8.1 Conduction System of the Heart
The sinoatrial (SA) node is the primary pacemaker of the heart because it is able to spontaneously generate action potentials (inherent automaticity). These action potentials are conducted rapidly through the right atrial myocardium to the atrioventricular (AV) node, which delays the impulse before conducting it to the ventricles via the bundle of His and Purkinje fibers (Fig. 8.1). This provides an orderly contraction sequence from apex to base for efficient ejection of blood from the ventricles.
– The SA node spontaneously generates action potentials at a rate of ~80 to 100/min.
– The AV node also has inherent automaticity but at a slower rate than the SA node. If the SA node fails, the AV node will take over the pacemaker activity of the heart.
– The delay of the cardiac impulse at the AV node gives the contracting atria adequate time to empty their contents into the ventricles before ventricular contraction is initiated.
Note: The typical resting heart rate is 65 to 75 beats/min. This is due to vagal slowing of the heart below the intrinsic rate set by the SA node.
Cardioversion
Cardioversion is a procedure for delivering an electrical shock to the heart via paddles or electrodes to convert a pathologically increased heart rate (tachycardia) or other arrhythmia to a normal rhythm. It does this by causing all of the cardiac muscle cells to contract simultaneously. This brief interruption to the arrhythmia gives the SA node an opportunity to regain control over the pacing of the heart.
Arrhythmias
An arrhythmia is an abnormal heart rate or rhythm due to a fault in the normal, coordinated propagation of action potentials through the heart. There are many causes of arrhythmias, including coronary artery disease, hypertension, structural abnormalities, scarring of heart tissue (e.g., following a myocardial infarction), diabetes, hyperthyroidism, and drugs (e.g., caffeine and alcohol). Arrhythmias can be asymptomatic, or they may cause a fluttering sensation in the chest, a sensation of a racing/abnormally slow heartbeat, dyspnea (shortness of breath), dizziness, or syncope (fainting). Complications of arrhythmias include stroke and heart failure. There are four main classes of antiarrhythmic drugs, the selection of which will depend on the particular arrhythmia. Class I drugs are Na+-channel blockers, class II drugs are β-blockers, class III drugs are K+-channel blockers, and class IV drugs are Ca2+-channel blockers. In addition to antiarrhythmic drugs, warfarin, an anticoagulant agent, is used in certain arrhythmias (e.g., atrial fibrillation) to prevent thromboembolic stroke.
Nondrug therapies for arrhythmias
Surgical interventions have an important role in place of, or in addition to, drug therapy for arrhythmias. Catheter ablation of the source or conduction path of the arrhythmia by application of radiofrequency current applied through a large-tip electrode on a steerable catheter may be useful for supraventricular tachycardias, atrial arrhythmias, atrial fibrillation, and ventricular tachycardia. In patients with sinus node dysfunction or AV nodal block, or heart block persisting following an ablative procedure, implantation of a permanent pacemaker may be indicated. In ventricular dysrhythmias, implantation of a defibrillator is superior to drug therapy in certain patient populations.
Fig. 8.1 
Cardiac conduction system.
Contraction of cardiac muscle is modulated by the cardiac conduction system. This system of specialized myocardial cells generates excitatory impulses in the sinoatrial (SA) node that are conducted through the atria to the atrioventricular (AV) node, where the impulse is delayed before conducting it to the ventricles via the bundle of His and Purkinje fibers.
From Atlas of Anatomy, © Thieme 2008, Illustration by Markus Voll.
8.2 Events Causing Contraction of Cardiac Muscle
Contraction of cardiac muscle occurs when the excitation produced by an action potential is transmitted to cardiac myofibrils.
Cardiac Action Potentials
The general features of action potentials are discussed in Chapter 1. The ionic conductances that are a feature of action potential phases at the SA node, cardiac muscle, and branches of the conduction system are discussed in this section.
Fig. 8.2 Action potential phases at the sinoatrial node (A). Action potential phases at the atrial and ventricular myocardium, bundle of His, and Purkinje fibers (B).
Action Potential Phases at the Sinoatrial Node
Refer to Fig. 8.2.
Phase 0
– This slow upstroke of the action potential shows membrane depolarization (it becomes less negative).
– It results from an increase in Ca2+ conductance, causing inward Ca2+ flow.
Phases 1 and 2
– These phases do not occur at the SA node.
Phase 3
– This is the repolarization phase.
– It results from an increase in K+ conductance, which causes outward K+ flow and repolarization of the membrane toward the K+ equilibrium potential.
Phase 4
– The SA node does not have a stable resting membrane potential. During phase 4, it slowly depolarizes (which is responsible for its inherent automaticity).
– It results from an increase in Na+ conductance, causing inward Na+ flow and a decrease in K+ conductance.
Note: The events at the AV node are similar to those at the SA node but slower. As a result, the AV node normally does not generate its own action potentials. This is because action potentials are conducted to the AV node more frequently than its own slow inherent rate of action potential generation.
Action Potential Phases at the Atrial and Ventricular Myocardium, Bundle of His, and Purkinje Fibers
Refer to Fig. 8.2.
Phase 0
– This rapid upstroke of the action potential shows membrane depolarization (it becomes less negative).
– It results from an increase in Na+ conductance, causing rapid inward Na+ flow.
– This inward Na+ flow stops after a few milliseconds due to inactivation of Na+ channels.
Phase 1
– This is an early slight membrane repolarization (membrane becomes more negative).
– It results from outward K+ flow (due to a favorable electrochemical gradient) and a decrease in Na+ conductance.
Phase 2
– This is the plateau of depolarization.
– In this phase, there is increased Ca2+ conductance. This creates an approximate balance between inward Ca2+ flow and outward K+ flow.
– Phase 2 is responsible for the long duration of cardiac action potentials (150–250 msec) compared with those of nerve and skeletal muscle (1–2 msec), which have no such plateau phase.
Phase 3
– This is the repolarization phase.
– It results from a decrease in Ca2+ conductance and an increase in K+ conductance. The net effect of this is a rapid outward K+ flow, which repolarizes the membrane toward the K+ equilibrium potential.
Phase 4
– This is the resting membrane potential.
– It is determined by high K+ conductance, and its value is therefore close to the K+ equilibrium potential (−96mV). At this potential, K+ outflow and K+ inflow are equal.
Table 8.1 compares the net ionic conductances of the atrial and ventricular myocardium, bundle branches, and Purkinje fibers and those at the SA node.
Excitation–Contraction Coupling
– Depolarization of the cardiac muscle cell membrane triggers an action potential that passes through T tubules.
– During phase 2 (plateau) of the action potential, there is increased Ca2+ conductance, causing inward Ca2+ flow.
– This inward Ca2+ flow initiates the release of Ca2+ from the sarcoplasmic reticulum (Ca2+-induced Ca2+ release). Such releases increase intracellular [Ca2+].
– Ca2+ binds to troponin C, and tropomysin moves out of its blocking position, allowing actin and myosin to form cross-bridges.
– The thick and thin filaments of actin and myosin slide past each other, resulting in cardiac muscle cell contraction.
– The contraction ends when Ca2+ ATPase facilitates the reuptake of Ca2+ into the sarcoplasmic reticulum, reducing the intracellular [Ca2+].
Note: The force of contraction of cardiac muscle cells is proportional to the amount of Ca2+ release, which varies depending on conditions.
8.3 Measuring the Electrical Activity of the Heart: The Electrocardiogram
Recording an ECG
The electrocardiogram (ECG) is a representation of the electrical activity in the heart (Fig. 8.3). It is measured by recording voltages through surface electrodes, which “look” at the heart from different positions. A wave of depolarization moving toward a lead causes an upward deflection of the ECG.
Interpretation of ECG Waves, Segments, and Intervals
Waves
– The P wave corresponds to atrial depolarization.
– The QRS complex corresponds to ventricular depolarization, which occurs from apex to base.
Note: Repolarization of the atria is masked by the QRS complex.
– The T wave corresponds to ventricular repolarization, which occurs from base to apex.
Fig. 8.3 Electrocardiogram (ECG) curve.
The ECG depicts electrical activity as waves, segments, and intervals.
Fig. 8.4 Cardiac impulse spreading.
The P wave corresponds to atrial depolarization. The PQ segment is an isoelectric period between atrial depolarization and the beginning of ventricular depolarization (impulse delayed at AV node). The Q wave of the QRS complex corresponds to depolarization of the septum from left to right. The R and S waves of the QRS complex corresponds to ventricular depolarization (in opposite directions). The ST segment is an isoelectric period between ventricular depolarization and repolarization. The T wave corresponds to ventricular repolarization.
Figure 8.4 depicts cardiac impulse spreading and how this translates to waves of the ECG.
Segments
– The PQ segment is an isoelectric period between the P wave and the QRS complex. During this time, the wave of depolarization is traveling through the AV node into the bundle of His.
– The ST segment corresponds to the plateau phase of the cardiac action potential when all ventricular fibers are simultaneously depolarized.
Intervals
– The PQ interval corresponds to the conduction of the action potential through the AV node.
– The QT interval corresponds to ventricular depolarization and repolarization.
Cardiac axis
The cardiac axis is the direction of propagation through the ventricles when the QRS complex is at a maximum. The mean electrical axis is calculated by finding the QRS complex that is biphasic (deflections of the QRS complex are equally positive and negative), then finding the lead that is perpendicular to the biphasic lead that has a positive net deflection. This lead corresponds to the mean electrical axis. A normal axis is between −30 and +90 degrees. A value below −30° is left axis deviation and a value above +90° is right axis deviation. Many factors can alter the cardiac axis, including abnormal cardiac anatomy or position, infarction, ischemia, pulmonary embolism, cardiomyopathy, and conduction abnormalities.
Information Provided by the ECG
Table 8.2 lists the information that may and may not be gathered by analysis of an ECG tracing.
