Cardiac mitochondria power the mechanical twin pump that delivers nutrients, O2, hormones, and other factors to all cells of the body while extruding waste products and carbon dioxide. The heart itself is fed by its own coronary circulatory system. The sinoatrial node pacemaker self-initiates an action potential that spreads throughout the heart to cause muscle contraction and relaxation. A depolarization wave transiently opens voltage-gated Na+ channels and then induces Ca2+ release via L-type Ca2+ channels in the sarcoplasmic reticulum, which primarily results in a polarized state long enough to increase myofibrillar Ca2+ for contraction that propels blood ejection. Action potential repolarization occurs with closure of L-type Ca2+ channels and the influx of K+ so that myocytes lengthen and relax. Na+ entry stops with depolarization and Na+ is extruded by Na+-K+-ATPase. The excitation-contraction coupling of the action potential with cell Ca2+ influx and efflux is mediated by fast Ca2+ release via ryanodine receptors in the sarcoplasmic reticulum with reuptake and extrusion by Ca2+-ATPases. The binding of Ca2+ to troponin C causes the myosin filament to slide over the actin filament which shortens the muscle cells in unison. The rise and fall in both cell Ca2+ and in the generated left ventricular pressure can be measured together in isolated hearts. Cardiac mitochondria dynamically buffer large amounts of Ca2+ as calcium phosphates. The buffering system capacity is assessed by measuring the change in ionized mitochondrial Ca2+ and the Ca2+ retention capacity and is dynamically responsive to energy availability. Excess mitochondrial ionized Ca2+ is slowly removed, mostly by mitochondrial Na+-Ca2+ exchange. Studies suggest that during mitochondrial stress due to cardiac ischemia, mitochondrial Ca2+-H+ and K+-H+ exchangers remove excess Ca2+ and K+ while inducing proton influx (H+ leak); this stimulates respiration and reduces release of superoxide radicals and hydrogen peroxide. Nitric oxide, whether produced in the cell or in mitochondria, can react with excess superoxide to form the toxin peroxynitrite that can damage lipids, proteins, and nucleotides, both within mitochondria and within the cell.