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Electrophysiological consequences of hypothermic hyperkalemic elective cardiac arrest
N M Cohen1, C A Allen, M K Belz
1Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond.
Insights
Hypothermic hyperkalemic cardioplegia (CPG) during cardiopulmonary bypass (CPB) increases arrhythmias. A new porcine model reveals CPG significantly slows ventricular activation and injures the heart's conduction system, impacting cardiac surgery safety.
Area of Science:
- Cardiovascular Research
- Cardiac Electrophysiology
- Surgical Innovation
Background:
- Pharmacological cardioplegic solutions improve cardiac surgery safety during cardiopulmonary bypass (CPB).
- However, hypothermic hyperkalemic cardioplegia (CPG) is linked to increased postoperative arrhythmias and conduction abnormalities.
- Existing models lack sensitivity to CPG-induced electrophysiological derangements.
Purpose of the Study:
- To develop and validate a large animal porcine model of CPB sensitive to CPG-induced electrophysiological (EP) changes.
- To quantify the spatial and temporal effects of CPG on ventricular activation.
- To assess CPG's impact on the heart's specialized conducting system and myocardium.
Main Methods:
- A customized computerized mapping system with up to 84 epicardial electrodes was used in a porcine CPB model.
- High-resolution measurement of spatial and temporal parameters of ventricular activation.
- Comparison between CPG arrest and hypothermia-alone control groups.
Main Results:
- CPG significantly slowed ventricular activation compared to hypothermia alone (p < 0.05).
- CPG induced profound, persistent changes in the spatial distribution and speed of ventricular activation.
- While traditional EP parameters were unchanged, CPG demonstrated injury to the specialized conducting system.
Conclusions:
- CPG induces injury to the heart's specialized conducting system and, to a lesser extent, the myocardium.
- The developed porcine model accurately reflects CPG-induced EP disturbances.
- This model provides a platform for testing novel CPG strategies to enhance myocardial preservation during CPB.
Abstract:
While the development of pharmacological cardioplegic solutions for myocardial protection during cardiopulmonary bypass (CPB) have significantly lengthened the safe operating time for cardiac surgical procedures, the introduction of hypothermic hyperkalemic cardioplegia (CPG) has markedly increased the incidence of postoperative arrhythmias and conduction abnormalities. Using a customized modification of a computerized mapping system, we have developed a large animal porcine model of CPB that is exquisitely sensitive to the electrophysiological (EP) derangements imposed by ischemia and cardiac arrest. This model is able to measure spatial and temporal parameters of ventricular activation with high resolution, using an array of up to 84 epicardial electrodes that can be reproducibly placed on the surface of the heart utilizing known epicardial anatomical markers (e.g., coronary arteries). With this system we have measured the spectrum of clinically observed EP disturbances caused by CPG, from slowed intraventricular conduction to complete heart block. Compared to the control group of hypothermia alone, 2 hours of crystalloid CPG arrest had a significant slowing effect on ventricular activation (p < 0.05). CPG was accompanied, in each animal, by profound changes in the spatial distribution of ventricular activation and persistent slowing of ventricular activation. Traditional EP parameters of effective refractory period and pacing threshold were unchanged by CPG. Smaller temporal and spatial changes were observed in the control group, but were always reversed by 90 minutes of warm reperfusion. We conclude that CPG induces injury of the specialized conducting system and, to a lesser degree, the myocardium. This model will afford us the opportunity to test new methods of CPG to further improve myocardial preservation during CPB.