Chapter 19: Study guide - asses your knowledge

Two subdivisions of cardiovascular system

Pulmonary circuit (lungs) and systemic circuit (body)

Great vessels

Superior vena cava (SVC; Superior Vena Cava), inferior vena cava (IVC; Inferior Vena Cava), pulmonary trunk, pulmonary veins, aorta → connect to heart chambers

Heart location

Thoracic cavity, mediastinum, size of fist, base (top), apex (bottom)

Pericardium

Double

Heart wall layers

Epicardium (outer), myocardium (middle, thickest), endocardium (inner)

Myocardium thickness

Thicker in ventricles; vortex enables twisting contraction

Fibrous skeleton

Connective tissue framework; supports valves, electrical insulation

Atria and ventricles

Separated by interatrial septum, interventricular septum; sulci mark boundaries

Four valves

Right atrioventricular valve (right AV valve; Tricuspid Valve), left atrioventricular valve (left AV valve; Bicuspid Valve or Mitral Valve), pulmonary valve, aortic valve

Valve structure

Atrioventricular valves (AV valves) have papillary muscles and tendinous cords to prevent prolapse

Blood flow path

Body → right atrium → right ventricle → lungs → left atrium → left ventricle → body

Coronary arteries

Supply myocardium; branches reduce myocardial infarction (MI; Myocardial Infarction) risk via collateral circulation

Blood flow in coronary arteries

Greatest during heart relaxation

Myocardial veins

Drain into coronary sinus, supplemented by small cardiac veins

Cardiomyocytes

Striated, short, branched, intercalated discs; rely on aerobic respiration

Conduction system

Sinuatrial node (SA node; Sinuatrial Node) → atria → atrioventricular node (AV node; Atrioventricular Node) → atrioventricular bundle (AV bundle; Atrioventricular Bundle or Bundle of His) → bundle branches → subendocardial branches (Purkinje Fibers)

Systole

Contraction of the heart

Diastole

Relaxation of the heart

Sinus rhythm

Normal rhythm

Ectopic focus

Abnormal pacemaker

Nodal rhythm

Atrioventricular node (AV node) takes over

SA node depolarization

Spontaneous pacemaker potentials via ion channel activity

Excitation path

Atria → atrioventricular node (AV node; Atrioventricular Node) (delay) → ventricles (atrioventricular bundle, bundle branches, subendocardial fibers)

Ventricular twisting

Aided by vortex; tendinous cords prevent prolapse

Action potentials

Long refractory period; shaped by sodium (Na⁺), calcium (Ca²⁺), potassium (K⁺) channel activity

Electrocardiogram (ECG; Electrocardiogram) waves

P wave (atrial depolarization), QRS complex (ventricular depolarization), T wave (ventricular repolarization)

Sphygmomanometer

Measures blood pressure (BP; Blood Pressure) in millimeters of mercury (mm Hg)

Flow principles

Pressure

Valve mechanics

Open/close by pressure gradients

Cardiac cycle

Four phases: ventricular filling, isovolumetric contraction, ventricular ejection, isovolumetric relaxation

Phase events

Electrical (ECG), mechanical (contraction/relaxation), sound (valves), volume/pressure changes

Time values

Atrial systole ~0.1 seconds, ventricular systole ~0.3 seconds, quiescent period ~0.4 seconds

Volume terms

End

Ventricular balance

Equal output prevents systemic/pulmonary imbalances

Innervation

Sympathetic (accelerates), parasympathetic (slows)

Cardiac output (CO; Cardiac Output)

Heart rate (HR; Heart Rate) × stroke volume (SV; Stroke Volume); resting HR ~70 beats per minute (bpm; beats per minute), changes with age

Abnormal HR

Tachycardia (fast heart rate), bradycardia (slow heart rate)

Chronotropic agents

Positive (increase HR), negative (decrease HR)

Sympathetic/parasympathetic effects

Norepinephrine increases HR, acetylcholine decreases HR

Intrinsic SA node rate

~100 beats per minute, lowered by vagal tone

Brainstem centers

Regulate HR via autonomic output

Receptors

Proprioceptors (activity), baroreceptors (pressure), chemoreceptors (chemistry)

Hormonal/drug effects

Epinephrine, glucagon, digitalis, potassium (K⁺), calcium (Ca²⁺) modify HR/contractility

Preload

Stretch

Contractility

Force

Afterload

Resistance (all affect SV)

Frank

Starling law

Inotropic agents

Positive (increase force), negative (decrease force)

Calcium and potassium effects

Modify contractility

Exercise effects

Increases cardiac output (CO); trained athletes → high stroke volume (SV), low resting heart rate (HR)