2.1 Cardiac anatomy & the conduction system

Gross cardiac anatomy

The heart is a four-chambered muscular pump enclosed in the pericardium and seated in the mediastinum. Its two thin-walled atria act as receiving and priming chambers, while the two thick-walled ventricles are the working pumps. Deoxygenated systemic blood enters the right atrium through the superior and inferior vena cavae and the coronary sinus, passes the tricuspid valve into the right ventricle, and is ejected through the pulmonic valve into the pulmonary arteries to be oxygenated in the lungs. Oxygen-rich blood returns through the pulmonary veins to the left atrium, crosses the mitral (bicuspid) valve into the left ventricle, and is driven through the aortic valve into the aorta and systemic circulation.

The two atrioventricular (AV) valves, tricuspid on the right and mitral on the left, are tethered by chordae tendineae to papillary muscles that contract during systole to prevent valve prolapse and backflow. The semilunar valves (pulmonic and aortic) guard the ventricular outflow tracts and snap shut in early diastole. The left ventricle has the thickest wall because it must generate enough pressure to perfuse the entire body, whereas the right ventricle pumps against the low-resistance pulmonary circuit. The interatrial and interventricular septa divide the right and left sides of the heart; the membranous upper interventricular septum lies very close to the AV node and bundle of His, which is why septal infarcts can disrupt conduction. Venous blood from the myocardium itself collects in the coronary sinus, which empties into the right atrium near the tricuspid valve.

Coronary circulation

The myocardium is fed by coronary arteries that arise from the aortic root just above the aortic valve cusps (the sinuses of Valsalva). For the CRAT exam, know which artery supplies which wall, because the ischemic wall determines both the ECG leads that change and the arrhythmias that follow.

Because the RCA usually feeds both the SA and AV nodes, an inferior wall MI often produces sinus bradycardia or AV block. The LAD is nicknamed the "widowmaker" because it supplies such a large anterior territory along with the conduction fascicles, so its occlusion is both extensive and dangerous.

Coronary dominance describes which artery gives rise to the posterior descending artery (PDA). About 70% of people are right-dominant, meaning the PDA arises from the RCA, so in most patients the RCA also supplies the posterior wall; in left-dominant hearts the LCx gives off the PDA. This anatomy explains why inferior and posterior MIs, and the nodal blocks that accompany them, are so often traced back to the RCA.

The conduction system

Every normal heartbeat begins as an electrical impulse that travels a fixed anatomic pathway:

• Sinoatrial (SA) node is the dominant pacemaker, located high in the right atrium near the junction with the superior vena cava. Its intrinsic firing rate is 60-100 beats per minute.
• Internodal and interatrial tracts carry the impulse across atrial muscle; Bachmann's bundle conducts it to the left atrium, and atrial depolarization produces the P wave.
• Atrioventricular (AV) node sits in the floor of the right atrium within the triangle of Koch. It deliberately delays conduction by about 0.1 second, giving the atria time to empty into the ventricles; this delay forms the flat PR segment. Its intrinsic escape rate is 40-60 bpm.
• Bundle of His penetrates the fibrous skeleton and is the only normal electrical bridge between the atria and the ventricles.
• Right and left bundle branches run down the interventricular septum; the left bundle splits into anterior and posterior fascicles.
• Purkinje fibers rapidly distribute the impulse throughout the ventricular myocardium, producing near-simultaneous contraction and a narrow QRS. Their intrinsic escape rate is 20-40 bpm.

Conduction velocity varies dramatically along this pathway. It is fastest in the Purkinje fibers (about 2-4 m/s) and slowest in the AV node (about 0.05 m/s), and that slow nodal conduction is the anatomic basis of the AV delay. The fibrous skeleton of the heart electrically insulates the atria from the ventricles, so under normal conditions the bundle of His is the only route by which an impulse can cross into the ventricles. This is why AV blocks interrupt the beat at a predictable location, and why a narrow QRS tells you the ventricles were activated through the normal His-Purkinje system rather than from an ectopic ventricular focus, which would spread cell-to-cell and produce a wide QRS.

Pacemaker hierarchy and overdrive suppression

All of these tissues can depolarize on their own, but the fastest one sets the heart rate. Because the SA node fires fastest, it repeatedly depolarizes the slower latent pacemakers before they can reach threshold, a phenomenon called overdrive suppression. Each conducted beat resets and hyperpolarizes the subsidiary cells, keeping them electrically quiet.

This creates a protective pacemaker hierarchy: if the SA node fails, slows, or its impulse is blocked, the next-fastest site takes over as an escape rhythm, the AV junction at 40-60 bpm, and failing that, the ventricular Purkinje system at 20-40 bpm. Escape beats and escape rhythms are therefore safety mechanisms, not the primary disease. The technician's job is to recognize that a slow junctional or ventricular rhythm may be rescuing a heart whose higher pacemaker has failed. Understanding this ladder, where faster rates suppress slower ones and slower ones stand ready as backups, explains much of the rhythm interpretation that follows in later chapters.