Heat Stroke Triggers Electrocardiographic (ECG) Abnormalities in a Conscious Rat Model

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Heat stroke (HS) is a potentially fatal injury that affects thousands of individuals every year. Multiple organs, including the heart, may be damaged as a result of HS. We showed previously that HS rats exhibit tachycardia, elevated cardiac Troponin I, and histological cardiac damage. Several observational studies and numerous case reports have described electrocardiogram (ECG) abnormalities among human HS patients, but these abnormalities have not been thoroughly investigated in animal HS models. This study identified the type of ECG abnormalities elicited in HS rats. Adult male Fisher 344 rats weighing 278.1±3.9 grams were previously implanted with radiotelemetry for continuous recording of core temperature (Tc), heart rate (HR), blood pressure, and Lead II ECG. After surgical recovery, rats were passively heated at an ambient temperature of 39°C until Tc reached 42.0±0.1°C (TcMax). Injury severity was classified as mild, moderate, or severe based on Tc responses during 24‐h of recovery. Baseline ECG recordings prior to heat exposure were normal. Severe and moderate rats had higher HR than mild rats at TcMax (mild 567±5; moderate 608±4; severe 611±15 bpm; p<0.05). Amplitude of the R wave during 1‐h of recovery was less for severe than mild and moderate rats (mild 1.58±0.12; moderate 1.60±0.10; severe 1.20±0.11 mV; p<0.05). ST depression was frequently observed prior to and shortly after TcMax and worsened with increasing injury severity. ST elevation was noted in two severe rats. ECG recordings taken the day after HS demonstrated an absence of T waves among severe rats and some moderate rats. These results demonstrate that ECG abnormalities occur as HS injury progresses and persist throughout acute recovery, which may be indicative of damage or dysfunction of the heart. Importantly, two rats died within 24‐h of HS recovery; one had extensive morphological ECG alterations whereas the other had a normal ECG, suggesting that cardiovascular dysfunction does not solely determine mortality but may contribute. In conclusion, ECG recordings should be monitored after HS for assessment of injury severity and potential cardiovascular dysfunction. Author views are not official US Army or DoD policy.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.