**7.1 Oxygen supplementation after ROSC**

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

**9**

*Cardiopulmonary Resuscitation: Recent Advances DOI: http://dx.doi.org/10.5772/intechopen.91866*

**7.2 Post-resuscitation ventilation**

**7.3 Hemodynamic support**

**7.4 Temperature management**

Hypercapnia and hypocapnia should be avoided.

ties and complexities of individual physiology [72, 73].

intravenous infusion in OHCA cardiac arrest [74].

**8. Physiological monitoring during CPR**

**7.5 Post-cardiac arrest seizures prophylaxis and treatment**

to cause irreversible brain damage and hyperoxia has been implicated in neurological injury due to increased free radicals. With the availability of current literature, emphasis should be given to prevent further hypoxia after cardiac arrest [71].

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.

Hemodynamic support is necessary to maintain organ perfusions. Vital organs like brain, kidneys, and heart are most vulnerable to get affected by low perfusion states. A state of post-cardiac arrest shock is mostly due to cardiogenic shock and needs inotropic support. Vasopressors are also supplemented to achieve hemodynamic goals like maintaining the mean arterial pressure (MAP). The cutoff value for mean arterial pressure has not been suggested by any large RCTs or systemic reviews but most of the observational studies and data from other critical patients suggest maintaining a MAP > 65 mm Hg. Other goals like urine output have also been targeted. Hemodynamic goals should be individualized based on comorbidi-

Targeted temperature management (TTM) has been the keystone of postcardiac arrest care to prevent neurological injury and improving the outcome of the patients. The current evidence suggests maintenance of optimum core body temperature of 32–36°C for 24 h after cardiac arrest in initial shockable rhythm in which patients remained unresponsive after ROSC. TTM has also been suggested in OHCA for non-shockable rhythm. There is no role of inducing hypothermia by cold

Post-cardiac arrest seizures and status epilepticus have been linked with poor neurological outcomes. Post-cardiac arrest seizures can be due to brain damage during cardiac arrest. Seizures can further exacerbate the neurological injury. There is no sufficient literature to comment on the routine use of seizures prophylaxis after cardiac arrest. Based on the available current literature, the task force suggests against the routine use of seizures prophylaxis in IHCA and OHCA situations. There is a strong recommendation to treat post-cardiac arrest seizures. Various antiepileptic drugs have been used solely or in combinations in different dosing regimens to treat seizures to prevent further neurological injury and improve survival [75].

Current CPR guidelines suggest a common approach to all the patients irrespective of the varied underlying physiological differences among patients and clinical

to cause irreversible brain damage and hyperoxia has been implicated in neurological injury due to increased free radicals. With the availability of current literature, emphasis should be given to prevent further hypoxia after cardiac arrest [71].
