**7.2 Post-resuscitation ventilation**

*Sudden Cardiac Death*

**6.3 Antiarrhythmic drugs**

*6.3.1 Amiodarone*

*6.3.2 Lidocaine*

*6.3.3 Magnesium sulfate*

arrest is discouraged [70].

logical morbidities and mortalities.

**7.1 Oxygen supplementation after ROSC**

recurrent VT/pulseless VT after 1 shock."

by 0.5 mg/min for the next 18 h.

benefits have been shown with its use [69].

**7. Recent advances in post-resuscitation care**

no improvement in short term benefits like ROSC and admission to discharge criteria or any long term benefits in quality of life/neurological outcomes. The combination of epinephrine and vasopressin has also been non-superior to epinephrine

Antiarrhythmic drugs are used in refractory ventricular dysrhythmias during cardiac arrest. Refractory ventricular arrhythmias are defined as the "persistent or

Amiodarone is a mainly a class III antiarrhythmic drug but also shows class I, II, and IV antiarrhythmic properties which showed benefits in ROSC. Although, no long term benefits were observed in survival to discharge benefits by the drug administration compared to placebo [68]. Amiodarone should only be used in the case when cardioversion/defibrillation and epinephrine administration have failed to revert the fatal arrhythmias to sinus rhythm. The dosing regimen during CPR is 300 mg intravenous/intraosseous bolus followed by the second dose of 150 mg failing the initial bolus dose to convert the rhythm. After successful cardioversion, amiodarone infusion should be continued for 6 h at the rate of 1 mg/min followed

Lidocaine is a local anesthetic which has been used as a substitute of amiodarone during a cardiac arrest for refractory VF/pulseless VT in cases of unavailability of the later. The initial dose is 1–1.5 mg/kg by the intravenous or intraosseous route. The evidence for the use of lidocaine during cardiac arrest is lacking and no survival

Magnesium sulfates have been used in torsade's de points caused by low serum magnesium levels. There is no survival benefit with the routine use of magnesium sulfate during cardiac arrest and routine use of magnesium sulfate during cardiac

There has been considerate literature available in post-resuscitation care from 2010 in various domains of resuscitation. All the post-resuscitation care interventions are aimed to increase the survival to discharge ratio and decrease the neuro-

Hypoxia during a cardiac arrest has been the cause of neurological injury and post-cardiac arrest morbidity. The optimum level of blood oxygenation for improving the neurological outcome has been studied but no RCTs and systemic reviews are available to support or refute normoxia or hyperoxia. Hypoxia has been well known

alone in improving clinical outcomes in patients [65–67].

**8**

Cardiac arrest has been associated with brain injury as well as injury to other organs including lungs. The optimal PCO2 to prevent further injury to the brain is critically important and need to optimize our ventilator strategy. Normocarbia is preferred in post-cardiac arrest to maintain the physiological homeostasis and acid-base balance. Ventilatory strategies should be individualized to patients. Hypercapnia and hypocapnia should be avoided.
