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Amount ejected by ventricle in 1 minute
Cardiac Output = Heart Rate x Stroke Volume
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Cardiac reserve: difference between a persons
maximum and resting CO
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19-1
about 4 to 6L/min at rest
vigorous exercise  CO to 21 L/min for fit person and
up to 35 L/min for world class athlete
 with fitness,  with disease
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Pulse = surge of pressure in artery
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Tachycardia: resting adult HR above 100
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stress, anxiety, drugs, heart disease or  body temp.
Bradycardia: resting adult HR < 60
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19-2
infants have HR of 120 bpm or more
young adult females avg. 72 - 80 bpm
young adult males avg. 64 to 72 bpm
HR rises again in the elderly
in sleep and endurance trained athletes
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Positive chronotropic agents  HR
Negative chronotropic agents  HR
Cardiac center of medulla oblongata
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19-3
an autonomic control center with two neuronal pools: a
cardioacceleratory center (sympathetic), and a
cardioinhibitory center (parasympathetic)
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Cardioacceleratory center
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19-4
stimulates sympathetic cardiac nerves to SA node, AV node
and myocardium
these nerves secrete norepinephrine, which binds to adrenergic receptors in the heart
(positive chronotropic effect)
CO peaks at HR of 160 to 180 bpm
Sympathetic n.s. can  HR up to 230 bpm, (limited by
refractory period of SA node), but SV and CO  (less filling
time)
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Cardioinhibitory center stimulates vagus nerves
 right vagus nerve - SA node
 left vagus nerve - AV node
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secretes ACH (acetylcholine) which binds to muscarinic
receptors
 nodal cells hyperpolarized, HR slows
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vagal tone: background firing rate holds HR to sinus rhythm of
70 to 80 bpm
 severed vagus nerves (intrinsic rate-100bpm)
 maximum vagal stimulation  HR as low as 20 bpm
19-5
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Higher brain centers affect HR
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cerebral cortex, limbic system, hypothalamus
 sensory or emotional stimuli (rollercoaster, IRS audit)
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Proprioceptors
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inform cardiac center about changes in activity, HR 
before metabolic demands arise
Baroreceptors signal cardiac center
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aorta and internal carotid arteries
 pressure , signal rate drops, cardiac center  HR
 if pressure , signal rate rises, cardiac center  HR
19-6
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Chemoreceptors
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19-7
sensitive to blood pH, CO2 and oxygen
aortic arch, carotid arteries and medulla oblongata
primarily respiratory control, may influence HR
 CO2 (hypercapnia) causes  H+ levels, may create acidosis
(pH < 7.35)
Hypercapnia and acidosis stimulates cardiac center to  HR
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Affect heart rate
Neurotransmitters - cAMP 2nd messenger
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catecholamines (NE and epinephrine)
 potent cardiac stimulants
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Drugs
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Hormones
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19-8
caffeine inhibits cAMP breakdown
nicotine stimulates catecholamine secretion
TH  adrenergic receptors in heart,  sensitivity
to sympathetic stimulation,  HR
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Electrolytes
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K+ has greatest effect
 hyperkalemia
 myocardium less excitable, HR slow and irregular
 hypokalemia
 cells hyperpolarized, requires increased stimulation
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Calcium
 hypercalcemia
 decreases HR
 hypocalcemia
 increases HR
19-9
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Governed by three factors:
preload
2. contractility
3. afterload
1.
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Example
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19-10
 preload or contractility causes  SV
 afterload causes  SV
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Amount of tension in ventricular myocardium
before it contracts
 preload causes  force of contraction
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Frank-Starling law of heart - SV EDV
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19-11
exercise  venous return, stretches myocardium (
preload) , myocytes generate more tension during
contraction,  CO matches  venous return
ventricles eject as much blood as they receive
 more they are stretched ( preload) the harder they contract
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Contraction force for a given preload
Positive inotropic agents
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factors that  contractility
 hypercalcemia, catecholamines, glucagon, digitalis
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Negative inotropic agents
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factors that  contractility are
 hyperkalemia, hypocalcemia
19-12
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Pressure in arteries above semilunar valves
opposes opening of valves
 afterload  SV
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19-13
any impedance in arterial circulation  afterload
Continuous  in afterload (lung disease,
atherosclerosis, etc.) causes hypertrophy of
myocardium, may lead it to weaken and fail
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What’s the difference
between arteries and
veins?
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It’s NOT oxygen
saturation!
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If the heart is the
body’s “pump,” then
the “plumbing” is the
system of arteries,
veins, and capillaries.
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Arteries carry blood
away from the heart.
Veins carry blood
toward the heart.
Capillaries allow for
exchange between the
bloodstream and tissue
cells.
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Most common route
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heart  arteries  arterioles 
capillaries  venules  veins
Portal system
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20-17
blood flows through two
consecutive capillary
networks before returning to
heart
 hypothalamus - anterior
pituitary
 found in kidneys
 between intestines - liver
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Point where 2 blood
vessels merge
Arteriovenous shunt
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Venous anastomosis
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artery flows directly into
vein
most common, blockage
less serious
alternate drainage of organs
Arterial anastomosis
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20-18
collateral circulation
(coronary)
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Blood flow: amount of blood flowing through a tissue
in a given time (ml/min)
Perfusion: rate of blood flow per given mass of tissue
(ml/min/g)
Important for delivery of nutrients and oxygen, and
removal of metabolic wastes
Hemodynamics
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20-19
physical principles of blood flow based on pressure and
resistance
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Force that blood exerts against a vessel wall
Measured at brachial artery of arm
Systolic pressure: BP during ventricular systole
Diastolic pressure: BP during ventricular diastole
Normal value, young adult: 120/75 mm Hg
Pulse pressure: systolic - diastolic
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Mean arterial pressure (MAP) is an estimate of
tissue perfusion:
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20-20
important measure of stress exerted on small arteries
Formula is: MAP ≈ DP + ⅓(DP-SP)
Less than 60 mmHg leads to tissue damage
20-21
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Importance of arterial elasticity
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20-22
expansion and recoil maintains steady flow of blood
throughout cardiac cycle, smoothes out pressure
fluctuations and  stress on small arteries
BP rises with age: arteries less distensible
BP determined by cardiac output, blood volume
and peripheral resistance
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Hypertension
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chronic resting BP > 140/90
consequences
 can weaken small arteries and cause aneurysms
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Hypotension
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chronic low resting BP
caused by blood loss, dehydration, anemia
An aneurysm (or aneurism) is a localized, blood-filled
dilation (balloon-like bulge) of a blood vessel caused by
disease or weakening of the vessel wall. Most common in
the aorta and the arteries at the base of the brain.
20-23
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Blood viscosity - by RBC’s and albumin
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Vessel length
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 viscosity with anemia, hypoproteinemia
 viscosity with polycythemia , dehydration
pressure and flow  with distance (friction)
Vessel radius - very powerful influence over flow (ml/min)
most adjustable variable, controls resistance quickly
 vasoconstriction and vasodilation
 arterioles can constrict to 1/3 of fully relaxed radius
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20-24
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20-25
Local control
Neural control
Hormonal control
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Local control
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20-26
Autoregulation – the ability of tissues to regulate their own
blood supply.
Metabolic wastes stimulate vasodilation
Neural control
Hormonal control
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Vasomotor center of medulla oblongata:
sympathetic control stimulates most vessels to
constrict, but dilates vessels in skeletal and
cardiac muscle
 integrates three autonomic reflexes
 baroreflexes (pressure)
 chemoreflexes (esp. pH)
 medullary ischemic reflex (brain perfusion)
 stress, pain, anger
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20-27
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Changes in BP detected by stretch receptors
(baroreceptors), in large arteries above heart
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aortic arch
aortic sinuses (behind aortic valve cusps)
carotid sinus (base of each internal carotid artery)
Autonomic negative feedback response
baroreceptors send constant signals to brainstem
  BP causes rate of signals to rise, inhibits vasomotor center,
 sympathetic tone, vasodilation causes BP 
  BP causes rate of signals to drop, excites vasomotor center,
 sympathetic tone, vasoconstriction and BP 
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20-28
20-29