Influence of Anaesthesia on the Regional Distribution of Perfusion and Ventilation in the Lung

1970 ◽  
Vol 38 (4) ◽  
pp. 451-460 ◽  
Author(s):  
G. H. Hulands ◽  
R. Greene ◽  
L. D. Iliff ◽  
J. F. Nunn

1. Distribution of lung volume, pulmonary ventilation and perfusion were studied in supine patients before and during anaesthesia with paralysis and artificial ventilation. Inspired gas and pulmonary blood flow were measured with 133xenon and the chest was scanned with vertically moving counters at a lung volume of 1 litre above functional residual capacity. 2. Ventilation/unit lung volume was slightly greater and perfusion/unit lung volume substantially greater during anaesthesia in the dependent parts of the lungs. The spread of ventilation/perfusion ratios in supine conscious patients was small in comparison with that reported in upright conscious patients. During anaesthesia and artificial ventilation, the inequality of ventilation to perfusion was marginally increased in three of the four patients. 3. Ventilation/perfusion inequality alone was insufficient to explain the alveolar—arterial Po2 difference usually observed during anaesthesia.

1990 ◽  
Vol 68 (5) ◽  
pp. 2013-2018 ◽  
Author(s):  
C. F. Mackenzie ◽  
M. Skacel ◽  
G. M. Barnas ◽  
W. J. Brampton ◽  
C. A. Alana

We evaluated the importance of cardiogenic gas mixing in the acini of 13 dogs during 2 min of apnea. 133Xe (1-2 mCi in 4 ml of saline) was injected into an alveolar region through an occluded pulmonary artery branch, and washout was measured by gamma scintillation scanning during continued occlusion or with blood flow reinstated. The monoexponential rate constant for Xe washout (XeW) was -0.4 +/- 0.08 (SE) min-1 at functional residual capacity (FRC) with no blood flow in the injected region. It decreased by more than half at lung volumes 500 ml above and 392 ml below FRC. With intact pulmonary blood flow, XeW was -1.0 +/- 0.08 (SE) min-1 at FRC, and it increased with decreasing lung volume. However, if calculated Xe uptake by the blood was subtracted from the XeW measured with blood flow intact, resulting values at FRC and at FRC + 500 ml were not different from XeW with no blood flow. Reasonable calculation of Xe blood uptake at 392 ml below FRC was not possible because airway closure, increased shunt, and other factors affect XeW. After death, no significant XeW could be measured, which suggests that XeW caused by molecular diffusion was small. We conclude that 1) the effect of heart motion on the lung parenchyma increases acinar gas mixing during apnea, 2) this effect diminishes above or below FRC, and 3) there is probably no direct effect of pulmonary vascular pulsatility on acinar gas mixing.


1992 ◽  
Vol 72 (6) ◽  
pp. 2292-2297 ◽  
Author(s):  
K. C. Beck ◽  
J. Vettermann ◽  
K. Rehder

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.


1979 ◽  
Vol 237 (6) ◽  
pp. H705-H712 ◽  
Author(s):  
J. R. Hales ◽  
L. B. Rowell ◽  
R. B. King

Radioactive microspheres (containing six different nuclide labels) were used to measure blood flow (BF) to most major organs of eight conscious baboons during heat stress. Cardiac output (CO), arterial mean pressure, and arterial PO2, PCO2, and pH did not change, but heart rate increased and stroke volume fell as body temperature increased by as much as 2.56 degrees C. Skin BF increased in all regions sampled so that the fraction of CO distributed to skin (not including feet and hands) increased from 3% (control) to 14%. Increased skin BF was compensated for by decreases in splanchnic (intestines, stomach, pancreas, and spleen) (35%), renal (27%), and possibly muscle BF. There was no change in BF to the brain, spinal cord, coronary, or subcutaneous adipose tissue during heating. Therefore, baboons show a generalized redistribution of BF during heat stress, so that increments in skin BF are provided without increases in CO, whereas man depends on changes in both; despite this latter difference between the baboon and man, the similarity in magnitude of the splanchnic and renal vasoconstriction between the two primates may indicate that the baboon would be a suitable animal model for investigations into mechanisms of changes in regional blood flow in man during heat stress.


1997 ◽  
Vol 200 (19) ◽  
pp. 2539-2545
Author(s):  
J Herman ◽  
T Wang ◽  
A W Smits ◽  
J W Hicks

As for most ectothermic vertebrates, the breathing pattern of turtles is episodic, and pulmonary blood flow (Qpul) and heart rate (fH) normally increase several-fold during spontaneous ventilation. While some previous studies suggest that these cardiovascular changes are caused by stimulation of pulmonary stretch receptors (PSRs) during ventilation, it has been noted in other studies that blood flows often change prior to the initiation of breathing. Given the uncertainty regarding the role of PSRs in the regulation of central vascular blood flows, we examined the effect of manipulating lung volume (and therefore PSR stimulation) on blood flows and heart rate in the freshwater turtle Trachemys scripta. Turtles were instrumented with blood flow probes on the left aortic arch and the left pulmonary artery for measurements of blood flow, and catheters were inserted into both lungs for manipulation of lung volume. In both anaesthetized and fully recovered animals, reductions or increases in lung volume by withdrawal of lung gas or injection of air, N2, O2 or 10% CO2 (in room air) had no effect on blood flows. Furthermore, simulations of normal breathing bouts by withdrawal and injection of lung gas did not alter Qpul or fH. We conclude that stimulation of PSRs is not sufficient to elicit cardiovascular changes and that the large increase in Qpul and fH normally observed during spontaneous ventilation are probably caused by a simultaneous feedforward control of central origin.


PEDIATRICS ◽  
1973 ◽  
Vol 52 (2) ◽  
pp. 179-187
Author(s):  
Richard L'E Orme ◽  
Elizabeth A. Featherby ◽  
Henrique Rigatto ◽  
Francisco J. Cervantes ◽  
June P. Brady

We have devised a method of measuring pulmonary capillary blood flow (Qpc eff) suitable for infants with idiopathic respiratory distress syndrome (IRDS). The uptake of nitrous oxide is measured during a 40-second period of rebreathing 40% nitrous oxide in oxygen from a 40- to 80-ml bag. The rate of uptake of nitrous oxide is divided by the solubility in cord blood and the mean alveolar concentration to give Qpc eff. We studied 14 preterm infants, 7 hours to 14 days of age, on 73 occasions; nine had classical IRDS and five were healthy preterm infants (controls). During the first five days of life Qpc eff was significantly lower in infants with IRDS than in the control infants, 106 ml/kg/min compared with 177 ml/kg/min (P < 0.001). Qpc eff was not related to arterial Po2, Pco2, or pH but was inversely related to the inspired oxygen concentration needed to keep the arterial Po2 within normal limits (P < 0.02). Qpc eff showed a highly significant increase with age in infants with IRDS (P < 0.001). This method provides a reasonably rapid, safe and noninvasive technique for estimating effective pulmonary blood flow in sick infants.


Respiration ◽  
1975 ◽  
Vol 32 (3) ◽  
pp. 189-209 ◽  
Author(s):  
J. Coudert ◽  
M. Paz-Zamora ◽  
L. Barragan ◽  
L. Briançon ◽  
H. Spielvogel ◽  
...  

1983 ◽  
Vol 55 (1) ◽  
pp. 205-211 ◽  
Author(s):  
G. M. Burma ◽  
G. M. Saidel

As the basis for comparing rebreathing methods of estimating pulmonary blood flow (Q) and tissue-capillary volume (Vtc), we use a dynamic mass-balance model for gas species having different physicochemical properties (e.g., He, CO, C2H2). The model accounts for the effects of ventilation and perfusion inhomogeneities, breathing pattern variation, lung and rebreathing-bag volumes, and recirculation. Also, we examine the variability of the estimates caused by random error. In addition to analyzing two well-known methods, we show how an appropriate synthesis of these methods can lead to improved estimates.


1982 ◽  
Vol 52 (4) ◽  
pp. 914-920 ◽  
Author(s):  
E. M. Baile ◽  
P. D. Pare ◽  
L. A. Brooks ◽  
J. C. Hogg

We have examined the relationship between regional pulmonary vascular resistance (PVRr) and regional lung volume (VLr) to determine whether the decrease in blood flow in the dependent lung (zone 4) was related to lung volume. Regional blood flow (Qr) was measured with radiolabeled macroaggregates at functional residual capacity (FRC) and at transpulmonary pressure of 10 cmH2O (PL10) in 10 anesthetized supine dogs. VLr was determined at FRC by measuring lung density in frozen lung slices and was calculated at PL10 using each dog's pressure-volume curve. We found that when PVRr was expressed as a function of VLr there was not a single relationship between the two. Instead we found two separate U-shaped curves, one at FRC and one at PL10 indicating that the increased vascular resistance at the lung base remained when the lung volume was made uniform by inflation to PL10. This suggests that there is no simple relationship between VLr and PVRr.


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