Physiology
Cardiac Output, Blood
Flow, and Blood
Pressure
ww.cambodiamed.com
Cardiac Output
Cardiac Output (CO)
Is volume of blood pumped/min by each ventricle
Heart Rate (HR) = 70 beats/min
Stroke volume (SV) = blood pumped/beat by
each ventricle
◦ Average is 70-80 ml/beat
CO = SV x HR
Total blood volume is about 5.5L
ww.cambodiamed.com
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)
• Mechanisms that affect HR: chronotropic effect
• Positive increases; negative decreases
• 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
• NE & Epi stimulate
opening of
pacemaker HCN
channels
Fig 14.1
• This depolarizes SA
faster, increasing HR
• ACh promotes
opening of K+
channels
• The resultant K+
outflow counters Na+
influx, slows
depolarization &
decreasing HR
14-6
Regulation of Cardiac Rate continued
• Vagus nerve:
• Decrease activity: increases heart rate
• Increased activity: slows heart
• 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
• SV is inversely proportional to TPR
• Ejection fraction is SV/ EDV (~80ml/130ml=62%)
• 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
• 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
Extrinsic Control of Contractility
• Parasympathetic stimulation
• Negative chronotropic effect
• Through innervation of the SA node and myocardial cell
• Slower heart rate means increased EDV
• Increases SV through Frank-Starling law
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
Venous Return continued
• Veins hold most of
blood in body (70%)
& are thus called
capacitance vessels
• Have thin walls &
stretch easily to
accommodate more
blood without
increased pressure
(=higher compliance)
• Have only 010 mm Hg pressure
Fig 14.6
14-16
Blood Volume
• Constitutes small
fraction of total body
fluid
• 2/3 of body H20 is inside
cells (intracellular
compartment)
• 1/3 total body H20 is in
extracellular
compartment
• 80% of this is interstitial
fluid; 20% is blood
plasma
Fig 14.8
14-18
Exchange of Fluid between
Capillaries & Tissues
• Distribution of ECF between blood & interstitial
compartments is in state of dynamic equilibrium
• Movement out of capillaries is driven by hydrostatic
pressure exerted against capillary wall
• Promotes formation of tissue fluid
• Net filtration pressure= hydrostatic pressure in capillary (17-37
mm Hg) - hydrostatic pressure of ECF (1 mm Hg)
14-19
Exchange of Fluid between
Capillaries & Tissues
• Movement also affected by colloid osmotic pressure
• = osmotic pressure exerted by proteins in fluid
• Difference between osmotic pressures in & outside of
capillaries (oncotic pressure) affects fluid movement
• Plasma osmotic pressure = 25 mm Hg; interstitial osmotic pressure =
0 mm Hg
14-20
Overall Fluid Movement
• Is determined by net filtration pressure & forces opposing
it (Starling forces)
• Pc + Pi (fluid out) - Pi + Pp (fluid in)
• Pc = Hydrostatic pressure in capillary
• Pi = Colloid osmotic pressure of interstitial fluid
• Pi = Hydrostatic pressure in interstitial fluid
• Pp = Colloid osmotic pressure of blood plasma
14-21
Fig 14.9
14-22
Edema
• Normally filtration, osmotic reuptake, & lymphatic
drainage maintain proper ECF levels
• Edema is excessive accumulation of ECF resulting
from:
•
•
•
•
High blood pressure
Venous obstruction
Leakage of plasma proteins into ECF
Myxedema (excess production of glycoproteins in
extracellular matrix) from hypothyroidism
• Low plasma protein levels resulting from liver disease
• Obstruction of lymphatic drainage
14-23
Regulation of Blood Volume by Kidney
• Urine formation begins with filtration of plasma in
glomerulus
• Filtrate passes through & is modified by nephron
• Volume of urine excreted can be varied by changes in
reabsorption of filtrate
• Adjusted according to needs of body by action of hormones
14-24
ADH (vasopressin)
• ADH released by Post Pit
when osmoreceptors detect
high osmolality
• From excess salt intake
or dehydration
• Causes thirst
• Stimulates H20
reabsorption from urine
• ADH release inhibited by
low osmolality
Fig 14.11
14-25
Aldosterone
• Is steroid hormone secreted by adrenal cortex
• Helps maintain blood volume & pressure through
reabsorption & retention of salt & water
• Release stimulated by salt deprivation, low blood
volume, & pressure
14-26