Fibrinolytic therapy in pulmonary embolism: an evidence-based treatment algorithm.

Patients presenting with pulmonary embolism (PE) have a wide spectrum of clinical severity. Although some patients may present with frank hemodynamic collapse and cardiac arrest, others may present with an asymptomatic PE that is discovered incidentally during workup of another condition. Fibrinolytic therapy is an option in the treatment of patients with PE due to its ability to rapidly dissolve thromboemboli clots. However, the use of fibrinolytics in the treatment of PE is a controversial topic that has left many practicing physicians confused on how to best treat these patients. A rational approach to deciding whether fibrinolytic therapy is indicated is based on an assessment of the benefit that each particular patient will derive from fibrinolytic therapy weighed against that patients risk for major bleeding and intracranial hemorrhage. There is a clear benefit/risk ratio for fibrinolytic therapy in patients with PE who present with cardiac arrest and in those who are hemodynamically unstable from a massive PE. With proper risk assessment, select patients with stable hemodynamics and right ventricular dysfunction may also benefit from fibrinolytic therapy. There is no benefit to fibrinolytic treatment in patients with stable hemodynamics and normal right ventricular function. This article sets out to review the literature on fibrinolytic therapy in the treatment of patients with PE and will propose an evidence based treatment algorithm.

Should etomidate be used for rapid-sequence intubation induction in critically ill septic patients?

Etomidate is an agent often used by emergency medicine physicians for rapid-sequence intubation induction of critically ill patients because of its reliable pharmacokinetics and cardiovascular stability. Etomidate is known to inhibit endogenous cortisol production through inhibition of 11beta-hydroxylase. Previous studies in undifferentiated emergency department patients and healthy, elective surgical patients have shown this effect to be only transient and not clinically significant. Recent retrospective studies in the pediatric and adult intensive care literature have shown an association between a single induction dose of etomidate in critically ill septic patients and sustained suppression of the adrenal axis with an increase in mortality. It is unknown at this time if any increase in mortality associated with etomidate-induced adrenal suppression would be offset by concomitant corticosteroid administration. Aggressive resuscitation of septic patients with fluids, antibiotics, and vasopressors has been shown to significantly reduce mortality and may allow for the use of alternative agents that had previously been discouraged because of concern for hemodynamic collapse during intubation. A prospective randomized trial in septic patients of etomidate induction with early corticotropin stimulation testing or corticosteroid supplementation vs the use of alternative induction agents with enough power to detect differences in mortality is needed to further address this clinical dilemma.

Atrial fibrillation in the Wolff-Parkinson-White syndrome: ECG recognition and treatment in the ED.

Estimated to occur in 0.1% to 0.3% of the population, Wolff-Parkinson-White syndrome (WPW) is a condition where atrial impulses bypass the atrioventricular node and activate the ventricular myocardium directly via an accessory pathway. Clinical clues to the diagnosis include a young patient with previous episodes of palpitations, rapid heart rate, or syncope. Although several different rhythm presentations are possible, atrial fibrillation is a not infrequent dysrhythmia seen in the WPW patient. Electrocardiographic features suggestive of WPW atrial fibrillation include irregularity of the rhythm; a very rapid ventricular response; presence of a delta wave; and a wide, bizarre QRS complex. Stable patients suspected of having this condition should not receive agents that predominantly block atrioventricular conduction, but they may be treated with procainamide or ibutilide. If instability is present, electrical cardioversion is required.

Activity-dependent plasticity of calcium clearance from crayfish motor axons.

Previous studies of a crayfish explant culture demonstrated that regenerating motor axons with high impulse activity develop more rapid clearance of cytoplasmic free Ca(2+) than those with low impulse activity. We examined whether Ca(2+) clearance in mature axons also showed activity-dependent plasticity. We studied the phasic and tonic axons of the motor bundle innervating the crayfish closer muscle that display large differences in impulse activity. To compare their Ca(2+) regulation, we applied the Ca(2+) ionophore Br-23187 (1 microM) and measured the increase in intracellular free Ca(2+) concentration ([Ca(2+)](i)) with fura-2. After 55 min of ionophore application, the increase in [Ca(2+)](i) in the phasic axons (1,326 +/- 192 nM) was significantly greater than in the tonic axons (359 +/- 148 nM). This resulted from stronger Ca(2+) clearance in the tonic axon rather than less Ca(2+) influx because blocking Ca(2+) clearance by Na/Ca exchange and mitochondria eliminated these differences in [Ca(2+)](i). Next we determined whether Ca(2+) clearance from the phasic axon could be strengthened by a prolonged increase in impulse activity. The phasic axon was stimulated in vivo at 5 Hz for 1 h/day for 5 days, and 1-3 days after stimulation, Ca(2+) clearance was again examined. After 55 min of Br-23187 (1 microM) exposure, the increase in [Ca(2+)](i) in the stimulated phasic axon was only 232 plus minus 123 nM, which was much less than in the control phasic axons and similar to that in the tonic axons. Thus Ca(2+)-clearance mechanisms adapt to changes in impulse activity both in growing and mature axons.