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Chapter 19: The Circulatory
System: The Heart
Gondelon/Photo Researchers, Inc.
Circulatory System
• Circulatory system
• Blood
• Heart
• Blood
Cardiovascular system
Vessels
19-3
Circulatory System: The Heart
1.Overview of Cardiovascular System
2.Gross Anatomy of the Heart
3.Cardiac Conduction System and Cardiac
Muscle
4.Electrical and Contractile Activity of Heart
5.Blood Flow, Heart Sounds, and Cardiac
Cycle
6.Cardiac Output
19-2
Circulatory System: The Heart
• Cardiology – the scientific study of the heart and the
treatment of its disorders
• For Information on the field of Cardiology visit:
http://www.aamc.org/students/considering/careers.
htm
Circulatory System: The Heart
• Two Major Circuits of the Circulatory System
1. Pulmonary Circuit
2. Systemic Circuit
• Pulmonary Circuit occupies the Right Side
of Heart
• Systemic Circuit occupies the Left Side of
the Heart
Circulatory System: The Heart
• Two Major divisions of Circulatory System
1.Pulmonary Circuit
• Pumps blood through the Lungs
• Carries blood to lungs for gas exchange and back to
heart
• Right side of heart
2.Systemic Circuit
• Pump blood through the Body
• Supplies oxygenated blood to all tissues of the body and
returns it to the heart
• Left side of heart
Fig. 19.1
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CO2
O2
Pulmonary circuit
O2-poor,
CO2-rich
blood
O2-rich,
CO2-poor
blood
Systemic circuit
CO2
O2
Cardiovascular System Circuit
• Pulmonary Circuit
• Systemic Circuit
• First, low O2 blood from the •
body enters heart
• Second, heart pumps blood•
to the lungs
First, high O2 blood from lungs
returns to heart
Second, heart pumps blood to
all body systems
• Veins carry blood to the heart
• Arteries carry blood from the heart
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Fig. 19.1
CO2
1. Heart pumps
blood to the lungs
O2
2.High O2 blood from
lungs returns to
Pulmonary circuit
heart
O2-poor,
CO2-rich
blood
1. Low O2 blood
from the body
enters heart
O2-rich,
CO2-poor
blood
Systemic circuit
CO2
O2
2.Heart pumps
blood to all body
systems
Cardiovascular System Circuit
• Pulmonary Circuit
• Right side of Heart
• Systemic Circuit
• Left side of Heart
• Low O2 blood enters heart
via inferior and superior
vena cava
• Blood leaves heart to lungs
via pulmonary trunk
(arteries)
• High O2 blood from lungs
enters heart via pulmonary
veins
• Blood sent to all organs of the
body via aorta
• Veins carry blood to the heart
• Arteries carry blood from the heart
Fig. 19.1
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
CO2
O2
2.High O2 blood from
1. Blood leaves
lungs enters heart
heart to lungs via
via pulmonary
pulmonary trunk
Pulmonary circuit veins
(arteries)
O2-poor,
CO2-rich
blood
1. Low O2 blood
enters heart via
inferior and
superior vena
cava
O2-rich,
CO2-poor
blood
Systemic circuit
CO2
O2
2.Blood sent to all
organs of the body
via aorta
Cardiovascular System Circuit
• Pulmonary Circuit
• Systemic Circuit
• Left side of Heart
• Right side of Heart
• Inferior and Superior Vena • High O2 blood from the
Cava return blood to the
pulmonary veins enters the
Right Atrium of the heart
Left Atrium of the heart
• The Right Ventricle pumps • The Left Ventricle of the
blood to lungs via
heart pumps blood to the
Pulmonary Trunk (arteries)
body via Aorta
• Blood enters the heart through the Atria
• Blood leaves the heart through the Ventricles
Fig. 19.1
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
CO2
O2
1. The Right
2.High O2 blood from
Ventricle pumps
the pulmonary veins
blood to lungs via
enters the Left
Pulmonary
Atrium of the heart
Trunk (arteries) Pulmonary circuit
O2-poor,
CO2-rich
blood
O2-rich,
CO2-poor
blood
Systemic circuit
1. Inferior and
Superior Vena
Cava return blood
to the Right
Atrium of the
heart
CO2
O2
2.The Left
Ventricle of the
heart pumps blood
to the body via
Aorta
Fig. 19.1
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
CO2
O2
• Systemic Circuit
• Pulmonary Circuit
• Uses Left side of
• Uses Right side of Heart
Heart
• Blood enters PC
Pulmonary circuit
• Blood enters SC
through the Right Atrium
through the Left
• Blood leaves PC through
Atrium
the Right Ventricle
• Blood leaves SC
Systemic circuit
through the Left
Ventricle
O2-poor,
CO2-rich
blood
O2-rich,
CO2-poor
blood
CO2
O2
Cardiovascular System Circuit
• Veins carry blood to the heart
• Arteries carry blood from the heart
and
• Blood enters the heart through the Atria
• Blood leaves the heart through the Ventricles
Therefore,
• Veins return blood to the Atria
• Arteries carry blood from the Ventricles
Cardiovascular System Circuit:
Unity of Form and Function
• Atrium are Superior
• Ventricles are Inferior
• The Atria are thinned walled, little muscle
• The Ventricles are thick walled, very
muscular
• The Left Ventricle is much larger than the
right Ventricle
Position, Size, and Shape
• Heart located in
Mediastinum
- Tilts to the left
• Base
- wide, superior
portion of heart
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Aorta
Pulmonary
trunk
Superior
vena cava
Right lung
Base of
heart
Parietal
pleura (cut)
Pericardial
sac (cut)
• Apex
- inferior end tapers to
point
• Approximately size of fist
Apex
of heart
Diaphragm
(c)
Figure 19.2c
19-5
Fig. 19.2c
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Aorta
Pulmonary
trunk
Superior
vena cava
Base of
heart
Right lung
Parietal
pleura (cut)
Pericardial
sac (cut)
Apex
of heart
(c)
Diaphragm
Fig. 19.2a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Sternum
3rd rib
Diaphragm
(a)
Pericardial Cavity
• Body cavity containing the heart
• Lined by the Pericardium
- Anchored to diaphragm inferiorly and sternum anteriorly
• Filled with 5 - 30 mL of Pericardial Fluid
• Functions:
- Allows heart to beat without friction,
- Provides room to expand
- Resists excessive expansion
Fig. 19.2b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Posterior
Lungs
Thoracic
vertebra
Pericardial
cavity
Left
ventricle
Right
ventricle
Interventricular
septum
Sternum
(b)
Anterior
Pericardium
Structure:
•Pericardium
– Double-walled membrane sac (pericardial sac) that
encloses the heart
a. Parietal Pericardium
• Outer wall of pericardial sac; lines pericardial cavity
• Superficial fibrous layer of connective tissue
• Serous membrane layer - recall: serous membranes
line body cavities that do not open to the outside
b. Visceral Pericardium (Epicardium)
• Inner wall of pericardial cavity; covers the heart
• Serous lining of sac turns inward at base of heart to
cover the heart surface
19-7
Pericardium and Heart Wall
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pericardial
cavity
Pericardial
sac:
Fibrous
layer
Serous
layer
Epicardium
Myocardium
Endocardium
Epicardium
Pericardial sac
Figure 19.3
19-8
Fig. 19.3b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Pericardial
cavity
Pericardial
sac:
Fibrous
layer
Serous
layer
Epicardium
Heart Wall
• The Heart Wall is Composed of 3 Tissue
Layers:
1. Epicardium
2. Myocardium
3. Endocardium
Superficial
Deep
Heart Wall
1.Epicardium
• The Visceral Pericardium
• Serous membrane covering heart
• Adipose in thick layer in some places
• Coronary Blood Vessels travel
through this layer
- Supply the heart tissue with blood
19-10
Heart Wall
2.Myocardium
• Layer of cardiac muscle
• Fibrous skeleton of the heart
- framework of collagenous and elastic fibers
- provides structural support and attachment for cardiac
muscle and anchor for valve tissue
- electrical insulation between atria and ventricles
important in timing and coordination of contractile activity
Fig. 19.6
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
(a)
(b)
Photo and illustration by Roy Schneider, University of Toledo. Plastinated heart model for illustration courtesy of Dr. Carlos Baptista, University of Toledo
Heart Wall
3.Endocardium
– Smooth inner lining of heart and blood
vessels
– Covers the valve surfaces
– Continuous with endothelium of blood
vessels
Fig. 19.4a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Epicardium:
Fat in interventricular
sulcus
Left ventricle
Right ventricle
Anterior interventricular
artery
(a) Anterior view, external anatomy
© The McGraw-Hill Companies, Inc.
Fig. 19.4b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Superior vena cava
Base of heart
Inferior vena cava
Right atrium
Interatrial septum
Left atrium
Opening of coronary sinus
Right AV valve
Left AV valve
Trabeculae carneae
Coronary blood vessels
Right ventricle
Tendinous cords
Papillary muscles
Left ventricle
Epicardial fat
Endocardium
Myocardium
Interventricular septum
Epicardium
Apex of heart
(b) Posterior view, internal anatomy
© The McGraw-Hill Companies, Inc.
2. Gross Anatomy of the Heart
A.External Structure
B.Internal Structure
Is this an Anterior or Posterior view of the Heart?
(a)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Fig. 19.6a
A. External Anatomy - Anterior
Aortic arch
Ascending
aorta
Superior vena cava
Left pulmonary
artery
Branches of the
right pulmonary
artery
Pulmonary trunk
Left pulmonary
veins
Right pulmonary
veins
Left auricle of Left Atrium
Right auricle
Right atrium
Right ventricle
Inferior vena cava
Left ventricle
Apex of heart
Fig. 19.5a
(a) Anterior view
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
B. External Anatomy -Posterior
Aorta
Left pulmonary
artery
Superior
vena cava
Right pulmonary
artery
Left pulmonary
veins
Right pulmonary
veins
Left atrium
Right atrium
Inferior vena cava
Fat
Left ventricle
Apex of heart
Right ventricle
(b) Posterior view
Fig. 19.5b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Structure of Cardiac Muscle
• Cardiocytes
– Cells of the heart
– Form the Myocardium, compose the heart
walls
– A type of muscle cell
• Striated
• Involuntary
– Repair of damage of cardiac muscle is
almost entirely by fibrosis (scarring)
19-28
Structure of Cardiac Muscle:
Cardiocytes
• Histological Differentiation
–Striated
–Branched Cells
–Contain Glycogen
–Intercalated Disks
Fig. 19.11a
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Striations
Nucleus
Intercalated discs
(a)
© Ed Reschke
Fig. 19.11b
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Striated myofibril
(b)
Glycogen Nucleus Mitochondria Intercalated discs
Structure of Cardiac Muscle:
Cardiocytes
• Intercalated Disks
– Tightly join cardiocytes end to end
1. Interdigitating Folds – cell membrane folds interlock
with each other, and increase surface area of contact
2. Mechanical Cell-to-Cell Junctions
– Fascia Adherens – broad band of protein anchors
the actin of the thin myofilaments to the plasma
membrane
– Desmosomes - weldlike mechanical junctions
between cells
41
42
Structure of Cardiac Muscle:
Cardiocytes
• Intercalated Disks
– Tightly join cardiocytes end to end
3. Gap Junctions - specialized cell-to-cell junctions that allow
ion to flow between cells
- Electrical Junctions – adjacent cells can stimulate
neighbors
- entire myocardium of either two atria or two ventricles
acts like single unified cell
- crucial for synchronized heart beat
Fig. 19.11c
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Intercellular space
Desmosomes
Gap junctions
(c)
Metabolism of Cardiac Muscle
• Cardiac Muscle depends almost
exclusively on Aerobic Respiration to
make ATP
• Cardiocytes:
– Rich in Myoglobin - a specialized form of
hemoglobin
– Rich in Glycogen - the fuel for Aerobic Respiration
– Highly Developed Mitochondria - The
organelle for Cellular Respiration
- fill 25% of cell
19-30
Metabolism of Cardiac Muscle
• Cardiac Muscle Adaptable to Organic Fuels
– fatty acids (60%), glucose (35%), ketones, lactic acid and
amino acids (5%)
• Fatigue Resistant
– makes little use of anaerobic fermentation or oxygen debt
mechanisms
– avoids producing bi-products of anaerobic respiration like
lactic acid
– does not fatigue for a lifetime
• More vulnerable to oxygen deficiency
than lack of a specific fuel
19-30
Cardiac Conduction System:
Coordination of the Heart Beat
• System of specialized cells, innervations,
and cell junctions working together to
coordinate the heart beat
• Very important processes for an efficient
heart beat
• Main Components of system include:
– an Internal Pacemaker of specialized cardiocytes
– Nervelike Conduction Pathways through myocardium
• Work together to generate and conduct
rhythmic electrical signals through the
myocardium
19-31
Cardiac Conduction System
• Internal Pacemaker of specialized
cardiocytes:
• Sinoatrial (SA) Node
–
–
–
–
Group of modified cardiocytes known as the Pacemaker
Located in right atrium near base of Superior Vena Cava
Initiates each heartbeat and determines heart rate
signals spread throughout atria
19-31
Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 SA node fires.
Right atrium
2 Excitation spreads through
atrial myocardium.
2
1
Sinoatrial node
(pacemaker)
Left
atrium
2
Atrioventricular
node
Atrioventricular
bundle
Purkinje
fibers
3
Bundle
branches
4
5
3 AV node fires.
4 Excitation spreads down AV
bundle.
5 Purkinje fibers distribute
excitation through
ventricular myocardium.
Purkinje fibers
Figure 19.12
19-32
Cardiac Conduction System
• Internal Pacemaker of specialized
cardiocytes:
• Atrioventricular (AV) Node
– Specialized cardiocytes located near the right AV valve at
lower end of interatrial septum
– Propagate electrical signal to the ventricles
– Fibrous skeleton acts as an insulator to prevent currents
from getting to the ventricles from any other route
• Atrioventricular (AV) Bundle (bundle of His)
– Bundle of conducting tissue that travels from AV node
through interventricular septum
– Bundle branches into RV and LV at apex
19-31
Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 SA node fires.
Right atrium
2 Excitation spreads through
atrial myocardium.
2
1
Sinoatrial node
(pacemaker)
Left
atrium
2
Atrioventricular
node
Atrioventricular
bundle
Purkinje
fibers
3
Bundle
branches
4
5
3 AV node fires.
4 Excitation spreads down AV
bundle.
5 Purkinje fibers distribute
excitation through
ventricular myocardium.
Purkinje fibers
Figure 19.12
19-32
Cardiac Conduction System
• Internal Pacemaker of specialized
cardiocytes:
• Purkinje Fibers
– Nervelike processes that spread from Bundle of His and
distribute throughout ventricular myocardium
– Distribute excitation through ventricular myocardium
– Conduct signal from cell to cell through gap junctions
19-31
Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 SA node fires.
Right atrium
2 Excitation spreads through
atrial myocardium.
2
1
Sinoatrial node
(pacemaker)
Left
atrium
2
Atrioventricular
node
Atrioventricular
bundle
Purkinje
fibers
3
Bundle
branches
4
5
3 AV node fires.
4 Excitation spreads down AV
bundle.
5 Purkinje fibers distribute
excitation through
ventricular myocardium.
Purkinje fibers
Figure 19.12
19-32
Nerve Supply to Heart
• The heart also receives sympathetic and
parasympathetic innervation
• Important for adaptation and modification of
cardiac output
– modifies heart rate
– modifies heart contractility (contraction
strength)
Nerve Supply to Heart
• Sympathetics
• Sympathetic stimulation:
- Raises heart rate
- Increases contractility
- Dilates coronary arteries
Increases Cardiac Output
• Sympathetic Innervation:
- Sympathetic pathway to the heart originates in the lower
cervical to upper thoracic segments of the spinal cord
- Continues to adjacent sympathetic chain ganglia
- Some pass through cardiac plexus in mediastinum
- Continue as cardiac nerves to the heart
- Fibers terminate in SA and AV nodes, as well as the aorta,
pulmonary trunk, and coronary arteries
19-33
Nerve Supply to Heart
• Parasympathetics
• Parasympathetic stimulation:
- Reduces heart rate
- Decreases contractility
Increases Cardiac Output
• Parasympathetic Innervation:
- pathway begins with nuclei of the vagus nerves (CN X) in the
medulla oblongata
- extend to cardiac plexus and continue to the heart by way of
the cardiac nerves
- fibers of right vagus nerve lead to the SA node
- fibers of left vagus nerve lead to the AV node
- little or no vagal stimulation of the myocardium
19-33
Cardiac Rhythm
• Cycle of events in heart – special names
– systole – atrial or ventricular contraction
– diastole – atrial or ventricular relaxation
• Sinus Rhythm - normal heartbeat triggered by
the SA node
– set by SA node at 60 – 100 bpm
– adult at rest is 70 to 80 bpm (vagal tone)
• Ectopic Focus - another part of heart fires before
SA node
– caused by hypoxia, electrolyte imbalance, caffeine,
nicotine, and other drugs
19-34
Abnormal Heart Rhythms
• Spontaneous firing from part of heart other
than SA node
– ectopic foci - regions of spontaneous firing
• Nodal Rhythm – if SA node is damaged, heart rate is set
by AV node, 40 to 50 bpm
• Intrinsic Ventricular Rhythm – if both SA and AV nodes
are not functioning, rate set at 20 to 40 bpm
– this requires pacemaker to sustain life
• Arrhythmia – any abnormal cardiac rhythm
– failure of conduction system to transmit signals
(heart block)
• bundle branch block
• total heart block (damage to AV node)
19-35
Cardiac Arrhythmias
• Atrial Flutter – ectopic foci in atria
– atrial fibrillation
– atria beat 200 - 400 times per minute
• Premature Ventricular Contractions (PVCs)
– caused by stimulants, stress or lack of sleep
• Ventricular Fibrillation
– serious arrhythmia caused by electrical signals
reaching different regions at widely different times
• heart can’t pump blood and no coronary perfusion
– kills quickly if not stopped
• defibrillation - strong electrical shock whose intent is to
depolarize the entire myocardium, stop the fibrillation, and
reset SA nodes to sinus rhythm
19-36
Pacemaker Physiology
• The SA node spontaneously signals
– The heart rhythm and contraction is automatic and
originates in the heart itself
– Nervous stimulation can adjust heart contraction
• The SA node regularly signals
– The SA node is able to maintain a metronome like
beat
– The rhythm is maintained through polarization and
depolarization of the SA node cell membranes
19-37
Pacemaker Physiology
• The cell membrane maintains a Membrane Potential
– Membrane Potential is an unequal charge between the inside
and the outside of the membrane
– The membrane potential is maintained by ion channels
regulating the flow of ions across the cell membrane
• Membrane potential is similar to a battery
– Just as a battery has positive and negative poles, so does the
membrane (extracellular and intracellular poles)
– The cell membrane can conduct an electrical signal, just like a
battery
• Polarization and Depolarization
– Polarization - the charge difference between the poles increases
– Depolarization - the charge difference between the poles equalizes
19-37
Pacemaker Physiology
• Regular polarization and depolarization of the membrane regulates
the cardiac rhythm:
1. Depolarization
– Depolarization has two stages:
a. Gradual depolarization called the Pacemaker Potential
b. Rapid depolarization facilitated by Fast Calcium-Sodium Ion
Channels
2. Repolarization
- The resting membrane potential is restored
19-37
1. Depolarization
a. Gradual depolarization called the Pacemaker Potential
– The resting membrane potential is -60 mV (The intracellular charge
is negative compared to the outside)
– Na+ ions passively flow through ion channels into the cell
– The inside of the cell becomes less negative
b. Rapid depolarization facilitated by Fast Calcium-Sodium
Ion Channels
– When potenital reaches threshold of -40 mV, voltage-gated fast
Ca2+ and Na+ channels open and ions rush into the cell
• Rapid Depolarization continues until the MP reaches 0 mV
• Each depolarization of the SA node sets off one heartbeat
– at rest, fires every 0.8 seconds or 75 bpm
19-37
1. Repolarization
• The RMP of -60 mV is restored
– When the membrane depolarizes and the MP
reaches 0 mV, K+ channels then open and K+
leaves the cell
– The intracellular charge becomes more negative
causing repolarization to RMP -60 mV
– At RMP -60 mV, K+ channels close
• Pacemaker potential starts over as
inflow of Na+ ions once again leads to
the gradual depolarization of the
Pacemaker Potential
19-37
SA Node Potentials
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Membrane potential (mV)
+10
0
–10
Fast K+
outflow
Fast
Ca2+–Na+
inflow
–20
Action
potential
Threshold
–30
–40
Pacemaker
potential
–50
–60
Slow Na+
inflow
–70
0
.4
.8
1.2
1.6
Time (sec)
Figure 19.13
19-38
Impulse Conduction to Myocardium
• Signal from SA node stimulates L and R atria to contract
almost simultaneously
• Signal delayed through AV node
– cardiocytes have fewer gap junctions
– delays signal 100 msec which
– allows ventricles to fill
• Signal travels through AV bundle and Purkinje fibers
– ventricular myocardium depolarizes and contracts in near unison
– papillary muscles contract tightening chordae tendineae closing AV valves
• Ventricular systole progresses up from the apex
– spiral arrangement of cardiocytes ‘wrings’ out ventricles
19-39
Myocardiocyte Physiology
• Cardiocytes have a stable RMP of 90 mV
– cadiocyte Na+ ion channels are voltage gated, do not
‘leak’ like SA node Na+ ion channels
– depolarize only when stimulated
• Three phases of Mycardiocyte
Contraction:
1. Depolarization Phase
2. Plateau Phase
3. Repolarization Phase
19-40
Myocardiocyte Physiology
1. Depolarization Phase
– nodal stimulus opens voltage regulated Na+ gates,
Na+ rushes in, membrane depolarizes rapidly
– Na+ gates close quickly at +30 mV
2. Plateau Phase
– Ca2+ channels are slow to close and SR is slow to
uptake Ca2+ from the cytosol
– sustains contraction for expulsion of blood from heart
– lasts 200 to 250 msec
3. Repolarization Phase
– Ca2+ channels close, K+ channels open
– rapid diffusion of K+ out of cell returns it to resting
potential
19-40
Action Potential of a Cardiocyte
1) Na+ gates open
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
3
2) Rapid
depolarization
gates close
4
0
Membrane potential (mV)
3)
Na+
+20
–80
5) Ca2+ channels close,
K+ channels open
(repolarization)
Voltage-gated Na+ channels open.
2
Na+ inflow depolarizes the membrane
and triggers the opening of still more Na+
channels, creating a positive feedback
cycle and a rapidly rising membrane voltage.
3
Na+ channels close when the cell
depolarizes, and the voltage peaks at
nearly +30 mV.
4
Ca2+ entering through slow Ca2+
channels prolongs depolarization of
membrane, creating a plateau. Plateau falls
slightly because of some K+ leakage, but most
K+ channels remain closed until end of
plateau.
5
Ca2+ channels close and Ca2+ is transported
out of cell. K+ channels open, and rapid K+
outflow returns membrane to its resting
potential.
Myocardial
relaxation
–20
–40
1
5
Action
potential
2
Myocardial
contraction
–60
4) Slow Ca2+ channels
open
Plateau
Absolute
refractory
period
1
0
.15
Time (sec)
.30
Figure 19.14
19-41
Action Potential of a Cardiocyte
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
• Long absolute
refractory period
3
+20
4
Membrane potential (mV)
0
- 250 msec compared to
1 – 2 msec in skeletal
muscle
- prevents wave
summation and tetanus
which would stop the
pumping action of the
heart
Plateau
2
Na+ inflow depolarizes the membrane
and triggers the opening of still more Na+
channels, creating a positive feedback
cycle and a rapidly rising membrane voltage.
3
Na+ channels close when the cell
depolarizes, and the voltage peaks at
nearly +30 mV.
4
Ca2+ entering through slow Ca2+
channels prolongs depolarization of
membrane, creating a plateau. Plateau falls
slightly because of some K+ leakage, but most
K+ channels remain closed until end of
plateau.
5
Ca2+ channels close and Ca2+ is transported
out of cell. K+ channels open, and rapid K+
outflow returns membrane to its resting
potential.
Myocardial
relaxation
2
Myocardial
contraction
–60
–80
Voltage-gated Na+ channels open.
5
Action
potential
–20
–40
1
Absolute
refractory
period
1
0
.15
Time (sec)
.30
Figure 19.14
19-41
Electrocardiogram (ECG or EKG)
• composite of all action potentials of nodal and
myocardial cells detected, amplified and recorded
by electrodes on arms, legs and chest
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
0.8 second
R
R
Millivolts
+1
PQ
ST
segment segment
T wave
P wave
0
PR Q
interval S
QT
interval
QRS interval
Figure 19.15
–1
Atria
contract
Ventricles
contract
Atria
contract
Ventricles
contract
19-42
ECG Deflections
• P wave
– SA node fires, atria depolarize and contract
– atrial systole begins 100 msec after SA signal
• QRS complex
– ventricular depolarization
– complex shape of spike due to different thickness
and shape of the two ventricles
• ST segment - ventricular systole
– plateau in myocardial action potential
• T wave
– ventricular repolarization and relaxation
19-43
Electrical Activity of Myocardium
1)
atrial depolarization begins
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Key
2)
atrial depolarization
complete (atria contracted)
Wave of
depolarization
Wave of
repolarization
R
P
P
Q
S
3)
ventricles begin to
depolarize at apex; atria
repolarize (atria relaxed)
4 Ventricular depolarization complete.
1 Atria begin depolarizing.
R
4)
ventricular depolarization
complete (ventricles
contracted)
Q
S
2 Atrial depolarization complete.
5 Ventricular repolarization begins at apex
and progresses superiorly.
R
R
5)
6)
ventricles begin to
repolarize at apex
ventricular repolarization
complete (ventricles
relaxed)
T
P
P
T
P
P
Q
3 Ventricular depolarization begins at apex
and progresses superiorly as atria repolarize.
Q
S
6 Ventricular repolarization complete; heart
is ready for the next cycle.
Figure 19.16
19-45
Normal Electrocardiogram (ECG)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
0.8 second
R
R
+1
Millivolts
PQ
segment
ST
segment
T wave
P wave
0
Q
PR
S
interval
QT
interval
QRS interval
–1
Atria
contract
Ventricles
contract
Atria
contract
Figure 19.15
Ventricles
contract
19-44
Diagnostic Value of ECG
• Abnormalities in conduction pathways
• Myocardial infarction
• Nodal damage
• Heart enlargement
• Electrolyte and hormone imbalances
19-46
Cardiac Cycle
• Cardiac Cycle - one complete contraction and
relaxation of all four chambers of the heart
• Atrial systole (contraction) occurs while
ventricles are in diastole (relaxation)
• Atrial diastole occurs while ventricles in
systole
• Quiescent Period all four chambers relaxed at
same time
• questions to solve – how does pressure affect
blood flow? and how are heart sounds
produced?
19-48
Principles of Pressure and Flow
• Two main variables that govern fluid movement:
1. Pressure - causes a fluid to flow (fluid dynamics)
– pressure gradient - pressure difference between two points
– measured
sphygmomanometer
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 Volume
increases
2. Resistance - opposes fluid flow
– great vessels have positive
blood pressure
– ventricular pressure must rise
above this resistance for blood
to flow into great vessels
2 Pressure
decreases
3 Air flows in
P1
P2>P1
Pressure gradient
P2
(a)
1 Volume
decreases
2 Pressure
increases
3 Air flows out
P1
P2<P1
Pressure gradient
(b)
P2
Figure 19.18
19-49
Pressure Gradients and Flow
• Fluid only flows down its pressure gradient from high pressure to
low pressure
• Events occurring on left side of heart
–
–
–
–
when ventricle relaxes and expands, its internal pressure falls
if bicuspid valve is open, blood flows into left ventricle
when ventricle contracts, internal pressure rises
AV valves close and the aortic valve is pushed open and blood
flows into aorta from left ventricle
• Opening and closing of valves are governed by these
pressure changes
– AV valves limp when ventricles relaxed
– semilunar valves under pressure from blood in vessels when
ventricles relaxed
19-50
Operation of Heart Valves
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Atrium
Atrioventricular
valve
Ventricle
Atrioventricular valves open
Atrioventricular valves closed
(a)
Figure 19.19
Aorta
Pulmonary
artery
Semilunar
valve
19-51
Semilunar valves open
(b)
Semilunar valves closed
Valvular Insufficiency
• Valvular Insufficiency (incompetence) - any failure of a
valve to prevent reflux (regurgitation) the backward flow of
blood
– Valvular Stenosis – cusps are stiffened and opening is
constricted by scar tissue
• result of rheumatic fever autoimmune attack on the mitral and aortic
valves
• heart overworks and may become enlarged
– Mitral Valve Prolapse – insufficiency in which one or both mitral
valve cusps bulge into atria during ventricular contraction
• hereditary in 1 out of 40 people
• may cause chest pain and shortness of breath
– Heart Murmur – abnormal heart sound produced by regurgitation
of blood through incompetent valves
19-52
Heart Sounds
• Auscultation - listening to sounds made by body
• Two stages of heart sounds
1. First Heart Sound (S1)
• louder and longer “lubb”
• occurs with closure of AV valves
2. Second Heart Sound (S2)
• softer and sharper “dupp”
• occurs with closure of semilunar valves
19-53
Cardiac Cycle
• Four Phases of Cardiac Cycle
1. Ventricular Filling
2. Isovolumetric Contraction
3. Ventricular Ejection
4. Isovolumetric Relaxation
• Total duration of the cardiac cycle is 0.8
sec in a heart beating 75 bpm
19-54
1. Ventricular Filling
• During diastole, ventricles expand
– their pressure drops below that of the atria
– AV valves open and blood flows into the ventricles
• Ventricular filling occurs in three phases:
– rapid ventricular filling - first one-third
• blood enters very quickly
– diastasis - second one-third
• marked by slower filling
• P wave occurs at the end of diastasis
– atrial systole - final one-third
• atria contract
• End-diastolic volume (EDV) – amount of blood
contained in each ventricle at the end of ventricular filling
– 130 mL of blood
19-55
2. Isovolumetric Contraction
• Atria repolarize and relax
– remain in diastole for the rest of the cardiac cycle
• Ventricles depolarize, create the QRS complex, and
begin to contract
• AV valves close as ventricular blood surges back
against the cusps
• Heart sound S1 occurs at the beginning of this phase
• ‘Isovolumetric’ because even though the ventricles
contract, they do not eject blood
– because pressure in the aorta (80 mm Hg) and in pulmonary
trunk (10 mm Hg) is still greater than in the ventricles
• Cardiocytes exert force, but with all four valves closed,
19-56
3. Ventricular Ejection
• Ejection of blood begins when the ventricular pressure exceeds arterial
pressure and forces semilunar valves open
– pressure peaks in left ventricle at about 120 mm Hg and 25 mm Hg
the right
in
• Blood spurts out of each ventricle rapidly at first – rapid ejection
• then more slowly under reduced pressure – reduced ejection
• ventricular ejections last about 200 – 250 msec
– corresponds to the plateau phase of the cardiac action potential
• T wave occurs late in this phase
• stroke volume (SV) of about 70 mL of blood is ejected of the 130 mL in
each ventricle
– ejection fraction of about 54%
– as high as 90% in vigorous exercise
19-57
4. Isovolumetric Relaxation
• early ventricular diastole
– when T wave ends and the ventricles begin to expand
• elastic recoil and expansion would cause pressure to
drop rapidly and suck blood into the ventricles
– blood from the aorta and pulmonary briefly flows backwards
– filling the semilunar valves and closing the cusps
– creates a slight pressure rebound that appears as the dicrotic
notch of the aortic pressure curve
– heart sound S2 occurs as blood rebounds from the closed
semilunar valves and the ventricle expands
– ‘isovolumetric’ because semilunar valves are closed and AV
valves have not yet opened
• ventricles are therefore taking in no blood
– when AV valves open, ventricular filling begins again
19-58
Major Events of Cardiac Cycle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Diastole
120
100
Pressure (mm Hg)
Systole
Diastole
• ventricular
filling
Aortic
pressure
Aortic
valve
opens
80
Left
ventricular
pressure
60
AV
valve
closes
40
Left atrial
pressure
20
Aortic valve
closes
(dicrotic notch)
AV
valve
opens
0
Ventricular
volume (mL)
• isovolumetric
contraction
End-diastolic
volume
120
90
60
End-systolic volume
R
R
T
P
P
ECG
Q
Q
S
S
• ventricular
ejection
Heart
sounds
S2
S3
Phase of
cardiac cycle
1a
0
S1
1b
.2
1c
.4
Ventricular filling
1a Rapid filling
1b Diastasis
1c Atrial systole
2
S2
3
4
.6
.8
Time (sec)
2
Isovolumetric
contraction
S3
1a
S1
1b
.2
1c
2
.4
3
Ventricular
ejection
4
Isovolumetric
relaxation
• isovolumetric
relaxation
Figure 19.20
19-60
Unbalanced Ventricular Output
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 Right ventricular
output exceeds left
ventricular output.
2 Pressure backs up.
3 Fluid accumulates in
pulmonary tissue.
pulmonary edema
1
2
3
Figure 19.21a
19-62
(a) Pulmonary edema
Unbalanced Ventricular Output
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 Left ventricular
output exceeds right
ventricular output.
2 Pressure backs up.
3 Fluid accumulates in
systemic tissue.
peripheral edema
1
2
3
(b) Systemic edema
Figure 19.21b
19-63
Congestive Heart Failure
• Congestive Heart Failure (CHF) - results from the failure
of either ventricle to eject blood effectively
– usually due to a heart weakened by myocardial infarction, chronic
hypertension, valvular insufficiency, or congenital defects in heart
structure.
• Left Ventricular Failure – blood backs up into the lungs
causing pulmonary edema
– shortness of breath or sense of suffocation
• Right Ventricular Failure – blood backs up in the vena
cava causing systemic or generalized edema
– enlargement of the liver, ascites (pooling of fluid in abdominal
cavity), distension of jugular veins, swelling of the fingers, ankles,
and feet
19-64
• Leads to total heart failure
Cardiac Output (CO)
• Cardiac Output (CO) – the amount ejected by ventricle in
1 minute
– about 4 to 6 L/min at rest
CO = HR x SV
Cardiac Output = Heart Rate x Strove Volume
• Cardiac Output is directly proportional the Heat Rate and
Stroke Volume
• Cardiac Reserve – the difference between a person’s
maximum and resting CO
– increases with fitness, decreases with disease
19-65
Heart Rate
• Pulse – surge of pressure produced by each heart beat
that can be felt by palpating a superficial artery with the
fingertips
–
–
–
–
infants have HR of 120 bpm or more
young adult females avg. 72 - 80 bpm
young adult males avg. 64 to 72 bpm
heart rate rises again in the elderly
• Tachycardia - resting adult heart rate above 100 bpm
– stress, anxiety, drugs, heart disease, or fever
– loss of blood or damage to myocardium
• Bradycardia - resting adult heart rate of less than 60 bpm
– in sleep, low body temperature, and endurance trained athletes
• positive chronotropic agents – factors that raise the heart rate
• negative chronotropic agents – factors that lower heart rate
19-66
Chronotropic Effects of the
Autonomic Nervous System
1. Cardiac Centers in the Reticular Formation of the
Medulla Oblongata initiate autonomic output to the heart
2. Cardiostimulatory Effect – some neurons of the cardiac
center transmit signals to the heart by way of
sympathetic pathways
3. Cardioinhibitory Effect – others transmit
parasympathetic signals by way of the vagus nerve
19-67
Chronotropic Effects of the ANS
• Sympathetic postganglionic fibers (Adrenergic)
– Release norepinephrine
– Binds to β-adrenergic fibers in the heart
– Activates c-AMP second-messenger system in cardiocytes and
nodal cells
– Leads to opening of Ca2+ channels in plasma membrane
– Increased Ca2+ inflow accelerates depolarization of SA node
– cAMP accelerates the uptake of Ca2+ by the sarcoplasmic
reticulum allowing the cardiocytes to relax more quickly
– by accelerating both contraction and relaxation, norepinephrine
and cAMP increase the heart rate as high as 230 bpm
– diastole becomes too brief for adequate filling
– both stroke volume and cardiac output are reduced
19-68
Chronotropic Effects of the ANS
• Parasympathetic Vagus Nerves (Cholinergic) inhibitory
effects on the SA and AV nodes
– Acetylcholine (ACh) binds to muscarinic receptors
– opens K+ gates in the nodal cells
– as K+ leaves the cells, they become hyperpolarized and fire less
frequently
– heart slows down
– Parasympathetics do not need a second messenger system
• Vagal Tone – holds down heart rate to 70 – 80 bpm at
rest
– steady background firing rate of the vagus nerves
– without influence from the cardiac centers, the heart has a
intrinsic “natural” firing rate of 100 bpm
19-69
Inputs to Cardiac Center
• Cardiac centers in the Medulla receive input from many
sources and integrate it into the ‘decision’ to speed or
slow the heart
• Medulla receives input from muscles, joints, arteries, and
brainstem
– Proprioceptors in the muscles and joints
• inform cardiac center about changes in activity, HR increases before
metabolic demands of muscle arise
– Paroreceptors signal cardiac center
• pressure sensors in aorta and internal carotid arteries
• blood pressure decreases, signal rate drops, cardiac center
increases heart rate
• if blood pressure increases, signal rate rises, cardiac center
decreases heart rate
19-70
Inputs to Cardiac Center
• Higher Brain Centers affect heart
rate
– cerebral cortex, limbic system, hypothalamus
• sensory or emotional stimuli
Inputs to Cardiac Center
– Chemoreceptors
• in aortic arch, carotid arteries and medulla oblongata
• sensitive to blood pH, CO2 and O2 levels
• more important in respiratory control than cardiac control
– if CO2 accumulates in blood or CSF (hypercapnia), reacts with water
and causes increase in H+ levels
– H+ lowers the pH of the blood possibly creating acidosis (pH < 7.35)
• hypercapnia and acidosis stimulate the cardiac center to
increase heart rate
• also respond to hypoxemia – oxygen deficiency in the blood
– usually slows down the heart
• chemoreflexes and baroreflexes, responses to
fluctuation in blood chemistry, are both negative
feedback loops
19-71
Chronotropic Chemicals
• Chemicals affect heart rate as well as
neurotransmitters from cardiac nerves
– blood born adrenal catecholamines (NE and
epinephrine) are potent cardiac stimulants
• Drugs that stimulate heart
– nicotine stimulates catecholamine secretion
– thyroid hormone increases number adrenergic
receptors on heart so more responsive to sympathetic
stimulation
– caffeine inhibits cAMP breakdown prolonging
adrenergic effect
19-72
Chronotropic Chemicals
• Electrolytes
– K+ has greatest chronotropic effect
• hyperkalemia – excess K+ in cardiocytes
– myocardium less excitable, heart rate slows and
becomes irregular
• hypokalemia – deficiency K+ in cardiocytes
– cells hyperpolarized, require increased stimulation
– Calcium
• hypercalcemia – excess of Ca2+
– decreases heart rate and contraction strength
• hypocalcemia – deficiency of Ca2+
– increases heart rate and contraction strength
19-73
Stroke Volume (SV)
CO = HR x SV
Cardiac Output = Heart Rate x Strove Volume
•Three variables govern stroke volume:
1. Preload
2. Contractility
3. Afterload
SV = EDV - ESV
Stroke Volume = End Diastolic Volume - End Systolic Volume
EDV = Capacity of blood before LV systole
EVS = Capacity of blood left in LV after systole
19-74
Stroke Volume (SV)
SV = EDV - ESV
Stroke Volume = End Diastolic Volume - End Systolic Volume
- EDV = Capacity of blood before LV systole
- EVS = Capacity of blood left in LV after systole
•
Factors that increase EDV and reduce ESV increase stroke
volume and CO
• increased preload or contractility causes increases
stroke volume
• increased afterload causes decrease stroke volume
1. Preload
• Preload – the amount of tension in ventricular
myocardium immediately before it begins to
contract
–
–
–
–
increased preload causes increased force of contraction
exercise increases venous return and stretches myocardium
cardiocytes generate more tension during contraction
increased cardiac output matches increased venous return
• Frank-Starling law of heart - SV EDV
– stroke volume is proportional to the end diastolic volume
– ventricles eject as much blood as they receive
– the more they are stretched, the harder they contract
19-75
2. Contractility
• Contractility refers to how hard the myocardium contracts
for a given preload
• Positive Inotropic Agents increase contractility
– hypercalcemia can cause strong, prolonged contractions and even
cardiac arrest in systole
– catecholamines increase calcium levels
– glucagon stimulates cAMP production
– digitalis raises intracellular calcium levels and contraction strength
• Negative Inotropic Agents reduce contractility
– hypocalcemia can cause weak, irregular heartbeat and cardiac
arrest in diastole
– hyperkalemia (high K+) reduces strength of myocardial action
potentials and the release of Ca2+ into the sarcoplasm
– vagus nerves have effect on atria but too few nerves to ventricles
for a significant effect
19-76
3. Afterload
• Afterload – the blood pressure in the aorta and
pulmonary trunk immediately distal to the semilunar
valves
– opposes the opening of these valves
– limits stroke volume
• Hypertension (High peripheral Blood Pressure
– increases afterload and opposes ventricular ejection
• Anything that impedes arterial circulation can also
increase afterload
– lung diseases that restrict pulmonary circulation
– cor pulmonale – right ventricular failure due to obstructed
pulmonary circulation
• in emphysema, chronic bronchitis, and black lung disease
19-77
How to Prepare for the Practical
• Read and Review Chapter 19, images, and the Lecture
Slides
• Read and Review Chapter 19 Lab Handout and Slides
• ID the anatomical structures listed on your lab handout
• Review blood flow
• Review www.mhhe.com/saladin5 Resources
• Review anatomical models and software in LC
• Come prepared for WET LAB
• Please see me if you object to conducting dissections or
handling pigs