A heartbeat isn't triggered by a nerve impulse sent down from the brain each time, the way a muscle contraction usually is. The heart generates its own electrical signal, from specialised tissue inside the heart itself, and that signal has to travel through a precise, one-way sequence in a fraction of a second for the heart's four chambers to contract in the coordinated order that actually moves blood, rather than all contracting uselessly at once.
A built-in pacemaker, and a deliberate delay
The signal originates at the sinoatrial (SA) node, a small cluster of specialised cells in the right atrium that spontaneously generates an electrical impulse roughly sixty to a hundred times a minute at rest, functioning as the heart's natural pacemaker. That signal spreads rapidly across both atria, triggering them to contract and push blood into the ventricles below — but before the signal can reach the ventricles, it passes through the atrioventricular (AV) node, which deliberately slows the signal down for a fraction of a second, giving the atria time to finish emptying into the ventricles before the ventricles themselves are triggered to contract.
Why the delay, and the exact path after it, both matter
After the AV node's brief delay, the signal accelerates rapidly through a specialised conduction pathway — the Bundle of His, then the left and right bundle branches, then a network of Purkinje fibres — spreading through the ventricle walls fast enough that both ventricles contract together, from the bottom up, squeezing blood efficiently out through the arteries rather than contracting unevenly or from the top down, which would be far less effective at actually pushing blood forward. The entire sequence, from the SA node's initial signal to full ventricular contraction, normally takes well under a second, timed precisely enough that any disruption to the pathway or its timing — a blocked signal, an extra unwanted pathway, cells firing out of sequence — is what produces the range of conditions doctors group together as arrhythmias.
What we're still unsure about
Many arrhythmias are well understood and precisely mapped to a specific point of failure in this conduction pathway, but a meaningful share of cardiac rhythm disorders, particularly some forms of atrial fibrillation, don't trace to one single, clearly identifiable defect and instead appear to involve a more complex, still incompletely understood interplay between the heart's structure, its electrical properties, and other physiological factors. Precisely predicting which patients will develop a serious arrhythmia before it happens, based on their individual cardiac conduction patterns, remains an active, unresolved area of cardiology research rather than a fully solved diagnostic problem.
This sits inside Cardiac Physiology & the Cardiac Cycle, one of seven topics in Physiology, one of four domains in Medicine, one of seventeen subjects the app can quiz you on.