copyright 2009, john wiley & sons, inc. chapter 20: the cardiovascular system: the heart
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Copyright 2009, John Wiley & Sons, Inc.
Chapter 20: The Cardiovascular
System: The Heart
Copyright 2009, John Wiley & Sons, Inc.
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
Copyright 2009, John Wiley & Sons, Inc.
Copyright 2009, John Wiley & Sons, Inc.
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
Copyright 2009, John Wiley & Sons, Inc.
Pericardium and Heart Wall
Copyright 2009, John Wiley & Sons, Inc.
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
Copyright 2009, John Wiley & Sons, Inc.
Chambers of the Heart
2 atria – receiving chambers Auricles increase capacity
2 ventricles – pumping chambers Sulci – grooves
Contain coronary blood vessels Coronary sulcus Anterior interventricular sulcus Posterior interventricular sulcus
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Structure of the Heart
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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
Copyright 2009, John Wiley & Sons, Inc.
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
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Internal Anatomy of the Heart
Copyright 2009, John Wiley & Sons, Inc.
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
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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
Copyright 2009, John Wiley & Sons, Inc.
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
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Fibrous skeleton
Dense connective tissue that forms a structural foundation, point of insertion for muscle bundles, and electrical insulator between atria and ventricles
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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
Copyright 2009, John Wiley & Sons, Inc.
Copyright 2009, John Wiley & Sons, Inc.
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 No valves guarding entrance to atria
As atria contracts, compresses and closes opening
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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
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
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Copyright 2009, John Wiley & Sons, Inc.
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
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Coronary Circulation
Copyright 2009, John Wiley & Sons, Inc.
Cardiac Muscle Tissue and the Cardiac Conduction System Histology
Shorter and less circular than skeletal muscle fibers 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
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Copyright 2009, John Wiley & Sons, Inc.
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
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Conduction system
1. Begins in sinoatrial (SA) node in right atrial wall Propagates through atria via gap junctions Atria contact
2. Reaches atrioventricular (AV) node in interatrial septum3. Enters atrioventricular (AV) bundle (Bundle of His)
Only site where action potentials can conduct from atria to ventricles due to fibrous skeleton
4. Enters right and left bundle branches which extends through interventricular septum toward apex
5. Finally, large diameter Purkinje fibers conduct action potential to remainder of ventricular myocardium
Ventricles contract
Frontal plane
Right atrium
Right ventricle
Left atrium
Left ventricle
Anterior view of frontal section
Frontal plane
Left atrium
Left ventricle
Anterior view of frontal section
SINOATRIAL (SA) NODE1
Right atrium
Right ventricle
Frontal plane
Left atrium
Left ventricle
Anterior view of frontal section
SINOATRIAL (SA) NODE
ATRIOVENTRICULAR(AV) NODE
1
2
Right atrium
Right ventricle
Frontal plane
Left atrium
Left ventricle
Anterior view of frontal section
SINOATRIAL (SA) NODE
ATRIOVENTRICULAR(AV) NODE
ATRIOVENTRICULAR (AV)BUNDLE (BUNDLE OF HIS)
1
2
3
Right atrium
Right ventricle
Frontal plane
Left atrium
Left ventricle
Anterior view of frontal section
SINOATRIAL (SA) NODE
ATRIOVENTRICULAR(AV) NODE
ATRIOVENTRICULAR (AV)BUNDLE (BUNDLE OF HIS)
RIGHT AND LEFTBUNDLE BRANCHES
1
2
3
4
Right atrium
Right ventricle
Frontal plane
SINOATRIAL (SA) NODE
ATRIOVENTRICULAR(AV) NODE
Left atrium
Left ventricle
Anterior view of frontal section
ATRIOVENTRICULAR (AV)BUNDLE (BUNDLE OF HIS)
RIGHT AND LEFTBUNDLE BRANCHES
PURKINJE FIBERS
1
2
3
4
5
Right atrium
Right ventricle
Copyright 2009, John Wiley & Sons, Inc.
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
Copyright 2009, John Wiley & Sons, Inc.
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
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Action Potentials and Contraction
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
Copyright 2009, John Wiley & Sons, Inc.
Action Potentials and Contraction
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
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
Copyright 2009, John Wiley & Sons, Inc.
Action Potential in a ventricular contractile fiber
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
Depolarization Repolarization
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
Depolarization Repolarization
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
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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
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Correlation of ECG Waves and Systole
Systole – contraction/ diastole – relaxation1. Cardiac action potential arises in SA node
P wave appears2. 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
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
Action potentialin SA node
P
P
2
1
Depolarization ofventricular contractilefibers produces QRScomplex
Atrial systole(contraction)
Depolarization of atrialcontractile fibersproduces P wave
0.2 0.40Seconds
0.20Seconds
0.20
Seconds
Action potentialin SA node
R
SQ
P
P
2
3
P
1
Ventricular systole(contraction)
Depolarization ofventricular contractilefibers produces QRScomplex
Atrial systole(contraction)
Depolarization of atrialcontractile fibersproduces P wave
0.2 0.40Seconds
0.2 0.40Seconds
0.20Seconds
0.20
Seconds
Action potentialin SA node
R
SQ
P
P
P
2
3
4
P
1
5Repolarization ofventricular contractilefibers produces Twave
Ventricular systole(contraction)
Depolarization ofventricular contractilefibers produces QRScomplex
Atrial systole(contraction)
Depolarization of atrialcontractile fibersproduces P wave
0.60.2 0.40Seconds
0.2 0.40Seconds
0.2 0.40Seconds
0.20Seconds
0.20
Seconds
Action potentialin SA node
R
SQ
P
P
P
PT
2
3
4
5
P
1
6Ventricular diastole(relaxation)
5Repolarization ofventricular contractilefibers produces Twave
Ventricular systole(contraction)
Depolarization ofventricular contractilefibers produces QRScomplex
Atrial systole(contraction)
Depolarization of atrialcontractile fibersproduces P wave
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
Action potentialin SA node
R
SQ
P
P
P
PT
P
2
3
4
5
6
P
Copyright 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
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
(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
2
1
2
Atrial depolarization
Begin atrial systole
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
End (ventricular) diastolic volume
0.3 sec0.1sec 0.4 sec
Ventricularsystole
Relaxationperiod
Atrialsystole
S1 S2 S3 S4
2
3
1
2
3
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
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
41
2
3
4
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
End (ventricular) diastolic volume
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
4
5
1
2
3
4
5
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
End (ventricular) diastolic volume
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
4
6
1
2
3
4
5
6
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
Begin ventricular ejection
End (ventricular) diastolic volume
5
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
Strokevolume
0.3 sec0.1sec 0.4 sec
Ventricularsystole
Relaxationperiod
Atrialsystole
S1 S2 S3 S4
4
7
1
2
3
4
5
6
7
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
Begin ventricular ejection
End (ventricular) systolic volume
End (ventricular) diastolic volume
6
5
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
Strokevolume
0.3 sec0.1sec 0.4 sec
Ventricularsystole
Relaxationperiod
Atrialsystole
S1 S2 S3 S4
8 1
2
3
4
5
6
7
8
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
Begin ventricular ejection
End (ventricular) systolic volume
Begin ventricular repolarization
End (ventricular) diastolic volume
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
Strokevolume
0.3 sec0.1sec 0.4 sec
Ventricularsystole
Relaxationperiod
Atrialsystole
S1 S2 S3 S4
8
9
1
2
3
4
5
6
7
8
9
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
Begin ventricular ejection
End (ventricular) systolic volume
Begin ventricular repolarization
Isovolumetric relaxation
End (ventricular) diastolic volume
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
Strokevolume
0.3 sec0.1sec 0.4 sec
Ventricularsystole
Relaxationperiod
Atrialsystole
S1 S2 S3 S4
10
1
2
3
4
5
6
7
8
9
10
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
Begin ventricular ejection
End (ventricular) systolic volume
Begin ventricular repolarization
Isovolumetric relaxation
Ventricular fillingEnd (ventricular) diastolic volume
8
9
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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
Copyright 2009, John Wiley & Sons, Inc.
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
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Regulation of stroke volume
3 factors ensure left and right ventricles pump equal volumes of blood
1. Preload
2. Contractility
3. Afterload
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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
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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
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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
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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
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Autonomic regulation
Originates in cardiovascular center of medulla oblongata Increases or decreases frequency of nerve impulses in
both sympathetic and parasympathetic branches of ANS Noreprinephrine 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
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Nervous System Control of the Heart
Copyright 2009, John Wiley & Sons, Inc.
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
Copyright 2009, John Wiley & Sons, Inc.
Copyright 2009, John Wiley & Sons, Inc.
End of Chapter 20
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