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Spontaneous Circulation: What to Do After the Heart Starts

Bruen, Charles MD

doi: 10.1097/01.EEM.0000476281.09979.8b
Spontaneous Circulation

Dr. Bruenis a cardiac intensivist and emergency physician at Regions Hospital in St. Paul, MN, and an assistant professor at the University of Minnesota with a special interest in emergency cardiovascular care. He completed a combined emergency medicine/internal medicine residency and fellowships in critical care and emergency cardiology at Hennepin County Medical Center. Visit his website, http://resusreview.com, follow him @resusreview, and read his past columns athttp://bit.ly/SponCirc.

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Figure

We drill ACLS algorithms over and over, but return of spontaneous circulation (ROSC) is not the end of the code. The last link in the chain of life is post-arrest (post-ROSC) care. Doing this right is critical for patients' survival and neurologic recovery.

Once perfusion is restored, organ function remains impaired. The body develops a post-arrest syndrome. Like sepsis, it is a maladaptive inflammatory response that worsens cardiac function from myocardial stunning, impairs vasoregulation, and causes systemic hypotension beyond the ischemic injury.

Maintaining adequate blood pressure and perfusion is critical to reversing organ ischemia. A goal of 65-70 mm Hg mean arterial blood pressure (MAP) is reasonable. Outcomes are best if patients can achieve this level of perfusion without vasopressors, but they should be used to reach this goal if needed.

Additional hypoxemia is devastating to an already-injured brain, and most patients are treated with high levels of FiO2 to maintain adequate oxygen tension. Hyperoxia is also associated, however, with increasing hospital mortality and poor neurologic status. A PaO2 of 100-150 mm Hg avoids the adverse outcomes of hypoxia and hyperoxia.

Carbon dioxide also has adverse outcomes outside of the range 40-45 mm Hg. Hypercapnia increases cerebral blood flow, which increases intracranial pressure, while hypocapnia causes cerebral vasoconstriction and decreased cerebral blood flow and oxygen delivery.

Hyperglycemia is common after cardiac arrest. The post-arrest phase is a hypermetabolic state in which hypoglycemia rapidly leads to harm. Targeting a level of less than 140 mg/dL and avoiding hypoglycemia is ideal.

Precautions against agitation and fever reduce brain tissue metabolism and are beneficial. Up to 36 percent of comatose survivors of cardiac arrest are found to have seizure activity, and most of these are in status. Status itself is a strong predictor of mortality, reflecting not only the initial insult of global ischemia but also the fact that seizures represent the state of most intense metabolic activity possible for the brain. Prophylactic anticonvulsants are not beneficial, but aggressive treatment is needed if seizures occur.

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ACS as the Cause

Revascularization is indicated if acute coronary syndrome was the original cause of the cardiac arrest. Around 50 percent of patients with arrest have a culprit lesion identified during angiography. It can be difficult to distinguish ACS from other causes of arrest such as sepsis, trauma, metabolic disorder, and hemorrhage.

Except under extremely rare circumstances, patients without a pulse gain little from cardiac catheterization. Resuscitated patients showing evidence of STEMI on ECG should be considered for emergent PCI. This is also true for patients with shockable initial rhythms (ventricular tachycardia/ventricular fibrillation) regardless of post-ROSC ECG findings, if they meet the criteria of over age 85 (previously 75), no history of terminal illness, no evidence of intracranial hemorrhage or major trauma, and pH greater than 7.0.

Unfortunately, catheterization lab mortality metrics are a real concern for your hospital and interventionist cardiologist. Interventional cardiologists will be reluctant to intervene on a patient until some hemodynamic or neurologic stability has been established, at least until the reporting criteria can be changed at the federal level.

Table

Table

Unless the patient meets STEMI criteria, a post-arrest catheterization can be delayed up to six hours without affecting survival or morbidity. This means that it might be reasonable to defer a 3 a.m. case until 8 a.m. PCI, however, should be performed before reaching the goal therapeutic hypothermia temperature if indicated in a comatose patient, which means they should go for angiography during the early post-arrest period.

Temperature management following cardiac arrest has seen dramatic changes recently. (http://emn.online/Apr15SponCirc.) Two landmark trials published in the New England Journal of Medicine in 2002 were responsible for treatment with therapeutic hypothermia at 33°C becoming widespread.

The Targeted Temperature Management Trial published in 2013 evaluated the equivalence (noninferiority) of using 36°C mild hypothermia for out-of-hospital cardiac arrest. (New Engl J Med 2013;369 [23]:2197.) It enrolled twice as many patients than previous RCTs for adequate power. It also added avoidance of hyperthermia after completion of 24 hours of temperature management and standardized neurological assessment. Hypothermia was so ingrained when the study started that several IRBs turned it down for being unethical. The results were neutral: no benefit of either temperature in any outcome, including adverse events.

Many criticisms were lobbed at the trial, mainly questioning the severity of illness of the enrolled patients and the applicability of the study. The patients in the study had a very short time to BLS (less than one minute) and more than 70 percent of patients received bystander CPR. Nevertheless, this study supports a protocol of mild hypothermia and avoidance of hyperthermia, and many institutions have changed their protocols.

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