Chapter 19: Part 2
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Transcript Chapter 19: Part 2
Amount ejected by ventricle in 1 minute
Cardiac Output = Heart Rate x Stroke Volume
Cardiac reserve: difference between a persons
maximum and resting CO
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
Pulse = surge of pressure in artery
Tachycardia: resting adult HR above 100
stress, anxiety, drugs, heart disease or body temp.
Bradycardia: resting adult HR < 60
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
Positive chronotropic agents HR
Negative chronotropic agents HR
Cardiac center of medulla oblongata
19-3
an autonomic control center with two neuronal pools: a
cardioacceleratory center (sympathetic), and a
cardioinhibitory center (parasympathetic)
Cardioacceleratory center
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)
Cardioinhibitory center stimulates vagus nerves
right vagus nerve - SA node
left vagus nerve - AV node
secretes ACH (acetylcholine) which binds to muscarinic
receptors
nodal cells hyperpolarized, HR slows
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
Higher brain centers affect HR
cerebral cortex, limbic system, hypothalamus
sensory or emotional stimuli (rollercoaster, IRS audit)
Proprioceptors
inform cardiac center about changes in activity, HR
before metabolic demands arise
Baroreceptors signal cardiac center
aorta and internal carotid arteries
pressure , signal rate drops, cardiac center HR
if pressure , signal rate rises, cardiac center HR
19-6
Chemoreceptors
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
Affect heart rate
Neurotransmitters - cAMP 2nd messenger
catecholamines (NE and epinephrine)
potent cardiac stimulants
Drugs
Hormones
19-8
caffeine inhibits cAMP breakdown
nicotine stimulates catecholamine secretion
TH adrenergic receptors in heart, sensitivity
to sympathetic stimulation, HR
Electrolytes
K+ has greatest effect
hyperkalemia
myocardium less excitable, HR slow and irregular
hypokalemia
cells hyperpolarized, requires increased stimulation
Calcium
hypercalcemia
decreases HR
hypocalcemia
increases HR
19-9
Governed by three factors:
preload
2. contractility
3. afterload
1.
Example
19-10
preload or contractility causes SV
afterload causes SV
Amount of tension in ventricular myocardium
before it contracts
preload causes force of contraction
Frank-Starling law of heart - SV EDV
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
Contraction force for a given preload
Positive inotropic agents
factors that contractility
hypercalcemia, catecholamines, glucagon, digitalis
Negative inotropic agents
factors that contractility are
hyperkalemia, hypocalcemia
19-12
Pressure in arteries above semilunar valves
opposes opening of valves
afterload SV
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
What’s the difference
between arteries and
veins?
It’s NOT oxygen
saturation!
If the heart is the
body’s “pump,” then
the “plumbing” is the
system of arteries,
veins, and capillaries.
Arteries carry blood
away from the heart.
Veins carry blood
toward the heart.
Capillaries allow for
exchange between the
bloodstream and tissue
cells.
Most common route
heart arteries arterioles
capillaries venules veins
Portal system
20-17
blood flows through two
consecutive capillary
networks before returning to
heart
hypothalamus - anterior
pituitary
found in kidneys
between intestines - liver
Point where 2 blood
vessels merge
Arteriovenous shunt
Venous anastomosis
artery flows directly into
vein
most common, blockage
less serious
alternate drainage of organs
Arterial anastomosis
20-18
collateral circulation
(coronary)
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
20-19
physical principles of blood flow based on pressure and
resistance
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
Mean arterial pressure (MAP) is an estimate of
tissue perfusion:
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
Importance of arterial elasticity
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
Hypertension
chronic resting BP > 140/90
consequences
can weaken small arteries and cause aneurysms
Hypotension
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
Blood viscosity - by RBC’s and albumin
Vessel length
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
20-24
20-25
Local control
Neural control
Hormonal control
Local control
20-26
Autoregulation – the ability of tissues to regulate their own
blood supply.
Metabolic wastes stimulate vasodilation
Neural control
Hormonal control
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
20-27
Changes in BP detected by stretch receptors
(baroreceptors), in large arteries above heart
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
20-28
20-29