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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice during craniotomy for supratentorial cerebral tumors by the Kety and Schmidt technique. The anaesthetic procedures included halothane, enflurane isoflurane and continuous infusion with midazolam, etomidate, althesin and neurolept anaesthesia (dehydrobenzpyridol). Moderate hypocapnia was used and the anaesthesia was supplemented with nitrous oxide and fentanyl. In general, both CBF and CMRO2 were decreased. However, with inhalation anaesthetics an increase in concentration resulted in an increase in CBF (halothane) or unchanged CBF (isoflurane and enflurane) and a decrease in CMRO2. With the hypnotic agents a dose related decrease in CMRO2 was observed, while CBF either was unchanged (midazolam) or decreased (Althesin and etomidate).
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PMID:Measurement of cerebral blood flow (CBF) with the Kety and Schmidt technique during craniotomy. 184 39

Experiments were undertaken to test the comparability of changes in respiratory frequency and tidal volume during hypoxia and hypercapnia in rats with and without intact peripheral chemoreceptors and with intact vagi. Neural organisation of respiratory control was perturbed by anemic decerebration, achieved by ligation of the common carotid and basilar arteries. Ischemia of the brain was produced as far candal as the rostral pontine nuclei involved in respiratory control but left the medulla well perfused. The dominant respiratory effect in animals breathing air or oxygen was polypnea with hypocapnia (mean PaCO2 when breathing air 24.7 mmHg, when breathing oxygen 29.6 mmHg). After decerebration the increase of ventilation produced by breathing 10% O2 in N2 was reduced compared with responses in the intact state but levels of ventilation (V1) in hypoxia were similar to those before decerebration. After decerebration, the increase of ventilation produced by breathing 5% CO2 was greatly reduced and the level of V1 in animals breathing CO2 was significantly less than in the intact state. Intermediate changes were seen in animals breathing 2-3% CO2 which converted the hypocapnia (PaCO2 30.9 mmHg) to eucapnia (PaCO2 46.4 mmHg). In the intact state, hypoxia dominantly caused increased frequency (f) and hypercapnia caused increased tidal volume (VT); after decerebration, hypoxia produced reduction of VT while hypercapnia produced reduction of f. Bilateral carotid sinus nerve section in decerebrate animals eliminated the ventilatory response to hypoxia but left the responses to hypercapnia unaltered. The results point to differences in the mechanisms by which hypoxia and hypercapnia influence respiration in both intact and decerebrate animals with carotid sinus and vagus nerves functional. The differences can now be interpreted in terms of specific neural features of respiratory control.
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PMID:Respiratory patterns in anesthetised rats before and after anemic decerebration. 185 90

The purpose of this study was to compare psychologic and physiologic variables during intense dyspnea to those at times of no or low dyspnea in people with asthma. Thirty-six adults ranging from 19 to 76 years old were tested when they first came to the emergency department in acute dyspnea and again when they had no or low dyspnea just prior to discharge. Clinical signs found to be higher during high dyspnea than low dyspnea were respiratory rate, pulse, wheezing, and accessory muscle use. Peak expiratory flow rates and oxygen saturation were significantly lower, while anxiety, depression, somatization, and hostility were higher during times of high dyspnea. The panic/fear, fatigue, dyspnea, hyperventilation/hypocapnia, congestion, and rapid breathing subscales of the Asthma Symptom Checklist were also higher during high dyspnea compared to low dyspnea.
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PMID:Psychologic and physiologic aspects of acute dyspnea in asthmatics. 185 43

The authors examined in 60 patients with acute pulmonary embolism values of blood gases and acid-base equilibrium, incl. 30 from arterialized capillary blood, in another 30 subjects from arterial blood. On analysis of capillary blood hypoxaemia was present in all subjects, on analysis of arterial blood only in 63%. Respiratory alkalosis was found on capillary examination in 37%, on arterial examination in 23% of the patients. Hypoxaemia and hypocapnia thus are not specific phenomena in acute pulmonary embolism, in particular when accurate blood collection for analysis is respected, and normal values of paO2 and paCO2 do not rule out the presence of pulmonary embolism. In the development of hypoxaemia in patients with pulmonary embolism participates above all an incomplete right-to-left pulmonary shunt, as revealed during calculation of the magnitude of the shunt by means of the so-called oxygen method in 30 patients with embolism, as compared with a group of 10 healthy subjects.
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PMID:[The importance of blood gas analysis and acid-base equilibrium in pulmonary embolism]. 190 44

The effects of acute changes in arterial carbon dioxide and oxygen tension, produced by altering the inspired gas mixtures while maintaining constant-volume intermittent positive pressure ventilation, on global function, regional left ventricular function, and coronary hemodynamics were studied in eight sheep during halothane anesthesia. Hypercapnia (Paco2, 73.5 +/- 2.3 mm Hg, mean +/- SD) increased heart rate, stroke volume, and cardiac output but decreased systolic shortening in the base of the left ventricle. Hypocapnia (PaO2, 24 +/- 1.5 mm Hg) decreased cardiac output and coronary flow below levels seen with hypercapnia but not below levels seen with normocapnia. Systolic shortening decreased in both apical and basal regions, and left ventricular relaxation was impaired as evidenced by a reduction of the nadir of LV dP/dt. Hypoxemia (PaO2, 39 +/- 1.5 mm Hg) elicited a hyperdynamic response of the circulation, increased coronary blood flow, and exhausted the coronary flow reserve. Neither changes in PaCO2 nor changes in PaO2 caused postsystolic shortening, although hypercapnia caused nonuniformity of contraction in the left ventricle. Thus, marked alterations in oxygen and carbon dioxide tensions do not cause left ventricular dysfunction, even though moderate hypoxia reduces the coronary flow reserve.
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PMID:Effects of altered PaO2 and PaCO2 on left ventricular function and coronary hemodynamics in sheep. 190 14

The authors previously reported that hypocapnia increased myocardial oxygen demand under droperidol-fentanyl (D-F) anesthesia. In this study, we observed myocardial oxygen tension, hemodynamics, and coronary arterial-venous blood content differences of oxygen and lactate before and after hyperventilation in dogs with and without a narrowed coronary artery under halothane anesthesia. We studied the functional and metabolic responses of the heart to hypocapnia under halothane in comparison with D-F anesthesia. In the intact heart, heart rate, LV dp/dt max and myocardial energy demand (heart rate x systolic aortic pressure x LV dp/dt max), which increased during hypocapnia under D-F anesthesia, were unchanged during hypocapnia under halothane anesthesia. Aortic pressure and coronary flow were unchanged under both types of anesthesia. Though subendocardial oxygen tension decreased significantly, myocardial lactate extraction was unchanged under both types of anesthesia. In the heart with a constricted coronary artery, subendocardial oxygen tension and lactate extraction ratio decreased significantly during hypocapnia under both types of anesthesia. Myocardial lactate production was observed in six of eleven dogs in which myocardial energy demand increased under D-F anesthesia. Myocardial lactate production was observed in one dog under halothane anesthesia. Coronary arterial-venous blood oxygen content difference increased under D-F anesthesia, but not under halothane anesthesia. In summary, hypocapnia increased myocardial oxygen demand under D-F anesthesia but not under halothane anesthesia. In the intact heart under both types of anesthesia, hypocapnia deteriorated myocardial oxygen supply-demand relations, but the evidence of myocardial anaerobic metabolism was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of hypocapnia on hemodynamics and myocardial metabolism in anesthetized dogs]. 190 56

We have studied, in six normal subjects, the effect of nitrous oxide sedation on the ventilatory pattern and oxygen saturation using pulse oximetry (SpO2) after hyperventilation to an end-tidal carbon dioxide partial pressure (PE'CO2) of 3 kPa. This value of PE'CO2 was shown to be less than the apnoeic threshold of all these subjects when their ventilation vs PE'CO2 response curves were plotted. All subjects became apnoeic when told to relax following hyperventilation while breathing 75% nitrous oxide for 90 s. Apnoea was defined as cessation of breathing for 20 s or more. The mean duration of apnoea was 78 s (range 29-130 s). All subjects demonstrated arterial desaturation (mean SpO2 75%, range 44-87%). In contrast, following hyperventilation with air, no apnoea was seen in any subject, although there was some evidence of desaturation (mean SpO2 92.5%, range 88-98%). It was concluded that subjects who are sedated with nitrous oxide behave similarly to those who are anaesthetized rather than to those who were fully conscious, in that they become apnoeic below the apnoeic threshold point. The reduction in SpO2 after hyperventilation was explained almost entirely by apnoea and may explain abnormalities of respiratory control and hypoxaemia in patients recovering from general anaesthesia or sedation accompanied by hypocapnia. This mechanism may be of importance in obstetric patients after breathing Entonox, when apnoea and hypoxaemia may reduce oxygen delivery to the fetus.
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PMID:Nitrous oxide sedation causes post-hyperventilation apnoea. 190 55

The cardiorespiratory responses to exercise and forced hyperventilation were measured in 17 unselected patients with syndrome X (angina, positive exercise test, normal coronary arteriogram, no other cardiovascular disease) and compared with those in 15 healthy subjects. Forced hyperventilation produced hypocapnia and metabolic alkalosis but no chest pain or electrocardiographic change. Patients with syndrome X showed reduced maximum oxygen consumption with an increased respiratory exchange ratio at peak exercise, confirming that exercise was limited by skeletal muscle perfusion--and thus that the increase in cardiac output with exercise is limited in syndrome X as in heart failure. Arterial carbon dioxide tension (PCO2) homoeostasis during exercise was normal but the ventilatory cost of carbon dioxide excretion was increased in syndrome X (as in heart failure). End tidal PCO2 measurements correlated only poorly with arterial PCO2 in individual patients with syndrome X, providing a possible explanation for previous reports, based on end tidal PCO2 of inappropriate hyperventilation. Patients with syndrome X did not show inappropriate hyperventilation but they did show hyperventilation that was appropriate to maintain normal arterial PCO2 in the face of reduced cardiac reserve.
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PMID:Syndrome X and hyperventilation. 193 59

A new index of cerebral hemodynamics, cerebral hemodynamic reserve (CHR), was evaluated in 12 comatose adults with severe, acute, traumatic, diffuse swelling of the brain, who underwent continuous monitoring with a fiberoptic catheter of the saturation difference in arteriojugular oxyhemoglobin. CHR was assessed as the ratio of changes in global cerebral oxygen extraction to changes in cerebral perfusion pressure (CPP) as a result of spontaneous increases in intracranial pressure (ICP). During the course of hyperventilation (Pco2 in the range of 20 mm Hg) for ICP control below 20 mm Hg, 34 observations were made over the initial 48 hours postinjury. Despite normal CPP, in 25 of the observations (73.5%), ICP elevations to the range of 20 mm Hg were associated with compromised CHR, as evidenced by decreases in jugular oxygenation directly attributed to the ICP increases. In the remaining nine observations (26.5%), CHR was preserved, as evidenced by no changes or increases in jugular oxygenation when ICP increased. The CHR improved on the second day, suggesting an improved tolerance of the cerebral hemodynamics to ICP increases. Before the ICP elevations, in most of the observations, the global cerebral blood flow was estimated as being optimally decreased (by hypocapnia), in relation to cerebral oxygen consumption. This was reflected by the occurrence of baseline normalized cerebral oxygen extraction. It is concluded that in this group of patients, under circumstances of profound hyperventilation, ICP elevations within the normal CPP range may result in decreased cerebral oxygenation, even when the normal CPP would imply otherwise. It is suggested that CHR assessment may provide information regarding the status of intracranial "tightness," insofar as cerebral circulation and oxygenation are concerned.
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PMID:Continuous monitoring of cerebral oxygenation in acute brain injury: assessment of cerebral hemodynamic reserve. 196 6

Propofol was used for 1,350 sessions of electro-convulsive therapy (ECT). After 0.5 mg of intravenous atropine, patients received 1 to 1.5 mg.kg-1 bolus of propofol over a period of 20 seconds or less. This was convenient for loss of the eye-lash reflex. A bolus of 15 to 20 mg suxamethonium was given, in non allergic patients, to prevent trauma from the seizure. The patient was hyperventilated with pure oxygen through a facial mask. The electric shock was delivered bitemporally after a dental protection had been inserted. For each patient, the following data were noted: sex, use of tricyclic antidepressant drugs, atopy, amount of administered propofol and the effective intensity of the electric shock. The 99 patients were given 16.27 +/- 14 ECT sessions. Among them 26 took antidepressant drugs and 34 were atopic. There was no difference, except for weight, between the 25 men and 74 women. The mean dose of propofol was 1.37 +/- 0.3 mg.kg-1. The dose decreased with increasing age. There was no statistical relationship between the amount of propofol and intensity of the electric shock required to set off a seizure. The use of antidepressant drugs, and atopy did not influence the required amount of propofol. Speed of injection seemed to be the determining factor for narcosis with low doses of propofol. Hyperoxia and hypocapnia induced by hyperventilating with pure oxygen seemed to facilitate occurrence and duration of seizures. Although propofol has been said to reduce the length of seizures, there is controversy concerning the ECT efficacy criteria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of propofol in 1350 anesthetized patients for electroconvulsive therapy]. 200 69


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