Cardiorespiratory arrest

Levels greater than 40 mcg/mL-seizuresand cardiorespiratory arrest... 

Correia D, Rodrigues De Resende LA et al (2006) Power spectral analysis of heart rate variability in HIV-infected and AIDS patients. Pacing CUn Electrophysiol 29(l) 53-58 Craddock C, Pasvol G et al (1987) Cardiorespiratory arrest and autonomic neuropathy in AIDS. Lancet 2(8549) 16-18... 

Petito C, Feldmann E, Pulsinelli W, et al. 1987. Delayed hippocampal damage in humans following cardiorespiratory arrest. Neurology 37 1281-1286. 

Respiratory and metabolic acidosis can develop in patients with cardiorespiratory arrest, with chronic lung disease and shock, and with metabolic acidosis and respiratory failure. 

Cardiac effects Cardiorespiratory arrest or anaphylaxis has occurred, possibly because of excessively rapid administration in some cases. Rapid injection of undiluted miconazole may produce transient tachycardia or arrhythmia. 

Aseptic meningitis syndrome-The incidence of this syndrome was 6%. Fever, headache, meningismus, and photophobia were the most commonly reported symptoms a combination of these 4 symptoms occurred in 5% of patients. Headache - Headache is frequently seen after any of the first few doses and may occur in any of the aforementioned neurologic syndromes or by itself. Seizures - Seizures, some accompanied by loss of consciousness or cardiorespiratory arrest, or death, have occurred independently or in conjunction with any of the neurologic syndromes described below. Patients predisposed to seizures may include those with the following conditions Acute tubular necrosis/uremia fever infection a precipitous fall in serum calcium fluid overload hypertension hypoglycemia, history of seizures and electrolyte imbalances those who are taking a medication concomitantly that may, by itself, cause seizures. 

A fatal interaction between ritonavir and MDMA (methylenedioxymethamphetamine, ecstasy) has been reported in an HIV-positive man (see Henry et ah, 1998). The patient had allegedly taken MDMA on several occasions without untoward effects. However, several weeks after ritonavir was added to his regular medication with zidovudine and lamivudine, he took some MDMA for recreational purposes and died of a cardiorespiratory arrest within hours. Toxicology showed that the plasma MDMA concentration was about ten times that expected from the ingested dose. Inhibition of CYP2D6, the principal pathway for MDMA metabolism, by ritonavir was thought to be the most likely cause. 

Petito CK, Feldmann E, Pulsinelli WA, Plum F (1987) Delayed hippocampal damage in humans following cardiorespiratory arrest. Neurology 37 1281-1286 Pevny L, Rao MS (2003) The stem-cell menagerie. Trends Neurosci 26 351-359 Picard-Riera N, Nait-Oumesmar B, Baron-Van Evercooren A (2004) Endogenous adult neural stem cells limits and potential to repair the injured central nervous system. J Neurosci Res 76 223-231... 

A 30-year-old woman with a history of bronchial asthma and cocaine abuse had a cardiorespiratory arrest preceded by sudden dyspnea 1 hour after cocaine inhalation. Direct laryngoscopy showed edema of the glottis. After extended cardiopulmonary resuscitation, she went into a deep coma with dilated non-reactive pupils. Toxicological analysis showed cocaine and amphetamines in her urine. She was brain dead 11 hours later and her organs were used for transplantation. Her liver was given to a 14-year-... 

A 32-year-old HIV-positive man, who added ritonavir 600 mg bd to his antiretroviral regimen of zidovudine and lamivudine, became unwell within hours after having taken two and a half tablets of ecstasy, estimated to contain 180 mg of MDMA. He was hypertonic, sweating profusely, tachypneic, tachycardic, and cyanosed. Shortly after he had a tonic-clonic seizure and a cardiorespiratory arrest. Attempts at resuscitation were unsuccessful. Blood concentrations obtained post-mortem showed an MDMA concentration of 4.56 mg/1, in the range of that reported in a patient with a life-threatening illness and symptoms similar to this patient after an overdose of 18 tablets of MDMA. 

Mehta et al, 1990 Sriramachari, 2004 Varma and Guest, 1993 Varma and Mulay, 2006). Dureja and Saxena (1987), two of the earliest physicians who were involved in the rescue, graded symptoms into four categories (1) minor eye ailments, throat irritation and cough (2) severe conjunctivitis, keratitis, acute bronchitis and drowsiness (3) severe pulmonary edema and (4) convulsions followed by cardiorespiratory arrest. Similar findings were reported by others (Kamat et al., 1985 Misra et al., 1987). 

Torsade de pointes and cardiorespiratory arrest have been reported in a patient with congenital long QT syndrome who took azithromycin (20). In a prospective study of 47 previously healthy people, there was a modest statistically insignificant prolongation of the QT interval without clinical consequences after the end of a course of azithromycin 3 g/day for 5 days (21). 

Anaphylactoid reactions can occur after the intravenous administration of Cremophor (SEDA-22, 526) when it is used as a diluent of alfadolone/afaxolone (SED-11,211) (2), ciclosporin (3), paclitaxel (4), propanidid (SED-11, 211) (5,6), teniposide (7), and vitamin K (8,9). Cardiorespiratory arrest after intravenous miconazole has been attributed to the histamine-releasing properties of Cremophor (10). 

Cardiorespiratory arrest can occur only 15 minutes after drug ingestion (16). This risk is enhanced if ethanol is taken concomitantly. 

An 81-year-old man underwent CT scanning of the head with intravenous contrast enhancement (100 ml of the non-ionic contrast medium iopamidol). After the injection he complained of sweating and nausea and had a cardiorespiratory arrest. Immediate resuscitation and intravenous dexamethasone and adrenaline were not successful. Mast cell tryptase activity in a sample taken 4 hours after death was high. At autopsy, the coronary and pulmonary arteries were patent. The right heart chambers were moderately enlarged. The lungs were hyperemic and edematous and there was obstructive edema of the larynx. 

An 18-month-old infant died after swallowing an unknown amount of 2% viscous lidocaine. He rapidly became unwell at home, with convulsions, followed by an asystolic cardiorespiratory arrest. He was intubated and resuscitated by paramedics, but continued to have seizures. He was given anticonvulsants and cardiorespiratory resuscitation was unsuccessful. Toxicological tests identified high concentrations of lidocaine and its metabolites. 

Collapse after rapid intravenous injection has been described, as have some cases of tachycardia, ventricular tachycardia, and even, in a few instances, cardiorespiratory arrest, attributable to the histamine-releasing properties of Cremophor (SED-12, 679) (2). 

Acute overdose can produce cardiorespiratory arrest and death (SEDA-22, 7). 

During dialysis a patient received an accidental infusion of 30 ml of a 5.25% solution of hypochlorite. This led to cardiorespiratory arrest and massive hemolysis with hyperkalemia, although the patient eventually recovered (7). 

Symptoms of overdose include nausea, vomiting, transient visual or auditory deficits, drowsiness, and seizures followed by severe cardiac arrhythmias, shock, or cardiorespiratory arrest. Hypotension may be severe and intractable, producing metabolic acidosis and end-organ failure. Cardiac conduction disturbances include complete atrioventricular dissociation, QRS and QT prolongation, severe bradycardia, and ventricular fibrillation. Acute ingestions of 30-50 mg kg of chloroquine in adults and as little as 300 mg in children are potentially fatal. 

The major manifestations of barbiturate intoxication are CNS, cardiovascular, and respiratory depression. Severe intoxication results in coma, hypothermia, hypotension, and cardiorespiratory arrest. 

Mixed respiratory and metabolic acidosis may develop in patients with cardiorespiratory arrest, in those with chronic lung disease who are in shock, and in metabolic acidosis patients who develop respiratory failure. This mixed disorder should be treated by responding to both the respiratory and metabolic acidosis. Improved oxygen delivery must be initiated to improve hypercarbia and hypoxia. Mechanical ventilation may be needed to reduce PaC02. During the initial stage of therapy, appropriate amounts of alkali should be given to reverse the metabolic acidosis (see section on treatment of metabolic acidosis earlier in this chapter). 

A. With the more toxic agents oxyphenbutazone, phenylbutazone, mefe-namic acid, or piroxicam, and with massive ibuprofen or fenoprofen overdose, seizures, coma, renal failure, and cardiorespiratory arrest may occur. Hepatic dysfunction, hypoprothrombinemia, and metabolic acidosis ate also reported. 

Acute ingestion commonly causes gastrointestinal upset, variable CNS depression (confusion, disorientation, obtundation, and coma with respiratory failure), and occasionally hypotension with tachycardia and prolonged QT interval. The pupils may be miotic, and the presentation may mimic an opiate poisoning. Cardiorespiratory arrest has been associated with severe intoxication, and the morbidity and mortality from valproic acid poisoning seem to be related primarily to hypoxia and refractory hypotension. 

In 1990, the CSM in the UK noted that, of 26 reports they had on record of hypokalaemia with unnamed xanthines or beta2 agonists, 9 occurred in patients receiving both groups of drugs. In 5 of these 9 cases, the hypokalaemia had no clinical consequence. However, in 2 cases it resulted in cardiorespiratory arrest, in another case confusion, and in a further case intestinal pseudo-obstruction. ... 

A case of an amniotic fluid embolism causing a maternal cardiorespiratory arrest was temporally associated with ingestion of castor oil by a woman at week 40 of gestation, although causality could not be determined (Steingrub et al. 1988). 

The most severe and acute form of lead poisoning which usually follows ingestion or inhalation of large amounts of lead is acute encephalopathy which may arise precipitously with the onset of intractable seizures, coma, cardiorespiratory arrest, and death within 48 hours. 

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