(1/582) Arousal from sleep shortens sympathetic burst latency in humans.
1. Bursts of sympathetic activity in muscle nerves are phase-locked to the cardiac cycle by the sinoaortic baroreflexes. Acoustic arousal from non-rapid eye movement (NREM) sleep reduces the normally invariant interval between the R-wave of the electrocardiogram (ECG) and the peak of the corresponding sympathetic burst; however, the effects of other forms of sleep disruption (i.e. spontaneous arousals and apnoea-induced arousals) on this temporal relationship are unknown. 2. We simultaneously recorded muscle sympathetic nerve activity in the peroneal nerve (intraneural electrodes) and the ECG (surface electrodes) in seven healthy humans and three patients with sleep apnoea syndrome during NREM sleep. 3. In seven subjects, burst latencies were shortened subsequent to spontaneous K complexes (1.297 +/- 0.024 s, mean +/- s. e.m.) and spontaneous arousals (1.268 +/- 0.044 s) compared with latencies during periods of stable NREM sleep (1.369 +/- 0.023 s). In six subjects who demonstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst latency relative to sleep with stable electroencephalogram (EEG) and breathing (1.313 +/- 0.038 vs. 1.342 +/- 0.026 s); however, following apnoea-induced EEG perturbations, burst latencies were reduced (1.214 +/- 0.034 s). 4. Arousal-induced reduction in sympathetic burst latency may reflect a temporary diminution of baroreflex buffering of sympathetic outflow. If so, the magnitude of arterial pressure perturbations during sleep (e.g. those caused by sleep disordered breathing and periodic leg movements) may be augmented by arousal. (+info)
(2/582) Firing properties of single vasoconstrictor neurones in human subjects with high levels of muscle sympathetic activity.
1. Single-unit recordings were made from 19 postganglionic muscle vasoconstrictor axons via tungsten microelectrodes in the peroneal nerve in seven healthy subjects with many multi-unit sympathetic discharges at rest ('high group', 75 +/- 5 multi-unit bursts per 100 heart beats, mean +/- s.e.m.). The results were compared with previous data from 14 units in subjects with 21 +/- 2 multi-unit bursts per 100 heart beats ('low group'). 2. In the 'high group' the units fired spontaneously in 35 +/- 4 % of all cardiac intervals. One unit only ever fired once per cardiac interval, 14 units (74 %) generated maximally two to three spikes, and four units (21 %) up to four to five spikes. Of those cardiac intervals in which a unit fired, a single spike occurred in 78 %, two spikes in 18 %, three spikes in 4 % and four spikes in less than 1 % of cardiac intervals. Measured as the inverse of all interspike intervals, the mean rate was 0.33 +/- 0.04 Hz and the mean intraburst frequency 22.2 +/- 1.6 Hz. Most results were similar to those in the 'low group', but in the 'low group' heart rate was higher (64.5 vs. 50.4 beats min-1) and mean firing frequency was higher (0.49 +/- 0.06 Hz). 3. During increases of multi-unit burst activity evoked by sustained inspiratory-capacity apnoea the firing probability of nine units in the 'high group' increased from 33 +/- 6 to 56 +/- 3 % of the cardiac intervals. Simultaneously, the incidence of single spikes decreased and the incidence of multiple spikes per cardiac interval increased, resulting in an increase of mean firing frequency from 0. 23 +/- 0.04 Hz at rest to 1.04 +/- 0.14 Hz during the apnoea. 4. We conclude that single muscle vasoconstrictor neurones usually fire only a solitary spike during sympathetic bursts both in subjects with a high and in subjects with a low number of bursts at rest. Presumably, differences in the numbers of bursts are due mainly to differences in firing probability and recruitment of sympathetic fibres. During acute increases of multi-unit activity, both increases in discharge frequency and recruitment of additional neurones contribute to the increased intensity of an individual sympathetic burst. (+info)
(3/582) Inadvertent inhalation anaesthesia during surgery under retrobulbar eye block.
I describe a case of inadvertent inhalation anaesthesia during surgery under retrobulbar anaesthesia and its management. Some of the hazards of supplementary oxygen delivery during monitored anaesthetic care and the actions taken to prevent this mishap recurring are discussed. (+info)
(4/582) Mechanisms of acute cardiovascular response to periodic apneas in sedated pigs.
This study was designed to evaluate the importance of sympathoadrenal activation in the acute cardiovascular response to apneas and the role of hypoxemia in this response. In addition, we evaluated the contribution of the vagus nerve to apnea responses after chemical sympathectomy. In six pigs preinstrumented with an electromagnetic flow probe and five nonpreinstrumented pigs, effects of periodic nonobstructive apneas were tested under the following six conditions: room air breathing, 100% O2 supplementation, both repeated after administration of hexamethonium (Hex), and both repeated again after bilateral vagotomy in addition to Hex. With room air apneas, during the apnea cycle, there were increases in mean arterial pressure (MAP; from baseline of 108 +/- 4 to 124 +/- 6 Torr, P < 0.01), plasma norepinephrine (from 681 +/- 99 to 1,825 +/- 578 pg/ml, P < 0.05), and epinephrine (from 191 +/- 67 to 1,245 +/- 685 pg/ml, P < 0.05) but decreases in cardiac output (CO; from 3.3 +/- 0.6 to 2.4 +/- 0.3 l/min, P < 0.01) and cervical sympathetic nerve activity. With O2 supplementation relative to baseline, apneas were associated with small increases in MAP (from 112 +/- 4 to 118 +/- 3 Torr, P < 0.01) and norepinephrine (from 675 +/- 97 to 861 +/- 170 pg/ml, P < 0.05). After Hex, apneas with room air were associated with small increases in MAP (from 103 +/- 6 to 109 +/- 6 Torr, P < 0.05) and epinephrine (from 136 +/- 45 to 666 +/- 467 pg/ml, P < 0.05) and decreases in CO (from 3.6 +/- 0.4 to 3.2 +/- 0. 5 l/min, P < 0.05). After Hex, apneas with O2 supplementation were associated with decreased MAP (from 107 +/- 5 to 100 +/- 5 Torr, P < 0.05) and no other changes. After vagotomy + Hex, with room air and O2 supplementation, apneas were associated with decreased MAP (from 98 +/- 6 to 76 +/- 7 and from 103 +/- 7 to 95 +/- 6 Torr, respectively, both P < 0.01) but increased CO [from 2.7 +/- 0.3 to 3. 2 +/- 0.4 l/min (P < 0.05) and from 2.4 +/- 0.2 to 2.7 +/- 0.2 l/min (P < 0.01), respectively]. We conclude that sympathoadrenal activation is the major pressor mechanism during apneas. Cervical sympathetic nerve activity does not reflect overall sympathoadrenal activity during apneas. Hypoxemia is an important but not the sole trigger factor for sympathoadrenal activation. There is an important vagally mediated reflex that contributes to the pressor response to apneas. (+info)
(5/582) Assessment of effect of nasal continuous positive pressure on laryngeal opening using fibre optic laryngoscopy.
AIM: To assess the effect of nasal continuous positive airways pressure (CPAP) on the dimensions of the laryngeal opening. METHODS: Nine preterm infants who had previously received ventilatory support for respiratory distress syndrome (RDS) were studied. All were receiving nasal CPAP. The laryngeal opening was visualised using a fibre optic video camera system. The ratio of width to length of the opening was measured on and off CPAP. RESULTS: In eight of the infants the width: length ratio increased on CPAP; mean change for group +24.4% (95% CI +11.9 to +37.9). CONCLUSIONS: Nasal CPAP seems to dilate the larynx. This may explain the selective beneficial effects of CPAP on mixed and obstructive apnoea. (+info)
(6/582) Haemoptysis after breath-hold diving.
Pulmonary oedema has been described in swimmers and self-contained underwater breathing apparatus (Scuba) divers. This study reports three cases of haemoptysis secondary to alveolar haemorrhage in breath-hold divers. Contributory factors, such as haemodynamic modifications secondary to immersion, cold exposure, exercise and exposure to an increase in ambient pressure, could explain this type of accident. Furthermore, these divers had taken aspirin, which may have aggravated the bleeding. (+info)
(7/582) Effects of capsaicin pretreatment on expiratory laryngeal closure during pulmonary edema in lambs.
The present study, performed in nonsedated, conscious lambs, consisted of two parts. In the first part, we 1) examined for the first time whether a respiratory response to pulmonary C-fiber stimulation could be elicited in nonsedated newborns and 2) determined whether this response could be abolished by capsaicin pretreatment. Then, by using capsaicin-desensitized lambs, we studied whether pulmonary C fibers were involved in the sustained, active expiratory upper airway closure previously observed during pulmonary edema. Airflow and thyroarytenoid and inferior pharyngeal constrictor muscle electromyographic activities were recorded. In the first set of experiments, a 5-10 microg/kg capsaicin bolus intravenous injection in seven intact lambs consistently led to a typical pulmonary chemoreflex, showing that C fibers are functionally mature in newborn lambs. In the second series of experiments, eight lambs pretreated with 25-50 mg/kg subcutaneous capsaicin did not exhibit any respiratory response to 10-50 microg/kg intravenous capsaicin injection, implicating C fibers in the response. Finally, in the above capsaicin-desensitized lambs, we observed that halothane-induced high-permeability pulmonary edema did not cause the typical response of sustained expiratory upper airway closure seen in the intact lamb. We conclude that functionally mature C fibers are present and responsible for a pulmonary chemoreflex in response to capsaicin intravenous injection in nonsedated lambs. Capsaicin pretreatment abolishes this reflex. Furthermore, the sustained expiratory upper airway closure observed during halothane-induced pulmonary edema in intact nonsedated lambs appears to be related to a reflex involving stimulation of pulmonary C fibers. (+info)
(8/582) Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs.
There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 +/- 25%, P < 0.05), systemic vascular resistance (SVR; +33 +/- 16%, P < 0.0005), and heart rate (HR; +5 +/- 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; -16 +/- 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater ( approximately 14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes. (+info)