Post-cardiac arrest syndrome
Post-cardiac arrest syndrome, also known as post-resuscitation syndrome, reflects a state of whole body ischaemia and subsequent reperfusion injury. Components include neurological dysfunction, transient myocardial dysfunction (myocardial stunning), and a systemic inflammatory response syndrome (SIRS).
In early reperfusion following cardiac arrest or severe hypoperfusion, the heart is initially hyperkinetic due to circulating catecholamines, with ensuing global hypokinesis. This transient myocardial dysfunction is responsive to inotropic drugs and usually resolves within 24-72 hours. Coronary blood flow is not reduced, indicating a true stunning phenomenon rather than permanent injury or infarction.
Note that this is a diagnosis of exclusion, and we must rule out other conditions including acute coronary syndrome prior to attributing cardiac dysfunction to post-cardiac arrest syndrome.
Hypothermia and repolarisation abnormalities
ECG changes in hypothermia relate to slowed potassium efflux in phase 1 and 2 of the cardiac action potential, correlating with early membrane repolarisation. This results in predominantly ventricular repolarisation abnormalities, manifesting on the ECG as prominent J waves, QT prolongation, and loss of normal T wave morphology. Bradycardia is common and may be the only initial feature.
Repeat ECG at 33°C (91.4°F)
- Note resolution of previously seen J waves in V4, V5 and aVR
- QT interval has shortened to within normal limits
- T waves are now visualised in both lateral precordial and inferior leads
Complications of rewarming
Disproportionate hypotension often occurs during rewarming, due to a combination of severe dehydration, fluids shifts, and peripheral vasodilation as a result of active external rewarming. An after drop in temperature is common and was seen in this patient — when the extremities are rewarmed, cold, acidaemic blood that has pooled in vasoconstricted extremities of the hypothermic patient returns to core circulation, causing a drop in temperature and pH. This can theoretically predispose to arrhythmias but usually is clinically insignificant. Focussing active external rewarming on the trunk can reduce these complications.
Failure to rewarm should raise suspicion for other contributing causes of hypothermia, including sepsis (especially in the elderly patient), adrenal insufficiency, and hypothermia.
Electrolyte concentrations can be unpredictable during rewarming and should be closely monitored. Severe hypothermia (< 30°C) is associated with insulin resistance, and these patients are predisposed to hypoglycaemia on rewarming as insulin sensitivity normalises. It would be prudent to give a glucose infusion (100ml/hour of 10% dextrose) until core temperature is above 34°C.
Cardiac function in hypothermia
There are sparse human studies on the effects of hypothermia on myocardial contractility. Limited studies in patients undergoing cardiothoracic surgery suggest there is little change in left ventricular contractility with cooling to 32-34°C, but beyond this point both contractility and heart rate fall leading to substantial reductions in cardiac output. Due to slowed metabolism and peripheral vasoconstriction, lower cardiac output is required to maintain vital organ perfusion in hypothermic patients.