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

During CO2 hysteroscopy the intracavitary pressure increases up to 80 mmHg. This can result in a CO2 embolism, especially after injury/lesion of the endometrium. A 49-year-old female Caucasian patient underwent curettage, and the following day while a hysteroscopy was being performed in general anesthesia a CO2 embolism occurred, with bradyarrhythmia, drop of arterial blood pressure, superior vena cava syndrome, metallic heartsound and hypercapnia. It was possible to achieve recompensation of the right heart failure with drug therapy. Other causes (lung embolism, hypoventilation, increased CO2 production, cardiac causes) could be excluded.
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PMID:[CO2 embolism during hysteroscopy]. 211 Nov 2

The authors made two series of experiments in rabbits, using liquid ventilation. The first group was ventilated manually using RM 101 solution with an equilibration period of 30 and 60 sec., Tv = 10 ml/kg after previous administration of 30 ml/kg RM 101 at the beginning. The second group was ventilated using a specially developed liquid ventilator--part of the animals was ventilated with an equilibration interval of 30-90 sec., Tv = 10 ml/kg with administration of an initial dose od 30 ml/kg of RM 101 solution, a part of the animals in a continual manner, i.e. without an equilibration period and without administration of the initial dose of the solution. From the results it is apparent that the optimal way as regards blood gases and minimal manner of liquid ventilation. When this method was used during the 180 minutes of liquid ventilation paO2, paCO2 and pH were within the normal range. The other methods of liquid ventilation led rapidly to hypercapnia and a drop of pH as well as to serious changes in the circulation (hypertension, bradyarrhythmia).
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PMID:[Liquid ventilation. 2]. 813 49

Birth asphyxia represents a serious problem worldwide, resulting in 1 million deaths and an equal number of neurologic sequelae annually. It is therefore important to develop new and better ways to treat asphyxia. In the present study we tested the effect of reoxygenation with room air or 100% oxygen following experimental pneumothorax induced asphyxia on blood oxidative stress indicators, early neurologic outcome and cerebral histopathology of newborn piglets. 26 animals were studied in three experimental groups: sham-operated (SHAM, n = 6), reoxygenation with room air after pneumothorax (RORA, n = 10) and reoxygenation with 100% oxygen after pneumothorax (RO100, n = 10). In RORA and RO100 asphyxia was induced under anesthesia with bilateral intrapleural room air insufflation. Gasping, bradyarrhythmia, arterial hypotension, hypoxemia, hypercarbia and severe combined acidosis occurred 62 +/- 6 (RORA) and 65 +/- 7 min (RO100) after the start of the experiments, when the pneumothorax was relieved and ten min of reoxygenation period was started with mechanical ventilation with room air (RORA) or 100% oxygen (RO100). Then the spontaneously breathing animals were followed on room air during the next three hours. Blood oxidative stress indicators--as oxidized and reduced glutathione, plasma hemoglobin and malondialdehyde concentrations--were also measured at different stages of the experiments and early neurologic examinations (neurological score: 20 = normal, 5 = brain dead) were performed at the end of the study. Then the brains were fixed and stained. In SHAM blood gases and acid/base status differed significantly from values measured in RORA and RO100. In RO100 PaO2 was significantly higher at 5 (13.8 +/- 1.8 kPa) and 10 min (13.2 +/- 2.0 kPa) than in RORA (8.7 +/- 0.9, 9.2 +/- 1.0 kPa), respectively. All the measures of oxidative stress indicators remained unchanged in the study groups (SHAM, RORA, RO100). Neurologic examination scores from SHAM were 18 +/- 0, from RORA 13.5 +/- 1.0 and from RO100 9.5 +/- 1.3 (significant differences between SHAM and RORA and RO100, significant difference between RORA and RO100). Cerebral histopathology showed marked damage with similar severity in both asphyxiated groups. We conclude that blood oxidative stress indicators and cerebral histopathology did not differ significantly after 10 min reoxygenation either with room air or with 100% oxygen following pneumothorax induced asphyxia, but reoxygenation with 100% oxygen might impair the early neurologic outcome of newborn pigs.
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PMID:[Reoxigenation after neonatal asphyxia with 21% or 100% oxygen in piglets]. 1114 59

Although it is unwise to recommend any preanaesthetic drug or regimen to be used routinely without consideration for the individual patient, the procedure being undertaken or the other drugs that will be used during the anaesthetic, of all anaesthetic-related drugs that might be under review, atropine is probably one of the least 'toxic' and least likely to cause life-threatening complications when used correctly. In most small veterinary practices there isn't the luxury of a dedicated anaesthetist available to monitor and manage each anaesthetised patient and the best form of cardiac monitor available may be an audible rate monitor. In this situation the advantages combined with the usual indications probably far outweigh the disadvantages of using atropine prophylactically. If a choice must be made, a sinus tachycardia under anaesthesia is probably preferable to a profound bradyarrhythmia. Absolute contraindications for using atropine are rare; the drug, when used alone, has low incidence of toxicity at clinically recommended doses in dogs and cats. Further, the new inhalation agents available to veterinarians (enflurane and isoflurane) do not sensitise the heart to the effect of catecholamines, so that the predominance of sympathetic tone produced when atropine is used is unlikely to precipitate dysarrthythmias during gaseous anaesthesia. Rhythm disturbances that occur under halothane anaesthesia when atropine is used, suggest there is some other cause, or agent, that is arrhythmogenic, such as an alpha 2 agonist, excessively deep level of anaesthesia, hypercapnia or hypoxaemia. Notwithstanding the above arguments, my preference, as a specialist anaesthetist, is that a drug is given only as required (not before) and that when, for example, any unusual heart rhythm occurs, all possible reasons for the occurrence (such as excessively deep anaesthesia or hypoventilation) are eliminated before other drugs like atropine or antiarrhythmics are administered.
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PMID:Preanaesthetic use of atropine in small animals. 1122 64

Birth asphyxia is a serious problem worldwide, resulting in 1 million deaths and an equal number of neurologic sequelae annually. It is therefore important to develop new and better ways to treat asphyxia. In the present study we tested the effects of reoxygenation with room air or with 100% oxygen (O2) after experimental pneumothorax-induced asphyxia on the blood oxidative stress indicators, early neurologic outcome, and cerebral histopathology of newborn piglets. Twenty-six animals were studied in three experimental groups: 1) sham-operated animals (SHAM, n = 6), 2) animals reoxygenated with room air after pneumothorax (R21, n = 10), and 3) animals reoxygenated with 100% O2 after pneumothorax (R100, n = 10). In groups R21 and R100, asphyxia was induced under anesthesia with bilateral intrapleural room air insufflation. Gasping, bradyarrhythmia, arterial hypotension, hypoxemia, hypercarbia, and combined acidosis occurred 62 +/- 6 min (R21) or 65 +/- 7 min (R100; mean +/- SD) after the start of the experiments; then pneumothorax was relieved, and a 10-min reoxygenation period was started with mechanical ventilation with room air (R21) or with 100% O2 (R100). The newborn piglets then breathed room air spontaneously during the next 3 h. Blood oxidative stress indicators (oxidized and reduced glutathione, plasma Hb, and malondialdehyde concentrations) were measured at different stages of the experiments. Early neurologic outcome examinations (neurologic score of 20 indicates normal, 5 indicates brain-dead) were performed at the end of the study. The brains were next fixed, and various regions were stained for cerebral histopathology. In the SHAM group, the blood gas and acid-base status differed significantly from those measured in groups R21 and R100. In group R100, arterial PO2 was significantly higher after 5 (13.8 +/- 5.6 kPa) and 10 min (13.2 +/- 6.3 kPa) of reoxygenation than in group R21 (8.7 +/- 2.8 kPa and 9.2 +/- 3.1 kPa). The levels of all oxidative stress indicators remained unchanged in the study groups (SHAM, R21, and R100). The neurologic examination score in the SHAM group was 18 +/- 0, in group R21 it was 13.5 +/- 3.1, and in group R100 it was 9.5 +/- 4.1 (significant differences between SHAM and R21 or R100, and between R21 and R100). Cerebral histopathology revealed marked damage of similar severity in both asphyxiated groups. We conclude that the blood oxidative stress indicators and cerebral histopathology did not differ significantly after a 10-min period of reoxygenation with room air or with 100% O2 after pneumothorax-induced asphyxia, but reoxygenation with 100% O2 might impair the early neurologic outcome of newborn piglets.
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PMID:Impaired early neurologic outcome in newborn piglets reoxygenated with 100% oxygen compared with room air after pneumothorax-induced asphyxia. 1138 43

The autonomic consequences of seizures can be severe. Death can follow from autonomic overactivity that causes a parasympathetically mediated bradyarrhythmia. We studied the cardiovascular consequences of unilateral and bilateral stimulation of the distal segments of transected vagus nerve in rats anesthetized with urethane. The range of stimulation rates tested is comparable to the firing rates observed in vagus nerve during seizures. There was a consistent inverse relation between stimulus rate and heart rate with nodal block appearing at 5-10 Hz and minimum HR levels (cardiac standstill) occurring at 50 Hz. Cardiac standstill could last many seconds. Blood pressure during VNS was maintained during lower frequency VNS, but collapsed at frequencies > or =20 Hz to dramatically impair ventricular filling. Recovery of heart rate and blood pressure after VNS was rapid. In the presence of sympathetic co-activation (pharmacological or hypercapnia and/or hypoxia), mean arterial pressure was better maintained and there was much better ventricular filling, but cardiac performance was worse (e.g. ejection fraction derived from echocardiography). The combination of sympathetic and parasympathetic overactivity was sometimes associated with prolonged (> or =20 s) apneic periods during VNS. We conclude that an abrupt increase in parasympathetic activity on the order of 5 times the background of parasympathetic tone can produce transient bradyarrhythmias, and increases on the order of 20 times can produce cardiac standstill, sometimes accompanied by apnea. Our findings suggest that parasympathetically mediated bradyarrhythmia must be accompanied by airway obstruction to sustain parasympathetic overactivity and produce hypoxia to ultimately cause death.
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PMID:Vagus nerve stimulation-induced bradyarrhythmias in rats. 1965 41