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Chapter 14
Lecture
Outline
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Chapter 14 Outline
Cardiac
Output
Blood Volumes
Vascular Resistance to Blood Flow
Blood Flow to the Heart and Skeletal Muscles
Blood Flow to the Brain and Skin
Blood Pressure
Hypertension, Shock, and Congestive Heart Failure
14-2
Cardiac Output
14-3
Cardiac Output (CO)
Is
volume of blood pumped/min by each ventricle
Stroke volume (SV) = blood pumped/beat by each
ventricle
Heart rate (HR) = the number of beats/minute
CO = SV x HR
Total blood volume is about 5.5L
14-4
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
14-5
Regulation of Cardiac Rate continued
 Norepinephrine
and
epinephrine stimulate
opening of pacemaker
HCN channels
 This depolarizes SA
node faster,
increasing HR
 ACh promotes opening
of K+ channels
 The resultant K+
outflow counters
Na+ influx, slowing
depolarization and
decreasing HR
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
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) = resistance 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 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
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
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 and
contraction would be weak
 In (b, c and d) there is increasing interaction of actin and myosin
allowing more force to be developed
14-12
Extrinsic Control of Contractility
 At
any given EDV,
contraction depends
upon level of
sympathoadrenal
activity
 Norepi. and Epi.
produce an increase
in HR and contraction
(positive inotropic
effect)
 Due to increased
Ca2+ in
sarcomeres
14-13
14-14
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
14-15
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
14-16
Blood Volume
14-17
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
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)
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
14-20
Overall Fluid Movement
Is
determined by net filtration pressure and forces
opposing it (Starling forces)
+ I)– (Pi + p)
[fluid out] – [fluid in]
Pc = Hydrostatic pressure in capillary
i = Colloid osmotic pressure of interstitial fluid
Pi = Hydrostatic pressure in interstitial fluid
p = Colloid osmotic pressure of blood plasma
(Pc
14-21
14-22
Edema
 Normally
filtration, osmotic reuptake, and lymphatic drainage
maintain proper ECF levels
 Edema is excessive accumulation of fluid resulting from:
 High arterial blood pressure
 Venous obstruction
 Leakage of plasma proteins into interstitial fluid
 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 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
14-24
ADH (vasopressin)
 ADH
released by Post
Pit when osmoreceptors
in hypothalamus detect
high osmolality
 From excess salt
intake or dehydration
 Causes thirst
 Stimulates H2O
reabsorption from
urine
 Homeostasis maintained
by these
countermeasures
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
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
14-27
Angiotensin II
Fig
14.12 shows
when and how
Angio II is
produced, and
its effects
14-28
Atrial Natriuretic Peptide (ANP)
Expanded
blood volume is detected by stretch
receptors in left atrium and causes release of ANP
ANP inhibits aldosterone, promoting salt and water
excretion to lower blood volume
And promotes vasodilation
14-29
Atrial Natriuretic Peptide (ANP) continued
 ANP,
together
with decreased
ADH, acts in a
negative
feedback
system to lower
blood volume
and venous
return
14-30
Vascular Resistance to Blood Flow
14-31
Vascular Resistance to Blood Flow
Determines
how much blood flows through a tissue or
organ
Vasodilation decreases resistance, increases blood
flow
Vasoconstriction does opposite
14-32
14-33
Physical Laws Describing Blood Flow
 Blood
flows through vascular system when there is pressure
difference (P) at its two ends
 Flow rate is directly proportional to difference (P = P1 - P2)
14-34
Physical Laws Describing Blood Flow continued
 Flow
rate is inversely proportional to resistance
 Flow = P/R
 Resistance is directly proportional to length of vessel (L) and
viscosity of blood ()
 Inversely proportional to 4th power of radius
 So diameter of vessel is very important for resistance
 Poiseuille's Law describes factors affecting blood flow
 Blood
flow = Pr4()
L(8)
14-35
14-36
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
14-37
Total Peripheral Resistance
 Sum
of all vascular
resistances within the
systemic circulation is
total peripheral
resistance
 Arteries supply tissues
and organs in parallel
circuits
 Changes in
resistance in these
circuits determines
relative blood flow
14-38
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
14-39
Extrinsic Regulation of Blood Flow continued
Parasympathetic
effects cause vasodilation
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
14-40
Paracrine Regulation of Blood Flow
The
endothelium produces several paracrine
regulators that promote relaxation:
Nitric oxide (NO), bradykinin, prostacyclin
NO is involved in setting resting “tone” of vessels
 Levels are increased by Parasymp activity
 Vasodilator drugs such as nitroglycerin or
Viagra act thru NO
Endothelin 1 is vasoconstrictor produced by
endothelium
14-41
Intrinsic Regulation of Blood Flow
(Autoregulation)
Maintains
fairly constant blood flow despite BP
variation
Myogenic control mechanisms occur in some tissues
because vascular smooth muscle contracts when
stretched and relaxes when not stretched
e.g. decreased arterial pressure causes cerebral
vessels to dilate and vice versa
14-42
Intrinsic Regulation of Blood Flow
(Autoregulation) continued
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 causing the tissue to appear red=reactive
hyperemia
A similar inc. in blood flow occurs in sk. Muscle and
other organs as a result of inc. metabolism=active
hyperemia
14-43
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
14-44
Regulation of Coronary Blood Flow
Blood
flow to heart is affected by Symp activity
Norep. causes vasoconstriction; Epi causes
vasodilation
Dilation accompanying exercise is due mostly to
intrinsic regulation
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
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
14-47
14-48
14-49
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
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
14-51
Changing patterns of blood flow in the brain.
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
14-53
Blood Pressure
14-54
Blood Pressure (BP)
 Arterioles
play role in blood distribution and control of BP
 Blood flow to capillaries and BP is controlled by diameter of
arterioles
 Capillary BP is decreased because they are downstream of high
resistance arterioles
14-55
Blood Pressure (BP)
Capillary
BP is also low because of large total crosssectional area
14-56
Blood Pressure (BP)
Is
controlled mainly by 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
14-57
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 Act. Pot.
Baroreceptors send Act. Pot. to vasomotor and
cardiac control centers in medulla
Is most sensitive to decrease and sudden changes in
BP
14-58
14-59
14-60
Atrial Stretch Receptors
Are
activated by increased venous return and act to
reduce BP and in response:
Stimulate reflex tachycardia (slow HR)
Inhibit ADH release and promote secretion of ANP
14-61
Measurement of Blood Pressure
 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
 Cuff constricts artery creating turbulent flow and noise as
blood passes constriction during systole and is blocked
during diastole
 1st Korotkoff sound is heard at pressure that blood is 1st
able to pass thru cuff; last occurs when one can no long hear
systole because cuff pressure = diastolic pressure
14-62
Measurement of Blood Pressure continued
 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
14-63
The indirect, or auscultatory, method of blood
pressure measurement:
14-64
Pulse Pressure
pressure = (systolic pressure) – (diastolic
pressure)
Mean arterial pressure (MAP) represents average
arterial pressure during cardiac cycle
Has to be approximated because period of diastole
is longer than period of systole
MAP = diastolic pressure + 1/3 pulse pressure
Pulse
14-65
Hypertension, Shock, and
Congestive Heart Failure
14-66
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
14-67
Essential Hypertension
Increase
in peripheral resistance is universal
CO and HR are elevated in many
Secretion of renin, Angio II, and aldosterone is variable
Sustained high stress (which increases Symp activity)
and 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 H2O
14-68
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"
14-69
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 II-receptor blockers
14-70
Possible Causes of Secondary
Hypertension
Kidney
disease—kidney disease; renal artery disease
Endocrine disorder—excess catecholamines; excess
aldosterone
Nervous system disorder—inc. intracranial pressure;
damage to vasomotor center
Cardiovascular disorder—complete heart block;
arteriosclerosis of aorta
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
14-72
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
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
14-74
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
14-75
Congestive Heart Failure
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, and diuretics
14-76