Cardiopulmonary arrest

The most frequent symptoms of anaphylaxis in patients with mastocytosis are decreased blood pressure and tachycardia. Also observed are dizziness, dyspnea, flushing, nausea and diarrhea [4]. Severe reactions are typical for patients with mastocytosis. In 55 patients with insect sting allergy and confirmed mastocytosis, 81% of patients experienced severe anaphylaxis with shock or cardiopulmonary arrest, whereas clinical reactions of this severity occurred in only 17% of 504 patients without evidence for mastocytosis and normal tryptase levels [29]. In another study in... 

Patients who are acutely intoxicated with an opioid usually present with miosis, euphoria, slow breathing and slow heart rate, low blood pressure, and constipation. Seizures may occur with certain agents such as meperidine (Demerol ). It is critically important to monitor patients carefully to avoid cardiac/ respiratory depression and death from an excessive dose of opioids. One strategy is to reverse the intoxication by utilizing naloxone (Narcan ) 0.4 to 2 mg IV every 2 to 3 minutes up to 10 mg. Alternatively, the IM/SC route may be used if IV access is not available. Because naloxone is shorter-acting than most abused opioids, it may need to be readministered at periodic intervals otherwise the patient could lapse into cardiopulmonary arrest after a symptom-free interval of reversed... 

Cardiopulmonary arrest is the abrupt cessation of spontaneous and effective ventilation and circulation after a cardiac or respiratory event. Cardiopulmonary resuscitation (CPR) provides artificial ventilation and circulation until it is possible to provide advanced cardiac life support (ACLS) and reestablish spontaneous circulation. 

Cardiopulmonary arrest in adults usually results from arrhythmias. The most common arrhythmias are ventricular fibrillation (VF) and pulseless ventricular tachycardia (PVT), often in patients after myocardial infarction (MI) or pulmonary embolism (PE). In children, cardiopulmonary arrest is often the terminal event of progressive shock or respiratory failure. 

The onset of cardiopulmonary arrest may be characterized by symptoms of anxiety, mental status changes, or unconsciousness cold, clammy extremities dyspnea, shortness of breath, or no respiration chest pain diaphoresis, and nausea or vomiting. 

Rapid diagnosis of cardiopulmonary arrest is vital to the success of CPR. Patients must receive early intervention to prevent cardiac rhythms from degenerating into less treatable arrhythmias. 

Cardiopulmonary arrest is diagnosed initially by observation of clinical manifestations consistent with cardiac arrest. The diagnosis is confirmed by evaluating vital signs, especially heart rate and respirations. Electrocardiography (ECG) is useful for determining the cardiac rhythm, which in turn determines drug therapy. 

FIGURE 7-1. Advanced cardiac life support (ACLS) treatment algorithm for adult cardiopulmonary arrest. (CPR, cardiopulmonary resuscitation PEA, pulseless electrical activity PVT, pulseless ventricular tachycardia VF, ventricular fibrillation.)... 

Vasopressin is a potent vasoconstrictor that increases blood pressure and systemic vascular resistance. It may have several advantages over epinephrine. First, the metabolic acidosis that frequently accompanies cardiopulmonary arrest can blunt the vasoconstrictive effect of epinephrine this does not occur with vasopressin. Second, stimulation of P receptors by epinephrine can increase myocardial oxygen demand and complicate the postresuscitative phase of CPR. Vasopressin can also have a beneficial effect on renal blood flow in the kidney, causing vasodilation and increased water reabsorption. 

Cardiovascular Effects. One of the patients described by Letz et al. (1984) (see Section 2.2.3.1) who had a terminal cardiopulmonary arrest had acute myocardial interstitial edema, myocardial inflammation, and Gram-positive sporulating rods at necropsy. The second patient initially had a normal electrocardiogram, but as his renal and hepatic function deteriorated, eventually developed supraventricular tachycardia and asystole. 

Death. 1,2-Dibromoethane can be fatal to humans after oral or dermal exposure. Acute deaths following toxic doses are related to cardiopulmonary arrest or, if affected individuals survive for a period of time, to hepatic and renal failure. These results are supported by animal studies in which acute death occurred after oral, dermal, and inhalation exposure. 

Two fatalities occurred after reentry of a home fumigated with sulfuryl fluoride. The male experienced severe dyspnea and cough, followed by generalized seizure and cardiopulmonary arrest within 24 hours. The female initially had weakness, nausea, and repeated vomiting within 4 days, there was severe hypoxemia and diffuse pulmonary infiltrates. Ventricular fibrillation and death occurred on day 6. The concentration of sulfuryl fluoride gas was not available, and the difference in time of death for the two individuals was not explainable. 

Superinfection (especially enterococcal orfungal), nephropathy, cardiopulmonary arrest, chest pain, and cerebral thrombosis may occur. 

Cardiac arrest IV Initially, 1 mEq/kg (as 7.5%-8.4% solution). May repeat with 0.5 mEq/kg qlOmin during continued cardiopulmonary arrest. Use in the postresuscitation phase is based on arterial blood pH, partial pressure of carbon dioxide in arterial blood (PaCOj) and base deficit calculation. 

Respiratory Effects. Case reports of humans who died after ingesting chromium(VI) compounds have described respiratory effects as part of the sequelae leading to death. A 22-month-old boy who ingested an unknown amount of sodium dichromate died of cardiopulmonary arrest. Autopsy revealed pleural effusion, pulmonary edema, severe bronchitis, and acute bronchopneumonia (Ellis et al. 1982). Autopsy of a 17-year-old male who committed suicide by ingesting 29 mg chromium(VI)/kg as potassium dichromate revealed congested lungs with blood-tinged bilateral pleural effusions (Clochesy 1984 Iserson et al. 1983). Respiratory effects were not reported at nonlethal doses. 

Cardiovascular Effects. Case reports of humans who died after ingesting chromium(VI) compounds have described cardiovascular effects as part of the sequelae leading to death. A 22-month-old boy who ingested an unknown amount of sodium dichromate died of cardiopulmonary arrest. 

Johri S, Rashid H, Daniel PJ, Soni A. Cardiopulmonary arrest secondary to haloperidol. Am J Emerg Med 2000 18(7) 839. 

Dysrhythmias seem to be the most likely cause of sudden death from cocaine, but cardiac conduction disorders are more common in patients with acute cocaine toxicity. Severe cocaine toxicity also causes acidemia and cardiac dysfunction (96). Four patients developed seizures, psychomotor agitation, and cardiopulmonary arrest two of these are briefly summarized here. 

A 43-year-old man injected a large dose of cocaine in a suicide attempt and had a seizure and cardiopulmonary arrest, from which he was resuscitated. His arterial blood pH was 6.72 and his electrocardiogram showed a wide complex tachycardia. An infusion of sodium bicarbonate maintained the blood pH at 7.50 and the electrocardiogram became normal. The bicarbonate infusion was discontinued after 12 hours. 

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