PubMed · 6807454
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G S Sykes, P M Molloy, P Johnson. 1982-07-24. Birth asphyxia.. https://doi.org/10.1136/bmj.285.6337.289-c
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OBJECTIVE: Status asthmaticus with respiratory failure is a potentially fatal complication of bronchial asthma. To prevent a fatality in status asthmaticus with respiratory failure, treatment with intravenous isoproterenol or mechanical ventilation has been advocated. These interventions also have serious potential complications, however, and while continuous inhalation of beta agonists has shown promise, the optimal therapy of severe status asthmaticus remains unclear. This paper describes our experience with a treatment protocol used in status asthmaticus with respiratory failure that seeks to avoid intravenous isoproterenol or assisted ventilation. STUDY DESIGN: Case series of pediatric intensive care patients with severe respiratory failure due to status asthmaticus. Six children and adolescents experienced a total of nine episodes of severe respiratory failure due to status asthmaticus. RESULTS: In seven of the nine episodes the patients were managed without either intravenous isoproterenol or mechanical ventilation. Hypercarbia persisted for an average of 25 hours (range 17 to 40 hours) in these seven episodes. All subjects recovered without notable sequelae. In two episodes, clinical and blood gas deterioration led to mechanical ventilation. Ventilation was required for 112 and 42 hours, respectively, in these episodes and the patients developed either pneumothorax or pneumomediastinum during ventilation. CONCLUSION: Using a protocol initiated in 1978 for correction of hypoxia and acidemia, many patients with severe respiratory failure from status asthmaticus can be treated without isoproterenol or mechanical ventilation. Since those treatments have significant risks, consideration should be given to this intervention before resorting to them.
Systemic toxicity of local anesthetics causes cardiac and central nervous system (CNS) depression that could be enhanced in the presence of respiratory acidosis. We examined a potential suppression of baroreflex function with bupivacaine and ropivacaine during hypercapnic acidosis or hypocapnic alkalosis. Baroreflex sensitivity (BRS) was randomly tested in rats with one of 13 conditions during intravenous administration of saline (control), bupivacaine 1, 2, or 3 mg/kg, or ropivacaine 2, 4, or 6 mg/kg. The effects of bupivacaine (3 mg/kg) or ropivacaine (6 mg/kg) on BRS were also examined during hypercapnic acidosis or hypocapnic alkalosis. The BRS was assessed using a value of delta heart rate/ delta mean arterial pressure after infusion of phenylephrine (3 micrograms/kg). Both bupivacaine and ropivacaine (at the largest dose) significantly suppressed BRS. Acute respiratory acidosis (pHa 7.24 +/- 0.04, Paco2 63 +/- 4 mm Hg) enhanced BRS. The BRS enhanced during acidosis was also suppressed with bupivacaine and ropivacaine, but less so than in the absence of acidosis. The presence of hypocapnic alkalosis (pHa 7.55 +/- 0.03, Paco2 25 +/- 2 mm Hg) did not affect BRS and reversed BRS suppression caused by both drugs. Thus, bupivacaine and ropivacaine affect neuronal control mechanisms for maintaining cardiovascular stability, and acute changes of respiration could significantly modify such suppression.