Biomedical subjects

J C Kay

Publications and source records attributed to J C Kay.

30 records · Page 2Linked to original sources

PubMed1981

Single versus multiple pulmonary emboli: different haemodynamic and blood gas results.

We evaluated haemodynamic and blood gas changes following the intravenous infusion of starch microemboli (63-74 mu). Comparisons were made between dogs receiving a single embolus and dogs receiving an equal quantity of embolus divided into small doses given at 30 minute intervals (multiple emboli). The most significant finding was that the same quantity of embolus produces different effects. In the dogs receiving a single embolus of 150 mg kg-1 of starch. Pao2 fell from 11.3 to 7.6 kPa (85 to 57 torr)(p less than 0.025) and Qs/Qt increased from 11 to 34 per cent (p less than 0.01). In the multiple emboli dogs, after a total dose of 150 mg kg-1 of starch, there was a small but not significant fall in Pao2 from 11.6 to 10.8 kPa (87 to 81 torr), and Qs/Qt did not change significantly. In the single embolus dogs Q increased significantly after an embolus of 100 mg kg-1 of starch (p less than 0.05). after a single embolus of 150 mg kg-1, Q was variable; 3 dogs showed a decrease, and 2 an increase, however the mean change was not significant. In the multiple emboli dogs, Q decreased significantly (p less than 0.005).

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PubMed1981

The effect of PCO2 on hypoxic pulmonary vasoconstriction.

Lung areas with a low V/Q ratio cause hypoxaemia. The low alveolar oxygen concentration may cause local hypoxic pulmonary vasoconstriction (HPV) which reduces perfusion, raises the V/Q ratio, and hence reduces the tendency to a low PaO2. By changing PCO2, the HPV response can be altered. We examined this relationship in anaesthetized dogs by using a tracheal divider to separate hypoxic (nitrogen ventilated) from oxygenated (100 per cent oxygen ventilated) lung. Relative perfusion was assessed from total 133Xe exhaled from each lung area after intravenous infusions. When PaCO2 was changed by changing ventilation, we found that an increasing PaCO2 increased HPV and also PaO2. At a PaCO2 of 3.3 kPa, HPV was abolished and PaO2 fell. We also changed PaCO2 by altering PICO2 to one or both lung areas while ventilation remained constant throughout the experiment. Again as PaCO2 increased, HPV and PaCO2 increased. When PaCO2 fell and end tidal carbon dioxide in the hypoxic lung (PETCO2) remained elevated by maintaining PICO2 in the hypoxic lung and removing CO2 from the oxygenated lung) HPV was maintained. Thus it is the alveolar concentration of CO2 in the hypoxic lung which is important in modifying HPV. We conclude that in this model a low PETCO2 (3.3 kPa) in hypoxic lung will reduce HPV, and will result in more severe hypoxaemia. This may have relevance in both anaesthetized and intensive care unit patients when a higher PaO2 may be obtained by increasing hypoxic lung PETCO2. The effect of PETCO2 on PaO2 will be influenced by other variables, but when hypoventilated or hypoxic exist, increasing PETCO2 may reinforce hypoxic pulmonary vasoconstriction and thus may increase PaO2.

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PubMed1981

Hypoxemia following pulmonary embolism: a dog model of altering regional perfusion.

We studied the role played by a shift in perfusion to hypoxic lung areas after pulmonary embolism in pst embolic hypoxemia. A tracheal divider was used to separate hypoxic (N2 ventilated) from oxygenated (100 per cent O2 ventilated) lung in anaesthetized dogs. Relative perfusion was assessed from total 133Xenon (133Xe) exhaled from each lung area after intravenous infusions. When one lung area was ventilated with N2 and the other with O2 at a normal PaCO2 to allow hypoxic pulmonary vasoconstriction (HPV), there was a significant (P less than 0.001) shift away from the hypoxic side. Starch or blood clots were then infused to produce pulmonary emboli. Starch emboli were distributed predominantly to the oxygenated lung. After blood clot embolization in normocapnic dogs, pulmonary artery pressure increased 15 torr, perfusion to the hypoxic lung increased from 14 +/- 2 to 23 +/- 1 per cent, and PaCO2 fell from 278 to 186 torr. When the degree of HPV was reduced in another group of dogs by hypocapnea, a similar increase in pulmonary artery pressure (14 torr) created by blood clot embolism did not shift perfusion or create hypoxemia. In all dogs the perfusion shift to hypoxic lung was sufficient to account for all the post embolic hypoxemia. In this dog model, post embolic hypoxemia is explained by preferential distribution of emboli to oxygenated lung followed by perfusion shift to hypoxic lung as the effect of HPV is overcome by pulmonary hypertension.

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PubMed1980

Pulmonary embolism distribution to ventilated and unventilated lungs in the dog: a cause of hypoxaemia.

To examine a possible mechanism which could cause arterial hypoxaemia following pulmonary embolism, we collapsed and did not ventilate one lung in each of eleven dogs, to produce hypoxic pulmonary vasoconstriction. In five dogs (Starch Group), PaO2 fell from 10 to 7.7 kPa (76.6 to 58.4 torr) as shunt fraction (Qs/Qt) rose from 19 to 31 per cent. Mean pulmonary artery pressure (ppa), paCO2 and VD/VT remained constant. Starch emboli (63--74 micron) were taken injected. PPA increased significantly and PaO2 dropped further to 5 kPa (37.8 torr) as Qs/Qt rose to 57 per cent. VD/VT increased and PaCO2 remained constant. Microscopic examination of the lungs showed that three times as many emboli went to the ventilated lung compared to the unventilated lung. Six dogs (Blood Clot Group) received 51Cr labelled autologous blood clot. Changes after emboli in PPA, PaO2, Qs/QT, PaCO2 and VD/VT were similar to the results in the Starch group. 125I serum albumin was then injected and the dogs were sacrificed. The lungs were monogenized separately and the 51Cr and 125I counted. The 51Cr counts indicated 66 per cent of the blood clot emboli went to the ventilated lung. Following embolization, the 125I counts suggested a shift in perfusion to the unventilated lung. We conclude from these results that emboli are preferentially distributed to ventilated lung. After embolization PPA increases. At least in this pulmonary embolism model the increased PPA may overcome hypoxic pulmonary vasoconstriction, redistribute blood to non-ventilated lung and create arterial hypoxaemia.

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PubMed1980

Reappraisal of extravascular lung thermal volume as a measure of pulmonary edema.

Previous papers have evaluated extravascular thermal volume of the lung (ETVL) as a measure of lung water by using median transit time (tmed) rather than the correct mean transit time (tmean). Calculation of ETVL using tmean (ETVLmean) and tmed (ETVLmed) gave an excellent relationship, ETVLmean = 1.48 ETVLmed - 0.74 (r = 0.99). This allowed us to calculate a new ratio of ETVLmean to PETW = 1.55 +/- 0.17, WHERE PETW is the postmortem value of pulmonary extravascular tissue weight. Thermistors were placed in dogs to determine the contribution of chest wall, pleural and pericardial fluid, left heart, bronchi, and lung gas to the ETVL measurement. We found ETVLmean greater than PETW because of thermal distributioninto left heart (18 +/- 2% of ETVL), bronchi (estimate 7% of ETVL), pulmonary arteries and veins (estimate 7% of ETVL), and perhaps a small portion of chest wall. We could not detect any portion of lung gas or pleural or pericardial effusions as a part of the ETVL measurement. When the distribution into left heart, bronchi, pulmonary arteries, and veins is removed ETVLmean/PETW = 1.07.

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PubMed1978

The linear relation of cerebral blood flow to arterial oxygen saturation in hypoxic hypoxia induced with nitrous oxide or nitrogen.

This study has demonstrated a linear relationship between cerebral blood flow and arterial oxygen saturation (Sao2) in the cerebral blood flow response in the hypoxic range of Pao2 values, which we believe is documented for the first time. The cerebral blood flow increased 1.02 per cent for each percentage decrease in Sao2 in hypoxia induced with nitrogen. Hypoxia induced with nitrous oxide increased cerebral blood flow at the rate of 2.09 per cent for each one per cent decrease in Sao2 which was dramatically more than the increase associated with hypoxia induced with nitrogen. Increased survival rates at lower Sao2 levels suggested that nitrous oxide also exerts a protective effect on dog myocardium. The mechanism by which hypoxia increases cerebral blood flow is unclear but the prevalent theory is one of neurogenic control which causes cerebral blood flow to increase as the intracellular hydrogen ion ([H+]I) increases in the progressive lactacidosis of hypoxia. The demonstration of a linear relationship between cerebral blood flow and Sao2 will provide the statistician, the researcher and the clinician with a useful tool for the neurophysiological assessment of cerebral blood flow.

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PubMed1975

The effects of continuous positive pressure ventilation on pulmonary oedema, gas exchange and lung mechanics.

The effect of continuous positive pressure ventilation was studied in 23 dogs in whom pulmonary oedema was induced by rapid intravenous infusion of dextran 40. CPPV slowed but did not prevent the formation of oedema. CPPV prevented or reversed the formation of liver-like areas in the dependent lobes, maintaining the oedematous lung compliant and aerated. This led to a reduction of shunt and an increase in PaO2. The use of CPPV decreased cardiac output and body oxygen consumption. Mixed venous oxygen tension was higher in dogs ventilated by CPPV and these dogs tolerated fulminant frothy oedema without distress.

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PubMed1975

Lung mechanics in hypervolemic pulmonary edema.

Extravascular thermal volume of the lung (ETVL) is a double indicator dilution technique of use in measuring pulmonary edema. ETVL and lung mechanics measurements were followed to find a less invasive monitor of pulmonary edema than the double indicator dilution technique. Pulmonary edema was induced by overloading the dogs' circulation with dextran. Phases of overload were defined on the basis of a previous electron microscopic study (Noble et al., Can. Anesthetists Soc. J. 21:275, 1974) of lung biopsies relating anatomic changes to physiologic measurements of ETVL and central blood volume (CBV). Congestion occurred when CBV was elevated and ETVL was not, interstitial edema when ETVL was elevated but smaller than 60% above control and alveolar edema when ETVL greater than 85% above control. Once the dogs were in alveolar edema, they were mechanically ventilated with 4, 8, 12, and 16 cmH2O end-tidal pressure (CPPV). Mean functional residual capacity (FRC) for all 15 dogs did not change up to the time CPPV was applied. Pulmonary resistance did not rise until alveolar edema was present. Once in pulmonary edema, lung compliance always fell as lung water increased. In individual dogs, the compliance fall was directly proportional to the rising lung water. However, the variations in slope and beginning point among dogs made it difficult to predict the amount of lung water from dynamic compliance values. PaO2 fell markedly in alveolar edema as a result of a widened A-a gradient. CPPV did not decrease lung water but did increase FRC and PaO2.

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PubMed1974