scholarly journals Gas exchange and ventilation–perfusion relationships in the lung

2014 ◽  
Vol 44 (4) ◽  
pp. 1023-1041 ◽  
Author(s):  
Johan Petersson ◽  
Robb W. Glenny
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Gas Exchange ◽  
Minute Ventilation ◽  
Work Of Breathing ◽  
Arterial Oxygen Tension ◽  
Supplemental Oxygen ◽  
Arterial Oxygen ◽  
Respiratory Drive ◽  
Clinical Scenarios

This review provides an overview of the relationship between ventilation/perfusion ratios and gas exchange in the lung, emphasising basic concepts and relating them to clinical scenarios. For each gas exchanging unit, the alveolar and effluent blood partial pressures of oxygen and carbon dioxide (PO2andPCO2) are determined by the ratio of alveolar ventilation to blood flow (V′A/Q′) for each unit. Shunt and lowV′A/Q′ regions are two examples ofV′A/Q′ mismatch and are the most frequent causes of hypoxaemia. Diffusion limitation, hypoventilation and low inspiredPO2cause hypoxaemia, even in the absence ofV′A/Q′ mismatch. In contrast to other causes, hypoxaemia due to shunt responds poorly to supplemental oxygen. Gas exchanging units with little or no blood flow (highV′A/Q′ regions) result in alveolar dead space and increased wasted ventilation,i.e.less efficient carbon dioxide removal. Because of the respiratory drive to maintain a normal arterialPCO2, the most frequent result of wasted ventilation is increased minute ventilation and work of breathing, not hypercapnia. Calculations of alveolar–arterial oxygen tension difference, venous admixture and wasted ventilation provide quantitative estimates of the effect ofV′A/Q′ mismatch on gas exchange. The types ofV′A/Q′ mismatch causing impaired gas exchange vary characteristically with different lung diseases.

Ventilation with Constant Versus Decelerating Inspiratory Flow in Experimentally Induced Acute Respiratory Failure

1996 ◽  
Vol 84 (4) ◽  
pp. 882-889. ◽  
Author(s):  
Agneta M. Markstrom ◽  
Michael Lichtwarck-Aschoff ◽  
Bjorn A. Svensson ◽  
K. Anders Nordgren ◽  
Ulf H. Sjostrand
Keyword(s):  
Carbon Dioxide ◽  
Gas Exchange ◽  
Tidal Volume ◽  
Airway Pressure ◽  
Arterial Oxygen Tension ◽  
Inspiratory Flow ◽  
Arterial Oxygen ◽  
Positive End Expiratory Pressure ◽  
Residual Capacity ◽  
Inspiratory Flow Pattern

Background Recognition of the potential for ventilator-associated lung injury has renewed the debate on the importance of the inspiratory flow pattern. The aim of this study was to determine whether a ventilatory pattern with decelerating inspiratory flow, with the major part of the tidal volume delivered early, would increase functional residual capacity at unchanged (or even reduced) inspiratory airway pressures and improve gas exchange at different positive end-expiratory pressure levels. Methods Surfactant depletion was induced by repeated bronchoalveolar lavage in 13 anesthetized piglets. Decelerating and constant inspiratory flow ventilation was applied at positive end-expiratory pressure levels of 22, 17, 13, 9, and 4 cm H(2)O. Tidal volume, inspiration-to-expiration ratio, and ventilatory frequency were kept constant. Airway pressures, gas exchange, functional residual capacity (using a wash-in/washout method with sulfurhexafluoride), central hemodynamics, and extravascular lung water (using the thermo-dye-indicator dilution technique) were measured. Results Decelerating inspiratory flow yielded a lower arterial carbon dioxide tension compared to constant flow, that is, it improved alveolar ventilation. There were no differences between the flow patterns regarding end-inspiratory occlusion airway pressure, end-inspiratory lung volume, static compliance, or arterial oxygen tension. No differences were seen in hemodynamics and oxygen delivery. Conclusions The decelerating inspiratory flow pattern increased carbon dioxide elimination, without any reduction of inspiratory airway pressure or apparent improvement in arterial oxygen tension. It remains to be established whether these differences are sufficiently pronounced to justify therapeutic consideration.

Hypoxemia and pulmonary gas exchange during hemodialysis

1981 ◽  
Vol 50 (2) ◽  
pp. 259-264 ◽  
Author(s):  
R. W. Patterson ◽  
A. R. Nissenson ◽  
J. Miller ◽  
R. T. Smith ◽  
R. G. Narins ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Oxygen Tension ◽  
Minute Ventilation ◽  
Arterial Oxygen Tension ◽  
Pulmonary Gas Exchange ◽  
Arterial Oxygen ◽  
Exchange Relationships ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Alveolar Oxygen

With measured values of arterial blood gas tensions, of expired respiratory gas fractions, and volume of the expired ventilation, the determinants of alveolar oxygen tension (PAO2) were used to evaluate their influence on the development of the arterial hypoxemia that occurs in spontaneously breathing patients undergoing hemodialysis using an acetate dialysate. Dialysis produced no significant changes in the alveolar-arterial O2 tension gradient (AaDO2). The extracorporeal dialyzer removed an average of 30 ml.m-2.min-1 of CO2. Accordingly the pulmonary gas exchange ratio (R) dropped from a mean predialysis value of 0.81 to 0.62 (P less than 0.001). The arterial CO2 tension remained constant throughout, whereas the minute ventilation, both total (P less than 0.01) and alveolar (P less than 0.01), decreased during dialysis. This decrease in ventilation accounts for more than 80% of the fall in PAO2. During dialysis there was a decrease (P less than 0.001) in arterial oxygen tension (PaO2), which varied among the individuals from 9 to 23% of control. During the postdialysis hour PaO2 returns to control values concomitant with increase in ventilation. The quantitative gas exchange relationships among R, alveolar ventilation, and AaDO2 predict the PaO2 values actually measured.

Time Course and Pattern of Pulmonary Flow Distribution following Unilateral Airway Occlusion in Sheep

1998 ◽  
Vol 94 (4) ◽  
pp. 453-460 ◽  
Author(s):  
B. Johansen ◽  
M. N. Melsom ◽  
T. Flatebø ◽  
G. Nicolaysen
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Oxygen Tension ◽  
Time Course ◽  
Arterial Oxygen Tension ◽  
Flow Distribution ◽  
Blood Gases ◽  
Carbon Dioxide Tension ◽  
Arterial Oxygen ◽  
Contralateral Lung

1. Unilateral bronchial occlusion causes ipsilateral hypoxic pulmonary vasoconstriction, which shifts blood flow towards the other lung. We studied the time course of flow diversion following acute bronchial occlusion, and the temporal effect of the latter on blood gases and vertical distribution of blood flow within the two lungs. 2. Serial infusions of radioactive or fluorescent microspheres were given to each of seven adult standing sheep before, during occlusion of the left mainstem bronchus for up to 6 min, and after release of occlusion. Pulmonary and systemic arterial pressures were recorded continuously and arterial and mixed venous blood gases were determined intermittently. Post-mortem, the lungs were inflated, dried and cut into slices. Relative blood flow at the time of infusion was expressed as the weight-normalized intensity of each tracer in each slice or lung divided by the weight-normalized intensity in the two lungs. 3. Within 30 s, 1 min and 2 min after onset of occlusion, flow in the occluded lung had decreased to 68–84% (range), 51–78% and 43–79% respectively, of the initial value. In the contralateral lung, flow increased by 10–24%, 14–37% and 23–39% respectively. The distribution of flow along the gravitational axis within each lung varied widely between animals, both before and during occlusion. The during-occlusion profiles in the occluded lung differed from those in the non-occluded lung. In either lung, during-occlusion profiles could not be predicted with certainty from the pre-occlusion profiles. Two minutes post-occlusion, inter- and intra-lung flow distribution were nearly the same as before occlusion. Arterial oxygen tension fell in the first minute of occlusion, but never below 7.5 kPa, and increased slowly thereafter. Arterial carbon dioxide tension increased slightly throughout the occlusion period. No appreciable changes in systemic or pulmonary artery pressure were observed. Post-occlusion, arterial oxygen tension was still sub-normal, while carbon dioxide tension continued to increase. 4. We conclude that acute unilateral bronchial occlusion diverts blood flow within 30 s towards the contralateral lung. This rapidly occurring flow diversion prevents the development of severe arterial hypoxaemia. The variable and largely unpredictable distribution of blood flow in the hyperfused non-occluded lung might explain some of the gas-exchange abnormalities observed in physiologically hyperfused lungs and in patients with one hyperfused lung.

Mechanisms of improvement in pulmonary gas exchange during isovolemic hemodilution

1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fractal Dimension ◽  
Gas Exchange ◽  
Spatial Correlation ◽  
Pulmonary Blood Flow ◽  
Minute Ventilation ◽  
Flow Distribution ◽  
Pulmonary Gas Exchange ◽  
Normal Lung ◽  
Blood Flow Distribution

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.

PERIODIC BREATHING AND APNEA IN PRETERM INFANTS. II. HYPOXIA AS A PRIMARY EVENT

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 219-228
Author(s):  
Henrique Rigatto ◽  
June P. Brady
Keyword(s):  
Preterm Infants ◽  
Oxygen Tension ◽  
Minute Ventilation ◽  
Arterial Oxygen Tension ◽  
Blood Gases ◽  
Periodic Breathing ◽  
Capillary Blood ◽  
Arterial Oxygen ◽  
Primary Event ◽  
The Relationship

We studied nine healthy preterm infants during the first 35 days of life to define the relationship between periodic breathing, apnea, and hypoxia. For this purpose we compared ventilation/apnea (V/A), minute ventilation, and alveolar and capillary blood gases during periodic breathing induced by hypoxia and during spontancous periodic breathing in room air. We induced periodic breathing by giving the baby in sequence 21, 19, 17, and 15% O2 to breathe for 5 minutes each, and also by giving 21, 15, and 21% O2. We measured ventilation with a nosepiece and a screen flowmeter. With a decrease in arterial oxygen tension, preterm infants (1) hypoventilated, (2) breathed periodically more frequently, and (3) showed a decrease in V/A due to an increase in the apneic interval. In one baby this led to apnea lasting 30 seconds. These findings support our hypothesis that preterm infants breathing periodically hypoventilate and suggest that hypoxia may be a primary event leading to periodic breathing and apnea.

PULMONARY FUNCTION, DEDUCED FROM URINARY NITROGEN TENSIONS

PEDIATRICS ◽  
1967 ◽  
Vol 40 (6) ◽  
pp. 937-938
Author(s):  
M. E. A.
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Pulmonary Function ◽  
Partial Pressure ◽  
Urine Sample ◽  
Pulmonary Blood Flow ◽  
Lung Perfusion ◽  
Alveolar Ventilation ◽  
Arterial Oxygen ◽  
Urinary Nitrogen

THE elegant studies reported by Led-better, Homma, and Farhi in this issue are entitled `'Readjustment in Distribution of Alveolar Ventilation and Lung Perfusion in the Newborn." It must come as a great surprise to the reader to discover that the only measurement actually made was the partial pressure of nitrogen in the infants' urine. How could one conclude that there were significant imbalances between the distribution of alveolar ventilation and pulmonary blood flow (VA/Q) in the first days of life in normal infants from a urine sample? It is all the more astounding in the light of previous (and seemingly more direct) studies of alveolar-arterial oxygen and carbon dioxide differences which led others to consider the differences largely explained by anatomical right-to-left shunts.

Effect of continuous postive-pressure ventilation (CPPV) on edema formation in dog lung

1975 ◽  
Vol 39 (4) ◽  
pp. 672-679 ◽  
Author(s):  
P. Caldini ◽  
J. D. Leith ◽  
M. J. Brennan
Keyword(s):  
Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Arterial Oxygen Tension ◽  
Lung Parenchyma ◽  
Arterial Oxygen ◽  
Morphometric Measurements ◽  
Edema Formation ◽  
Significant Difference ◽  
Pulmonary Arterial

The effect of CPPV on edema formation in lungs perfused at constant blood flow was studied in whole dogs and in isolated dog lungs. In intact animals, subjected to an increase in left atrial pressure relative to pleural pressure of 40 Torr, pulmonary shunts correlate inversely (r = -0.82) with the level of end-expiratory pressure (PEE). CPPV had no significant effect on total extravasation of liquid even though PEE higher than 20 Torr was effective in preventing liquid from accumulating in the airways. In isolated lobes, perfused at constant blood flow and at a venous pressure of zero, accumulation of liquid occurred when PEE was increased above 8–10 Torr. At comparable levels of pulmonary arterial pressure, an increase in PEE resulted in lesser accumulation of liquid than when pulmonary venous pressure was elevated. Morphometric measurements revealed no significant difference in the distribution of accumulated liquid within the lung parenchyma between lobes made edematous either by raising venous pressuure or by raising PEE. It would appear that CPPV, while beneficial in improving arterial oxygen tension in pulmonary edema, does not prevent extravasation of liquid in lungs perfused at constant blood flow. High levels of PEE appear to damage the lung by favoring accumulation of liquid in the extravascular spaces of the lung.

Pulmonary Effects of Sustained Periods of High-G Acceleration Relevant to Suborbital Spaceflight

2021 ◽  
Vol 92 (8) ◽  
pp. 633-641
Author(s):  
Ross D. Pollock ◽  
Caroline J. Jolley ◽  
Nadia Abid ◽  
John H. Couper ◽  
Luis Estrada-Petrocelli ◽  
...  
Keyword(s):  
Work Of Breathing ◽  
Arterial Oxygen Saturation ◽  
Regional Distribution ◽  
Blood Gases ◽  
Respiratory Physiology ◽  
Arterial Oxygen ◽  
Relative Distribution ◽  
Respiratory Drive ◽  
Impedance Tomography ◽  
Arterial Blood

AbstractBACKGROUND: Members of the public will soon be taking commercial suborbital spaceflights with significant Gx (chest-to-back) acceleration potentially reaching up to 6 Gx. Pulmonary physiology is gravity-dependent and is likely to be affected, which may have clinical implications for medically susceptible individuals.METHODS: During 2-min centrifuge exposures ranging up to 6 Gx, 11 healthy subjects were studied using advanced respiratory techniques. These sustained exposures were intended to allow characterization of the underlying pulmonary response and did not replicate actual suborbital G profiles. Regional distribution of ventilation in the lungs was determined using electrical impedance tomography. Neural respiratory drive (from diaphragm electromyography) and work of breathing (from transdiaphragmatic pressures) were obtained via nasoesophageal catheters. Arterial blood gases were measured in a subset of subjects. Measurements were conducted while breathing air and breathing 15 oxygen to simulate anticipated cabin pressurization conditions.RESULTS: Acceleration caused hypoxemia that worsened with increasing magnitude and duration of Gx. Minimum arterial oxygen saturation at 6 Gx was 86 1 breathing air and 79 1 breathing 15 oxygen. With increasing Gx the alveolar-arterial (A-a) oxygen gradient widened progressively and the relative distribution of ventilation reversed from posterior to anterior lung regions with substantial gas-trapping anteriorly. Severe breathlessness accompanied large progressive increases in work of breathing and neural respiratory drive.DISCUSSION: Sustained high-G acceleration at magnitudes relevant to suborbital flight profoundly affects respiratory physiology. These effects may become clinically important in the most medically susceptible passengers, in whom the potential role of centrifuge-based preflight evaluation requires further investigation.Pollock RD, Jolley CJ, Abid N, Couper JH, Estrada-Petrocelli L, Hodkinson PD, Leonhardt S, Mago-Elliott S, Menden T, Rafferty G, Richmond G, Robbins PA, Ritchie GAD, Segal MJ, Stevenson AT, Tank HD, Smith TG. Pulmonary effects of sustained periods of high-G acceleration relevant to suborbital spaceflight. Aerosp Med Hum Perform. 2021; 92(7):633641.

scholarly journals Bidirectional Ductal Shunting and Preductal to Postductal Oxygenation Gradient in Persistent Pulmonary Hypertension of the Newborn

Children ◽  
2020 ◽  
Vol 7 (9) ◽  
pp. 137
Author(s):  
Amy Lesneski ◽  
Morgan Hardie ◽  
William Ferrier ◽  
Satyan Lakshminrusimha ◽  
Payam Vali
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Arterial Oxygen Tension ◽  
Persistent Pulmonary Hypertension ◽  
Arterial Oxygen ◽  
Meconium Aspiration ◽  
Arterial Blood Gas ◽  
Arterial Blood

Background: The aim was to evaluate the relationship between the direction of the patent ductus arteriosus (PDA) shunt and the pre- and postductal gradient for arterial blood gas (ABG) parameters in a lamb model of meconium aspiration syndrome (MAS) with persistent pulmonary hypertension of the newborn (PPHN). Methods: PPHN was induced by intermittent umbilical cord occlusion and the aspiration of meconium through the tracheal tube. After delivery, 13 lambs were ventilated and simultaneous 129 pairs of pre- and postductal ABG were drawn (right carotid and umbilical artery, respectively) while recording the PDA and the carotid and pulmonary blood flow. Results: Meconium aspiration resulted in hypoxemia. The bidirectional ductal shunt had a lower postductal partial arterial oxygen tension ([PaO2] with lower PaO2/FiO2 ratio—97 ± 36 vs. 130 ± 65 mmHg) and left pulmonary flow (81 ± 52 vs. 133 ± 82 mL/kg/min). However, 56% of the samples with a bidirectional shunt had a pre- and postductal saturation gradient of < 3%. Conclusions: The presence of a bidirectional ductal shunt is associated with hypoxemia and low pulmonary blood flow. The absence of a pre- and postductal saturation difference is frequently observed with bidirectional right-to-left shunting through the PDA, and does not exclude a diagnosis of PPHN in this model.

Effect of acute hypoxia on respiration and brain stem blood flow in the piglet

1991 ◽  
Vol 70 (1) ◽  
pp. 251-259 ◽  
Author(s):  
R. A. Darnall ◽  
G. Green ◽  
L. Pinto ◽  
N. Hart
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Extracellular Fluid ◽  
Respiratory Drive ◽  
Peripheral Chemoreceptor ◽  
Before And After ◽  
Spontaneously Breathing ◽  
Local Brain

Changes in local brain stem perfusion that alter extracellular fluid Pco2 and/or [H+] near central chemoreceptors may contribute to the decrease in respiration observed during hypoxia after peripheral chemoreceptor denervation and to the delayed decrease observed during hypoxia in the newborn. In this study, we measured the changes in respiration and brain stem blood flow (BBF) during 2–4 min of hypoxic hypoxia in both intact and denervated piglets and calculated the changes in brain stem Pco2 and [H+] that would be expected to occur as a result of the changes in BBF. All animals were anesthetized, spontaneously breathing, and between 2 and 7 days of age. Respiratory and other variables were measured before and during hypoxia in all animals, and BBF (microspheres) was measured in a subgroup of intact and denervated animals at 0, 30, and 260 s and at 0 and 80 s, respectively. During hypoxia, minute ventilation increased and then decreased (biphasic response) in the intact animals but decreased only in the denervated animals. BBF increased in a near linear fashion, and calculated brain stem extracellular fluid Pco2 and [H+] decreased over the first 80 s both before and after denervation. We speculate that a rapid increase in BBF during acute hypoxia decreases brain stem extracellular fluid Pco2 and [H+], which, in turn, negatively modulate the increase in respiratory drive produced by peripheral chemoreceptor input to the central respiratory generator.

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