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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with a carcinoid tumour and a history suggestive of carcinoid syndrome, but with no biochemical evidence in support, had a cardiovascular collapse during an anaesthetic with propofol and suxamethonium. Subsequent investigations suggested an anaphylactoid reaction to suxamethonium, but there were features in common with a carcinoid crisis. The necessity for a second anaesthetic soon afterwards posed a dilemma. In the event of a similar reaction during another anaesthetic, a management plan beforehand should include ready availability of appropriate drugs and the use of sympathomimetic drugs that are less likely to exacerbate the situation.
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PMID:Anaphylactoid or carcinoid? 750 93

Cardiovascular collapse following intravascular bupivacaine may be resistant to treatment. The effect of amrinone on recovery from bupivacaine-induced severe cardiovascular depression was evaluated in 20 pigs (13-26 kg) in a placebo-controlled randomized double-blind study. Under 0.7% isoflurane anesthesia at FIO2 0.21, 0.5% bupivacaine 2 mg.kg-1.min-1 was infused until mean arterial pressure was 40% of the baseline. Cardiac output and heart rate decreased 75% and 50% from the baseline, respectively. The total dose of bupivacaine was 17 +/- 6 (SD) mg.kg-1 in the control and 19 +/- 5 mg.kg-1 in the amrinone group, resulting in mean plasma concentrations of 42 +/- 6 and 53 +/- 19 micrograms.ml-1, respectively. A bolus of amrinone 4 mg.kg-1 (n = 10) was given immediately after cardiovascular depression, followed by an infusion of 0.6 mg.kg-1.min-1. The control animals received corresponding volumes of physiologic saline (n = 10). After cardiovascular depression, the lungs were ventilated with FIO2 1.0 without anaesthetics or sympathomimetic support. Electric activity of the heart ceased in all control animals in 3.9 +/- 2 min after cardiovascular depression despite atropine and external cardiac compression. All animals in the control group and 5 of 10 animals in the amrinone group were given atropine (P less than 0.01). The animals receiving amrinone survived without cardiac compression (P less than 0.0001). During bupivacaine infusion, all animals developed burst suppression in the electroencephalogram. At the time of cardiovascular depression, in 8 of 10 control and in 6 of 10 amrinone animals, the electroencephalogram was isoelectric.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of amrinone on recovery from severe bupivacaine intoxication in pigs. 164 51

Pediatric asthma mortality is a perplexing and increasingly serious problem. Although many possible etiologic factors have been suggested, clear relationships are yet to be delineated. In addition to reviewing the literature, we studied the clinical and pathologic features of 14 local pediatric asthma deaths that occurred over a 7-year period. Thirteen of 14 children were African-American. Nine of 14 children (64.3) were older than 10 years of age, and 11 of 14 (78.6) were males. Based on a history of clinical features, 10 of the 14 children were characterized as severe asthmatics. Despite the fact that the majority of the children were regarded as severe asthmatics, only 1 of 14 had been evaluated with pulmonary function testing, and only 2 of 14 were receiving corticosteroids. Furthermore, only 2 of 14 were regarded as having good medical follow-up for their asthma. Ten of 14 children died suddenly secondary to asthma. One child was possibly abusing sympathomimetic inhalers, and none had evidence of toxic serum levels of theophylline. Six of 14 children (all adolescents) who died suddenly were negative on urine toxicology screening for cocaine, heroin, etc. Pathologic findings available for 10 children revealed mainly mucus plugging of the airways and collapse of various segments of the lungs, as well as pneumonia and pneumothorax in one child. In this group of children with sudden deaths (except for one child with pneumothorax), no other cause of death could be found.
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PMID:Childhood asthma mortality: the Brooklyn experience and a brief review. 180 55

Allergic reactions are often unpredictable, sudden in onset and may be potentially lethal. Clinical manifestations are confined to skin (rash, urticaria, angioedema), respiratory tract (laryngeal edema, bronchospasm) and cardiovascular system (hypotension, bradycardia, dysrhythymia). Because cardiovascular collapse is the most common life-threatening clinical feature, immediate and proper treatment is necessary. We have experienced two cases of intraoperative anaphylatic shock between September 1988 and April 1989. The precipitating factors were of nonanesthetic origin (case 1 was probably due to cephalothin and case 2 was due to dextran 40). Both cases manifestated with hypotension, bradycardia, cutaneous rash and urticaria. Recovery was smooth and without sequela after volume expansion and sympathomimetic drug. We discuss these two cases with a brief review.
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PMID:[Intraoperative anaphylactic shock--report of two cases]. 248 41

A 48-year-old man with a history of hypertension and diabetes mellitus was hospitalized with sudden onset of severe chest pain. He was in cardiogenic shock with a systolic pressure of 60 mm Hg. His electrocardiogram (ECG) showed ST-segment elevation in the precordial leads suggestive of acute anteroseptal myocardial infarction. The ST-segment returned to baseline after the systolic blood pressure rose to 100 mm Hg with the administration of sympathomimetic agents. Aortography and transesophageal echocardiography demonstrated type A aortic dissection and aortic regurgitation. Aortography and short-axis transesophageal echocardiography showed during diastole almost complete collapse of the true lumen of the ascending aorta caused by the intimal flap. The patient underwent surgical repair of the aortic dissection and implantation of Palmaz stents in the carotid arteries. Decreased blood pressure and the presence of aortic regurgitation accelerated the collapse of the true lumen during diastole in the ascending aorta, resulting in functional obstruction of the left main coronary artery, which may have been related to ST-segment changes in this case.
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PMID:A case of aortic dissection with transient ST-segment elevation due to functional left main coronary artery obstruction. 1071 27

Judging from the number of cases reported in the literature, severe bradycardia and/or asystole in association with central neuraxis blockade fortunately seems a rare complication. However, short periods of extreme bradycardia may go unnoticed and manifest cases, especially when outcome is favourable, may go unreported, and thus the real incidence may be much higher. Although the decrease in systemic blood pressure as a result of central neuraxis blockade is caused by various mechanisms, the most important factor causing severe hypotension, bradycardia and circulatory collapse is decreased venous return, and both prevention and treatment are aimed at preserving or restoring adequate venous return to the heart. Correction of preoperative hypovolaemia, limiting the extent of sensory blockade and positioning the patient so that gravity promotes venous return are the most significant preventive measures. Although a widespread custom, controversy exists regarding the efficacy of a preload; for certain categories of patients intravenous volume loading may be deleterious, and rather than a routine measure, the decision to administer a preload should be based on the clinical situation and the condition of the individual patient. For the treatment of mild bradycardia, anticholinergic drugs are the first choice. Hypotension may be treated by promoting venous return using gravity, by intravenous fluid infusion, by intravenous administration of sympathomimetic drugs, or by a combination of all three measures. In the event of sudden circulatory collapse, the first therapeutic measure that is usually immediately effective is elevation of the legs, thus promoting venous return.
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PMID:Mechanisms behind and treatment of sudden, unexpected circulatory collapse during central neuraxis blockade. 1098 74

Cocaine, derived from the leaves of the shrub Erythroxylon coca, which grows on the slopes of the Andes, remains one of the most widely abused illicit drugs (Johnson et al., 1993). Its abuse appears to be increasing and as a result, so is its trafficking across borders, with ever-increasing sophistication of concealment (Rouse, 1992). Over the past few years, cases of cocaine intoxication have been reported, resulting from ruptured packets of cocaine that have been swallowed, or inserted into the vagina or rectum by couriers (drug smugglers), so called 'body packers' or 'mules' (Westli and Mittleman, 1981; Ricaurte and Langston, 1995). Cocaine is a powerful sympathomimetic and central nervous system stimulant, an overdose of which causes primarily cardiac, neurological and psychiatric effects (Ricaurte and Langston, 1995). Acute toxicity is dose-related and is characterized in the first place by its sympathomimetic effects, which include tachycardia, hypertension and hyperthermia arrythmias, followed by seizures. Brainstem depression and cardio-respiratory collapse, stroke, coma, intracranial vasculitis, myocardial infarction and sudden death have all been reported in cocaine abuse (Ricaurte and Langston, 1995). We present a fatal case with neurological and psychiatric symptoms, but without the usual cardiac and systemic signs.
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PMID:Body packer: cocaine intoxication, causing death, masked by concomitant administration of major tranquilizers. 1105 42

Hemodynamic studies have demonstrated that the fall of blood pressure in shock caused by endotoxin in dogs does not result primarily from dilatation or "vasomotor collapse." Indeed, vasoconstriction is increased and may be excessive. Progression of shock has recently been blamed on such excessive vasoconstriction. For this reason the use of sympathomimetic drugs as vasopressor agents has been challenged and sympatholytic or adrenolytic agents have been recommended. In the present study, vasopressor and vasodilator drugs were used for the treatment of shock in dogs caused by endotoxin. Vasodilator drugs, when used after the onset of shock, hastened a fatal outcome but vasopressor agents were not detrimental when used in moderate doses. The effectiveness of the vasopressor agent is not necessarily due to a primary vasoconstrictor action on arteries and arterioles, as previously assumed.
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PMID:Treatment of endotoxic shock--the dilemma of vasopressor and vasodilator therapy. 1400 56

A small amount of Methamphetamine (MA) can produce behavioural changes such as euphoria, increased alertness, paranoia, decreased appetite and increased physical activity. In cardiovascular system, it can produce chest pain and hypertension which can result in cardiovascular collapse. In addition, MA causes accelerated heartbeat, elevated blood pressure. It can also cause irreversible damage to blood vessels in the brain. A number of sympathomimetic amines are capable of causing myocardial damage, but the cardio-toxic action of MA has been of particular interest since standardized dosage consistently produces myocardial lesions. As this drug is a choice of many teenagers and young adults, the damage to their health, as well as their future aspects could be greatly affected, therefore more evidence must be sought to convince them the negative root and show them the optimism of recovery and salvation. To clarify the effect of Methamphetamine (MA) on myocardium, 56 male Wister rats aged four weeks were divided equally into MA, Methamphetamine withdrawal (MW), Placebo (P) and Control (C) group were examined following daily intra-peritoneal administration of MA at a dose of 5 mg/kg body weight for 2, 4, 8 and 12 weeks. Normal saline was similarly injected in P group. Light microscopic changes was seen in the myocardium of MA treated group including eosinophilic degeneration, atrophy, hypertrophy, disarray, edema, cellular infiltration, myolysis, granulation tissue, fibrosis and vacuolization. On the other hand, the withdrawal group showed evidence of gradual recovery of those myocardial changes. Optimism is therefore generated about possibility of returning towards normal by withdrawing of this drug by the addicts.
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PMID:Histopathological studies of cardiac lesions after long term administration of methamphetamine in high dosage--Part II. 1934 31

Excited delirium syndrome (ExDS) is defined by marked agitation and confusion with sympathomimetic surge and incessant physical struggle, despite futility, which may lead to profound pathophysiologic changes and sudden death. Severe metabolic derangements, including lactic acidosis, rhabdomyolysis, and hyperthermia, occur. The pathophysiology of excited delirium is a subject of ongoing basic science and clinical research. Positive associations with ExDS include male gender, mental health disorders, and substance abuse (especially sympathomimetics). Excited delirium syndrome patients often exhibit violent, psychotic behavior and have "superhuman" strength which can result in the patient fighting with police and first responders. Continued struggle can cause a patient with ExDS to experience elevated temperature (T) and acidosis which causes enzymes to fail, leading to sudden death from cardiovascular collapse and multi-system organ failure. Therefore, effective early sedation is optimal to stop this fulminant process. Treatment of ExDS must be focused on rapidly, safely, and effectively sedating the patient and providing intensive, supportive care. Benzodiazepines, like midazolam, may not be ideal to sedate ExDS patients since their onset takes several minutes, and their side effects include loss of airway control and respiratory depression. Injectable antipsychotic medications have a relatively slow onset and may cause prolongation of the QTc interval. Ketamine is the ideal medication to sedate patients with ExDS. Ketamine has a rapid, predictable onset within three to four minutes when given by intramuscular (IM) injection. It does not adversely affect airway control, breathing, heart rate, or blood pressure (BP). In this retrospective case series, prehospital scenarios in which ExDS patients received ketamine by paramedics for sedation, and their subsequent treatment in the emergency department (ED) and hospital, are described. It is demonstrated that ketamine administered by paramedics in the prehospital setting of a community hospital based Emergency Medical Services (EMS) system is a safe and effective treatment for ExDS. Scaggs TR , Glass DM , Hutchcraft MG , Weir WB . Prehospital ketamine is a safe and effective treatment for excited delirium in a community hospital based EMS system. Prehosp Disaster Med. 2016;31(5):563-569.
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PMID:Prehospital Ketamine is a Safe and Effective Treatment for Excited Delirium in a Community Hospital Based EMS System. 2751 1


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