Following a severe brain injury the goal of the clinician is to prevent secondary brain injury. This entails increasing oxygen delivery to the brain by preventing hypoxia and increasing cerebral perfusion. Hyperosmolar therapy, including mannitol and hypertonic saline, is often used to decrease ICP.
When patients present to the Emergency Department with acute upper GI bleeding, the natural inclination is to quickly pull the transfusion trigger. However, a 2013 study gives us pause:
Dynamic hyperinflation (autoPEEP, air trapping, etc.) is a process leading to an increase in end-expiratory lung volumes and increased airway pressures. This process may occur secondary to obstructive lung pathology and/or an increase in minute-ventilation without sufficient time for expiration. The pathologic effects of dynamic hyperinflation include an increased work-of-breathing, barotrauma, pneumothorax, and an increase in intrathoracic pressure leading to a decrease in cardiac output and possible hemodynamic collapse. Rapid identification of this process is crucial for reversing it.
In the setting of a severe asthma exacerbation that is refractory to medical mangagment and noninvasive ventilation, mechanical ventilation can be life-saving. However, the ventilator can quickly kill your patient if careful thought is not taken to address the unique respiratory needs and pulmonary physiology inherent to severe asthma.
When treating acute, wide-complex tachycardia deemed to be stable, monomorphic ventricular tachycardia, two agents remain prevalent among emergency medicine physicians: amiodarone and procainamide. This post examines some of the evidence behind these agents in achieving successful conversion of stable, monomoprhic VT.