Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In anaesthesiology of today, due to the increased use of strong analgetics, it is necessary to have an effective antagonist for mini- mizing the danger of respiratory depression in postoperative period. Naloxone, ( Narcan , R-Endo Laboratories Inc., Subsidiary of E. J. du Pont de Nemours and Co., (Inc.), USA), a new narcotic antagonist was investigated in this study. It has been applied to 58 patients in cases of respiratory depression at the end of anaesthesia in which fentanyl was given, (these cases constituted 14% of all anaesthesias). Fentanyl was given intravenously in fractional doses, (fig 1), during NLA, and other general anaesthesias, for operation and diagnostic examination ( exeption of cardiosurgery), in children and adolescents from two month-to nineteen years of age, (tab. 1.). Naloxone was given intravenously, in fractional doses from 1 microgram to 5 micrograms/kg body weight. As a criterium of an antidepressive effect of Naloxone--in addition to clinical evaluation, blood gases analyses and continuous capnographic recording has been accepted. In all 58 cases diminition of respiratory depression was observed 2-3 min. after injected each dose of Naloxone. Respiratory rate increased from 15 to 22/min. concentration of CO2 in expired gases decreased from 5-6% to 4,5%, (fig. 2 and 3), and regain of consciousness, and return of intensive reaction to endotracheal tube stimulation was observed. Naloxone produced neither changes in the cardiovascular system, nor side effects. Based on these results Naloxone has been suggested as an effective narcotic antagonist. It increase of the possibility of applying strong analgetics in children--allowing to keep a steady level of anaesthesia with easy elimination respiratory depression in the desired period of time.
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PMID:[Naloxone as a drug for improving anesthesia results in children]. 26 40

In anaesthetised and tracheotomised pig, the reflex of panting has been evaluated. The thermal tachypnea showed two phases: initially respiratory frequency increases likely to body temperature but at 41,4 degrees C is observed apnea. When temperature rose above 42 degrees C the respiratory frequency further increased the changes in blood CO2, O2 and pH were not significant. During apnea is present a slight alkalosis.
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PMID:[Thermal tachypnea in pigs]. 55 28

During sleep some patients with airways obstruction and hypoxaemia developed tachypnoea. This could not be explained by the severity of their abnormality of lung function, their CO2 responsiveness, the nature of their lung disease or their personality. This nocturnal tachypnoea correlated best with a raised resting arterial blood PCO2, and was not seen hypoxaemic patients with a normal PCO2 who showed the usual fall in respiratory rate when asleep. We suggest that in patients with both hypoxaemia and hypercapnia sleep removes a cortical inhibitory mechanism which slows breathing durigng waking hours, and is linked to the arterial blood PCO2.
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PMID:Sleeping ventilatory patterns in patients with severe chronic airflow obstruction causing respiratory failure. 95 25

1. Single fibre pulmonary stretch receptor discharge was recorded in dogs on cardiopulmonary bypass. 2. Inhalation of CO2 depressed pulmonary stretch receptor discharge despite the absence of changes in arterial PCO2. This effect was particularly marked with airway CO2 levels below 5%. 3. Changing arterial PCO2, without changing airway CO2, had only small and insignificant effects on pulmonary stretch receptor discharge. 4. The effect of changes in airway CO2 on pulmonary stretch receptor discharge was rapid and correlated well in time with the reflex tachypnoea produced when CO2 was inhaled in conditions of cardiopulmonary bypass. 5. Stimulation of the central end of the cut vagus nerve was triggered from simultaneously recorded action potentials from a single pulmonary stretch receptor. 6. In these conditions, the reflex response to CO2 could be simulated provided that the pulmonary stretch receptor had an end-expiratory discharge. 7. It is suggested that the vagally mediated tachypnoeic response to changes in airway CO2 seen in conditions of cardiopulmonary bypass is due to the effect of CO2 on the end-expiratory discharge of pulmonary stretch receptors.
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PMID:The direct effect on pulmonary stretch receptor discharge produced by changing lung carbon dioxide concentration in dogs on cardiopulmonary bypass and its action on breathing. 97 77

Ventilation while breathing air and in response to hypoxia was studied in unanesthetized cats after carotid body chemo-defferentation. Hypoxic exposure (FIO2 equal to 0.07-0.12) of chemo-deafferented animals rapidly produced a high frequency, low tidal volume tachypnea. Tachypneic breathing, although usually associated with an increased expired ventilation, was accompanied by an increase in PACO2. In contrast to intact cats, behavioral arousal during hypoxic exposure was not observed after chemo-deafferentation. The response to milder hypoxia (FIO2 equal to 0.14-0.16) occurred with an increased latency, and there resulted a less marked depression of tidal volume and stimulation of respiratory frequency. Elevation of PACO2 to 5 mm Hg above the resting value, by addition of CO2 to the inspired gas, prevented the appearance of tachypnea upon subsequent reduction of FIO2 from 0.21 to 0.07. Depletion of central catecholamine stores, by administration of reserpine, did not prevent the tachypneic response to hypoxia. Following administration of anesthesia (pentobarbital, 30 mg/kg, IP), hypoxic exposure (FIO2 equal to 0.10) led to depression of both respiratory frequency and tidal volume, resulting in apnea within 1.5 minutes. It is concluded that hypoxia (FLO2 equal to 0.07-0.16) acts, in a concentration-related manner, as a powerful stimulant to central respiratory frequency generation and as a depressant of the tidal volume in the unanesthetized cat.
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PMID:Hypoxia-induced tachypnea in carotid-deafferented cats. 112 49

1 The effects of clonidine infused into the IIIrd cerebral ventricle, the hypothalamus or intravenously were studied on behaviour, electrocortical activity, body, comb and leg temperatures, respiration and carbon dioxide elimination in adult and young fowls (Gallus domesticus). 2 Behavioural and electrocortical slow wave sleep were induced by clonidine infused into IIIrd cerebral ventricle, the hypothalamus or intravenously. Suprisingly, sleep elicited by intravenous clonidine was much longer-lasting than that induced by an identical dose given intraventricularly. 3 Body temperature was lowered by clonidine given intraventricularly or infused into the hypothalamus. Depending on initial comb temperature and ambient temperature, comb temperature was elevated, unaffected or lowered as body temperature fell; temperature of the unfeathered legs also rose as body temperature declined after clonidine. 4 Following clonidine, but before any considerable decline of body temperature, tachypnoea and wing abduction developed; during recovery of body temperature, the wings were lowered and applied closely to the trunk and the feathers partly erected. 5 CO2 elimination fell more swiftly than body temperature following intrahypothalamic clonidine in young chicks; initial recovery developed sooner than that of body temperature, but eventual recovery was delayed compared to that for body temperature. The effects of clonidine were much more marked in young chicks studied at an ambient temperature below thermoneutrality as compared to thermoneutrality. 6 The soporific effects of clonidine were attenuated by intraventricular phentolamine; its hypothermic effects were prevented by phenoxybenzamine and prevented or attenuated by phentolamine. Intraventricular atropine, haloperidol, methysergide and propranolol were ineffective. 7 Larger doses of intraventricular phentolamine elicited shivering, tachypnoea and wing abduction; body temperature was elevated, to the extent even of lethal hyperthermia. Intraventricular atropine also elevated body temperature. 8 Clonidine infused intravenously, intraventricularly or into the hypothalamus, replaced the behavioural and electrocortical arousal evoked with dexamphetamine, by sleep associated with slow wave electrocortical activity.
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PMID:Central effects of clonidine 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride in fowls. 121 58

We tested the efficacy of nocturnal nasal ventilation (NNV) using the BIPAP ventilator in patients with restrictive thoracic diseases by withdrawing them from NNV for an average of 1 wk. One male and five female patients were enrolled in the study; four with restrictive chest wall diseases, and two with muscular dystrophies. All patients had chronic CO2 retention (PaCO2 greater than 50 mm Hg) and had been improved by using NNV for at least 2 months before the study. Four patients were switched to the BIPAP ventilator from standard portable volume ventilators at least 1 month prior to the study without changes in gas exchange or symptoms. After withdrawal of NNV, patients had no deterioration in daytime vital signs, pulmonary functions, maximal inspiratory or expiratory pressures, or arterial blood gases compared with measures made immediately before withdrawal and 1 wk after resumption. However, patients had more dyspnea at rest, increased daytime somnolence, more morning headaches, less daytime energy, and felt less rested in the morning during withdrawal of NNV. Furthermore, nocturnal monitoring demonstrated greater tachycardia, tachypnea, oxygen desaturation, and hypoventilation during withdrawal of NNV. We conclude that NNV administered by the BIPAP ventilator is effective in ameliorating nocturnal hypoventilation and daytime symptoms in patients with chronic CO2 retention caused by severe restrictive thoracic diseases. These data also suggest that the efficacy of NNV may depend more on amelioration of nocturnal hypoventilation than on resting of ventilatory muscles.
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PMID:Efficacy of nocturnal nasal ventilation in patients with restrictive thoracic disease. 173 43

Using the recruitment threshold technique, we measured the CO2 responsiveness of the unloaded respiratory pump in 14 mechanically ventilated patients prior to weaning. The CO2 recruitment threshold (CO2RT) was compared with the arterial CO2 tension during unassisted breathing (CO2SB) and with the PaCO2 during mechanical ventilation (CO2MV) at machine settings determined by the primary physician. Based on these comparisons, we tested the hypotheses that (1) patients without weaning-induced respiratory distress (group 1) maintain CO2SB near CO2RT, (2) patients with weaning-induced respiratory distress (group 2) retain CO2SB above CO2RT, thereby manifesting incomplete load compensation, and (3) CO2MV is ventilator setting dependent and provides insufficient information about the ventilatory requirement during weaning. Respiratory distress was prospectively defined as sustained tachypnea (rate greater than or equal to 30) or intense dyspnea (Borg scale rating) and limited weaning in nine of 14 patients. The average CO2RT was 40 mm Hg in both groups. All patients in group 1 maintained CO2SB near CO2RT (p greater than 0.1). Seven of nine patients in group 2 retained CO2 by greater than or equal to 3 mm Hg above CO2RT (p less than 0.01). There was no significant difference between CO2MV and CO2SB in either group. We conclude that CO2RT provides a better reference of the adequacy of ventilatory load compensation during weather than CO2MV.
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PMID:The control of breathing during weaning from mechanical ventilation. 190 19

To illustrate the abilities of several physiologic events to indicate a change in metabolic status, dinitrophenol was used to induce hyperthermia. Ten dogs were divided into two groups, one being mechanically ventilated and the other allowed to breathe spontaneously. End-tidal CO2 (ETCO2) and CO2 production, O2 consumption, mean blood pressure, and rectal temperature were monitored continuously in both groups. Respired volume was measured with a pneumotachograph. An infrared-absorption CO2 analyzer measured inspired and expired CO2 concentrations. An ultraviolet-absorption analyzer measured inspired and expired O2 concentrations. Of the physiologic events measured, CO2 production and O2 consumption were the earliest and most reliable indicators of increased metabolism and consequent approaching hyperthermia in the spontaneously breathing and mechanically ventilated animals. In the spontaneously breathing animals ETCO2 transiently decreased due to transient tachypnea. In the mechanically ventilated animals ETCO2 increased steadily. Mean blood pressure increased more in the mechanically ventilated animals than in the spontaneously breathing animals. The increase in rectal temperature required 6 minutes or more to occur, whereas the increases in CO2 production and O2 consumption appeared in only about 2 minutes. It is concluded that ETCO2 is a reliable indicator of increased metabolism in mechanically ventilated subjects only, but CO2 production and O2 consumption are excellent indicators of increasing metabolism in spontaneously breathing and mechanically ventilated subjects.
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PMID:End-tidal CO2, CO2 production, and O2 consumption as early indicators of approaching hyperthermia. 212 12

During exercise, the oxygen consumption above which aerobic energy production is supplemented by anaerobic mechanisms, causing a sustained increase in lactate and metabolic acidosis, is termed the anaerobic threshold (AT). The oxygen consumption at the AT depends on factors that affect oxygen delivery to the tissues. It is increased when oxygen flow is enhanced and decreased when oxygen flow is diminished. Its value is quite low in patients with heart disease. The AT is an important functional demarcation since the physiological responses to exercise are different above the AT compared to below the AT. Above the AT, in addition to the development of metabolic acidosis, exercise endurance is reduced, VO2 kinetics are slowed so that a steady state is delayed, and VE increases disproportionately to the metabolic requirement and a progressive tachypnea develops. The AT can be measured directly from the lactate concentration with precise threshold detection from a log-log transformation of lactate and VO2. This threshold also defines the VO2 above which the lactate/pyruvate ratio increases. As bicarbonate changes reciprocally with lactate, its measurement can also be used to estimate the lactate threshold. But most convenient are gas exchange measurements made during exercise testing which can be used to noninvasively detect the lactate or anaerobic threshold. These methods are based on the physical-chemical event of buffering lactic acid with bicarbonate, and the increased CO2 output which occurs in association with the acute development of a metabolic acidosis.
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PMID:The anaerobic threshold: definition, physiological significance and identification. 355 13


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