Download Human Physiology

Chapter 14
Cardiac Output,
Blood Flow,
and Blood
Pressure
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Cardiac Output
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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
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Regulation of Cardiac Rate
Without
neuronal influences, SA node will drive heart at
rate of its spontaneous activity
Normally Symp and Parasymp activity influence HR
(chronotropic effect)
Autonomic innervation of SA node is main controller of HR
Symp and Parasymp nerve fibers modify rate of
spontaneous depolarization
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Regulation of Cardiac Rate continued
 NE
and Epi stimulate
opening of pacemaker
HCN channels
 This depolarizes SA
faster, increasing HR
 ACH promotes opening
of K+ channels
 The resultant K+
outflow counters Na+
influx, slowing
depolarization and
decreasing HR
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14-6
Regulation of Cardiac Rate continued
Cardiac
control center of medulla coordinates activity of
autonomic innervation
Sympathetic endings in atria and ventricles can stimulate
increased strength of contraction
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14-7
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14-8
Regulation of Stroke Volume
EDV
is workload (preload) on heart prior to contraction
SV is directly proportional to preload and 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
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14-10
Frank-Starling Law of the Heart
 States
that strength of
ventricular contraction
varies directly with
EDV
 Is an intrinsic
property of
myocardium
 As EDV increases,
myocardium is
stretched more,
causing greater
contraction and SV
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14-11
Extrinsic Control of Contractility
 At
any given EDV,
contraction depends upon
level of sympathoadrenal
activity
 NE and Epi produce an
increase in HR and
contraction (positive
inotropic effect)
 Due to increased
Ca2+ in sarcomeres
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14-13
Venous Return
 Is
return of blood to heart
via veins
 Controls EDV and thus SV
and CO
 Dependent on:
 Blood volume and
venous pressure
 Vasoconstriction caused
by Symp
 Skeletal muscle pumps
 Pressure drop during
inhalation
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Venous Return continued
 Veins
hold most of blood
in body (~70%) and are
thus called capacitance
vessels
 Have thin walls and
stretch easily to
accommodate more
blood without
increased pressure
(=higher compliance)
 Have only 010 mm Hg pressure
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14-16
Blood and Body Fluid Volumes
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Blood Volume
 Constitutes small
fraction of total body fluid
 2/3 of body H2O is inside cells (intracellular compartment)
 1/3 total body H2O is in extracellular compartment
 80% of this is interstitial fluid; 20% is blood plasma
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14-18
Exchange of Fluid between Capillaries and
Tissues
Distribution of
ECF between blood and 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)
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14-19
Exchange of Fluid between Capillaries and
Tissues
Movement
also affected by colloid osmotic pressure
= osmotic pressure exerted by proteins in fluid
Difference between osmotic pressures in and outside of
capillaries (oncotic pressure) affects fluid movement
Plasma osmotic pressure = 25 mm Hg; interstitial
osmotic pressure = 0 mm Hg
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14-20
Edema
 Normally
filtration, osmotic reuptake, and 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
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14-23
Regulation of Blood Volume by Kidney
Urine
formation begins with filtration of plasma in
glomerulus
Filtrate passes through and 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
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ADH (vasopressin)
 ADH
released by Post Pit
when osmoreceptors detect
high osmolality
 From excess salt intake
or dehydration
 Causes thirst
 Stimulates H2O
reabsorption from urine
 ADH release inhibited by
low osmolality
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14-25
Aldosterone
Is
steroid hormone secreted by adrenal cortex
Helps maintain blood volume and pressure through
reabsorption and retention of salt and water
Release stimulated by salt deprivation, low blood volume,
and pressure
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14-26
Renin-Angiotension-Aldosterone System
When
there is a salt deficit, low blood volume, or pressure,
angiotensin II is produced
Angio II causes a number of effects all aimed at
increasing blood pressure:
Vasoconstriction, aldosterone secretion, thirst
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Factors Affecting Blood Flow
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Vascular Resistance to Blood Flow
Determines
how much blood flows through a tissue or organ
Vasodilation decreases resistance, increases blood flow
Vasoconstriction does opposite
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14-32
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Physical Laws Describing Blood Flow continued
 Mean
arterial pressure
and vascular resistance
are the 2 major factors
regulating blood flow
 Blood is shunted
from one organ to
another by degree of
constriction of their
arterioles
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14-37
Extrinsic Regulation of Blood Flow
Sympathoadrenal
activation causes increased CO and
resistance in periphery and viscera
Blood flow to skeletal muscles is increased
Because their arterioles dilate in response to Epi and
their Symp fibers release ACh which also dilates their
arterioles
Thus blood is shunted away from visceral and skin to
muscles
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14-39
Extrinsic Regulation of Blood Flow continued
Parasympathetic
effects are vasodilative
However, Parasymp only innervates digestive tract,
genitalia, and salivary glands
Thus Parasymp is not as important as Symp
Angiotenin II and ADH (at high levels) cause general
vasoconstriction of vascular smooth muscle
Which increases resistance and BP
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14-40
Aerobic Requirements of the Heart
Heart
(and brain) must receive adequate blood supply at all
times
Heart is most aerobic tissue--each myocardial cell is within
10 m of capillary
Contains lots of mitochondria and aerobic enzymes
During systole coronary, vessels are occluded
Heart gets around this by having lots of myoglobin
Myoglobin is an O2 storage molecule that releases O2
to heart during systole
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14-44
Regulation of Coronary Blood Flow
Blood
flow to heart is affected by Symp activity
NE causes vasoconstriction; Epi causes vasodilation
Dilation accompanying exercise is due mostly to intrinsic
regulation
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14-45
Regulation of Blood Flow Through Skeletal
Muscles
At
rest, flow through skeletal muscles is low because of
tonic sympathetic activity
Flow through muscles is decreased during contraction
because vessels are constricted
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14-46
Circulatory Changes During Exercise
At
beginning of exercise, Symp activity causes vasodilation
via Epi and local ACh release
Blood flow is shunted from periphery and visceral to
active skeletal muscles
Blood flow to brain stays same
As exercise continues, intrinsic regulation is major
vasodilator
Symp effects cause SV and CO to increase
HR and ejection fraction increases vascular resistance
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14-47
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Cerebral Circulation
Gets
about 15% of total resting CO
Held constant (750ml/min) over varying conditions
Because loss of consciousness occurs after few secs of
interrupted flow
Is not normally influenced by sympathetic activity
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14-50
Cerebral Circulation
Regulated
almost exclusively by intrinsic mechanisms
When BP increases, cerebral arterioles constrict; when
BP decreases, arterioles dilate (=myogenic regulation)
Arterioles dilate and constrict in response to changes in
CO2 levels
Arterioles are very sensitive to increases in local neural
activity (=metabolic regulation)
 Areas of brain with high metabolic activity receive
most blood
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14-51
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14-52
Cutaneous Blood Flow
 Skin
serves as a heat exchanger
for thermoregulation
 Skin blood flow is adjusted to
keep deep-body at 37oC
 By arterial dilation or
constriction and activity of
arteriovenous anastomoses
which control blood flow
through surface capillaries
 Symp activity closes
surface beds during cold
and fight-or-flight, and
opens them in heat and
exercise
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Blood Pressure
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Blood Pressure (BP)
 Arterioles play
role in blood distribution and control of BP
 Blood flow to capillaries and BP is controlled by aperture of arterioles
 Capillary BP is decreased because they are downstream of high
resistance arterioles
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14-55
Blood Pressure (BP)
Is
controlled mainly by volume HR, SV, and peripheral
resistance
An increase in any of these can result in increased BP
Sympathoadrenal activity raises BP via arteriole
vasoconstriction and by increased CO
Kidney plays role in BP by regulating blood volume and
thus stroke volume
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Baroreceptor Reflex
Is
activated by changes in BP
Which is detected by baroreceptors (stretch receptors)
located in aortic arch and carotid sinuses
Increase in BP causes walls of these regions to stretch,
increasing frequency of APs
Baroreceptors send APs to vasomotor and cardiac
control centers in medulla
Is most sensitive to decrease and sudden changes in BP
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14-58
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Hypertension
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Hypertension
Blood
pressure in excess of normal range for age and gender
(> 140/90 mmHg)
Afflicts about 20% of adults
Most common type is primary or essential hypertension
Caused by complex and poorly understood processes
Secondary hypertension is caused by known disease
processes
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14-67
Dangers of Hypertension
Patients
are often asymptomatic until substantial vascular
damage occurs
Contributes to atherosclerosis
Increases workload of the heart leading to ventricular
hypertrophy and congestive heart failure
Often damages cerebral blood vessels leading to stroke
These are why it is called the "silent killer"
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Treatment of Hypertension
Often
includes lifestyle changes such as cessation of
smoking, moderation in alcohol intake, weight reduction,
exercise, reduced Na+ intake, increased K+ intake
Drug treatments include diuretics to reduce fluid volume,
beta-blockers to decrease HR, calcium blockers, ACE
inhibitors to inhibit formation of Angio II, and Angio IIreceptor blockers
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Circulatory Shock
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Circulatory Shock
Occurs
when there is inadequate blood flow to, and/or O2
usage by, tissues
Cardiovascular system undergoes compensatory changes
Sometimes shock becomes irreversible and death ensues
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Hypovolemic Shock
Is
circulatory shock caused by low blood volume
E.g. from hemorrhage, dehydration, or burns
Characterized by decreased CO and BP
Compensatory responses include sympathoadrenal
activation via baroreceptor reflex
Results in low BP, rapid pulse, cold clammy skin, low
urine output
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14-73
Septic Shock
Refers
to dangerously low blood pressure resulting from
sepsis (infection)
Mortality rate is high (50-70%)
Often occurs as a result of endotoxin release from bacteria
Endotoxin induces NO production causing vasodilation
and resultant low BP
Effective treatment includes drugs that inhibit production
of NO
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Other Causes of Circulatory Shock
Severe
allergic reaction can cause a rapid fall in BP called
anaphylactic shock
Due to generalized release of histamine causing
vasodilation
Rapid fall in BP called neurogenic shock can result from
decrease in Symp tone following spinal cord damage or
anesthesia
Cardiogenic shock is common following cardiac failure
resulting from infarction that causes significant myocardial
loss
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