Download The Nervous System

Overview of the Cardiovascular System
Topics to be addressed:
Blood
Anatomy of Blood Vessels
Anatomy of the Heart
The Conduction System
The Cardiac Cycle
Cardiodynamics
Blood Flow and its Regulation
Adaptation and Disorders of the Cardiovascular System
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Cardiodynamics:
Control of Cardiac Output
Cardiac Output = the volume of blood pumped by the left ventricle in one minute
= number of beats/minute X volume pumped with each beat
= Heart Rate X Stroke Volume
CO = HR X SV
Determines oxygen available to tissues
Typically measured in ml/min or L/min
At rest, CO~5 liters/min; can rise to 30 liters/min during strenuous activity
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Cardiodynamics :
Control of Cardiac Output
Some basic terms to know
End-diastolic volume (EDV): the
amount of blood in the left
ventricle just before contraction
End-systolic volume (ESV): the
amount of blood left in the left
ventricle after contraction (it
doesn’t all get pumped)
Stroke volume (SV) : the amount
pumped out of the left ventricle
during systole
SV=EDV-ESV
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Cardiodynamics:
Factors that affect Cardiac Output
CO = HR X SV
HR = heart rate (beats/min)
SV = stroke volume (milliliters pumped out/beat)
CO = HR X SV
SV = EDV-ESV
CO = HR X (EDV – ESV)
Cardiac output can be adjusted with changes to one or more variables
Heart rate (speeding up or slowing down)
End diastolic volume (how much blood fills ventricle between beats)
End systolic volume (how much ventricle pumps out each beat)
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CO = HR X SV
Factors Affecting Cardiac Output:
control of heart rate
Autonomic innervation is the primary factor affecting HR
Cardiovascular center of medulla oblongata in the brainstem drives the autonomic
nervous system: one part of this, the Cardiac Center, regulates heart activity
Medulla
cardioacceleratory center
controls sympathetic neurons, causes them to release more norepinephrine at SA node
(increases heart rate); NE binds to Beta-1 adrenergic receptors on SA node cells.
cardioinhibitory center
controls parasympathetic neurons of vagus nerve, leading to acetylcholine release at SA
node (slows heart rate); ACh binds to muscarinic receptors on SA node cells.
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Autonomic Innervation of the Heart
Note that
parasympathetic fibers
innervate the SA and AV
nodes
Sympathetic fibers
innervate both nodes,
atrial muscle and
ventricular muscle
Drug Target:
Circulating epinephrine
mimics this sympathetic
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nervous system effect
HOW is heart rate controlled?
Autonomic axons adjust heart rate by slowing down or speeding up the
rate of spontaneous depolarization of pacemaker cells
Parasympathetic
Chronotropic
drugs are used
to alter heart
rate
Sympathetic
(and hormones)
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CO = HR X SV
Factors Affecting Cardiac Output:
control of stroke volume
CO = HR X SV
CO = HR X (EDV – ESV)
Stroke volume can be
adjusted by changing the
EDV, the ESV, or both
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CO = HR X SV
Factors Affecting Cardiac Output:
control of stroke volume
SV = EDV - ESV
Two main factors influence the End Diastolic Volume:
Factors that cause more blood to return to heart result in larger
fill volume (the EDV)
Filling time: duration of ventricular diastole
Longer fill time results in larger fill volume
Related to heart rate
Venous return: rate of blood flow during ventricular diastole
Vasoconstriction is a critical factor affecting venous
return
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The Sympathetic Nervous System Innervates Blood Vessels
and Controls Vessel Diameter
Sympathetic fibers are always “talking” to the smooth
muscle in the walls of blood vessels… this is called
sympathetic “tone”. This continuous rate of action
potential firing leads to continuous release of transmitter
and sustained low level of contraction of the smooth
muscle, and thus partial vasoconstriction of the vessel.
Increased sympathetic activity increases the degree of
constriction to reduce blood flow = Vasoconstriction
Decreased sympathetic activity decreases the degree of
constriction, dilating the vessel to increase blood flow
= Vasodilation
Sympathetic Transmitter: Norepinephrine
Receptor Type : Alpha-1 adrenergic
Seeley, Stevens, Tate, Anatomy & Physiology
8th ed, McGraw Hill, 2008
Usually, vasodilation of blood vessels occurs because local
chemicals in active tissues (eg. skeletal muscle) trigger the smooth
muscle cells to relax, increasing blood flow and providing more
oxygen and nutrients to the tissue.
How does vasoconstriction increase venous return?
Vasoconstriction mobilizes blood
in the capacitance vessels
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Clinical treatments to Improve Venous Return
Compression cuffs
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CO = HR X SV
Factors Affecting Cardiac Output:
control of stroke volume
SV = EDV - ESV
Three main factors influence the End Systolic Volume:
Factors that cause more blood to be pumped from ventricle affect
volume left in ventricle after systole (the EDV)
Preload :Ventricular stretching during diastole
Contractility: Force produced during contraction, at a given preload
Afterload: Tension the ventricle needs to produce to open the aortic
valve and eject blood
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Preload affects stroke volume
Preload is the degree of ventricular stretching during diastole
Directly proportional to EDV : more blood in ventricle = more stretch
Stretch affects the ability of muscle cells to produce tension
ANPS 19
Skeletal Muscle Mechanics lecture
The amount of stretch on a sarcomere influences
its ability to develop tension.
This is especially true for contractile cells of the
heart, and is called the
Frank-Starling Law of the Heart
The more blood in the ventricle, the greater the
stretch on the ventricle wall and the stronger the
contraction
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Contractility affects stroke volume
Contractility – how hard the ventricle contracts is affected by factors that
adjust calcium levels in the muscle cells
Sympathetic nervous system activity affects contraction strength
Stimulation of the sympathetic nerves causes release of norepinephrine on the
heart cells, leading the ventricles to contract with more force, and pump out
more blood (Increasing stroke volume and thus decreasing ESV)
Hormones from the bloodstream (epinephrine, norepinephrine, thyroid
hormone) affect contraction strength
Note two ways that heart function is controlled clinically:
BETA BLOCKERS : Contractile cells have Beta-1 adrenergic receptors to
respond to epinephrine and norepinephrine
CALCIUM CHANNEL BLOCKERS : decrease calcium entry or release in
contractile cells; less calcium=less actin/myosin interaction=less tension
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Afterload affects stroke volume
Afterload – the aortic pressure that must be overcome in order for the
ventricle to eject blood
Any factor that restricts arterial blood flow increases peripheral
resistance, and affects the heart as afterload
(valve stenosis, high blood pressure, atherosclerosis, etc.)
As afterload increases, stroke volume decreases, and therefore ESV
increases
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Ejection Fraction
an important clinical measure of heart function
the percentage of EDV represented by SV: a weak heart pumps out less
Example:
left ventricle volume at end of diastole (EDV): 100 ml
left ventricle volume at end of systole (ESV) : 40 ml
stroke volume (EDV-ESV) : 60 ml
ejection volume (SV/EDV) : 60%
Typical Ejection Fraction Numbers:
50-75%
Heart's pumping ability is Normal
36-49%
Heart's pumping ability is Below Normal
35% and Below
Heart's pumping ability is Low
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Review: Main Factors Affecting Cardiac Output
CO = HR X SV
CO=HR X (EDV-ESV)
1.
Heart Rate Control Factors
Autonomic nervous system (sympathetic + parasympathetic)
Circulating hormones
2. Stroke Volume Control Factors
EDV- end diastolic volume
filling time
rate of venous return
ESV- end systolic volume
preload (stretch on ventricle wall)
contractility (calcium availability within muscle cell)
afterload (downstream resistance)
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Review: Main Factors Affecting Cardiac Output
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