Ca²⁺ sparks are spatially localized intracellular Ca²⁺ release events that were first described in 1993. Sparks have been ascribed to sarcoplasmic reticulum Ca²⁺ release channel (ryanodine receptor, RyR) opening induced by Ca²⁺ influx via L-type Ca²⁺ channels or by spontaneous RyR openings and have been thought to reflect Ca²⁺ release from a cluster of RyR. Here we describe a pharmacological approach to study sparks by exposing ventricular myocytes to caffeine with a rapid solution-switcher device. Sparks under these conditions have properties similar to naturally occurring sparks in terms of size and intracellular Ca²⁺ concentration ([Ca²⁺]_i) amplitude. However, after the diffusion of caffeine, sparks first appear close to the cell surface membrane before coalescing to produce a whole cell transient. Our results support the idea that a whole cell [Ca²⁺]_i transient consists of the summation of sparks and that Ca²⁺ sparks consist of the opening of a cluster of RyR and confirm that characteristics of the cluster rather than the L-type Ca²⁺ channel-RyR relation determine spark properties.