Cardiac Arrest: Difference between revisions

BLS the cornerstone to the treatment of cardiac arrest. Early and high quality CPR is critical to survival. In the hospital setting trained expert en technical equipment can facilitate cardiac arrest management. The only intervention besides proper BLS and early defibrillation to increase survival is the administration of adrenaline. The ALS protocol deviates into two strategies encountered in the setting of cardiac arrest; a shock protocol and no-shock protocol. During both protocols it is important to establish intravascular access as soon as possible, as an alternative intraosseous injection of drugs can be performed. Furthermore assessment of airway management and ventilation is essential. Oxygen should be administered as soon as possible and be titrated tot the arterial blood oxygen saturation. Tracheal intubation is the optimal method of providing and maintaining a clear and secure airway. Intubation should be performed by experienced personnel to reduce complications and delay between intubation and chest compressions. When there is return of spontaneous circulation the resuscitation team should stabilize the patient to prevent recurrence of cardiac arrest.  

When a shockable rhythm is detected, it is important to minimize the time between chest compressions and defibrillation. When the shock is delivered immediately resume with chest compressions to minimize delay. Even after successful shock the heart can be stunned and effective circulation can only be maintained through chest compressions. After the first round of shock and compressions reassess rhythm and act according to the protocol. After the third shock has been given, adrenaline 1mg and amiodarone 300mg can be administered intravenously. Further adrenaline 1mg can be administered every 3-5 minutes, there is no further indication for anti-arrhythmic drugs during resuscitation.

When asystole or pulseless electrical activity is detected CPR should be started immediately simultaneously with 1mg intravenous adrenaline. Assess the rhythm after 2 minutes of chest compressions and continue according to the rhythm. Continue with adrenaline injections every 3-5 minutes if no return of spontaneous circulation has been achieved. There is no place for further medical intervention.  

After cardiac arrest and return of spontaneous circulation the whole body ischemia/reperfusion affects all organ systems. Multiple organ failure, increased risk of infection, neurocognitive dysfunction, myocardial dysfunction are common problems encounter after a cardiac arrest and resembles the problems encountered with sepsis. After resuscitation strict control of oxygenation, cardiac output and glucose metabolism can improve outcome after cardiac arrest. Studies have indicated that a period of 12-24 h after cardiac arrest therapeutic hypothermia (32-34oC) can increase neurological outcome. This can be achieved by internal infusion or external cooling. Cooling should be initiated quickly after return of circulation. When cooled the temperature should be maintained without to much fluctuations. Warming of the patient should occur very slowly (0.25oC to 0.5oC per hour) to prevent rapid plasma electrolyte concentration, intravascular volume and metabolic rate change.  

Prognosis after cardiac arrest is difficult and not fully predictable. Survival after cardiac arrest is poor, mainly due to neurological damage. Clinical examination of the patient can give information on the prognosis of the patient after cardiac arrest. The absence of both papillary light and corneal reflex at >72h predicts poor outcome. In patients that are not treated with therapeutic hypothermia absence of vestibulo-ocular reflexes at >24h and a Glasgow coma scale motor score of 2 or less >72 are possible prognostic markers of a worse outcome. Furthermore myoclonus status is associated with poor outcome, but recovery can occur, and is therefore not useful in prognostication. Electrophysiological studies measuring somatosensory evoked potentials after 24 hours, absence of N20 cortical response to median nerve stimulation predict poor outcome.