Even brief hypoxia from cardiac arrest can cause lasting memory deficits

By Wayne Kuznar, for MDLinx
Published May 25, 2018

Key Takeaways

Even hypoxia lasting less than 7 minutes due to cardiac arrest can result in a reduction in hippocampal volume and significant memory deficits. Researchers led by Vess Stamenova, PhD, Women’s College Hospital, Toronto, Ontario, Canada, found a 10% average reduction in hippocampal volume in individuals who suffered out-of-hospital cardiac arrest and who were deemed neurologically intact on discharge compared with matched controls with myocardial infarction (MI). They reported their findings in Resuscitation.

The study suggests that a detailed neuropsychologic assessment should be performed for brief cardiac arrest survivors, according to the authors. “Patients should be referred for a neurological assessment, even in the absence of deficits on neurological screening tests, so that comprehensive assessments of memory are completed and appropriate rehabilitation referrals made,” wrote Dr. Stamenova and colleagues.

The investigators conducted neuropsychologic assessments and brain magnetic resonance imaging (MRI) on nine patients who had an MI not complicated by cardiac arrest and nine with ST-segment elevation MI who had sustained brief (< 7 minutes) cardiac arrest at the Rambam Medical Center in Haifa, Israel. Patients who had cardiac arrests lasting for a brief period before receiving cardiopulmonary resuscitation (CPR) were tested 2 to 4 years after the incident. The average time to test was 46 months in the MI group and 27 months in the group suffering cardiac arrest.

The volumes of both the left (P < 0.05) and the right (P < 0.05) hippocampus were significantly reduced by 15% to 20% in the patients with cardiac arrest relative to MI patients.

Neuropsychologic assessments included tests for general intelligence, visual processing, memory, executive functions, working memory, and recollection and familiarity.

Patients suffering cardiac arrest showed lower performance on several memory measures compared with MI patients. Significant differences between the two groups were observed only in the memory domain, with cardiac arrest patients performing worse (medians mostly in low-average to borderline range) than MI patients (medians in average to superior range). There was no significant difference between groups on assessments of recollection and familiarity, although cardiac arrest sufferers had a lower recognition hit rate (P < 0.05).

The reductions in hippocampal volume were also significantly correlated with measures of verbal memory, which were significant only in the cardiac arrest group. In this group, significant correlations were observed between the right hippocampus and immediate free recall (r=0.826, P=0.011), immediate cued recall (r=0.812, P=0.014), delayed cued recall (r=0.707, P=0.049), and the estimate of recollection (r=0.863, P=0.027). The recollection estimate was also strongly correlated with the left hippocampus (r=0.942, P=0.005).

The association between hippocampal volume and memory “provides support for the idea that the reductions in hippocampal volume were likely causing the decline in memory, even though the evidence here is only correlational,” wrote the investigators.

They concluded that “even brief episodes of hypoxia (< 7 minutes to CPR; average=2.6 minutes) lead to significant reductions in hippocampal volume and associated mild memory deficits that persist years after the cardiac arrest.”

Dr. Stamenova said that a comprehensive neurologic consult would be beneficial to patients since individual cognitive screening measures—such as the Cerebral Performance Category Scale, Mini Mental Status Examination, and the Montreal Cognitive Assessment—cannot sufficiently detect the memory problems faced by cardiac arrest survivors.

This study was funded by a Marie-Curie IRG grant, the Centre for Stroke Recovery, and the Sandra A. Rotman program in Cognitive Neuroscience.

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