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CVS - Physio
CVS - Physio
CVS - Physio
andwairi7@just.edu.jo
M2 L0
Outline
• Cardiovascular System Function
• Functional Anatomy of the Heart
• Myocardial Physiology
• Cardiac Cycle
• Cardiac Output Controls & Blood
Pressure
Cardiovascular System Function
• Functional components of the cardiovascular
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system:
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– Heart
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– Blood Vessels
– Blood
Cardiovascular System Function
• Functional Anatomy that create the
“pump”: c
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• Chambers
• Valves
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• Intrinsic Conduction System
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Myocardial Thickness and Function
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Atrioventricular Valve Function
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Semilunar Valve Function
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Intrinsic Conduction System
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• Autorhythmic cells:
– Initiate action potentials
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– Have unstable resting potentials called
pacemaker potentials
– Use calcium influx (rather than sodium) for
rising phase of the action potential
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Pacemaker and Action Potentials of the Heart
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Intrinsic Conduction System
• Consists of
“pacemaker” cells
and conduction
pathways
– Coordinate the
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contraction of the
atria and
ventricles
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The sinoatrial node is the normal pacemaker
of the heart.
1. The sinoatrial node (SA node), a small, specialized region in the right
atrial wall near the opening of the superior vena cava.
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2. The atrioventricular node (AV node), a small bundle of specialized
cardiac muscle cells located at the base of the right atrium near the septum,
just above the junction of the atria and ventricles.
4. Purkinje fibers, small terminal fibers that extend from the bundle of His
and spread throughout the ventricular myocardium.
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Heart Physiology: Sequence of Excitation
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Autorhythmic Cells (Pacemaker Cells)
• Characteristics of Pacemaker Cells
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– Unstable membrane potential
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• “bottoms out” at -60mV
• “drifts upward” to -40mV, forming a pacemaker potential
– Myogenic
• The upward “drift” allows the membrane to reach threshold
potential (-40mV) by itself
• This is due to
1. Slow leakage of K+ out & faster leakage Na+ in
» Causes slow depolarization
» Occurs through If channels (f=funny) that open at negative
membrane potentials
É and start closing as membrane
approaches threshold potential
iii 2. Ca2+ channels opening as membrane approaches threshold
» At threshold additional Ca2+ ion channels open causing more
rapid depolarization
» These deactivate shortly after and
3. Slow K+ channels open as membrane depolarizes causing an
efflux of K+ and a repolarization of membrane
Extrinsic Innervation of the Heart
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• Heart is stimulated by the
sympathetic
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Cardiac Muscle
• Characteristics
Cell
– Striated
– Short branched cells Hey go
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– Intercalated discs BE
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Summary of Action Potentials
Skeletal Muscle vs Cardiac Muscle
Electrocardiography
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Heart Sounds
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– Second sound occurs when SL valves close
at the beginning of ventricular diastole
(relaxation)
due to vibration
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Cardiac Cycle
• Cardiac cycle is the sequence of events as
blood enters the atria, leaves the
ventricles and then starts over
• Synchronizing this is the Intrinsic Electrical
Conduction System
• Influencing the rate is done by the
sympathetic and parasympathetic
divisions of the ANS
Cardiac Cycle: Coordinating the activity
• Electrical
Conduction
Pathway
Cardiac Cycle: Coordinating the activity
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Cardiac Cycle: Phases
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Cardiac Cycle
Blood Volumes & Pressure is
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Cardiac Output
• Cardiac Output (CO) is the volume pumped by
the left ventricle each minute
– influenced by
• Stroke Volume (SV)
EDV – ESV = SV
135ml – 65ml = 70ml
• Heart Rate (HR) bpm
80 bmp
– CO = SV x HR
70ml/b x 72bpm = 5040 ml/min
=5.04L/min
– How is this controlled to account for changing
conditions? (exercise, disease, stress…)
• What influences SV?
• What influences HR?
Cardiac Output
Factors influencing stroke volume
1- Pre Load HenxsRet D
The amount of stretch
within the contractile
myocardial fibers
represents the “load”
placed on the muscle
fibers before they head
contract
They respond unite
according to length-
tension patterns
observed in muscle tissue
by Frank, then by Starling
Became known as the Frank-Starling Law of the Heart
“The heart will pump all the blood that is returned to it”
• Venous return, driven by:
– Skeletal muscle pump
– Respiratory pump
– Atrial Suction
Effect of sympathetic stimulation on stroke volume.
(a) Normal stroke volume.
(b) Stroke volume during sympathetic stimulation
(c) Stroke volume with combination of sympathetic stimulation and increased end
diastolic volume.
Cardiac Output
• Influencing stroke volume
inverse proportional to
to
– Afterload Resistance
• This is the amount of pressure that is sitting on the semilunar
valves that must be overcome before ventricular ejection can
occur
• The more pressure that must be built up during Isovolumetric
ventricular contraction reduces the time that ejection can occur
– Reduces the ejection fraction (SV/EDV)
» Normal 70ml/135ml = 52%
» Elevated aortic pressure causes the reduction from normal
» 60ml/135ml = 44%
• indirect relationship
– Higher aortic pressure = lower stroke volume
• Causes?
– Elevated blood pressure
– Loss of compliance in aorta (loss of elasticity)
• Factors influencing stroke volume
– Contractility Direct 2625biond to 5
• Stronger contraction = larger stroke volume
• Due to inotropic agents
– Epinephrine, Norepinephrine, Digitalis* are (+) inotropic
agents
– ACh is a (-) inotropic agent
conflates
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thenotion
*digitalis – a cardiac glycoside drug that lowers Na +/K+ ATPase activity and
therefore the NCX transporter activity, resulting in elevated ICF Ca 2+ which
creates a stronger graded contraction.
Cardiac Output
• Inotropic Agents
Blood Flow & Blood Pressure Controls
3 4