Introduction

If too little potassium is present, the contractions become broader, and there results in fusion of the beats. If too much potassium is present...then the contraction of the ventricle is imperfect, and by increasing the quantity of potassium salt the beat becomes weaker and weaker till it stops.

Sidney Ringer (1883) From Moore (Moore, 1911) pvii

The origins of cardioplegia can be traced to 1883, with Sidney Ringer studying the effect of potassium on frog hearts, though the term was not introduced until 1957 by Lam. Myocardial protection has evolved over the last 60 years through intermittent cross-clamping, topical cooling, and more recently, crystalloid, whole blood cardioplegia, and lidocaine-containing solutions to induce and sustain diastolic relaxation, minimize energy consumption, and prevent ischemia-reperfusion injury. Simply stated, the aim of cardioplegia in myocardial protection is to curtail the postischemic myocardial dysfunction associated with ischemic arrest in cardiac surgery. Delivery techniques regarding antegrade versus retrograde, frequency, and temperature of cardioplegia remain polarizing topics. Protection methods are guided by the ability to minimize detectable injury to the contractile apparatus and release of injury biomarkers. This chapter reviews the rationale for various cardioplegia solutions and describes strategies for myocardial protection in common operations.