201 Circulation

8/2/2019 201 Circulation

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Chapter 14

Cardiac Output, Blood Flow, and Blood

Pressure

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Is volume of blood pumped/min by each ventricle

Stroke volume (SV) = blood pumped/beat by eachventricle

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 driveheart at rate of its spontaneous activity

Normally Symp & Parasymp activity influence HR

(chronotropic effect) Autonomic innervation of SA node is main

controller of HR

Symp & Parasymp nerve fibers modify rate ofspontaneous depolarization

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Regulation of Cardiac Rate continued

NE & Epi stimulateopening of pacemakerHCN channels This depolarizes SA

faster, increasing HR

ACH promotes openingof K+ channels The resultant K+ outflow

counters Na+ influx,slowing depolarization &decreasing HR

Fig 14.1

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Cardiac control centerof medulla coordinatesactivity 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 diastoleTotal 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 tocontraction

SV is directly proportional to preload & contractility

Strength of contraction varies directly with EDV

Total peripheral resistance = afterload whichimpedes ejection from ventricle

Ejection fraction is SV/ EDVNormally is 60%; useful clinical diagnostic tool

Regulation of Stroke Volume

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Frank-Starling Law of the Heart

States that strengthof ventricularcontraction variesdirectly with EDV

Is an intrinsicproperty ofmyocardium

As EDV increases,myocardium isstretched more,causing greatercontraction & 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 beweak

In (b, c & d) there is increasing interaction of actin & myosin allowingmore force to be developed

Fig 14.3

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Extrinsic Control of Contractility

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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Fig 14.5

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Venous Return

Is return of blood toheart via veins

Controls EDV & thus

SV & CO Dependent on:

Blood volume &venous pressure

Vasoconstrictioncaused by Symp

Skeletal muscle pumps

Pressure drop duringinhalation

Fig 14.7 14-15


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Venous Return continued

Veins hold most ofblood in body (70%)& are thus calledcapacitance vessels

Have thin walls &stretch easily toaccommodate more

blood withoutincreased pressure

(=highercompliance) 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 & interstitialcompartments is in state of dynamic equilibrium

Movement out of capillaries is driven by hydrostatic

pressure exerted against capillary wallPromotes 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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Click here to playFluid Exchange AcrossThe Walls of Capillaries

RealMedia Movie

E h f Fl id b C ill i
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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 & forcesopposing it (Starling forces)

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

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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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t
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egu at on o oo o ume yKidney

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 ofhormones

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ADH (vasopressin)

ADH released by Post

Pit when

osmoreceptors detect

high osmolality

From excess salt intakeor dehydration

Causes thirst

Stimulates H20

reabsorption from urine ADH release inhibited

by low osmolality

Fig 14.11

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Aldosterone

Is steroid hormone secreted by adrenal cortex

Helps maintain blood volume & pressure throughreabsorption & retention of salt & water

Release stimulated by salt deprivation, low bloodvolume, & pressure

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R i A i t i Ald t
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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 atincreasing blood pressure:

Vasoconstriction, aldosterone secretion, thirst

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Fig 14.12

shows when

& how

Angio II is

produced, &its effects

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 tissueor 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(DP) at its two ends Flow rate is directly proportional to difference (DP = P1 - P2)

Fig 14.13

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Ph i l L D ibi Bl d Fl
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Physical Laws Describing Blood Flow

Flow rate is inversely proportional to resistance Flow = DP/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 = DPr4

()L(8)

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Fig 14.14. Relationship

between blood flow,radius & resistance

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E i i R l i f Bl d Fl
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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 Sympfibers 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 vasodilativeHowever, Parasymp only innervates digestive tract,

genitalia, & salivary glands

Thus Parasymp is not as important as Symp Angiotenin II & ADH (at high levels) cause general

vasoconstriction of vascular smooth muscle

Which increases resistance & BP

Extrinsic Regulation of Blood Flowcontinued

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i l i f l d l
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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
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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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n r ns c egu a on o oo ow
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Metabolic control mechanism matches blood flow to

local tissue needs

Low O2 or pH or high CO2, adenosine, or K+ fromhigh metabolism cause vasodilation which increases

blood flow (= active hyperemia)

n r ns c egu a on o oo ow(Autoregulation) continued

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A bi R i f h H
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Aerobic Requirements of the Heart

Heart (& brain) must receive adequate blood supplyat all times

Heart is most aerobic tissue--each myocardial cell is

within 10 m of capillaryContains lots of mitochondria & aerobic enzymes

During systole coronary, vessels are occluded

Heart gets around this by having lots ofmyoglobin Myoglobin is an 02 storage molecule that releases 02 to heart

during systole

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R l i f C Bl d Fl
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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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Ci l t Ch D i E i
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Circulatory Changes During Exercise

At beginning of exercise, Symp activity causesvasodilation 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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C b l Ci l ti
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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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C b l Ci l ti


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Cerebral Circulation

Is regulated almost exclusively by intrinsicmechanisms

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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Cutaneous Blood Flow
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Cutaneous Blood Flow

Skin serves as a heat

exchanger forthermoregulation

Skin blood flow is adjustedto keep deep-body at 37oC

By arterial dilation orconstriction & activity ofarteriovenous anastomoseswhich control blood flowthrough surface capillaries

Symp activity closes surfacebeds during cold & fight-or-flight, & opens them in heat &exercise

Fig 14.22 14-50
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Blood Pressure

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Blood Pressure (BP)


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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)
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Blood Pressure (BP)

Capillary BP is also low because of large total cross-

sectional area

Fig 14.24

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Blood Pressure (BP)
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Blood Pressure (BP)

Is controlled mainly by HR, SV, &peripheralresistance

An increase in any of these can result in increased BP

Sympathoadrenal activity raises BP via arteriolevasoconstriction & by increased CO

Kidney plays role in BP by regulating blood volume& thus stroke volume

14-54

Baroreceptor Reflex
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Baroreceptor Reflex

Is activated by changes in BPWhich is detected bybaroreceptors (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& cardiaccontrol centers

in medulla

Is most sensitive to decrease & sudden changes in

BP

14-55

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Fig 14.26 14-56


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Fig 14.27

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Atrial Stretch Receptors


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Atrial Stretch Receptors

Are activated by increased venous return & act toreduce BP

Stimulate reflex tachycardia (slow HR)

Inhibit ADH release & promote secretion of ANP

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Measurement of Blood Pressure


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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 sphygmomanometercuff 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 topass thru cuff; last occurs when can no long hear systole becausecuff pressure = diastolic pressure

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Measurement of Blood Pressure i d
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Measurement of Blood Pressure continued

Blood pressure cuff is

inflated above systolicpressure, occluding artery

As cuff pressure islowered, blood flows onlywhen systolic pressure is

above cuff pressure,producing Korotkoffsounds

Sounds are heard until

cuff pressure equalsdiastolic pressure, causingsounds to disappear

Fig 14.29 14-60

Pulse Pressure
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Pulse Pressure

Pulse pressure = (systolic pressure)(diastolicpressure)

Mean arterial pressure (MAP) represents average

arterial pressure during cardiac cycleHas to be approximated because period of diastole is

longer than period of systole

MAP = diastolic pressure + 1/3 pulse pressure
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201 Circulation

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