Once the AV nodal delay concludes, the electrical impulse is unleashed into the rapid ventricular conduction system.
The High-Voltage QRS Complex
The impulse travels down the Bundle of His, divides into the right and left bundle branches, and spreads through the Purkinje fiber network into the ventricular myocardium. Because the ventricular muscle mass is substantially larger than that of the atria and the depolarization occurs rapidly and synchronously, it produces a high-voltage deflection on the surface ECG—the QRS complex.
Excitation-Contraction Coupling
At the cellular level, depolarization opens L-type calcium channels (dihydropyridine receptors) in the sarcolemma. A small amount of extracellular calcium enters the cell and triggers a much larger release of calcium from the sarcoplasmic reticulum through ryanodine receptors. This process is known as calcium-induced calcium release (CICR). The rise in intracellular calcium allows binding to troponin C, which removes tropomyosin inhibition and enables actin-myosin cross-bridge cycling, resulting in contraction.
Isovolumetric Contraction
As the sarcomeres shorten, ventricular pressure rises sharply. During this phase all four valves remain closed because ventricular pressure has not yet exceeded the pressures in the aorta and pulmonary artery. This period of pure pressure generation without a change in volume is called isovolumetric contraction.
Understanding the transition from the QRS complex to mechanical systole is essential. Any delay or abnormality in ventricular depolarization can directly affect the timing and force of contraction, with immediate consequences for stroke volume.