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Biomedical subjects

W H Noble

Publications and source records attributed to W H Noble.

At least 37 records · Page 2Linked to original sources
PubMed1984

Lung water increases with fluid administration during CPPV after pulmonary microembolization.

Hypoxemia created by pulmonary microemboli is improved by continuous positive-pressure ventilation (CPPV) but at a cost of reducing cardiac output (Q). In this high pulmonary vascular resistance (PVR), pulmonary edema setting, the authors attempted to increase the Q, which had been reduced by CPPV, with an infusion of dextran. In 14 dogs, 0.125 g/kg of starch microemboli (63-74 microns in diameter) were infused. CPPV at 15 cm H2O then was applied and PaO2 increased from 53 +/- 4 to 69 +/- 3 mmHg, but Q decreased from 2.9 +/- 0.2 to 1.7 +/- 0.2 1/min. Seven of these dogs (control group) were monitored for 3 h. In the remaining seven dogs (volume group), dextran 40 was infused until Q returned to pre-CPPV values, and monitoring was continued for 3 h. With return of Q to pre-CPPV levels, indices of tissue oxygenation (O2 transport, PVO2, O2 consumption and metabolic acidosis) were significantly improved. However lung water was increased significantly by the volume infusion, so that at 3 h lung water in the volume group was double the value in the control group. The authors conclude that volume infusion in the face of a high PVR may correct the reduced Q of CPPV and improve tissue oxygenation, but it also may increase pulmonary edema.

Animals↗
PubMed1983

Hypoxaemia created by pulmonary oedema after pulmonary microemboli in dogs.

Pulmonary microemboli may play a role in the adult respiratory distress syndrome, creating both pulmonary oedema and hypoxaemia. We measured the time course of pulmonary oedema and hypoxaemia after pulmonary microemboli of 63-74 mu starch were infused into dogs. Dogs were divided into two groups: six dogs that did not develop pulmonary oedema, and seven that did. Immediately after emboli there was no difference between groups in the large fall in PaO2 or the rise in Qs/Qt. Therefore the hypoxaemia of pulmonary embolism is not created by pulmonary oedema. As pulmonary oedema increased with time in the oedematous dogs, PaO2 fell further. There was no further reduction in PaO2 in the dogs who did not develop pulmonary oedema. We conclude that hypoxaemia after pulmonary embolism may be worsened if pulmonary oedema occurs, but the immediate large reduction in PaO2 after embolism is not created by pulmonary oedema.

Animals↗
PubMed1983

Lung water.

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Extracellular Space↗
PubMed1983

Nitroglycerin relaxes large airways.

This study documents the effect of intravenous nitroglycerin (NTG) on tracheal smooth muscle in 12 patients undergoing coronary artery surgery. The pressure within a water-filled tracheal cuff was monitored continuously, as well as systemic and pulmonary arterial pressures. A significant decrease in cuff pressure after intravenous NTG (4.0 +/- 0.3 micrograms/kg) was detected before cardiopulmonary bypass (CPB). During CPB, with exclusion of the pulmonary arterial circulation, the tracheal cuff response to NTG administered into the oxygenator persisted and was not significantly different from that noted before CPB. Thus, the large airway (tracheal) response to NTG was independent of the pulmonary circulation and probably is mediated by the bronchial circulation. The response during CPB indicated that the tracheal smooth muscle retains tone and can respond to NTG even when the lungs are collapsed with no pulmonary arterial perfusion. These data were obtained from patients with no clinical evidence of reversible airway obstruction and indicate only that NTG relaxed human tracheal smooth muscle in vivo. These data do not demonstrate the efficacy of intravenous NTG in patients with asthma.

Adult↗
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).

Animals↗
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.

Animals↗
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.

Animals↗
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.

Animals↗
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.

Animals↗
PubMed1978

Influence of elevated pulmonary vascular resistance on the relationship between central venous pressure and pulmonary artery occluded pressure following cardiopulmonary bypass.

This study has demonstrated that CVP measurement is an unreliable index of left ventricular filling pressure in unselected patients undergoing A-C bypass procedures. The influence of altered PVR on the disparity between right and left ventricular filling pressures is not of prime importance. The inconsistent relationship between CVP and PAo is primarily a result of ventricular dysfunction and not altered PVR. This suggests that following A-C bypass surgery patients cannot be grouped with respect to altered PVR as the variable which determines whether CVP will be a reliable guide to changes in left atrial pressure. Routine use of Swan-Ganz catheters would improve the precision of monitoring and fluid administration in all patients following CPB. However, it would also increase the cost and complexity of routine care and add a very low incidence of complications to all patients having cardiac surgery. At present, we monitor high risk patients from the time of surgery and advocate early insertion of Swan-Ganz catheters in low risk patients if they are not responding to appropriate management.

Blood Pressure↗
PubMed1978

Postperfusion lung syndrome. Comparison of Travenol bubble and membrane oxygenators.

To examine the role of the oxygenator in the postperfusion lung syndrome, we studied 16 patients undergoing aorta-coronary bypass with a bubble oxygenator and 14 similar patients with a membrane oxygenator both before and for 2 days after the operation. To maintain the same pulmonary artery occluded pressure and hemoglobin level at the end of the surgical procedure, significantly more blood was required in the bubble than in the membrane group. Postoperative pulmonary dysfunction in the bubble group was characterized by increased pulmonary vascular resistance (PVR) and lung water. The increase in lung water was present after bubble oxygenation on three successive measurements, whereas there was no increase in lung water above control value at any measurement time in the membrane group. The bubble group had a significantly greater increase in PVR at the immediate postoperative study time than did the membrane group. PVR returned to control value for the duration of study. These differences in lung water and PVR measurements may be related to greater blood component trauma with a Travenol bubble oxygenator than with a membrane lung.

Blood↗
PubMed1977

Lung water estimation using an external sensing catheter.

A method for measuring pulmonary oedema (ETVL) is described using sodium ions as the intravascular indicator and heat as the extravascular indicator. The technique offers the advantage of virtually unlimited repeatability, relatively uncomplicated instrumentation and no blood loss. There is also the potential for differentiating between pulmonary oedema and pulmonary congestion and determining the efficacy of therapy. A sensing catheter to detect blood conductivity and temperature changes is required. Ideally the sensing catheter should be situated at a point just distal to the aortic valve. However, a commercially manufactured detecting catheter we had built proved troublesome to insert because of its relatively large diameter. Therefore, an external sensing catheter has been constructed to measure ETVL and the values obtained have been compared with those from an internal catheter. There was no difference between the internal and external catheter QT, but ETVL was consistently overestimated by 2.46 +/- 0.26 ml/kg. However, this value can be related to the internal value and can be used for clinical studies.

Animals↗
PubMed1977

Extravascular lung water accumulation in patients following coronary artery surgery.

We studied patients undergoing A-C Bypass with haemodilution. The bubble oxygenator was primed with either two units of plasma and lactated Ringer's solution (PLASMA) or with lactated Ringer's solution (RINGER'S) alone. We found no difference in pulmonary function or lung water determinations between the Ringer's and the Plasma groups. When all patients were grouped together we found no significant increase in lung water (ETVL)5 immediately post-operatively. This suggests lung water did not increase during cardiopulmonary bypass. By the following morning there was a highly significant increase in lung water which was related to changes in the balance between hydrostatic pressure and colloid osmotic pressure and which continued through the second post-operative day. Pulmonary dysfunction, as measured by gas exchange, was not a major problem except in one patient whose lung water increase exceeded 3 ml H2O/kg of total body weight (52 per cent increase) and in whom there was increased shunting. We consider the increase in lung water important, since it may reduce lung compliance and further lung water accumulation. Since the increased lung water was associated with a change in the balance of Starling's forces (PMV - COPMV), treatment designed to reduce that balance should reduce lung water accumulation.

Adult↗