Cardiovascular system includes the heart and blood vessels.
Circulatory system encompasses the heart, blood vessels, and the blood itself.
The circulatory system has two major divisions:
Pulmonary circuit: The right side of the heart carries blood to the lungs for gas exchange and returns it to the heart.
Systemic circuit: The left side of the heart supplies oxygenated blood to all tissues of the body and returns it to the heart.
Basic Concepts
Cardiology: The study of the heart and its disorders.
Heart: A pump that keeps blood flowing through the vessels.
Vessels: Deliver blood to body tissues and return it to the heart.
Types of vessels:
Arteries: Vessels that carry blood away from the heart.
Veins: Vessels that carry blood toward the heart.
Capillaries: Microscopic vessels that connect the smallest arteries to the smallest veins.
Pulmonary and Systemic Circuits
Left side of heart:
Fully oxygenated blood arrives from the lungs via pulmonary veins.
Blood is sent to all organs of the body via the aorta.
Right side of heart:
Oxygen-poor blood arrives from the inferior and superior venae cavae.
Blood is sent to the lungs via the pulmonary trunk.
Position, Size, and Shape of the Heart
The heart is located in the mediastinum, between the lungs.
Base: The wide, superior portion of the heart where large vessels attach; mainly formed by the Left Atrium.
Apex: The tapered inferior end, which tilts to the left.
Size:
In adults: weighs 10 ounces, 3.5 inches wide at the base, 5 inches from base to apex.
At any age, the heart is about the size of a fist.
The Pericardium
Pericardium: A double-walled sac that encloses the heart.
Allows the heart to beat without friction.
Provides room to expand, yet resists excessive expansion.
Anchored to the diaphragm inferiorly and the sternum anteriorly.
Layers of the pericardium:
Fibrous pericardium: The outer wall, not attached to the heart.
Serous pericardium:
Parietal layer: Lines the fibrous pericardium.
Visceral layer (epicardium): Covers the heart surface.
Pericardial cavity: The space between the parietal and visceral layers of the serous pericardium, filled with 5 to 30 mL of pericardial fluid.
Pericarditis: Painful inflammation of the membranes.
The Heart Wall
Epicardium (visceral layer of serous pericardium):
Serous membrane covering the heart.
Adipose in a thick layer in some places.
Coronary blood vessels travel through this layer.
Myocardium:
Layer of cardiac muscle proportional to workload.
Muscle spirals around the heart, producing a wringing motion (vortex of the heart).
Fibrous skeleton of the heart: Framework of collagenous and elastic fibers.
Provides structural support and attachment for cardiac muscle and anchor for valve tissue.
Electrical insulation between atria and ventricles which is important in timing and coordination of contractile activity.
Endocardium:
Smooth inner lining of the heart and blood vessels.
Covers the valve surfaces and is continuous with the endothelium of blood vessels.
The Chambers of the Heart
Four chambers:
Right and left atria:
Two superior chambers.
Receive blood returning to the heart.
Auricles (seen on the surface) enlarge the chamber.
Right and left ventricles:
Two inferior chambers.
Pump blood into arteries.
Surface Features of the Heart
Coronary sulcus: Separates the atria and ventricles.
Interventricular sulcus: Overlies the interventricular septum that divides the right ventricle from the left.
Sulci contain coronary arteries.
Internal Structures of the Heart Chambers
Interatrial septum: The wall that separates the atria.
Pectinate muscles: Internal ridges of myocardium in the right atrium and both auricles.
Interventricular septum: The muscular wall that separates the ventricles.
Trabeculae carneae: Internal ridges in both ventricles; may prevent ventricle walls from sticking together after contraction.
Valves of the Heart
Valves ensure one-way flow of blood through the heart.
Each valve has two or three fibrous flaps—cusps or leaflets.
Atrioventricular (AV) valves: Control blood flow between atria and ventricles.
Right AV valve: Has three cusps (tricuspid valve).
Left AV valve: Has two cusps (mitral valve, formerly ‘bicuspid’).
Tendinous cords / Chordae tendineae: Cords connecting AV valves to papillary muscles on the floor of ventricles.
Prevent AV valves from flipping or bulging into atria when ventricles contract.
Semilunar valves: Control flow into great arteries; open and close because of blood flow and pressure.
Pulmonary semilunar valve: In the opening between the right ventricle and the pulmonary trunk.
Aortic semilunar valve: In the opening between the left ventricle and the aorta.
Each has three cusps shaped like shirt pockets.
During ventricular contraction and blood ejection, cusps are pressed up against arterial walls.
When ventricles relax, blood flows back toward ventricles and fills cusps, causing valves to close.
Blood Flow Through the Chambers
Ventricles relax:
Pressure drops inside the ventricles.
Semilunar valves close as blood attempts to back up into the ventricles from the vessels.
AV valves open.
Blood flows from atria to ventricles.
Ventricles contract:
AV valves close as blood attempts to back up into the atria.
Pressure rises inside of the ventricles.
Semilunar valves open and blood flows into great vessels.
Detailed Blood Flow Through the Heart
Blood enters the right atrium from the superior and inferior venae cavae.
Blood in the right atrium flows through the right AV valve into the right ventricle.
Contraction of the right ventricle forces the pulmonary valve open.
Blood flows through the pulmonary valve into the pulmonary trunk.
Blood is distributed by the right and left pulmonary arteries to the lungs, where it unloads CO2 and loads O2.
Blood returns from the lungs via the pulmonary veins to the left atrium.
Blood in the left atrium flows through the left AV valve into the left ventricle.
Contraction of the left ventricle (simultaneous with step 3) forces the aortic valve open.
Blood flows through the aortic valve into the ascending aorta.
Blood in the aorta is distributed to every organ in the body, where it unloads O2 and loads CO2.
Blood returns to the right atrium via the venae cavae.
Coronary Circulation
5% of blood pumped by the heart is pumped to the heart itself through the coronary circulation to sustain its strenuous workload.
Approximately 250 mL of blood per minute.
Needs abundant O_2 and nutrients.
The heart has its own supply of vessels to deliver blood to the myocardium—the coronary circulation.
Two coronary arteries, right and left, arise from the aortic sinuses in the initial portion of the ascending aorta and supply oxygenated blood to the muscle and other tissues of the heart.
Flow through coronary arteries is greatest when the heart relaxes.
Contraction of the myocardium compresses the coronary arteries and obstructs blood flow.
Opening of the aortic valve flap during ventricular systole covers the openings of the coronary arteries, blocking blood flow into them.
During ventricular diastole, blood in the aorta surges back toward the heart and into the openings of the coronary arteries.
Arterial Supply
Left Coronary Artery (LCA) branches off the ascending aorta.
Anterior interventricular branch: Supplies blood to both ventricles and the anterior two-thirds of the interventricular septum.
Circumflex branch:
Passes around the left side of the heart in the coronary sulcus.
Gives off the left marginal branch and then ends on the posterior side of the heart.
Supplies the left atrium and posterior wall of the left ventricle.
Right Coronary Artery (RCA) branches off the ascending aorta.
Supplies the right atrium and sinuatrial node (pacemaker).
Right marginal branch: Supplies the lateral aspect of the right atrium and ventricle.
Posterior interventricular branch: Supplies the posterior walls of both ventricles and the interventricular septum.
Angina and Heart Attack
Angina pectoris: Chest pain from partial obstruction of coronary blood flow.
Pain caused by ischemia of cardiac muscle.
Obstruction partially blocks blood flow.
The myocardium shifts to anaerobic fermentation, producing lactate and thus stimulating pain.
Myocardial Infarction (MI): Sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation.
Atheroma (blood clot or fatty deposit) often obstructs coronary arteries.
Cardiac muscle downstream of the blockage dies.
Heavy pressure or squeezing pain radiating into the left arm.
Some painless heart attacks may disrupt electrical conduction pathways, leading to fibrillation and cardiac arrest.
Silent heart attacks occur in diabetics and the elderly.
MI is responsible for about 27% of all deaths in the U.S.
Venous Drainage
Venous Drainage: The route by which blood leaves an organ.
5% to 10% of coronary blood drains directly into heart chambers (mostly the right ventricle) by way of the small cardiac veins.
Most coronary blood returns to the right atrium by way of the coronary sinus, which has three main inputs: great cardiac, posterior interventricular, and left marginal veins.
Great cardiac vein:
Travels alongside the anterior interventricular artery.
Collects blood from the anterior portion of the heart.
Empties into the coronary sinus.
Middle cardiac vein (posterior interventricular):
Found in the posterior sulcus.
Collects blood from the posterior portion of the heart.
Drains into the coronary sinus.
Left marginal vein:
Empties into the coronary sinus.
Coronary sinus:
Large transverse vein in the coronary sulcus on the posterior side of the heart.
Collects blood and empties into the right atrium.
Coronary Circulation Summary
The 1st branches of the Aorta: Left and Right Coronary Artery
They provide arterial (O2 rich) blood to the heart. Block Ischemia MI (Myocardial Infarction)
Coronary Arteries:
Left Coronary Artery: Circumflex artery, Anterior interventricular artery
Right Coronary Artery: AV nodal artery, Marginal Artery, Posterior Interventricular artery
All 3 drain into the Coronary Sinus which drains into the Right Atrium
Associations
Both the Circumflex artery and the Coronary Sinus are in the Coronary Sulcus
Both the Anterior interventricular artery and the Great Cardiac Vein are in the anterior interventricular sulcus
Both the Posterior Interventricular artery and the Middle Cardiac Vein are in the Posterior interventricular sulcus
Both the Right Coronary Artery and the Small Cardiac Vein are in the sulcus inferior to the Right Auricle.
Anatomical Markings
Rough area of the atria: Pectinate Muscle
Rough area of the ventricle: Trabeculae Carnea
Fossa ovalis Remnant of foramen ovale
Ligamentum Arteriosum Remnant of Ductus arteriosus
Auricle means ear
Between the Auricles: Anterior to Posterior; Pulmonary Trunk and Ascending Aorta
Structure of Cardiac Muscle
Heartbeat is myogenic—the signal originates in the heart itself.
The heart is autorhythmic—it has a built-in pacemaker and electrical system, so it does not rely on the nervous system for its rhythm.
Cardiomyocytes: Striated, short, thick, branched cells, one central nucleus surrounded by a light-staining mass of glycogen.
Repair of damage to cardiac muscle is almost entirely by fibrosis (scarring).
Intercalated discs: Join cardiomyocytes end to end with three features: interdigitating folds, mechanical junctions, and electrical junctions.
Interdigitating folds: Folds interlock with each other and increase the surface area of contact.
Mechanical junctions tightly join cardiomyocytes.
Fascia adherens: Broad band in which the actin of the thin myofilaments is anchored to the plasma membrane. Each cell is linked to the next via transmembrane proteins.
Desmosomes: Mechanical linkages that prevent contracting cardiomyocytes from being pulled apart from each other.
Electrical junctions (gap junctions): Allow ions to flow between cells; can stimulate neighbors.
The entire myocardium of either the two atria or the two ventricles acts like a single, unified cell.
Metabolism of Cardiac Muscle
Cardiac muscle depends almost exclusively on aerobic respiration to make ATP.
Rich in myoglobin and glycogen.
Huge mitochondria: fill 25% of cell.
Fatigue resistant because it makes little use of anaerobic fermentation or oxygen debt mechanisms; does not fatigue for a lifetime.
Cardiac muscle is adaptable to different organic fuels.
Nerve-like processes spread throughout the ventricular myocardium.
Cardiomyocytes then pass the signal from cell to cell through gap junctions.
Electrical and Contractile Activity of the Heart
Cycle of events in the heart:
Systole: Contraction.
Diastole: Relaxation.
Although “systole” and “diastole” can refer to the contraction and relaxation of either type of chamber, they usually refer to the action of the ventricles.
Sinus rhythm: The normal heartbeat triggered by the SA node.
Adult at rest is typically 70 to 80 bpm (vagal tone).
Ectopic focus: A region of spontaneous firing other than the SA node.
May govern heart rhythm if the SA node is damaged.
Nodal rhythm: If the SA node is damaged, the heart rate is set by the AV node (40 to 50 bpm).
Other ectopic focal rhythms are 20 to 40 bpm and too slow to sustain life.
Spiral Orientation of Myocardial Muscle
Signals travel very quickly through the AV bundle and subendothelial conducting network.
The entire ventricular myocardium depolarizes and contracts in near unison.
Ventricular systole progresses up from the apex of the heart.
The spiral arrangement of the myocardium twists the ventricles slightly, like someone wringing out a towel.
Pacemaker Physiology
SA node fires spontaneously at regular intervals.
Mechanism:
The SA node does not have a stable resting membrane potential.
Pacemaker potential: Starts at -60 mV and drifts upward due to slow Na^+ inflow; this gradual depolarization is the pacemaker potential (prepotential).
When it reaches a threshold of -40 mV, voltage-gated Ca^{2+} and Na^+ channels open.
Faster depolarization occurs, peaking at 0mV.
K^+ channels then open and K^+ leaves the cell, causing repolarization.
Once K^+ channels close, the pacemaker potential starts over.
When the SA node fires, it sets off the heartbeat.
As the internal pacemaker, it typically fires every 0.8 seconds, setting the resting rate at 75 bpm.
Impulse Conduction to Myocardium
The signal from the SA node stimulates the atria to contract almost simultaneously.
Reaches the AV node in 50 ms.
The signal slows down through the AV node due to thin cardiomyocytes with fewer gap junctions.
Delays the signal 100 ms, which allows the ventricles time to fill.
Signals travel very quickly through the AV bundle and subendothelial conducting network.
The entire ventricular myocardium depolarizes and contracts in near unison.
Ventricular systole progresses up from the apex of the heart; the spiral arrangement of the myocardium twists the ventricles slightly, like someone wringing out a towel.
Electrical Behavior of the Myocardium
Action potentials of cardiomyocytes differ from those of nodal cells, neurons, and muscle fibers.
Cardiomyocytes have a stable resting potential of −90 mV and depolarize only when stimulated.
Mechanism of cardiomyocyte action potential:
Depolarization: Stimulus opens voltage-regulated Na^+ gates (Na^+ rushes in), membrane depolarizes rapidly Action potential peaks at +30 mV Na^+ gates close quickly.
Plateau: Voltage-gated slow Ca^{2+} channels open, admitting Ca^{2+}, which triggers the opening of Ca^{2+} channels on the sarcoplasmic reticulum (SR). Lasts 200 to 250 ms; sustains contraction for expulsion of blood from the heart.
Repolarization: Ca^{2+} channels close. K^+ channels open, causing rapid diffusion of K^+ out of the cell, returning it to resting potential. The action potential peaks at +30 mV. Na^+ gates close quickly.
Cardiac muscle has a long absolute refractory period of 250 ms (compared to 1 to 2 ms in skeletal muscle).
Prevents wave summation and tetanus, which would stop the pumping action of the heart.
The Electrocardiogram (ECG or EKG)
Detects electrical currents in the heart using electrodes (leads) on the skin and an electrocardiograph to amplify and record the signals.
The record is called an electrocardiogram (ECG or EKG)—a composite of all action potentials of nodal and myocardial cells detected.
The ECG has three principal deflections:
P wave: Depolarization of the atria; atrial systole begins 100 ms after the start of the P wave.
PQ segment: Time (approximately 160 ms) between P and Q deflections; represents the time required for signals to pass from the SA node to the AV node.
QRS complex: Depolarization of the ventricles; ventricular systole begins shortly after.
ST segment: Between S and T deflections; time that ventricles are contracting.
Atrial repolarization also occurs, but the weak signal is obscured.
T wave: Repolarization of the ventricles immediately prior to diastole.
Normal Electrocardiogram
P wave: SA node fires, atria depolarize and contract; atrial systole begins 100 ms after the SA signal.
PR interval: Signal conduction through the AV node, before activating ventricles.
QRS complex: Ventricular depolarization; complex shape of spike due to different thicknesses and shapes of the two ventricles.
QT interval: Duration of ventricular depolarization; shorter during exercise.
ST segment: Ventricular systole; corresponds to the plateau in the myocardial action potential.
T wave: Ventricular repolarization and relaxation.
Cardiac Arrhythmias
Deviations of the ECG from normal can indicate:
Myocardial infarction (MI)
Abnormalities in conduction pathways
Heart enlargement
Electrolyte and hormone imbalances
Ventricular fibrillation:
Random electrical signals result in no pumping action; a hallmark of myocardial infarction (MI) and quickly fatal.
Serious arrhythmia caused by electrical signals traveling randomly.
The heart cannot pump blood; no coronary perfusion.
Hallmark of a heart attack (MI).
Kills quickly if not stopped.
Defibrillation: A strong electrical shock with the intent to depolarize the entire myocardium and reset the heart to sinus rhythm.
Not a cure for artery disease but may allow time for other corrective action.
Atrial fibrillation: Chaotic depolarizations that do not stimulate the ventricles; common in the elderly and alcoholics.
Weak rippling contraction in atria due to chaotic signals; atria fail to stimulate ventricles.
Heart block: Failure of any part of the cardiac conduction system to conduct signals, usually the result of disease or degeneration of the conduction system.
Failure of part of the conduction system; includes bundle branch block (bundle branch failure) and total heart block (AV node failure).
Premature ventricular contraction: Ventricular ectopic focus with an extra beat; may result from stress, lack of sleep, or stimulants.
Ventricular ectopic focus fires and sets off an extra beat.
Blood Flow, Heart Sounds, and the Cardiac Cycle
Cardiac cycle: One complete contraction and relaxation of all four chambers of the heart.
Two main variables govern fluid movement: pressure causes flow, and resistance opposes it.
Blood pressure is measured with a sphygmomanometer.
Flow requires a pressure gradient: The difference in pressure between two points.
Fluid flows from a high-pressure point to a low-pressure point.
Inverse relationship between volume and pressure:
Higher volume = lower pressure
Lower volume = higher pressure
Pressure Gradients and Flow
Events occurring on the left side of the heart:
When the ventricle relaxes and expands, its internal pressure falls.
If the mitral valve is open, blood flows into the left ventricle.
When the ventricle contracts, internal pressure rises.
AV valves close, the aortic valve is pushed open, and blood flows into the aorta from the left ventricle.
The opening and closing of valves are governed by these pressure changes.
AV valves are limp when ventricles are relaxed.
Semilunar valves are under pressure from the blood in vessels when ventricles are relaxed.
Operation of the Heart Valves
Atrioventricular valves open when the atrium has a higher pressure then the ventricle.
Atrioventricular valves close when the ventricle has a higher pressure then the atrium.
The first heart sound is produced hen the Atrioventricular valves close.
Semilunar valves open when the ventricles contract overcoming the pressure in the Pulmonary artery and Aorta.
Semilunar valves close when the ventricles relax and the pressure in the Pulmonary artery an Aorta is higher then the ventricles.
The second heart sound is produced when the semilunar valves close.
Valvular Insufficiency Disorders
Valvular insufficiency (incompetence): Any failure of a valve to prevent reflux (regurgitation), the backward flow of blood.
Valvular stenosis: Cusps are stiffened, and the opening is constricted by scar tissue.
Result of rheumatic fever, an autoimmune attack on the mitral and aortic valves.
The heart overworks and may become enlarged.
Heart murmur: An abnormal heart sound produced by the regurgitation of blood through incompetent valves.
Mitral valve prolapse: Insufficiency in which one or both mitral valve cusps bulge into the atria during ventricular contraction.
Hereditary in 1 out of 40 people.
May cause chest pain and shortness of breath.
Heart Sounds
Auscultation: Listening to sounds made by the body.
First heart sound (S1): Louder and longer “lubb,” occurs with closure of AV valves, turbulence in the bloodstream, and movements of the heart wall.
Second heart sound (S2): Softer and sharper “dupp,” occurs with closure of semilunar valves, turbulence in the bloodstream, and movements of the heart wall.
S3: Rarely heard in people over 30.
Phases of the Cardiac Cycle
The entire cardiac cycle is completed in less than 1 second.
Phases of the cardiac cycle:
Ventricular filling
Isovolumetric contraction
Ventricular ejection
Isovolumetric relaxation
Detailed Look at Each Phase of the Cardiac Cycle
Ventricular filling:
Ventricles expand, and their pressure drops below that of the atria.
AV valves open, and blood flows into the ventricles.
Filling occurs in three phases:
Rapid ventricular filling: First one-third.
Diastasis: Second one-third; slower filling.
The P wave occurs at the end of diastasis.
Atrial systole: Final one-third; atria contract.
End-diastolic volume (EDV) remains in each ventricle; about 130 mL of blood.
Isovolumetric contraction:
The atria repolarize, relax, and remain in diastole for the rest of the cardiac cycle.
Ventricles depolarize, causing the QRS complex, and begin to contract.
AV valves close as ventricular blood surges back against the cusps.
Heart sound S1 occurs at the beginning of this phase.
Called isovolumetric because, although ventricles contract, they do not eject blood.
Pressures in the aorta and pulmonary trunk are still greater than those in the ventricles.
Cardiomyocytes exert force, but with all four valves closed, the blood cannot go anywhere.
Ventricular ejection:
Begins when ventricular pressure exceeds arterial pressure, and semilunar valves open.
Pressure peaks in the left ventricle at about 120 mm Hg and 25 mm Hg in the right.
At first, rapid ejection: Blood spurts out of the ventricles quickly; then, reduced ejection: Slower flow under less pressure.
Ejection lasts about 200 to 250 ms; corresponds to the plateau phase of the cardiac action potential.
The T wave of the ECG occurs late in this phase.
Stroke volume (SV)—the amount ejected—is about 70 mL.
As a percentage of EDV (the ejection fraction), this is about 54%.
The 60 mL of remaining blood is the end-systolic volume (ESV).
Isovolumetric relaxation:
The T wave ends, and ventricles begin to expand.
Blood from the aorta and pulmonary trunk briefly flows backward, filling cusps and closing semilunar valves.
Creates a pressure rebound that appears as the dicrotic notch in the graph of artery pressure.
Heart sound S2 occurs.
Called isovolumetric because semilunar valves are closed, and AV valves have not yet opened, so there is no change in blood volume.
When AV valves open, ventricular filling begins again.
Duration of Systole
Atrial systole lasts about 0.1 second.
Ventricular systole lasts about 0.3 seconds.
Quiescent period: When all four chambers are in diastole; lasts about 0.4 seconds.
The total duration of the cardiac cycle is therefore 0.8 seconds in a heart beating 75 bpm.
Congestive Heart Failure (CHF)
Normally, the right and left sides of the heart eject the same volume of blood, even though they are under different pressures.
Congestive heart failure (CHF) results from the failure of either ventricle to eject blood effectively.
Usually due to a heart weakened by myocardial infarction, chronic hypertension, valvular insufficiency, or congenital defects in the heart structure.
Necessity of Balanced Ventricular Output
Left ventricular failure: Blood backs up into the lungs, causing pulmonary edema.
Shortness of breath or sense of suffocation.
Right ventricular failure: Blood backs up in the vena cava, causing systemic or generalized edema.
Enlargement of the liver, ascites (pooling of fluid in the abdominal cavity), distension of the jugular veins, swelling of the fingers, ankles, and feet.
Eventually leads to total heart failure.
Autonomic Innervation of the Heart
Sympathetic stimulation increases heart rate and contraction strength and dilates coronary arteries.
Parasympathetic stimulation decreases heart rate.
Heart rhythm and contraction are controlled by two cardiac centers in the medulla oblongata.
Cardioacceleratory center: Communicates with the heart via right and left cardiac nerves carrying sympathetic postganglionic nerve fibers.
Cardioinhibitory center: Communicates with the heart via right and left vagus nerves carrying parasympathetic preganglionic nerve fibers.
The body’s total volume of blood (4 to 6 L) passes through the heart every minute
CO varies with activity; vigorous exercise increases CO to 21 L/min for a fit person and up to more than 40 L/min for a world-class athlete
Factors Affecting Cardiac Output
Positive chronotropic agents: Factors that raise the heart rate.
Negative chronotropic agents: Factors that lower the heart rate.
Positive inotropic agents increase contractility.
Negative inotropic agents decrease contractility.
Hypercalcemia can cause strong, prolonged contractions and even cardiac arrest in systole.
Catecholamines increase calcium levels.
3 variables govern stroke volume: Preload, Contractility, Afterload
Increased preload or contractility increases stroke volume.
Increased afterload decreases stroke volume.
Preload
The amount of tension in ventricular myocardium immediately before it begins to contract.
Increased preload causes increased force of contraction.
The more they are stretched, the harder they contract
Afterload
Afterload: The sum of all forces opposing the ejection of blood from the ventricle.
The largest part of afterload is blood pressure in the aorta and pulmonary trunk.
Opposes the opening of semilunar valves.
Limits stroke volume.
Hypertension increases afterload and opposes ventricular ejection.
Contractility
Contractility refers to how hard the myocardium contracts for a given preload.
Understanding preload, contractility, and afterload
If you think of the heart as a balloon, it will help you understand stroke volume.
Blowing up the balloon
Preload is the stretching of muscle fibers in the ventricles. This stretching results from blood volume in the ventricles at end-diastole. According to Starling's law, the more the heart muscles stretch during diastole, the more forcefully they contract during systole. Think of preload as the balloon stretching as air is blown into it. The more air,