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Biomedical subjects

J R Rigg

Publications and source records attributed to J R Rigg.

35 records · Page 2Linked to original sources
PubMed1978

Variation in the disposition of morphine after i.m. administration in surgical patients.

The disposition of morphine when administered by i.m. injection was studied in 36 patients receiving morphine as part of premedication before general anaesthesia, and in five patients who received morphine as a postoperative analgesic after median sternotomy for coronary artery surgery (PCA group). Maximum plasma concentration of morphine (CP max) was 75.3 +/- 6.0 (mean elimination rate constant (k) 4.85 X 10(-3) min-1 and half-life (T1/2) = 143 min for the preanaesthetic group. The corresponding values for PCA group were CPmax = 58.0 +/- 18.0 ng ml-1 (range 30--130 ng ml-1), k = 5.63 X 10(-3) min-1 and T 1/2 = 123 min. Analysis of variance showed no differences between the groups. Within the preanaesthetic group, there was a significant difference in k between males (k = 4.01 X 10(-3) min-1) and females (6.30 X 10(-3) min-1, P less than 0.01). The corresponding T 1/2 for males was 173 min; and 110 min for females. The variation in the disposition of morphine is thought to be the result of variations in resting muscle blood flow and inadvertent injection into adipose tissue. There were no significant differences between males and females in the preanaesthetic group with respect to age, Cpmax or time from injection to Cpmax.

Adult↗
PubMed1978

Ventilatory effects and plasma concentration of morphine in man.

The relationship between the plasma concentration of morphine and morphine-induced changes in ventilation and the ventilatory response to carbon dioxide was studied in 17 healthy adults undergoing elective surgery under general anaesthesia. Each subject was given morphine sulphate 0.15 mg kg-1 i.m.; ventilation (Ve), end-tidal PCO2(PE'CO2), mixed venous PCO2(PVCO2) and ventilatory response to carbon dioxide (delta Ve/deltaPCO2) were measured before and within 90 min after injection. Mixed venous PCO2 and deltaVe/deltaPCO2 were measured by standard rebreathing methods; plasma morphine concentration was measured by radioimmunoassay. Maximum plasma morphine ranged from 30 to 120 ng ml-1, between 4 and 60 min after injection. There was a significant increase in mixed venous PCO2 (P less than 0.001), and PE'CO2 (P less than 0.01) after morphine while Ve decreased insignificantly. Morphine displaced the carbon dioxide response curve to the right (P less than 0.01) and delta Ve/delta PCO2 decreased from 12.3 to 10.0 litre min-1 kPa-1 (P less than 0.05). The magnitude of changes in Ve and deltaVe/deltaPCO2 were not related to the peak plasma concentration of morphine or to the mean concentration immediately before and after the carbon dioxide response measurement. Plasma concentrations of morphine, under the conditions of the present study, are not an objective indicator of pharmacological activity between one patient and another.

Adult↗
PubMed1978

Low ventilatory response to carbon dioxide not associated with increased depression by morphine.

Ventilation (Ve), end-tidal (Pe' CO2), mixed venous PCO2 (PVCO2) and the ventilatory response to carbon dioxide (deltaVE/deltaPCO2) were measured before and within 90 min after morphine 0.15 mg kg-1 i.m. given to 17 adult patients undergoing elective surgery under general anaesthesia. The hypothesis that patients with a low ventilatory response to carbon dioxide are more susceptible to the ventilatory depressant effects of morphine was tested. Morphine induced increases in PE'CO2 and PVCO2 were not correlated with either the slope or the position of hte preinjection response to carbon dioxide. Mean delta Ve/deltaPCO2 was depressed after morphine (P less than 0.05), but individual responses varied widely. Seven patients whose control delta Ve/PCO2 was 9.9 litre min-1 kPa-1 or less decreased delta Ve/deltaPCO2 after morphine. In four patients, delta Ve/deltaPCO2 increased after morphine; however, in each case, PE'CO2 and PVCO2 increased also. Morphine displaced the carbon dioxide response to the right (P less than 0.001) but no correlation was found betwen either the magnitude of the displacement or change in slope and control delta Ve/deltaPCO2. The results suggest that patients with a low value for delta Ve/deltaPCO2 are not more susceptible to the ventilatory depressant action of morphine.

Adult↗
PubMed1978

Effect of curare on maximum static PV relationships of the respiratory system.

The effect of respiratory muscle weakness on the maximum static pressure-volume (PV) characteristics of the respiratory system was studied in four healthy males infused slowly with d-tubocurarine (dtc). Inspiratory capacity (IC), expiratory reserve volume (ERV), maximum static inspiratory and expiratory mouth pressures at four lung volumes, and handgrip were measured during induction of, and recovery from muscle weakness. The maximum effect of dtc varied among the muscle groups tested; peripheral muscles were most severely affected, expiratory muscles moderately, and inspiratory muscles least affected. At each level of weakness studied, decreases of IC and ERV were proportional to decreases of maximum static mouth pressures. Vital capacity, measured at each level of weakness was much less than values predicted from the static mechanical properties of the respiratory system. Our findings suggest that the marked change in the extremes of lung volume during submaximal neuromuscular blockade (SMNB) is due, in part, to unequal distribution of muscle weakness, reflected by decreased ability to change ribcage dimensions even at modest levels of SMNB.

Abdomen↗
PubMed1977

Interaction of mental factors with hypercapnic ventilatory drive in man.

1. The effect of mental arithmetic tasks on ventilation, breathing pattern, oxygen intake and carbon dioxide output was studied during air breathing and carbon dioxide rebreathing in healthy subjects. 2. Ventilation and breathing frequency increased significantly on performance of the task during 4 min air breathing and 4 min rebreathing; tidal volume was unchanged. The slopes of the ventilatory, frequency and tidal volume responses to carbon dioxide changed little during task performance. 3. During 15 min air breathing, oxygen intake was unchanged with task performance. Carbon dioxide output increased significantly with task performance, as a result of wash-out of carbon dioxide from body stores by the increased ventilation. 4. Mental arithmetic had no effect on the coefficients of variation of the slope and position variables of the ventilatory, frequency and tidal volume responses to carbon dioxide. It is concluded that task performance does not improve the reproducibility of these responses.

Female↗
PubMed1977

Future of anesthesia.

The authors present an account of some of the problems facing the specialty of anesthesia, which suggests that the interdependence of these problems and of their solutions should be recognized. Recruitment, job satisfaction and clinical standards will be improved as a result of greater involvement by anesthetists in preanesthetic care as part of the health care team. Teaching programs require appropriate expansion and modification. The incorporation of a physician-assistant program is essential to the future of anesthesia.

Anesthesiology↗
PubMed1976

Recovery of ventilatory response to carbon dioxide after thiopentone, morphine and fentanyl in man.

Ventilatory responses to CO2 (delta VI/delta PCO2) were measured half, one, two and four hours after infusions of thiopentone, morphine, fentanyl and saline in healthy men in order to test the idea that variation in clinical recovery and control of breathing after anaesthetic drugs are associated with interindividual differences in control measurements of delta VI/delta PCO2. Ventilatory response to CO2 was profoundly reduced one half hour after each drug, in contrast to the observation during air breathing that ventilation and end tidal PCO2 had returned to within 10 per cent of control. Mean delta VI/delta PCO2 increased progressively at one, two, and four hours, returning to near control after thiopentone, but remaining less than 80 per cent of control four hours after morphine and fentanyl. From the regression equations of each ventilatory response, ventilation at PCO2 of 58 and 70 mmHg (VI58 and VI70) were computed to estimate displacement of the response curves by the drugs. Following thiopentone there was no significant change of V158. In contrast ther was a highly siginificant fall of VI58 one half hour after fentanyl (p less than 0.01), with progressive return towards control at one, two, and four hours; similar changes were observed after morphine. For each drug, changes of VI70 were substantially greater than corresponding changes of V158. At all times during these recovery measurements, subjects were conscious and co-operative and, by traditional clinical criteria, were judged to have recovered from the effects of the drugs. Differences between high and low responding subjects were assessed by plotting control measurements against values obtained half and one hour after drugs. No systematic differences were found. These findings suggest that delta VI/delta PCO2 is a sensitive indicator of central nervous activity, but do not support the concepts that individuals with low delta VI/delta PCO2 might be more susceptible to the ventilatory depressant effects of anaesthetic drugs, or that low delta VI/delta PCO2 might be associated with delayed return of spontaneous breathing after general anaesthesia. Plasma thiopentone levels at half, one, and four hours were highly reproducible, in contrast to the wide variation of delta VI/delta PCO2 among subjects in this study. These findings together support the notion that wide variation in clinical recovery from anaesthesia may have a primary physiological basis in addition to variation caused by interindividual differences in drug dosage, biotransformation and excretion.

Adult↗
PubMed1976

Respiratory frequency response to progressive isocapnic hypoxia.

1. Ventilatory, tidal volume and frequency responses to progressive isocapnic hypoxia have been measured in twenty-nine healthy subjects by a rebreathing technique. 2. A strong correlation was found between ventilatory response to hypoxia (deltaVI/DELTASaO2) and frequency response to hypoxia (deltaf/deltaSaO2) (r=0-82, P less than 0-001). There was a lesser correlation between deltaV1/deltaSaO2 and tidal volume response (deltaVT/deltaSaO2) (r=0-50, P less than 0-01). These findings suggest that the wide range of ventilatory response to hypoxia among subjects is mainly determined by differences in frequency response and contrast with previous findings in studies of the response to progressive hypercapnia. 3. The breathing pattern during progressive hypoxia and hypercapnia was compared in ten subjects. Ventilation/tidal volume plots were constructed and patterns of response were further analysed in terms of inspiratory duration (TI), expiratory duration (TE) and mean inspiratory flow rate (VI). 4. Increments in ventilation during hypoxia were achieved with a greater respiratory frequency and a smaller tidal volume than during hypercapnia in eight of the ten subjects studied. In two subjects no difference in breathing pattern during hypoxia and hypercapnia was observed. 5. Changes in respiratory frequency during progressive hypoxia were achieved in all subjects by a progressive shortening of TI and TE. By contrast, TI remained constant during hypercapnia until VT had increased to 3-5 times the eupnoeic value; during hypercapnia the increase in frequency was achieved mainly by a progressive shortening of TE. 6. It is concluded that different mechanisms may be involved in altering respiratory frequency when ventilation is driven progressively by these different chemical stimuli.

Carbon Dioxide↗