Download Cardiovascular Dynamics Abbreviated File

Cardiovascular dynamics-abbreviated
• For bio 260
• Source:mixed
Topics to be covered
• Chapter 18-The Heart
• Chapter 19-Blood vessels
• Physio Ex-Cardiovascular Dynamics-Print data
w/explanations.
• Physio Ex-Frog Cardiovascular Physiology-read
only.
Topics to be covered
• Chapter 18-The Heart
• Chapter 19-Blood vessels
• Physio Ex-Cardiovascular Dynamics-Print data
w/explanations.
• Physio Ex-Frog Cardiovascular Physiology-read
only.
Cardiac Output
14-3
Cardiac Output (CO)
• Is volume of blood pumped/min by each ventricle
• Stroke volume (SV) = blood pumped/beat by each
ventricle
• CO = SV x HR
• Total blood volume is about 5.5L
14-4
Regulation of Cardiac Rate
• Without neuronal influences, SA node will drive
heart at rate of its spontaneous activity
• Normally Symp & Parasymp activity influence HR
(chronotropic effect)
• Autonomic innervation of SA node is main
controller of HR
– Symp & Parasymp nerve fibers modify rate of
spontaneous depolarization
14-5
Regulation of Cardiac Rate continued
• Cardiac control center of medulla coordinates
activity of autonomic innervation
• Sympathetic endings in atria & ventricles can
stimulate increased strength of contraction
14-7
14-8
Stroke Volume
• Is determined by 3 variables:
– End diastolic volume (EDV) = volume of blood in
ventricles at end of diastole
– Total peripheral resistance (TPR) = impedance to blood
flow in arteries
– Contractility = strength of ventricular contraction
14-9
Regulation of Stroke Volume
• EDV is workload (preload) on heart prior to
contraction
– SV is directly proportional to preload & contractility
• Strength of contraction varies directly with EDV
• Total peripheral resistance = afterload which
impedes ejection from ventricle
• Ejection fraction is SV/ EDV
– Normally is 60%; useful clinical diagnostic tool
14-10
Frank-Starling Law of the Heart
• States that strength of
ventricular contraction
varies directly with
EDV
Fig 14.2
– Is an intrinsic property
of myocardium
– As EDV increases,
myocardium is
stretched more, causing
greater contraction &
SV
14-11
Frank-Starling Law of the Heart continued
• (a) is state of myocardial sarcomeres just before filling
– Actins overlap, actin-myosin interactions are reduced & contraction would be weak
• In (b, c & d) there is increasing interaction of actin & myosin allowing more
force to be developed
Fig 14.3
14-12
Extrinsic Control of Contractility
• At any given EDV,
contraction depends
upon level of
sympathoadrenal
activity
– NE & Epi produce an
increase in HR &
contraction (positive
inotropic effect)
• Due to increased Ca2+ in
sarcomeres
Fig 14.4
14-13
Fig 14.5
14-14
Venous Return
• Is return of blood to
heart via veins
• Controls EDV & thus SV
& CO
• Dependent on:
– Blood volume & venous
pressure
– Vasoconstriction
caused by Symp
– Skeletal muscle pumps
– Pressure drop during
inhalation
Fig 14.7
14-15