A&P II (The Cardiovascular System)

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Human Anatomy & Physiology

Second Edition

Chapter 17

The Cardiovascular System I:The Heart

PowerPoint® Lectures created by Suzanne Pundt, University of Texas at Tyler

Module 17.1 Overview of the Heart

The Cardiovascular System

Cardiovascular system:

Consists of heart, blood vessels, and blood

Heart pumps blood (liquid carrying oxygen and nutrients) into blood vessels (system of tubes that distributes it throughout cardiovascular system)

Location and Basic Structure of the Heart (1 of 7)

Heart—somewhat cone-shaped organ; situated slightly to left side in thoracic cavity; posterior to sternum in mediastinum; rests on diaphragm (Figure 17.1a)

Apex—point of cone; points toward left hip; flattened base is posterior side (not inferior) facing posterior rib cage (Figure 17.1c)

Relatively small, only about size of fist; generally weighs from 250 to 350 grams (slightly less than 1 pound)

Location and Basic Structure of the Heart (2 of 7)

Figure 17.1a Location and basic anatomy of the heart in the thoracic cavity.

Location and Basic Structure of the Heart (3 of 7)

Figure 17.1c Location and basic anatomy of the heart in the thoracic cavity.

Location and Basic Structure of the Heart (4 of 7)

Chambers and external anatomical features (Figure 17.1b and 17.2):

Chambers—superior right and left atria (singular, atrium) and inferior right and left ventricles

Externally, indentation known as atrioventricular sulcus is boundary between atria and ventricles

Interventricular sulcus—external depression between right and left ventricles

Location and Basic Structure of the Heart (5 of 7)

Figure 17.1b Location and basic anatomy of the heart in the thoracic cavity.

Location and Basic Structure of the Heart (6 of 7)

Figure 17.2 The chambers of the heart.

Location and Basic Structure of the Heart (7 of 7)

Both right and left atria receive blood from veins (blood vessels that bring blood to heart)

Blood drains from atria to ventricles; ventricles pump blood into arteries (carry blood away from heart)

Great vessels—main veins and arteries; bring blood to and from heart

Vessels and organs that transport oxygenated blood are color-coded red in textbook; those that carry deoxygenated blood are blue

Circulation of Blood through the Pulmonary and Systemic Circuits (1 of 8)

Heart pumps blood through two separate sets of vessels (circuits) (Figure 17.3a)

Heart is divided functionally into right and left sides

Right side of heart is pulmonary pump; pumps blood into series of blood vessels leading to and within lung; collectively called pulmonary circuit

Circulation of Blood through the Pulmonary and Systemic Circuits (2 of 8)

Pulmonary arteries of pulmonary circuit deliver oxygen-poor and carbon dioxide-rich (deoxygenated) blood to lungs

Gas exchange takes place between tiny air sacs in lung (alveoli) and smallest vessels of pulmonary circuit (pulmonary capillaries)

Oxygen diffuses from air in alveoli into blood in pulmonary capillaries

Carbon dioxide diffuses from blood in pulmonary capillaries to air in alveoli, to be expired

Veins of pulmonary circuit deliver this oxygen-rich (oxygenated) blood to left side of heart

Circulation of Blood through the Pulmonary and Systemic Circuits (3 of 8)

Figure 17.3a The pulmonary and systemic circuits.

Circulation of Blood through the Pulmonary and Systemic Circuits (4 of 8)

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Circulation of Blood through the Pulmonary and Systemic Circuits (5 of 8)

Left side of heart is systemic pump; receives oxygenated blood from pulmonary veins; pumps it into blood vessels that serve rest of body (systemic circuit) (Figure 17.3b)

In systemic circuit, arteries deliver oxygenated blood to smallest blood vessels (systemic capillaries)

Here gas exchange occurs again, in reverse:

Oxygen diffuses from blood into tissues

Carbon dioxide diffuses from tissues into blood

Circulation of Blood through the Pulmonary and Systemic Circuits (6 of 8)

Blood delivers nutrients, picks up wastes to be excreted, and distributes hormones to their target cells throughout body

As result of gas exchange in tissues, blood is deoxygenated and veins of systemic circuit then deliver it back to right side of heart, to be pumped into pulmonary circuit

Pulmonary circuit is low-pressure circuit because it pumps blood only to lungs; systemic circuit is a high-pressure circuit because it has to pump blood to entire rest of body

Circulation of Blood through the Pulmonary and Systemic Circuits (7 of 8)

Figure 17.3b The pulmonary and systemic circuits.

Circulation of Blood through the Pulmonary and Systemic Circuits (8 of 8)

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Functions of the Heart

Heart helps maintain homeostasis of pressure that blood exerts on blood vessels (blood pressure)

Rate and force of heart’s contraction are major factors that influence blood pressure and blood flow to organs

Heart (specifically atria) also acts as endocrine organ; produces atrial natriuretic peptide (ANP)

ANP lowers blood pressure by decreasing sodium ion retention in kidneys

Reduces osmotic water reabsorption and volume and pressure of blood in blood vessels

Module 17.2 Heart Anatomy and Blood Flow Pathway

The Pericardium, Heart Wall, and Heart Skeleton (1 of 7)

Pericardium—membranous structure surrounding heart (Figure 17.4):

Fibrous pericardium—outer layer

Composed of collagen bundles that make it tough; anchor heart to diaphragm and great vessels

Low distensibility—doesn’t change shape or size considerably when stretching forces applied; helps to prevent chambers of heart from overfilling with blood

Cardiac Tamponade

If pericardial cavity becomes filled with excess fluid, cardiac tamponade may result

Potential causes: trauma, certain cancers, kidney failure, recent thoracic surgery, and HIV

Regardless of cause, result is same—fibrous pericardium is strong but not very flexible, so excess fluid in pericardial cavity squeezes heart; reduces capacity of ventricles to fill with blood, decreasing amount of blood pumped with each beat

Treatment may include removal of excess fluid via needle inserted into pericardial cavity

The Pericardium, Heart Wall, and Heart Skeleton (2 of 7)

Serous pericardium—thin inner serous membrane; produces serous fluid:

Parietal pericardium—fused to inner surface of fibrous pericardium; encases heart-like sac; at great vessels, it folds under itself and forms another layer that adheres directly to heart

Visceral pericardium—innermost layer; also known as epicardium; considered most superficial layer of heart wall

The Pericardium, Heart Wall, and Heart Skeleton (3 of 7)

Pericardial cavity—between parietal and visceral pericardia; contains very thin layer of serous fluid (pericardial fluid); fluid acts as lubricant, decreasing friction as heart moves

Visceral pericardium rests on top of thin layer of areolar connective tissue; contains large fat deposits

Myocardium—deep to connective tissue; second and thickest layer of heart wall

The Pericardium, Heart Wall, and Heart Skeleton (4 of 7)

Myocardium components: cardiac muscle tissue and fibrous skeleton

Cardiac muscle tissue consists of cardiac muscle cells (myocytes) and their surrounding extracellular matrix

Cardiac muscle cells are attached to and woven through fibrous skeleton; composed of dense irregular collagenous connective tissue; fibrous skeleton functions:

Giving cardiac muscle cells something on which to pull when they contract

Providing structural support

Acting as insulator for heart’s electrical activity

The Pericardium, Heart Wall, and Heart Skeleton (5 of 7)

Lumen of heart is lined by endocardium; third and deepest layer of heart wall

Composed of special type of simple squamous epithelium (endothelium) and several layers of connective tissue with elastic and collagen fibers

Endothelial cells of endocardium are continuous with endothelial cells that line blood vessels; share many functions

The Pericardium, Heart Wall, and Heart Skeleton (6 of 7)

Figure 17.4a The pericardium and the layers of the heart wall.

The Pericardium, Heart Wall, and Heart Skeleton (7 of 7)

Figure 17.4b, c The pericardium and the layers of the heart wall.

Thoracotomy

Thoracic cavity is opened in surgical procedure known as thoracotomy

Performed when surgeon must gain access to thoracic organs, surrounding blood vessels, or anterior side of thoracic vertebral column

Generally involves incision in chest wall and cutting through either sternum or ribs; separated and held apart with instrument called retractor (or “rib spreader”); creates “window” into thoracic cavity

When procedure is completed, chest wall is closed, and chest tube must be inserted to prevent air from leaking into thoracic cavity and potentially causing collapse of lung

The Heart’s Great Vessels, Chambers, and Valves (1 of 21)

Heart consists of four chambers: two atria and two ventricles (Figures 17.5–17.7):

Atria receive blood from veins, and pump blood into ventricles through valves

Valves have flaps that close when ventricles contract; keep blood from moving backward

Contracting ventricles then eject blood into arteries; carry blood through either systemic or pulmonary circuit

The Heart’s Great Vessels, Chambers, and Valves (2 of 21)

Great vessels—bring blood to and away from heart; largest in body (Figure 17.5):

Major systemic veins: two veins that drain majority of systemic circuit are superior and inferior venae cavae; both have large openings into posterior aspect of right atrium:

Superior vena cava (SVC)—drains deoxygenated blood from veins superior to diaphragm

Inferior vena cava (IVC)—drains deoxygenated blood from veins inferior to diaphragm

The Heart’s Great Vessels, Chambers, and Valves (3 of 21)

Pulmonary trunk—largest vessel in pulmonary circuit; receives deoxygenated blood pumped from right ventricle

Originates from right ventricle on anterior aspect of heart, nearly along midline

Splits into right and left pulmonary arteries; bring deoxygenated blood to right and left lungs, respectively

Pulmonary arteries branch extensively inside lungs to become tiny pulmonary capillaries where gases are exchanged

The Heart’s Great Vessels, Chambers, and Valves (4 of 21)

Oxygenated blood in pulmonary capillaries returns to heart via a set of pulmonary veins

Most people have four; two from each lung

Drain oxygenated blood into posterior part of left atrium

Aorta supplies entire systemic circuit with oxygenated blood

Largest and thickest artery in systemic circuit and in entire body

Arises from left ventricle as ascending aorta; curves to left and makes U-turn as aortic arch

The Heart’s Great Vessels, Chambers, and Valves (5 of 21)

Figure 17.5a The external anatomy of the heart.

The Heart’s Great Vessels, Chambers, and Valves (6 of 21)

Figure 17.5b The external anatomy of the heart.

The Heart’s Great Vessels, Chambers, and Valves (7 of 21)

Figure 17.5c The external anatomy of the heart.

The Heart’s Great Vessels, Chambers, and Valves (8 of 21)

Largest structures in heart are four chambers (Figure 17.6):

Ventricles are larger than atria and have much thicker walls; makes ventricles much stronger pumps

Greater strength is needed to generate pressure that pumps blood around pulmonary and systemic circuits

The Heart’s Great Vessels, Chambers, and Valves (9 of 21)

Atria are not symmetrical in size, shape, or location:

Right atrium is larger, thinner-walled, and more anterior than left atrium

Left atrium is thicker-walled, somewhat smaller, and located mostly on posterior side of heart; makes up much of heart’s base (posterior surface)

Externally, each atrium has muscular pouch (auricle); named for resemblance to external ear; expand to give atria more space to hold blood; auricle of right atrium is much larger than that of left atrium

The Heart’s Great Vessels, Chambers, and Valves (10 of 21)

Atria (continued)

Pectinate muscles—muscular ridges on anterior side of internal surface of right atrium

Left atrium is mostly formed by pulmonary veins, and internally its walls are smooth

Interatrial septum—thin wall that separates two atria

Fossa ovalis—small indentation in septum; remnant of hole (foramen ovale) in interatrial septum of fetal heart

The Heart’s Great Vessels, Chambers, and Valves (11 of 21)

Ventricles—like atria, ventricles are asymmetrical; right ventricle is wider with thinner walls than left ventricle because of pressure differences in pulmonary and systemic circuits

Right ventricle has little resistance against which to pump; left ventricle pumps against much greater resistance

Left ventricle has to work harder than right ventricle; therefore has greater muscle mass; walls are about three times thicker than those of right ventricle; Structure-Function Core Principle

The Heart’s Great Vessels, Chambers, and Valves (12 of 21)

The Heart’s Great Vessels, Chambers, and Valves (13 of 21)

Ventricles (continued)

Internally, both ventricles have ridged surface created by irregular protrusions of cardiac muscle tissue (trabeculae carneae)

Each ventricle also contains finger-like projections of muscle (papillary muscles); attach by tendon-like cords (chordae tendineae) to valves between atria and ventricles

Interventricular septum—thick, muscular wall; separates right and left ventricles; contracts with rest of ventricular muscle; helps expel blood into pulmonary trunk and aorta

The Heart’s Great Vessels, Chambers, and Valves (14 of 21)

Figure 17.6a The internal anatomy of the heart.

The Heart’s Great Vessels, Chambers, and Valves (15 of 21)

Figure 17.6b The internal anatomy of the heart.

The Heart’s Great Vessels, Chambers, and Valves (16 of 21)

Blood flow through heart must occur in only one direction so deoxygenated blood goes to pulmonary circuit and oxygenated blood goes to systemic circuit

Two types of valves prevent blood from flowing backward

No valves needed between atria and veins that drain blood into them (Figure 17.7)

Backflow of blood generally doesn’t occur in veins draining into atria

Atria are under very low pressure; blood mostly flows into atria with help of gravity and pressure in veins

The Heart’s Great Vessels, Chambers, and Valves (17 of 21)

Forceful ventricular contractions could drive blood backward into atria; prevented by valves between atria and ventricles (right and left atrioventricular (AV) valves)

AV valves consist of flaps (cusps); composed of endocardium overlying core of collagenous connective tissue

Each valve is named for number of cusps:

Tricuspid valve—between right atrium and right ventricle contains three cusps

Bicuspid valve—between left atrium and left ventricle has two cusps; more commonly called mitral valve (clinical name)

The Heart’s Great Vessels, Chambers, and Valves (18 of 21)

Chordae tendineae—fibrous, tendon-like structures attached to inferior end of each cusp

Attached to papillary muscles that contract just before ventricles begin ejecting blood

Creates tension on chordae tendineae keeping valves closed

The Heart’s Great Vessels, Chambers, and Valves (19 of 21)

Backflow of blood into ventricles from pulmonary artery and aorta can also occur

Blood flows backward when ventricles relax as result of higher pressure in arteries and gravity; semilunar valves prevent this

“Semilunar” refers to half-moon shape of their three cusps; also composed of endocardium and central collagenous core

Named according to artery in which they reside

Pulmonary valve—between right ventricle and pulmonary trunk

Aortic valve—posterior to pulmonary; between left ventricle and aorta

The Heart’s Great Vessels, Chambers, and Valves (20 of 21)

Figure 17.7a Anatomy of the atrioventricular and semilunar valves.

The Heart’s Great Vessels, Chambers, and Valves (21 of 21)

Figure 17.7b Anatomy of the atrioventricular and semilunar valves.

The Big Picture of Blood Flow through the Heart (1 of 2)

Figure 17.8 The Big Picture of Blood Flow through the Heart.

The Big Picture of Blood Flow through the Heart (2 of 2)

Figure 17.8 The Big Picture of Blood Flow through the Heart.

Valvular Heart Diseases (1 of 2)

Valvular heart diseases impair function of one or more of valves; may be congenital (present at birth) or acquired from disease process (infection, cancer, or disorders of immune system)

Two major types of valvular defects: insufficiency and stenosis

Insufficient valve—fails to close fully; allows blood to leak backward

Stenotic valve—calcium deposits in cusps; makes them hard and inflexible; blood flows through stenotic valve with difficulty; often heart has to pump harder to eject blood through it

Valvular Heart Diseases (2 of 2)

Both types of valvular heart diseases may cause heart murmur (audible “swooshing” of blood when heart beats)

Other signs and symptoms vary with type and severity of disease; may include enlargement of heart, fatigue, dizziness, and heart palpitations

Mitral and aortic valves are most commonly affected by valvular heart disease

The Coronary Circulation (1 of 14)

Heart’s chambers are filled with blood, but myocardium is too thick for oxygen and nutrients to diffuse from inside chambers to all of organ’s cells

For this reason, heart is supplied by a set of blood vessels collectively called coronary circulation (Figure 17.9)

The Coronary Circulation (2 of 14)

Coronary vessels (coronary arteries):

Ascending aorta—main systemic artery into which left ventricle pumps blood

Immediately after ascending aorta emerges from left ventricle, two branches (right and left coronary arteries) arise; travel in right and left atrioventricular sulci, respectively

The Coronary Circulation (3 of 14)

Right coronary artery travels inferiorly and laterally along right atrioventricular sulcus; gives off several branches that supply right atrium and ventricle (Figure 17.9a):

Largest branch is marginal artery; typically arises near inferior margin (border) of heart

After marginal artery branches off, right coronary artery curls around to posterior heart; travels in posterior interventricular sulcus as posterior interventricular artery

The Coronary Circulation (4 of 14)

Shortly after left coronary artery emerges from ascending aorta, it generally branches into two vessels:

Anterior interventricular artery (left anterior descending artery, or LAD) travels along anterior interventricular sulcus; at apex of heart, it generally curls around and travels short distance along posterior interventricular sulcus

Circumflex artery curves along left atrioventricular sulcus and flexes around heart; supplies left atrium and parts of left ventricle; in some people, replaces right coronary artery in supplying branch that becomes posterior interventricular artery

The Coronary Circulation (5 of 14)

Coronary arterial supply is complicated by formation of anastomoses (systems of channels formed between blood vessels)

Coronary arteries may form anastomoses with one another, with branches from pericardium, or even with arteries from outside coronary circulation entirely

When blood flow to myocardium is insufficient, occasionally new anastomoses will form to provide alternate routes of blood flow (collateral circulation) to myocardium

Collaterals help protect muscle cells from damage that could result from blocked vessels

The Coronary Circulation (6 of 14)

Figure 17.9a The coronary circulation.

The Coronary Circulation (7 of 14)

Coronary vessels (coronary veins) (Figure 17.9b):

Majority of heart’s veins empty into large venous structure on posterior heart (coronary sinus); drains into posterior right atrium

Coronary sinus receives blood from three major veins:

Great cardiac vein

Small cardiac vein

Middle cardiac vein

The Coronary Circulation (8 of 14)

Coronary sinus receives blood from three major veins (continued):

Large great cardiac vein ascends along anterior interventricular sulcus; travels to posterior side of heart along left atrioventricular sulcus; drains left atrium and much of both ventricles

Small cardiac vein travels along right atrioventricular sulcus; drains right atrium and parts of right ventricle

Middle cardiac vein travels along posterior interventricular groove; drains mostly posterior left ventricle

The Coronary Circulation (9 of 14)

Figure 17.9b The coronary circulation.

The Coronary Circulation (10 of 14)

Build-up of fatty material (plaques) in coronary arteries results in coronary artery disease (CAD); leading cause of death worldwide

CAD decreases blood flow to myocardium; results in inadequate oxygenation of myocardium; known as myocardial ischemia

When present, symptoms generally come in form of chest pain (angina pectoris)

The Coronary Circulation (11 of 14)

Most dangerous potential consequence of CAD is myocardial infarction (MI; heart attack)

MIs occur when plaques in coronary arteries rupture and clot forms; obstructs blood flow to myocardium; myocardial tissue supplied by that artery infarct (die)

Symptoms include chest pain that radiates along dermatomes to left arm or left side of neck, shortness of breath, sweating, anxiety, and nausea and/or vomiting

Note: women may not present with chest pain; may suffer back, jaw, or arm pain instead

The Coronary Circulation (12 of 14)

Survival after MI depends on extent and location of damage

Cardiac muscle cells generally do not undergo mitosis

Dead cells are replaced with fibrous, noncontractile scar tissue

Death of part of myocardium increases workload of remaining heart muscle

Risk factors for CAD and MI include smoking, high blood pressure, poorly controlled diabetes, high levels of certain lipids in blood, obesity, age over 40 for males and over 50 for females, genetics, and male gender

The Coronary Circulation (13 of 14)

CAD is definitively diagnosed via angiography; small tube is fed through artery in systemic circuit into ascending aorta, and into coronary arteries; special dye is injected into arteries, and their condition is examined by x-ray

Treatments include lifestyle modifications and appropriate medications; if these approaches fail, invasive treatments are considered (next slide)

The Coronary Circulation (14 of 14)

Coronary angioplasty—commonly performed invasive procedure; balloon is inflated in blocked artery; piece of wire-mesh tubing (stent) may be inserted into artery to keep it open

Coronary artery bypass grafting—more invasive treatment; other vessels are grafted onto diseased coronary artery to bypass blockage and provide alternate route for blood flow

Module 17.3 Cardiac Muscle Tissue Anatomy and Electrophysiology

Electrophysiology (1 of 2)

Heart does not require conscious intervention to elicit cardiac muscle to contract; cardiac muscle exhibits autorhythmicity; sets its own rhythm without need for input from nervous system

Cardiac muscle cells contract in response to electrical excitation in form of action potentials

Unlike skeletal muscle and many smooth muscle cells, cardiac muscle cells do not require stimulation from nervous system to generate action potentials

Electrophysiology (2 of 2)

Cardiac electrical activity is coordinated by very small, unique population of cardiac muscle cells (pacemaker cells)

These cells rhythmically and spontaneously generate action potentials; spread to other type of cardiac muscle cell (contractile cells)

Histology of Cardiac Muscle Tissue and Cells (1 of 6)

Cardiac muscle cells, like skeletal muscle fibers, have striations (alternating light and dark bands when viewed under microscope) (Figure 17.10)

As with skeletal muscle fibers, striations are due to arrangement of contractile proteins within cardiac muscle cells

Structural similarities reflect physiological similarities; skeletal and cardiac muscle tissues have same general function; both generate tension through sliding-filament mechanism of contraction; Structure-Function Core Principle

Histology of Cardiac Muscle Tissue and Cells (2 of 6)

Cardiac muscle cells (continued)

Typically branched cells with single nucleus; shorter and wider than skeletal muscle fibers

Contain abundant myoglobin (protein that carries oxygen)

Nearly half of cytoplasmic volume is composed of mitochondria; reflect high energy demands

Histology of Cardiac Muscle Tissue and Cells (3 of 6)

Cardiac muscle cells (continued)

Possess unique structures (intercalated discs) that join adjacent cardiac muscle cells; join pacemaker cells to contractile cells, and contractile cells to one another

Intercalated discs contain

Desmosomes—hold cardiac muscle cells together

Gap junctions—allow ions to rapidly pass from one cell to another, permitting communication among cardiac muscle cells; Cell-Cell Communication Core Principle

Histology of Cardiac Muscle Tissue and Cells (4 of 6)

Figure 17.10 Cardiac muscle cells.

Histology of Cardiac Muscle Tissue and Cells (5 of 6)

Like skeletal muscle fibers and other excitable cells, cardiac muscle cells contain selective gated ion channels in sarcolemma

Opening and closing action of these ion channels is responsible for both pacemaker and contractile cardiac action potentials

Histology of Cardiac Muscle Tissue and Cells (6 of 6)

Types of gated ion channels:

Voltage-gated sodium ion channels—open in response to voltage changes across membrane; in all cardiac muscle cells except certain pacemaker cells

Calcium ion channels—demonstrate voltage-gated opening but time-gated closing; close after certain period regardless of voltage

All types of cardiac muscle cells have one or more types of potassium ion channels; some ligand-gated; others voltage-gated

Study Boost: Revisiting Electrophysiology (1 of 3)

Terminology:

Voltage—difference in electrical potential between two points

Membrane potential—voltage (charge) difference that exists across membranes of all cells, including excitable cells

Resting membrane potential—membrane potential of excitable cell at rest (not being stimulated); averages between −60 and −90 mV: difference in concentration of ions across plasma membrane

Study Boost: Revisiting Electrophysiology (2 of 3)

Terminology (continued):

Current—flow of ions or electrons with chemical or electrical gradient

Depolarization—change in resting membrane potential to value less negative than when at rest; occurs when positive charges (generally, sodium and/or calcium ions) rush into cell

Repolarization—return of cell to its negative resting membrane potential; occurs when positive charges (potassium ions) leave cell

Study Boost: Revisiting Electrophysiology (3 of 3)

Review of ion gradients (Gradients Core Principle):

Concentration of sodium and calcium ions in extracellular fluid (ECF) is higher than in cytosol; concentration of potassium ions in ECF is lower than in cytosol

Sodium and calcium ions tend to follow their concentration gradients to enter cell when their channels open

Potassium ions follow their concentration gradient and leave cell when their channels open

Sodium and potassium ion gradients are maintained by Na+/K+ pump; calcium ion gradient by separate active transport pump

Electrophysiology of Cardiac Muscle Tissue (1 of 38)

Pacemaker cells undergo rhythmic, spontaneous depolarizations that lead to action potentials; spread quickly through heart by cardiac conduction system (group of interconnected pacemaker cells) (Figures 17.11–7.12)

Electrophysiology of Cardiac Muscle Tissue (2 of 38)

Action potentials are transmitted from pacemaker cells to contractile cells through intercalated discs that unite them

Gap junctions in these discs allow electrical activity generated by pacemaker cells to rapidly spread to all cardiac muscle cells via electrical synapses

Permits heart to contract as unit and produce coordinated heartbeat; reason cells of heart are sometimes referred to as functional syncytium (term for large, multinucleated cell)

Electrophysiology of Cardiac Muscle Tissue (3 of 38)

Pacemaker cells make up only about 1% of total number of cardiac muscle cells

Three populations of these cells in heart; capable of spontaneously generating action potentials, thereby setting pace of heart

Three cell populations are collectively called cardiac conduction system

Electrophysiology of Cardiac Muscle Tissue (4 of 38)

Pacemaker potential—much different from that of contractile cell (Figure 17.11):

Depolarization in pacemaker cell occurs much more slowly; due in part to lack of voltage-gated sodium ion channels in pacemaker sarcolemma

Pacemaker cell action potentials lack plateau phase and membrane potential oscillates—never remains at resting level; instead occurs in cycle, with last event triggering first

Occurs because of nonspecific cation channels; unique to pacemaker cells

Electrophysiology of Cardiac Muscle Tissue (5 of 38)

Pacemaker potential (continued)

Slow initial depolarization phase—pacemaker potential starts with plasma membrane in hyperpolarized state—at minimum membrane potential

Opens nonspecific cation channels in membrane; allow sodium ions to leak into cell and potassium ions to leak out

Results in overall slow depolarization to threshold

Full depolarization phase—when membrane reaches threshold, voltage-gated calcium ion channels open; allows calcium ions to enter cell; causes membrane to fully depolarize

Electrophysiology of Cardiac Muscle Tissue (6 of 38)

Pacemaker potential (continued)

Repolarization phase—calcium ion channels are time-gated for closing; after certain time (about 100–150 msec), they close; at same time, voltage-gated potassium ion channels begin to open; allows potassium ions to exit cell, and membrane begins to repolarize

Minimum potential phase—potassium ion channels remain open until membrane reaches its minimum potential (membrane is hyperpolarized); opens nonspecific cation channels, and cycle begins again

Electrophysiology of Cardiac Muscle Tissue (7 of 38)

Figure 17.11 A pacemaker cell action potential.

Electrophysiology of Cardiac Muscle Tissue (8 of 38)

Figure 17.11 A pacemaker cell action potential.

Electrophysiology of Cardiac Muscle Tissue (9 of 38)

Cardiac conduction system includes three populations of pacemaker cells (Figure 17.12):

Sinoatrial node (SA node)—in upper right atrium, slightly inferior and lateral to opening of superior vena cava

Under normal conditions, SA node has fastest intrinsic rate of depolarization—about 60 or more times per minute

Rate is subject to influence from sympathetic and parasympathetic nervous systems

Electrophysiology of Cardiac Muscle Tissue (10 of 38)

Cardiac conduction system cells populations (continued):

Atrioventricular node (AV node)— posterior and medial to tricuspid valve; slower than SA node; intrinsic rate of only about 40 action potentials per minute

Purkinje fiber system—slowest group of pacemaker cells; depolarize only about 20 times per minute; atypical pacemakers because their action potentials rely on different ion channels and they function in slightly different way

Electrophysiology of Cardiac Muscle Tissue (11 of 38)

Purkinje fiber system:

Atrioventricular bundle (AV bundle)—penetrates heart’s fibrous skeleton in inferior interatrial septum and superior interventricular septum

Right and left bundle branches—course along right and left sides of interventricular septum, respectively

Terminal branches—penetrate ventricles and finally come into contact with contractile cardiac muscle cells

Electrophysiology of Cardiac Muscle Tissue (12 of 38)

Figure 17.12 The cardiac conduction system.

Electrophysiology of Cardiac Muscle Tissue (13 of 38)

Pacing Heart: Sinus rhythm—each population of pacemaker cells can potentially pace heart (make it beat at certain rate); one that depolarizes fastest sets heart rate; other pacemakers will pace heart only if fastest pacemaker ceases to function

SA node is normal pacemaker of entire heart; electrical rhythms generated and maintained by SA node are known as sinus rhythms

AV node and Purkinje fiber system normally only conduct action potentials generated by SA node; if SA node ceases to function, AV node can successfully pace heart, albeit somewhat slowly

Electrophysiology of Cardiac Muscle Tissue (14 of 38)

Note that AV bundle of Purkinje system is only connection between AV node and ventricles

If blocked, SA node cannot pace ventricles even if functioning normally

Purkinje fiber system is capable of pacing heart, but its slow rate of depolarization is not adequate to sustain life beyond short period of time

Occasionally, group of regular contractile cells or pacemaker cells other than SA node will attempt to pace heart at same time as SA node; “extra” pacemaker is called ectopic pacemaker; can cause irregular heart rhythms

Electrophysiology of Cardiac Muscle Tissue (15 of 38)

Under normal conditions, SA node generates action potential; spreads rapidly via gap junctions to surrounding atrial cells

Impulses are conducted by specialized atrial conducting fibers to AV node; altogether require about 0.03 second

Once impulse reaches AV node, conduction slows considerably as result of:

Low number of gap junctions between AV nodal cells

Presence of nonconducting fibrous skeleton that surrounds AV node

Electrophysiology of Cardiac Muscle Tissue (16 of 38)

This slow conduction (AV node delay) generally lasts about 0.13 second

Allows atria to depolarize (and contract) before ventricles; gives ventricles time to fill with blood

Also helps to prevent current from flowing backward from AV bundle into AV node and atria

Action potential is then conducted from AV bundle to right and left bundle branches

Depolarization spreads along Purkinje fibers to contractile cardiac muscle cells of ventricles

Electrophysiology of Cardiac Muscle Tissue (17 of 38)

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Electrophysiology of Cardiac Muscle Tissue (18 of 38)

Contractile cells—great majority (99%) of cardiac muscle cells

Action potential in contractile cardiac muscle cell results from reversal in membrane potential—inside of plasma membrane swings from negative (about −85 mV) to momentarily positive (ranging from 0 to +20 mV)

Voltage-gated ion channels in sarcolemma and unequal concentrations of sodium and potassium ions on either side of membrane drive ions in or out of cell through channels

Electrophysiology of Cardiac Muscle Tissue (19 of 38)

Sequence of events of contractile cell action potential proceeds as follows (Figure 17.13):

Rapid depolarization phase—pacemaker cell action potentials cause voltage changes in adjacent cells; voltage-gated sodium ion channels in sarcolemma are activated; causes rapid and massive influx of sodium ions; leads to rapid membrane depolarization

Initial repolarization phase—small, initial repolarization immediately after depolarization spike; due to abrupt inactivation of sodium ion channels and to very small outflow of potassium ions through selected potassium ion channels (open only briefly)

Electrophysiology of Cardiac Muscle Tissue (20 of 38)

Sequence of events (continued):

Plateau phase—depolarization is sustained at about 0 mV in plateau phase; critically important phase is mostly due to slow opening of calcium ion channels and resulting influx of calcium ions

Repolarization phase—final phase of action potential; both sodium and calcium ion channels return to resting states and most of potassium ion channels open; allows positively charged potassium ions to exit cardiac muscle cell; membrane potential returns to its resting value of about −85 mV

Electrophysiology of Cardiac Muscle Tissue (21 of 38)

Figure 17.13 A contractile cell action potential.

Electrophysiology of Cardiac Muscle Tissue (22 of 38)

Figure 17.13 A contractile cell action potential.

Electrophysiology of Cardiac Muscle Tissue (23 of 38)

Sequence of events of contractile cell action potential resembles that of skeletal muscle fiber action potential with one important exception: plateau phase

If cardiac action potentials lasted only about 1–5 msec, like skeletal muscle fiber action potentials, resting heart rate would be about 15 times faster than it should be at rest

Plateau phase lengthens cardiac action potential to about 200–300 msec; slows heart rate; provides time required for heart to fill with blood

Electrophysiology of Cardiac Muscle Tissue (24 of 38)

Electrophysiology of Cardiac Muscle Tissue (25 of 38)

Plateau phase also increases strength of heart’s contraction; prolonged action potential makes muscle twitch last longer; can develop more force; allows more calcium ions to enter cell; needed for contraction via sliding-filament mechanism

Plateau phase also effectively prevents tetany (sustained contraction) in heart by lengthening refractory period (time during which excitable cell cannot be stimulated to contract again)

Electrophysiology of Cardiac Muscle Tissue (26 of 38)

Refractory period in cardiac muscle cells is so long that cells cannot maintain sustained contraction; allows heart to relax and ventricles to refill with blood before cardiac muscle cells are stimulated to contract again

Electrophysiology of Cardiac Muscle Tissue (27 of 38)

Excitation-contraction coupling—mechanism for cardiac muscle cell contraction is very similar to that of skeletal muscle fiber; occurs by sliding-filament mechanism

In stimulated cardiac muscle cell, depolarization propagates through sarcolemma and dives into cell along T-tubules; causes sarcoplasmic reticulum to release calcium ions

Ions bind to troponin; allows actin and myosin to bind and crossbridge cycle to begin

Electrophysiology of Cardiac Muscle Tissue (28 of 38)

Excitation-contraction coupling (continued)

Sarcoplasmic reticulum of cardiac muscle cells is much less extensive than in skeletal muscle fibers; does not release enough calcium ions to produce reliably strong contraction

Remaining calcium ions needed for contraction diffuse into cell during action potential through calcium ion channels from extracellular fluid in T-tubules

For this reason, concentration of calcium ions in cardiac extracellular fluid plays significant role in determining strength of contraction; one reason why calcium ion homeostasis is so critical

Electrophysiology of Cardiac Muscle Tissue (29 of 38)

Electrocardiogram (ECG)—important clinical tool for examining health of heart; graphic depiction of electrical activity occurring in all cardiac muscle cells over period of time (Figure 17.14)

Recorded by placing electrodes on surface of patient’s skin: six on chest and two on each extremity

Electrical changes are shown on ECG as deflections (waves); show changes in electrical activity—if there is no net difference, there is no deflection shown

One of most obvious changes in heart revealed by ECG is disturbance in electrical rhythm (dysrhythmia or arrhythmia)

Electrophysiology of Cardiac Muscle Tissue (30 of 38)

ECG recording generally consists of five waves; each represents active depolarization or repolarization of different parts of heart

Small, initial P wave represents depolarization of all cells within atria except SA node; P wave nearly always registers as upward deflection on ECG

Electrophysiology of Cardiac Muscle Tissue (31 of 38)

ECG (continued)

Large QRS complex represents ventricular depolarization; actually three separate waves:

Q wave is first downward deflection

R is large upward deflection

S is following downward deflection

Small T wave occurs after S wave of QRS complex; represents ventricular repolarization; T wave is upward deflection under normal conditions

Electrophysiology of Cardiac Muscle Tissue (32 of 38)

Figure 17.14 A normal electrocardiogram (ECG) tracing.

Electrophysiology of Cardiac Muscle Tissue (33 of 38)

Periods between waves represent important phases of action potentials and of spread of electrical activity through heart

Intervals include component of at least one wave

Segments do not include any wave components

Electrophysiology of Cardiac Muscle Tissue (34 of 38)

Three intervals of note:

R-R interval—time between two successive R waves; entire duration of generation and spread of action potential through heart; can be measured to determine heart rate

P-R interval—period from beginning of P wave to beginning of R wave; time it takes for depolarization generated by SA node to spread through atria to ventricles; includes AV node delay

Q-T interval—time from beginning of QRS complex to end of T wave; action potentials spread through ventricular cells

Electrophysiology of Cardiac Muscle Tissue (35 of 38)

Figure 17.14 A normal electrocardiogram (ECG) tracing.

Electrophysiology of Cardiac Muscle Tissue (36 of 38)

S-T segment—between end of S wave and beginning of T wave

Flat because it is recorded during plateau phase of ventricles; no net changes occur in electrical activity

Elevation or depression of S-T segment is seen with many clinical conditions, most notably myocardial ischemia and myocardial injury and infarction

Electrophysiology of Cardiac Muscle Tissue (37 of 38)

Figure 17.14 A normal electrocardiogram (ECG) tracing.

Electrophysiology of Cardiac Muscle Tissue (38 of 38)

Figure 17.14 A normal electrocardiogram (ECG) tracing.

Dysrhythmias (1 of 7)

Cardiac dysrhythmias have three basic patterns:

Disturbances in heart rate:

Bradycardia—heart rate under 60 beats per minute

Tachycardia—heart rate over 100 beats per minute; sinus tachycardia is regular, fast rhythm

Dysrhythmias (2 of 7)

Disturbances in conduction pathways—normal conduction pathway may be disrupted by accessory pathways between atria and ventricles or by blockage along conduction system (heart block)

Blockage common at AV node;

P-R interval is longer than normal, due to increased time for impulses to spread to ventricles through AV node

Extra P waves present; indicates some action potentials from SA node are not being conducted through AV node at all

Dysrhythmias (3 of 7)

Disturbances in conduction pathways (continued):

AV node blockage

Another common location for heart blocks is along right or left bundle branch; generally widen QRS complex; depolarization takes longer to spread through ventricles

Dysrhythmias (4 of 7)

In fibrillation

Electrical activity in heart essentially goes haywire; causes parts of heart to depolarize and contract while others are repolarizing and not contracting

Fibrillating muscle is often visually compared to writhing movement of plastic bag full of earthworms

Dysrhythmias (5 of 7)

Fibrillation (continued):

Atrial fibrillation—generally not life threatening because atrial contraction isn’t necessary for ventricular filling; manifests on ECG tracing as “irregularly irregular” rhythm (no discernible pattern) that lacks P waves

Dysrhythmias (6 of 7)

Ventricular fibrillation—immediately life-threatening and manifests on ECG with chaotic activity

Treated with defibrillation (electric shock to heart); depolarizes all ventricular muscle cells simultaneously and throws cells into their refractory periods

Ideally, SA node will resume pacing heart after shock is delivered

Dysrhythmias (7 of 7)

Ventricular fibrillation is not same as “flat-lining”; condition called asystole

Defibrillation is not used for asystole because heart is not fibrillating; no electrical activity to reset

Treated with CPR and pharmacological agents that stimulate heart such as atropine and epinephrine

Module 17.4 Mechanical Physiology of the Heart: The Cardiac Cycle

Introduction to Mechanical Physiology

Mechanical physiology—actual processes by which blood fills cardiac chambers and is pumped out of them

Cardiac muscle cells contract as unit to produce one coordinated contraction (heartbeat); muscle cells are arranged in spiral pattern, producing “wringing” action in heart when it contracts

Pressure changes caused by contractions drive blood flow through heart, with valves preventing backflow

Cardiac cycle—sequence of events within heart from one heartbeat to next

Pressure Changes, Blood Flow, and Valve Function (1 of 21)

Blood flows in response to pressure gradients (Gradients Core Principle); as ventricles contract and relax, pressure in chambers changes, causing blood to push on valves and open or close them (Figure 17.15):

When ventricles contract, their pressures rise above those in right and left atria and in pulmonary trunk and aorta; causes blood to flow from ventricles to vessels and produces two changes in valves:

Both AV valves are forced shut by blood pushing against them

Both semilunar valves are forced open by outgoing blood

Pressure Changes, Blood Flow, and Valve Function (2 of 21)

Figure 17.15a Pressure changes, blood flow, and valve function.

Pressure Changes, Blood Flow, and Valve Function (3 of 21)

When ventricles relax, opposite occurs; pressures in ventricles fall below those in atria and in pulmonary trunk and aorta

Higher pressure in atria forces AV valves open, allowing blood to drain from atria into relaxed ventricles

Higher pressures in pulmonary trunk and aorta push cusps of semilunar valves closed

Pressure Changes, Blood Flow, and Valve Function (4 of 21)

Figure 17.15b Pressure changes, blood flow, and valve function.

Pressure Changes, Blood Flow, and Valve Function (5 of 21)

Stethoscope—clinical device that can be used to listen to (auscultate) rhythmic heart sounds (Figure 17.16):

Under normal conditions, blood flow through open AV and semilunar valves is relatively quiet; sounds occur only when valves close

Sounds are not due to actual valve “slamming shut”; likely result from vibrations of ventricular and blood vessel walls

There are two heart sounds: S1, or “lub,” when AV valves close, and S2, “dub,” when semilunar valves close; S1 is typically longer and louder than S2, although it’s lower in frequency

Pressure Changes, Blood Flow, and Valve Function (6 of 21)

Figure 17.16 Heart sounds.

Heart Murmurs and Extra Heart Sounds (1 of 2)

One of more common findings on chest auscultation is audible sound called heart murmur; occurs when blood flow through heart is turbulent

Heart murmurs are generally caused by defective valves; may also result from defective chordae tendineae or holes in interatrial or interventricular septum

Children, however, often have heart murmurs that do not represent defects

Heart Murmurs and Extra Heart Sounds (2 of 2)

Chest auscultation may also reveal extra heart sounds

S3—can occur just as blood begins to flow into ventricles, right after S2; results from recoil of ventricular walls as they are stretched and filled

S4—heard when most of blood has finished draining from atria to ventricles, just before S1; typically results from blood being forced into stiff or enlarged ventricle

Both S3 and S4 may represent pathology; can also occasionally be heard in healthy heart

Pressure Changes, Blood Flow, and Valve Function (7 of 21)

Each cardiac cycle consists of one period of relaxation (diastole) and one period of contraction (systole) for each chamber of heart (Figures 17.17, 17.18)

Atrial and ventricular diastoles and systoles occur at different times as result of AV node delay; both sides of heart are working to pump blood into their respective circuits simultaneously

Cycle is divided into four main phases; defined by actions of ventricles and positions of valves: filling, contraction, ejection, and relaxation

Pressure Changes, Blood Flow, and Valve Function (8 of 21)

Ventricular filling phase of cardiac cycle—period during which blood drains from atria into ventricles

Pressures in left and right ventricles are lower than in atria, pulmonary trunk, and aorta

Higher pressures in pulmonary trunk and aorta cause semilunar valves to be closed; prevents flow of blood from pulmonary trunk and aorta back into ventricles

Pressure Changes, Blood Flow, and Valve Function (9 of 21)

Atrioventricular valves open because of higher atrial pressure; blood flows down pressure gradient from atria into ventricles

Nearly 80% of total blood volume of atria drains passively in this manner into ventricles

Initially, atria are in diastole, but as blood continues to drain into ventricles, pressure gradient becomes smaller and filling slows

Pressure Changes, Blood Flow, and Valve Function (10 of 21)

At this point, atrial systole takes place and contracting atria eject variable volume of blood into ventricles—as much as remaining 20% of blood volume and as little as few percent

At end of atrial systole, each ventricle contains about 120 ml of blood (end-diastolic volume (EDV)); ventricular volume at end of ventricular diastole

Pressure Changes, Blood Flow, and Valve Function (11 of 21)

Figure 17.17 Events of the cardiac cycle.

Pressure Changes, Blood Flow, and Valve Function (12 of 21)

Beginning of ventricular systole occurs during shortest phase of cardiac cycle (isovolumetric contraction)

Pressure in ventricles rises rapidly as ventricles begin to contract; high pressure closes AV valves and causes S1 heart sound

Ventricular pressure is not yet high enough to push open semilunar valves, so both sets of valves are closed and ventricular volume does not change (same volume = isovolumetric)

Pressure Changes, Blood Flow, and Valve Function (13 of 21)

Figure 17.17 Events of the cardiac cycle.

Pressure Changes, Blood Flow, and Valve Function (14 of 21)

At beginning of ventricular ejection phase

Pressure in ventricles rises to level higher than in pulmonary trunk and aorta; pushes semilunar valves open; rapid outflow of blood from ventricles occurs

As phase continues, pressure in pulmonary trunk and aorta approaches that in ventricles; at this point, ejection of blood into vessels decreases considerably

Approximately 70 ml of blood pumped from each ventricle; about 50 ml of blood remains in each ventricle (end-systolic volume (ESV))

Pressure Changes, Blood Flow, and Valve Function (15 of 21)

Figure 17.17 Events of the cardiac cycle.

Pressure Changes, Blood Flow, and Valve Function (16 of 21)

Final phase (isovolumetric relaxation) is brief; occurs as ventricular diastole begins and pressure declines in ventricles

Semilunar valves snap shut; S2 heart sound is heard

Pressure in ventricles is still somewhat higher than in atria; AV valves remain closed

Blood is neither being ejected from nor entering into ventricles; volume briefly remains constant

Pressure Changes, Blood Flow, and Valve Function (17 of 21)

Figure 17.17 Events of the cardiac cycle.

Pressure Changes, Blood Flow, and Valve Function (18 of 21)

Figure 17.17 Events of the cardiac cycle.

Pressure Changes, Blood Flow, and Valve Function (19 of 21)

Figure 17.18 Comparison of pressure changes in left and right ventricles during the cardiac cycle.

Pressure Changes, Blood Flow, and Valve Function (20 of 21)

Figure 17.19 Cardiac cycle diagram showing an overview of electrical and mechanical events in the heart during the cardiac cycle.

Concept Boost: Deconstructing the Wigger’s Diagram (1 of 2)

Figure 17.20 Electrical and mechanical events in the left side of the heart during each phase of the cardiac cycle.

Concept Boost: Deconstructing the Wigger’s Diagram (2 of 2)

Figure 17.20 Electrical and mechanical events in the left side of the heart during each phase of the cardiac cycle.

Pressure Changes, Blood Flow, and Valve Function (21 of 21)

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Module 17.5 Cardiac Output and Regulation

Introduction to Cardiac Output and Regulation

Heart undergoes average of 60–80 cardiac cycles (beats) per minute; value known as heart rate (HR)

HR is one determinant of cardiac output (CO); amount of blood pumped into pulmonary and systemic circuits in 1 minute

CO is also determined by amount of blood pumped in one heartbeat (stroke volume (SV))

Determination of Cardiac Output (1 of 2)

Stroke volume (SV) and heart rate (HR) must be known to calculate cardiac output for ventricle:

SV can be calculated by subtracting amount of blood in ventricle at end of contraction (end-systolic volume, or ESV) from amount of blood in ventricle after it has filled during diastole (end-diastolic volume, or EDV)

In average heart, resting stroke volume is equal to about 70 ml:

120 ml (EDV) −50 ml (ESV) = 70 ml (SV)

Determination of Cardiac Output (2 of 2)

To find cardiac output, multiply heart rate by stroke volume:

72 beats/min (HR) × 70 ml/beat (SV) = 5040 ml/min, or ~5 liters/min (CO)

Resting cardiac output averages about 5 liters/min; right ventricle pumps about 5 liters into pulmonary circuit and left ventricle pumps same amount into systemic circuit in 1 minute

Normal adult blood volume is about 5 liters; entire supply of blood passes through heart every minute

Factors that Influence Stroke Volume (1 of 7)

Stroke volume averages about 70 ml per beat; may range from 50 to 120 ml; exact stroke volume may be difficult to measure directly; often measurement called ejection fraction is used in its place

Ejection fraction—percentage of blood (out of total amount) that is ejected with each ventricular systole; equal to stroke volume divided by EDV; normal ejection fraction is about 50–65%, and this value should be equal for each ventricle

Three factors that influence stroke volume: preload, heart contractility, and afterload

Factors that Influence Stroke Volume (2 of 7)

Preload refers to length or degree of stretch of sarcomeres in ventricular cells before they contract; largely determined by EDV (amount of blood that has drained into ventricle by end of filling phase)

Two factors influence EDV:

Length of time ventricle spends in diastole

Amount of blood returning to right ventricle from systemic circuit (venous return)

Factors that Influence Stroke Volume (3 of 7)

Preload (continued)

EDV increases when:

Ventricles spend more time in diastole, because there is more time for them to fill with blood

Left ventricle pumps blood more forcefully into systemic circuit, because additional blood returns to right atrium more rapidly, increasing venous return

Factors that Influence Stroke Volume (4 of 7)

Relationship between preload and stroke volume is explained by mechanism known as Frank-Starling law

According to this law, increased ventricular muscle cells stretch, leads to more forceful contraction

Stretching causes more optimal overlap of actin and myosin filaments in muscle cells; enables stronger contraction and higher stroke volume

Ensures that volume of blood discharged from heart is equal to volume that enters it; particularly important during exercise, when cardiac output must increase to meet body’s needs

Factors that Influence Stroke Volume (5 of 7)

Contractility—heart’s intrinsic pumping ability, or ability to generate tension; difficult to measure directly; can be estimated clinically by examining velocity of blood being ejected from ventricles

Increasing contractility will increase stroke volume and therefore decrease ESV

Decreasing contractility will do opposite: decreasing stroke volume and increasing ESV (assuming that preload and afterload remain constant)

Factors that Influence Stroke Volume (6 of 7)

Contractility (continued):

Agents that affect contractility are known as inotropic agents

Factors that increase heart rate, such as sympathetic nervous stimulation, often also affect contractility and so increase force of contraction

When heart rate is too high, contractility decreases, as does preload; as heart is beating too rapidly to develop significant tension during each contraction decrease in both stroke volume and cardiac output occurs

Stroke volume and heart rate generally increase together

Factors that Influence Stroke Volume (7 of 7)

Afterload refers to force that right and left ventricles must overcome in order to eject blood into their respective arteries

Largely determined by blood pressure in arteries of both pulmonary and systemic circuits

As afterload increases, ventricular pressure must be greater to exceed pressure in arterial pulmonary and systemic vessels and open semilunar valves

Increase in afterload therefore generally causes decrease in stroke volume and rise in ESV of ventricles; conversely, decrease in afterload generally corresponds to higher stroke volume and lower ESV

How Changes in Preload, Contractility, and Afterload Affect Stroke Volume (1 of 3)

Factors that determine stroke volume—preload, contractility, and afterload—illustrated using only the left ventricle for simplicity.

How Changes in Preload, Contractility, and Afterload Affect Stroke Volume (2 of 3)

High preload leads to high EDV; volume of blood stretches cardiac muscle cells; combined with increased contractility, leads to more forceful contraction

Since afterload is low, this forceful contraction isn’t pumping against great deal of resistance

A forceful contraction against low resistance leads to high stroke volume and low ESV

How Changes in Preload, Contractility, and Afterload Affect Stroke Volume (3 of 3)

Notice that low preload leads to low EDV, so cardiac muscle cells are much less stretched; combined with diminished contractility, heart contracts weakly

Since afterload is high, weak contraction is pumping against great deal of resistance

A weak contraction against high resistance leads to low stroke volume, and more blood left in ventricle after contraction (high ESV)

Ventricular Hypertrophy (1 of 2)

Long-standing increases in preload and afterload are associated with enlargement of ventricles (ventricular hypertrophy)

Cardiac muscle cells of ventricles need to generate more tension to continue pumping blood against higher afterload; cells respond same as skeletal muscle fibers when they have to generate more tension—make more myofibrils and more organelles, and as result get bigger

Ventricular Hypertrophy (2 of 2)

Right ventricular hypertrophy most often results from respiratory disease or high blood pressure in pulmonary circuit; left ventricular hypertrophy generally results from high blood pressure in systemic circuit

Ventricular hypertrophy can increase effectiveness of heart’s pumping up to certain point; condition decreases heart lumen and so filling space

Increases risk for many other cardiac conditions, including heart failure

Factors that Influence Heart Rate

Other determinant of cardiac output is heart rate; under normal conditions, rate at which SA node generates action potentials determines heart rate:

Factors that influence rate at which SA node depolarizes are known as chronotropic agents

Anything that increases rate at which this node fires is called positive chronotropic agent; include sympathetic nervous system, certain hormones, and elevated body temperature

One with opposite effect is known as negative chronotropic agent; include parasympathetic nervous system and decreased body temperature

Regulation of Cardiac Output (1 of 11)

Although heart is autorhythmic, it still requires regulation to ensure that cardiac output meets body’s needs at all times

Regulated primarily by nervous and endocrine systems, which influence both heart rate and stroke volume (Figure 17.21)

Two branches of autonomic nervous system (ANS) regulate our automatic functions

Regulation of Cardiac Output (2 of 11)

Role of sympathetic division of ANS includes following:

Innervates heart via set of sympathetic nerves that stem from ganglia located along spinal cord

Neurons release neurotransmitter norepinephrine; increases cardiac output with both positive chronotropic and inotropic effects

Regulation of Cardiac Output (3 of 11)

Norepinephrine’s positive chronotropic effect increases heart rate by raising rate at which SA node fires, up to 180–200 or more times per minute

Also increases entry of calcium ions into cardiac muscle cells

Higher calcium ion concentration increases contractility of cardiac muscle cells

In turn raises stroke volume

Together, these two effects can dramatically increase cardiac output

Regulation of Cardiac Output (4 of 11)

Parasympathetic nervous system exerts essentially opposite effects on heart; innervates heart by left and right vagus nerves (CN X)

Release acetylcholine; primarily affects SA node, decreasing rate of action potential generation

Slows heart rate and can even stop heart temporarily if parasympathetic stimulation is strong enough

Vagus nerves primarily innervate atrial muscle; have less effect on ventricular contractility than on heart rate; therefore have only weak negative inotropic effects

Regulation of Cardiac Output (5 of 11)

Figure 17.21 Innervation and nervous regulation of the heart.

Regulation of Cardiac Output (6 of 11)

Hormonal regulation of cardiac output occurs in various forms

Adrenal medulla is activated by sympathetic nervous system, and in response it secretes hormones epinephrine and norepinephrine into bloodstream

Hormones have same effects as sympathetic nervous system neurotransmitters—positive inotropic and chronotropic agents—but effect is longer-lasting than sympathetic stimulation

Other hormones that also have positive inotropic and chronotropic effects include thyroid hormone and glucagon produced by pancreas

Regulation of Cardiac Output (7 of 11)

Amount of water in blood (blood volume) plays significant role in determining heart’s preload and therefore its strength of contraction

Hormones such as aldosterone and antidiuretic hormone increase blood volume and preload, and so raise cardiac output

Atrial natriuretic peptide, decreases blood volume and preload, and therefore reduces cardiac output

Regulation of Cardiac Output (8 of 11)

Other factors that influence cardiac output (Figure 17.22):

Concentration of certain electrolytes in extracellular fluid plays large role in determining length and magnitude of action potential and cardiac output

Body temperature influences CO; SA node fires more rapidly at higher body temperatures and more slowly at lower body temperatures

Regulation of Cardiac Output (9 of 11)

Other factors that influence cardiac output (continued):

Age and physical fitness influence heart rate and cardiac output; younger children and elderly often have higher resting heart rate; trained athletes often have much lower resting heart rate

Exercise increases stroke volume, so for body to maintain constant cardiac output, heart rate must decrease

Regulation of Cardiac Output (10 of 11)

Figure 17.22 Regulation of cardiac output.

Heart Failure (1 of 4)

Heart failure—as any condition that reduces heart’s ability to function effectively as pump:

Causes of heart failure include reduced contractility due to myocardial ischemia and/or myocardial infarction, valvular heart diseases, any disease of heart muscle itself (known as cardiomyopathy), and electrolyte imbalances

Heart failure generally results in decreased stroke volume, which in turn reduces cardiac output

Heart Failure (2 of 4)

Signs and symptoms of heart failure generally depend on type of heart failure and side of heart that is affected

In left ventricular failure, blood often backs up within pulmonary circuit; known as pulmonary congestion

Backup of blood flow increases pressure in these vessels, driving fluid out of pulmonary capillaries and into lungs; called pulmonary edema

Heart Failure (3 of 4)

Both right and left ventricular failure may produce similar finding in systemic circuit: peripheral edema, in which blood backs up in systemic capillaries (systemic congestion)

This backup forces fluid out of capillaries and into tissues; often causes visible swelling, especially in legs and feet, where fluid collects as result of gravity

Peripheral edema is exacerbated by fact that kidneys retain excess fluid during heart failure (in order to increase preload and compensate for lower cardiac output)

Heart Failure (4 of 4)

Treatment—generally aimed at increasing cardiac output

Lifestyle modifications may include weight loss and mild exercise plus dietary sodium and fluid restrictions

Drug therapy increases cardiac output in one of at least three ways: decreasing abnormally high preload by promoting fluid loss from kidneys, increasing heart’s contractility so that it pumps more effectively, and decreasing afterload so that ventricles have to pump against lower pressure

In some cases, heart transplant and/or surgically implanted pacemaker that electrically stimulates and paces heart may be necessary

Regulation of Cardiac Output (11 of 11)

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