169 Ch 20_lecture_presentation

© 2012 Pearson Education, Inc.

PowerPoint® Lecture Presentations prepared byJason LaPresLone Star College—North Harris

20The Heart


An Introduction to the Cardiovascular System

• Learning Outcomes

• 20-1 Describe the anatomy of the heart, including vascular supply and pericardium structure,

and trace the flow of blood through the heart, identifying the major blood vessels,

chambers, and heart valves.

• 20-2 Explain the events of an action potential in cardiac muscle, indicate the importance of calcium ions to the contractile

process, describe the conducting system of the heart, and identify the electrical events associated with a normal electrocardiogram.



• Learning Outcomes

• 20-3 Explain the events of the cardiac cycle, including atrial and ventricular systole and

diastole, and relate the heart sounds to specific events in the cycle.

• 20-4 Define cardiac output, describe the factors that influence heart rate and stroke volume,

and explain how adjustments in stroke volume and cardiac output are coordinated at different levels of physical activity.



• The Pulmonary Circuit

• Carries blood to and from gas exchange surfaces of

lungs

• The Systemic Circuit

• Carries blood to and from the body

• Blood alternates between pulmonary circuit and

systemic circuit



• Three Types of Blood Vessels

1. Arteries

• Carry blood away from heart

2. Veins

• Carry blood to heart

3. Capillaries

• Networks between arteries and veins



• Capillaries

• Also called exchange vessels

• Exchange materials between blood and tissues

• Materials include dissolved gases, nutrients, waste

products


Figure 20-1 An Overview of the Cardiovascular System

PULMONARY CIRCUIT SYSTEMIC CIRCUIT

Pulmonary arteries

Pulmonary veins Systemic veins

Systemic arteries

Capillariesin lungs

Rightatrium

Rightventricle

Capillariesin trunk

and lowerlimbs

Capillariesin head,neck, upperlimbs

Leftatrium

Leftventricle



• Four Chambers of the Heart

1. Right atrium

• Collects blood from systemic circuit

2. Right ventricle

• Pumps blood to pulmonary circuit

3. Left atrium

• Collects blood from pulmonary circuit

4. Left ventricle

• Pumps blood to systemic circuit


20-1 Anatomy of the Heart

• The Heart

• Great veins and arteries at the base

• Pointed tip is apex

• Surrounded by pericardial sac

• Sits between two pleural cavities in the mediastinum


Figure 20-2a The Location of the Heart in the Thoracic Cavity

Trachea

First rib (cut)

Base of heart

Right lung

Diaphragm

Thyroid gland

Left lung

Apex of heart

Parietal pericardium(cut)

An anterior view of the chest, showing the position of the heart andmajor blood vessels relative to the ribs, lungs, and diaphragm.



• The Pericardium

• Double lining of the pericardial cavity

• Visceral pericardium

• Inner layer of pericardium

• Parietal pericardium

• Outer layer

• Forms inner layer of pericardial sac



• The Pericardium

• Pericardial cavity

• Is between parietal and visceral layers

• Contains pericardial fluid

• Pericardial sac

• Fibrous tissue

• Surrounds and stabilizes heart


Figure 20-2b The Location of the Heart in the Thoracic Cavity

Right ventricle

Aorticarch

Posterior mediastinum

Aorta (arch segment removed)

Left pulmonary artery

Left pulmonary vein

Pulmonary trunk

Left ventricle

Epicardium

Pericardial sac

Anterior mediastinum

Pericardial cavity

Right atrium

Left atrium

Right pulmonary artery

Right pulmonary vein

Superior vena cava

Esophagus

Right pleural cavity

Bronchus of lung

Rightlung Left

lung

Left pleural cavity

A superior view of the organs in the mediastinum; portions of the lungs havebeen removed to reveal blood vessels and airways. The heart is situated in the anterior part of the mediastinum, immediately posterior to the sternum.


Figure 20-2c The Location of the Heart in the Thoracic Cavity

Wrist (correspondsto base of heart)

Inner wall (correspondsto epicardium)

Air space (correspondsto pericardial cavity)

Outer wall (correspondsto parietal pericardium)

Balloon

Cut edge ofparietal pericardium

Fibrous tissue ofpericardial sac

Parietal pericardium

Areolar tissueMesothelium

Cut edge of epicardium

Apex of heart

Base of heart

Fibrousattachment

to diaphragm

The relationship between the heart and the pericardial cavity; compare with the fist-and-balloon example.



• Superficial Anatomy of the Heart

• Atria

• Thin-walled

• Expandable outer auricle (atrial appendage)



• Superficial Anatomy of the Heart

• Sulci

• Coronary sulcus divides atria and ventricles

• Anterior interventricular sulcus and posterior

interventricular sulcus

• Separate left and right ventricles

• Contain blood vessels of cardiac muscle


Figure 20-3a The Superficial Anatomy of the HeartLeft commoncarotid artery

Brachiocephalictrunk

Ascendingaorta

Superiorvena cava

Auricleof rightatrium

Fat andvessels incoronary

sulcus

Left subclavian artery

Arch of aorta

Ligamentumarteriosum

Descendingaorta

Left pulmonaryartery

Pulmonarytrunk

Auricle ofleft atrium

Fat and vesselsin anteriorinterventricularsulcus

LEFTVENTRICLE

RIGHTVENTRICLE

RIGHTATRIUM

Major anatomical features on the anterior surface.


Figure 20-3a The Superficial Anatomy of the Heart

Ascendingaorta

Parietalpericardium

Superiorvena cava

Auricle ofright atrium

RIGHT ATRIUM

Right coronaryartery

Coronary sulcus

RIGHT VENTRICLE

Marginal branchof right coronary artery


Pulmonarytrunk

Fibrouspericardium

Parietal pericardiumfused to diaphragm

Anteriorinterventricular

sulcus

LEFTVENTRICLE

Major anatomical features on the anterior surface.


Figure 20-3b The Superficial Anatomy of the Heart Arch of aorta

Right pulmonaryartery

Superiorvena cava

Rightpulmonaryveins (superiorand inferior)

Inferiorvena cava

Fat and vessels in posteriorinterventricular sulcus

RIGHTVENTRICLE

LEFTVENTRICLE

RIGHTATRIUM

LEFTATRIUM

Left pulmonary artery

Left pulmonary veins

Fat and vessels incoronary sulcus

Coronarysinus

Major landmarks on the posterior surface. Coronaryarteries (which supply the heart itself) are shown inred; coronary veins are shown in blue.


Figure 20-3c The Superficial Anatomy of the Heart

Base of heart

Apex ofheart

Ribs

Heart position relative to the rib cage.

1

2

3

4

5

6

7

89

10

1

2

3

4

5

6

7

8910



• The Heart Wall

1. Epicardium

2. Myocardium

3. Endocardium



• Epicardium (Outer Layer)

• Visceral pericardium

• Covers the heart



• Myocardium (Middle Layer)

• Muscular wall of the heart

• Concentric layers of cardiac muscle tissue

• Atrial myocardium wraps around great vessels

• Two divisions of ventricular myocardium

• Endocardium (Inner Layer)

• Simple squamous epithelium


Figure 20-4a The Heart Wall

Mesothelium

Endocardium

Areolar tissue

Endothelium

Mesothelium

Dense fibrous layer

Parietal pericardium

Pericardial cavity

Areolar tissue

Areolar tissue

Connective tissues

Cardiac muscle cells

Myocardium(cardiac muscle tissue)

Epicardium(visceral pericardium)


Figure 20-4b The Heart Wall

Atrialmusculature

Cardiac muscle tissueforms concentric layersthat wrap around theatria or spiral within thewalls of the ventricles.

Ventricularmusculature



• Cardiac Muscle Tissue

• Intercalated discs

• Interconnect cardiac muscle cells

• Secured by desmosomes

• Linked by gap junctions

• Convey force of contraction

• Propagate action potentials


Figure 20-5a Cardiac Muscle Cells

Cardiac muscle cells

Nucleus

Cardiac musclecell (sectioned)

Bundles ofmyofibrils

Cardiac muscle cell

Mitochondria

Intercalateddisc (sectioned)

Intercalated discs


Figure 20-5b Cardiac Muscle Cells

Intercalated disc

Gap junction

Opposing plasmamembranes

Desmosomes

Structure of an intercalated disc


Figure 20-5c Cardiac Muscle Cells

Intercalated discs

Cardiac muscle tissue

Cardiac muscle tissue LM 575



• Characteristics of Cardiac Muscle Cells

1. Small size

2. Single, central nucleus

3. Branching interconnections between cells

4. Intercalated discs


Table 20-1 Structural and Functional Differences between Cardiac Muscle Cells and Skeletal Muscle Fibers



• Internal Anatomy and Organization

• Interatrial septum separates atria

• Interventricular septum separates ventricles



• Internal Anatomy and Organization

• Atrioventricular (AV) valves

• Connect right atrium to right ventricle and left

atrium to left ventricle

• Are folds of fibrous tissue that extend into

openings between atria and ventricles

• Permit blood flow in one direction

• From atria to ventricles



• The Right Atrium

• Superior vena cava

• Receives blood from head, neck, upper limbs, and chest

• Inferior vena cava

• Receives blood from trunk, viscera, and lower limbs

• Coronary sinus

• Cardiac veins return blood to coronary sinus

• Coronary sinus opens into right atrium




• Foramen ovale

• Before birth, is an opening through interatrial septum

• Connects the two atria

• Seals off at birth, forming fossa ovalis




• Pectinate muscles

• Contain prominent muscular ridges

• On anterior atrial wall and inner surfaces of right

auricle


Figure 20-6a The Sectional Anatomy of the Heart

Descending aorta

Left common carotid artery

Left subclavian artery

Ligamentum arteriosum

Pulmonary trunk

Pulmonary valve

Left pulmonaryarteries

Left pulmonaryveins

Interatrial septumAortic valve

Cusp of left AV(mitral) valve

LEFT VENTRICLE

Interventricularseptum

Trabeculaecarneae

Moderator band

Aortic arch

LEFTATRIUM

Brachiocephalictrunk

Superiorvena cava

Rightpulmonary

arteries

Ascending aorta

Fossa ovalis

Opening ofcoronary sinus

RIGHT ATRIUM

Pectinate muscles

Conus arteriosus

Cusp of right AV(tricuspid) valve

Chordae tendineae

Papillary muscles

RIGHT VENTRICLE

Inferior vena cava


Figure 20-6c The Sectional Anatomy of the Heart

A frontal section, anterior view.

Inferior vena cava

RIGHT VENTRICLE

Papillary muscles

Cusps of right AV(tricuspid) valve

Pectinate muscles

RIGHT ATRIUM

Fossa ovalis

Ascending aorta

Cusp of left AV(bicuspid) valve


LEFT VENTRICLE

Chordae tendineae

Left coronary arterybranches (red)and great cardiacvein (blue)

Cusp of aortic valve

Coronary sinus

Trabeculae carneae



• The Right Ventricle

• Free edges attach to chordae tendineae from

papillary muscles of ventricle

• Prevent valve from opening backward

• Right atrioventricular (AV) valve

• Also called tricuspid valve

• Opening from right atrium to right ventricle

• Has three cusps

• Prevents backflow



• The Right Ventricle

• Trabeculae carneae

• Muscular ridges on internal surface of right (and left)

ventricle

• Includes moderator band

• Ridge contains part of conducting system

• Coordinates contractions of cardiac muscle cells


Figure 20-6b The Sectional Anatomy of the Heart

The papillary muscles and chordaetendinae supporting the right AV(tricuspid) valve. The photographwas taken from inside the rightventricle, looking toward a lightshining from the right atrium.

Chordae tendineae

Papillary muscles



• The Pulmonary Circuit

• Conus arteriosus (superior end of right ventricle)

leads to pulmonary trunk

• Pulmonary trunk divides into left and right

pulmonary arteries

• Blood flows from right ventricle to pulmonary trunk

through pulmonary valve

• Pulmonary valve has three semilunar cusps



• The Left Atrium

• Blood gathers into left and right pulmonary veins

• Pulmonary veins deliver to left atrium

• Blood from left atrium passes to left ventricle through

left atrioventricular (AV) valve

• A two-cusped bicuspid valve or mitral valve



• The Left Ventricle

• Holds same volume as right ventricle

• Is larger; muscle is thicker and more powerful

• Similar internally to right ventricle but does not have

moderator band



• The Left Ventricle

• Systemic circulation

• Blood leaves left ventricle through aortic valve

into ascending aorta

• Ascending aorta turns (aortic arch) and becomes

descending aorta


Figure 20-6c The Sectional Anatomy of the Heart

A frontal section, anterior view.

Inferior vena cava

RIGHT VENTRICLE

Papillary muscles

Cusps of right AV(tricuspid) valve

Pectinate muscles

RIGHT ATRIUM

Fossa ovalis

Ascending aorta

Cusp of left AV(bicuspid) valve


LEFT VENTRICLE

Chordae tendineae

Left coronary arterybranches (red)and great cardiacvein (blue)

Cusp of aortic valve

Coronary sinus

Trabeculae carneae



• Structural Differences between the Left and

Right Ventricles

• Right ventricle wall is thinner, develops less pressure

than left ventricle

• Right ventricle is pouch-shaped, left ventricle is round

ANIMATION The Heart: Heart Anatomy


Figure 20-7a Structural Differences between the Left and Right Ventricles

Left ventricle

Rightventricle

Posteriorinterventricular sulcus

Fat in anteriorinterventricular sulcus

A diagrammatic sectional view through the heart,showing the relative thicknesses of the two ventricles.Notice the pouchlike shape of the right ventricle andthe greater thickness of the left ventricle.


Figure 20-7b Structural Differences between the Left and Right Ventricles

Dilated Contracted

Diagrammatic views of the ventricles justbefore a contraction (dilated) and just after acontraction (contracted).

Left ventricle

Rightventricle



• The Heart Valves

• Two pairs of one-way valves prevent backflow

during contraction

• Atrioventricular (AV) valves

• Between atria and ventricles

• Blood pressure closes valve cusps during ventricular

contraction

• Papillary muscles tense chordae tendineae to prevent

valves from swinging into atria



• The Heart Valves

• Semilunar valves

• Pulmonary and aortic tricuspid valves

• Prevent backflow from pulmonary trunk and aorta

into ventricles

• Have no muscular support

• Three cusps support like tripod



• Aortic Sinuses

• At base of ascending aorta

• Sacs that prevent valve cusps from sticking to

aorta

• Origin of right and left coronary arteries

ANIMATION The Heart: Valves


Figure 20-8a Valves of the Heart

Rel

axe

d v

entr

icle

s

Right AV(tricuspid)

valve (open)

Transverse Sections, Superior View,Atria and Vessels Removed

POSTERIOR

RIGHTVENTRICLE

Cardiacskeleton

Left AV (bicuspid)valve (open)

LEFTVENTRICLE

Aortic valve(closed)

Pulmonaryvalve (closed)ANTERIOR

Aortic valve closed

When the ventricles are relaxed, the AV valves are open and the semilunar valves are closed. The chordae tendineae are loose, and the papillary muscles are relaxed.


Figure 20-8a Valves of the Heart

Aortic valve(closed)

LEFTATRIUM

Left AV (bicuspid)valve (open)

Chordaetendineae (loose)

Papillary muscles(relaxed)

LEFT VENTRICLE(relaxed and fillingwith blood)

Pulmonaryveins

Frontal Sections through Left Atrium and Ventricle

Rel

axe

d v

entr

icle

s


Figure 20-8b Valves of the Heart

Co

ntr

acti

ng

ven

tric

les

Aortic valve open

RIGHTVENTRICLE

Right AV(tricuspid) valve

(closed)

Cardiacskeleton

Left AV(bicuspid) valve

(closed)LEFTVENTRICLE

Aortic valve(open)

Pulmonaryvalve (open)

When the ventricles are contracting, the AV valves are closed and the semilunar valves are open. In the frontal section notice the attachment of the left AV valve to the chordae tendineae and papillary muscles.


Figure 20-8b Valves of the Heart

Co

ntr

acti

ng

ven

tric

les

Aorta

Aortic sinus

LEFTATRIUM

Aortic valve(open)

Left AV (bicuspid)valve (closed)

Chordae tendineae(tense)

Papillary muscles(contracted)

Left ventricle(contracted)



• Connective Tissues and the Cardiac Skeleton

• Connective Tissue Fibers

1. Physically support cardiac muscle fibers

2. Distribute forces of contraction

3. Add strength and prevent overexpansion of heart

4. Provide elasticity that helps return heart to original

size and shape after contraction



• The Cardiac Skeleton

• Four bands around heart valves and bases of

pulmonary trunk and aorta

• Stabilize valves

• Electrically insulate ventricular cells from atrial cells



• The Blood Supply to the Heart

• = Coronary circulation

• Supplies blood to muscle tissue of heart

• Coronary arteries and cardiac veins



• The Coronary Arteries

• Left and right

• Originate at aortic sinuses

• High blood pressure, elastic rebound forces blood

through coronary arteries between contractions



• Right Coronary Artery

• Supplies blood to:

• Right atrium

• Portions of both ventricles

• Cells of sinoatrial (SA) and atrioventricular nodes

• Marginal arteries (surface of right ventricle)

• Posterior interventricular artery



• Left Coronary Artery

• Supplies blood to:

• Left ventricle

• Left atrium

• Interventricular septum



• Two Main Branches of Left Coronary Artery

1. Circumflex artery

2. Anterior interventricular artery

• Arterial Anastomoses

• Interconnect anterior and posterior interventricular

arteries

• Stabilize blood supply to cardiac muscle



• The Cardiac Veins

• Great cardiac vein

• Drains blood from area of anterior interventricular artery into

coronary sinus

• Anterior cardiac veins

• Empty into right atrium

• Posterior cardiac vein, middle cardiac vein, and

small cardiac vein

• Empty into great cardiac vein or coronary sinus


Figure 20-9a Coronary Circulation

Aorticarch

Ascendingaorta


Atrial arteries

Anteriorcardiac veins

Smallcardiac vein

Marginalartery

Left coronaryartery

Pulmonarytrunk

Circumflexartery

Anteriorinterventricularartery

Greatcardiacvein

Coronary vessels supplyingand draining the anteriorsurface of the heart.


Figure 20-9b Coronary Circulation

Coronary sinusCircumflex artery

Great cardiac vein

Marginal artery

Posteriorinterventricular

artery

Posteriorcardiac

vein

Leftventricle

Middle cardiac vein Marginal artery


Small cardiacvein

Coronary vessels supplying and drainingthe posterior surface of the heart.


Figure 20-9c Coronary Circulation

Posterior interventricular artery

Posteriorcardiac vein

Marginal artery

Great cardiac vein

Circumflex artery


Left pulmonaryveins

Left pulmonaryartery

Right pulmonaryartery

Superiorvena cava

Right pulmonaryveins

Left atrium

Right atrium

Inferior vena cava

Coronary sinus

Middle cardiac vein

Right ventricle

A posterior view of the heart; the vessels have beeninjected with colored latex (liquid rubber).


Figure 20-10 Heart Disease and Heart Attacks

Narrowing of Artery

Lipid depositof plaque

Cross-section

Tunicaexterna

Tunicamedia

Cross-section

Normal Artery



• Heart Disease - Coronary Artery Disease

• Coronary artery disease (CAD)

• Areas of partial or complete blockage of coronary circulation

• Cardiac muscle cells need a constant supply of oxygen and nutrients

• Reduction in blood flow to heart muscle produces a corresponding reduction in cardiac performance

• Reduced circulatory supply, coronary ischemia, results from partial or complete blockage of coronary arteries




• Usual cause is formation of a fatty deposit, or atherosclerotic plaque, in the wall of a coronary vessel

• The plaque, or an associated thrombus (clot), then narrows the passageway and reduces blood flow

• Spasms in smooth muscles of vessel wall can further decrease or stop blood flow

• One of the first symptoms of CAD is commonly angina pectoris




• Angina Pectoris

• In its most common form, a temporary ischemia develops when the workload of the heart increases

• Although the individual may feel comfortable at rest, exertion or emotional stress can produce a sensation of pressure, chest constriction, and pain that may radiate from the sternal area to the arms, back, and neck




• Myocardial infarction (MI), or heart attack

• Part of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxygen

• The death of affected tissue creates a nonfunctional area known as an infarct

• Heart attacks most commonly result from severe coronary artery disease (CAD)



• Heart Disease - Coronary Artery Disease• Myocardial infarction (MI), or heart attack

• Consequences depend on the site and nature of the circulatory blockage

• If it occurs near the start of one of the coronary arteries:

• The damage will be widespread and the heart may stop beating

• If the blockage involves one of the smaller arterial branches:

• The individual may survive the immediate crisis but may have many complications such as reduced contractility and cardiac arrhythmias




• Myocardial infarction (MI), or heart attack

• A crisis often develops as a result of thrombus formation at a plaque (the most common cause of an MI), a condition called coronary thrombosis

• A vessel already narrowed by plaque formation may also become blocked by a sudden spasm in the smooth muscles of the vascular wall

• Individuals having an MI experience intense pain, similar to that felt in angina, but persisting even at rest



• Heart Disease - Coronary Artery Disease• Myocardial infarction (MI), or heart attack

• Pain does not always accompany a heart attack, therefore, the condition may go undiagnosed and may not be treated before a fatal MI occurs

• A myocardial infarction can usually be diagnosed with an ECG and blood studies

• Damaged myocardial cells release enzymes into the circulation, and these elevated enzymes can be measured in diagnostic blood tests

• The enzymes include:

• Cardiac troponin T,

• Cardiac troponin I,

• A special form of creatinine phosphokinase, CK-MB




• Treatment of CAD and Myocardial Infarction

• About 25% of MI patients die before obtaining medical

assistance

• 65% of MI deaths among those under age 50 occur

within an hour after the initial infarction





• Risk Factor Modification

• Stop smoking

• High blood pressure treatment

• Dietary modification to lower cholesterol and

promote weight loss

• Stress reduction

• Increased physical activity (where appropriate)





• Drug Treatment

• Drugs that reduce coagulation and therefore the risk of thrombosis, such as aspirin and coumadin

• Drugs that block sympathetic stimulation (propranolol or metoprolol)

• Drugs that cause vasodilation, such as nitroglycerin

• Drugs that block calcium movement into the cardiac and vascular smooth muscle cells (calcium channel blockers)

• In a myocardial infarction, drugs to relieve pain, fibrinolytic agents to help dissolve clots, and oxygen





• Noninvasive Surgery

• Atherectomy

• Blockage by a single, soft plaque may be reduced with the aid of a long, slender catheter inserted into a coronary artery to the plaque





• Noninvasive Surgery

• Balloon angioplasty

• The tip of the catheter contains an inflatable balloon

• Once in position, the balloon is inflated, pressing the plaque against the vessel walls

• Because plaques commonly redevelop after angioplasty, a fine tubular wire mesh called a stent may be inserted into the vessel, holding it open





• Coronary Artery Bypass Surgery (CABG)

• In a coronary artery bypass graft, a small section is removed from either a small artery or a peripheral vein and is used to create a detour around the obstructed portion of a coronary artery

• As many as four coronary arteries can be rerouted this way during a single operation

• The procedures are named according to the number of vessels repaired, so we speak of single, double, triple, or quadruple coronary bypasses



Normal Heart

Advanced Coronary Artery DiseaseA color-enhanced DSA scan showing advancedcoronary artery disease. Blood flow to the ven-tricular myocardium is severely restricted.

A color-enhanced digital subtractionangiography (DSA) scan of a normalheart.



OccludedCoronaryArtery

DamagedHeartMuscle


20-2 The Conducting System

• Heartbeat

• A single contraction of the heart

• The entire heart contracts in series

• First the atria

• Then the ventricles



• Cardiac Physiology

• Two Types of Cardiac Muscle Cells

1. Conducting system

• Controls and coordinates heartbeat

2. Contractile cells

• Produce contractions that propel blood



• The Cardiac Cycle

• Begins with action potential at SA node

• Transmitted through conducting system

• Produces action potentials in cardiac muscle cells

(contractile cells)

• Electrocardiogram (ECG or EKG)

• Electrical events in the cardiac cycle can be recorded

on an electrocardiogram



• The Conducting System

• A system of specialized cardiac muscle cells

• Initiates and distributes electrical impulses that

stimulate contraction

• Automaticity

• Cardiac muscle tissue contracts automatically



• Structures of the Conducting System

• Sinoatrial (SA) node - wall of right atrium

• Atrioventricular (AV) node - junction between atria

and ventricles

• Conducting cells - throughout myocardium



• Conducting Cells

• Interconnect SA and AV nodes

• Distribute stimulus through myocardium

• In the atrium

• Internodal pathways

• In the ventricles

• AV bundle and the bundle branches



• Prepotential

• Also called pacemaker potential

• Resting potential of conducting cells

• Gradually depolarizes toward threshold

• SA node depolarizes first, establishing heart rate

ANIMATION The Heart: Conduction System


Figure 20-11a The Conducting System of the Heart

AV bundle

Components of the conductingsystem

Purkinjefibers

Bundlebranches

Atrioventricular(AV) node

Internodalpathways

Sinoatrial(SA) node


Figure 20-11b The Conducting System of the Heart

Changes in the membrane potential of a pacemakercell in the SA node that is establishing a heart rate of72 beats per minute. Note the presence of a prepotential, a gradual spontaneous depolarization.

Time (sec)

Prepotential(spontaneous depolarization)

Threshold



• Heart Rate

• SA node generates 80–100 action potentials per

minute

• Parasympathetic stimulation slows heart rate

• AV node generates 40–60 action potentials per

minute



• The Sinoatrial (SA) Node

• In posterior wall of right atrium

• Contains pacemaker cells

• Connected to AV node by internodal pathways

• Begins atrial activation (Step 1)


Figure 20-12 Impulse Conduction through the Heart (Step 1)

Time = 0

SAnode

SA node activityand atrialactivation begin.



• The Atrioventricular (AV) Node

• In floor of right atrium

• Receives impulse from SA node (Step 2)

• Delays impulse (Step 3)

• Atrial contraction begins



Elapsed time = 50 msec

AVnode

Stimulus spreads acrossthe atrial surfaces andreaches the AV node.



Elapsed time = 150 msec

Bundlebranches

AVbundle

There is a 100-msec delayat the AV node. Atrialcontraction begins.



• The AV Bundle

• In the septum

• Carries impulse to left and right bundle branches

• Which conduct to Purkinje fibers (Step 4)

• And to the moderator band

• Which conducts to papillary muscles



Elapsed time = 175 msecModerator

band

The impulse travels alongthe interventricular septumwithin the AV bundle andthe bundle branches to thePurkinje fibers and, via themoderator band, to thepapillary muscles of theright ventricle.



• Purkinje Fibers

• Distribute impulse through ventricles (Step 5)

• Atrial contraction is completed

• Ventricular contraction begins



Elapsed time = 225 msecPurkinje

fibers

The impulse is distributedby Purkinje fibers andrelayed throughout theventricular myocardium.Atrial contraction iscompleted, and ventricularcontraction begins.



• Abnormal Pacemaker Function

• Bradycardia - abnormally slow heart rate

• Tachycardia - abnormally fast heart rate

• Ectopic pacemaker

• Abnormal cells

• Generate high rate of action potentials

• Bypass conducting system

• Disrupt ventricular contractions



• The Electrocardiogram (ECG or EKG)

• A recording of electrical events in the heart

• Obtained by electrodes at specific body locations

• Abnormal patterns diagnose damage



• Features of an ECG

• P wave

• Atria depolarize

• QRS complex

• Ventricles depolarize

• T wave

• Ventricles repolarize



• Time Intervals between ECG Waves

• P–R interval

• From start of atrial depolarization

• To start of QRS complex

• Q–T interval

• From ventricular depolarization

• To ventricular repolarization


Figure 20-13a An Electrocardiogram

Electrode placement forrecording a standard ECG.


Figure 20-13b An Electrocardiogram

800 msec

SQ

QRS interval(ventricles depolarize)

Millivolts

R

P–R segmentT wave

(ventricles repolarize)

R

P wave(atria

depolarize)S–T

segment

S–Tinterval

Q–Tinterval

P–Rinterval


Figure 20-14 Cardiac Arrhythmias

Premature Atrial Contractions (PACs)

Paroxysmal Atrial Tachycardia (PAT)

Atrial Fibrillation (AF)

PPP

PPPPPP


Figure 20-14 Cardiac Arrhythmias

Premature Ventricular Contractions (PVCs)

Ventricular Tachycardia (VT)

Ventricular Fibrillation (VF)

PPP

P

TTT



• Contractile Cells

• Purkinje fibers distribute the stimulus to the contractile

cells, which make up most of the muscle cells in the

heart

• Resting Potential

• Of a ventricular cell about –90 mV

• Of an atrial cell about –80 mV


Figure 20-15a The Action Potential in Skeletal and Cardiac Muscle

Rapid Depolarization The Plateau RepolarizationCause: Na+ entryDuration: 3–5 msecEnds with: Closure of voltage-gated fast sodium channels

Cause: Ca2+ entryDuration: ~175 msecEnds with: Closure of slow calcium channels

Cause: K+ lossDuration: 75 msecEnds with: Closure of slow potassium channels

Relativerefractoryperiod

Stimulus

Events in an action potential in a ventricular musclecell.

KEY

Absolute refractoryperiod

Relative refractoryperiod


Time (msec)

mV


Figure 20-15b The Action Potential in Skeletal and Cardiac Muscle

mV

SKELETALMUSCLE

CARDIACMUSCLE

Action potentialmV

Contraction

Tension

Time (msec)

Time (msec)

ContractionTension

Actionpotential

KEY


Relative refractoryperiod

Action potentials and twitchcontractions in a skeletal muscle(above) and cardiac muscle (below).



• Refractory Period

• Absolute refractory period

• Long

• Cardiac muscle cells cannot respond

• Relative refractory period

• Short

• Response depends on degree of stimulus



• Timing of Refractory Periods

• Length of cardiac action potential in ventricular cell

• 250–300 msec

• 30 times longer than skeletal muscle fiber

• Long refractory period prevents summation and

tetany



• The Role of Calcium Ions in Cardiac

Contractions

• Contraction of a cardiac muscle cell

• Is produced by an increase in calcium ion

concentration around myofibrils




Contractions

1. 20% of calcium ions required for a contraction

• Calcium ions enter plasma membrane during plateau

phase

2. Arrival of extracellular Ca2+

• Triggers release of calcium ion reserves from

sarcoplasmic reticulum (SR)




Contractions

• As slow calcium channels close

• Intracellular Ca2+ is absorbed by the SR

• Or pumped out of cell

• Cardiac muscle tissue

• Very sensitive to extracellular Ca2+ concentrations



• The Energy for Cardiac Contractions

• Aerobic energy of heart

• From mitochondrial breakdown of fatty acids and

glucose

• Oxygen from circulating hemoglobin

• Cardiac muscles store oxygen in myoglobin


20-3 The Cardiac Cycle

• The Cardiac Cycle

• Is the period between the start of one heartbeat

and the beginning of the next

• Includes both contraction and relaxation



• Two Phases of the Cardiac Cycle

• Within any one chamber

1. Systole (contraction)

2. Diastole (relaxation)


Figure 20-16 Phases of the Cardiac Cycle

Cardiaccycle

370msec

100 msec

0msec800

msec

Start


Figure 20-16a Phases of the Cardiac Cycle

Cardiaccycle

100 msec

0msec800

msec

Atrial systole begins:Atrial contraction forces a small amount ofadditional blood into relaxed ventricles.

Start


Figure 20-16b Phases of the Cardiac Cycle

Cardiaccycle

100 msec

Atrial systole ends,atrial diastolebegins


Figure 20-16c Phases of the Cardiac Cycle

Cardiaccycle

Ventricular systole—first phase: Ventricularcontraction pushes AVvalves closed but doesnot create enoughpressure to opensemilunar valves.


Figure 20-16d Phases of the Cardiac Cycle

Cardiaccycle

370msec

Ventricular systole—second phase: Asventricular pressure risesand exceeds pressurein the arteries, thesemilunar valvesopen and bloodis ejected.


Figure 20-16e Phases of the Cardiac Cycle

Cardiaccycle

370msec

Ventricular diastole—early:As ventricles relax, pressure inventricles drops; blood flows backagainst cusps of semilunar valvesand forces them closed. Bloodflows into the relaxed atria.


Figure 20-16f Phases of the Cardiac Cycle

Cardiaccycle

Ventriculardiastole—late:All chambers arerelaxed.Ventricles fillpassively.

800msec



• Blood Pressure

• In any chamber

• Rises during systole

• Falls during diastole

• Blood flows from high to low pressure

• Controlled by timing of contractions

• Directed by one-way valves



• Cardiac Cycle and Heart Rate

• At 75 beats per minute (bpm)

• Cardiac cycle lasts about 800 msec

• When heart rate increases

• All phases of cardiac cycle shorten, particularly diastole



• Phases of the Cardiac Cycle

• Atrial systole

• Atrial diastole

• Ventricular systole

• Ventricular diastole



• Atrial Systole

1. Atrial systole

• Atrial contraction begins

• Right and left AV valves are open

2. Atria eject blood into ventricles

• Filling ventricles

3. Atrial systole ends

• AV valves close

• Ventricles contain maximum blood volume

• Known as end-diastolic volume (EDV)



• Ventricular Systole

4. Ventricles contract and build pressure

• AV valves close cause isovolumetric contraction

5. Ventricular ejection

• Ventricular pressure exceeds vessel pressure opening the

semilunar valves and allowing blood to leave the ventricle

• Amount of blood ejected is called the stroke volume (SV)



• Ventricular Systole

6. Ventricular pressure falls

• Semilunar valves close

• Ventricles contain end-systolic volume (ESV), about 40%

of end-diastolic volume


Figure 20-17 Pressure and Volume Relationships in the Cardiac CycleATRIAL

SYSTOLEATRIAL

DIASTOLE

VENTRICULARDIASTOLE

VENTRICULARSYSTOLE

Strokevolume

End-diastolicvolume

Le

ftv

en

tric

ula

rv

olu

me

(m

L)

Pre

ss

ure

(mm

Hg

)

Aortic valveopens

Aorta

Leftventricle

Left atrium Left AVvalve closes AV valves open; passive ventricular

filling occurs.

Isovolumetric relaxation occurs.

Semilunar valves close.

Ventricular ejection occurs.

Isovolumetric ventricular contraction.

Atrial systole ends; AV valves close.

Atria eject blood into ventricles.

Atrial contraction begins.

ATRIAL DIASTOLE

Time (msec)



• Ventricular Diastole

7. Ventricular diastole

• Ventricular pressure is higher than atrial pressure

• All heart valves are closed

• Ventricles relax (isovolumetric relaxation)

8. Atrial pressure is higher than ventricular pressure

• AV valves open

• Passive atrial filling

• Passive ventricular filling


Figure 20-17 Pressure and Volume Relationships in the Cardiac CycleATRIAL

SYSTOLEATRIAL DIASTOLE

VENTRICULARSYSTOLE

VENTRICULAR DIASTOLE

AV valves open; passive ventricularfilling occurs.

Isovolumetric relaxation occurs.

Semilunar valves close.

Ventricular ejection occurs.

Isovolumetric ventricular contraction.

Atrial systole ends; AV valves close.

Atria eject blood into ventricles.

Atrial contraction begins.

Time (msec)

End-systolicvolume

Aortic valvecloses

Dicroticnotch

Left AVvalve opens

Le

ftv

en

tric

ula

rv

olu

me

(m

L)

Pre

ss

ure

(mm

Hg

)



• Heart Sounds

• S1

• Loud sounds

• Produced by AV valves

• S2

• Loud sounds

• Produced by semilunar valves

ANIMATION The Heart: Cardiac Cycle



• S3, S4

• Soft sounds

• Blood flow into ventricles and atrial contraction

• Heart Murmur

• Sounds produced by regurgitation through valves


Figure 20-18a Heart Sounds

Aorticvalve

Pulmonaryvalve

Valve locationSounds heard

LeftAVvalve

RightAVvalve

Placements of a stethoscope forlistening to the different soundsproduced by individual valves

Valve location

Sounds heard




Figure 20-18b Heart Sounds

Semilunarvalves close

AV valvesopen

AV valvesclose

“Dubb”“Lubb”

The relationship between heart sounds and key events in thecardiac cycle

Heart sounds

Pre

ss

ure

(mm

Hg

)

Aorta

Semilunarvalves open

Leftventricle

Leftatrium

S1

S4S4

S2S3


20-4 Cardiodynamics

• Cardiodynamics

• The movement and force generated by cardiac contractions

• End-diastolic volume (EDV)

• End-systolic volume (ESV)

• Stroke volume (SV)

• SV = EDV – ESV

• Ejection fraction

• The percentage of EDV represented by SV


Figure 20-19 A Simple Model of Stroke Volume

Filling

Ventriculardiastole

End-diastolicvolume (EDV)

Pumping

Ventricularsystole

Strokevolume

End-systolicvolume(ESV)

Start



Filling

Ventriculardiastole

When the pump handle israised, pressure within thecylinder decreases, andwater enters through aone-way valve. This corresponds to passive filling during ventricular diastole.

Start



At the start of the pumpingcycle, the amount of water inthe cylinder corresponds to theamount of blood in a ventricleat the end of ventriculardiastole. This amount is knownas the end-diastolic volume(EDV).

End-diastolicvolume (EDV)



Pumping

As the pump handle ispushed down, water is forcedout of the cylinder. This cor-responds to the period ofventricular ejection.

Ventricularsystole



When the handle is depressed asfar as it will go, some water willremain in the cylinder. That amountcorresponds to the end-systolicvolume (ESV) remaining in theventricle at the end of ventricularsystole. The amount of waterpumped out corresponds to thestroke volume of the heart; thestroke volume is the differencebetween the EDV and the ESV.

Strokevolume

End-systolicvolume(ESV)


20-4 Cardiodynamics

• Cardiac Output (CO)

• The volume pumped by left ventricle in 1 minute

• CO = HR SV

• CO = cardiac output (mL/min)

• HR = heart rate (beats/min)

• SV = stroke volume (mL/beat)


20-4 Cardiodynamics

• Factors Affecting Cardiac Output

• Cardiac output

• Adjusted by changes in heart rate or stroke volume

• Heart rate

• Adjusted by autonomic nervous system or hormones

• Stroke volume

• Adjusted by changing EDV or ESV


Figure 20-20 Factors Affecting Cardiac Output

End-systolicvolume

End-diastolicvolume

HormonesAutonomicinnervation

STROKE VOLUME (SV) = EDV – ESVHEART RATE (HR)

CARDIAC OUTPUT (CO) = HR SV

Factors AffectingHeart Rate (HR)

Factors AffectingStroke Volume (SV)


20-4 Cardiodynamics

• Autonomic Innervation

• Cardiac plexuses innervate heart

• Vagus nerves (N X) carry parasympathetic

preganglionic fibers to small ganglia in cardiac plexus

• Cardiac centers of medulla oblongata

• Cardioacceleratory center controls sympathetic neurons

(increases heart rate)

• Cardioinhibitory center controls parasympathetic neurons

(slows heart rate)


20-4 Cardiodynamics

• Autonomic Innervation

• Cardiac reflexes

• Cardiac centers monitor:

• Blood pressure (baroreceptors)

• Arterial oxygen and carbon dioxide levels (chemoreceptors)

• Cardiac centers adjust cardiac activity

• Autonomic tone

• Dual innervation maintains resting tone by releasing ACh and NE

• Fine adjustments meet needs of other systems


Figure 20-21 Autonomic Innervation of the Heart

Cardioinhibitorycenter

Cardioacceleratorycenter

Vagal nucleus

Medullaoblongata

Vagus (N X)

Spinal cord

Parasympathetic

Parasympatheticpreganglionicfiber

Synapses incardiac plexus

Parasympatheticpostganglionicfibers

Cardiac nerve

Sympatheticpostganglionic fiber

Sympatheticpreganglionicfiber

Sympatheticganglia (cervicalganglia andsuperior thoracicganglia [T1–T4])

Sympathetic


20-4 Cardiodynamics

• Effects on the SA Node

• Membrane potential of pacemaker cells

• Lower than other cardiac cells

• Rate of spontaneous depolarization depends on:

• Resting membrane potential

• Rate of depolarization


Figure 20-22a Autonomic Regulation of Pacemaker Function

Prepotential(spontaneous

depolarization)

Normal (resting)

Membranepotential

(mV)

Threshold

Heart rate: 75 bpm

Pacemaker cells have membrane potentials closer to thresholdthan those of other cardiac muscle cells (–60 mV versus–90 mV). Their plasma membranes undergo spontaneousdepolarization to threshold, producing action potentials at afrequency determined by (1) the resting-membrane potentialand (2) the rate of depolarization.


20-4 Cardiodynamics

• Effects on the SA Node

• Sympathetic and parasympathetic stimulation

• Greatest at SA node (heart rate)

• ACh (parasympathetic stimulation)

• Slows the heart

• NE (sympathetic stimulation)

• Speeds the heart


Figure 20-22b Autonomic Regulation of Pacemaker Function

Parasympathetic stimulation releases ACh, whichextends repolarization and decreases the rate ofspontaneous depolarization. The heart rate slows.

Slower depolarization

Hyperpolarization

Parasympathetic stimulation

Heart rate: 40 bpm

Membranepotential

(mV)

Threshold


Figure 20-22c Autonomic Regulation of Pacemaker Function

Sympathetic stimulation releases NE, which shortensrepolarization and accelerates the rate of spontaneousdepolarization. As a result, the heart rate increases.

Time (sec)

More rapiddepolarization

Reduced repolarization

Sympathetic stimulation

Heart rate: 120 bpm

Membranepotential

(mV)

Threshold


20-4 Cardiodynamics

• Atrial Reflex

• Also called Bainbridge reflex

• Adjusts heart rate in response to venous return

• Stretch receptors in right atrium

• Trigger increase in heart rate

• Through increased sympathetic activity


20-4 Cardiodynamics

• Hormonal Effects on Heart Rate

• Increase heart rate (by sympathetic stimulation of

SA node)

• Epinephrine (E)

• Norepinephrine (NE)

• Thyroid hormone


20-4 Cardiodynamics

• Factors Affecting the Stroke Volume

• The EDV amount of blood a ventricle contains at the

end of diastole

• Filling time

• Duration of ventricular diastole

• Venous return

• Rate of blood flow during ventricular diastole


20-4 Cardiodynamics

• Preload

• The degree of ventricular stretching during ventricular

diastole

• Directly proportional to EDV

• Affects ability of muscle cells to produce tension


20-4 Cardiodynamics

• The EDV and Stroke Volume

• At rest

• EDV is low

• Myocardium stretches less

• Stroke volume is low

• With exercise

• EDV increases

• Myocardium stretches more

• Stroke volume increases


20-4 Cardiodynamics

• The Frank–Starling Principle

• As EDV increases, stroke volume increases

• Physical Limits

• Ventricular expansion is limited by:

• Myocardial connective tissue

• The cardiac (fibrous) skeleton

• The pericardial sac


20-4 Cardiodynamics

• End-Systolic Volume (ESV)

• Is the amount of blood that remains in the ventricle

at the end of ventricular systole


20-4 Cardiodynamics

• Three Factors That Affect ESV

1. Preload

• Ventricular stretching during diastole

2. Contractility

• Force produced during contraction, at a given preload

3. Afterload

• Tension the ventricle produces to open the semilunar

valve and eject blood


20-4 Cardiodynamics

• Contractility

• Is affected by:

• Autonomic activity

• Hormones


20-4 Cardiodynamics

• Effects of Autonomic Activity on Contractility

• Sympathetic stimulation

• NE released by postganglionic fibers of cardiac nerves

• Epinephrine and NE released by adrenal medullae

• Causes ventricles to contract with more force

• Increases ejection fraction and decreases ESV


20-4 Cardiodynamics

• Effects of Autonomic Activity on Contractility

• Parasympathetic activity

• Acetylcholine released by vagus nerves

• Reduces force of cardiac contractions


20-4 Cardiodynamics

• Hormones

• Many hormones affect heart contraction

• Pharmaceutical drugs mimic hormone actions

• Stimulate or block beta receptors

• Affect calcium ions (e.g., calcium channel blockers)


20-4 Cardiodynamics

• Afterload

• Is increased by any factor that restricts arterial

blood flow

• As afterload increases, stroke volume decreases


Figure 20-23 Factors Affecting Stroke Volume

Preload

Factors Affecting Stroke Volume (SV)

Venous return (VR)VR = EDV FT = EDV

Filling time (FT) Increased bysympatheticstimulation

Decreased byparasympathetic

stimulation

Increased by E, NE,glucagon,

thyroid hormones

Contractility (Cont)of muscle cellsCont = ESV Increased by

vasoconstrictionDecreased byvasodilation

Afterload (AL)AL = ESVEnd-systolic

volume (ESV)End-diastolicvolume (EDV)

STROKE VOLUME (SV)ESV = SV

VR = EDV FT = EDV

Cont = ESV

AL = ESV

ESV = SVEDV = SVEDV = SV


20-4 Cardiodynamics

• Summary: The Control of Cardiac Output

• Heart Rate Control Factors

• Autonomic nervous system

• Sympathetic and parasympathetic

• Circulating hormones

• Venous return and stretch receptors


20-4 Cardiodynamics

• Summary: The Control of Cardiac Output

• Stroke Volume Control Factors

• EDV

• Filling time, and rate of venous return

• ESV

• Preload, contractility, afterload


20-4 Cardiodynamics

• Cardiac Reserve

• The difference between resting and maximal

cardiac output


20-4 Cardiodynamics

• The Heart and Cardiovascular System

• Cardiovascular regulation

• Ensures adequate circulation to body tissues

• Cardiovascular centers

• Control heart and peripheral blood vessels

• Cardiovascular system responds to:

• Changing activity patterns

• Circulatory emergencies


Figure 20-24 A Summary of the Factors Affecting Cardiac Output

Hormones

Factors affecting heart fate (HR) Factors affecting stroke volume (SV)

CARDIAC OUTPUT (CO) = HR SV

STROKE VOLUME (SV) = EDV – ESVHEART RATE (HR)

AfterloadEnd-systolicvolume

End-diastolicvolume

Vasodilation orvasoconstriction

ContractilityPreload

HormonesAutonomicinnervation

Fillingtime

Venousreturn

Changes inperipheralcirculation

Bloodvolume

Skeletalmuscleactivity

Autonomicinnervation

Atrialreflex

169 Ch 20_lecture_presentation

Health & Medicine

Transcript of 169 Ch 20_lecture_presentation