Clinical meaning
Cardiac arrhythmias are disorders of the heart's electrical conduction system that alter the rate, rhythm, or sequence of cardiac activation. Understanding the cellular electrophysiology underlying both normal conduction and arrhythmia generation is essential in nursing practice to interpret rhythm strips, anticipate clinical deterioration, and implement ACLS protocols effectively.
Normal cardiac electrical activity originates in the sinoatrial (SA) node, a crescent-shaped cluster of specialized pacemaker cells in the right atrial wall near the junction of the superior vena cava. SA node cells exhibit automaticity: they spontaneously depolarize during diastole (phase 4 depolarization) due to the funny current (If), a mixed sodium-potassium inward current activated by hyperpolarization. When the membrane potential reaches threshold (approximately -40 mV), slow calcium channels (L-type Ca2+) open, generating the action potential upstroke. The SA node fires at an intrinsic rate of 60 to 100 beats per minute, establishing normal sinus rhythm.
The impulse propagates through atrial myocytes to the atrioventricular (AV) node, located in the triangle of Koch at the base of the right atrial septum. The AV node introduces a critical delay of 0.12 to 0.20 seconds (represented by the PR interval on ECG), allowing atrial contraction to complete before ventricular activation begins (the atrial kick contributes approximately 20 to 30% of cardiac output). The impulse then travels rapidly through the bundle of His, which splits into the right bundle branch and left bundle branch (the left further dividing into left anterior and left posterior fascicles), and finally through the Purkinje fibers, which deliver the impulse to ventricular myocytes for coordinated contraction from apex to base.