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

Since 1983, many papers tell of the usefulness of isoflurane for induced hypotension. It can induce and maintain stable arterial hypotension during neurosurgery, or any other surgical procedure requiring induced hypotension. Its use has proved to be simple. Although other hypotensive techniques are possible, especially if only moderate hypotension is required, the mechanism of action of isoflurane is very appealing: it reduces arterial pressure by reducing the peripheral resistances, without reducing the output, unlike halothane or trinitrin. Moreover, as it is anaesthetic, it reduces the overall oxygen consumption, such that if there were a fall in output one could assume that it was related to the level of oxygen consumption. When there is no severe hypocapnia, isoflurane, quite unlike sodium nitroprusside, lowers cerebral oxygen consumption without affecting cerebral blood flow rate. It does however increase intracranial pressure, like all the other hypotensive agents used. It does not increase filling pressures and has no effect on blood gas movements, unlike sodium nitroprusside and trinitrin which increase filling pressures and the intrapulmonary shunt. It is not toxic either, unlike sodium nitroprusside. The expensiveness of the drug is balanced by its many advantages, all the more so as this cost can be reduced by using a filter-system for some cases (e.g. middle ear surgery), or by using some drug combinations which need yet to be defined. However, there exist some disadvantages which may, in fact, be due to experimental conditions: failure of induced hypotension, coronary ischaemia, doubtful cerebral protection in case of focal areas of ischemia, different degrees of organ vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Can isoflurane be advised for controlled hypotension?]. 306 28

We have previously demonstrated a 40% increase in myocardial blood flow (MBF) during hypercapnia but no significant decrease of MBF during hypocapnia. The present study was undertaken to evaluate if epinephrine infusion, which increases both myocardial oxygen consumption (MVo2) and myocardial performance, might influence the effects of hypocapnia and hypercapnia on MBF. Induction of hypocapnia was performed by hyperventilation in closed-chest dogs anesthetized with pentobarbital. By adding carbon dioxide to the inspiratory gas, normocapnia and hypercapnia were created. Epinephrine infusion (0.8 microgram X kg-1 X min-1) increased MBF and cardiac output (CO) by 90 and 140%, respectively, while MVo2 was increased by 45%. Epinephrine had a direct coronary vasodilating effect in excess of myocardial needs evidenced by increased oxygen content of the coronary sinus blood. During epinephrine infusion, induction of hypocapnia effected no change of MBF, while myocardial oxygen extraction increased significantly. Although oxygen saturation (So2) and Po2 in the coronary sinus blood decreased, these values remained well above those with hypocapnia without epinephrine infusion, thereby excluding impaired oxygen supply to the heart. Hypercapnia induced an increase of MBF by nearly 40% despite the coronary vasodilatation already induced by epinephrine infusion.
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PMID:Effects of hypo- and hyper-capnia on myocardial blood flow and metabolism during epinephrine infusion in the dog. 308

This study examined the effect of hypocapnia (PaCO2 20 mm Hg) on cerebral metabolism and the electroencephalogram (EEG) findings in 12 dogs during nitroglycerin (NTG)-induced hypotension. Previous studies suggest that NTG is a more potent cerebral vasodilator than sodium nitroprusside or trimethaphan. It was speculated that combining hypocapnia with NTG-induced hypotension would cause less disturbance of cerebral metabolism and the EEG than the disturbances previously reported when hypocapnia was combined with hypotension induced by sodium nitroprusside or trimethaphan. All 12 dogs were examined at 1) normocapnia with normotension; 2) hypocapnia with normotension; and 3) hypocapnia combined with NTG-induced hypotension to mean arterial blood pressure (MABP) levels of 60, 50, and 40 mm Hg. In six dogs the cerebral metabolic rate of oxygen was determined, and the EEG was evaluated using compressed spectral analysis. Brain tissue metabolites were calculated in the other six dogs. During normotension, hypocapnia caused no deterioration of cerebral metabolism or of the EEG. Hypocapnia combined with NTG-induced hypotension caused a decrease of the power of the alpha and beta 2 spectra of the EEG at MABP's of 60 mm Hg or less. At an MABP of 40 mm Hg, brain tissue phosphocreatine and the cerebral energy charge decreased, while the brain tissue lactate:pyruvate ratio increased. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites returned to initial values, but the power of the EEG alpha and beta 2 spectra was decreased compared to baseline values. The cerebral metabolic disturbances and EEG alterations seen here with hypocapnia plus NTG-induced hypotension were similar to those previously reported with hypocapnia plus sodium nitroprusside-induced hypotension, and less than those previously reported with hypocapnia plus trimethaphan-induced hypotension. For hyperventilated patients, administration of NTG may be a better hypotensive treatment than trimethaphan, but similar in effect to sodium nitroprusside.
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PMID:Cerebral effects of hypocapnia plus nitroglycerin-induced hypotension in dogs. 308 20

It has been suggested that generalized endothelial damage and permeability changes, induced by prolonged activation of the complement system and ensuing release of lysosomal enzymes, prostaglandins and toxic oxygen products, underlie the genesis of the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF). The effects in New Zealand white rabbits were investigated of a 4 h infusion of activated complement and its combination with a short hypoxic episode on respiratory function, leukocyte count, platelet count and morphology of the lungs, heart, liver, kidney and spleen. Prolonged activation of the complement system induced hyperventilation with respiratory alkalosis and hypocapnia, depletion of granulocytes (PMN), and a variable accumulation PMN in the capillaries of all organs examined, in combination with interstitial, and, in the liver, cellular oedema. Electron microscopy of the lungs revealed degranulation of PMN, endothelial swelling and widening of the alveolar septa. The combination of hypoxia and systemic complement activation appeared to aggravate this microvascular injury with the occurrence of protein rich alveolar oedema and haemorrhage in the lungs and accumulation of PMN debris containing macrophages in the spleen. The alterations in respiratory function and pulmonary morphology in these rabbits, imitate the clinical and morphological characteristics of the early phase of ARDS. The inflammatory reaction, found in all other organs examined, might represent the early phase of MOF. If so, ARDS and MOF -- clinically closely interconnected syndromes -- might be interpreted as manifestations of the same syndrome and as the clinical expression of an uncontrolled whole body inflammation.
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PMID:Acute generalized microvascular injury by activated complement and hypoxia: the basis of the adult respiratory distress syndrome and multiple organ failure? 309 Oct 57

Isoflurane (ISF)-induced hypotension causes equal reductions of cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) so that no disturbance of cerebral energy stores or metabolites occurs. While hypocapnia during ISF-induced hypotension causes a further reduction of CBF, the effects on cerebral energy stores and metabolites produced by combining hypocapnia with ISF-induced hypotension are not known. This study examined the effect of hypocapnia (PaCO2 = 20 mmHg) on CMRO2, the electroencephalogram (EEG), and levels of adenine nucleotides, phosphocreatine, lactate, pyruvate, and glucose in brain tissue in 12 dogs during ISF-induced hypotension. All dogs were examined at: normocapnia with normotension; hypocapnia with normotension; hypocapnia combined with ISF-induced hypotension to cerebral perfusion pressures of 60, 50, and 40 mmHg; and restoration of normocapnia with normotension. In six dogs CMRO2 was determined, and the EEG was evaluated using compressed spectral analysis. In the other six dogs brain tissue metabolites were determined. Hypocapnia combined with ISF-induced hypotension (all levels) caused a decrease of the power of the beta-2 spectra, an increase of the power of the alpha and beta-1 spectra, but no change in total power of the EEG. There was no change in cerebral energy stores or brain tissue metabolites. CMRO2 was reduced by approximately 27%. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites remained unchanged and CMRO2, and the power of the alpha, beta-1, and beta-2 spectra of the EEG returned to control values. These results suggest no adverse effect on cerebral metabolism or function during hypocapnia combined with ISF-induced hypotension.
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PMID:Cerebral metabolism and EEG during combination of hypocapnia and isoflurane-induced hypotension in dogs. 309 38

It has been postulated that a coronary vasoconstriction during hypocapnia might be opposed by a compensating coronary vasodilatation due to impaired myocardial oxygen supply. The present study was performed first to examine whether a maximal decline in coronary sinus (CS) oxygen content was reached during hypocapnia. During hypercapnia a myocardial "over perfusion" has been demonstrated. The second purpose of the present study was to examine whether a myocardial "over perfusion" is essential to maintain a sufficient myocardial tissue oxygen supply during hypercapnia. Closed-chest dogs were anesthetized with pentobarbital and hypocapnia was induced by hyperventilation. Nitrogen gas and carbon dioxide could both be added to the inspiratory gas to create arterial hypoxemia (arterial SO2 65%) and hypercapnia, respectively. Arterial hypoxemia during hypocapnia increased myocardial blood flow (MBF) by 50%, while CS SO2 decreased significantly. The decrease in CS SO2 demonstrates a reserve capacity of myocardial oxygen extraction during hypocapnia, thereby ruling out any major coronary vasoconstriction during hypocapnia. Hypercapnia during normoxemia increased MBF, myocardial oxygen delivery, and CS SO2 substantially, but this was not observed when hypercapnia was created during arterial hypoxemia. From the present results we conclude that hypocapnia does not cause any major coronary vasoconstriction, while hypercapnia results in a myocardial "over perfusion," which is a luxury perfusion not essential to maintain sufficient myocardial oxygen supply during hypercapnia.
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PMID:Myocardial oxygen supply during hypocapnia and hypercapnia in the dog. 309 94

In 14 patients with supratentorial cerebral tumours with midline shift less than or equal to 10 mm, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice on the contralateral side of the craniotomy, using a modification of the Kety & Schmidt method. For induction of anaesthesia, thiopental, fentanyl and pancuronium were used. The anaesthesia was maintained with enflurane 1% in nitrous oxide 67%. Moderate hypocapnia to a level averaging 4.3 kPa was achieved. The patients were divided into two groups. In Group 1 (n = 7), 1% enflurane was used throughout the anaesthesia, and CBF and CMRO2 measured about 70 min after induction averaged 30.1 ml 100 g-1 min-1 and 1.98 ml O2 100 g-1 min-1, respectively. During the second CBF study 1 h later, CBF and CMRO2 were unchanged (P greater than 0.05). In Group 2 (n = 7), the inspiratory enflurane concentration was increased from 1 to 2% after the first CBF measurement. In this group a significant decrease in CMRO2 was observed, while CBF was unchanged. In six patients EEG was recorded simultaneously with the CBF measurements. In patients subjected to increasing enflurane concentration (Group 2), a suppression in the EEG activity was observed without spike waves. It is concluded that enflurane induces a dose-related decrease in CMRO2 and suppression in the EEG activity, whereas CBF was unchanged.
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PMID:CBF and CMRO2 during craniotomy for small supratentorial cerebral tumours in enflurane anaesthesia. A dose-response study. 310 85

The results of the investigation of the acid-base state of the arterial and venous blood have proved that during the emotional stress compensated metabolic acidosis develops. Respiratory alkalosis which is a compensatory shift results in the pronounced hypocapnia. The given state of the acid-base equilibrium is found under conditions of simultaneous transport violation and oxygen use by tissues.
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PMID:[Acid-base equilibrium of the blood and oxygen metabolism during stress]. 311 Oct 50

Effects of hypocapnia on cerebral oxygen consumption (CMRO2) and blood flow (CBF) in cerebral ischemia were studied in 19 patients. The CMRO2 did not change significantly during hypocapnia within the whole group of patients, because 10 out of 19 cases showed a decrease (p less than 0.001) and other 9 showed an increase (p less than 0.01) of CMRO2 during hypocapnia. The first 10 showed higher resting CMRO2 (p less than 0.001) and arteriovenous differences of oxygen content (AVDO2; p less than 0.02) than the other 9. However, the resting CBF and CO2 reactivity to hypocapnia were not different between them, and clinical situations were also similar. A dissociation between flow and metabolism was suggested in the first 10 with rather preserved CMRO2, while reduced metabolic demands were suggested in the other 9. Different responses of CMRO2 to hypocapnia are expected in cerebral ischemia, i.e. in cases with rather preserved CMRO2 it decreases despite an AVDO2 increase, suggesting a capability of CMRO2 to respond to CBF reduction, while it increases in cases with more decreased CMRO2, as the AVDO2 increase exceeds the CBF reduction to maintain the decreased CMRO2 for a further CBF reduction. The vascular CO2 reactivity, therefore, might be maintained to be constant between these patients.
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PMID:Effect of hypocapnia on cerebral oxygen metabolism and blood flow in ischemic cerebrovascular disorders. 311 60

1. The effects of hypercapnia and hypocapnia on brain intracellular pH (pHi) and metabolism were investigated in new-born lambs under barbiturate anaesthesia. 2. 31P nuclear magnetic resonance (n.m.r.) spectroscopy was used to determine brain pHi and the relative concentrations of compounds containing mobile phosphorus nuclei including phosphocreatine (PCr), nucleoside triphosphates (NTP) and inorganic phosphate (Pi). Simultaneous measurements were made of the molar ratio of glucose to oxygen uptake by the brain. 3. During normocapnia (arterial partial pressure of CO2 Pa, CO2, 39 +/- 1 mmHg mean +/- S.E. of mean, n = 9) brain pHi was 7.13 +/- 0.02. Hypercapnia (Pa, CO2, 98 +/- 3 mmHg) was associated with a fall in brain pHi to 6.94 +/- 0.03 (n = 19, P less than 0.001), whereas no significant change in brain pHi occurred during hypocapnia (Pa, CO2, 16 +/- 1 mmHg; brain pHi 7.15 +/- 0.01). 4. During hypercapnia there was an increase in the ratio of Pi to NTP from 1.09 +/- 0.08 to 1.47 +/- 0.06 (P less than 0.001) and a decrease in the ratio PCr/Pi from 1.60 +/- 0.08 to 0.93 +/- 0.04 (P less than 0.001). There was a linear correlation between Pi/NTP and brain pHi. 5. Alterations in arterial PCO2 had no significant effect on the molar ratio of glucose to oxygen uptake by the brain, which remained close to unity. 6. The change in brain pHi observed during hypercapnia can be accounted for by the known physico-chemical buffering capacity of brain tissue. Homoeostasis of brain pHi during hypocapnia provides further evidence that additional regulatory mechanisms operate in these circumstances. 7. The observed changes in PCr and Pi can be accounted for in part by the [H+] dependence of the creatine kinase reaction.
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PMID:Brain intracellular pH and metabolism during hypercapnia and hypocapnia in the new-born lamb. 311 75


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