Ventilating the acutely injured lung.
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Biomedical subjects
Publications and source records attributed to H B Fairley.
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A prospective study of acute hypoxic respiratory failure was carried out by nine centers in a collaborative NIH study from 1 September 1975 to 1 March 1977. Serious hypoxic respiratory failure was defined in 713 patients by the presence of (1) endotracheal intubation and positive airway pressure for at least 24 hours, and (2) the administration of at least 50 percent oxygen. The 490 patients between 12 to 65 years of age had a mortality of 61 percent. Mortality increased with increasing organ failure: one organ system failure (lung only) 40 percent; two, 54 percent; three, 72 percent; four, 84 percent, five, 100 percent. Only 103 patients died with isolated lung failure, whereas 353 died of a combination of lung and other organ failures. Both the overall mortality (66 percent) and the mortality of those with only isolated lung failure (40 percent) were much higher than anticipated for the selection criteria.
The effects of three anesthetic techniques on liver function were compared in patients with mild alcoholic hepatitis who required surgery, both peripheral and superficial. Thirty patients were randomly assigned to receive one of three anesthetics: thiopental, nitrous oxide and oxygen, enflurane, plus muscle relaxant; thiopental, nitrous oxide and oxygen, narcotic, plus muscle relaxant; or spinal anesthesia with tetracaine. Measurements of hepatic function were made preoperatively (on the day of operation) and on the first and third postoperative days. Levels of serum bilirubin, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, and lactate dehydrogenase liver isoenzyme were similar in the three groups on both postoperative days. They were not significantly different from those obtained preoperatively, although mean values decreased by the first postoperative day and again on the third. The data suggest that the choice among the three anesthetic methods studied could be based on factors other than the presence of mild alcoholic hepatitis and that, when peripheral surgery is required, one may not anticipate a worsening of any biochemical disorder in the first three postoperative days.
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To determine the effects of tidal volume (VT) and positive end-expiratory pressure (PEEP) on pulmonary oxygen exchange during endobronchial (one-lung) anesthesia, the authors studied the effects of VT at 8 and 16 per cent total lung capacity (TLC), at zero end-expiratory pressure (ZEEP), and at 10 cmH2O PEEP in 16 patients in the lateral position. Anesthesia was maintained with halothane and oxygen. During two-lung ventilation (FIO2 0.99), mean PaO2 and physiologic shunt (Qs/Qt) were 421 +/- 12 mmHg and 0.22 +/- 0.02, respectively. During one-lung ventilation, PaO2 decreased and venous admixture (or Qs/Qt) increased in every patient. The magnitude of this decrease correlated directly with preoperative forced expiratory volume in one second (FEV1) (r = 0.66, P less than 0.005). A VT of 16 per cent of TLC at ZEEP resulted in the highest mean PaO2 (210 +/- 30 mmHg) and lowest Qs/Qt (0.35 +/- 0.02), probably as a result of end-inspiratory alveolar recruitment with the least pulmonary blood flow redistribution. When 10 cmH2O PEEP was applied during 16 per cent TLC ventilation, mean PaO2 decreased from 210 +/- 35 to 162 +/- 25 mmHg (P less than 0.05). PEEP did not significantly affect PaO2 during 8 per cent TLC ventilation. At both levels of VT, PEEP reduced mean Qt by approximatley 10 per cent (P less than 0.01) and increased compliance (P less than 0.01). However, PEEP did not significantly affect mean Qs/Qt or mean arterial or pulmonary arterial pressures at either level of VT. There was considerable variation in PaO2 and Qs/Qt among patients.
To determine the effects of a step change in end-expiratory pressure on functional residual capacity (FRC) and lung-thorax compliance (CLT), 10 cm H2O positive end-expiratory pressure (PEEP) was applied in eight patients who needed mechanical ventilation for acute pulmonary failure. Of the total change in FRC, 66 +/- 5.3 per cent (mean +/- SEM) was complete within the next breath, and 90 per cent change was achieved in 4.6 +/- 1.4 breaths (24 +/- 6.4 sec). There was no statistically significant difference between times to 90 per cent FRC change with application and with removal of PEEP. In another 13 patients, PEEP was increased in 5 cm H2O steps from 3 to 18 cm H2O. Mean FRC at 3 cm H2O PEEP was 1.51 +/- 0.20 1 (55 +/- 7.0 per cent predicted supine value). Mean CLT did not change significantly until 18 cm H2O PEEP was reached, at which point it decreased (P < 0.005). The static compliance derived from change in FRC (deltaFRC/deltaPEEP) increased with increments of PEEP (P < 0.05) compared with the initial level. At PEEP levels of 8 and 13 cm H2O, mean FRC was larger than would be predicted from mean CLT (P < 0.005), but it was not significantly different at 3 cm H2O PEEP. The lung component accounted for 62 +/- 3.7 per cent of the lung-thorax compliance difference. These data define a time-dependent increase in lung volume that resembles pressure-volume hysteresis in normal man. Possible mechanisms include surface tension changes, recruitment of nonventilated lung, and stress relaxation of lung and chest wall. This study may explain the greater efficiency of PEEP compared with large tidal-volume ventilation in increasing PaO2 in patients with acute pulmonary failure.
A precise method for rapid measurement of functional residual capacity (FRC) during mechanical ventilation that uses the simultaneous exchange of argon and nitrogen is described. Circuit leaks were immediately recognizable upon completion of a run, and pneumotachygraphic inaccuracies due to turbulent flows, changes in viscosity, and time delays between pneumotachygraph and mass spectrometer signals were avoided. For 166 duplicate determinations, the first measurement of FRC differed from the second by 0.5 +/- 0.5 per cent (mean +/- SE). The technique does not affect pulmonary gas exchange. During 35 consecutive determinations of FRC (with an inspired oxygen of 50 per cent), mixed expired oxygen and carbon dioxide tensions varied less than 7 and 1.5 torr, respectively.
The usefulness of lung-thorax compliance (or elastance) as an index of pulmonary compliance (or elastance) was examined in 15 patients being ventilated for acute respiratory failure. Mean lung-thorax elastance (ELT) was 27.9 +/- 2.6 cm H2O/L, and the chest wall accounted for 34 +/- 2 percent of the mean total value. Changes in ELT caused by increments of positive end-expiratory pressure correlated only with changes in pulmonary elastance (r = 0.96; P less than 0.001) and not with chest wall elastance, although individual patients varied as to the contribution of the chest wall component. Lung-thorax elastance increased in direct proportion (1:1) to increases in pulmonary elastance, whereas the changes in lung-thorax compliance were only half those in pulmonary compliance. We conclude that elastance is a more useful clinical index than compliance.
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Kirby and Downs are to be congratulated for introducing a technique that has greatly extended the principles of the old Engström ventilator. IMV permits diagnostic distinction and therapeutic choice between lung distention, for mechanical improvement and oxygen exchange, and mechanical ventilation for pH homeostasis. They have stimulated great interest on the part of manufacturers and clinicians. Factual physiological support is still relatively slim, hypotheses greatly outstripping their supporting data. Much of the existing data are as yet either poorly based or, in one or two instances, in error. Where data do exist, their clinical importance is frequently unclear--effects on cardiac output being a good example. The obvious popularity of this technique certainly justifies its further study, and I look forward to seeing the results. I hope that, if studies being carried out in our own intensive care unit are subject to a similar degree of criticism, my resilience will equal that of the authors of these very interesting chapters.
An increased alveolar-arterial Po2 difference and a decreased in functional residual capacity are common intraoperatively and postoperatively. There is an associated increase in ventilation/perfusion maldistribution and in intrapulmonary shunt, and this may occur without roentgenographic evidence of atelectasis. The intraoperative mechanism is a function of general anesthesia and is corrected within the first few hours after most types of peripheral surgery. Postoperative hypoxemia is most exaggerated in the elderly, the obese, those with preoperative cardiopulmonary disease, and after operations on the upper abdomen and thoraex. After these procedures, arterial Po2 does not return to normal until after the second postoperative day. Anesthetic technique and intraoperative maneuvers do not influence this postoperative course, but regional analgesia is more effect than narcotics for maintaining postoperative pulmonary function. Low concentrations of supplementary O2 are usually effective in maintaining a normal arterial Po2 and should be administered routinely to those at hazard postoperatively, combined with a vigorous nursing "stir-up" regimen.
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In 12 patients requiring therapy with mechanical ventilation for acute respiratory failure, total static compliance (Cst) increased from 29 +/- 4 ml/cm H2O at a tidal volume (TV) of 5 ml/kg to 42 +/- 7 ml/cm H2O at a TV of 15 ml/kg. Similarly, Cst increased from 42 +/- 7 ml/cm H2O to 52 +/- 8 ml/cm H2O between 0 and 6 cm H2O of positive end-expiratory pressure (PEEP). At high levels of pulmonary inflation (ie, high PEEP and large TV) compliance decreased. The changes of total respiratory compliance with TV were mainly due to changes in pulmonary compliance. With PEEP, the functional residual capacity increased, and specific compliance did not change. Two mechanisms may be responsible for the changes in compliance. First, varying TV or PEEP will alter the position of tidal ventilation on the pressure-volume curve, resulting in an increase in compliance with increasing TV and PEEP up to a point, where overdistention occurs and compliance decreases. Secondly, the function of the surface-lowering substance may be altered in acute pulmonary parenchymal disease, thus disturbing the regulation of surface tension over the range of pulmonary inflation studied.
In order to evaluate the effects of ultrasonic nebulization on airway resistance in respiratory failure, ten patients requiring mechanical ventilation for acute pulmonary failure were each ventilated with two humidification systems, one producing inspired air saturated with vapour at 35 degrees C, the other nebulizing water droplets ultrasonically. There was no statistically significant difference in pulmonary resistance at inspiratory flow rates of 40, 60, AND 80 1/min. A separate comparison between humidifiers in those patients with the highest resistances did not reveal any difference in response to method of humidification. In contrast to studies in other contexts, these data fail to show any significant difference, from the standpoint of effects on resistance, in the use of ultrasonic mist humidification during mechanical ventilation for respiratory failure.
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