Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of induced hypercarbia on the cardiovascular system during steady-state halothane-nitrous oxide anaesthesia was investigated in 4 male patients without cardiac disease. Heart rate, cardiac index, systemic and pulmonary blood pressures rose as pCO2 was increased. Stroke volume, systemic and pulmonary vascular resistance remained unchanged. Oxygen consumption decreased and oxygen saturation of mixed venous blood increased. In conclusion the primary effect of hypercarbia was an increased heart rate and a resultant increase of cardiac output. The pressure changes merely reflect the effect on cardiac output. Under these circumstances a regulatory role of mixed venous pO2 on cardiac output is highly unlikely.
 ...
PMID:Cardiovascular effects of induced hypercarbia during halothane-nitrous oxide anaesthesia. 107 49

The haemodynamic responses to hypocapnia and hypercapnia have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia (1% halothane in oxygen) and under nitrous oxide anaesthesia (30% oxygen in nitrous oxide). In the absence of significant variations of either myocardial contractility or left ventricular end-diastolic pressure, the changes of stroke volume and cardiac output (diminution because of hypocapnia, augmentation because of hypercapnia) were determined by alterations of systemic vascular resistance (augmentation because of hypocapnia, diminution because of hypercapnia).
 ...
PMID:Effect of CO2 on myocardial contractility and aortic input impedance during anaesthesia. 109 15

Pulmonary arterial input impedance spectra were computed in goats in whom the appropriate pressure and flow transducers had been chronically implanted. In response to either hypocapnia or hypercapnia, under anesthesia (1% halothane in a 70% nitrous oxide--30% oxygen mixture) there were no significant modifications of impedance at zero frequency; no consistent or significant changes in the impedance moduli at frequencies between 2 and 14 Hz were observed; the position of the first impedance minimum or the subsequent maximum was not modified; however, pulmonary vascular resistance increased significantly with hypercapnia. Although the load opposing right ventricular ejection was not modified by variation of Paco2, right ventricular work was reduced in response to hypocapnia and augmented in response to hypercapnia.
 ...
PMID:Effects of changes in PaCO2 on pulmonary input impedance. 111 Feb 43

The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.
 ...
PMID:Circulatory effects of halothane and halothane-nitrous oxide anesthesia in the dog: spontaneous ventilation. 111 85

The effects of isoflurane and halothane on intraocular pressure (IOP) were studied in 28 children. Measurements were made during spontaneous ventilation and at a various levels of reduced PaCO2 achieved by controlled ventilation. Control IOP values were determined prior to anesthesia following premedication with chloral hydrate, pentobarbital, pentobarbital with meperidine. At roughly equivalent levels of anesthesia, mean IOP values during spontaneous ventilation ranged frm 16.3 to 17.6 torr for each anesthetic. These values were significantly less (P less than 0.01) than control values only in those patients receiving chloral hydrate who did not cooperate. In contrast, no significant change in IOP was found in more sedated and cooperative patients who received pentobarbital and meperidine. Moderate hypocarbia and hypercarbia over a range of PaCO2 greater than 42 torr had little influence on IOP. We conclude that IOP's during isoflurane and halothane anesthesia do not differ significantly from IOP in the sedated, cooperative, healthy pediatric patient.
 ...
PMID:Intraocular pressures in children during isoflurane and halothane anesthesia. 111 65

The effect of sympathetic stimulation (stellate ganglion) on dog cerebral and cephalic blood flows was studied via a cervical or a thoracic approach to the stellate ganglion under sodium pentobarbital or chloralose anesthesia. Two different stimulation voltages (3v and 5v) of monophasic pulses were applied for 1 minute. Venous outflow was measured at the confluence of the sagittal, straight and lateral sinuses with the lateral sinuses occluded and with them patent. When the lateral sinuses were occluded, stellate ganglion stimulation resulted in a marked decrease in common carotid blood flow to 38 plus or minus 2.5% (SE) of control and dilation of the ipsilateral pupil, but cerebral blood flow did not change. Similar effects were observed with each of the anatomic approaches, anesthetics, and voltages used and in dogs with low cerebral vascular tone induced by hypercapnia. When the lateral sinuses were kept patent, sympathetic nerve stimulation decreased the venous outflow to 89 plus or minus 2.9% of control and clamping both of the external jugular veins increased venous outflow to 120 plus or minus 2.7% of control. When the lateral sinuses were kept patent and the extracranial venous pressure was increased by clamping both of the external jugular veins, the decrease in venous outflow in response to sympathetic stimulation was even larger: venous outflow was only 65 plus or minus 4.9% of control. We conclude that stimulation of the stellate ganglion has no effect on the cerebral vasculature. Sympathetic stimulation significantly decreases venous blood flow measured at the confluence of the sinuses only when communications between the intracranial and extracranial venous vasculatures are present.
 ...
PMID:Effect of sympathetic nerve stimulation on cerebral and cephalic blood flow in dogs. 112 72

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in seven chronically tracheostomized dogs awake and during anesthesia with pentobarbital (30 mg/kg, iv), ketamine, or thiopental (10 and 15 mg/kg, respectively, followed by infusion). Isocapnic hypoxic ventilatory drive (HVD) was expressed as the parameter A such that the higher the A, the greater the hypoxic drive. HVD(A) was significantly reduced from 259 +/- 28 (mean +/- SEM) in awake dogs, to 96 +/- 14 after pentobarbital, 161 +/- 27 after thiopental, and 213 +/- 23 after ketamine. Hypercapnic ventilatory drive (HCVD) as measured by S (slope of the VE-PACO2 response curve) was significantly reduced from 1.3 +/- .32 in awake dogs to 0.4 +/- .13 after pentobarbital, 0.5 +/- .12 after thiopental, and 0.6 +/- .11 after ketamine. In addition, hypercapnia-induced augmentation of hypoxic drive was markedly diminished by the two barbiturates but was unaffected by ketamine. Therefore, ketamine at this dose level afforded greater protection during exposure to hypoxia than did barbiturates. (Key words: Ventilation, hypoxic response; Hypoxia, ventilation; Oxygen, ventilatory response; Carbon dioxide, ventilatory response; Anesthetics, intravenous, ketamine; Anesthetics, intravenous, thiopental; Hypnotics, barbiturates, pentobarbital.)
 ...
PMID:Hypoxic ventilatory drive in dogs during thiopental, ketamine, or pentobarbital anesthesia. 119 May 38

In dogs, plasma renin activity (PRA) was increased by anesthesia, by hypercapnia and by extreme hypoxia (paO2 47.6 mm Hg). Relatively moderate hypoxia (paO2 47.6 mm Hg) and artificial respiration had no appreciable influence on PRA. It appears that the sympathomimetic stimulus of CO2 has an important bearing on PRA.
 ...
PMID:[Proceedings: Experimentally induced effects on the plasma renin activity]. 121 77

Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) were measured in rats under nitrous oxide anaesthesia, using a 133Xenon modification of the Kety and Schmidt inert gas technique with sampling of cerebral venous blood from the retroglenoid vein. Extracerebral contamination of the venous blood sampled was studied by comparing the rates at which the activity of 133Xenon decreased in blood and tissues. Contamination was avoided by gentle compression of the contralateral retroglenoid vein during sampling. CBF and CMRo2 of the rat brain were 80+/-2 and 7.6+/-0.2 ml-(100g)-1-min-1, respectively. These values are about 25% lower than those previously obtained for cerebral cortical tissue under similar conditions. Induced hypercapnia (Paco2 about 70 mm Hg) or hypocapnia (Paco2 15-20 mm Hg) gave rise to expected changes in CBF but did not alter CMRo2. The CMRo2 of the rat brain is at least twice that of the human brain. This species difference, which is similar to that previously reported for the oxygen uptake of cerebral tissue in vitro, probably reflects on inverse relationship between brain weight and neuronal packing density.
 ...
PMID:A method for determining blood flow and oxygen consumption in the rat brain. 125 48

In a Mapleson D circuit the carbon dioxide content of gases, sampled at the breathing bag or near the bellows of the ventilator, is virtually constant throughout the phases of respiration. Assuming that after induction of anaesthesia the fresh gas inflow, if kept constant, is essentially equal in volume to the gas vented at the expiratory valve, CO2 output can be calculated by multiplying the fresh gas inflow by the CO2 content of the vented gas measured with a suitable CO2 analyzer. Anaesthesia with nitrous oxide-oxygen, supplemented with low doses of alphaprodine or halothane was compared in two groups of young patients who underwent dental surgery and who were breathing spontaneously. While the CO2 output in the group supplemented with alphaprodine increased from about 100 to 130 ml/m2/min, the halothane group showed a constant CO2 output of about 90 ml/m2/min followed by a significant rise within 5 minutes after halothane was discontinued. In 42 patients on controlled ventilation, no significant difference was found in the CO2 output estimated one hour after induction of anaesthesia in nitrous oxide-oxygen anaesthesia supplemented by halothane, ethrane or alphaprodine. The values obtained were 87 +/- 11 ml/m2/min for halothane (11 patients), 98 +/- 19 ml/m2/min for ethrane (14) and 93 +/- 13 ml/m2/min for the narcotic supplemented anaesthesia (17). The mean CO2 output for all 42 patients was 93 +/- 14 ml/m2/min. Six markedly obese patients under the same anaesthetic technique had a CO2 output of 114 +/- 17 ml/m2/min; however, their CO2 output was similar to normal patients when calculated on the basis of body weight. A marked increase in CO2 output to a mean of 160 +/- 25 ml/m2/min was found in eight patients undergoing operation while on hyperalimentation. The technique described appears suitable to monitor CO2 output under anaesthesia. In order to avoid hypercarbia when using a partial rebreathing system, the fresh gas inflow must be increased above recommended values in cases with increased metabolic activity (e.g. patients receiving hyperalimentation). In obese patients the fresh gas inflow should be calculated on the basis of body weight.
 ...
PMID:Carbon dioxide output in anaesthesia. 125 73


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>