8.4 Heart Structure, Cardiac Cycle, Electrical Activity, Heart Defects & Special Senses

Heart Structure, Cardiac Cycle, Electrical Activity, Heart Defects & Special Senses

Quick Answer: The heart is a four-chambered, two-sided pump whose valves partition the cardiac cycle into systole and diastole. Electrical excitation originates in the SA node, is delayed at the AV node, travels through the bundle of His and Purkinje fibers, and is recorded as the ECG. The PA-CAT Bulletin sample item frames a myocardial infarction of the ventricular septum as an injury to the bundle of His/bundle branches — a conduction defect reflected in the QRS. The special senses close the chapter.

Heart Structure and Valves

The right side pumps deoxygenated blood to the lungs; the left side pumps oxygenated blood to the systemic circulation. The four valves ensure unidirectional flow:

• Atrioventricular (AV) valves — tricuspid (right, three leaflets) and mitral (bicuspid) (left, two leaflets). Closed during ventricular systole; their closure produces the S1 ("lub") heart sound. Chordae tendineae and papillary muscles prevent prolapse.
• Semilunar valves — pulmonary and aortic. Closed during ventricular diastole; their closure produces the S2 ("dub") heart sound.

The coronary circulation supplies the myocardium. The left main coronary artery divides into the left anterior descending (LAD) and left circumflex; the right coronary artery supplies the SA node (in ~60% of people), the AV node, and much of the right ventricle. Most coronary perfusion occurs during diastole, when the intramyocardial pressure is lowest. Coronary flow is regulated chiefly by metabolic vasodilation (adenosine, hypoxia, CO₂).

The Cardiac Cycle and Pressure-Volume Loop

The cardiac cycle has four phases per ventricle: (1) ventricular filling during diastole with the mitral open; (2) isovolumetric contraction with all valves closed and pressure climbing; (3) ventricular ejection once the aortic valve opens at ~80 mmHg, ejecting the stroke volume and peaking near 120 mmHg; and (4) isovolumetric relaxation after the aortic valve closes (S2), with pressure falling to ~5 mmHg before the mitral reopens.

The pressure-volume (PV) loop of the left ventricle plots ventricular pressure against volume through one cycle:

• Filling — mitral opens at low pressure; volume rises from ESV to EDV.
• Isovolumetric contraction — mitral closes (S1), all valves shut, pressure climbs with no volume change.
• Ejection — aortic opens at ~80 mmHg; volume falls as stroke volume (SV = EDV − ESV) is ejected; peak ~120 mmHg.
• Isovolumetric relaxation — aortic closes (S2), all valves shut, pressure falls to ~5 mmHg, then mitral opens.

Preload is the ventricular end-diastolic volume (or wall stress); afterload is the aortic pressure against which the ventricle ejects. Contractility (inotropy) is the intrinsic force of contraction, raised by sympathetic stimulation and catecholamines. Stroke volume = EDV × ejection fraction; cardiac output = HR × SV.

Electrical Activity and the ECG

The SA node in the right atrium is the normal pacemaker (~60–100 bpm). Its depolarization propagates through atrial muscle to the AV node in the floor of the right atrium. The AV node is the only electrical connection between atria and ventricles; its deliberate delay (~100 ms) lets atrial systole finish before ventricular contraction begins. The impulse then enters the bundle of His (AV bundle), which divides into the left and right bundle branches traveling along the interventricular septum, finally distributing through the Purkinje fibers to the ventricular myocardium. Accessory pathways (e.g., the bundle of Kent in Wolff-Parkinson-White) bypass the AV node and can produce reentrant tachycardias with a delta wave and shortened PR interval.

The ECG maps these events: the P wave is atrial depolarization; the PR interval (normal 0.12–0.20 s) includes atrial depolarization plus the AV nodal delay; the QRS complex is ventricular depolarization; the ST segment is the ventricular plateau (elevations or depressions suggest ischemia); and the T wave is ventricular repolarization.

MI, the Ventricular Septum, and the Bundle of His

The PA-CAT Bulletin of Information, rev. 20240815, includes a sample item describing a myocardial infarction that damages the ventricular septum and asking about immediate changes in cardiac electrical conduction. Because the bundle of His and its bundle branches run along the interventricular septum, septal infarction can directly injure this conduction tissue, producing heart block or a bundle branch block. On ECG, a right or left bundle branch block broadens and notches the QRS (the "RSR'" or "M-shaped" pattern in V1 for RBBB, a wide QRS with deep S waves in V1 and broad R in lateral leads for LBBB). A septal infarct also typically produces pathologic Q waves and ST elevation in V1–V2 and may progress to third-degree (complete) AV block if the bundle of His is severed, requiring transcutaneous or transvenous pacing.

Congenital and Valvular Heart Defects

Common congenital defects:

• Ventricular septal defect (VSD) — the most common congenital heart defect; left-to-right shunt causes a holosystolic murmur at the lower left sternal border. Large shunts can lead to pulmonary hypertension and Eisenmenger syndrome if uncorrected.
• Atrial septal defect (ASD) — left-to-right shunt at the atrial level; fixed splitting of S2.
• Patent ductus arteriosus (PDA) — continuous "machinery" murmur; indomethacin closes, prostaglandin E1 keeps open.
• Coarctation of the aorta — upper-extremity hypertension with radio-femoral delay; rib notching on imaging.
• Tetralogy of Fallot — PROVe: Pulmonary stenosis, Right ventricular hypertrophy, Overriding aorta, VSD. "Tet spells" improve with squatting (increases systemic vascular resistance).

Valvular defects:

• Aortic stenosis — systolic ejection murmur, slow-rising carotid pulse, delayed carotid upstroke (pulsus parvus et tardus).
• Aortic regurgitation — diastolic decrescendo murmur, wide pulse pressure, bounding pulses (water-hammer).
• Mitral stenosis — diastolic rumble, opening snap, loud S1; often sequela of rheumatic fever.
• Mitral regurgitation — holosystolic murmur radiating to the axilla.

Special Senses (Summary)

• Vision — Light activates photopigments in rods (rhodopsin, high sensitivity, achromatic) and cones (three opsins, color). Phototransduction is unusual: light hyperpolarizes the photoreceptor by closing cGMP-gated Na⁺ channels, reducing glutamate release onto bipolar cells. The retina's fovea is cone-dense and color-acute.
• Hearing — Pressure waves travel through the external auditory canal → tympanic membrane → ossicles (malleus, incus, stapes) → oval window → cochlear fluid. Frequency is mapped tonotopically along the basilar membrane (high frequencies at the base, low at the apex). Hair cells depolarize when their stereocilia bend against the tectorial membrane, releasing glutamate onto the cochlear nerve (CN VIII).
• Taste — Five basic qualities (sweet, salty, sour, bitter, umami) sensed by taste buds. Sweet/umami/bitter use G protein-coupled receptors (T1R, T2R families); salty (ENaC) and sour (H⁺/proton channels) use ion channels. Afferents travel via CN VII (anterior two-thirds), IX (posterior third), and X (epiglottis).
• Smell — Olfactory receptor neurons in the olfactory epithelium (CN I) are bipolar neurons with cilia bearing GPCR odorant receptors; they regenerate throughout life. Axons pass through the cribriform plate to the olfactory bulb — the only sensory pathway that bypasses the thalamus on its way to cortex.

This chapter closes the Physiology survey of respiratory, reproductive, cardiac, and sensory systems tested in PA-CAT Physiology (~16% of the 240-item exam). For the Bulletin's sample item, remember: septal MI → bundle of His/bundle branch injury → conduction block with widened, abnormal QRS.