Depolarizing potassium cardioplegia does not afford optimal cardioprotection in pediatric
or adult patients requiring complicated operative procedures. Polarizing adenosine-lidocaine
cardioplegia has been shown to be cardioprotective without hyperkalemia. Our aim was
to examine the effects of changing extracellular potassium levels in adenosine-lidocaine
cardioplegia on arrest and reanimation properties.
Isolated-perfused rat hearts (n = 96) were arrested at 32 degrees C to 33 degrees
C for 1 or 2 hours with intermittent 200 mumol/L adenosine and 500 mumol/L lidocaine
in modified Krebs-Henseleit buffer with 0.1, 3.0, 5.9, 10, and 16 mmol/L potassium
or with 16 or 25 mmol/L potassium in Krebs-Henseleit buffer (n = 8 for each group).
Membrane potentials were estimated in the arrested ventricular myocardium (n = 42),
and recovery function was measured in working mode during 60 minutes' reperfusion.
Arrest was interrupted by breakout beats in the adenosine-lidocaine hypokalemic (0.1
and 3 mmol/L potassium) and non-adenosine-lidocaine hyperkalemic (16 and 25 mmol/L
potassium) groups. The membrane potentials for the non-adenosine-lidocaine 16 and
25 mmol/L potassium groups were -51 and -39 mV, and those for the adenosine-lidocaine
groups (0.1, 3.0, 5.9, 10, and 16 mmol/L potassium) were -183, -94, -75, -65, and
-49 mV, respectively. After 1 hour of arrest, coronary vascular resistance increased
linearly in adenosine-lidocaine cardioplegia with increasing potassium levels (5.9,
10, and 16 mmol/L), and the slope increased more than 2-fold after 2 hours. Nearly
40% of hearts in the adenosine-lidocaine (0.1 mmol/L potassium) and non-adenosine-lidocaine
25 mmol/L potassium groups failed to recover after 1 hour arrest. After 2 hours, hearts
in the polarizing (5.9 mmol/L potassium) adenosine-lidocaine group increased coronary
vascular resistance by only 30% and spontaneously recovered 107% heart rate, 92% systolic
pressure, 81% aortic flow, and 113% coronary flow (all metrics returned 85% to 100%
at 15 minutes) with no reperfusion arrhythmias. In contrast, hearts in the adenosine-lidocaine
(3, 10, and 16 mmol/L potassium) groups were all slow to recover (15% to 40% return
at 15 minutes) and experienced arrhythmias. Increasing potassium levels in adenosine-lidocaine
cardioplegia from 5.9 to 16 mmol/L resulted in a 67% loss of left ventricular contractility.
Polarizing adenosine-lidocaine cardioplegia (5.9 mmol/L potassium) administered intermittently
at 33 degrees C provides superior arrest and reanimation profiles under normokalemic
conditions when the myocardial cell membrane potential is close to its resting state.
Copyright 2010 The American Association for Thoracic Surgery. Published by Mosby,
Inc. All rights reserved.