Medication for in-hospital cardiac arrest

Reviewed by Jessica Munoz DPN, RN, CEN

In-hospital cardiac arrest (IHCA) continues to be significant in numbers and is linked to a high death rate. Attention has been focused on cardiovascular conditions with high death rates, such as myocardial infarctions, stroke, and out-of-hospital cardiac arrests (OHCA). Over 290,000 adults suffer in-hospital cardiac arrest every year in the United States. Cohort data from the United States shows that the average age of victims suffering in-hospital cardiac arrest is 66 years, 58% are male, and the current pattern is most often (81%) non-shockable (ie, asystole or pulseless electrical activity). The most common cause of IHCA is cardiac (50%–60%), followed by respiratory insufficiency (15%–40%). Attempts to stop in-hospital cardiac arrest need not only a mechanism for recognizing the worsening condition of patients but also a suitable interventional response (eg, rapid response teams). ¹

In-hospital cardiac arrest remains a major clinical issue, with survival to discharge typically ranging from about 15–20%, depending on patient population and hospital setting. The survival rate may exceed 30% after a person witnessing pulseless VF or VT responds to one or two direct countershocks. However, survival after in-hospital asystole, pulseless electrical activity, or refractory VF/VT (defined as not responsive to two countershocks) may be considerably lower (< 5–10%).

IHCA treatment

A multidisciplinary team is required for the proper assessment and treatment of the patient’s current clinical conditions. The team has nurses, cardiologists, critical care providers, neurologists, lab technicians, and some other specialists who provide simultaneous care and expertise.³ The in-hospital cardiac arrest treatment consists of chest compressions, ventilation, early defibrillation, and treatment of reversible causes, such as hyperkalemia, hypoxia, or suspected massive pulmonary embolism in select cases.

According to clinical trials, vasopressor use during cardiac arrest may improve return of spontaneous circulation (ROSC), but has shown limited or inconsistent improvement in neurologically intact survival to hospital discharge. There is evidence, however, that the use of vasopressor agents favors initial ROSC.⁴

Epinephrine and vasopressin
VF and pulseless VT

Epinephrine

Epinephrine hydrochloride has α-adrenergic receptor–stimulating vasoconstrictive properties that are beneficial in cardiac arrest by increasing coronary and cerebral perfusion during CPR. These epinephrine effects subsequently increase cerebral and coronary perfusion pressure during CPR. However, the value and safety of β-adrenergic effects are disputed, as they increase cardiac workload and reduce subendocardial perfusion. Epinephrine is widely used in resuscitation and has been shown to improve return of spontaneous circulation (ROSC), with a smaller and less consistent effect on survival to hospital discharge and neurologically intact survival.

Vasopressin

Vasopressin is a potent vasoconstrictor that acts on V1 receptors to increase vascular tone during cardiac arrest. Despite promising randomized studies, additional lower-level studies, and multiple well-performed animal studies, large randomized controlled human trials failed to show an increase in rates of ROSC or survival when vasopressin was compared with epinephrine as the initial vasopressor for treatment of cardiac arrest.

Asystole and pulseless electrical activity

Vasopressors

The studies described above enrolled patients with PEA and asystole and failed to show that either vasopressin or epinephrine is superior for the treatment of PEA regardless of the order of administration. A post hoc analysis suggested possible survival differences between vasopressin and epinephrine; however, no evidence of improved neurologically intact survival was found, and these findings did not change guideline recommendations.

Vasopressin is not recommended for asystole or PEA in current ACLS guidelines. Epinephrine is the recommended vasopressor during treatment of these rhythms. Further research is required. Epinephrine may be administered every 3 to 5 minutes during resuscitation.⁴

Summary

Ideally, if ACLS providers can intervene during the pre-arrest period, they can prevent pulseless arrest. If the arrest occurs, good ACLS begins with high-quality BLS. During the resuscitation process, the rescuers must provide chest compressions with the required rate and depth, allowing the chest to recoil completely between the compressions and keeping the interruption as little as possible. Rescuers should be careful not to provide excessive ventilation, particularly once an advanced airway is in place. Resuscitation drugs, particularly epinephrine, improve ROSC, while survival to hospital discharge and neurologically intact survival remain strongly dependent on high-quality CPR and early defibrillation.⁴

References

1. https://pmc.ncbi.nlm.nih.gov/articles/PMC6482460/
2. https://clinicaltrials.gov/study/NCT00411879?tab=table
3. https://www.ncbi.nlm.nih.gov/books/NBK321499/
4. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.105.166557