1. Chapter 20: The Cardiovascular System: The Heart
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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
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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
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5. Pericardium and Heart Wall
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6. Layers of the Heart Wall
Epicardium (external layer)
Visceral layer of serous pericardium
Smooth, slippery texture to outermost surface
Myocardium
95% of heart is cardiac muscle
Endocardium (inner layer)
Smooth lining for chambers of heart, valves and continuous with lining of large blood vessels
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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
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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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11. Internal Anatomy of the Heart
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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
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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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16. 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
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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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19. Systemic and pulmonary circulation - 2 circuits in series
Essay Question on Chapter 20 Examination
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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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
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23. 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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Autorhythmic Fibers
Specialized cardiac muscle fibers
Self-excitable
Repeatedly generate action potentials that trigger heart contractions
2 important functions
Act as pacemaker
Form conduction system
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Conduction system
Essay Question on Chapter 20 Examination
Begins in sinoatrial (SA) node in right atrial wall
Propagates through atria via gap junctions
Atria contact
Reaches atrioventricular (AV) node in interatrial septum
Enters atrioventricular (AV) bundle (Bundle of His)
Only site where action potentials can conduct from atria to ventricles due to fibrous skeleton
Enters right and left bundle branches which extends through interventricular septum toward apex
Finally, large diameter Purkinje fibers conduct action potential to remainder of ventricular myocardium
Ventricles contract
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27. 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 LEFT
BUNDLE 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 LEFT
BUNDLE BRANCHES
PURKINJE FIBERS 1 2 3 4 5
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 1 2
Right atrium
Right ventricle
Frontal plane
Left atrium
Left ventricle
Anterior view of frontal section
SINOATRIAL (SA) NODE 1
Right atrium
Right ventricle
Frontal plane
Right atrium
Right ventricle
Left atrium
Left ventricle
Anterior view of frontal section

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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
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29. Action Potentials and Contraction
Action potential initiated by SA node spreads out to excite “working” fibers called contractile fibers
Depolarization
Plateau
Repolarization
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30. Action Potentials and Contraction
Depolarization – contractile fibers have stable resting membrane potential
Voltage-gated fast Na+ channels open – Na+ flows in
Then deactivate and Na+ inflow decreases
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
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31. Action Potentials and Contraction
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
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32. Action Potential in a ventricular contractile fiber
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33. Depolarization
Repolarization
Refractory period
Contraction
Membrane
potential (mV)
Repolarization due to closure
of Ca2+ channels and K+ outflow
when additional voltage-gated
K+ channels open
Rapid depolarization due to
Na+ inflow when voltage-gated
fast Na+ channels open
Plateau (maintained depolarization) due to Ca2+ inflow
when voltage-gated slow Ca2+ channels open and
K+ outflow when some K+ channels open
0.3 sec
+ 20
–20
–40
– 60
– 80
–100 2 1 3
Depolarization
Repolarization
Refractory period
Contraction
Membrane
potential (mV)
Rapid depolarization due to
Na+ inflow when voltage-gated
fast Na+ channels open
Plateau (maintained depolarization) due to Ca2+ inflow
when voltage-gated slow Ca2+ channels open and
K+ outflow when some K+ channels open
0.3 sec
+ 20
–20
–40
– 60
– 80
–100 2 1
Depolarization
Repolarization
Refractory period
Contraction
Membrane
potential (mV)
Rapid depolarization due to
Na+ inflow when voltage-gated
fast Na+ channels open
0.3 sec
+ 20
–20
–40
– 60
– 80
–100 1

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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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35. Correlation of ECG Waves and Systole
Systole – contraction/ diastole – relaxation
Cardiac action potential arises in SA node
P wave appears
Atrial contraction/ atrial systole
Action potential enters AV bundle and out over ventricles
QRS complex
Masks atrial repolarization
Contraction of ventricles/ ventricular systole
Begins shortly after QRS complex appears and continues during S-T segment
Repolarization of ventricular fibers
T wave
Ventricular relaxation/ diastole
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36. 1 6
Ventricular diastole
(relaxation) 5
Repolarization of
ventricular contractile
fibers produces T
wave
Ventricular
systole
(contraction)
Depolarization of
fibers produces QRS
complex
Atrial systole
Depolarization of atrial
contractile fibers
produces P wave
0.6
0.2
0.4
0.8
Seconds
Action potential
in SA node R S Q P T 2 3 4 1 5
Repolarization of
ventricular contractile
fibers produces T
wave
Ventricular
systole
(contraction)
Depolarization of
fibers produces QRS
complex
Atrial systole
Depolarization of atrial
contractile fibers
produces P wave
0.6
0.2
0.4
Seconds
Action potential
in SA node R S Q P T 2 3 4 1
Ventricular
systole
(contraction)
Depolarization of
ventricular contractile
fibers produces QRS
complex
Atrial systole
Depolarization of atrial
contractile fibers
produces P wave
0.2
0.4
Seconds
Action potential
in SA node R S Q P 2 3 4 1
Depolarization of
ventricular contractile
fibers produces QRS
complex
Atrial systole
(contraction)
Depolarization of atrial
contractile fibers
produces P wave
0.2
0.4
Seconds
Action potential
in SA node R S Q P 2 3 1
Atrial systole
(contraction)
Depolarization of atrial
contractile fibers
produces P wave
0.2
Seconds
Action potential
in SA node P 2 1
Depolarization of atrial
contractile fibers
produces P wave
0.2
Seconds
Action potential
in SA node P

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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
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38. 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 4 7 1 2 3 5 6
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
Begin ventricular ejection
End (ventricular) systolic volume 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 8 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
Begin ventricular repolarization 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 8 9 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
Begin ventricular repolarization
Isovolumetric relaxation 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 10 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
Ventricular filling 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 4 6 1 2 3 5
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction
Begin ventricular ejection 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 4 5 1 2 3
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization
Isovolumetric contraction 1 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 2
Atrial depolarization
Begin atrial systole 1 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
End (ventricular) diastolic volume
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 2 3
Atrial depolarization
Begin atrial systole 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4 4 1 2 3
Atrial depolarization
Begin atrial systole
End (ventricular) diastolic volume
Ventricular depolarization 1 20 40 60 80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P R Q S
Dicrotic wave
Left atrial
pressure
Aortic
Left
ventricular T
130
Atrial
contraction
Isovolumetric
relaxation
Ventricular
ejection
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec
0.4 sec
systole
Relaxation
period S1 S2 S3 S4
Atrial depolarization

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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
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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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41. Regulation of stroke volume
3 factors ensure left and right ventricles pump equal volumes of blood
Preload
Contractility
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
Duration of ventricular diastole
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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45. 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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47. Nervous System Control of the Heart
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48. 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
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End of Chapter 20
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