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Chapter 14
Cardiac Output, Blood Flow, and
Blood Pressure
14-1
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Chapter 14 Outline
Cardiac Output
Blood & Body Fluid Volumes
Factors Affecting Blood Flow
Blood Pressure
Hypertension
Circulatory Shock
14-2
Cardiac Output
14-3
Cardiac Output (CO)
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Is volume of blood pumped/min by
each ventricle
Heart Rate (HR) = 70 beats/min
Stroke volume (SV) = blood
pumped/beat by each ventricle
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Average is 70-80 ml/beat
CO = SV x HR
Total blood volume is about 5.5L
14-4
Regulation of Cardiac Rate
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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
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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
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NE & Epi stimulate
opening of
pacemaker HCN
channels
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Fig 14.1
This depolarizes SA
faster, increasing
HR
ACh promotes
opening of K+
channels
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The resultant K+
outflow counters
Na+ influx, slows
depolarization &
decreasing HR
14-6
Regulation of Cardiac Rate
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Vagus nerve:
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continued
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
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Is determined by 3 variables:
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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
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EDV is workload (preload) on heart prior to
contraction
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Strength of contraction varies directly with EDV
Total peripheral resistance = afterload which
impedes ejection from ventricle
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SV is directly proportional to preload & contractility
SV is inversely proportional to TPR
Ejection fraction is SV/ EDV (~80ml/130ml=62%)
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Normally is 60%; useful clinical diagnostic tool
14-10
Frank-Starling Law of the Heart
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States that
strength of
ventricular
contraction varies
directly with EDV
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Is an intrinsic
property of
myocardium
As EDV increases,
myocardium is
stretched more,
causing greater
contraction & SV
Fig 14.2
14-11
Frank-Starling Law of the Heart
continued
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(a) is state of myocardial
sarcomeres just before
filling
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Actins overlap, actinmyosin 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
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At any given EDV,
contraction
depends upon level
of
sympathoadrenal
activity
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NE & Epi produce
an increase in HR &
contraction (positive
inotropic effect)
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Due to increased
Ca2+ in sarcomeres
Fig 14.4
14-13
Extrinsic Control of Contractility
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Parasympathetic stimulation
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Negative chronotropic effect
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Through innervation of the SA node and
myocardial cell
Slower heart rate means increased EDV
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Increases SV through Frank-Starling law
Fig 14.5
14-14
Venous Return
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Is return of blood to
heart via veins
Controls EDV & thus
SV & CO
Dependent on:
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Blood volume & venous
pressure
Vasoconstriction caused
by Symp
Skeletal muscle pumps
Pressure drop during
inhalation
Fig 14.7
14-15
Venous Return
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continued
Veins hold most of
blood in body
(70%) & are thus
called capacitance
vessels
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Have thin walls &
stretch easily to
accommodate more
blood without
increased pressure
(=higher
compliance)
Fig 14.6
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Have only 010 mm Hg pressure
14-16
Blood & Body Fluid Volumes
14-17
Blood Volume
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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
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80% of this is
interstitial fluid; 20%
is blood plasma
Fig 14.8
14-18
Exchange of Fluid between
Capillaries & Tissues
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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
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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
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Movement also affected by colloid osmotic
pressure
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= osmotic pressure exerted by proteins in fluid
Difference between osmotic pressures in &
outside of capillaries (oncotic pressure) affects
fluid movement
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Plasma osmotic pressure = 25 mm Hg; interstitial
osmotic pressure = 0 mm Hg
14-20
Overall Fluid Movement
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Is determined by net filtration pressure & forces
opposing it (Starling forces)
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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
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Normally filtration, osmotic reuptake, &
lymphatic drainage maintain proper ECF levels
Edema is excessive accumulation of ECF
resulting from:
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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
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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
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Adjusted according to needs of body by action of
hormones
14-24
ADH (vasopressin)
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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
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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
Renin-Angiotension-Aldosterone System
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Decreased BP and flow (low blood volume)
Kidney secreted Renin (enzyme)
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Angiotensin I to AngiotensinII
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Juxaglomerular apparatus
By angiotensin-converting enzyme (ACE)
Angio II causes a number of effects all
aimed at increasing blood pressure:
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Vasoconstriction, aldosterone secretion, thirst
14-27
Angiotensin
II
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Fig 14.12
shows when
& how Angio
II is
produced, &
its effects
14-28
Atrial Natriuretic Peptide (ANP)
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Expanded blood volume is detected by
stretch receptors in left atrium &
causes release of ANP
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Inhibits aldosterone, promoting salt &
water excretion to lower blood volume
Promotes vasodilation
14-29
Factors Affecting Blood Flow
14-30
Vascular Resistance to Blood Flow
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Determines how much blood flows through a
tissue or organ
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Vasodilation decreases resistance, increases
blood flow
Vasoconstriction does opposite
14-31
14-32
Physical Laws Describing Blood Flow
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Blood flows
through vascular
system when there
is pressure
difference (DP) at
its two ends
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Flow rate is directly
proportional to
difference
(DP = P1 - P2)
Fig 14.13
14-33
Physical Laws Describing Blood Flow
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Flow rate is inversely proportional to resistance
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Flow = DP/R
Resistance is directly proportional to length of
vessel (L) & viscosity of blood ()
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Inversely proportional to 4th power of radius
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So diameter of vessel is very important for resistance
Poiseuille's Law describes factors affecting
blood flow
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Blood flow = DPr4()
L(8)
14-34
Fig 14.14. Relationship
between blood flow,
radius & resistance
14-35
Extrinsic Regulation of Blood Flow
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Sympathoadrenal activation causes
increased CO & resistance in periphery &
viscera
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Blood flow to skeletal muscles is increased
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Because their arterioles dilate in response to Epi
& their Symp fibers release ACh which also
dilates their arterioles
Thus blood is shunted away from visceral & skin
to muscles
14-36
Extrinsic Regulation of Blood Flow
continued
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Parasympathetic effects are vasodilative
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However, Parasymp only innervates
digestive tract, genitalia, & salivary glands
Thus Parasymp is not as important as Symp
Angiotensin II & ADH (at high levels)
cause general vasoconstriction of
vascular smooth muscle
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Which increases resistance & BP
14-37
Paracrine Regulation of Blood Flow
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Endothelium produces several paracrine
regulators that promote relaxation:
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Nitric oxide (NO), bradykinin, prostacyclin
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NO is involved in setting resting “tone” of vessels
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Levels are increased by Parasymp activity
Vasodilator drugs such as nitroglycerin or Viagra act
thru NO
Endothelin 1 is vasoconstrictor produced
by endothelium
14-38
Intrinsic Regulation of Blood Flow
(Autoregulation)
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Maintains fairly constant blood flow despite BP
variation
Myogenic control mechanisms occur in some
tissues because vascular smooth muscle
contracts when stretched & relaxes when not
stretched
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E.g. decreased arterial pressure causes cerebral
vessels to dilate & vice versa
14-39
Intrinsic Regulation of Blood Flow (Autoregulation)
continued
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Metabolic control mechanism matches
blood flow to local tissue needs
Low O2 or pH or high CO2, adenosine, or
K+ from high metabolism cause
vasodilation which increases blood flow (=
active hyperemia)
14-40
Aerobic Requirements of the Heart
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Heart (& brain) must receive adequate blood
supply at all times
Heart is most aerobic tissue--each myocardial
cell is within 10 m of capillary
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Contains lots of mitochondria & aerobic enzymes
During systole coronary vessels are occluded
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Heart gets around this by having lots of myoglobin
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Myoglobin is an 02 storage molecule that releases 02 to
heart during systole
14-41
Regulation of Coronary Blood Flow
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Blood flow to heart is affected by Symp
activity
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NE causes vasoconstriction; Epi causes
vasodilation
Dilation accompanying exercise is due
mostly to intrinsic regulation
14-42
Regulation of Blood Flow Through
Skeletal Muscles
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At rest, flow through skeletal muscles is low
because of tonic sympathetic activity
Flow through muscles is decreased during
contraction because vessels are constricted
14-43
Circulatory Changes During Exercise
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At beginning of exercise, Symp activity causes
vasodilation via Epi & local ACh release
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Blood flow is shunted from periphery & visceral to
active skeletal muscles
Blood flow to brain stays same
As exercise continues, intrinsic regulation is
major vasodilator
Symp effects cause SV & CO to increase
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HR & ejection fraction increases vascular resistance
14-44
Fig 14.19
14-45
Fig 14.20
14-46
Cerebral Circulation
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Gets about 15% of total resting CO
Held constant (750ml/min) over
varying conditions
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Because loss of consciousness occurs
after few secs of interrupted flow
Is not normally influenced by
sympathetic activity
14-47
Cerebral Circulation
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Is regulated almost exclusively by intrinsic
mechanisms
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When BP increases, cerebral arterioles
constrict; when BP decreases, arterioles
dilate (=myogenic regulation)
Arterioles dilate & constrict in response to
changes in C02 levels
Arterioles are very sensitive to increases in
local neural activity (=metabolic regulation)
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Areas of brain with high metabolic activity receive most
blood
14-48
Fig 14.21
14-49
Cutaneous Blood Flow
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Skin serves as a heat
exchanger for
thermoregulation
Skin blood flow is
adjusted to keep deepbody at 37oC
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By arterial dilation or
constriction & activity of
arteriovenous anastomoses
which control blood flow
through surface capillaries
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Symp activity closes surface
beds during cold & fight-orflight, & opens them in heat
& exercise
Fig 14.22
14-50
Blood Pressure
14-51
Blood Pressure (BP)
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Arterioles play role in
blood distribution &
control of BP
Blood flow to
capillaries & BP is
controlled by
aperture of arterioles
Capillary BP is
decreased because
they are downstream
of high resistance
arterioles
Fig 14.23
14-52
Blood Pressure (BP)
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Capillary BP
is also low
because of
large total
crosssectional
area
Fig 14.24
14-53
Blood Pressure (BP)
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Is controlled mainly by HR, SV, & peripheral
resistance
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An increase in any of these can result in increased
BP
Sympathoadrenal activity raises BP via arteriole
vasoconstriction & by increased CO
Kidney plays role in BP by regulating blood
volume & thus stroke volume
14-54
Baroreceptor Reflex
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Is activated by changes in BP
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Which is detected by baroreceptors (stretch
receptors) located in aortic arch & carotid sinuses
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Increase in BP causes walls of these regions to stretch,
increasing frequency of APs
Baroreceptors send APs to vasomotor & cardiac control
centers in medulla
Is most sensitive to decrease & sudden
changes in BP
14-55
Fig 14.26
14-56
Fig 14.27
14-57
Atrial Stretch Receptors
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Are activated by increased venous return & act
to reduce BP
Stimulate reflex tachycardia (slow HR)
Inhibit ADH release & promote secretion of ANP
14-58
Measurement of Blood Pressure
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Is via auscultation (to examine by listening)
No sound is heard during laminar flow (normal, quiet,
smooth blood flow)
Korotkoff sounds can be heard when
sphygmomanometer cuff pressure is greater than
diastolic but lower than systolic pressure
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Cuff constricts artery creating turbulent flow & noise as
blood passes constriction during systole & is blocked during
diastole
1st Korotkoff sound is heard at pressure that blood is 1st
able to pass thru cuff; last occurs when can no long hear
systole because cuff pressure = diastolic pressure
14-59
Measurement of Blood Pressure
continued
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Blood pressure cuff
is inflated above
systolic pressure,
occluding artery
As cuff pressure is
lowered, blood flows
only when systolic
pressure is above
cuff pressure,
producing Korotkoff
sounds
Sounds are heard
until cuff pressure
equals diastolic
pressure, causing
sounds to disappear
Fig 14.29
14-60
Fig 14.30
14-61
Pulse Pressure
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Pulse pressure = (systolic pressure) –
(diastolic pressure)
Mean arterial pressure (MAP) represents
average arterial pressure during cardiac
cycle
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Has to be approximated because period of
diastole is longer than period of systole
MAP = diastolic pressure + 1/3 pulse
pressure
14-62
Hypertension
14-63
Hypertension
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Is blood pressure in excess of normal range for
age & gender (> 140/90 mmHg)
Afflicts about 20 % of adults
Primary or essential hypertension is caused by
complex & poorly understood processes
Secondary hypertension is caused by known
disease processes
14-64
Essential Hypertension
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Constitutes most of hypertensives
Increase in peripheral resistance is universal
CO & HR are elevated in many
Secretion of renin, Angio II, & aldosterone is
variable
Sustained high stress (which increases Symp
activity) & high salt intake act synergistically in
development of hypertension
Prolonged high BP causes thickening of arterial
walls, resulting in atherosclerosis
Kidneys appear to be unable to properly excrete
Na+ and H20
14-65
Dangers of Hypertension
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Patients are often asymptomatic until
substantial vascular damage occurs
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Contributes to atherosclerosis
Increases workload of the heart leading to
ventricular hypertrophy & congestive heart failure
Often damages cerebral blood vessels leading to
stroke
These are why it is called the "silent killer"
14-66
Treatment of Hypertension
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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, & Angio II-receptor
blockers
14-67
Circulatory Shock
14-68
Circulatory Shock
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Occurs when there is inadequate blood flow to,
&/or O2 usage by, tissues
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Cardiovascular system undergoes compensatory
changes
Sometimes shock becomes irreversible & death
ensues
14-69
Hypovolemic Shock
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Is circulatory shock caused by low blood
volume
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E.g. from hemorrhage, dehydration, or burns
Characterized by decreased CO & BP
Compensatory responses include
sympathoadrenal activation via baroreceptor
reflex
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Results in low BP, rapid pulse, cold clammy skin, low
urine output
14-70
Septic Shock
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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
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Endotoxin induces NO production causing
vasodilation & resultant low BP
Effective treatment includes drugs that inhibit
production of NO
14-71
Other Causes of Circulatory Shock
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Severe allergic reaction can cause a rapid fall in
BP called anaphylactic shock
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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
14-72
Congestive Heart Failure
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Occurs when CO is insufficient to maintain
blood flow required by body
Caused by MI (most common), congenital
defects, hypertension, aortic valve stenosis,
disturbances in electrolyte levels
Compensatory responses are similar to those of
hypovolemic shock
Treated with digitalis, vasodilators, & diuretics
14-73