
In patients with respiratory failure measurements of pulmonary gas exchange are of importance. The bedside automatic lung parameter estimator (ALPE) of pulmonary gas exchange is based on changes in inspired oxygen (FiO2) assuming that these changes do not affect pulmonary circulation. This assumption is investigated in this study. Forty-two out of 65 patients undergoing coronary artery bypass grafting (CABG) had measurements of mean pulmonary arterial pressure (MPAP), cardiac output and pulmonary capillary wedge pressure thus enabling the calculation of pulmonary vascular resistance (PVR) at each FiO2 level. The research version of ALPE was used and FiO2 was step-wise reduced a median of 0.20 and ultimately returned towards baseline values, allowing 6-8 min' steady state period at each of 4-6 levels before recording the oxygen saturation (SpO2). FiO2 reduction led to median decrease in SpO2 from 99 to 92 %, an increase in MPAP of 4 mmHg and an increase in PVR of 36 dyn s cm(-5)....
Effects of active vasoconstriction and total flow on perfusion distribution in the rabbit lung
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 1997
We analyzed the effects of hypoxic vasoconstriction and total flow on the distribution of pulmonary perfusion in 38 isolated left rabbit lungs perfused under zone 3 conditions. Lungs were suspended in an upright position, oriented to the apicobasal line. Distributions of regional perfusion rates (RPR) along the vertical and horizontal axes were determined using nonradioactive microspheres labeled with heavy metal elements, which were detectable with X-ray fluorescence spectrometry. Changing the O2 concentration of a respirator and an extracorporeal membrane oxygenator independently, respective influences of active vasoconstriction induced by alveolar hypoxia and pulmonary artery hypoxia (PA hypoxia) on the RPR distribution were examined at a flow rate of 0.4 ml ⋅ min−1 ⋅ g wet lung tissue−1. To analyze the effects of changes in total flow, we investigated the RPR distribution at a perfusion rate of 1.2 ml ⋅ min−1 ⋅ g wet lung tissue−1. The RPR distribution in the absence of hypoxia ...
The hypoxic pulmonary vasoconstriction: From physiology to clinical application in thoracic surgery
Saudi Journal of Anaesthesia, 2021
More than 70 years after its original report, the hypoxic pulmonary vasoconstriction (HPV) response continues to spark scientific interest on its mechanisms and clinical implications, particularly for anesthesiologists involved in thoracic surgery. Selective airway intubation and one-lung ventilation (OLV) facilitates the surgical intervention on a collapsed lung while the HPV redirects blood flow from the “upper” non-ventilated hypoxic lung to the “dependent” ventilated lung. Therefore, by limiting intrapulmonary shunting and optimizing ventilation-to-perfusion (V/Q) ratio, the fall in arterial oxygen pressure (PaO2) is attenuated during OLV. The HPV involves a biphasic response mobilizing calcium within pulmonary vascular smooth muscles, which is activated within seconds after exposure to low alveolar oxygen pressure and that gradually disappears upon re-oxygenation. Many factors including acid-base balance, the degree of lung expansion, circulatory volemia as well as lung disease...
Regulation of hypoxic pulmonary vasoconstriction: basic mechanisms
2010
µm) lack a complete muscular media. We tested the hypothesis that these thinwalled vessels do not participate in the hypoxic pressor response. Isolated canine lobes were pump perfused at precisely known microvascular pressures. A videomicroscope, coupled to a computerized image-enhancement system, permitted accurate diameter measurements of subpleural arterioles and venules, with each vessel serving as its own control. While vascular pressure was maintained constant throughout the protocol, hypoxia caused an average reduction of 25% of microvessel diameters. The constriction was reversed when nitric oxide was added to the hypoxic gas mixture. The nitric oxide reversal, combined with a lack of lobar blood flow redistribution as measured by fluorescent microspheres, shows that the constriction was active. This response suggests the unexpected potential for active intra-acinar ventilationperfusion matching.