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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemodynamic characteristics, arrhythmogenicity, and dose-related hemodynamic responses to intravenous dopamine (group I) and dobutamine (group II) were examined in 16 swine at three different core body temperatures (38.5 degrees C, 35 degrees C, and 30 degrees C). The animals were anesthetized with isoflurane and mechanically ventilated. Cooling and re-warming were accomplished by a femoral-jugular A-V shunt. The animals were cooled down to 30 degrees C and stabilized for 1 hour before intravenous infusion of dopamine (group I, n = 8) or dobutamine (group II, n = 8) was started at 2, 5, 10, 15, 20, and 30 micrograms/kg/min. Hemodynamic responses to the two inotropes were continuously monitored with a bedside monitor equipped with a PC mode for customized data collection and analysis. Computerized arrhythmia detection was performed. Our findings were: (1) profound hypothermia (30 degrees C) causes significant depression of hemodynamic functions; (2) IV infusion of dopamine and dobutamine can be used safely and effectively for inotropic support during profound hypothermia, and the optimal dosage for improving cardiac output is 10-20 micrograms/kg/min; (3) no risk of inducing arrhythmia was noted with IV infusion of both inotropes up to a maximum dosage of 30 micrograms/kg/min, even though significant sinus tachycardia was consistently seen at 30 micrograms/kg/min.
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PMID:Effects of hypothermia on hemodynamic responses to dopamine and dobutamine. 146 14

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Sinus node responses to perfusion pressure changes, ischaemia and hypothermia were evaluated in 22 isolated blood-perfused dog atria. Sinus cycle length (SCL) was measured and sinoatrial conduction time (SACT) was estimated using the premature atrial stimulation technique (PAS) and the constant atrial pacing method (CAP). There was a good correlation between the results obtained with both techniques (r = 0.8297) but CAP had less depressing action on sinus node automaticity. Increasing the perfusion pressure from 100 to 200 mmHg did not influence estimated SACT nor SCL. However, a reduction in perfusion pressure (from 100 to 50 mmHg) markedly shortened SCL without significantly decreasing estimated SACT. Lowering temperature from 37 to 25 degrees C caused a linear increase in estimated SACT and SCL. Occlusion of the sinus node artery induced a sinus tachycardia which was not blocked by sotalol. Estimated SACT was significantly shorter 1 min after occlusion and longer 3 min after occlusion; this increase was significantly inhibited by atropine infusion. Thus, the increase in estimated SACT seen after occlusion might be related to cholinergic activity. However, the sinus tachycardia following a decrease in perfusion pressure might be due to activation of the stretch-receptors while the one seen after reduction in blood flow and occlusion of the sinus node artery seems more likely to be a consequence of ischaemia.
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PMID:Sinus node responses to perfusion pressure changes, ischaemia and hypothermia in the isolated blood-perfused dog atrium. 398 49

Clostridium botulinum can colonize and produce botulinal toxin in the human infant intestine, which the toxin then permeates to cause generalized flaccid paralysis, and occasionally, sudden death. This study was undertaken to test the hypothesis that toxins produced by other intestinal clostridia, e.g., C. difficile, might also cause systemic illness and sometimes death in infants (J Pediatr 100:568, 1982). Because this hypothesis could not be evaluated clinically until the systemic manifestations of C. difficile toxins in primates were known, infant rhesus monkeys were given 6 to 11 micrograms/kg of the recently purified C. difficile toxins A or B, either intravenously or intraperitoneally. The animals showed no abnormalities for several hours, but then developed lethargy, hypotonia, hypothermia, and, shortly before death, sudden elevation of serum concentrations of potassium, magnesium, and phosphorus and of enzymes that derived mainly from skeletal muscle, heart and brain. Five of six animals died quietly 3.5 to 8.0 hours after onset of symptoms. Death appeared to result from cessation of breathing, after which the sinus tachycardia then deteriorated to a flat ECG. Necropsy findings were insufficient to explain the cause of death. It appears that in infant monkeys microgram amounts of C. difficile toxins A and B can produce a rapid quiet death, the cause of which is undetectable at necropsy, a situation pathologically reminiscent of crib death in human infants, although the possible clinical identity of these two conditions has yet to be established.
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PMID:Rapid death of infant rhesus monkeys injected with Clostridium difficile toxins A and B: physiologic and pathologic basis. 669 Jun 74

The author reviewed records of 10 patients who had experienced acute loxapine overdose. The most frequent medical complications were CNS depression, sinus tachycardia, hypertension, and hypothermia; 6 patients had had generalized major motor seizures, 1 had had recurrent paroxysmal atrial tachycardia, and 2 had had transient renal insufficiency from rhabdomyolysis and myoglobinuria. Other clinical effects from loxapine overdose were predominantly anticholinergic. The author recommends that loxapine-overdose patients receive ECG monitoring and treatment of medical complications in an intensive care unit.
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PMID:Seizures induced by acute loxapine overdose. 725 88

Fifty patients with drug-resistant, recurrent tachyarrhythmias causing Wolff-Parkinson-White syndrome underwent surgery between 1990 and 1992. All recognized surgical methods for accessory pathway destruction were performed. Epicardial electric shock ablation was first used as a method of surgically destroying an accessory atrioventricular pathway in 1983. This technique avoids the need for cardioplegia and hypothermia during operation. The procedure is based on the application of a series of two to five electrical shocks (50-150 J) to the region of the atrioventricular groove where the accessory pathway has been previously located. Some 32 patients with a left free wall accessory pathway underwent this operation. Cardioplegia and hypothermia were not required in 22 patients with an accessory pathway located in the left lateral position. In the second group comprising ten patients with a left lateral accessory pathway, four were diagnosed as having a second pathway and four had concomitant heart pathology such as coronary artery disease -- one had an atrial septal defect and another had a ventricular septal defect. Accessory pathway ablation was carried out in these ten patients using epicardial electric shock under normothermic cardiopulmonary bypass. Concomitant heart pathology was corrected at the second stage of the operation under cardiopulmonary bypass with cardioplegia and hypothermia. Postoperative electrophysiological studies confirmed that the accessory pathway had been destroyed in all patients. The only side effects of epicardial electric shock application were transient ST elevation < 1 mm in four patients, transient atrioventricular bloc in two and moderate sinus tachycardia in three.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epicardial electric shock ablation of the left lateral accessory pathway. 857 41

During winter time in the period from 1993 to 1998, 18 elderly patients: 11 female and 7 male aged 65-88 years, were treated because of hypothermia. Rectal temperature on admission was 20-34.5 degrees C. Ten patients suffered from moderate hypothermia (35-32 degrees C), and eight suffered of severe hypothermia (< 32 degrees C). Arterial hypotension was recorded in 7, and shock in 11 patients. In all of them, and in 18 controls, an electrocardiogram was analyzed with the special reference to the corrected Q-T interval. Decompensated metabolic acidosis was observed in 7/8 patients with severe hypothermia and in 4/10 with moderate hypothermia. Among patients with moderate hypothermia, sinus tachycardia was present in 2, sinus bradycardia in 2, idioventricular rhythm in 2 and atrial fibrillation in 4/10 patients. In patients with severe hypothermia, sinus tachycardia was present in 2, sinus bradycardia in 3, idioventricular rhythm in one, and atrial fibrillation in 2/8 patients. In moderate hypothermia Osborn's or Tomaszewski's J wave was present in 7/10, and it only appeared in 3/10 patients; in severe hypothermia it was present in 6/8 and only appeared in 2/8 patients. The corrected Q-T interval in the group with hypothermia ranged 0.450-0.688 s, in the control group 0.343-0.444 s. The X minimum (s) in the group with hypothermia was 0.508 +/- 0.079, in the control group it was 0.371-0-139 s, and the difference was statistically significant (p < 0.001). The X maximum (s) in the group with hypothermia was 0.576 +/- 0.067 s, in the control group 0.390 +/- 0.019 s, and the difference was also statistically significant (p < 0.0001). In both groups the most significant prolongation of the corrected Q-T interval in the majority of patients was found in anteroseptal leads. The dispersion of the corrected Q-T interval in the group with hypothermia was 87.19 +/- 28.44 ms, in the control group it was 32.06 +/- 8.94 ms, and the difference was statistically significant (p < 0.001).
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PMID:The corrected Q-T interval in the elderly with urban hypothermia. 1064 46

A 20-year-old woman with borderline personality disorder was referred to the emergency department by a psychiatric clinic. After taking 10 g of nutmeg she complained of stomach ache and dizziness. A physical examination showed mild hypothermia and sinus tachycardia. She was admitted for observation and discharged after 24 h to the psychiatric clinic without sequelae. Nutmeg is a spice. Relatively unknown are the hallucinogenic and euphoric effects for which it is used by drug abusers and students. Symptoms appear 6 h after ingestion of at least 10 g of nutmeg and are related to its effects on the central nervous system. Use of the drug can lead to anxiety and feelings of doom and even to psychosis. Dry mouth, nausea and dizziness may also occur. A physical examination may show hypothermia, tachycardia or hypertension or, in rarer cases, hypotension and shock. Symptoms disappear without sequelae after 24-48 h. Treatment consists of supportive measures. In the event of haemodynamic instability, cardiovascular monitoring is indicated.
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PMID:[Unusual use of nutmeg]. 2085 16

A 27-year-old woman with a history of depression and previous overdose presented within 60 min of ingestion of 50 g of caffeine powder. Initially alert but hypotensive and tachycardic, the patient developed a broad complex tachycardia followed by a seizure and multiple ventricular fibrillation (VF) arrests. Following multiple defibrillations for VF, eight cycles of cardiopulmonary resuscitation and treatment with amiodarone, lidocaine, magnesium and potassium supplementation, the patient went to the intensive care unit (ICU). While there, the patient had further VF and required haemofiltration for a profound metabolic acidaemia with cardiac rhythm instability. She developed a postcardiac arrest systemic inflammatory response syndrome with episodes of acute pulmonary oedema, profound vasoplegia, hypothermia and coagulopathy. After 5 days in the ICU, the patient was stable enough to be transferred to the ward, with a persistent sinus tachycardia, and was discharged 3 days later with cardiology and psychiatry follow-up.
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PMID:Survival of a highly toxic dose of caffeine. 2339 22

BACKGROUND The clinical presentation of pulmonary embolism (PE) is highly variable, ranging from no symptoms to shock or sudden death, often making the diagnosis a challenge. An electrocardiogram (EKG) is not a definitive diagnostic tool; however, it can alter the clinical suspicion of acute PE. PE has nonspecific electrocardiographic patterns ranging from a normal EKG in almost 33% of patients to sinus tachycardia, S1Q3T3 pattern (McGinn-White Sign), right axis deviation, and incomplete right bundle branch block (RBBB). ST-segment elevation associated with PE is exceedingly rare, and to date, only a few cases have been reported. CASE REPORT We present a case of a middle-aged male patient with no medical comorbidities other than obesity, who presented with initial symptoms and EKG findings concerning an ST-elevation myocardial infarction (STEMI). He was later found to have rather patent coronary arteries on cardiac catheterization but bilateral sub-massive pulmonary embolism on computed tomography angiogram (CTA) of the chest. CONCLUSIONS The differential diagnosis of STEMI is broad, including, but not limited to, Prinzmetal's angina, takotsubo cardiomyopathy, Brugada syndrome, left ventricular aneurysm, hypothermia, hyperkalemia, and acute pericarditis. Pulmonary embolism may present with abnormal EKG and biomarkers that appear to be an acute coronary syndrome, even STEMI. Physicians must maintain a high index of clinical suspicion through risk stratification to identify PE in these settings, as the frequency of such an occurrence is extremely low. A bedside echocardiogram can be an invaluable diagnostic tool in such cases.
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PMID:Pulmonary Embolism Presenting as ST-Elevation Myocardial Infarction: A Diagnostic Trap. 3324 83


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