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)

Hypercarbia was induced in 12 patients anesthetized with either halothane or fluroxene in an inspired concentration of approximately 1.3 MAC (1% halothane and 4-5% fluroxene). The six patients receiving halothane anesthesia responded to hypercarbia with a pronounced tachycardia, an increased arterial pressure and an electrocardiographically monitored threshold level for ventricular arrhythmias at a Paco2 level averaging 98 mmHg. The six patients receiving fluroxene anesthesia responded to hypercarbia with both tachycardia and hypertension, but in spite of an average Paco2 level of 109 mmHg, no ventricular arrhythmias could be provoked. It is therefore suggested that within the non-narcotic level of hypercarbia a threshold level for cardiac arrhythmias does not exist under fluroxene anesthesia.
 ...
PMID:Effects of respiratory acidosis on the arrhythmia threshold during fluroxene and halothane anesthesia. 23 95

We investigated the impact of enflurane and halothane (1.1 MAC) on heart rate and blood pressure responses to experimental hypoxaemia (PETo2 6.0 kPa [45 torr]) and small increments in PCO2 (1.3--1.6 KPa [10--12 torr]). The results reaffirm that circulatory signs of mild hypercarbia are vitually abolished by these anaesthetics. The important new observation is that signs of acute moderate hypoxaemia are also markedly depressed. Although potential modifying factors such as surgical stimulation were not evaluated, this study indicates that human subjects anaesthetized with enflurane or halothane lack reliable cardiovascular signs of acute hypoxaemia.
 ...
PMID:Cardiovascular signs of acute hypoxaemia and hypercarbia during enflurane and halothane anaesthesia in man. 50 44

To elucidate the effects of halothane on chemical regulation of ventilation in man, the authors studied the ventilatory responses to isocapnic hypoxia and hyperoxic hypercapnia in 33 human subjects while fully conscious and during sedation or anesthesia with halothane, .1, 1.1, or 2 MAC. In each group, the ventilatory effect of intravenous administration of doxapram, .4 mg/kg, was also measured. Halothane, 1.1 and 2 MAC, totally abolished the hypoxic response and nearly abolished the response to doxapram, while leaving the response to CO2 relatively brisk. Halothane, .1 MAC, decreased the responses to hypoxia and doxapram to less than a third of control, but did not alter the response to CO2. It is concluded that halothane selectivity impairs two ventilatory responses mediated by peripheral chemoreceptors in man.
 ...
PMID:Ventilatory responses to hypoxia and hypercapnia during halothane sedation and anesthesia in man. 69 78

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in six dogs each with a tracheostomy, awake and during anaesthesia with halothane, enflurane and isoflurane (1-2.5 MAC). Isocapnic hypoxic ventilatory response (HVR) was expressed as the parameter A, such that the greater the value of A, the greater the hypoxic response. In the anaesthetized dogs HVR (A) was reduced significantly from the awake value of 2010 +/- 172 (mean + SEM) to 630 +/- 173 by 1 MAC halothane, 495 +/- 105 by 1 MAC enflurane and 952 +/- 157 by 1 MAC isoflurane (PL0.05). All three anaesthetic agents produced significant depression of HUR at 1 MAC, but enflurane was more depressant than isoflurane. At 1.5 MAC all three anaesthetics produced equal and significant depression of HVR at equianalgesic concentrations. Further increases in anaesthetic concentration caused no increase in depression. Hypercapnic drive, as measured by the slope of the VE/PACO2 response curve, was reduced significantly from 9.75 litre min-1 kPa-1 +/- 2.4 in awake dogs to 0.83 +/- 0.56 after 1 MAC halothane, 0.68 +/- 0.53 after 1 MAC enflurane and 1.58 +/- 0.75 after 1 MAC isoflurane. In addition, hypercapnia-induced augmentation of the hypoxic drive was abolished by 1 MAC halothane or enflurane and diminished markedly by 1 MAC isoflurane. It may be clinically significant that hypoxia and hypercapnia during anaesthesia with these agents did not produce optimal stimulation of ventilation.
 ...
PMID:Depression of hypoxic ventilatory response by halothane, enflurane and isoflurane in dogs. 92 74

The effects of halothane and enflurane anesthesia under conditions of normo-, hyper-, and hypocarbia on the autoregulation of cerebral blood flow (CBF) in the goat were evaluated. The goat was selected because of its unique arterial blood supply to the head and the development of a method by which CBF may be continuously measured. The study revealed that 1 MAC of halothane or enflurane anesthesia at normocarbia abolished cerebral autoregulation, CBF increasing or decreasing with increasing or decreasing peripheral blood pressure. Reduction of anesthesia to 0.5 MAC partially restored cerebral autoregulatory capability. The effect of 1 MAC and 0.5 MAC anesthesia on cerebral autoregulation of blood flow was potentiated by hypercarbia and antagonized by hypocarbia, indicating that the vascular response to blood CO2 fluctuations remained intact.
 ...
PMID:Absence of autoregulation of cerebral blood flow during halothane and enflurane anesthesia. 94 20

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 normal ventilatory response to the sudden imposition of sustained hypoxia is characterized by an acute increase followed by a modest decline in ventilation. Since subanesthetic concentrations of potent inhalational anesthetics greatly attenuate the acute response, we hypothesized that ventilation might decrease to less than normoxic levels when hypoxia is sustained. We therefore measured the ventilatory response to 20 min of sustained hypoxia (PETO2 45 mmHg) at two levels of strict isocapnia--normocapnia (PETCO2 1-2 mmHg above resting) and hypercapnia (PETCO2 49 mmHg)--in eight healthy male subjects during inhalation of 0.1 MAC isoflurane or carrier gas (control). An abrupt end-tidal step from normoxia to isocapnic hypoxia was induced using a dynamic end-tidal forcing system. Isoflurane and control experiments were performed on separate days; the order of isoflurane and control days and the order of normocapnia and hypercapnia within days were randomized. Subjects were studied while fasted, always at the same time of day, and were required to watch a documentary videotape to minimize differences in level of consciousness. With normocapnia, there was no difference in ventilation at any time between isoflurane and control (prehypoxic 9.6 +/- 1.5 vs. 9.5 +/- 2.6 1/min, peak hypoxic 24.7 +/- 10.4 vs. 26.2 +/- 10.4 1/min, final hypoxic 15.0 +/- 4.4 vs. 15.9 +/- 3.5 1/min; mean +/- SD). With hypercapnia, prehypoxic ventilation increased to the same level for isoflurane and control (24.8 +/- 6.7 vs. 24.8 +/- 9.6 1/min). Although peak hypoxic ventilation was slightly less in isoflurane than in control hypercapnic experiments, this was not significant (49.6 +/- 16.3 vs. 56.5 +/- 24.3 1/min; P = .22).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Does a subanesthetic concentration of isoflurane blunt the ventilatory response to hypoxia? 146 64

Rings of canine bronchi were studied in vitro to determine the effects of halothane on the responses of airway smooth muscle to hypercapnia and hypocapnia. Bronchi were first contracted to 50% of maximal active force with acetylcholine (ACh), 5-hydroxytryptamine (5HT), potassium chloride (KCl), or the muscarinic agonist McN-A-343 (McN). The CO2 concentration of the bathing solution was then changed from 6% to either 1% (hypocapnia) or 10% (hypercapnia). In the absence of halothane, changes in CO2 concentration had no significant effect on muscles contracted with ACh. With all other contractile agonists, increasing the CO2 concentration caused bronchial relaxation, while decreasing the CO2 concentration caused contraction. In the presence of 2 MAC halothane, hypocapnia relaxed bronchi contracted with the muscarinic agonists ACh or McN; the responses to hypocapnia of bronchi contracted with KCl and 5HT were not significantly changed by halothane. Halothane had no effect on the responses of the bronchi to hypercapnia. We conclude that airway smooth muscle contracted with cholinergic agonist relaxes in response to hypocapnia when exposed to 2 MAC halothane; this mechanism may contribute to the depression of hypocapnic bronchoconstriction caused by halothane in vivo.
 ...
PMID:Halothane alters the response of isolated airway smooth muscle to carbon dioxide. 156 97

The electroencephalographic (EEG) effects of a new inhaled anesthetic are of interest because of the potential of such agents to produce excitatory (convulsant) activity and because of the potential usefulness of the EEG as an indicator of anesthetic depth and cerebral activity. Accordingly, we examined the EEG in 12 healthy, young male volunteers during desflurane anesthesia. Each subject had a baseline recording and then steady-state exposure to 6, 9, and 12% (0.83, 1.24, and 1.66 MAC) desflurane in O2 alone, and to 3, 6, and 9% desflurane in O2 with 60% N2O. The sequence of doses and the presence of N2O were randomized. We used mechanical ventilation to maintain normocapnia at each dose level. We also tested the effects of hypercapnia secondary to spontaneous ventilation. Additionally, at 1.24 MAC, subjects' lungs were hyperventilated to a PCO2 of 25.8 +/- 0.7 mmHg and exposed to rhythmic, loud clapping to attempt to provoke excitatory phenomena. Finally, after at least 6 h exposure to desflurane, we repeated measurements at 0.83 and 1.66 MAC to assess possible tolerance. Four channels of EEG were monitored visually, and at each dose, a quantitative EEG analysis was performed. Desflurane produced EEG changes comparable to those observed with equipotent levels of isoflurane. No epileptiform activity was seen. Desflurane significantly suppressed EEG activity; prominent burst suppression was seen at 1.24 MAC and higher. Substitution of N2O for 0.42 MAC desflurane reduced the degree of EEG suppression relative to the equipotent administration of desflurane and O2. Quantitative EEG measures for the early doses and for the later, repeated exposures did not differ.
 ...
PMID:The electroencephalographic effects of desflurane in humans. 200 Oct 21

The changes in intracranial pressure which occur following a change in one of the constituent volumes within the skull are governed by the Monro-Kellie doctrine, stated in the late 18th century and describes how an increase in one of the constituent volumes must be reflected by a reciprocal decrease in another volume to avoid any change in pressure and that if this does not occur, there is a rapid rise in intracranial pressure. Cerebral blood flow is affected by many physiological and pharmacological factors, and is relevant as a change in cerebral blood flow results in a similar alteration in cerebral arterial volume which will affect intracranial dynamics. Another important concept to be understood is cerebral perfusion pressure, how it is related to intracranial and arterial pressures and its relevance during the conduct of any neuroanaesthetic. Both carbon dioxide and the volatile agents are potent vasodilating agents and will cause a catastrophic rise in intracranial pressure and fall in cerebral perfusion pressure if hypercapnia develops in the presence of more than one MAC of a volatile agent. The volatile agents are reviewed and it is stressed that while isoflurane may have advantages over the older volatile agents it is not without complication and nitrous oxide which has always been regarded as an innocuous agent may also have some significant intracranial affects. The use of propofol, as an infusion and the neuromuscular blocking agents and narcotics are described. Recently the use of induced hypotension during clipping of cerebral aneurysms has been questioned and this view and the treatment of vasospasm is discussed in some detail.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Neuro anaesthesia--a review of the basic principles and current practices. 222 16


1 2 3 4 Next >>