Influence of Changes in Mixed Venous Oxygen Tension(PvO2) by Extracorporeal Membrane Oxygenation(ECMO) on Hypoxic Pulmonary Vasoconstriction

1992 ◽  
Vol 25 (1) ◽  
pp. 1
Author(s):  
Duk Hwan Choi ◽  
Seong Deok Kim
Keyword(s):  
Extracorporeal Membrane Oxygenation ◽  
Oxygen Tension ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Membrane Oxygenation ◽  
Pulmonary Vasoconstriction ◽  
Mixed Venous

PAO2 and PVO2 interaction on hypoxic pulmonary vasoconstriction

1982 ◽  
Vol 53 (1) ◽  
pp. 134-139 ◽  
Author(s):  
R. D. Pease ◽  
J. L. Benumof ◽  
F. R. Trousdale
Keyword(s):  
Oxygen Tension ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Small Compartment ◽  
Pulmonary Vasoconstriction ◽  
Lung Compartment ◽  
Anesthetized Dogs ◽  
Fraction Of Inspired Oxygen ◽  
Alveolar Oxygen ◽  
Inspired Oxygen ◽  
Mixed Venous

We sought to determine why large lung compartment hypoxic pulmonary vasoconstriction fails to redistribute blood flow at a low fraction of inspired oxygen (FIO2) level (0.06) when the remaining small lung compartment is ventilated with room air. In 10 pentobarbital-anesthetized dogs, we decreased large compartment FIO2 from 1.0 to 0.06 while the small compartment FIO2 was constant at 0.21, 0.3, 0.5, or 1.0. When small compartment FIO2 was 0.21 and 0.3, large compartment FIO2 decreases from 1.0 to 0.15–0.10 caused a disproportionate increase in large compartment pulmonary vascular resistance (PVR) and further large compartment FIO2 decreases from 0.15–0.10 to 0.06 caused a decrease in large compartment PVR while small compartment PVR continued to increase. When small compartment FIO2 was 0.5, large compartment FIO2 decreases caused an increase and then no change in large compartment PVR, while small compartment PVR remained constant. When small compartment FIO2 was 1.0, all large compartment FIO2 decreases caused increases in large compartment PVR, while small compartment PVR remained constant. When small compartment FIO2 was 0.21 and 0.3, small compartment alveolar oxygen tension (PAO2) and PVR were always inversely related. When small compartment FIO2 was 0.21, 0.3, and 0.5, large compartment PVR either decreased or remained constant whenever mixed venous oxygen tension (PVO2) was less than 30–32 Torr and large compartment PAO2 was less than 50–60 Torr. We conclude that both small compartment hypoxic pulmonary vasoconstriction and primarily failure of large compartment hypoxic pulmonary vasoconstriction occurred when large compartment FIO2 was low (0.06) and small compartment FIO2 was 0.21 or 0.3.

Hypoxic Pulmonary Vasoconstriction in Nonventilated Lung Areas Contributes to Differences in Hemodynamic and Gas Exchange Responses to Inhalation of Nitric Oxide 

1997 ◽  
Vol 86 (6) ◽  
pp. 1254-1261 ◽  
Author(s):  
Albert Benzing ◽  
Georg Mols ◽  
Thomas Brieschal ◽  
Klaus Geiger
Keyword(s):  
Nitric Oxide ◽  
Gas Exchange ◽  
Oxygen Tension ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Arterial Oxygen ◽  
Mixed Venous Blood ◽  
Respiratory Response ◽  
Pulmonary Vasoconstriction ◽  
Wide Range ◽  
Mixed Venous

Background Enhancement of hypoxic pulmonary vasoconstriction (HPV) in nonventilated lung areas by almitrine increases the respiratory response to inhaled nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS). Therefore the authors hypothesized that inhibition of HPV in nonventilated lung areas decreases the respiratory effects of NO. Methods Eleven patients with severe ARDS treated by venovenous extracorporeal lung assist were studied. Patients' lungs were ventilated at a fraction of inspired oxygen (F[I(O2)]) of 1.0. By varying extracorporeal blood flow, mixed venous oxygen tension (P[O2]; partial oxygen pressure in mixed venous blood [PV(O2)]) was adjusted randomly to four levels (means, 47, 54, 64 and 84 mmHg). Extracorporeal gas flow was adjusted to prevent changes in mixed venous carbon dioxide tension [PV(CO2)]). Hemodynamic and gas exchange variables were measured at each level before, during, and after 15 ppm NO. Results Increasing PV(O2) from 47 to 84 mmHg resulted in a progressive decrease in lung perfusion pressure (PAP-PAWP; P < 0.05) and pulmnonary vascular resistance index (PVRI; P < 0.05) and in an increase in intrapulmonary shunt (Q[S]/Q[T]; P < 0.05). PV(CO2) and cardiac index did not change. Whereas the NO-induced reduction in PAP-PAWP was smaller at high PV(O2), NO-induced decrease in Q(S)/Q(T) was independent of baseline PV(O2). In response to NO, arterial P(O2) increased more and arterial oxygen saturation increased less at high compared with low PV(O2). Conclusion In patients with ARDS, HPV in nonventilated lung areas modifies the hemodynamic and respiratory response to NO. The stronger the HPV in nonventilated lung areas the more pronounced is the NO-induced decrease in PAP-PAWP. In contrast, the NO-induced decrease in Q(S)/Q(T) is independent of PV(O2) over a wide range of PV(O2) levels. The effect of NO on the arterial oxygen tension varies with the level of PV(O2) by virtue of its location on the oxygen dissociation curve.

Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange

1996 ◽  
Vol 81 (4) ◽  
pp. 1535-1543 ◽  
Author(s):  
Serge Brimioulle ◽  
Philippe Lejeune ◽  
Robert Naeije
Keyword(s):  
Gas Exchange ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Gas Exchange ◽  
Lung Model ◽  
Arterial Oxygenation ◽  
Blood Gas ◽  
Stimulus Response ◽  
Pulmonary Vasoconstriction ◽  
Lung Compartment ◽  
Mixed Venous

Brimioulle, Serge, Philippe Lejeune, and Robert Naeije.Effects of hypoxic pulmonary vasoconstriction on pulmonary gas exchange. J. Appl. Physiol. 81(4): 1535–1543, 1996.—Several reports have suggested that hypoxic pulmonary vasoconstriction (HPV) might result in deterioration of pulmonary gas exchange in severe hypoxia. We therefore investigated the effects of HPV on gas exchange in normal and diseased lungs. We incorporated a biphasic HPV stimulus-response curve observed in intact dogs (S. Brimioulle, P. Lejeune, J. L. Vachièry, M. Delcroix, R. Hallemans, and R. Naeije, J. Appl. Physiol. 77: 476–480, 1994) into a 50-compartment lung model (J. B. West, Respir. Physiol. 7: 88–110, 1969) to control the amount of blood flow directed to each lung compartment according to the local hypoxic stimulus. The resulting model accurately reproduced the blood gas modifications caused by HPV changes in dogs with acute lung injury. In single lung units, HPV had a moderate protective effect on alveolar oxygenation, which was maximal at near-normal alveolar[Formula: see text] (75–80 Torr), mixed venous[Formula: see text] (35 Torr), and[Formula: see text] at which hemoglobin is 50% saturated (24 Torr). In simulated diseased lungs associated with 40–60 Torr arterial [Formula: see text], however, HPV increased arterial [Formula: see text]by 15–20 Torr. We conclude that HPV can improve arterial oxygenation substantially in respiratory failure.

scholarly journals How Do We Monitor Oxygenation during the Management of PPHN? Alveolar, Arterial, Mixed Venous Oxygen Tension or Peripheral Saturation?

Children ◽  
2020 ◽  
Vol 7 (10) ◽  
pp. 180
Author(s):  
Praveen Chandrasekharan ◽  
Munmun Rawat ◽  
Satyan Lakshminrusimha
Keyword(s):  
Oxygen Tension ◽  
Oxygen Delivery ◽  
Randomized Clinical Trials ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Venous Catheter ◽  
Supplemental Oxygen ◽  
Target Range ◽  
Randomized Controlled Studies ◽  
Pulmonary Vasodilator ◽  
Mixed Venous

Oxygen is a pulmonary vasodilator and plays an important role in mediating circulatory transition from fetal to postnatal period. Oxygen tension (PO2) in the alveolus (PAO2) and pulmonary artery (PaO2) are the main factors that influence hypoxic pulmonary vasoconstriction (HPV). Inability to achieve adequate pulmonary vasodilation at birth leads to persistent pulmonary hypertension of the newborn (PPHN). Supplemental oxygen therapy is the mainstay of PPHN management. However, optimal monitoring and targeting of oxygenation to achieve low pulmonary vascular resistance (PVR) and optimizing oxygen delivery to vital organs remains unknown. Noninvasive pulse oximetry measures peripheral saturations (SpO2) and a target range of 91–95% are recommended during acute PPHN management. However, for a given SpO2, there is wide variability in arterial PaO2, especially with variations in hemoglobin type (HbF or HbA due to transfusions), pH and body temperature. This review evaluates the role of alveolar, preductal, postductal, mixed venous PO2, and SpO2 in the management of PPHN. Translational and clinical studies suggest maintaining a PaO2 of 50–80 mmHg decreases PVR and augments pulmonary vasodilator management. Nevertheless, there are no randomized clinical trials evaluating outcomes in PPHN targeting SpO2 or PO2. Also, most critically ill patients have umbilical arterial catheters and postductal PaO2 may not be an accurate assessment of oxygen delivery to vital organs or factors influencing HPV. The mixed venous oxygen tension from umbilical venous catheter blood gas may assess pulmonary arterial PO2 and potentially predict HPV. It is crucial to conduct randomized controlled studies with different PO2/SpO2 target ranges for the management of PPHN and compare outcomes.

The potential of accurate SVO2 monitoring during venovenous extracorporeal membrane oxygenation: an in vitro model using ultrasound dilution

Perfusion ◽  
2007 ◽  
Vol 22 (4) ◽  
pp. 239-244 ◽  
Author(s):  
Joshua Walker ◽  
Johanna Primmer ◽  
Bruce E. Searles ◽  
Edward M. Darling
Keyword(s):  
Extracorporeal Membrane Oxygenation ◽  
Oxygen Saturation ◽  
Ecmo Circuit ◽  
Ultrasound Dilution ◽  
Membrane Oxygenation ◽  
Mixed Venous Saturation ◽  
Venovenous Extracorporeal Membrane Oxygenation ◽  
Line Oxygen ◽  
Mixed Venous ◽  
Vv Ecmo

Introduction. Some degree of recirculation occurs during venovenous extracorporeal membrane oxygenation (VV ECMO) which, (1) reduces oxygen (O2) delivery, and (2) renders venous line oxygen saturation monitoring unreliable as an index of perfusion adequacy. Ultrasound dilution allows clinicians to rapidly monitor and quantify the percent of recirculation that is occurring during VV ECMO. The purpose of this paper is to test whether accurate patient mixed venous oxygen saturation (SVO2) can be calculated once recirculation is determined. It is hypothesized that it is possible to derive patient mixed venous saturations by integrating recirculation data with the ECMO circuit arterial and venous line oxygen saturation data. Methods. A test system containing sheep blood adjusted to three venous saturations (low-30%, med-60%, high-80%) was interfaced via a mixing chamber with a standard VV ECMO circuit. Recirculation, arterial line and venous line oxygen saturations were measured and entered into a derived equation to calculate the mixed venous saturation. The resulting value was compared to the actual mixed venous saturation. Results. Recirculation was held constant at 30.5 ± 2.0% for all tests. A linear regression comparison of “actual” versus “calculated” mixed venous saturations produced a correlation coefficient of R2 = 0.88. Direct comparison of actual versus calculated saturations for all three test groups respectively are as follows; Low: 31.8 ± 3.95% vs. 37.0 ± 6.7% (NS), Med: 61.7 ± 1.5% vs. 72.3 ± 1.8% (p < 0.05), High: 84.4 ± 0.9% vs. 91.2 ± 1.1% (p < 0.05). Discussion. There was a strong correlation between actual and calculated mixed venous saturations; however, significant differences between actual and calculated values where observed at the Med and High groups. While this data suggests that using quantified recirculation data to calculate SVO2 is promising, it appears that a straightforward derivative of the oxygen saturation-based equation may not be sufficient to produce clinically accurate calculations of actual mixed venous saturations. Perfusion (2007) 22, 239—244.

Hypoxic pulmonary vasoconstriction in dogs: effects of lung segment size and oxygen tension

1981 ◽  
Vol 51 (6) ◽  
pp. 1543-1551 ◽  
Author(s):  
B. E. Marshall ◽  
C. Marshall ◽  
J. Benumof ◽  
L. J. Saidman
Keyword(s):  
Oxygen Tension ◽  
Standard Error ◽  
Perfusion Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Left Lung ◽  
Lower Lobe ◽  
Left Lower Lobe ◽  
Physiological Basis ◽  
Test Segment ◽  
Pulmonary Vasoconstriction

Six pentobarbital-anesthetized dogs were prepared with endobronchial tubes and electromagnetic flow probes. The effects of changing inspired oxygen concentrations (FIO2 = 1, 0.21, 0.15, 0.1, 0.075, 0.05, and 0) were tested on test segments of different size corresponding to left lower lobe, left upper lobe-lingula, left lung, right lung, right lung plus left lower lobe, right lung plus left upper lobe-lingula, and whole lung. In each test the rest of the lung received oxygen. Hypoxic pulmonary vasoconstriction is demonstrated by both diversion of blood flow away from hypoxic test segments and by increased perfusion pressure. Flow diversion (FD%) decreases with the size of the hypoxic test segment (%QSN) from a maximum of 75% for very small segments to zero when the whole lung is hypoxic. FD% increases linearly as alveolar oxygen tension (PAO2) of the test segment is decreased in the range of 130--28 Torr. When mixed venous oxygen tension (PVO2) is less than 45 Torr FD% is reduced. These relationships are described by FD% = [74.99 - 0.0778 (%QSN) - 0.00661 (%QSN)2] [1.268 - 0.0096 (PAO2)] [0.47 + 0.012 (PVO2)], with r = 0.92 and standard error for prediction of 8.4%. Pulmonary perfusion pressure changes (PPH/PPN) increase with the size of the hypoxic test segments from 0 with very small segments to approximately 2.2 for the hypoxic whole lung. For all test segments PPH/PPN increases linearly with PAO2. These relationships are described by PPH/PPN = 1 + [0.0043 (%QSN) + 0.000072 (%QSN)2] [1.234 - 0.0096 (PAO2)], with r = 0.91 and standard error for prediction of 0.3 units. Responses to hypoxic pulmonary vasoconstriction in dogs are therefore shown to be predictable and continuous, and the physiological basis for action of each of the variables is discussed.

Prostaglandin I2 supports blood flow to hypoxic alveoli in anesthetized dogs

1984 ◽  
Vol 56 (5) ◽  
pp. 1246-1251 ◽  
Author(s):  
R. S. Sprague ◽  
A. H. Stephenson ◽  
A. J. Lonigro
Keyword(s):  
Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Prostaglandin I2 ◽  
Flow Measurements ◽  
Pulmonary Vasoconstriction ◽  
Cyclooxygenase Activity ◽  
Hypoxic Vasoconstriction ◽  
Anesthetized Dogs ◽  
Alveolar Hypoxia ◽  
Mixed Venous

In an animal model of unilateral alveolar hypoxia, inhibition of cyclooxygenase activity, estimates of immunoreactive 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and administration of prostaglandin I2 (PGI2) were used to evaluate the hypothesis that endogenous PGI2 opposes hypoxic pulmonary vasoconstriction, thereby producing redistribution of blood flow to hypoxic alveoli and reductions in systemic PO2. In anesthetized dogs, one lung was ventilated with 100% N2 and the other with 100% O2. Thermal dilution coupled with electromagnetic flow measurements permitted estimates of blood flow to each lung. Indomethacin or meclofenamate reduced flow to the N2-ventilated lungs (P less than 0.05) and increased systemic PO2 (P less than 0.05). Simultaneously, aortic concentrations of immunoreactive 6-keto-PGF1 alpha decreased 63 +/- 8% (P less than 0.001). Following cyclooxygenase inhibition, incremental doses of PGI2 (0.01, 0.025, and 0.10 micrograms X kg-1 X min-1) increased flow to the N2-ventilated lungs and reduced systemic PO2 (P less than 0.001) without affecting mixed venous PO2. These results suggest that systemic PO2 was reduced because of increased venous admixture. We conclude that PGI2 attenuates hypoxic vasoconstriction which allows flow to be maintained to hypoxic alveoli, resulting in reduced systemic PO2.

Regional Matching of Ventilation and Perfusion during Lobar Bronchial Occlusion in Man

1995 ◽  
Vol 88 (2) ◽  
pp. 179-184 ◽  
Author(s):  
N. W. Morrell ◽  
K. S. Nijran ◽  
T. Biggs ◽  
W. A. Seed
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Arterial Oxygen Saturation ◽  
Regional Distribution ◽  
Lower Lobe ◽  
Fibreoptic Bronchoscopy ◽  
Arterial Oxygen ◽  
Mixed Venous Blood ◽  
Pulmonary Vasoconstriction ◽  
Ventilation And Perfusion ◽  
Mixed Venous

1. Ventilation—perfusion balance in the presence of airway obstruction will depend on the efficiency of hypoxic pulmonary vasoconstriction beyond obstructed airways and the matching of redistributed blood flow and ventilation to the rest of the lung. This study investigated the relative importance of these mechanisms in man during experimental bronchial occlusion. 2. The bronchus to the left lower lobe was temporarily occluded with a balloon-tipped catheter during fibreoptic bronchoscopy in eight supine normal volunteers. Respiratory gas tensions were measured within the occluded lobe with a respiratory mass spectrometer. The distribution of ventilation and perfusion was assessed under control conditions and after 5 min of bronchial occlusion by computer analysis of the regional distribution of radioactivity during inhalation of 81mKr gas and following injection of 99mTc-labelled macroaggregated albumin respectively. 3. Respiratory gas partial pressures within the occluded lobes rapidly stabilized at mixed venous gas tensions: Po2 43.4 ± 2.2 (SEM) mmHg, Pco2 40.2 ± 1.8 mmHg. During occlusions the arterial oxygen saturation fell from a baseline of 96.3 ± 0.46% to a nadir of 92.1 ± 0.43%. Bronchial occlusion produced underventilation in the left lung relative to perfusion, both in the region of the occluded lower lobe and at the lung apex. Relative overventilation occurred in the right lung. 4. It is concluded that arterial hypoxaemia during lobal bronchial occlusion is caused primarily by shunting of mixed venous blood, though the shunt fraction is reduced by approximately 50% by hypoxic pulmonary vasoconstriction. In lung adjacent to obstructed regions reduced compliance may impair ventilation more than perfusion to contribute to hypoxaemia. It seems likely that redistribution of ventilation and perfusion to unobstructed regions during lobar bronchial occlusion is dependent on mechanical factors rather than O2- or CO2-dependent changes in bronchial or vascular tone.

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