20 - Napa Valley College · Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Anatomy of the Heart The Left Ventricle Holds same volume as right ventricle

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings

C h a p t e r

20

The Heart

PowerPoint® Lecture Slides

prepared by Jason LaPres

Lone Star College - North Harris

Copyright © 2009 Pearson Education, Inc.,

publishing as Pearson Benjamin Cummings


Introduction to Cardiovascular System

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

Arteries

Carry blood away from heart

Veins

Carry blood to heart

Capillaries

Networks between arteries and veins



Capillaries

Also called exchange vessels

Exchange materials between blood and

tissues

Materials include dissolved gases, nutrients,

wastes



Figure 20–1 An Overview of the Cardiovascular System.



Four Chambers of the Heart

Right atrium

Collects blood from systemic circuit

Right ventricle

Pumps blood to pulmonary circuit

Left atrium

Collects blood from pulmonary circuit

Left ventricle

Pumps blood to systemic circuit


Figure 20–2c

Anatomy of 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


Figure 20–2c


The Pericardium

Double lining of the pericardial cavity

Parietal pericardium

Outer layer

Forms inner layer of pericardial sac

Visceral pericardium

Inner layer of pericardium



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



Figure 20–c2 The Location of the Heart in the Thoracic Cavity



Superficial Anatomy of the Heart

Atria

Thin-walled

Expandable outer auricle (atrial appendage)

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 Heart



Figure 20–3a The Superficial Anatomy of the Heart



Figure 20–3b The Superficial Anatomy of the Heart



Figure 20–3c The Superficial Anatomy of the Heart



The Heart Wall

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 20–4 The Heart Wall



Cardiac Muscle Tissue

Intercalated discs

Interconnect cardiac muscle cells

Secured by desmosomes

Linked by gap junctions

Convey force of contraction

Propagate action potentials



Figure 20–5 Cardiac Muscle Cells









Characteristics of Cardiac Muscle Cells

Small size

Single, central nucleus

Branching interconnections between cells

Intercalated discs







Internal Anatomy and Organization

Interatrial septum: separates atria

Interventricular septum: separates ventricles

Atrioventricular (AV) valves

Connect right atrium to right ventricle and left atrium to left

ventricle

The fibrous flaps that form bicuspid (2) and tricuspid (3)

valves

Permit blood flow in one direction: atria to ventricles

The Heart: Valves

20HeartValves_A_MOV.mov



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



The Right Atrium

Foramen ovale

Before birth, is an opening through interatrial

septum

Connects the two atria

Seals off at birth, forming fossa ovalis



The Right Atrium

Pectinate muscles

Contain prominent muscular ridges

On anterior atrial wall and inner surfaces of right

auricle



Figure 20–6a-b The Sectional Anatomy of the Heart.



Figure 20–6a-b The Sectional Anatomy of the Heart.



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



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

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.



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



Figure 20–7 Structural Differences between the Left and Right

Ventricles



Figure 20–7 Structural Differences between the Left and Right

Ventricles



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: prevent valves

from swinging into atria

Figure 20–8



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

Figure 20–8



Aortic Sinuses

At base of ascending aorta

Sacs that prevent valve cusps from sticking to

aorta

Origin of right and left coronary arteries



Figure 20–8a Valves of the Heart



Figure 20–8b Valves of the Heart



Figure 20–8c Valves of the Heart



Connective Tissues and the Cardiac

(Fibrous) Skeleton

Physically support cardiac muscle fibers

Distribute forces of contraction

Add strength and prevent overexpansion of heart

Elastic fibers return heart to original shape after

contraction



The Cardiac (Fibrous) 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

Coronary arteries and cardiac veins

Supplies blood to muscle tissue of heart



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

Circumflex artery

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

Empties 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



Figure 20–9b Coronary Circulation



Figure 20–9c Coronary Circulation



Figure 20–10 Coronary Circulation and Clinical Testing


The Conducting System

Heartbeat

A single contraction of the heart

The entire heart contracts in series

First the atria

Then the ventricles



Two Types of Cardiac Muscle Cells

Conducting system

Controls and coordinates heartbeat

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)

Electrical events in the cardiac cycle can be recorded on an

electrocardiogram (ECG)



Figure 20–11 An Overview of Cardiac Physiology



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



Figure 20–12 The Conducting System of the Heart



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 20–13 Impulse Conduction through the Heart



The Atrioventricular (AV) Node

In floor of right atrium

Receives impulse from SA node (Step 2)

Delays impulse (Step 3)

Atrial contraction 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






Purkinje Fibers

Distribute impulse through ventricles (Step 5)

Atrial contraction is completed

Ventricular contraction 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



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 20–14a An Electrocardiogram: Electrode Placement for Recording a Standard ECG



Figure 20–14b An Electrocardiogram: An ECG Printout



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 20–15 The Action Potential in Skeletal and Cardiac Muscle



Figure 20–15 The Action Potential in Skeletal and Cardiac Muscle



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 msecs:

– 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

20% of calcium ions required for a contraction

Calcium ions enter plasma membrane during plateau phase

Arrival of extracellular Ca2+

Triggers release of calcium ion reserves from sarcoplasmic

reticulum




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


The Cardiac Cycle

Cardiac cycle = The period between the

start of one heartbeat and the beginning of

the next

Includes both contraction and relaxation


The Cardiac Cycle

Phases of the Cardiac Cycle

Within any one chamber

Systole (contraction)

Diastole (relaxation)


The Cardiac Cycle

Figure 20–16 Phases of the Cardiac Cycle


The Cardiac Cycle

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


The Cardiac Cycle

Cardiac Cycle and Heart Rate

At 75 beats per minute

Cardiac cycle lasts about 800 msecs

When heart rate increases

All phases of cardiac cycle shorten, particularly

diastole


The Cardiac Cycle

Eight Steps in the Cardiac Cycle

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)


The Cardiac Cycle

Figure 20–17 Pressure and Volume Relationships in the Cardiac Cycle


The Cardiac Cycle


4. Ventricular systole

Isovolumetric ventricular contraction

Pressure in ventricles rises

AV valves shut

5. Ventricular ejection

Semilunar valves open

Blood flows into pulmonary and aortic trunks

Stroke volume (SV) = 60% of end-diastolic volume


The Cardiac Cycle



The Cardiac Cycle


6. Ventricular pressure falls

Semilunar valves close

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

of end-diastolic volume

7. Ventricular diastole

Ventricular pressure is higher than atrial pressure

All heart valves are closed

Ventricles relax (isovolumetric relaxation)


The Cardiac Cycle



The Cardiac Cycle


8. Atrial pressure is higher than ventricular

pressure

AV valves open

Passive atrial filling

Passive ventricular filling

Cardiac cycle ends

The Heart: Cardiac Cycle

20HeartCarCyc_A_MOV.mov


The Cardiac Cycle



The Cardiac Cycle

Heart Sounds

S1

Loud sounds

Produced by AV valves

S2

Loud sounds

Produced by semilunar valves

S3, S4

Soft sounds

Blood flow into ventricles and atrial contraction


The Cardiac Cycle

Heart Murmur

Sounds produced by regurgitation through

valves


The Cardiac Cycle

Figure 20–18 Heart Sounds


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

Cardiac output (CO)

The volume pumped by left ventricle in 1 minute


Cardiodynamics

Figure 20–19 A Simple Model of Stroke Volume


Cardiodynamics

Cardiac Output

CO = HR X SV

CO = cardiac output (mL/min)

HR = heart rate (beats/min)

SV = stroke volume (mL/beat)


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


Cardiodynamics

Figure 20–20 Factors Affecting Cardiac Output


Cardiodynamics

Factors Affecting the Heart Rate

Autonomic innervation

Cardiac plexuses: innervate heart

Vagus nerves (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)


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


Cardiodynamics

Figure 20–21 Autonomic Innervation of the Heart


Cardiodynamics

Effects on the SA Node

Sympathetic and parasympathetic stimulation

Greatest at SA node (heart rate)

Membrane potential of pacemaker cells

Lower than other cardiac cells

Rate of spontaneous depolarization depends on

Resting membrane potential

Rate of depolarization

ACh (parasympathetic stimulation)

Slows the heart

NE (sympathetic stimulation)

Speeds the heart


Cardiodynamics

Figure 20–22 Autonomic Regulation of Pacemaker Function


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


Cardiodynamics

Hormonal Effects on Heart Rate

Increase heart rate (by sympathetic

stimulation of SA node)

Epinephrine (E)

Norepinephrine (NE)

Thyroid hormone


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


Cardiodynamics

Preload

The degree of ventricular stretching during

ventricular diastole

Directly proportional to EDV

Affects ability of muscle cells to produce

tension


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


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


Cardiodynamics

End-Systolic Volume (ESV)

The amount of blood that remains in the

ventricle at the end of ventricular systole is

the ESV


Cardiodynamics

Three Factors That Affect ESV

Preload

Ventricular stretching during diastole

Contractility

Force produced during contraction, at a given preload

Afterload

Tension the ventricle produces to open the semilunar valve

and eject blood


Cardiodynamics

Contractility

Is affected by

Autonomic activity

Hormones


Cardiodynamics

Effects of Autonomic Activity on Contractility

Sympathetic stimulation

NE released by postganglionic fibers of cardiac nerves

Epinephrine and NE released by suprarenal (adrenal)

medullae

Causes ventricles to contract with more force

Increases ejection fraction and decreases ESV


Cardiodynamics

Effects of Autonomic Activity on

Contractility

Parasympathetic activity

Acetylcholine released by vagus nerves

Reduces force of cardiac contractions


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)


Cardiodynamics

Afterload

Is increased by any factor that restricts arterial

blood flow

As afterload increases, stroke volume

decreases


Cardiodynamics

Figure 20–23 Factors Affecting Stroke Volume


Cardiodynamics

Heart Rate Control Factors

Autonomic nervous system

Sympathetic and parasympathetic

Circulating hormones

Venous return and stretch receptors


Cardiodynamics

Stroke Volume Control Factors

EDV

Filling time

Rate of venous return

ESV

Preload

Contractility

Afterload


Cardiodynamics

Cardiac Reserve

The difference between resting and maximal

cardiac output


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


Cardiodynamics

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

Documents

20 - Napa Valley College · Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Anatomy of the Heart The Left Ventricle Holds same volume as right ventricle