Pulmonary exchange as related to altered pulmonary mechanics in anesthetized dogs

1964 ◽  
Vol 19 (4) ◽  
pp. 659-664 ◽  
Author(s):  
Clarence R. Collier ◽  
Jere Mead
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Lung Compliance ◽  
Surface Forces ◽  
Pulmonary Mechanics ◽  
Diffusing Capacity ◽  
Venous Admixture ◽  
Diffusion Capacity ◽  
Air Space ◽  
Anesthetized Dogs

Pulmonary mechanics and gas exchange were studied in supine anesthetized dogs, with and without periodic hyperinflations of the lungs, and after a single forced deflation. After a period without hyperinflations the lung compliance decreased to 66% of control values and patchy atelectasis was observed, but no changes were observed in diffusing capacity (Dl) or per cent venous admixture ( Qva/ Qt). Following a single forced deflation the compliance was 40% of control. Dl was 40% and Qva/ Qt 180% of control values, respectively. These data could be accounted for if there was an accompanying shift of blood flow from atelectatic to nonatelectatic areas, the compensation being very nearly complete for moderate, but less than complete for marked reductions in compliance. Alternative explanations of the apparent compensation are: 1) preferential initial atelectasis of regions with high ventilation-perfusion ratios (as proposed by Farhi) and 2) substantial reductions in compliance without closure of air space, as might result from changes in surface forces with time. aerotonometer; atelectasis; venous admixture; mechanics of breathing; compliance of dog lungs; diffusion capacity of dog lungs; ventilation perfusion; relationships of dog lungs Submitted on October 28, 1963

Ventilation-perfusion inequality during constant-flow ventilation

1987 ◽  
Vol 62 (3) ◽  
pp. 1255-1263 ◽  
Author(s):  
P. T. Schumacker ◽  
J. I. Sznajder ◽  
A. Nahum ◽  
L. D. Wood
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Lung Volume ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Asymmetric Distribution ◽  
Constant Flow ◽  
Arterial Pco2 ◽  
Continuous Stream ◽  
Anesthetized Dogs

Previous work by Lehnert et al. (J. Appl. Physiol. 53:483–489, 1982) has demonstrated that adequate alveolar ventilation can be maintained during apnea in anesthetized dogs by delivering a continuous stream of inspired ventilation through cannulas aimed down the main-stem bronchi. Because an asymmetric distribution of ventilation might introduce ventilation-perfusion (VA/Q) inequality, we compared gas exchange efficiency in nine anesthetized and paralyzed dogs during constant-flow ventilation (CFV) and conventional ventilation (intermittent positive-pressure ventilation, IPPV). Gas exchange was assessed using the multiple inert gas elimination technique. During CFV at 3 l X kg-1 X min-1, lung volume, retention-excretion differences (R-E*) for low- and medium-solubility gases, and the log standard deviation of blood flow (log SD Q) increased, compared with the findings during IPPV. Reducing CFV flow rate to 1 l X kg-1 X min-1 at constant lung volume improved R-E* and log SD Q, but significant VA/Q inequality compared with that at IPPV remained and arterial PCO2 rose. Comparison of IPPV and CFV at the same mean lung volume showed a similar reversible deterioration in gas exchange efficiency during CFV. We conclude that CFV causes significant VA/Q inequality which may be due to nonuniform ventilation distribution and a redistribution of pulmonary blood flow.

Pulmonary mechanics during induced pulmonary edema in anesthetized dogs

1959 ◽  
Vol 14 (2) ◽  
pp. 177-186 ◽  
Author(s):  
C. D. Cook ◽  
J. Mead ◽  
G. L. Schreiner ◽  
N. R. Frank ◽  
J. M. Craig
Keyword(s):  
Pulmonary Edema ◽  
Lung Compliance ◽  
Tidal Range ◽  
Pulmonary Mechanics ◽  
Vascular Congestion ◽  
Anesthetized Dogs ◽  
Trapped Gas ◽  
Aortic Obstruction ◽  
Gas Volume ◽  
Normal Lungs

In order to study the mechanisms underlying the changes in the mechanical properties of the lungs during pulmonary edema, pulmonary vascular congestion was produced in spontaneously breathing, anesthetized dogs by partial aortic obstruction and intravenous infusion. Brief periods of congestion were associated with small changes in the lung compliance compared with the progressive and striking compliance reduction (-78%) noted with more prolonged congestion. Lung volume at end-expiration showed little change if edema fluid and trapped gas as well as the ventilated gas volume were taken into account. When edematous lungs were forcibly inflated beyond the tidal range, it was found that the overall compliance at a distending pressure of 30 cm H2O was not much less (-6%) than that of normal lungs. Furthermore, edematous lungs manifested marked ‘static’ hysteresis during such maneuvers. These findings suggested that surface phenomena were responsible for the mechanical behavior of edematous lungs rather than vascular congestion, per se, or intrinsic tissue changes. This was borne out by experiments on excised lungs which showed that the elastic properties of edematous lungs were not significantly different from normal lungs when surface forces were minimized. Submitted on August 25, 1958

Intrapulmonary blood flow redistribution during hypoxia increases gas exchange surface area

1982 ◽  
Vol 52 (6) ◽  
pp. 1575-1580 ◽  
Author(s):  
R. L. Capen ◽  
W. W. Wagner
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Surface Area ◽  
Vascular Resistance ◽  
Diffusing Capacity ◽  
Capillary Recruitment ◽  
Blood Flow Redistribution ◽  
Exchange Surface

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary “derecruitment” occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.

scholarly journals Effect of lung hypoplasia on the cardiorespiratory transition in newborn lambs

2019 ◽  
Vol 127 (2) ◽  
pp. 568-578 ◽  
Author(s):  
Erin V. McGillick ◽  
Indya M. Davies ◽  
Stuart B. Hooper ◽  
Lauren T. Kerr ◽  
Marta Thio ◽  
...  
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Respiratory Function ◽  
Scientific Evidence ◽  
Management Strategies ◽  
Oxygenation Index ◽  
Fetal Lung ◽  
Lung Compliance ◽  
Lung Hypoplasia ◽  
Artery Blood Flow

Newborns with lung hypoplasia (LH) commonly have limited respiratory function and often require ventilatory assistance after birth. We aimed to characterize the cardiorespiratory transition and respiratory function in newborn lambs with LH. LH was induced by draining fetal lung liquid in utero [110–133 days (d), term = 147d, n = 6]. At ~133d gestation, LH and Control lambs ( n = 6) were instrumented and ventilated for 3 h to monitor blood-gas status, oxygenation, ventilator requirements, and hemodynamics during the transition from fetal to newborn life. Lambs with LH had significantly reduced relative wet and dry lung weights indicating hypoplastic lungs compared with Control lambs. LH lambs experienced persistent hypercapnia and acidosis during the ventilation period, had lower lung compliance, and had higher alveolar-arterial differences in oxygen and oxygenation index compared with Control lambs. As a result, LH lambs required greater respiratory support and more supplemental oxygen. Following delivery, LH lambs experienced periods of significantly lower pulmonary artery blood flow and higher carotid artery blood flow in association with the lower oxygenation levels. The detrimental effects of LH can be attributed to a reduction in lung size and poorer gas exchange capabilities. This study has provided greater understanding of the effect of LH itself on the physiology underpinning the transition from fetal to newborn life. Advances in this area is the key to identifying improved or novel management strategies for babies with LH starting in the delivery room, to favorably alter the fetal-to-newborn transition toward improved outcomes and reduced lifelong morbidity. NEW & NOTEWORTHY Current clinical management of newborns with lung hypoplasia (LH) is largely based on expert opinion rather than scientific evidence. We have generated physiological evidence for detrimental effects of LH on hemodynamics and respiratory function in newborn lambs, which mimics the morbidity observed in LH newborns clinically. The unfavorable consequences of LH can be attributed to a reduction in lung size and poorer gas exchange capabilities.

scholarly journals Ventilasi dan Perfusi, serta Hubungan antara Ventilasi dan Perfusi

2019 ◽  
Vol 2 (1) ◽  
pp. 29
Author(s):  
Afrita Amalia Laitupa ◽  
Muhammad Amin
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Oxygen Absorption ◽  
Critical Determinant ◽  
Lung Diffusion ◽  
Diffusion Capacity ◽  
Blood Flows ◽  
Functional Factors ◽  
Ventilation And Perfusion

Lung is a place for gas exchange where ventilation and perfusion occurs. Ventilation is the first step where sequential process of inhalation and exhalation take place. Meanwhile perfusion as the other step facilitates the gas exchange and tissue supply need. Blood flows through the lungs are equals as the amount of cardiac output where the factors that control cardiac output are mainly peripheral factors, also control pulmonary blood flow. In general condition, pulmonary blood vessels act as a passive tube, which can be increased with the increasing pressure and narrowed the pressure drop. Oxygen absorption level from lungs into bloodstream is a critical determinant for functional capacity, and an important factor wheter in normal conditions (including exercise) or even in illness state. Lung diffusion capacity is influenced by several geometric and functional factors. Gravitation influence systematic gradient in ventilation and perfusion distribution. Ventilation and blood flow variations at horizontal level also occur due to intrinsic anatomic variations and vascular geometry, as well as the differences in airway and vascular smooth muscle response which modifies the distribution. The change of integrity intrapleural chamber, hydrostatic pressure and osmotic imbalance, malfunction of surfactants, other intrinsic weakness of the branching system in the form of a progressive airway, and all the things that could potentially damage the structure of the lung can cause ventilation and diffusion dysfunction.

Persistent airway hyperresponsiveness after neonatal viral bronchiolitis in rats

1991 ◽  
Vol 70 (1) ◽  
pp. 375-383 ◽  
Author(s):  
R. Sorkness ◽  
R. F. Lemanske ◽  
W. L. Castleman
Keyword(s):  
Gas Exchange ◽  
Virus Infection ◽  
Airway Hyperresponsiveness ◽  
Sendai Virus ◽  
Lung Compliance ◽  
Airway Responsiveness ◽  
Pulmonary Mechanics ◽  
Small Airways ◽  
Human Infants ◽  
Lung Morphology

Viral bronchiolitis in human infants has been associated with permanent changes in small airways and gas exchange and an increased incidence of hyperresponsive airways later in life. Respiratory infection by Sendai virus in neonatal rats also has been reported to cause permanent changes in lung morphology and increased numbers of bronchiolar mast cells and eosinophils. We evaluated pulmonary mechanics, gas exchange, and airway responsiveness in rats at 7 and 13–16 wk after neonatal Sendai virus infection. Rats from the virus group had lower arterial PO2 and increased total lung resistance compared with controls. There were no significant differences between groups for arterial PCO2, dynamic lung compliance, quasi-static respiratory system compliance, or vital capacity. Rats from the infected group were significantly more sensitive to aerosolized methacholine than were controls, although both virus and control groups became less sensitive with age. We conclude that neonatal Sendai virus infection in rats results in persistent alterations in lung function and airway responsiveness. This phenomenon may be valuable for the study of the relationships among airway inflammation, lung morphology, and airway hyperresponsiveness, and it may be relevant to human airway disease.

Effect of negative-pressure breathing on lung mechanics and venous admixture

1964 ◽  
Vol 19 (4) ◽  
pp. 665-671 ◽  
Author(s):  
Tulio Velasquez ◽  
Leon E. Farhi
Keyword(s):  
Negative Pressure ◽  
Lung Compliance ◽  
Lung Mechanics ◽  
Positive Pressure ◽  
Venous Admixture ◽  
Respiratory Compliance ◽  
Anesthetized Dogs ◽  
Flow Through ◽  
Negative Pressure Breathing ◽  
Opening And Closing

Anesthetized dogs in the supine position show a spontaneous decrease in total respiratory compliance and an increase in venous admixture to the pulmonary circulation. Both these changes can be increased by negative-pressure breathing and reversed by positive-pressure breathing. If the changes in total respiratory compliance are due only to changes in lung compliance and these in turn result directly from the closure of alveoli, the relationship between compliance and inspiratory and expiratory pressure allows one to determine the scatter of opening and closing pressures in the alveoli. The venous admixture measures blood flow through collapsed alveoli, and its relationship to the negative pressure applied indicates the perfusion of the alveoli collapsing with each increment in negative pressure. By studying simultaneously changes in compliance and venous admixture, and using two basic assumptions, the dog's lungs can be described as a system composed of some elements receiving nearly 50% of the ventilation and 20% of the perfusion, relatively unstable mechanically, and having a very high Va/ Q ratio, while the remaining air spaces receive the same ventilation, but 80% of the perfusion. lung compliance; atelectasis; ventilation-perfusion ratio Submitted on October 28, 1963

Effect of regional alveolar hypoxia on gas exchange in dogs

1989 ◽  
Vol 67 (2) ◽  
pp. 730-735 ◽  
Author(s):  
K. B. Domino ◽  
M. P. Hlastala ◽  
B. L. Eisenstein ◽  
F. W. Cheney
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Lower Lobe ◽  
Dispersion Index ◽  
Anesthetized Dogs ◽  
Alveolar Hypoxia ◽  
The Right ◽  
Increased Blood Flow ◽  
Hypoxic Gas Mixture ◽  
Hypoxic Region

We studied the effects of left lower lobe (LLL) alveolar hypoxia on pulmonary gas exchange in anesthetized dogs using the multiple inert gas elimination technique (MIGET). The left upper lobe was removed, and a bronchial divider was placed. The right lung (RL) was continuously ventilated with 100% O2, and the LLL was ventilated with either 100% O2 (hyperoxia) or a hypoxic gas mixture (hypoxia). Whole lung and individual LLL and RL ventilation-perfusion (VA/Q) distributions were determined. LLL hypoxia reduced LLL blood flow and increased the perfusion-related indexes of VA/Q heterogeneity, such as the log standard deviation of the perfusion distribution (log SDQ), the retention component of the arterial-alveolar difference area [R(a-A)D], and the retention dispersion index (DISPR*) of the LLL. LLL hypoxia increased blood flow to the RL and reduced the VA/Q heterogeneity of the RL, indicated by significant reductions in log SDQ, R(a-A)D, and DISPR*. In contrast, LLL hypoxia had little effect on gas exchange of the lung when evaluated as a whole. We conclude that flow diversion induced by regional alveolar hypoxia preserves matching of ventilation to perfusion in the whole lung by increasing gas exchange heterogeneity of the hypoxic region and reducing heterogeneity in the normoxic lung.

Unequal distribution of pulmonary diffusing capacity in the anesthetized dog

1961 ◽  
Vol 16 (3) ◽  
pp. 499-506 ◽  
Author(s):  
Johannes Piiper ◽  
Pierre Haab ◽  
Hermann Rahn
Keyword(s):  
Experimental Data ◽  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Diffusing Capacity ◽  
Distribution Factor ◽  
Q Value ◽  
Diffusion Limitation ◽  
Unequal Distribution ◽  
Pulmonary Diffusing Capacity ◽  
Anesthetized Dogs

In anesthetized dogs the alveolar-arterial O2 pressure difference (AaD) was measured at alveolar O2 pressures of 45, 75, 106, 146, and 255 mm Hg. The AaD values observed could not be explained by the conventional “shunt factor,” “diffusion-limitation factor,” or “distribution factor.” However, the experimental data could be explained on the basis of the concept of unequal distribution of pulmonary diffusing capacity, D, to perfusion, Q. A procedure for estimation of the pattern of distribution of D to Q from experimental data is described. The results were compatible with the assumption that the lung consisted of a minimum of three functional compartments characterized by different D/Q ratios. A small portion of the perfusion (1.5%) probably behaved like a true shunt (D/Q = 0); 13% of the pulmonary blood flow passed through a compartment that shared in 2% of the total diffusing capacity only, resulting in a relatively small D/Q ratio for this compartment. The presence of this compartment gave rise to the largest part of the AaD at air breathing. The calculated D/Q value for the remaining, major compartment was so high that a measurable AaD due to diffusion limitation in this compartment could occur only at alveolar O2 pressures lower than 60 mm Hg. The validity of the assumptions and the significance of the results are discussed. Submitted on May 23, 1960

Modeling steady-state inert gas exchange in the canine trachea

1995 ◽  
Vol 79 (3) ◽  
pp. 929-940 ◽  
Author(s):  
S. C. George ◽  
J. E. Souders ◽  
A. L. Babb ◽  
M. P. Hlastala
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Sulfur Hexafluoride ◽  
Functional Dependence ◽  
Inert Gases ◽  
Diffusing Capacity ◽  
Relative Contribution ◽  
Airway Gas Exchange ◽  
And Diffusion

The functional dependence between tracheal gas exchange and tracheal blood flow has been previously reported using six inert gases (sulfur hexafluoride, ethane, cyclopropane, halothane, ether, and acetone) in a unidirectionally ventilated (1 ml/s) canine trachea (J. E. Souders, S. C. George, N. L. Polissar, E. R. Swenson, and M. P. Hlastala. J. Appl. Physiol. 79: 918–928, 1995). To understand the relative contribution of perfusion-, diffusion- and ventilation-related resistances to airway gas exchange, a dynamic model of the bronchial circulation has been developed and added to the existing structure of a previously described model (S. C. George, A. L. Babb, and M. P. Hlastala. J. Appl. Physiol. 75: 2439–2449, 1993). The diffusing capacity of the trachea (in ml gas.s-1.atm-1) was used to optimize the fit of the model to the experimental data. The experimental diffusing capacities as predicted by the model in a 10-cm length of trachea are as follows: sulfur hexafluoride, 0.000055; ethane, 0.00070; cyclopropane, 0.0046; halothane, 0.029; ether, 0.10; and acetone, 1.0. The diffusing capacities are reduced relative to an estimated diffusing capacity. The ratio of experimental to estimated diffusing capacity ranges from 4 to 23%. The model predicts that over the ventilation-to-tracheal blood flow range (10–700) attained experimentally, tracheal gas exchange is limited primarily by perfusion- and diffusion-related resistances. However, the contribution of the ventilation-related resistance increases with increasing gas solubility and cannot be neglected in the case of acetone. The increased role of diffusion in tracheal gas exchange contrasts with perfusion-limited alveolar exchange and is due primarily to the increased thickness of the bronchial mucosa.

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