Journal of intensive care medicine
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Acute respiratory failure is a common complication of drug abuse. It is more likely to develop in the setting of chronic lung disease or debility in those with limited respiratory reserve. Drugs may acutely precipitate respiratory failure by compromising respiratory pump function and/or by causing pulmonary pathology. ⋯ Alcohol, cocaine, amphetamines, opiates, and benzodiazepines are the most commonly abused drugs that may induce events leading to acute respiratory failure. While decontamination and aggressive supportive measures are indicated, specific therapies to correct seizures, metabolic acidosis, pneumothorax, infections, bronchospasm, and agitation should be considered. Drug-related respiratory failure when due to CNS depression alone may portend well, but in patients with drug-related significant pulmonary pathology, a protracted course of illness may be anticipated.
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Arginine vasopressin is a peptide produced in the posterior pituitary whose primary physiologic role is fluid homeostasis. Recent investigations have demonstrated a therapeutic role for arginine vasopressin in adult cardiac arrest as well as adult and pediatric vasodilatory shock. We review the physiology of arginine vasopressin and examine the supporting data behind the developing clinical applications of this naturally produced peptide.
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J Intensive Care Med · Jul 2004
Comparative Study Clinical TrialPulse oximetry in children with congenital heart disease: effects of cardiopulmonary bypass and cyanosis.
The objective of this prospective, observational study with consecutive sampling was to assess the reliability, bias, and precision of Nellcor N-395 (N) and Masimo SET Radical (M) pulse oximeters in children with cyanotic congenital heart disease and children with congenital heart disease recovering from cardiopulmonary bypass-assisted surgery admitted to a cardiovascular operating suite and pediatric intensive care unit at a tertiary care community hospital. Forty-six children with congenital heart disease were studied in 1 of 2 groups: (1) those recovering from cardiopulmonary bypass with a serum lactic acid > 2 mmol/L, and (2) those with co-oximetry measured saturations (SaO(2)) < 90% and no evidence of shock. Measurements of SaO(2) of whole blood were compared to simultaneous pulse oximetry saturations (SpO(2)). ⋯ There was a significant difference in bias (ie, average SpO(2) - SaO(2)) and precision (+/- 1 SD) between oximeters (N, 1.1 +/- 3.3 vs M, -0.2 +/- 4.1; P < .001) in the postcardiopulmonary bypass group but no significant difference in bias and precision between oximeters in the cyanotic congenital heart disease group (N, 2.9 +/- 4.6 vs M, 2.8 +/- 6.2; P = .848). The Nellcor N-395 pulse oximeter failed more often immediately after cardiopulmonary bypass than did the Masimo SET Radical pulse oximeter. SpO2 measured with both oximeters overestimated SaO2 in the presence of persistent hypoxemia.