Copyright 2009, John Wiley & Sons, Inc. Chapter 20: The Cardiovascular System: The Heart 2/7/20091

Copyright 2009, John Wiley & Sons, Inc.

Chapter 20: The Cardiovascular

System: The Heart

2/7/2009 1

Disorders: Homeostatic Imbalances End of Chapter 19 Study pp. 711-712 Anemia Sickle-Cell Disease Hemophilia Leukemia

Copyright 2009, John Wiley & Sons, Inc.2/7/2009 2


Anatomy of the Heart

Located in the mediastinum – anatomical region extending from the sternum to the vertebral column, the first rib and between the lungs

Apex at tip of left ventricle Base is posterior surface Anterior surface deep to sternum and ribs Inferior surface between apex and right border Right border faces right lung Left border (pulmonary border) faces left lung

2/7/2009 3



Pericardium

Membrane surrounding and protecting the heart Confines while still allowing free movement 2 main parts

Fibrous pericardium – tough, inelastic, dense irregular connective tissue – prevents overstretching, protection, anchorage

Serous pericardium – thinner, more delicate membrane – double layer (parietal layer fused to fibrous pericardium, visceral layer also called epicardium)

Pericardial fluid reduces friction – secreted into pericardial cavity

2/7/2009 5


Pericardium and Heart Wall

2/7/2009 6


Layers of the Heart Wall

1. Epicardium (external layer) Visceral layer of serous pericardium Smooth, slippery texture to outermost surface

2. Myocardium 95% of heart is cardiac muscle

3. Endocardium (inner layer) Smooth lining for chambers of heart, valves and

continuous with lining of large blood vessels

2/7/2009 7


Chambers of the Heart

2 atria – receiving chambers Auricles increase capacity

2 ventricles – pumping chambers Sulci – grooves

Contain coronary blood vessels Coronary sulcus – encircles most of heart; boundary

between atria and ventricles; rt. coronary, circumflex coronary and coronary sinus

Anterior interventricular sulcus – boundary between rt. and lt. ventricles; LAD

Posterior interventricular sulcus – distinction between rt. and lt. ventricles; rt. coronary

2/7/2009 8


Structure of the Heart

2/7/2009 9

20_03b


20_03c

2/7/2009 11


Right Atrium

Receives blood from Superior vena cava Inferior vena cava Coronary sinus

Interatrial septum has fossa ovalis Remnant of foramen ovale

Blood passes through tricuspid valve (right atrioventricular valve) into right ventricle

2/7/2009 12


Right Ventricle

Forms anterior surface of heart Trabeculae carneae – ridges formed by raised

bundles of cardiac muscle fiber Part of conduction system of the heart

Tricuspid valve connected to chordae tendinae connected to papillary muscles

Interventricular septum Blood leaves through pulmonary valve (pulmonary

semilunar valve) into pulmonary trunk and then right and left pulmonary arteries

2/7/2009 13


Internal Anatomy of the Heart

2/7/2009 14


20_04b

2/7/2009 15

20_04c


Left Atrium

About the same thickness as right atrium Receives blood from the lungs through pulmonary

veins Passes through bicuspid/ mitral/ left

atrioventricular valve into left ventricle

2/7/2009 17


Left Ventricle

Thickest chamber of the heart Forms apex Chordae tendinae attached to papillary muscles Blood passes through aortic valve (aortic

semilunar valve) into ascending aorta Some blood flows into coronary arteries,

remainder to body During fetal life ductus arteriosus shunts blood

from pulmonary trunk to aorta (lung bypass) closes after birth with remnant called ligamentum arteriosum

2/7/2009 18


Myocardial thickness

Thin-walled atria deliver blood under less pressure to ventricles

Right ventricle pumps blood to lungs Shorter distance, lower pressure, less resistance

Left ventricle pumps blood to body Longer distance, higher pressure, more resistance

Left ventricle works harder to maintain same rate of blood flow as right ventricle

2/7/2009 19


Fibrous skeleton

Dense connective tissue that forms a (1) structural foundation, (2) point of insertion for muscle bundles, and (3) electrical insulator between atria and ventricles

2/7/2009 20


Heart Valves and Circulation of Blood Atrioventricular valves

Tricuspid and bicuspid valves Atria contracts/ ventricle relaxed

AV valve opens, cusps project into ventricle In ventricle, papillary muscles are relaxed and chordae

tendinae slack Atria relaxed/ ventricle contracts

Pressure drives cusps upward until edges meet and close opening

Papillary muscles contract tightening chordae tendinae Prevents regurgitation

2/7/2009 21



Semilunar valves

Aortic and pulmonary valves Valves open when pressure in ventricle exceeds

pressure in arteries As ventricles relax, some backflow permitted but

blood fills valve cusps closing them tightly How blood is passed to coronary arteries

No valves guarding entrance to atria As atria contracts, compresses and closes

opening

2/7/2009 23

20_06d

All valves with atria removed; Semilunars closed

2/7/2009Copyright 2009, John Wiley &

Sons, Inc. 25


Systemic and pulmonary circulation - 2 circuits in series

Systemic circuit Left side of heart Receives blood from lungs Ejects blood into aorta Systemic arteries, arterioles Gas and nutrient exchange in systemic capillaries Systemic venules and veins lead back to right atrium

Superior vena cava, inferior vena cava, and coronary sinus Pulmonary circuit

Right side of heart Receives blood from systemic circulation Ejects blood into pulmonary trunk then pulmonary arteries Gas exchange in pulmonary capillaries Pulmonary veins takes blood to left atrium

2/7/2009 26



Coronary circulation

Myocardium has its own network of blood vessels Coronary arteries branch from ascending aorta

Anastomoses provide alternate routes or collateral circuits

Allows heart muscle to receive sufficient oxygen even if an artery is partially blocked

Coronary capillaries Coronary veins

Collects in coronary sinus Empties into right atrium

2/7/2009 28


Coronary Circulation

2/7/2009 29


Cardiac Muscle Tissue and the Cardiac Conduction System Histology

Shorter and less circular than skeletal muscle fibers But striated like skeletal muscle Branching gives “stair-step” appearance Usually one centrally located nucleus Ends of fibers connected by intercalated discs Discs contain desmosomes (hold fibers together) and gap

junctions (allow action potential conduction from one fiber to the next)

Mitochondria are larger and more numerous than skeletal muscle

Same arrangement of actin and myosin

2/7/2009 30



Autorhythmic Fibers

Specialized cardiac muscle fibers Self-excitable Repeatedly generate action potentials that

trigger heart contractions 2 important functions

1. Act as pacemaker

2. Form conduction system

2/7/2009 32


Conduction system

1. Begins in sinoatrial (SA) node in right atrial wall; at junction with SVC

Unstable resting potential; depolarize to threshold spontaneously

Spontaneous depolarization = pacemaker potential Propagates action potential through atria via gap

junctions Atria contact

2. Reaches atrioventricular (AV) node in interatrial septum; just anterior to coronary sinus

2/7/2009 33


Conduction system3. Enters atrioventricular (AV) bundle (Bundle of His)

Only site where action potentials can conduct from atria to ventricles;

elsewhere, fibrous skeleton electrically insulates the atria from the ventricles

4. Enters right and left bundle branches which extends through interventricular septum toward apex

5. Finally, large diameter Purkinje fibers rapidly conduct action potential to remainder of ventricular myocardium

Ventricles contract; pushing blood up and out

2/7/2009 34

Frontal plane

Right atrium

Right ventricle

Left atrium

Left ventricle

Anterior view of frontal section

Frontal plane

Left atrium

Left ventricle


SINOATRIAL (SA) NODE1

Right atrium

Right ventricle

Frontal plane

Left atrium

Left ventricle


SINOATRIAL (SA) NODE

ATRIOVENTRICULAR(AV) NODE

1

2

Right atrium

Right ventricle

Frontal plane

Left atrium

Left ventricle




ATRIOVENTRICULAR (AV)BUNDLE (BUNDLE OF HIS)

1

2

3

Right atrium

Right ventricle

Frontal plane

Left atrium

Left ventricle





RIGHT AND LEFTBUNDLE BRANCHES

1

2

3

4

Right atrium

Right ventricle

Frontal plane



Left atrium

Left ventricle



RIGHT AND LEFTBUNDLE BRANCHES

PURKINJE FIBERS

1

2

3

4

5

Right atrium

Right ventricle

2/7/2009 35


Conduction System

SA node acts as natural pacemaker Faster than other autorhythmic fibers Initiates 100 times per second

Nerve impulses from autonomic nervous system (ANS) and hormones modify timing and strength of each heartbeat Do not establish fundamental rhythm

2/7/2009 36


Action Potentials and Contraction

Action potential initiated by SA node spreads out to excite “working” fibers called contractile fibers

1. Depolarization

2. Plateau

3. Repolarization

2/7/2009 37



1. Depolarization – contractile fibers have stable resting membrane potential

Voltage-gated fast Na+ channels open – Na+ flows in Then deactivate and Na+ inflow decreases

2. Plateau – period of maintained depolarization Due in part to opening of voltage-gated slow Ca2+

channels – Ca2+ moves from interstitial fluid into cytosol

Ultimately triggers contraction Depolarization sustained due to voltage-gated K+

channels balancing Ca2+ inflow with K+ outflow

2/7/2009 38



3. Repolarization – recovery of resting membrane potential

Resembles that in other excitable cells Additional voltage-gated K+ channels open Outflow K+ of restores negative resting membrane

potential Calcium channels closing

4. Refractory period – time interval during which second contraction cannot be triggered

Lasts longer than contraction itself Tetanus (maintained contraction) cannot occur

Blood flow would cease

2/7/2009 39

Depolarization Repolarization

Refractory period

Contraction

Membranepotential (mV) Rapid depolarization due to

Na+ inflow when voltage-gatedfast Na+ channels open

0.3 sec

+ 20

0

–20

–40

– 60

– 80

–100

11


Refractory period

Contraction

Membranepotential (mV) Rapid depolarization due to

Na+ inflow when voltage-gatedfast Na+ channels open

Plateau (maintained depolarization) due to Ca2+ inflowwhen voltage-gated slow Ca2+ channels open andK+ outflow when some K+ channels open

0.3 sec

+ 20

0

–20

–40

– 60

– 80

–100

2

11

2


Refractory period

Contraction

Membranepotential (mV)

Repolarization due to closureof Ca2+ channels and K+ outflowwhen additional voltage-gatedK+ channels open

Rapid depolarization due toNa+ inflow when voltage-gatedfast Na+ channels open

Plateau (maintained depolarization) due to Ca2+ inflowwhen voltage-gated slow Ca2+ channels open andK+ outflow when some K+ channels open

0.3 sec

+ 20

0

–20

–40

– 60

– 80

–100

2

1

3

1

2

3

Action Potential in a ventricular contractile fiber


Electrocardiogram ECG or EKG Composite record of

action potentials produced by all the heart muscle fibers

Compare tracings from different leads with one another and with normal records

3 recognizable waves P, QRS, and T

2/7/2009 41


Correlation of ECG Waves and Systole Systole – contraction / diastole – relaxation

1. Cardiac action potential arises in SA node P wave appears

2. Atrial contraction/ atrial systole3. Action potential enters AV bundle and out over ventricles

QRS complex Masks atrial repolarization

4. Contraction of ventricles / ventricular systole Begins shortly after QRS complex appears and continues

during S-T segment5. Repolarization of ventricular fibers

T wave6. Ventricular relaxation / diastole

2/7/2009 42

1 Depolarization of atrialcontractile fibersproduces P wave

0.20

Seconds

Action potentialin SA node

P

1

Atrial systole(contraction)

Depolarization of atrialcontractile fibersproduces P wave

0.20Seconds

0.20

Seconds


P

P

2

1

Depolarization ofventricular contractilefibers produces QRScomplex



0.2 0.40Seconds

0.20Seconds

0.20

Seconds


R

SQ

P

P

2

3

P

1

Ventricular systole(contraction)




0.2 0.40Seconds

0.2 0.40Seconds

0.20Seconds

0.20

Seconds


R

SQ

P

P

P

2

3

4

P

1

5Repolarization ofventricular contractilefibers produces Twave





0.60.2 0.40Seconds

0.2 0.40Seconds

0.2 0.40Seconds

0.20Seconds

0.20

Seconds


R

SQ

P

P

P

PT

2

3

4

5

P

1

6Ventricular diastole(relaxation)

5Repolarization ofventricular contractilefibers produces Twave





0.60.2 0.40 0.8

Seconds

0.60.2 0.40Seconds

0.2 0.40Seconds

0.2 0.40Seconds

0.20Seconds

0.20

Seconds


R

SQ

P

P

P

PT

P

2

3

4

5

6

P

2/7/2009 43Copyright 2009, John Wiley &

Sons, Inc.


Cardiac Cycle

All events associated with one heartbeat Systole and diastole of atria and ventricles In each cycle, atria and ventricles alternately

contract and relax During atrial systole, ventricles are relaxed During ventricle systole, atria are relaxed

Forces blood from higher pressure to lower pressure During relaxation period, both atria and ventricles

are relaxed The faster the heart beats, the shorter the relaxation period Systole and diastole lengths shorten slightly

2/7/2009 44

1

0

20

40

60

80

100

120

(d) Volume in ventricle (mL)

(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure

Leftventricularpressure

T

130

60

0

Atrialcontraction

Atrialcontraction

Isovolumetriccontraction

Isovolumetricrelaxation

Ventricularejection

Ventricularfilling

(e) Phases of the cardiac cycle

0.3 sec0.1sec 0.4 sec

Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

1 Atrial depolarization1

0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling



Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

2

1

2

Atrial depolarization

Begin atrial systole

1

0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling


End (ventricular) diastolic volume


Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

2

3

1

2

3




0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling



Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

41

2

3

4




Ventricular depolarization


0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling



Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

4

5

1

2

3

4

5





Isovolumetric contraction


0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling



Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

4

6

1

2

3

4

5

6






Begin ventricular ejection


5

0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling


Strokevolume


Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

4

7

1

2

3

4

5

6

7







End (ventricular) systolic volume


6

5

0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling


Strokevolume


Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

8 1

2

3

4

5

6

7

8








Begin ventricular repolarization


0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling


Strokevolume


Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

8

9

1

2

3

4

5

6

7

8

9









Isovolumetric relaxation


0

20

40

60

80

100

120


(c) Heart sounds

(b) Pressure (mmHg)

(a) ECG P

R

QS

Dicrotic wave

Left atrialpressure

Aorticpressure


T

130

60

0

Atrialcontraction

Atrialcontraction



Ventricularejection

Ventricularfilling


Strokevolume


Ventricularsystole

Relaxationperiod

Atrialsystole

S1 S2 S3 S4

10

1

2

3

4

5

6

7

8

9

10









Isovolumetric relaxation

Ventricular fillingEnd (ventricular) diastolic volume

8

9

2/7/2009 45


Heart Sounds

Auscultation Sound of heartbeat comes

primarily from blood turbulence caused by closing of heart valves

4 heart sounds in each cardiac cycle – only 2 loud enough to be heard Lubb – AV valves close Dupp – SL valves close

S3 due to blood turbulence during rapid ventricular filling

S4 from blood turbulence during atrial systole

2/7/2009 46


Cardiac Output

CO = volume of blood ejected from left (or right) ventricle into aorta (or pulmonary trunk) each minute

CO = stroke volume (SV) x heart rate (HR) In typical resting male

5.25L/min = 70mL/beat x 75 beats/min Entire blood volume flows through pulmonary and

systemic circuits each minute Cardiac reserve – difference between maximum CO

and CO at rest Average cardiac reserve 4-5 times resting value

2/7/2009 47


Regulation of stroke volume

3 factors ensure left and right ventricles pump equal volumes of blood

1. Preload

2. Contractility

3. Afterload

2/7/2009 48


Preload

Degree of stretch on the heart before it contracts Greater preload increases the force of

contraction Frank-Starling law of the heart – the more the

heart fills with blood during diastole, the greater the force of contraction during systole

Preload proportional to end-diastolic volume (EDV) 2 factors determine EDV

1. Duration of ventricular diastole2. Venous return – volume of blood returning to right

ventricle

2/7/2009 49


Contractility

Strength of contraction at any given preload Positive inotropic agents increase contractility

Often promote Ca2+ inflow during cardiac action potential Increases stroke volume Epinephrine, norepinephrine, digitalis

Negative inotropic agents decrease contractility Anoxia, acidosis, some anesthetics, and increased K+ in

interstitial fluid

2/7/2009 50


Afterload

Pressure that must be overcome before a semilunar valve can open

Increase in afterload causes stroke volume to decrease Blood remains in ventricle at the end of systole

Hypertension and atherosclerosis increase afterload

2/7/2009 51


Regulation of Heart Beat

Cardiac output depends on heart rate and stroke volume

Adjustments in heart rate important in short-term control of cardiac output and blood pressure

Autonomic nervous system and epinephrine/ norepinephrine most important

2/7/2009 52


Autonomic regulation

Originates in cardiovascular center of medulla oblongata Increases or decreases frequency of nerve impulses in

both sympathetic and parasympathetic branches of ANS Norepinephrine has 2 separate effects

In SA and AV node speeds rate of spontaneous depolarization

In contractile fibers enhances Ca2+ entry increasing contractility

Parasympathetic nerves release acetylcholine which decreases heart rate by slowing rate of spontaneous depolarization

2/7/2009 53


Nervous System Control of the Heart

2/7/2009 54


Chemical regulation of heart rate

Hormones Epinephrine and norepinephrine increase heart rate and

contractility Thyroid hormones also increase heart rate and

contractility Cations

Ionic imbalance can compromise pumping effectiveness Relative concentration of K+, Ca2+ and Na+ important

2/7/2009 55


Clinical Connections

Pericarditis p. 720 Myocarditis and endocarditis p. 720 Myocardial ischemia and infarction p. 730 Heart murmurs p. 740 Congestive heart failure p. 742


Sons, Inc. 57

Disorders: Homeostatic imbalances Coronary artery disease pp. 750-752 Arrhythmias pp. 753-755


Sons, Inc. 58


End of Chapter 20

Copyright 2009 John Wiley & Sons, Inc.All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publishers assumes no responsibility for errors, omissions, or damages caused by the use of theses programs or from the use of the information herein.

2/7/2009 59

Documents

Copyright 2009, John Wiley & Sons, Inc. Chapter 20: The Cardiovascular System: The Heart 2/7/20091