Cardiovascular System: Cardiac Function - Anatomy & Physiology
Terms in this set (24)
Heart, blood vessels, and blood transport oxygen, nutrients, wastes, hormones, immune cells, and clotting proteins throughout the body.
Left ventricle → aorta → systemic circuit → vena cavae → right atrium → right ventricle → pulmonary artery → pulmonary circuit → pulmonary veins → left atrium → left ventricle.
Arteries carry blood away from the heart; arterioles have high resistance; capillaries are sites of exchange; venules and veins return blood to the heart.
Erythrocytes transport oxygen and CO2; leukocytes defend against pathogens; platelets aid clotting; plasma is the fluid and solute medium.
Heart's own capillaries supplied by coronary arteries arising from the aorta, providing nutrients to cardiac muscle cells.
Epicardium (outer membrane), myocardium (cardiac muscle), and endocardium (inner endothelial layer).
Valves ensure unidirectional blood flow by opening and closing passively based on pressure gradients, preventing backflow.
Atrioventricular (AV) valves: tricuspid (right) and bicuspid/mitral (left); Semilunar valves: aortic and pulmonary valves.
Prevent AV valves from everting by anchoring valve cusps during ventricular contraction.
Ability of pacemaker cells to generate spontaneous action potentials, coordinating heartbeat rhythm.
Sinoatrial (SA) node initiates action potentials at 70–80 AP/min, setting the heart rate.
SA node → atrial muscle → AV node (delay) → bundle of His → left and right bundle branches → Purkinje fibers → ventricular muscle contraction.
Contain desmosomes for mechanical strength and gap junctions for electrical coupling between cardiac cells.
1. Spontaneous depolarization (Na+ funny channels open)
2. Threshold reached (Ca2+ channels open)
3. Repolarization (K+ channels open)
Phase 0: Na+ influx
Phase 1: Na+ channels close
Phase 2: Ca2+ influx, K+ efflux
Phase 3: K+ efflux
Phase 4: resting potential
AP triggers Ca2+ entry via T tubules and sarcoplasmic reticulum, Ca2+ binds troponin, enabling crossbridge cycling and contraction.
P wave: atrial depolarization
QRS complex: ventricular depolarization and atrial repolarization
T wave: ventricular repolarization
1. Ventricular filling
2. Isovolumetric contraction
3. Ventricular ejection
4. Isovolumetric relaxation
First sound (lubb): AV valves closing
Second sound (dupp): Semilunar valves closing
Cardiac output (CO) = Stroke volume (SV) × Heart rate (HR)
Autonomic nervous system: parasympathetic lowers HR, sympathetic raises HR; hormones like epinephrine increase HR.
Ventricular contractility, end-diastolic volume (preload), and afterload influence stroke volume.
Increased end-diastolic volume stretches cardiac muscle fibers, leading to stronger contraction and increased stroke volume.
Norepinephrine binds β1 receptors, increasing Ca2+ channel opening and enhancing contraction strength.