Cardiac muscle, like skeletal muscle, contains myosin, actin, tropomyosin, and troponin in various isoforms. Even though cardiac muscle fibers resemble skeletal muscle fibers in that they are striated, they differ in that they form a functional syncytium, which means that all fibers are electrically connected via gap junctions. Pacemaker cells of the electrical conduction system can initiate depolarization, and thus contraction, throughout the myocardium without external neurohormonal control.
The cardiac conduction system consists of the sinoatrial (SA) node, atrioventricular (AV) nodes, AV bundle (Bundle of His), and left and right bundle branches and Purkinje fibers (Figure 149-1). A normal electrical impulse generally starts at the SA node and produces an action potential by allowing ions to cross the cell membrane to increase the resting membrane potential. As a result, electrical activation will cause adjacent myocardium to produce an action potential along the conduction pathway to elicit a normal heartbeat.
A, B: Cardiac conduction system.
(Reproduced with permission from Butterworth JF, Mackey DC, Wasnick JD, Morgan and Mikhail’s Clinical Anesthesiology, 5th ed. McGraw-Hill; 2013.)
ELECTRICAL ACTIVITY AND ACTION POTENTIAL OF THE HEART
Cardiac muscle cells have a resting potential of −90 mV, with the inside of cell being negatively charged and the outside being positively charged. Ions flow in and out of the cell by a concentration gradient, electrical gradient, or permeability of the membrane. Potassium is higher inside the cell (140 mmol/L) than outside (4 mmol/L), and has the highest permeability (more than sodium or chloride). Thus, potassium is the major determinant of the resting membrane potential.
During a depolarization episode, the inside of the cell becomes less negative (increase in the membrane potential) due to the influx of ions (Table 149-1). Two distinct action potentials are recognized as either fast action potentials or slow action potentials (Figure 149-1B). A fast action potential utilized by cardiac ventricular myocytes is divided into five phases. Each phase depends on the type of ions that cross the membrane and the availability or activation of the ion channel. When myocytes reach about −70 mV (“threshold”), fast sodium channels open and an influx of sodium ions increase the membrane potential to +30 mV (phase 0). A slight repolarization occurs when sodium channels are closed and potassium diffuse out of the cell (phase 1). Potassium diffusion is counterbalanced by the influx of calcium ions via the active calcium channels, creating a plateau phase (phase 2). Repolarization of the cell to resting potential follows when calcium channels close but potassium channels remain open for the outflow of potassium (phase 3). Ultimately, restoration of the resting potential commences the cycle and finishes with the next activation (phase 4). On the other hand, slow action potentials utilized by cells of the SA ...