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Biomedical subjects

W N Gardner

Publications and source records attributed to W N Gardner.

43 records · Page 3Linked to original sources

Very small, very short-latency changes in human breathing induced by step changes of alveolar gas composition.

1. Three healthy young males were maintained for sessions of about 1 hr in a state of mild asphyxia (PA,O2 approximately 55, PA,CO2 approximately 45 torr), i.e. with moderately strong drives from both arterial and intracranial chemoreceptors. Tidal volume (VT), breath duration (TT) and duration of inspiration (TI) were recorded, and ventilation (VE) and duration of expiration (TE) were derived breath by breath. 2. The arterial chemoreceptor component of the drive was briefly and abruptly reduced, perhaps silenced, by three separate procedures: the inspiratory pathway was connected for two breaths to a second gas supply line containing, B, hypoxia with Pi,CO2 zero (removal of hypercapnia with maintained hypoxia); C, pure oxygen (removal of asphyxia); and D, oxygen with 40 torr added PCO2 (removal of hypoxia with maintained hypercapnia). In controls, A, the second inspiratory line contained the maintenance mixture so that the switch involved no change of inspiratory gas composition. Each type of test was repeated twenty-four times on each subject. 3. Responses attributable to silencing of arterial chemoreceptors (i.e. with 1 1/2--3 breath latencies about equal to the lung-to-ear circulation time) are reported elsewhere. 4. Very small responses, occurring only half a respiratory cycle after first inhalation of the test mixture, were detected by pooling all responses of each kind from all subjects. When hypoxia was withdrawn, with (C) or without (D) simultaneous withdrawal of hypercapnia, VT and VE were reduced by 3 and 2% respectively, probably because gas mixtures containing high oxygen concentrations are appreciably more viscous than hypoxic mixtures and so require more effort to breathe in and out. When hypercapnia was withdrawn with (C) or without (B) simultaneous withdrawal of hypoxia, TE was significantly lengthened (mean, + 65 +/- 18 msec), 5. The change of TE was discussed in relation to known effects of CO2 on airway receptors in the dog.

Carbon Dioxide↗

The relation between tidal volume and inspiratory and expiratory times during steady-state carbon dioxide inhalation in man.

1. Ambiguities and discrepancies in the published descriptions of the patterns of breathing in man have been re-investigated.Steady-state hyperpnoea during rest was induced in normal subjects of both sexes by means of CO(2) inhalation, usually in high O(2), but sometimes in low (P(A, O2) approximately 200 and 55 torr respectively).2. The relations between mean tidal volume V(T) and mean times for inspiration T(I) and expiration T(E) were satisfactorily divided into lower and upper parts (ranges 1 and 2) in nineteen out of thirty-three experiments using an objective least-squares method, and polynomials were fitted separately to each of the following pairs of variables V(T,lower), T(I); V(T,lower), T(E); V(T,upper), T(I); V(T,upper), T(E).3. The breakpoints occurred when V(T) was about one third of vital capacity, but there was much variation between subjects.4. In range 2, V(T) was inversely related to both T(I) and T(E) and there appeared to be linkage between T(I) and T(E), all as described by Clark & Euler (1972). The relation suggested by Hey, Lloyd, Cunningham, Jukes & Bolton (1966) over range 2 was not confirmed.5. The main part of the relation described by Hey et al. (1966) is concerned with range 1. Here the relation between V(T) and T(I) was variable; slight, but significant negative correlation predominated. V(T) was, on the other hand, strongly and inversely related to T(E), and plots of (T(E) - T(I)) against V(T) over both ranges showed even less scatter. Hence (a) T(E) is probably related to V(T) through two mechanisms, one involving a link with T(I) and another prominent one being quite independent of T(I), (b) most changes of respiratory frequency in normal man are brought about by change of T(E) rather than of T(I), and (c) there is no region of constant frequency as implied by Clark & Euler (1972).

Adult↗

A quantitative description of the pattern of breathing during steady-state CO2 inhalation in man, with special emphasis on expiration.

1. Quantitative data on the pattern of breathing in normal men and women (Gardner, 1977) have been used to derive expressions that are based on known physiological mechanisms.2. The relations between the applied chemical drive to breathing (expressed as DeltaP(A, CO2) in high O(2)) and the several components of the volume-time patterns described in the companion paper were examined. Neither mean tidal volume (V(T)), nor mean inspiratory nor mean expiratory times (T(I), T(E)) were uniquely related to the chemical drive across the breakpoint, which could be demonstrated in two and suspected in the third of these plots.3. Mean inspiratory flow (V(T)/T(I)) was linearly related to P(A, CO2) over the whole range and, like minute ventilation (V), showed no breakpoint. The mean relation was V(T)/T(I) = 0.11 (P(A, CO2) - 35.2). V(T)/T(I) was highly correlated with V; in individuals with healthy lungs and under relatively stable conditions of compliance and resistance it may be accepted as a wholly inspiratory alternative to V as an index, on the efferent side, of the total prevailing chemical drive.4. The description of the relation between T(I) and V(T) was essentially the same as that of Clark & Euler (1972): in range 1, T(I) = either 1.29 - 0.07 V(T)or the constant 1.24 sec, and in range 2, T(I) = 0.65/(V(T) - 0.88) + 0.59.5. Expiration was described by an equation based on the inverse linkage between T(E) and chemical drive and the direct link between both mean and breath-by-breath values of T(I) and T(E): T(E) = pT(I) + q/(drive - r) in which p was 0.64 +/- 0.09, q was 11.1 +/- 2.64 sec. (torr CO(2))(-1) and r was -2.73 +/- 1.09 torr CO(2). All three parameters were necessary for an adequate description.6. It is argued that the first term of the T(E) equation represents influences related to lung volume exerted through the vagus, and that the second represents the effects of over-all chemical stimulation exerted through other pathways.

Adult↗

Severe hyponatraemia secondary to beer potomania complicated by central pontine myelinolysis.

A case of severe hyponatraemia in a 56-year-old male alcohol misuser secondary to beer potomania is presented. In view of severe volume depletion and the patient's inability to drink, normal saline was cautiously infused. Despite initial improvement, he subsequently deteriorated neurologically. Magnetic resonance imaging demonstrated the classical lesion of central pontine myelinolysis (CPM). The rate of correction of plasma sodium was within limits normally considered safe. Beer potomania should be considered as a cause of hyponatraemia in alcohol misusers. Recognition is important as the electrolyte imbalance repairs simply with cessation of alcohol intake and institution of normal diet. Correction of chronic hyponatraemia by infusion of normal or hypertonic saline should not be attempted unless life-threatening neurological complications supervene. When the balance of risks favours correction, caution should be exercised, as CPM may occur. Although a rate of correction of plasma sodium of up to 10 mM per 24-hour period has been associated with a low risk of precipitating CPM, this case illustrates that a completely safe rate of correction probably cannot be defined.

Alcoholism↗