Intrapartum fetal ECG electrodes.
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Biomedical subjects
Publications and source records attributed to D M Band.
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The CO2 production of 5 anaesthetized cats, ventilated to a constant PaCO2 and PaO2 by appropriate alteration of tidal volume and FIO2, was altered by means of an extracorporeal gas exchanger. Afferent chemoreceptor discharge was recorded from a single fibre preparation of the right carotid sinus nerve and the respiratory oscillations in firing were derived over 50 breath (2.5 min) periods. In response to an approximate doubling of CO2 production the discharge oscillation showed an increase in amplitude (P less than 0.05) but no change in mean level. When KCl was infused to produce a mean arterial [K+] of 5.9 mmol/L, while maintaining the same level of CO2 loading, the amplitude of the oscillation increased from 2.9 +/- 0.5 impulses/sec to 5.2 +/- 1.0 impulses/sec (P less than 0.05) and the mean increased from 2.6 +/- 0.4 impulses/sec to 3.9 +/- 0.2 impulses/sec (P less than 0.01). The implications of these findings are discussed.
Anaesthetized cats breathing 100% O2, air or 14% O2 received intravenous infusions of KCl (0.075 mmol/kg body weight per 30 sec). Ventilation increased significantly during the infusion and returned to control values within 10 sec of its completion. The ventilatory response to acute changes in arterial plasma potassium concentration is not abolished by hyperoxia. Some of these findings have already been briefly communicated (Band et al., in press).
The effect of hypoxia on the response of the carotid chemoreceptor to potassium has been investigated in anaesthetized cats. After an initial period of ventilation on air, FIO2 was reduced to 0.1-0.13 to give a mean PaO2 of 44 mm Hg. KCl was infused intravenously to raise arterial K+ to approximately 6 mM and hold it at that level. For 8 experiments in 7 cats, mean chemoreceptor discharge increased from 1.9 impulses.sec-1 on air, to 7.3 impulses.sec-1 during hypoxia to a peak of 12.2 impulses.sec-1 after the first 0.25 min of the potassium infusion. The initial speed of response and pattern of adaptation were similar to those seen in normoxic cats, but the combined effects of hypoxia and hyperkalaemia on carotid chemoreceptor discharge were greater than the sum of the individual effects.
The relationship between the respiratory oscillation in arterial pH and resulting respiratory oscillation in afferent chemoreceptor discharge has been investigated in anaesthetized, ventilated cats. The amplitude of the pH oscillations was reduced from a mean of 0.028 pH units to 0.016 by increasing respiratory frequency from 14/min to 20/min. For some chemoreceptors the amplitude of the discharge oscillations was unaffected by this change, whereas for others it was reduced. There was a significant correlation (P less than 0.05) between the reduction in the amplitude of discharge oscillations, caused by increasing respiratory rate, and the delay between the pH oscillation and the corresponding discharge oscillation. The implications of these findings are discussed.
1. In exercise the arterial plasma potassium rises; we have investigated the possibility that such rises might affect the carotid body chemoreceptor. 2. Intravenous infusions of KCl were used to produce hyperkalaemia in anaesthetized cats. 3. Intra-arterial catheter tip potassium electrodes were used to monitor changes in plasma potassium. 4. The effects of 5 min infusions of KCl on afferent carotid chemoreceptor preparations were studied. 5. Infusions of KCl, which produced increases in plasma potassium similar to those occurring in exercise in man, caused an initial large increase in mean firing frequency (237% of control). A phase of rapid adaptation of this response was followed by a phase of slower adaptation, but after 5 min of hyperkalaemia mean firing frequency was still significantly greater than control. The amplitude of the breath-by-breath oscillation in frequency appeared to increase in parallel with mean frequency so that the amplitude/mean ratio remained constant. 6. We conclude that plasma potassium changes during exercise may contribute to the chemical drive to breathe.
Intravenous injections of potassium chloride were given to anaesthetised cats to produce rises in arterial plasma potassium within the range of those occurring in man during exercise. Carotid chemoreceptor activity was recorded as action potentials from a single or few fibre preparation of the right sinus nerve. Arterial potassium was recorded continuously using a potassium electrode placed in the abdominal aorta. In response to the potassium injections there was an increase in carotid chemoreceptor activity, which closely followed the arterial potassium concentration, and an increase in ventilation. It is suggested that potassium released from muscle may be an important drive to ventilation in exercise.
The present experiments were designed to test the hypothesis that the increase in plasma potassium which occurs during exercise acts as a stimulus to respiration via the peripheral chemoreceptors. The effect of intravenous infusion of KCl on ventilation was measured in anaesthetised cats while they were loaded with CO2 intravenously via a bubble gas exchanger. Ventilation during K+ infusion was compared with that immediately before in 'intact' and peripherally chemodenervated cats. In the 'intact' group there was a highly significant increase in ventilation of approximately 25% (+253 +/- 22 ml/min, P less than 0.001), whereas in the chemodenervated group there was no significant change (+ 17 +/- 11 ml/min) in spite of similar increases in arterial K+ concentration. The results of these experiments indicate that K+ infusions stimulate ventilation and that this effect is abolished by peripheral chemodenervation.
Plasma ionized calcium has been measured in eighteen patients undergoing open heart surgery. No change in ionized calcium concentration was found during the period of cardiopulmonary bypass. In the early postbypass period, a wide range of ionized calcium concentrations was found, but this did not obviously affect myocardial performance. Factors influencing the ionized calcium concentration under these circumstances are discussed.
Five continuous records of arterial plasma potassium were obtained from three normal subjects during brief periods (5-7 min) of exercise (100 W). In two of these subjects hepatic venous blood samples were withdrawn at 0.5-1.0 min intervals and analysed in vitro for plasma potassium. Arterial plasma potassium rose rapidly at the start of exercise from 3.8 +/- 0.3 mmol/l (mean +/- SD) to plateau levels of 5.4 +/- 0.1 mmol/l. One of the above subjects and a further subject were studied after beta-blockade with propranolol. This resulted in an exaggerated rise in arterial plasma potassium during exercise. Hepatic venous potassium measurements indicated that the liver probably had little effect on potassium changes during exercise. The changes in arterial plasma potassium during exercise are rapid and substantial. If transmitted to the extracellular fluid these changes would alter cell transmembrane potential and might as a result alter receptor sensitivity.
Equimolar quantities of calcium chloride and calcium gluconate produced similar changes in plasma ionised calcium concentration when injected intravenously into anaesthetised ferrets or when added to human blood in vitro. In vivo changes were followed with a calcium electrode positioned in the animal's aorta, and this showed that the ionisation of calcium gluconate on its first pass through the circulation is as great as that of calcium chloride. This does not support the common suggestion that calcium chloride is preferable to calcium gluconate because of its greater ionisation.
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Plasma calcium ion concentration (cCa2+) in samples from 50 healthy volunteers was measured at four temperatures (21, 26, 31 and 37 degrees C) using a calcium electrode based on a neutral carrier ligand. A small negative correlation was found between temperature and cCa2+, the coefficient being -0.0017 mmol . l-1 . degrees C-1 (P less than 0.001). The significance of this in clinical, physiological and instrumentation fields is discussed. The effect on measured cCa2+ of overnight storage at 4 degrees C was slight, but did increase the variance of the results. It is suggested that the most accurate results of cCa2+ will be obtained from fresh samples measured at body temperature.
Ion-selective electrode catheters were used for continuous monitoring of epinephrine-induced changes in plasma potassium in different parts of the circulation of anesthetized greyhounds. Bolus injections and continuous infusions of epinephrine produced dose-related changes consisting of an initial transient increase followed by a decrease to levels below control. The latter part of the response was relatively short-lived in the case of bolus injections, but when the epinephrine was administered by continuous infusion, a progressive fall was maintained for the duration of the infusion. During the period when potassium levels were undergoing an acute change, marked differences were seen between concentrations in different parts of the circulation. Further studies are needed to delineate the incidence and extent of similar changes in humans, and their significance in producing dangerous dysrhythmias.
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A fast-responding, potassium-selective electrode catheter suitable for continuous intravascular monitoring is described. Traces illustrating its performance in human patients and anesthetized greyhounds are shown. There was no significant difference between off-line blood samples analysis (using an in vitro electrode) and results obtained with the in vivo electrode; mean absolute difference was 0.11 +/- 0.11 (SD) mM. The technique described is simple and reliable, and represents an advance on existing intermittent sampling methods for detailed monitoring of rapid changes in plasma potassium.
Changes in plasma potassium in the first 10 min after alterations in PaCO2 in anesthetized greyhounds were monitored continuously in vivo with potassium-selective electrode catheters. Elevation of PaCO2 resulted in a small transient fall in plasma potassium whereas reduction in PaCO2 resulted in a small transient rise in plasma potassium. Maximum changes occurred at approximately 5 min after alterations in PaCO2 with levels tending to return to control thereafter. Changes of similar magnitude in normal man would not be expected to have an adverse effect on cardiac function, but they may have greater significance in subjects with pre-existing abnormal potassium levels, during concurrent treatment with digoxin, and after sudden alterations in PaCO2 in chronic hypo- or hypercapnic conditions.