Transcript Heart

Fig. 12.1
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Carotid artery
Jugular vein
Aorta
Pulmonary trunk
Heart
Brachial artery
Inferior
vena cava
Femoral
artery
and vein
Fig. 12.2
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CO2 O2
Tissue
capillaries
Circulation to
tissues of head
Lung
CO2
Pulmonary
circulation
(to lungs)
Lung
capillaries
O2
Left side
of heart
Right side of heart
Circulation to
tissues of
lower body
Tissue
capillaries
CO2
O2
Systemic
circulation
(to body)
Fig. 12.3
Copyright © McGraw-Hill Education. Permission required for reproduction or display.
Larynx
Trachea
Rib
Superior vena cava
Aortic arch
Right lung
Pulmonary trunk
Left atrium
Left lung
Right atrium
Right ventricle
Left ventricle
Rib
Midclavicular
line
2nd intercostal
space
Apex of heart
Visceral pleura
Parietal pleura
Pleural cavity
Sternum
Apex of heart
Diaphragm
5th intercostal
space
Anterior view
(a)
(b)
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Fig. 12.10
Aortic arch
Left pulmonary artery
Superior
vena cava
Branches of
right pulmonary
arteries
4
Branches of left
pulmonary arteries
4
8
Pulmonary trunk
5
Aortic semilunar
valve
Pulmonary
veins
5
Pulmonary veins
Left atrium
6
3
Pulmonary semilunar
valve
Bicuspid valve
7
1
Right atrium
Left ventricle
Tricuspid valve
2
Interventricular septum
Right ventricle
Inferior
vena cava
(a)
1
Superior and
inferior vena
cava
2
Right
atrium
Tricuspid
valve
Right
ventricle
Pulmonary
semilunar
valve
3
4
Pulmonary
trunk
Pulmonary
arteries
Coronary sinus
Cardiac veins
Body tissues
(systemic
circulation)
Lung tissue
(pulmonary
circulation)
Heart tissue
(coronary
circulation)
Coronary
arteries
Aorta
(b)
8
Aortic
semilunar
valve
Left
ventricle
Bicuspid
valve
7
6
Left
atrium
Pulmonary
veins
5
Fig. 12.5b
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Aorta
Superior vena cava
Left pulmonary artery
Right pulmonary artery
Left pulmonary veins
Right pulmonary veins
Left atrium
Right atrium
Great cardiac vein
Inferior vena cava
Coronary sinus
Right coronary artery
Left Ventricle
Small cardiac vein
Posterior interventricular artery
(in posterior interventricular sulcus)
Middle cardiac vein
(in posterior interVentricular sulcus)
Right ventricle
Apex
(c)
Posterior view
Fig. 12.13
Copyright © McGraw-Hill Education. Permission required for reproduction or display.
Striations
Branching
muscle fibers
Intercalated disks
Nucleus of cardiac
muscle cell
T tubule
LM 400x
Sarcoplasmic
reticulum
(b)
Sarcomere
T tubule
Myofilbrils
Sarcoplasmic
reticulum
Mitochondrion
Sarcolemma
(cell membrane)
Connective tissue
(a)
Sarcomere
Nucleus of
cardiac muscle
cell
Mitochondrion
Myofibrils
(c)
b: ©Ed Reschke
Fig. 12.11
Copyright © McGraw-Hill Education. Permission required for reproduction or display.
Aortic arch
Aortic arch
Superior
vena cava
Aortic
semilunar
valve
Pulmonary
trunk
Left coronary
artery
Left atrium
Circumflex
artery
Right
atrium
Right
coronary
artery
Left marginal
artery
Anterior
interventricular
artery
Posterior
interventricular
artery
Right
marginal
artery
Left ventricle
Pulmonary
trunk
Left atrium
Right
atrium
Into
right
atrium
Middle
cardiac vein
Small
cardiac
vein
Right ventricle
Right ventricle
(a)
Superior
vena cava
Anterior view
(b)
Anterior view
Posterior vein
of left ventricle
Coronary
sinus
Great
cardiac
vein
Left
ventricle
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Fig. 12.14
Skeletal Muscle
Cardiac Muscle
Repolarization
phase
2
0
Plateau
phase
0
(mV)
(mV)
1
2
1
Depolarization
phase
Depolarization
phase
–85
–85
1
2
Repolarization
phase
1
Time (ms)
2
3
500
Time (ms)
Tension
Tension
3
4
1
2
1
Time (ms)
(a)
1 Depolarization phase
• Na+ channels open.
• K+ channels begin to open.
2 Repolarization phase
• Na+ channels close.
• K+ channels continue to open, causing
repolarization.
• K+ channels close at the end of
repolarization and return the membrane
potential to its resting value.
3 Refractory period effect on tension
• Maximum tension is obtained after the
refractory period (purple shaded area)
is completed allowing for increased
tension with additional stimulation.
(b)
2
Time (ms)
500
1 Depolarization phase
• Na+ channels open.
• Ca+ channels open.
2 Plateau phase
• Na+ channels close.
• Some K+ channels open, causing
repolarization.
• Ca2+ channels are open, producing the
plateau by slowing further repolarization.
3 Repolarization phase
• Ca2+ channels close.
• Many K+ channels open.
4 Refractory period effect on tension
• Cardiac muscle contracts and relaxes almost
completely during the refractory period (purple
shaded area).
Fig. 12.9
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Cardiac skeleton
Pulmonary semilunar valve
Aortic
semilunar valve
Bicuspid
valve
Tricuspid
valve
Cardiac muscle
of the right
ventricle
Cardiac muscle
of the left ventricle
Posterior view
Fig. 12.15
Copyright © McGraw-Hill Education. Permission required for reproduction or display.
1 Action potentials originate in the sinoatrial (SA) node
and travel across the wall of the atrium (arrows) from
the SA node to the atrioventricular (AV) node.
Sinoatrial
(SA) node
Left atrium
1
Atrioventricular
(AV) node
2 Action potentials pass through the AV node and
along the atrioventricular (AV) bundle, which extends
from the AV node, through the fibrous skeleton, into
the interventricular septum.
3 The AV bundle divides into right and left bundle branches,
and action potentials descend to the apex of each ventricle
along the bundle branches.
4 Action potentials are carried by the Purkinje fibers
from the bundle branches to the ventricular walls.
2
Right and left
bundle branches
Purkinje
fibers
Left ventricle
3
Atrioventricular
(AV) bundle
4
Apex
Fig. 12.16
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QRS complex
(mV)
R
T wave
P wave
Q
S
PQ interval
QT interval
Time (seconds)
Fig. 12.6
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Aortic arch
Superior vena cava
Left pulmonary artery
Pulmonary trunk
Branches of right
pulmonary artery
Right pulmonary veins
Aortic semilunar valve
Left pulmonary veins
Right pulmonary veins
Left atrium
Pulmonary
semilunar valve
Bicuspid (mitral) valve
Right atrium
Left ventricle
Coronary sinus
Chordae tendineae
Papillary muscles
Tricuspid valve
Interventricular septum
Right ventricle
Inferior vena cava
Anterior view
Fig. 12.7
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Bicuspid
valve
Tricuspid
valve
Chordae
tendineae
Papillary
muscles
Pulmonary
trunk
Pulmonary
semilunar
valve
Aorta
Aortic semilunar
valve
Left
ventricle
Right
ventricle
Right atrium
Anterior view
(a)
Tricuspid valve
Bicuspid valve
Superior view
(b)
a: ©VideoSurgery/Science Source; b: ©Oktay Ortakcioglu/iStock/360/Getty Images RF
Fig. 12.8
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Pulmonary veins
Pulmonary veins
Left atrium
Aorta
Aorta
Left atrium
Bicuspid valve
(closed)
Bicuspid valve
(open)
Aortic semilunar
Chordae tendineae valve (open)
(tension low)
Aortic semilunar
valve (closed)
Chordae tendineae
(tension high)
Papillary muscle
(relaxed)
Papillary muscle
(contracted)
Cardiac muscle
(relaxed)
Cardiac muscle
(contracted)
Left ventricle
(relaxed)
(a)
Anterior view
(b)
Anterior view
Left ventricle
(contracted)
Fig. 12.17
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Semilunar
valves closed
Semilunar
valves closed
AV valves
opened
1 The atria and ventricles are relaxed.
AV valves open, and blood flows into
the ventricles. The ventricles fill to
approximately 70% of their volume.
AV valves
opened
2 The atria contract and complete
ventricular filling.
Semilunar
valves closed
Semilunar
valves closed
AV valves
closed
5 At the beginning of ventricular
diastole, the ventricles relax, and the
semilunar valves close (the second
heart sound).
AV valves
closed
3 Contraction of the ventricles causes
pressure in the ventricles to increase.
Almost immediately, the AV valves
close (the first heart sound). The
pressure in the ventricles continues
to increase.
Semilunar
valves opened
AV valves
closed
4 Continued ventricular contraction
causes the pressure in the ventricles
to exceed the pressure in the pulmonary
trunk and aorta. As a result, the
semilunar valves are forced open,
and blood is ejected into the
pulmonary trunk and aorta.
Fig. 12.19
Copyright © McGraw-Hill Education. Permission required for reproduction or display.
Pulmonary
semilunar
valve
Aortic
semilunar
valve
Bicuspid
valve
Tricuspid Outline
valve
of heart
©Jose Luis Pelaez Inc/Blend Images LLC RF
Fig. 12.22
Copyright © McGraw-Hill Education. Permission required for reproduction or display.
1 Sensory neurons (green) carry
action potentials from baroreceptors
to the cardioregulatory center.
Chemoreceptors in the medulla
oblongata influence the
cardioregulatory center.
Cardioregulatory center and
chemoreceptors in medulla oblongata
Sensory nerve
fibers
2 The cardioregulatory center controls
the frequency of action potentials in
the parasympathetic neurons (red )
extending to the heart. The
parasympathetic neurons decrease
the heart rate.
1
Sensory
nerve
fibers
3 The cardioregulatory center controls
the frequency of action potentials in
the sympathetic neurons (blue)
extending to the heart. The
sympathetic neurons increase the
heart rate and the stroke volume.
4 The cardioregulatory center
influences the frequency of action
potentials in the sympathetic
neurons (blue) extending to the
adrenal medulla. The sympathetic
neurons increase the secretion of
epinephrine and some
norepinephrine into the general
circulation. Epinephrine and
norepinephrine increase the heart
rate and stroke volume.
Baroreceptors
in wall of internal
carotid artery
Carotid body
chemoreceptors
Baroreceptors
in aorta
2
SA node
3
Heart
Sympathetic
nerve fibers to
adrenal gland
4
Circulation
Adrenal medulla
Epinephrine and norepinephrine
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Fig. 12.20
3
4
Actions
Baroreceptors in the carotid arteries
and aorta detect an increase in blood
pressure.
Reactions
Effectors Respond:
The SA node and cardiac
muscle decrease activity and
heart rate and stroke volume
decrease.
The cardioregulatory center in the
brain decreases sympathetic
stimulation of the heart and adrenal
medulla and increases
parasympathetic stimulation of the
heart.
5
Homeostasis Disturbed:
Blood pressure increases.
Start here
6
Homeostasis Restored:
Blood pressure decreases.
Blood pressure
(normal range)
1
Blood pressure
(normal range)
2
Homeostasis Restored:
Blood pressure increases.
Homeostasis Disturbed:
Blood pressure decreases.
Actions
Baroreceptors in the carotid arteries
and aorta detect a decrease in blood
pressure.
The cardioregulatory center in the
brain increases sympathetic
stimulation of the heart and adrenal
medulla and decreases
parasympathetic stimulation of the
heart.
Reactions
Effectors Respond:
The SA node and cardiac
muscle increase activity
and heart rate and stroke
volume increase.
Copyright © McGraw-Hill Education. Permission required for reproduction or display.
Fig. 12.21
3
4
Actions
Chemoreceptors in the medulla
oblongata detect an increase in
blood pH (often caused by a
decrease in blood CO2). Control
centers in the brain decrease
stimulation of the heart and adrenal
medulla.
Effectors Respond:
The SA node and cardiac
muscle decrease activity and
heart rate and stroke volume
decrease.
5
Homeostasis Disturbed:
Blood pH increases.
Start here
6
Homeostasis Restored:
Blood pH decreases.
Blood pH
(normal range)
1
Blood pH
(normal range)
2
Reactions
Homeostasis Restored:
Blood pH increases.
Homeostasis Disturbed:
Blood pH decreases.
Actions
Chemoreceptors in the medulla
oblongata detect a decrease in blood
pH (often caused by an increase in
blood CO2). Control centers in the
brain increase stimulation of the
heart and adrenal medulla.
Reactions
Effectors Respond:
The SA node and cardiac
muscle increase activity and
heart rate and stroke volume
increase, increasing blood flow
to the lungs.
Fig. 12A
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Occluded coronary
artery
(left): ©Hank Morgan/Science Source; (right): ©SPL/Science Source
Page 345
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MUSCULAR
URINARY
Skeletal muscle activity is reduced
because of lack of blood flow to the brain
and because blood is shunted from blood
vessels that supply skeletal muscles to
those that supply the heart and brain.
Pallor of the skin results from intense
vasoconstriction of peripheral blood
vessels, including those in the skin.
URINARY
Blood flow to the kidney decreases
dramatically in response to sympathetic
stimulation. If the kidney becomes
ischemic, the kidney tubules can be
damaged, resulting in acute renal
failure and reduced urine production.
increased blood urea nitrogen,
increased blood levels of K+, and edema
are indications that the kidneys cannot
eliminate waste products and excess
water. If damage is not too great, the
period of reduced urine production
may last up to 3 weeks; then the rate
of urine production slowly returns to
normal as the kidney tubules heal.
DIGESTIVE
Intense sympathetic stimulation
reduces blood flow to the digestive
system to very low levels, which
often results in nausea and vomiting.
Myocardial
Infarctions
Symptoms
Chest pain that radiates down left arm
Tightness and pressure in chest
Difficulty breathing
Nausea and vomiting
Dizziness and fatigue
Treatment
Restore blood flow to cardiac muscle
Medication to reduce blood clotting
(aspirin) and increase blood flow (t-Pa)
Supplemental O2 to restore normal
O2 to heart tissue
Prevention and control of
hypertension
Angioplasty or bypass surgery
NERVOUS
Decreased blood flow to the brain, decreased
blood pressure, and pain due to ischemia of
heart muscle result in increased sympathetic
and parasympathetic stimulation of the
heart. Loss of consciousness occurs when
the blood flow to the brain decreases so that
not enough O2 is available to maintain normal
brain function, especially in the reticular
activating system.
ENDOCRINE
When blood pressure becomes
low, antidiuretic hormone (ADH) is
released from the posterior pituitary
gland, and renin, released from
the kidney, activates the renin
angiotensin-aldosterone mechanism.
ADH, secreted in large amounts, and
angiotensin II cause vasoconstriction
of peripheral blood vessels. ADH and
aldosterone act on the kidneys to
retain water and ions. increased blood
volume increases venous return, which
results in increased stroke volume and
blood pressure unless damage to the
heart is very severe.
LYMPHATIC AND IMMUNE
RESPIRATORY
Decreased blood pressure results in decreased blood flow to the lungs. the decrease in gas exchange
leads to increased blood co2 levels, acidosis, and decreased blood O2 levels. Initially, respiration
becomes deep and labored because of the elevated CO2 levels, decreased blood pH, and depressed
O2 levels. If the blood O2 levels decrease too much, the person loses consciousness. Pulmonary
edema can result when the pumping effectiveness of the left ventricle is substantially reduced..
White blood cells, including
macrophages, move to the area of
cardiac muscle damage and phagocytize
any dead cardiac muscle cells.