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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This retrospective study was undertaken to examine the management and outcome of children who developed isolated masseter muscle spasm (MMS) after the administration of intravenous succinylcholine during anesthetic induction. The inhalation anesthetics used for induction were continued in all of these cases. The medical records of 68 patients (male/female ratio, 1.7:1), identified from approximately 42,000 anesthetics given during the period 1980-1989, were reviewed. Fifty-seven children (2.3-12 yr old) were diagnosed as having isolated MMS, i.e., MMS without spasm of other muscles; 11 experienced generalized rigidity in combination with MMS. Anesthetic and postoperative management of these two groups differed. The overall incidence of MMS was 0.3% of inhalation anesthetics during which succinylcholine was given. Intraoperative arrhythmias occurred in 33% of the patients who developed isolated MMS and more frequently in older children. Most children experienced some degree of hypercarbia and/or metabolic acidosis, but the significance of these abnormalities in the spontaneously ventilating, fasting child is unknown. Serum creatine kinase levels when measured 18-24 h postoperatively were elevated in all but one child (n = 45). There was no long-term morbidity and no mortality. We conclude that failure of the masseter muscles to relax after succinylcholine is not uncommon in children. Based on our experience, and accepting that MMS may be part of the clinical spectrum of malignant hyperthermia, we believe that anesthesia can be continued safely in cases of isolated MMS when careful monitoring accompanies diagnostic evaluation. This differs from the current practice of discontinuing the anesthetic or switching to a nontriggering anesthetic technique.
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PMID:Masseter muscle spasm in children: implications of continuing the triggering anesthetic. 186 39

In a study of 100 patients undergoing rigid bronchoscopy under intravenous general anaesthesia with oxygen Venturi ventilation no major complications were observed. Minor complications included one adverse reaction to alphaxalone-alphadolone acetate (Althesin), one prolonged episode of laryngeal spasm after removal of the bronchoscope, and subsequent muscle pain attributed to suxamethonium in 36 patients. The last complication occurred significantly less frequently (p less than 0 . 025) in those patients who were pretreated with a small dose of a non-depolarising neuromuscular blocking agent. Serial arterial blood gas sampling in 10 patients showed adequate ventilation during bronchoscopy, but carbon dioxide retention developed in nine cases immediately after the bronchoscope was withdrawn. With adequate precautions, however, the procedure is safe and well tolerated, even in patients with severe impairment of respiratory function.
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PMID:Rigid bronchoscopy under intravenous general anaesthesia with oxygen Venturi ventilation. 681 87

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.
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PMID:Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates. 682 30

A 6-year old female child received succinylcholine (1 mg.kg-1) and isoflurane (concentrations of 1.5-2 percent) and developed at the end of surgery a hypermetabolic syndrome suggestive of malignant hyperthermia (MH) with masseter muscle spasm, muscle rigidity, tachypnea, systolic hypertension (140 mm Hg), tachycardia (205 beats.min-1), hypercarbia (end expiratory CO2 71 mmHg), and an increase in body temperature (39.2 degrees C). The child responded well to therapy which included cooling, hyperventilation with pure oxygen and dantrolene administration. However, blood creatine kinase and myoglobin elevations were moderate (respectively 375 IU.L-1 and 114 micrograms.L-1) and an in vitro halothane and caffeine contracture test was negative. Differential diagnostic proposals are discussed and compared to the clinical incident.
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PMID:Malignant hyperthermia suggestive hypermetabolic syndrome at emergence from anesthesia. 871 51

The impedance of a hemodynamic system is defined as the ratio of each harmonic component of blood pressure to that of flow. Calculation of impedance cures has been extensively performed in the systemic circulation, leading to the recognition of reflected pressure and flow waves and clarifying the shape of ultrasound waveforms. Impedance in the human cerebral circulation has not been measured primarily because of the relative inaccessibility of simultaneous flow and pressure data in the human cerebral circulation. We defined an impedance index using the transcranial Doppler waveform for that of flow and a noninvasive applanation measure of the carotid artery pressure waveform. Middle cerebral artery velocities and carotid artery pressure waveforms were simultaneously recorded in 16 vessels from 10 normal volunteers, 42 vessels in 14 patients with aneurysmal subarachnoid hemorrhage, and 14 vessels in 7 subjects during conditions of hypocapnia, normocapnia and hypercapnia. Impedance was calculated by dividing the harmonic associated with pressure divided by that of flow, and averaging 10 to 20 such calculations. Relative impedance curves were calculated by dividing by the impedance at the first harmonic. Impedance was also studied in an electrical model consisting of a Windkessel element containing inductance in series with a second Windkessel to model the large vessel and vascular bed, respectively. Model parameters were taken from the literature for these calculations. For the normal subjects, the shape of the impedance index curve was similar to those found in the systemic circulation. The impedance index curves for patients in vasospasm (middle cerebral velocity was greater than 180) showed a peak at the second or third harmonic, which appeared more frequently than the nonspasm group (p < 0.01). Furthermore, the ratio of the second harmonic to the first harmonic was significantly > 1.0 in the spasm group but significantly < 1.0 in the normal group (p < 0.05). Calculations from the electrical model replicated the appearance of these peaks at the second or third harmonic for vasospasm parameters. A statistically significant peak appeared at the second or third harmonic in the impedance index curves for patients in vasospasm, which was replicated quantitatively by our electrical model. Although such peaks can be explained in the systemic circulation by the presence of reflected waves, the distance to the reflection site is larger than expected for the cerebral circulation. This suggests the importance of the inertia of blood as a stenosis worsens and as the origin for the observed changes in the impedance index curves.
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PMID:An impedance index in normal subjects and in subarachnoid hemorrhage. 1105 55

1. Mechanisms that regulate the cerebral circulation have been intensively investigated in recent years. The role of several vasodilator mechanisms has been examined in the cerebral circulation, including nitric oxide (NO), trigeminal peptides and potassium channels, as well as the potent vasoconstrictor endothelin. These mediators appear to play a role in physiological and pathophysiological responses of the cerebral circulation. In the present review, we will focus on some recent developments in each of these areas. 2. Nitric oxide is an important regulator of cerebral vascular tone. Tonic production of NO maintains the cerebral vasculature in a dilated state. NO appears to be an important vasodilator during activation of neurons by excitatory amino acids, somatosensory stimulation and cortical spreading depression. Tonic production of NO appears to be critical in vasodilatation during hypercapnia, although NO may not directly mediate vasodilatation. NO produced by immunological NO-synthase appears to be important in dilatation following exposure to bacterial endotoxin. 3. Calcitonin gene-related peptide (CGRP), released from trigeminal perivascular sensory nerves in the brain, is an extremely potent dilator of brain vessels. CGRP may limit noradrenaline-induced constriction of cerebral vessels and contribute to dilatation during hypotension (autoregulation), reactive hyperaemia, seizures and cortical spreading depression. 4. Activation of potassium channels leads to hyperpolarization of cerebral vascular smooth muscle and appears to be a major mechanism for dilatation of cerebral arteries. Agents that increase the intracellular concentration of cyclic 3' 5'-adenosine monophosphate (cAMP) produce vasodilatation in part by activation of large conductance calcium-activated potassium channels (BKCa) and ATP-sensitive potassium channels (KATP). Activation of both KATP and BKCa channels also appears to contribute to vasodilatation during hypoxia. In contrast to KATP channels, BKCa channels appears to be active under basal conditions, contributing to tonic dilatation of cerebral blood vessels. 5. Endothelin is produced in the brain, but its role in the physiological regulation of cerebral blood flow is not known. Endothelin may contribute to the spasm of cerebral arteries following subarachnoid haemorrhage.
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PMID:Recent insights into the regulation of cerebral circulation. 880 May 65

A high incidence of unsuccessful attempts and complications has been reported when emergency tracheal intubation (ETI) is performed outside the hospital in severely injured children. The aim of this prospective series was to analyse the incidence and related risk factors of complications of emergency tracheal intubation. The time to complete successful ETI and occurrence of incidents, e.g. cough reflex, hypoxia or spasm were related to the experience of the physician performing intubation and the use of drugs to facilitate ETI. The incidence of hypoxia, hypercarbia, postintubation complications such as extubation stridor and long-term sequelae were noted. Of the 188 children, 78% were successfully intubated at the site of the accident, 10% upon arrival at a local hospital from where they were secondarily transferred and 12% upon admission to our trauma centre. The most severely injured children were intubated in the field in 98% of cases without failure, nor life-threatening complications related to ETI. The experience of the operator influenced the number of attempts and the time to complete successful intubation. Immediate incidents were noted in 25% of children, e.g. cough in 18%. The regimen of drugs, but not level of consciousness, influenced the incidence of immediate incidents; without drugs, more than 67% experienced incidents. Early tracheal intubation and controlled ventilation resulted in adequate ventilation upon arrival (mean PaO2 of 35.8+/-24 kPa, mean PaCO2 of 4.35+/-1 kPa). Long-term complications, including transient stridor upon extubation in 33% of the cases, and laryngeal granuloma or tracheal stenosis, were comparable to those in other series. ETI in shocked patients and pulmonary infection in hospital, but not the technique of ETI, increased the risks of long-term complications. Emergency tracheal intubation can be performed safely in the field, and results in adequate ventilation during transportation of severely injured children, provided that it can be performed by trained physicians using adequate drugs to facilitate intubation.
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PMID:Complications of emergency tracheal intubation in severely head-injured children. 1079 40

Malignant Hyperthermia (MH) has been a recognized complication of general anesthesia after the first case reports in the 1940's. Since then a great deal has been discovered about the genetics, pathophysiology and treatment of this once fatal syndrome. MH is the only clinical entity specifically related to and caused by anesthetic agents. MH once triggered during anesthesia results in a profound hyper metabolic state with rise in the core temperature, increased carbon dioxide production and oxygen consumption. Death will ensue if specific treatment is not started. The incidence of fulminant MH ranges from 1:62,000 to 1: 84,000 of general anesthesia cases if succinylcholine and inhalation agents are used. Massseter muscle spasm on induction of anesthesia, with an incidence of between 1:16,000 and 1:4,000, may be a predromal indication of the development of MH. Anesthetic agents, which may trigger MH in susceptible individuals, are the depolarizing muscle relaxant, succinyl choline and all the volatile anesthetic gasses. Nitrous oxide, intravenous induction agents, benzodiazepines, opioids, and the non-depolarizing relaxants do not trigger MH. MH susceptibility is associated with certain disorders, such as Duchene muscular dystrophy, and triggering agent should not be used in these patients. Inheritance is an autosomal dominant trait with variable penetrance. The pathogenesis of MH involves the loss of control of intracellular calcium ions in skeletal muscle with resultant protracted spasm and hyper metabolism. Clinically this will progress to hypercarbia, hypoxia, hyperthermia, hyperkalemia and death will result if specific treatment is not started. Management involves immediate discontinuation of the triggering anesthetics, hyperventilation with 100% oxygen and most importantly the definitive treatment with intravenous dantrolene.The importance of instigating the use of dantrolene in cases of MH cannot be overemphasized. MH is now treatable when once it would be fatal before the availability of dantrolene. Unless of an emergent nature, surgery should be canceled following the acute phase of MH. The patient should be admitted to intensive care for at least 24 hours and dantrolene continued as recurrence has been described. It is imperative that the patient and their family are counseled, Medalert bracelets provided and registration with the Malignant Hyperthermia Association of the United States (MHAUS), encouraged. The caffeine/halothane testing of muscle biopsies is currently the most definitive test for malignant hyperthermia susceptibility. The routine use in suspected cases or the immediate family of known cases remains a matter of contention.
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PMID:Malignant hyperthermia. 1450 52

Malignant hyperthermia (MH) is a rare but fatal complication that develops under general anesthesia. Reports on MH in patients over the age of 80 years are unusual. We experienced a case of MH in an 82-year-old patient during esophageal resection. Anesthesia was induced with propofol and succinylcholine, and maintained with sevoflurane. Neither masseter spasm nor rigidity of the limbs was seen during induction. Body temperature (BT) at induction was 36.0 degrees C. Three hours after incision, the level of end-tidal CO2 was elevated to 55 mmHg. We assumed that the rise in end-tidal CO2 had occurred due to secretions in the airway. However, the BT, which had risen at 3 h after incision, continued to rise, and about 60 min later, the BT exceeded 39.0 degrees C. A rise of more than 0.5 degrees C in less than 15 min was seen, and MH was suspected. With dantrolene administration, the BT decreased from 40.9 degrees C at maximum to 37.7 degrees C. With continuous infusion of dantrolene when the patient was transferred to the intensive care unit (ICU), BT remained within the normal range. The next day re-operation was performed, without further complications or recurrence of MH during the postoperative period. Because it is necessary to initiate treatment in the early stage of MH, as soon as possible, although MH prevalence is low in the elderly, it is important to suspect MH when hypercapnia and/or hyperthermia are seen.
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PMID:Malignant hyperthermia developing during esophageal resection in an 82-year-old man. 1901 91

The aim of the study was to establish ultrasound criteria of the differentiation between functional and morphological vasoconstriction of the vertebral artery (VA) using hypercapnia test in patients with signs of vertebral-basilar insufficiency. The inclusion criteria were the presence of clinical symptoms of vertebral-basilar disturbances of circulation and small diameter of VA (< or =2.9 mm). Fifty patients, aged from 17 to 57 years, were studied. Based on the form of Doppler 's spectrum of the blood flow in the small VA, patients were stratified into three groups: normal (N spectrum), peak-like split (PS spectrum) and high-resistance low-speed (HL spectrum). The increment of diameter by 0.2 mm and more, i.e. the functional vasoconstriction (spasm) during hypercapnia, was characteristic of patients with PS and N spectrum. The ROC-analysis revealed that the absence of VA increment during hypercapnia is a highly specific (90.9%) predictor of morphological vasoconstriction of VA. Quantitative criteria of VA hypoplasia were specified as well. Ultrasound angioscanning in the combination with hypercapnia test allows differentiation with a high probability between functional (spasm) and morphological (hypoplasia) vasoconstriction of VA.
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PMID:[Differential diagnosis of spasm and hypoplasia of the vertebral artery with ultrasound methods]. 2261 77


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