Effect of local pulmonary blood flow control on gas exchange: theory

1982 ◽  
Vol 53 (5) ◽  
pp. 1100-1109 ◽  
Author(s):  
B. J. Grant
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Flow Control ◽  
Pulmonary Blood Flow ◽  
Venous Blood ◽  
Pulmonary Gas Exchange ◽  
Mixed Venous Blood ◽  
Regulatory Effect ◽  
Local Ventilation ◽  
Blood Flow Control

The effect of local pulmonary blood flow control by local alveolar O2 tension on steady-state pulmonary gas exchange is analyzed with techniques derived from control theory. In a single homogeneous lung unit with normal inspired and mixed venous blood gas composition, the homeostatic effect on local ventilation-perfusion ratios (VA/Q) regulation occurs over a restricted range of VA/Q. The homeostatic effect is maximal at a moderately low VA/Q (about 0.4) due to the slope of the O2 dissociation curve. In a multicompartment lung with a lognormal distribution of VA/Q, regulation of arterial O2 tension varies with the extent of inhomogeneity. At mild degrees of inhomogeneity where local pulmonary blood flow (Q) control acts predominantly on the lower VA/Q of the Q distribution, the regulatory effect is best. At severe degrees of inhomogeneity where local Q control acts mainly on the higher VA/Q of the Q distribution, the regulatory effect is worse, and positive-feedback behavior may occur. Local Q control has the potential of reducing the deleterious effects of lung disease on pulmonary gas exchange particularly when it operates in association with other regulatory mechanisms.

Local pulmonary blood flow: control and gas exchange

1993 ◽  
Vol 94 (1) ◽  
pp. 91-107 ◽  
Author(s):  
Daniel W. Sheehan ◽  
Leon E. Farhi
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Flow Control ◽  
Pulmonary Blood Flow ◽  
Blood Flow Control

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.

Effect of intrapleural pressure on pulmonary shunt through atelectatic dog lung

1963 ◽  
Vol 205 (6) ◽  
pp. 1187-1192 ◽  
Author(s):  
T. N. Finley ◽  
T. R. Hill ◽  
J. J. Bonica
Keyword(s):  
Blood Flow ◽  
Spontaneous Breathing ◽  
Pulmonary Blood Flow ◽  
Venous Blood ◽  
Left Lung ◽  
Mixed Venous Blood ◽  
Pulmonary Shunt ◽  
Intrapleural Pressure ◽  
Flow Through ◽  
Mixed Venous

During spontaneous breathing of oxygen, the pulmonary shunt through the left lung, made atelectatic by occlusion of its airway, was calculated from the O2 and CO2 tension of the arterial and mixed venous blood. At intrapleural pressure swings of -3 to -12 cm H2O, the relative blood flow through the atelectatic lung was reduced to 21.6% of the pulmonary blood flow (normal 45%). With wider swings of intrapleural pressure, average -7.5 to -24 cm H2O, the relative blood flow through the atelectatic lung increased to 45% of the pulmonary blood flow, probably because resistance to blood flow increased in the overdistended right lung. The pulmonary shunt through atelectatic lung varied directly with the increased negativity of the intrapleural pressure.

Massive Pulmonary Infarction during Total Cardiopulmonary Bypass in Unanesthetized Spontaneously Breathing Lambs

1981 ◽  
Vol 4 (2) ◽  
pp. 76-81 ◽  
Author(s):  
T. Kolobow ◽  
R.G. Spragg ◽  
J.E. Pierce
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Ventilation ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Pulmonary Infarction ◽  
Cardiopulmonary Support ◽  
Mixed Venous

We provided total cardiopulmonary support for 1-18 hours in unanesthetized tethered lambs by peripheral vascular cannulation, using a roller pump and the spiral membrane lung. Respirations were allowed to remain spontaneous and unaided. A Swan-Ganz catheter was placed for retrograde pulmonary artery blood flow sampling. Within a few minutes following induced ventricular fibrillation the PCO2 of sampled blood flowing retrograde through the lungs fell below 10 mm Hg, the PO2 rose to near 150 mm Hg, the pH rose to above 7.8, and the glucose level fell to less than 20 mg %. All of these values later gradually shifted, approaching mixed venous blood values within minutes. After 1-18 hrs of perfusion the animals went into shock and were sacrificed. At autopsy, the lungs of animals breathing room air were beefy and hemorrhagic. In lambs that were «breathing» CO2 enriched air the retrograde pulmonary artery blood pH and PCO2 was usually maintained close to the mixed venous blood values. The observed pulmonary changes were considerably less abnormal, and the microscopic abnormalities were at times nonexistent. We believe the integrity of pulmonary blood flow is vital to the survival of the lungs as a functioning organ. Cessation of total forward pulmonary blood flow (unlike partial cardiopulmonary bypass), combined with spontaneous pulmonary ventilation, rapidly leads to massive, pulmonary infactions, shock, and death.

Pulmonary effects of intravenous atropine induce ventilation perfusion mismatch

2014 ◽  
Vol 92 (5) ◽  
pp. 399-404 ◽  
Author(s):  
Romolo J. Gaspari ◽  
David Paydarfar
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Blood Flow ◽  
Gas Analysis ◽  
Pulmonary Gas Exchange ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Anticholinergic Medications ◽  
Arterial Blood ◽  
Intravenous Atropine

Atropine is used for a number of medical conditions, predominantly for its cardiovascular effects. Cholinergic nerves that innervate pulmonary smooth muscle, glands, and vasculature may be affected by anticholinergic medications. We hypothesized that atropine causes alterations in pulmonary gas exchange. We conducted a prospective interventional study with detailed physiologic recordings in anesthetized, spontaneously breathing rats (n = 8). Animals breathing a normoxic gas mixture titrated to a partial arterial pressure of oxygen of 110–120 were exposed to an escalating dose of intravenous atropine (0.001, 0.01, 0.1, 5.0, and 20.0 mg/kg body mass). Arterial blood gas measurements were recorded every 2 min (×5) at baseline, and following each of the 5 doses of atropine. In addition, the animals regional pulmonary blood flow was measured using neutron-activated microspheres. Oxygenation decreased immediately following intravenous administration of atropine, despite a small increase in the volume of inspired air with no change in respiratory rate. Arterial blood gas analysis showed an increase in pulmonary dysfunction, characterized by a widening of the alveolar–arteriole gradient (p < 0.003 all groups except for the lowest dose of atropine). The microsphere data demonstrates an abrupt and marked heterogeneity of pulmonary blood flow following atropine treatment. In conclusion, atropine was found to decrease pulmonary gas exchange in a dose-dependent fashion in this rat model.

Effects of Vaporized Perfluorocarbon on Pulmonary Blood Flow and Ventilation/Perfusion Distribution in a Model of Acute Respiratory Distress Syndrome

2001 ◽  
Vol 95 (6) ◽  
pp. 1414-1421 ◽  
Author(s):  
Matthias Hübler ◽  
Jennifer E. Souders ◽  
Erin D. Shade ◽  
Nayak L. Polissar ◽  
Carmel Schimmel ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oleic Acid ◽  
Gas Exchange ◽  
Lung Injury ◽  
Repeated Measures ◽  
Pulmonary Blood Flow ◽  
Analysis Of Covariance ◽  
Inert Gas ◽  
Low Flow ◽  
Repeated Measures Analysis

Background Perfluorocarbon (PFC) liquids are known to improve gas exchange and pulmonary function in various models of acute respiratory failure. Vaporization has been recently reported as a new method of delivering PFC to the lung. Our aim was to study the effect of PFC vapor on the ventilation/perfusion (VA/Q) matching and relative pulmonary blood flow (Qrel) distribution. Methods In nine sheep, lung injury was induced using oleic acid. Four sheep were treated with vaporized perfluorohexane (PFX) for 30 min, whereas the remaining sheep served as control animals. Vaporization was achieved using a modified isoflurane vaporizer. The animals were studied for 90 min after vaporization. VA/Q distributions were estimated using the multiple inert gas elimination technique. Change in Qrel distribution was assessed using fluorescent-labeled microspheres. Results Treatment with PFX vapor improved oxygenation significantly and led to significantly lower shunt values (P &lt; 0.05, repeated-measures analysis of covariance). Analysis of the multiple inert gas elimination technique data showed that animals treated with PFX vapor demonstrated a higher VA/Q heterogeneity than the control animals (P &lt; 0.05, repeated-measures analysis of covariance). Microsphere data showed a redistribution of Qrel attributable to oleic acid injury. Qrel shifted from areas that were initially high-flow to areas that were initially low-flow, with no difference in redistribution between the groups. After established injury, Qrel was redistributed to the nondependent lung areas in control animals, whereas Qrel distribution did not change in treatment animals. Conclusion In oleic acid lung injury, treatment with PFX vapor improves gas exchange by increasing VA/Q heterogeneity in the whole lung without a significant change in gravitational gradient.

scholarly journals The beginnings of cardiac catheterization and the resulting impact on pulmonary medicine

2017 ◽  
Vol 313 (4) ◽  
pp. L651-L658 ◽  
Author(s):  
John B. West
Keyword(s):  
Blood Flow ◽  
Cardiac Catheterization ◽  
Nobel Prize ◽  
Venous Blood ◽  
Interventional Cardiology ◽  
Primary Objective ◽  
Mixed Venous Blood ◽  
Pulmonary Medicine ◽  
Fick Principle ◽  
The Right

The early history of cardiac catheterization has many interesting features. First, although it would be natural to assume that the procedure was initiated by cardiologists, two of the three people who shared the Nobel Prize for the discovery were pulmonologists, while the third was a urologist. The primary objective of the pulmonologists André Cournand and Dickinson Richards was to obtain mixed venous blood from the right heart so that they could use the Fick principle to calculate total pulmonary blood flow. Cournand’s initial catheterization studies were prompted by his reading of an account by Werner Forssmann, who catheterized himself 12 years before. His bold experiment was one of the most bizarre in medical history. In the earliest studies that followed, Cournand and colleagues first passed catheters into the right atrium, and then into the right ventricle, and finally, the pulmonary artery. At the time, the investigators did not appreciate the significance of the low vascular pressures, nor that what they had done would revolutionize interventional cardiology. Within a year, William Dock predicted that there would be a very low blood flow at the top of the upright lung, and he proposed that this was the cause of the apical localization of pulmonary tuberculosis. The fact that the pulmonary vascular pressures are very low has many implications in lung disease. Cardiac catheterization changed the face of investigative cardiology, and its instigators were awarded the Nobel Prize in 1956.

Gas exchange in dogs in the prone and supine positions

1992 ◽  
Vol 72 (6) ◽  
pp. 2292-2297 ◽  
Author(s):  
K. C. Beck ◽  
J. Vettermann ◽  
K. Rehder
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Prone Position ◽  
Pulmonary Blood Flow ◽  
Random Order ◽  
Arterial Pco2 ◽  
Supine Posture ◽  
Pulmonary Shunting ◽  
The Difference ◽  
Arterial Po2

To determine the cause of the difference in gas exchange between the prone and supine postures in dogs, gas exchange was assessed by the multiple inert gas elimination technique (MIGET) and distribution of pulmonary blood flow was determined using radioactively labeled microspheres in seven anesthetized paralyzed dogs. Each animal was studied in the prone and supine positions in random order while tidal volume and respiratory frequency were kept constant with mechanical ventilation. Mean arterial PO2 was significantly lower (P less than 0.01) in the supine [96 +/- 10 (SD) Torr] than in the prone (107 +/- 6 Torr) position, whereas arterial PCO2 was constant (38 Torr). The distribution of blood flow (Q) vs. ventilation-to-perfusion ratio obtained from MIGET was significantly wider (P less than 0.01) in the supine [ln SD(Q) = 0.75 +/- 0.26] than in the prone position [ln SD (Q) = 0.34 +/- 0.05]. Right-to-left pulmonary shunting was not significantly altered. The distribution of microspheres was more heterogeneous in the supine than in the prone position. The larger heterogeneity was due in part to dorsal-to-ventral gradients in Q in the supine position that were not present in the prone position (P less than 0.01). The decreased efficiency of oxygenation in the supine posture is caused by an increased ventilation-to-perfusion mismatch that accompanies an increase in the heterogeneity of Q distribution.

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