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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most serious complication of sickle cell trait (SCT) is sudden death during exertion. SCT often remains unrecognized in the 2.5 million African Americans affected. Exertional collapse and sudden death associated with SCT is characterized by rhabdomyolysis, heat stroke, and cardiac arrhythmia. There is a 40-fold increased risk of sudden death in affected soldiers during military basic training and there are many cases reported in athletes during preseason training. There have been no cases reported in soldiers beyond basic training. In the case presented, a soldier with 3 years of military service succumbed to SCT-associated sudden death during physical fitness testing.
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PMID:Exertional collapse and sudden death associated with sickle cell trait. 912 56

The National Association of Medical Examiners Ad Hoc Committee on the Definition of Heat-Related Fatalities recommends the following definition of "heat-related death": a death in which exposure to high ambient temperature either caused the death or significantly contributed to it. The committee also recommends that the diagnosis of heat-related death be based on a history of exposure to high ambient temperature and the reasonable exclusion of other causes of hyperthermia. The diagnosis may be established from the circumstances surrounding the death, investigative reports concerning environmental temperature, and/or measured antemortem body temperature at the time of collapse. In cases where the measured antemortem body temperature at the time of collapse was > or = 105 degrees F (> or = 40.6 degrees C), the cause of death should be certified as heat stroke or hyperthermia. Deaths may also be certified as heat stroke or hyperthermia with lower body temperatures when cooling has been attempted prior to arrival at the hospital and/or when there is a clinical history of mental status changes and elevated liver and muscle enzymes. In cases where the antemortem body temperature cannot be established but the environmental temperature at the time of collapse was high, an appropriate heat-related diagnosis should be listed as the cause of death or as a significant contributing condition.
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PMID:Criteria for the diagnosis of heat-related deaths: National Association of Medical Examiners. Position paper. National Association of Medical Examiners Ad Hoc Committee on the Definition of Heat-Related Fatalities. 909 94

The ambulance was called to a known asthmatic patient. On arrival, the team found a massively dyspnoeic, diaphoretic, non-cyanotic and somnolent patient. His medication consisted of oral theophylline (unknown dosage), fenoterol (metered-dose inhaler), as well as 8 mg oral prednisolone. On the day of emergency, the patient had been treated by two physicians who applied two doses of i.v. theophylline and one dose of s.c. terbutaline because of bronchoconstriction (dosage not documented). The patient's pulse was frequent with 200 beats/min, the blood pressure not measurable. Careful i.v. titration of metoprolol was started to decrease the patient's heart rate and increase diastolic filling and stroke volume. However, the patient showed a progressive circulatory collapse. Following diagnostic thoracocentesis to rule out a left-side pneumothorax, the patient required intubation and mechanical ventilation because of increasing cardiovascular instability. A tension pneumothorax developed immediately after mechanical ventilation and required rapid treatment with a chest tube. Nevertheless, CPR and intravenous infusion of catecholamines were necessary before the patient was referred to a medical intensive care unit where he died the same day in cardiogenic shock. Clinical signs and symptoms associated with an elevated theophylline plasma level make theophylline toxicity the probable causative event for the patient's emergency condition of acute theophylline intoxication.
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PMID:[Acute theophylline intoxication as differential diagnosis of pneumothorax in an asthma patient]. 913 51

Sinus tachycardia caused by circulating catecholamines in the setting of congestive heart failure may impair systemic perfusion because of decreased diastolic filling time. We report the case of a patient with Wolff-Parkinson-White syndrome with angina and cardiogenic shock who improved dramatically following administration of neostigmine. Cardiac output, blood pressure, and stroke volume increased as heart rate was reduced. A previous attempt at heart rate control, in the same patient, using a low dose beta-antagonist, precipitated hemodynamic collapse. The remarkable recovery of our patient suggests that acetylcholinesterase inhibitors may warrant further investigation in patients with severe sinus tachycardia.
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PMID:High dose neostigmine treatment of malignant sinus tachycardia. 917 Jan 42

Widespread hemorrhagic manifestations commonly occur in patients with severe heat stroke. The pathogenesis of hemostatic disorders in these patients is not fully understood, although it is believed to be multifactorial in origin. The present investigation was designed to study the changes in blood platelets caused by heat stress in an experimental model of five merino sheep. The experiments were performed in two groups of five merino sheep each. In one group the sheep were subjected to a combination of heat (elevated environmental temperature) and exertional stress, and allowed to proceed throughout the experiment until a state of near collapse was reached (Task A). In the other group (Task B) the animals were heated in the same manner as those in Task A and also subjected to exertional heat; however, when the temperature reached 43.6 +/- 0.2 degrees C, the critical core temperature (CCT), they were subjected to evaporative cooling in a climatic chamber. Serial changes in the platelet counts and platelet functions were measured throughout the duration of the experiments. At the core temperature (CT) of 42.1 degrees C and above there was a significant impairment of adhesion of platelets to glass beads. During the early phases of elevation of CT, platelets showed hyperaggregation in the presence of different agonists (such as, collagen, ADP, ristocetin); this was followed by hypoaggregation when the CCT was raised above 43.6 +/- 0.2 degrees C. However, these impairments of platelet functions occurring at elevated CT and CCT were found to reverse to normal within 24 hours after the animals were cooled to 39 degrees C. It was also found that the hyperaggregation of platelets to different agonists induced by raised CT could be partially prevented by prior in vitro treatment of platelets with apyrase, a known enzyme destroying of ADP. The results of these experiments indicate that heat stress induced by exposing merino sheep to elevated controlled temperature directly activates the platelets. This may be an important contributing factor in causing altered hemostasis in heat stroke activated directly by heat. This mechanism may be operating in altered hemostasis in heat stroke.
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PMID:Pathophysiology of bleeding in heat stress: an experimental study in sheep. 921 37

Heat stroke is a syndrome which reduces systemic vascular resistance and cardiac collapse. The gut plays an important role in shock. In hyperthermia, many of the same symptoms as heat stroke may be present, including inhibition of splanchnic vasoconstriction and endotoxemia. Furthermore, both conditions result in shock, in which the gut plays an important role. Detection of insufficient oxygenation of gut tissue, which sustains an earlier and more severe hypoxia, can warn of impending shock and can be performed by monitoring intramucosal pH (pHim). This index is very sensitive to tissue hypoxia and ischemia. In the present study both pHim, using tonometry, and gut blood flow during whole body heating (WBH) in pigs were measured. WBH was achieved by circulating warm water through a vinyl sheet covering the animal. Central venous pressure was maintained by fluid infusion. Body temperature was measured using a thermometer probe inserted into the right jugular vein. Mean arterial pressure, cardiac output and gut blood flow were also measured. pHim was evaluated using a tonometer placed into the midileum lumen. During WBH, cardiac index and mean arterial pressure increased, however systemic vascular resistance decreased. Gut blood flow was either maintained at the normal rate or increased. Intraarterial pH did not change significantly, however pHim significantly decreased from 7.30 at the beginning of WBH to approximately 7.05 after the body temperature reached 42.5 degrees C. These findings suggest that there was reduced oxygen delivery to the tips of the small intestinal villi during regional ischemia following WBH. In conclusion, insufficient tissue oxygen delivery as detected by a reduction in inramucosal pH is an important index in whole body heating.
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PMID:Changes in intramucosal pH and gut blood flow during whole body heating in a porcine model. 967 8

We report a case of accidental infant death presumably due to exertional self-overheating in bed. On a winter morning, a 9-month-old female baby was found dead in her bed at home. She had been confined to the bed overnight by her father, totally covered with a blanket and a thick quilt, because her night crying disturbed his sleep. The clothing and bedclothes were extremely wet with sweat. Many petechial hemorrhages were observed in the upper chest and thoracic viscera. The blood was concentrated, indicative of dehydration. Histological and immunohistochemical investigation revealed findings of shock and myolysis in the cardiac and skeletal muscles. There was no evidence of natural diseases. The main cause of death was diagnosed as circulatory collapse from overheating (hyperpyrexia and dehydration; heat stroke/exhaustion) probably precipitated by struggling in the closed space. Although there was no apparent evidence of battering or any other repetitive physical violence, this case was regarded as an atypical type of fatal child abuse.
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PMID:Infant death presumably due to exertional self-overheating in bed: an autopsy case of suspected child abuse. 971 Oct 68

Evidence from investigations of brain microcirculation (pial arterioles) reveals at least 3 different endothelium (EC) dependent mechanisms for dilation. Only one of the three can be triggered by acetylcholine (ACh) and in this vascular bed it is only this path that is dependent upon endothelial nitric oxide synthase (NOS) which produces nitric oxide (NO) from arginine. In this vascular bed the ACh sensitive path cannot be triggered by bradykinin (BK). This state of affairs appears to differ from that found in other beds or in endothelium cultured from conductance vessels. In the cerebral microcirculation there is considerable pharmacological evidence that the endothelium derived relaxing factor (EDRF) for ACh is not NO itself but may contain NO. In many experimental vascular settings the release of the NOS dependent EDRF is shear dependent. In the cerebral microcirculation there are several studies suggesting, in vivo, that this is correct. Among these are the following: (1) vessels narrow when shear is reduced after carotid ligation, and remain so along with unresponsiveness to ACh for at least ten minutes following resumption of flow. This may be important in developing stroke. The collapse is not passive due to low pressure. We know this because the narrowed vessels with their low intraluminal shear and pressure are still capable of large dilation by the NO donor, sodium nitropruside; (2) the antiplatelet effects of EC which are mediated, in part, by the EDRF for ACh are enhanced for 10 to 20 minutes following the transient increase and return of shear within these vessels. If the reverse is also true, reductions of shear may have important harmful proaggregant effects on platelets (and leukocytes) in the microvascular bed of developing infarcts. However most of the cited work depends upon pharmacological inhibitors of NOS to "prove" that NOS and an EDRF/NO are involved. In the last three years evidence in cats and rats shows that many of the NOS inhibitors also block K channels in cerebrovascular smooth muscle and that arginine, the "antidote" to the NOS inhibitors keeps the channels open. This latter work must force a reexamination of the conclusions reached in many studies.
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PMID:Is the EDRF in the cerebral circulation NO? Its release by shear and the dangers in interpreting the effects of NOS inhibitors. 978 59

Used worldwide since 1980 for the prevention of breast engorgement in the puerperium, in 1994 bromocriptine mesylate was withdrawn from the American market as an agent suitable for ablactation. The relevant recommendation of the Food and Drug Administration rested on case reports that described severe vasospastic reactions among users of the drug. Some patients so affected suffered stroke, intracranial bleeding, cerebral edema, convulsions, myocardial infarction, and puerperal psychosis. More recently, it has been suggested that the side effects of the drug may also include circulatory collapse secondary to cardiac dysrhythmia. This report describes two additional cases in this category. The antepartum clinical evaluation of these women suggested that they were predisposed to arrhythmias.
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PMID:Severe cardiac dysrhythmia in patients using bromocriptine postpartum. 1009 47

Ventilation-perfusion (V A/Q) distributions were evaluated in 24 patients with acute respiratory distress syndrome (ARDS), during airway pressure release ventilation (APRV) with and without spontaneous breathing, or during pressure support ventilation (PSV). Whereas PSV provides mechanical assistance of each inspiration, APRV allows unrestricted spontaneous breathing throughout the mechanical ventilation. Patients were randomly assigned to receive APRV and PSV with equal airway pressure limits (Paw) (n = 12) or minute ventilation (V E) (n = 12). In both groups spontaneous breathing during APRV was associated with increases (p < 0.05) in right ventricular end-diastolic volume, stroke volume, cardiac index (CI), PaO2, oxygen delivery, and mixed venous oxygen tension (PvO2) and with reductions (p < 0.05) in pulmonary vascular resistance and oxygen extraction. PSV did not consistently improve CI and PaO2 when compared with APRV without spontaneous breathing. Improved V A/Q matching during spontaneous breathing with APRV was evidenced by decreases in intrapulmonary shunt (equal Paw: 33 +/- 4 to 24 +/- 4%; equal V E: 32 +/- 4 to 25 +/- 2%) (p < 0.05), dead space (equal Paw: 44 +/- 9 to 38 +/- 6%; equal V E: 44 +/- 9 to 38 +/- 6%) (p < 0.05), and the dispersions of ventilation (equal Paw: 0.96 +/- 0.23 to 0.78 +/- 0.22; equal V E: 0.92 +/- 0.23 to 0.79 +/- 0.22) (p < 0.05), and pulmonary blood flow distribution (equal Paw: 0.89 +/- 0.12 to 0.72 +/- 0.10; equal V E: 0.94 +/- 0.19 to 0.78 +/- 0.22) (p < 0.05). PSV did not improve V A/Q distributions when compared with APRV without spontaneous breathing. These findings indicate that uncoupling of spontaneous and mechanical ventilation during APRV improves V A/Q matching in ARDS presumably by recruiting nonventilated lung units. Apparently, mechanical assistance of each inspiration during PSV is not sufficient to counteract the V A/Q maldistribution caused by alveolar collapse in patients with ARDS.
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PMID:Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome. 1019 72


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