Download Body System1 Cardiovascular System

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Body System1
Cardiovascular System
Prepared by Dr.Mustafa Al-Shehabat
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Capillary Beds
Circulatory System & Blood
General & Pulmonary Circulation
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Note Pulmonary arteries and veins (the exceptions)
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Location of the Heart
 Heart is located in the
mediastinum
 area from the sternum
to the vertebral column
and between the lungs
Heart Anatomy
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Fig.20.02b
Pericardial Layers of the Heart
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Heart Wall
 Epicardium – visceral layer of the serous pericardium
 Myocardium – cardiac muscle layer
 Endocardium – endothelial layer of the inner myocardial surface
External Heart: Major Vessels of the Heart
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Vessels returning blood to the heart include:
 Right and left pulmonary veins
 Superior and inferior venae cavae
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Vessels conveying blood away from the heart
include:
 Aorta
 Right and left pulmonary arteries
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Atria of the Heart
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Atria are the receiving chambers of the heart
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Blood enters right atria from superior and inferior venae
cavae and coronary sinus
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Blood enters left atria from pulmonary veins
Ventricles of the Heart
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Ventricles are the discharging chambers of the heart
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Right ventricle pumps blood into the pulmonary trunk
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Left ventricle pumps blood into the aorta
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Chambers
Borders
Surfaces
Sulci
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Heart Valves
One Way Direction
Atrioventricular Valves
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A-V valves open and allow blood to
flow from atria into ventricles when
ventricular pressure is lower than
atrial pressure
– occurs when ventricles are
relaxed, chordae tendineae are
slack and papillary muscles are
relaxed
•A-V valves close preventing backflow of
blood into atria
–occurs when ventricles contract,
pushing valve cusps closed, chordae
tendinae are pulled taut and papillary
muscles contract to pull cords and
prevent cusps from everting
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Fig. 20.06a,b
•
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Semilunar Valves
SL valves open with ventricular contraction
– allow blood to flow into pulmonary trunk and aorta
SL valves close with ventricular relaxation
– prevents blood from returning to ventricles, blood
fills valve cusps, tightly closing the SL valves
Aortic Sinuses
Nodule of semiluar
valve
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Right Atrium
• Receives All Venous Blood (front and behind).
•
Interatrial septum partitions the atria
musculi pectinati
(pectinate muscles)
Crista Terminalis
Right Ventricle
Forms most of anterior surface of heart
Interventricular septum: partitions ventricles
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Infindibulum
Tricuspid valve
Blood flows through into right ventricle
has three cusps composed of dense CT covered by endocardium
Pulmonary semilunar valve: blood flows into pulmonary trunk
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Left Ventricle
Forms the apex of heart
Bicuspid (Mitral) valve: blood passes through into left ventricle
has two cusps
Chordae tendineae anchor bicuspid valve to papillary muscles
(also has trabeculae carneae like right ventricle)
Aortic semilunar valve:
blood passes through valve into the ascending aorta
just above valve are the openings to the coronary arteries
Interventricular septum
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Cardiac cycle
Pathway of Blood Through the Heart and Lungs
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Heart Sounds
• Sounds of heartbeat
are from turbulence
in blood flow caused
by valve closure
– first heart sound
(lubb) is created with
the closing of the
atrioventricular valves
– second heart sound
(dupp) is created with
the closing of
semilunar valves
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The A-V valves
The Tricuspid valve and the mitral valve
The Semilunar valves
The aortic and the pulmonary artery valves
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Figure 9-1 Structure of the heart, and course of blood flow through the
heart chambers and heart valves.
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Figure 12-2
The heart is the pump
that propels the
blood through
the systemic and
pulmonary circuits.
Red color indicates
blood that is
fully oxygenated.
Blue color represents
blood that is only
partially oxygenated.
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Figure 12-3
The distribution of blood
in a comfortable, resting
person is shown here.
Dynamic adjustments in
blood delivery allow a
person to respond to
widely varying
circumstances,
including emergencies.
Figure 12-61
Dynamic adjustments
in blood-flow distribution
during exercise result
from changes in cardiac
output
and from changes in
regional
vasodilation/vasoconstric
tion.
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Figure 9-2 "Syncytial," interconnecting nature of cardiac muscle fibers.
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Figure 9-3 Rhythmical action potentials (in millivolts) from a Purkinje fiber and
from a ventricular muscle fiber, recorded by means of microelectrodes.
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Figure 12-17
The prolonged refractory period of cardiac muscle
prevents tetanus, and allows time for ventricles to
fill with blood prior to pumping.
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Figure 9-5 Events of the cardiac cycle for left ventricular function, showing changes in left
atrial pressure, left ventricular pressure, aortic pressure, ventricular volume, the
electrocardiogram, and the phonocardiogram.
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Figure 12-18
Systole:
ventricles contracting
Diastole:
ventricles relaxed
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Figure 12-19
Pressure and volume changes in the
left heart during a contraction cycle.
Figure 12-20
Pressure changes in the right heart during a contraction cycle.
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Figure 12-4
Though pressure is higher in the lower “tube,” the flow rates
in the pair of tubes is identical because they both have the
same pressure difference (90 mm Hg) between points P1 and P2.
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Figure 12-11
The sinoatrial node is
the heart’s pacemaker
because it initiates
each wave of excitation
with atrial contraction.
The action potential of a
myocardial pumping cell.
The rapid opening of voltage-gated
sodium channels is responsible for
the rapid depolarization phase.
Figure 12-12
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The Bundle of His and other parts
of the conducting system deliver
the excitation to the apex of the
heart so that ventricular contraction
occurs in an upward sweep.
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The action potential of a
myocardial pumping cell.
The prolonged “plateau” of
depolarization is due to the slow
but prolonged opening of
voltage-gated calcium channels
PLUS
closure of potassium channels.
Figure 12-12
The action potential of a
myocardial pumping cell.
Opening of potassium
channels results in the
repolarization phase.
Figure 12-12
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The action potential of a
myocardial pumping cell.
The rapid opening of voltage-gated
sodium channels is responsible for the
rapid depolarization phase.
The prolonged “plateau” of
depolarization is due to the slow
but prolonged opening of
voltage-gated calcium channels
PLUS
closure of potassium channels.
Opening of potassium
channels results in the
repolarization phase.
Figure 12-12
The action potential of an
autorhythmic cardiac cell.
Sodium ions “leaking” in through
the F-type [funny] channels
PLUS
calcium ions moving in through
the T [calcium] channels cause a
threshold graded depolarization.
The rapid opening of voltage-gated
calcium channels is responsible
for the rapid depolarization phase.
Reopening of potassium channels
PLUS
closing of calcium channels
are responsible for the
repolarization phase.
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Figure 12-13
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Figure 12-14
The relationship between the
electrocardiogram (ECG),
recorded as the difference
between currents at the left and
right wrists,
and
an action potential typical of
ventricular myocardial cells.
Figure 12-16
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Control of the Heart by the Sympathetic and Parasympathetic
Nerves
Increases HR
Increases Force of Heart Contraction
Increases Cardiac Output
Decreases HR
Decreases Strength of Heart Muscle
Pages 112-113,
and 121 from
Guyton and Hall
Figure 12-23
To speed up the heart rate:
deliver the sympathetic hormone, epinephrine, and/or
release more sympathetic neurotransmitter (norepinephrine), and/or
reduce release of parasympathetic neurotransmitter (acetylcholine).
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Figure 12-26
Sympathetic signals (norepinephrine and epinephrine) cause a stronger and
more rapid contraction and a more rapid relaxation.
Figure 12-22
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Figure 9-10 Cardiac sympathetic and parasympathetic nerves. (The vagus nerves
to the heart are parasympathetic nerves.)
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Figure 9-11 Effect on the cardiac output curve of different degrees of sympathetic
or parasympathetic stimulation.
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Figure 12-35
Sympathetic stimulation of alpha-adrenergic receptors causes
vasoconstriction to decrease blood flow to that location.
Sympathetic stimulation of beta-adrenergic receptors leads to
vasodilation to cause an increase in blood flow to that location.
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Figure 12-36
Diversity among signals that influence contraction/relaxation
in vascular circular smooth muscle implies a diversity of
receptors and transduction mechanisms.
Effects of
Function
Ions on Heart
Effect of Potassium Ions
Excess Potassium causes heart to dilate and HR to slow
Potassium decreases the resting membrane potential and result in
weak heart contraction
Effect of Calcium ions
Excess calcium causes spastic contraction
Calcium deficiency causes cardiac flaccidity
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Figure 9-12 Constancy of cardiac output up to a pressure level of 160 mm Hg. Only
when the arterial pressure rises above this normal limit does the increasing
pressure load cause the cardiac output to fall significantly.
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Figure 18-1 Anatomy of sympathetic nervous control of the circulation. Also shown by the
red dashed line is a vagus nerve that carries parasympathetic signals to the heart.
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Figure 18-2 Sympathetic innervation of the systemic circulation.
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Figure 18-3 Areas of the brain that play important roles in the nervous regulation
of the circulation. The dashed lines represent inhibitory pathways.
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Ref: Chapter 10 in Guyton and 12 in Vander
Rhythmical Excitation of the Heart
Specialized Excitatory and Conductive System of the
Heart
S-A node
A-V node
A-V bundle
Purkinjie fibers
Figure 12-10
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Figure 10-1 Sinus node, and the Purkinje system of the heart, showing also the A-V
node, atrial internodal pathways, and ventricular bundle branches.
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Figure 10-2 Rhythmical discharge of a sinus nodal fiber. Also, the sinus nodal action potential
is compared with that of a ventricular muscle fiber.
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Figure 14-2 Normal blood pressures in the different portions of the circulatory system when
a person is lying in the horizontal position.
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In response to the pulsatile contraction of the heart:
pulses of pressure move throughout the vasculature, decreasing
in amplitude with distance
Figure 12-29
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Figure 12-37
Capillary walls
are a single
endothelial cell
in thickness.
The capillary is
the primary point
exchange between
the blood and the
interstitial fluid
(ISF).
Intercellular clefts
assist the exchange.
Figure 12-38
Capillaries lack smooth muscle, but contraction/relaxation of circular smooth muscle
in upstream metarterioles and precapillary sphincters determine the volume of
blood each capillary receives.
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Figure 12-40
There are many, many capillaries, each with slow-moving
blood in it, resulting in adequate time and surface area
for exchange between the capillary blood and the ISF.
Figure 12-41
Filtration: movement of fluid and solutes out of the blood.
Absorption: movement of fluid and solutes into the blood.
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Figure 12-31
Cardiovascular Physiology
CO = HR x SV, as follows.
The heart is the pump that moves the blood. Its activity can be
expressed as “cardiac output (CO)” in reference to the amount
of blood moved per unit of time.
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Chapter 12:
Cardiovascular Physiology (cont.)
Mean arterial pressure, which drives the blood, is the sum of the diastolic
pressure plus one-third of the difference between the systolic and
diastolic pressures.
The autonomic system dynamically adjusts CO and MAP.
Blood composition and hemostasis are described.
Figure 14-3 Interrelationships among pressure, resistance, and blood flow.
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Figure 14-10 Vascular resistances: A, in series and B, in parallel.
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Figure 14-12 Effect of hematocrit on blood viscosity. (Water viscosity = 1.)
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Figure 15-11 Venous valves of the leg.
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Figure 15-7 Auscultatory method for measuring systolic and diastolic arterial
pressures.
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