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Blood cardioplegia delivery. Deleterious effects of potassium versus lidocaine
Insights
High potassium concentrations in cardioplegic solutions increase coronary vascular resistance and impede solution delivery. Adding lidocaine prevents these adverse effects, ensuring better myocardial protection during cardiac surgery.
Area of Science:
- Cardiovascular Surgery
- Cardiothoracic Anesthesia
- Cardiac Physiology
Background:
- Effective myocardial protection during cardiac surgery relies on uniform cardioplegic solution delivery.
- Limited data exist on how cardioplegic agents affect coronary vascular resistance (CVR) and solution distribution.
Purpose of the Study:
- To evaluate the impact of high potassium (K+) and lidocaine on CVR and cardioplegic (CP) solution delivery during hypothermic arrest.
- To assess the protective role of lidocaine against K+-induced changes in CVR and CP distribution.
Main Methods:
- An in vivo isolated dog heart model was used with three groups: high K+, lidocaine, and combined K+/lidocaine.
- Hypothermic blood cardioplegia was administered multi-dosely over 75 minutes.
- Coronary vascular resistance, CP flow, distribution, and myocardial metabolism were measured.
Main Results:
- High K+ (30 mEq/L) significantly increased CVR and reduced CP flow and distribution, particularly after the second infusion.
- Lidocaine, alone or combined with K+, prevented the adverse effects of high K+ on CVR and CP delivery.
- No significant differences were observed in myocardial oxygen consumption, lactate metabolism, or water content among groups.
Conclusions:
- High concentrations of K+ in cardioplegic solutions markedly increase CVR, impairing solution delivery and distribution.
- Lidocaine effectively mitigates these detrimental effects, suggesting its utility in cardioplegic formulations.
- Reassessment of cardioplegic solution additives is warranted to optimize CVR and distribution during cardiac arrest.
Abstract:
Delivery of cardioplegic (CP) solutions to all regions of the myocardium is critical for optimal myocardial protection during cardiac surgery. However, there are little data regarding the effects of CP agents upon coronary vascular resistance (CVR) and CP delivery. Accordingly, we evaluated blood CP (Hct 30) delivery and CVR during 75 minutes of multi-dose hypothermic blood CP arrest in an in vivo isolated dog heart preparation. Three groups of dogs were studied: K(K+ = 30 mEq/L; n = 6), L (Lidocaine = 400 mg/L; K+ = 4 mEq/L; n = 6), and KL (K+ = 30 mEq/L, Lidocaine 400 mg/L; n = 6) during total cardiopulmonary bypass and moderate systemic hypothermia (28 C). Basal CVR was calculated by measuring total coronary flow (HR 120/min; mean aortic pressure = 80 mmHg) in the empty beating heart. After aortic cross-clamping, the blood CP solution was infused into the aortic root at a constant pressure (80 mmHg) and constant temperature (16 +/- 2 C) for 60 seconds at 15 minute intervals for a total arrest time of 75 min. Total CP flow, CVR, O2 consumption, lactate extraction/production, and K+ balance during 75 minutes of arrest and 30 minutes of reperfusion were determined. The distribution of the CP solution in the left ventricle was measured with radioactive microspheres (9 +/- 1 mu). Biopsy specimens were taken to measure wet to dry ratios. Values are mean +/- SEM. Data were analyzed by BMDP-P2V. During the first CP infusion, after aortic cross-clamping, no differences in CVR or CP distribution were found among the three groups. However, CVR was increased significantly in the K group during the second CP infusion (O': 0.98 +/- 0.20 mmHg/ml/min/100 g; 15': 2.66 +/- 0.82; p less than 0.001). The CVR remained high for the remainder of the arrest period. Moreover, total, epi- and endocardial flow decreased significantly (54%, p less than 0.001). In groups L and KL, no significant changes in CVR were seen. Groups K and KL showed a significant K+ extraction during the first CP infusion. During the early reperfusion period, K+ washout occurred in these two groups, which was not seen in the L group. There was no significant difference between the three groups in myocardial O2 consumption, lactate metabolism, and water content during the arrest and the reperfusion period. In conclusion, high concentrations of K+ (30 mEq/L) can markedly increase CVR and impair blood CP delivery and distribution. These effects can be prevented by lidocaine. These findings warrant reassessment of the various additives to CP solutions and their effects on CVR and CP distribution during multi-dose hypothermic CP arrest.