Collapse arrest

Thus, we arrive at the conclusion that the standard scenario for supercontinuum generation in bulk media is incomplete. Although it correctly identifies the key quantities (peak intensity, plasma density generation rate) and processes (collapse arrest, MPI), our numerical experiments demonstrate that it doesn t explain the supercontinuum spectral properties. 

Consideration shonld also be given to the possibility that the flame arrester may ping, which conld prodnce a vacnnm condition in a low-pressnre tank when the tank is primped out, and implode (collapse) the tank. This may reqnire the installation of a vacnnm breaker or a pressnre-vacnnm conservation valve. If the tank contents are flammable and admission of air may resnlt in an ignitable mixture, it may be necessary to install an inert gas blanketing system on the tank, actuated by a pressnre controller, which would admit a sufficient flow of inerting gas when a vacnnm condition is detected. 

Initial features are mostly pulselessness, difficulty in ventilation, desaturation, and a decreased end-tidal CO2. Cutaneous symptoms are observed in 66-70% of patients in case of IgE-mediated reactions but in more than 90% in non-IgE-mediated reactions. On the contrary, cardiovascular collapse and bronchospasm are more frequent in IgE-dependent reactions (table 2). Severe anaphylaxis may be a primary cardiac arrest [9]. 

Nanoparticles of the semicondnctor titanium dioxide have also been spread as mono-layers [164]. Nanoparticles of TiOi were formed by the arrested hydrolysis of titanium iso-propoxide. A very small amount of water was mixed with a chloroform/isopropanol solution of titanium isopropoxide with the surfactant hexadecyltrimethylammonium bromide (CTAB) and a catalyst. The particles produced were 1.8-2.2 nm in diameter. The stabilized particles were spread as monolayers. Successive cycles of II-A isotherms exhibited smaller areas for the initial pressnre rise, attributed to dissolution of excess surfactant into the subphase. And BAM observation showed the solid state of the films at 50 mN m was featureless and bright collapse then appeared as a series of stripes across the image. The area per particle determined from the isotherms decreased when sols were subjected to a heat treatment prior to spreading. This effect was believed to arise from a modification to the particle surface that made surfactant adsorption less favorable. 

Figure 15.3 EEG/EMG recordings showing the differences between cataplexy (A) in an orexin l mouse, and a sleep attack (B) in an OX-jR mouse. Note how cataplexy (i.e. an abrupt arrest) is associated with a transition to REM sleep, but the sleep attack (i.e. a gradual arrest) shows the characteristics of non-REM sleep after the transition. In fact, based only on these EEG/EMG records, the sleep attack would not appear unusual, and it is the associated behavior, as revealed on the concurrent video recordings (i.e. the collapse into sleep without the typical preparatory behaviors), that reveals how this type of attack is similar to the overwhelming sleepiness experienced by the narcoleptic patient. Vertical arrows denote the times at which an arrest is behaviorally evident. Scale bar is 10 sec. Adapted from Willie et al. (2003).

The first stages of the collapse promised everything but that I would be arrested," Ambros told the court with a smile. It was the same smile that had greeted the vanguard of American soldiers that rolled into Gendorf, Bavaria, in 1945. 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

PVCs often cause no symptoms or only mild palpitations. The presentation of VT may vary from totally asymptomatic to pulseless hemodynamic collapse. Consequences of proarrhythmia range from no symptoms to worsening of symptoms to sudden death. VF results in hemodynamic collapse, syncope, and cardiac arrest. 

Cardiovascular Effects. In a recent report on the clinical treatment of phenol poisoning, Langford et al. (1998) provide a summary of a case report in which a woman accidentally consumed an ounce of 89% phenol which had been mistakenly been given to her in preparation for an in-office procedure. Her immediate reaction upon consuming the phenol was to clutch her throat and collapse, and within 30 minutes she was comatose and had gone into respiratory arrest. Treatment was initiated with an endotracheal intubation. Ventilation with a bag and mask led to the detection of a lamp oil odor. Within an hour she developed ventricular tachycardia which responded to cardioversion however, she subsequently developed (in the first 24 hours) supraventricular and ventricular dysrhythmias, metabolic acidosis, and experienced a grand mal seizure. After a 15-day hospital stay, she was completely recovered with no evidence of impaired motility or compromised gastrointestinal or cardiovascular systems. 

Significant drug interactions include light-headedness nervousness drowsiness dizziness apprehension confusion mood changes hallucinations tremors convulsions unconsciousness hypotension bradycardia cardiovascular collapse, which may lead to cardiac arrest febrile response soreness/infection at the injection site venous thrombosis or phlebitis extending from the site of injection extravasation vomiting respiratory depression/arrest. 

Other adverse cardiovascular and respiratory effects Orthostatic hypotension, with or without syncope, can occur with clozapine treatment. Rarely, collapse can be profound and accompanied by respiratory and/or cardiac arrest. Orthostatic hypotension is more likely to occur during initial titration in association with rapid dose escalation. In patients who have had even a brief interval off clozapine, start treatment with 12.5 mg once or twice daily (see Warnings). Because collapse, respiratory arrest, and cardiac arrest during initial treatment have occurred in patients receiving benzodiazepines or other psychotropic drugs, caution is advised when clozapine is initiated in patients taking a benzodiazepine or any other psychotropic drug. 

Anaphylactic or anaphylactoid reactions may occur following administration of any dose or course of muromonab-CD3. Serious and occasionally life-threatening systemic, cardiovascular, and CNS reactions have been reported. These have included the following Pulmonary edema, especially in patients with volume overload shock cardiovascular collapse cardiac or respiratory arrest seizures coma. Hence, a patient being treated with muromonab-CD3 must be managed in a facility equipped and staffed for cardiopulmonary resuscitation. 

Deflbrillation is one of the few interventions that has been shown to improve outcome from cardiac arrest. The cardiac arrhythmias commonly associated with sudden collapse are (1) asystole and (2) rapid and ineffective depolarization due to ventricular flbrillation (VF), pulseless ventricular tachycardia (VT), or supraventricular tachycardia with 1 1 ventricular response (as can occur with pre-excitation syndromes). The best strategy is to treat collapsed patients who have a broad-complex tachycardia at once by external Direct Current (DC) defibrillation. 

Although serious adverse reactions to lidocaine are uncommon, high dosage by any route may produce cardiovascular depression, bradycardia, hypotension, arrhythmias, heart block, cardiovascular collapse, and cardiac arrest,... 

Depression or cardiac excitability and contractility may cause AV block, ventricular arrhythmias, or cardiac arrest. Symptoms of local anesthetic CNS toxicity, such as dizziness, tongue numbness, visual impairment or disturbances, and muscular twitching appear to occur before cardiotoxiceffects. Cardiotoxic effects include angina, QT prolongation, PR prolongation, atrial fibrillation, sinus bradycardia, hypotension, palpitations, and cardiovascular collapse. 

Cardiovascular manifestations are usually depressant and are characterised by bradycardia, hypotension and cardiovascular collapse, which may lead to cardiac arrest. 

Adverse effects include ventricular fibrillation, hypotension or massive cardiac arrest due to overdose, dizziness, paraesthe-sia, drowsiness, seizures, disorientation, respiratory arrest, nausea, vomiting, circulatory collapse and blurred vision. 

Cardiac arrhythmias, circulatory collapse, and/or cardiac arrest have occurred after rapid administration... 

Hydrazine is toxic and readily absorbed by oral, dermal, or inhalation routes of exposure. Contact with hydrazine irritates the skin. eyes, and respiratory tract. Liquid splashed into die eyes may cause permanent damage to the cornea. Al high doses it can cause convulsions, but even low doses may result in central nervous system depression. Death from acute exposure results from convulsions, respiratory arrest, and cardiovascular collapse. Repeated exposure may affect the lungs, liver, and kidneys. Evidence is limited as to the effect of hydrazine on reproduction and/or development however, animal studies demonstrate that only doses that produce toxicity in pregnant rats result in embryo-toxicity. 

A 60-year-old white man was admitted for kidney transplantation. Immediately after reperfusion and intravenous methylprednisolone 500 mg, he developed severe bradycardia with hypotension and then cardiac arrest. After resuscitation, his clinical state improved quickly, but on the morning of the first postoperative day directly after the intravenous administration of methylprednisolone 250 mg, he had another episode of severe bradycardia, hypotension, and successful cardiopulmonary resuscitation. A third episode occurred 24 hours later after intravenous methylprednisolone 100 mg, again followed by rapid recovery after resuscitation. Two weeks later, during a bout of acute rejection, he was given intravenous methylprednisolone 500 mg, after which he collapsed and no heartbeat or breathing was detectable after cardiopulmonary resuscitation he was transferred to the intensive care unit, where he died a few hours later. 

Lasix is very strong and was reported to cause diarrhea, dehydration, dizziness, muscle cramps, circulatory disorders, vomiting, circulatory collapse, fainting, and cardiac arrest. It was considered far more safe to start with 20-mg and repeat every 4 hours than to use higher dosages for a shorter period of tome. Over 40-mg per dosage increased side effects dramatically ... 

At a manufacturing plant that used high-frequency, high-current welders for welding steel and aluminum parts, one of the welders took a break outdoors on a rainy day. When he walked back into the building and touched one of the welding machines to which power was turned on, he collapsed and died of cardiac arrest. 

Deaths from an overdose of PCP are usually caused by respiratory arrest, but death can also result from seizures, cardiovascular collapse, and extremely high fever, which leads to kidney, liver, and brain damage. High doses of PCP also result in extremely high blood pressure, which may cause a stroke. 

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