Sedation for Cardiac Arrest Patients 

January 5, 2023

Cardiac arrest is a major public health challenge worldwide 1. Despite significant advances in resuscitation methods, cardiac arrest is still linked to high rates of mortality and morbidity 2. Targeted temperature management (by inducing mild therapeutic hypothermia) is usually used to improve neurological outcomes of cardiac arrest patients. Since the first clinical studies, sedation has been used too for faster achievement and better maintenance of target temperature in cardiac arrest patients 3. By attenuating thermoregulatory defenses and shivering reactions, sedatives also tend to boost the body’s tolerance to induced cooling 4

For cardiac arrest patients who are successfully resuscitated, a major concern is whether their body received sufficient oxygen during resuscitation efforts, as lack of oxygen is damaging to cells. The brain is particularly vulnerable to low oxygen conditions. In animal studies of brain ischemia, it has been shown that barbiturate or propofol sedation may be neuroprotective. However, few studies have focused the effects of sedation on cerebral physiology and outcomes following cardiac arrest.  

A recent study sought to assess whether sedation would improve survival and neurological outcomes in mice following cardiac arrest. To this end, researchers sought to characterize the effects of two commonly used sedatives, propofol (2,6-di-isopropylphenol), a γ-aminobutyric receptor agonist, and dexmedetomidine, a selective α-adrenoceptor agonist, in mice resuscitated from experimentally induced cardiac arrest with continuous electroencephalography (EEG) monitoring and cerebral blood flow assessment. Results revealed that the early administration of sedation with propofol or dexmedetomidine improved survival and neurologic outcomes in mice resuscitated from cardiac arrest treated with hypothermia 5.  

The beneficial effects of early pharmacologic sedation were linked to the attenuation of cerebral hyperemia and the early recovery of EEG power during and following sedation. Clinically, these data may point to the ability of sedation to induce EEG slow-wave activity in comatose patients and improve neurologic outcomes following cardiac arrest. 

Some differences have been identified in clinical outcomes across different drugs. For example, propofol/remifentanil provides a faster recovery of consciousness than midazolam/fentanyl; however, it is associated with the need for more vasopressors to maintain stable hemodynamic properties 3. No other significant differences in clinical outcomes have been identified across drugs. 

Research has identified that sedative medications used in post-cardiopulmonary resuscitation patients can act as confounders 6 on the basis of the 72-hour bedside neurological examination. Not only that, but if the 72-hour examinations are confounded by sedation, the 24- and 48-hour examinations are even less reliable. Nevertheless, daily neurological examinations during this time period should still be carried out as they may uncover the presence of seizures or a number of other important neurological exam changes. 

In any case, across clinical settings, neuromonitoring may help titrate the effects of key drugs and detect earlier complications (such as a seizure). However, a wake-up test should be avoided during the first 24 hours following cardiac arrest 3

A number of limitations remain with regard to sedation for cardiac arrest patients. Several studies have demonstrated that deep sedation increases the mortality rate of intensive care unit patients. In addition, hypothermia impairs important physiological processes like hemostasis, immune defense, intestinal function, and wound healing 7. Thus, as a general rule, the benefits and drawbacks of sedation and temperature control need to be carefully weighed on a case-by-case basis.  

In the future, additional studies will be required to shed more light on the effects of sedation on neurologic recovery in cardiac arrest patients.  


1. Benjamin, E. J. et al. Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association. Circulation (2019). doi:10.1161/CIR.0000000000000659 

2. Geocadin, R. G. et al. Standards for Studies of Neurological Prognostication in Comatose Survivors of Cardiac Arrest: A Scientific Statement from the American Heart Association. Circulation (2019). doi:10.1161/CIR.0000000000000702 

3. Dell’Anna, M., Taccone, F. S., Halenarova, K. & Citerio, G. Sedation after cardiac arrest and during therapeutic hypothermia. Minerva Anestesiologica (2014). 

4. Oddo, M. Optimising sedation practices during post-resuscitation care. Resuscitation (2018). doi:10.1016/j.resuscitation.2018.05.003 

5. Ikeda, T. et al. Post–cardiac arrest Sedation Promotes Electroencephalographic Slow-wave Activity and Improves Survival in a Mouse Model of Cardiac Arrest. Anesthesiology 137, 716–732 (2022). doi: 10.1097/ALN.0000000000004390. 

6. Samaniego, E. A., Mlynash, M., Caulfield, A. F., Eyngorn, I. & Wijman, C. A. C. Sedation confounds outcome prediction in cardiac arrest survivors treated with hypothermia. Neurocrit. Care (2011). doi:10.1007/s12028-010-9412-8 

7. Kalbhenn, J., Knörlein, J. & Posch, M. J. “Do no further harm” – Why shall we sedate unresponsive patients? Intensive Care Medicine (2021). doi:10.1007/s00134-021-06422-1