What is the mechanism of fibrillary arrest in deep hypothermic circulatory arrest (DHCA)?

Mechanism of Fibrillary Arrest in Deep Hypothermic Circulatory Arrest (DHCA)

Fibrillary arrest in deep hypothermic circulatory arrest occurs primarily due to hypothermia-induced changes in cardiac electrophysiology, with the hypothermic heart becoming increasingly irritable and prone to ventricular fibrillation as temperatures decrease below 28°C. 1

Physiological Basis of Fibrillary Arrest

• Deep hypothermia reduces cerebral metabolic rate by approximately 6% for every 1°C reduction in brain temperature, which is the primary neuroprotective mechanism during circulatory arrest 1
• As core temperature decreases below 28°C, the heart becomes increasingly irritable and susceptible to ventricular arrhythmias, particularly ventricular fibrillation 1
• The hypothermic heart demonstrates altered calcium handling, ion channel function, and action potential duration, all of which contribute to electrical instability 1
• Conventional wisdom suggests that the hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation, though this is largely theoretical 1

Temperature Thresholds and Cardiac Effects

• DHCA typically involves cooling patients to temperatures ranging from 12° to 30°C using extracorporeal circulation 1
• At temperatures below 30°C, drug metabolism is significantly reduced, raising concerns about medication accumulation to potentially toxic levels if administered repeatedly 1
• Case reports document refractory ventricular arrhythmias with severe hypothermia, though animal models suggest that hearts at temperatures as low as 30°C may still respond to defibrillation 1
• The risk of ventricular fibrillation increases progressively as temperature decreases, with fibrillary arrest becoming more common below 25°C 2

Metabolic Changes Contributing to Fibrillary Arrest

• Hypothermia suppresses many chemical reactions associated with normal cardiac function, including:
  • Altered free radical production
  • Changes in excitatory amino acid release
  • Disrupted calcium shifts within cardiac cells
  • Potential mitochondrial damage 1
• These metabolic changes can lead to electrical instability and increased susceptibility to fibrillation 1, 2

Management Considerations During DHCA

• If ventricular fibrillation occurs during DHCA, defibrillation should be attempted, though the efficacy may be reduced at very low temperatures 1
• If VF persists after a single shock, it may be reasonable to perform further defibrillation attempts according to standard BLS algorithms concurrent with rewarming strategies 1
• Animal studies suggest that vasopressor medications (epinephrine or vasopressin) may increase rates of return of spontaneous circulation compared to placebo, though data remains limited 1
• Careful rewarming is essential, as rewarming from moderate-to-deep hypothermia has been associated with neuronal injury, neuroinflammation, and loss of cerebrovascular autoregulation 3

Clinical Implications and Safety Considerations

• The "safe" period for circulatory arrest appears to be limited to approximately 40 minutes, with stroke risk increasing after this threshold 4
• Mortality rates increase markedly after 65 minutes of circulatory arrest 4
• Institutional experience is an important factor in selecting brain protection techniques during DHCA 1
• Monitoring of brain function and metabolic suppression through electroencephalography, evoked potentials, and other methods can help guide the timing of circulatory arrest 1

DHCA remains an effective technique for cerebral protection during complex aortic surgeries when properly implemented, with outcomes comparable to other methods such as antegrade cerebral perfusion and retrograde cerebral perfusion 2.