Note Pulmonary arteries and veins the exceptions Heart is located in the mediastinum area from the sternum to the vertebral column and between the lungs Location of the Heart Heart Anatomy ID: 676205
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Slide1
Cardiovascular
System
mashehabat@just.edu.joSlide2Slide3
Note Pulmonary arteries and veins (the exceptions)Slide4
Heart is located in the
mediastinum
area
from the sternum to the vertebral column and
between
the lungs
Location of the HeartSlide5
Heart AnatomySlide6
Fig.20.02bSlide7
Pericardial Layers of the HeartSlide8
Heart Wall
Epicardium – visceral layer of the serous pericardium
Myocardium – cardiac muscle layer
Endocardium – endothelial layer of the inner myocardial surfaceSlide9
Vessels returning blood to the heart include:
Right and left pulmonary veins
Superior and inferior venae cavae
Vessels conveying blood away from the heart include:
Aorta
Right and left pulmonary arteries
External Heart: Major Vessels of the Heart Slide10
Atria of the Heart
Atria are the receiving chambers of the heart
Blood enters right atria from superior and inferior venae cavae and coronary sinus
Blood enters left atria from pulmonary veinsSlide11
Ventricles of the Heart
Ventricles are the discharging chambers of the heart
Right ventricle pumps blood into the pulmonary trunk
Left ventricle pumps blood into the aortaSlide12
Chambers
Borders
Surfaces
SulciSlide13Slide14
Heart Valves
One Way DirectionSlide15
Atrioventricular Valves
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 evertingSlide16
Fig. 20.06a,bSlide17
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
valveSlide18
Right Atrium
Receives All Venous Blood (front and behind).
Interatrial septum
partitions the atria
musculi pectinati
(pectinate muscles)
Crista Terminalis
Slide19
Infindibulum
Right Ventricle
Tricuspid valve
Blood flows through into right ventricle
has three cusps composed of dense CT covered by endocardium
Forms most of anterior surface of heart
Interventricular septum:
partitions ventricles
Pulmonary semilunar valve:
blood flows into pulmonary trunk Slide20
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 arteriesSlide21
Interventricular septumSlide22
Cardiac cycleSlide23
Pathway of Blood Through the Heart and LungsSlide24Slide25
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 valvesSlide26Slide27
The A-V valves
The Tricuspid valve and the mitral valve
The Semilunar valves
The aortic and the pulmonary artery valvesSlide28
Figure 9-1 Structure of the heart, and course of blood flow through the heart chambers and heart valves.
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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 representsblood that is only
partially oxygenated.
Figure 12-2Slide30
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 12-3Slide31
Dynamic adjustments
in blood-flow distribution
during exercise result from changes in cardiac output
and from changes in regional
vasodilation/vasoconstriction.
Figure 12-61Slide32Slide33
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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The prolonged refractory period of cardiac muscle
prevents tetanus, and allows time for ventricles to
fill with blood prior to pumping.
Figure 12-17Slide36
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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Systole:
ventricles contracting
Diastole:
ventricles relaxed
Figure 12-18Slide38
Pressure and volume changes in the left heart during a contraction cycle.
Figure 12-19Slide39
Pressure changes in the right heart during a contraction cycle.
Figure 12-20Slide40
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 P
1
and P
2
.
Figure 12-4Slide41Slide42
The sinoatrial node is
the heart’s pacemaker
because it initiates
each wave of excitation
with atrial contraction.
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.
Figure 12-11Slide43
Figure 12-12
The action potential of a
myocardial pumping cell.
The rapid opening of voltage-gated sodium channels is responsible for the rapid depolarization phase. Slide44
Figure 12-12
The prolonged “plateau” of
depolarization is due to
the slow
but prolonged opening of
voltage-gated calcium channels
PLUS
closure of potassium channels.
The action potential of a
myocardial pumping cell.Slide45
Figure 12-12
Opening of potassium
channels results in the
repolarization phase.
The action potential of a
myocardial pumping cell.Slide46
Figure 12-12
The action potential of a
myocardial pumping cell.
Opening of potassium
channels results in the
repolarization phase.
The prolonged “plateau” of
depolarization is due to
the slow
but prolonged opening of
voltage-gated calcium channels
PLUS
closure of potassium channels.
The rapid opening of voltage-gated sodium channels is responsible for the rapid depolarization phase. Slide47
Figure 12-13
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.
The action potential of an
autorhythmic cardiac cell.Slide48
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 12-14Slide49
Figure 12-16Slide50
Control of the Heart by the Sympathetic and Parasympathetic Nerves
Sympathetic stimulation
(
Norepinephrine
& Epinephrine)
Increases HR
Increases Force of Heart Contraction
Increases Cardiac Output
Parasympathetic Stimulation
Decreases HR
Decreases Strength of Heart Muscle
Pages 112-113, and 121 from Guyton and HallSlide51
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).
Figure 12-23Slide52
Sympathetic signals (norepinephrine and epinephrine) cause a stronger and more rapid contraction
and
a more rapid relaxation.
Figure 12-26Slide53
Figure 12-22Slide54
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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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.
Figure 12-35Slide58
Diversity among signals that influence contraction/relaxation
in vascular circular smooth muscle implies a diversity of
receptors and transduction mechanisms.
Figure 12-36Slide59
Effects of
Potassium and Calcium
Ions on Heart Function
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 Slide60
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 fibersSlide65
Figure 12-10Slide66
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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Figure 12-29
In response to the pulsatile contraction of the heart:
pulses of pressure move throughout the vasculature, decreasing in amplitude with distance Slide70
The capillary is
the primary point exchange between the blood and the
interstitial fluid (ISF).
Intercellular clefts assist the exchange.
Capillary walls
are a single
endothelial cell
in thickness.
Figure 12-37Slide71
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.
Figure 12-38Slide72
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 12-40Slide73
Absorption: movement of fluid and solutes into the blood.
Filtration: movement of fluid and solutes out of the blood.
Figure 12-41Slide74
Figure 12-31Slide75
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.Slide76
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.
Chapter 12:
Cardiovascular Physiology (cont.)
The autonomic system dynamically adjusts CO and MAP.
Blood composition and hemostasis are described.Slide77
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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