Cardiac Arrest: Difference between revisions

An obstruction of the airway is uncommon, but reversible and adequate recognition can prevent cardiac arrest.<cite>Fingerhut</cite> Airway obstruction is usually related with eating. In a mild obstruction patients can cough and speak and only frequent reassessment is advised. Patients that have a severe obstruction are unable to speak and have problems breathing and coughing. If a patient is still conscious five back blows can be applied between the shoulder blades whilst the patient leans forward. Otherwise five abdominal thrusts can be applied by clenching a fist and grasping it with the other hand. Place the hands it between the rib-cage and the umbilicus and pull sharply inward and upward whilst standing behind the patients.<cite>Guildner, Ruben</cite> If the patient loses consciousness start BLS.<cite>Koster2</cite>

[[File:MEWS.svg|thumb|500px|right|'''Figure 2.''' An example of a MEWS<cite>IHI</cite>.]]

The best way to prevent sudden death is to early detect deterioration of a patient and to act on early warning signs.<cite>Smith</cite> An early warning score (Figure 2) helps to create consensus among care providers about the sickness of a patient.<cite>Hodgetts, Hillman</cite> If the summed score is ≥ 3 a doctor should be notified. The notified doctor should assess the patient within 30 minutes and discuss a treatment plan. If the patient does not improve within 60 minutes a reassessment should follow with possible inclusion of a medical emergency team (MET) or intensive care specialist.<cite>Bellomo</cite>

During a cardiac arrest a structured assessment of the patient is required to detect the effects of the resuscitation, return of spontaneous circulation, reversible causes. To facilitate this assessment, an ABCDE approach can be used.<br>

'''Breathing:''' Hypoxaemia is a reversible cause and after assessment and securing the airway, ventilation of the patient should be optimized. Arterial blood oxygen saturation can be monitored to assess hypoxaemia. If necessary tracheal intubation, sedation and controllered ventilation should be instituted.<br>  

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 the chest compressions to minimize delay. Even after a 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. Continuous monitoring is required for return of spontaneous circulation or for asystole and initiation of the no-shock protocol.

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 intravenously 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 and myocardial dysfunction are common problems encountered after a cardiac arrest which resembles the problems encountered with sepsis. After resuscitation strict control of oxygenation, cardiac output and glucose metabolism can improve outcome after cardiac arrest. Treatment of the underlying cause of the cardiac resuscitation, for instance a myocardial infarction should be considered. Studies have indicated that therapeutic hypothermia (32-34^oC) during 12-24h after cardiac arrest can increase neurological outcome. This can be achieved by internal infusion or external cooling. Therapeutic hypothermia should be initiated in comatose patients quickly after return of circulation. When cooled the temperature should be maintained without to much fluctuations. Warming of the patient should occur very slowly (0.25^oC to 0.5^oC per hour) to prevent rapid plasma electrolyte concentration changes, intravascular volume and metabolic rate changes.

Prognosis after cardiac arrest is difficult and cannot be fully predicted. Survival after cardiac arrest is poor, mainly due to neurological damage, and two out of three patients admitted to the ICU following cardiac arrest die from neurological injury. Most prognostic markers have been studied in the era before therapeutic hypothermia. Therefore their value in patients that are actively cooled is incompletely understood. It is not possible to predict outcome reliable within 24 hours after cardiac arrest. Clinical examination of the patient can give information on the prognosis of the patient 24 hours after cardiac arrest. After 72 hours the absence of both pupillary light and corneal reflex predict 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 hours after return of spontaneous circulation are possible prognostic markers of a worse outcome. Furthermore myoclonal status is associated with poor outcome, but recovery can occur, and is therefore not useful in determining the prognosis. Electrophysiological studies measuring somatosensory evoked potentials (SSEP) after 24 hours, absence of bilateral N20 cortical response to median nerve stimulation predicts a poor outcome.

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