Cardiac Output, Blood Flow, and Blood Pressure

Cardiac Output, Blood Flow, and
Blood Pressure
www.freelivedoctor.com
14-1
 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)
 Is volume of blood pumped/min by

each ventricle
 Heart Rate (HR) = 70 beats/min
 Stroke volume (SV) = blood
pumped/beat by each ventricle
 Average is 70-80 ml/beat
 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 & Parasymp activity influence
HR (chronotropic effect)
 Mechanisms that affect HR: chronotropic
effect
 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
Fig 14.1
 NE & 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, slows
depolarization &
decreasing HR www.freelivedoctor.com
14-6
Regulation of Cardiac Rate continued
 Vagus nerve:
 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
 Is determined by 3 variables:
 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
 EDV is workload (preload) on heart prior to
contraction
 SV is directly proportional to preload & contractility
 Strength of contraction varies directly with EDV
 Total peripheral resistance = afterload which
impedes ejection from ventricle
 SV is inversely proportional to TPR
 Ejection fraction is SV/ EDV (~80ml/130ml=62%)
 Normally is 60%; useful clinical diagnostic tool
14-10
Frank-Starling Law of the Heart
 States that
strength of Fig 14.2
ventricular
contraction varies
directly with EDV
 Is an intrinsic
property of
myocardium
 As EDV increases,
myocardium is
stretched more,
causing greater
contraction & SV www.freelivedoctor.com
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 & contraction
would be weak
 In (b, c & d) there is
increasing interaction of
actin & myosin allowing
more force to be
developed
Fig 14.3 www.freelivedoctor.com
14-12
 At any given EDV,
contraction
depends upon level
of
sympathoadrenal
activity
 NE & Epi produce
an increase in HR &
contraction (positive
inotropic effect)
 Due to increased
Ca2+ in sarcomeres Fig 14.4
14-13
Extrinsic Control of Contractility
 Parasympathetic stimulation
 Negative chronotropic effect
 Through innervation of the SA node and
myocardial cell
 Slower heart rate means increased EDV
 Increases SV through Frank-Starling law
Fig 14.5
14-14
Venous Return
 Is return of blood to
heart via veins
 Controls EDV & thus
SV & CO
 Dependent on:
 Blood volume & venous
pressure
 Vasoconstriction caused
by Symp
 Skeletal muscle pumps
 Pressure drop during
inhalation
Figwww.freelivedoctor.com
14.7 14-15
Venous Return continued
 Veins hold most of

blood in body
(70%) & are thus
called capacitance
vessels
 Have thin walls &
stretch easily to
accommodate more
blood without
increased pressure
(=higher
compliance) Fig 14.6
 Have only 0- www.freelivedoctor.com
10 mm Hg pressure 14-16
Blood & Body Fluid Volumes
14-17
Blood Volume
 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
 80% of this is Fig 14.8
interstitial fluid; 20% www.freelivedoctor.com
14-18
Exchange of Fluid between
Capillaries & Tissues
 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
 Promotes formation of tissue fluid
 Net filtration pressure= hydrostatic pressure in
capillary (17-37 mm Hg) - hydrostatic pressure of
ECF (1 mm Hg) www.freelivedoctor.com 14-19
Exchange of Fluid between
Capillaries & Tissues
 Movement also affected by colloid osmotic

pressure
 = osmotic pressure exerted by proteins in fluid
 Difference between osmotic pressures in &
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 & forces
opposing it (Starling forces)
 Pc + Πi (fluid out) - Pi + Πp (fluid in)
 Pc = Hydrostatic pressure in capillary

 Πi = Colloid osmotic pressure of interstitial fluid
 Pi = Hydrostatic pressure in interstitial fluid
 Πp = Colloid osmotic pressure of blood plasma
14-21
Fig 14.9
14-22
Edema
 Normally filtration, osmotic reuptake, &
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
14-23
Regulation of Blood Volume by Kidney
 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
 Adjusted according to needs of body by action of
hormones
14-24
ADH (vasopressin)
 ADH released by Post Pit

when osmoreceptors
detect high osmolality
 From excess salt
intake or dehydration
 Causes thirst
 Stimulates H 0
2
reabsorption from
urine
 ADH release inhibited by
low osmolality Fig 14.11
14-25
Aldosterone
 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
 Decreased BP and flow (low blood volume)

 Kidney secreted Renin (enzyme)
 Juxaglomerular apparatus
 Angiotensin I to AngiotensinII
 By angiotensin-converting enzyme (ACE)
 Angio II causes a number of effects all
aimed at increasing blood pressure:
 Vasoconstriction, aldosterone secretion, thirst
14-27
II
 Fig 14.12
shows when
& how Angio
II is
produced, &
its effects
14-28
Atrial Natriuretic Peptide (ANP)
 Expanded blood volume is detected by

stretch receptors in left atrium &
causes release of ANP
 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
 Determines how much blood flows through a

tissue or organ
 Vasodilation decreases resistance, increases
blood flow
 Vasoconstriction does opposite
14-31
14-32
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)
Fig 14.13
14-33
Physical Laws Describing Blood Flow
 Flow rate is inversely proportional to resistance

 Flow = ∆P/R
 Resistance is directly proportional to length of
vessel (L) & viscosity of blood (η)
 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(π)

ηL(8)
14-34
Fig 14.14. Relationship
between blood flow,
radius &resistance
14-35
Extrinsic Regulation of Blood Flow
 Sympathoadrenal activation causes

increased CO & resistance in periphery &
viscera
 Blood flow to skeletal muscles is increased
 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
 Parasympathetic effects are vasodilative

 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
 Which increases resistance & BP
14-37
Paracrine Regulation of Blood Flow
 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
14-38
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 & relaxes when not
stretched
 E.g. decreased arterial pressure causes cerebral
vessels to dilate & vice versa
14-39
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 (=
active hyperemia)
14-40
Aerobic Requirements of the Heart
 Heart (& 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 & aerobic enzymes
 During systole coronary vessels are occluded
 Heart gets around this by having lots of myoglobin
 Myoglobin is an 02 storage molecule that releases 02 to
heart during systole
14-41
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
14-42
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
14-43
Circulatory Changes During Exercise
 At beginning of exercise, Symp activity causes

vasodilation via Epi & local ACh release
 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
 HR & ejection fraction increases vascular resistance
14-44
Fig 14.19
14-45
Fig 14.20
14-46
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
14-47
Cerebral Circulation
 Is regulated almost exclusively by intrinsic

mechanisms
 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)
 Areas of brain with high metabolic activity receive most
blood
14-48
Fig 14.21
14-49
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 & activity of
arteriovenous anastomoses
which control blood flow
through surface capillaries
 Symp activity closes surface
beds during cold & fight-or-
flight, & opens them in heat
& exercise
Fig 14.22
14-50
Blood Pressure
14-51
Blood Pressure (BP)
 Arterioles play role in

blood distribution &
control of BP
 Blood flow to
Fig 14.23
capillaries & BP is
controlled by
aperture of arterioles
 Capillary BP is
decreased because
they are downstream
of high resistance
arterioles www.freelivedoctor.com
14-52
Blood Pressure (BP)
 Capillary BP
is also low
because of
large total
cross-
sectional
area
Fig 14.24
14-53
Blood Pressure (BP)
 Is controlled mainly by HR, SV, & peripheral

resistance
 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
 Is activated by changes in BP
 Which is detected by baroreceptors (stretch
receptors) located in aortic arch & carotid sinuses
 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
14-56
Fig 14.27
14-57
Atrial Stretch Receptors
 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
 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
 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
 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
14-61
Pulse Pressure
 Pulse 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
14-62
Hypertension
14-63
Hypertension
 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
 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
 Patients are often asymptomatic until

substantial vascular damage occurs
 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
 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
 Occurs when there is inadequate blood flow to,

&/or O2 usage by, tissues
 Cardiovascular system undergoes compensatory
changes
 Sometimes shock becomes irreversible & death
ensues
14-69
Hypovolemic Shock
 Is circulatory shock caused by low blood

volume
 E.g. from hemorrhage, dehydration, or burns
 Characterized by decreased CO & BP
 Compensatory responses include
sympathoadrenal activation via baroreceptor
reflex
 Results in low BP, rapid pulse, cold clammy skin, low
urine output
14-70
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 & resultant low BP
 Effective treatment includes drugs that inhibit
production of NO
14-71
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
14-72
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, & diuretics
14-73

Cardiac Output, Blood Flow, and Blood Pressure

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Cardiac Output, Blood Flow, and Blood Pressure

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Cardiac Output, Blood Flow, and

 Is volume of blood pumped/min by

 (a) is state of myocardial

 Veins hold most of

 Distribution of ECF between blood &

 Movement also affected by colloid osmotic

 Pc + Πi (fluid out) - Pi + Πp (fluid in)

 Pc = Hydrostatic pressure in capillary

 Urine formation begins with filtration of

 ADH released by Post Pit

 Is steroid hormone secreted by adrenal

 Decreased BP and flow (low blood volume)

 Expanded blood volume is detected by

 Determines how much blood flows through a

 Flow rate is inversely proportional to resistance

 Blood flow = ∆Pr4(π)

 Sympathoadrenal activation causes

 Parasympathetic effects are vasodilative

 Endothelium produces several paracrine

 Maintains fairly constant blood flow despite BP

 Metabolic control mechanism matches

 Heart (& brain) must receive adequate blood

 Blood flow to heart is affected by Symp

 At rest, flow through skeletal muscles is low

 At beginning of exercise, Symp activity causes

 Gets about 15% of total resting CO

 Is regulated almost exclusively by intrinsic

 Arterioles play role in

 Is controlled mainly by HR, SV, & peripheral

 Are activated by increased venous return & act

 Is via auscultation (to examine by listening)

 Blood pressure cuff

 Pulse pressure = (systolic pressure) –

 Is blood pressure in excess of normal range for

 Constitutes most of hypertensives

 Patients are often asymptomatic until

 Occurs when there is inadequate blood flow to,

 Is circulatory shock caused by low blood

 Refers to dangerously low blood pressure

 Severe allergic reaction can cause a rapid fall in

 Occurs when CO is insufficient to maintain

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