Download - Physiology Of Circulation
Cardiac Output, Blood Flow, and Blood Pressure
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Outline
Cardiac Output Blood & Body Fluid Volumes Factors Affecting Blood Flow Blood Pressure Hypertension Circulatory Shock
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Cardiac Output
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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 Average is 70-80 ml/beat
CO = SV x HR Total blood volume is about 5.5L
Cardiac Output (CO)
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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
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Regulation of Cardiac Rate continued
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
Fig 14.1
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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
Regulation of Cardiac Rate continued
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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
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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
Regulation of Stroke Volume
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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 & SV
Fig 14.2
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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 14.314-12
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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 14.414-13
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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
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Fig 14.5
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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 Fig 14.7 14-15www.freelivedoctor.com
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)
Have only 0-10 mm Hg pressure
Fig 14.6
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Blood & Body Fluid Volumes
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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 interstitial fluid; 20% is blood plasma
Fig 14.8
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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)
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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
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Overall Fluid Movement
Is determined by net filtration pressure & forces opposing it (Starling forces)
Pc + i (fluid out) - Pi + p (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
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Fig 14.9
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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
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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
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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 H20
reabsorption from urine
ADH release inhibited by low osmolality
Fig 14.1114-25
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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
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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
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Fig 14.12 shows when & how Angio II is produced,
& its effects
Angiotensin II
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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
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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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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 14.1314-33
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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 () 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)
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Fig 14.14. Relationshipbetween blood flow, radius & resistance
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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
Extrinsic Regulation of Blood Flow
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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
Extrinsic Regulation of Blood Flow continued
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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
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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
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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)
Intrinsic Regulation of Blood Flow (Autoregulation) continued
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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 14-41www.freelivedoctor.com
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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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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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
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Fig 14.19
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Fig 14.20
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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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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
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Fig 14.2114-49
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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 14.2214-50
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Blood Pressure
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Blood Pressure (BP)
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
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Blood Pressure (BP)
Capillary BP is also low because of large total cross-sectional area
Fig 14.24 14-53
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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
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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
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Fig 14.27
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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
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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
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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
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Fig 14.3014-61
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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
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Hypertension
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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
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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
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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"
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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, & Angio II-receptor blockers
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Circulatory Shock
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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
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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 & 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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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
Septic Shock
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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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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
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