85. Functional Anatomy of Heart, Cardiac Muscle, Conducting System, and Cardiac Innervation – Quiz

📌 Professor’s Notes: Quick Revision

High-yield revision notes for rapid review before university examinations.

• The heart is an involuntary muscular pump that maintains blood circulation through coordinated contraction of cardiac muscle, an intrinsic conducting system, and autonomic innervation. The sinoatrial (SA) node acts as the normal pacemaker and generates rhythmic impulses throughout life.
• The heart is enclosed by the pericardium, which consists of an outer fibrous pericardium and an inner serous pericardium (parietal and visceral layers). The pericardial cavity normally contains 15–50 mL of lubricating fluid. Excess fluid causes pericardial effusion, while rapid accumulation produces cardiac tamponade, leading to impaired ventricular filling, reduced cardiac output, hypotension, and shock.
• The cardiac wall has three layers: epicardium, myocardium, and endocardium. The myocardium is thickest in the left ventricle because it pumps against systemic pressure. Atrial contraction contributes about 15–20% of ventricular filling. Cardiac valves ensure one-way blood flow; chordae tendineae and papillary muscles prevent prolapse of atrioventricular valves during systole.
• Cardiac muscle is involuntary, striated, branched, and connected by intercalated discs containing gap junctions. These junctions allow rapid electrical transmission, making the myocardium a functional syncytium. Cardiac muscle contains abundant mitochondria and depends mainly on aerobic metabolism. The sarcotubular system forms a diad (one T tubule and one terminal cisterna) at the Z line, unlike the triad in skeletal muscle.
• The Frank–Starling law states that, within physiological limits, increased ventricular filling increases myocardial fiber length and produces a stronger contraction. Stretch improves actin–myosin interaction, increases calcium sensitivity, and enhances calcium-induced calcium release, thereby increasing stroke volume and matching cardiac output to venous return.
• Excitation–contraction coupling depends on extracellular calcium. Calcium entering through T tubules triggers further calcium release from the sarcoplasmic reticulum. Calcium binds troponin C, initiating contraction. Hypercalcemia increases contractility and may cause systolic arrest, whereas hyperkalemia can produce diastolic arrest. Digoxin increases contractility by inhibiting the sodium–potassium adenosine triphosphatase pump, thereby increasing intracellular calcium.
• The conducting system consists of the SA node → internodal pathways → AV node → His bundle → right and left bundle branches → Purkinje fibers. The AV node produces a physiological delay of about 0.1 second, allowing ventricular filling. Purkinje fibers have the fastest conduction velocity (2–4 m/s), ensuring synchronous ventricular contraction.
• The heart receives autonomic innervation from both sympathetic and parasympathetic (vagus) nerves. The right vagus mainly affects the SA node, whereas the left vagus predominantly influences the AV node. Vagal stimulation causes negative chronotropic, dromotropic, bathmotropic, and mild inotropic effects. Sympathetic stimulation produces positive chronotropic, inotropic, dromotropic, and bathmotropic effects. Resting (basal) heart rate is mainly determined by vagal tone, while the intrinsic heart rate after autonomic blockade is about 100–110 beats/min.