BLOOD FLOW AND THE CONTROL OF BLOOD PRESSURE

Goal of cardiovascular regulation is the maintenance of adequate blood flow thru peripheral tissues and organs.
Under normal circumstances blood flow is equal to cardiac outut.
o When cardiac output goes up blood flow goes up more blood thru capillaries more blood to tissue
cells
o When cardiac output declines blood flow goes down less blood thru capillaries less blood to
tissue cells
The afterload of the heart is determined by the interplay between re!!ure and re!i!ta"ce (forces like friction
between blood and vessels that oppose blood flow)
PRESSURE
lood is incompressible
!ydrostatic pressure is generated by the force e"erted in all directions against blood
o #f there was no resistance in the cardiovascular system$ there would be no need for the heart to generate
pressure to force the blood thru the systemic and pulmonary systems
% pressure gradient does e"ist and blood flow! from a #i$# re!!ure to a low re!!ure
The flow rate is directl% roortio"al to the re!!ure $radie"t.
o The greater the pressure$ the faster the flow
o The lower the pressure$ the slower the flow
#n the !%!te&ic circuit (blood between heart and all tissues e"cept lungs)$ the pressure gradient is the
circulator% re!!ure 'CP(
o The pressure difference between the ba!e of t#e a!ce"di"$ aorta and the e"tra"ce to t#e ri$#t atriu&
o &irculatory pressure averages around )** &&H$
o This pressure is needed primarily to force blood through the arterioles (resistance vessels) and into
peripheral capillaries (where gas e"change takes place)
&irculatory pressure is divided into ' components(
o Blood re!!ure 'BP(
This is arterial pressure (elastic ) muscular arteries and arterioles) and ranges from an average
of *++mm !g to roughly ', mm !g at the start of the capillary network
o Caillar% re!!ure
-ressure within the capillary beds.
%long the length of a typical capillary (only place gas e"change is taking place)$ pressure declines
from roughly ', mm !g to *. mm !g
o +e"ou! re!!ure
-ressure within the venous system (venules ) veins)
-ressure gradient is low$ from the venules to the right atrium it is only around *. mm !g
%s the blood flows away from the heart (left ventricle) the &- decreases and is almost + mm !g when it returns
back to the right atrium
RES,STANCE
% resistance is a force that opposes movement
The resistance of the circulatory system opposes the movement of blood
o the greater the resistance$ the slower the blood flow
/or circulation to occur$ the &- must be great enough to overcome the total eri#eral re!i!ta"ce (the
resistance of the entire &-)
ecause the resistance of the venous system is very low$ we focus on the eri#eral re!i!ta"ce (the resistance
of the arterial system)
/or blood to flow into peripheral capillaries$ blood re!!ure must be great enough to overcome PR
The higher the -0$ the lower the rate of blood flow
1ources of -0 include(
o +a!cular re!i!ta"ce
The resistance of the blood vessels due to friction btwn blood and vessel walls
2argest component of -0 and depends on(
+e!!el le"$t#
o #ncreasing length increases friction b3c the longer the vessel$ the longer the
surface area contact with blood
o #n adults$ vessel length is constant
+e!!el dia&eter
*
o 4ecreasing diameter (vasoconstriction) decreases blood flow b3c in small
diameter vessels blood is slowed by friction in the narrow 5one closest to the
vessel wall
o #ncreasing diameter (vasodilation) increases blood flow b3c blood near the
center of the large diameter vessel will not encounter any resistance with the
vessel wall
4ifference in diameter has much more significant effects on resistance than difference in length
#f there are two vessels of equal diameter (one 6 7" longer than the other)$ the longer
vessel will offer 6"8s as much resistance to blood flow
With 6 vessels of equal length$ one 6"8s the diameter of the other$ the smaller one will
offer *9"8s as much resistance to blood flow
See Fi$- )./)0
:ost -0 occurs in the arterioles by altering the diameter of the vessels to control -0 ) blood flow
+a!odilatio" decreases -0 increases blood flow
+a!oco"!trictio" increases -0 decreases blood flow
o +i!co!it% of blood (how thick it is)
0esistance to blood flow due to the interactions among molecules and suspended materials in
blood
more water$ less viscous decrease -0 higher rate of blood flow
less water$ more viscous increase -0 lower rate of blood flow
Under normal circumstances$ the viscosity of blood remains stable
4ehydration less water more viscous decrease blood flow
%nemia due to blood loss too few 0&8s less viscous increase blood flow
-olycythemia too many 0&8s more viscous decrease blood flow
Turbule"ce
!igh flow rates$ irregular surfaces (plaque build up in vessels)$ or sudden changes in vessel diameter upset the
smooth flow of blood creates eddies and swirls ; turbule"ce
<ormally turbulence occurs when blood flows between atria and ventricles and between the ventricles and the
aortic and pulmonary trunks generating the third and fourth heart sounds
o Third sound by vibrations of the ventricular walls
o /ourth sound by the accelerated rush of blood into the ventricles
o The first and second heart sounds are created by the opening and closing of the heart valves
/irst sound due to %= valves closing and 1= valves opening (at beginning of systole) >2ub?
1econd sound due %= valves opening and 1= valves closing (at end of systole) >4ub?
Turbulent flow across a damaged or misaligned heart valve is responsible for heart
murmurs
0ushing$ gurgling$ or whooshing sound due to malfunctioning heart valves
o #ncomplete closure of valve causing regurgitation of blood
o 1tenotic valve (too narrow) usually heard @ust A/B0A systole
Turbulence develops in large arteries (aorta)$ when &B and arterial flow rates are high$ seldom occurs in smaller
vessels unless their walls are damaged
o 1car tissue from a damaged vessel
o 4evelopment of atherosclerotic plaque
o oth create turbulence and restrict blood flow
1EAN ARTER,AL PRESSURES or BP
%rterial pressures overcome -0 and maintain blood flow thru capillary beds
%rterial pressure is not stable
0ises during ventricular systole
/alls during ventricular diastole
See Fi$- )./.
-eak blood pressure measured duri"$ 2e"tricular !%!tole is called !%!tolic re!!ure
:inimum blood pressure at the e"d of 2e"tricular dia!tole is called dia!tolic re!!ure
6
When - is recorded by listening for 3orot4off !ou"d! in the brachial artery using a sphygmomanometer (-
cuff ) press. gauge$ along with a stethoscope)$ systolic and diastolic pressures are separated by a slashmark
o See Fi$- )./5
o 1ystolic press. ; *6+ mm !g
o 4iastolic press. ; .+ m !g
A"pressed as 1yst34iastol.
)6*78* 9 a2era$e7"or&al BP
The difference between the systolic press. and diastolic press. is called the ul!e re!!ure
o PP 9 S%!tolic re!! : Dia!tolic re!!
o -- ; *6+C.+ ; D+
To report a single valve for -$ the mean arterial pressure (:%-) is used
o :%- is calculated by adding *3' of the pulse pressure to the diastolic press
o :%- or :- ; diastolic E *3' (pulse pressure)
1AP or 1BP 9 dia!tlolic ;)7< '!%!tolic : dia!tolic(
:- ; .+ E *3' (*6+C.+) or .+ E (D+3')
1BP ; F'.'' or =<
o The :- is a function of cardiac output and total peripheral resistance
o 0emember T-0 depends on the diameter of the blood vessels and viscosity of blood
:- ; cardiac output " T-0
:- ; (!0 " 1=) " T-0
Ela!tic rebou"d
o %s systolic pressure climbs$ the atrial walls stretch (like an e"tra puff of air e"pands a partially inflated
balloon)
o This e"pansion allows the arterial system to accommodate some of the blood provided by the ventricular
system
o When diastole begins ) pressure falls$ the arteries recoil to their original dimensions
o ecause the aortic semilunar valve prevents the return of blood to the heart$ the arterial recoil pushes
blood toward the capillaries
o See Fi$- )./8
o :- provides us with information on the heart8s pumping efficiency and the condition of the vessels in the
systemic circuit
1ince systolic press indicates the contraction force of the heart and diastolic press indicates the
condition of the blood vessels$ and increase in the diastolic press indicates a decrease in vessel
elasticity (i.e. hardening of the arteries)
%s a person ages the elastic arteries lose their elasticityG therefore$ and as a persons gets older
there may be an increase in blood pressure is largely due to the overall loss of vessel elasticity
-artly due to increased deposits of cholesterol and other lipids in the blood vessel walls
H%erte"!io" is the presence of abnormally high blood pressure )<*78.
H%ote"!io" abnormally low blood pressure sometimes due to overaggressive treatment for hypertension
CARD,O+ASCULAR RE>ULAT,ON
!omeostatic mechanisms regulate cardiovascular activity to ensure that tissue blood flow meets the demand for
o"ygen and nutrients in the capillary beds (only place for gas e"change with tissues)
The ' variable factors that ensure these demands are cardiac outut? eri#eral re!i!ta"ce$ ) BP
When cells become active$ blood flow to that region must increase to deliver necessary B6 and nutrients and to
carry away &B6 and wastes generated by cellular respiration
o When cells are not as active$ blood flow to that region can be decreased
o 1ee /ig. *,C*,
Goal of cardiovascular regulation is to ensure blood flow changes occur
o %t an appropriate time
o #n the right area
o Without drastically altering blood pressure and blood flow to any vital organs 'See Fi$- )./)<(
'
/actors involved in the regulation of cardiovascular function include
o Local factor!
&hange the pattern of blood flow within capillary beds in response to chemical changes in the
interstitial fluids
The is an e"ample of autore$ulatio" within the &icrocirculatio" at the tissue level 'See Fi$-
)./< a"d )./).(
Arteriole! &etarteriole! 't#orou$#fare c#a""el!( true caillarie! 2e"ule!
Precaillar% !#i"cter! control blood flow at entrance to true capillaries via constriction
or dilation
+a!odilator!
/actors that promote dilation of recaillar% !#i"cter! called 2a!odilator!
When produced at the tissue level accelerate blood flow thru tissue of origin
A"amples(
o 4ecr. tissue B6 levels
o #ncr. tissue &B6 levels
o Generation of lactic acid or other acids by tissue cells
o 0elease of nitric acid from endothelial cells
o 0ising concentrations of HE or !E in interstitial fluid
o &hemicals released during local inflammation
!istamine ) nitric o"ide
o Alevated local temperatures
+a!oco"!trictor!
%ggregating platelets and damaged tissues produce compounds that stimulate
constriction of precapillary sphincters (prevent blood loss and can be in response to pain)
o -rostaglandins and thrombo"anes
o 1erotonin (platelet aggregation) and 1ubstance - (pain)
o Ce"tral &ec#a"i!&!
The nervous system is responsible for ad@usting cardiac output and peripheral resistance to
maintain adequate blood flow to vital tissues and organs
&enters responsible for these regulatory activities include(
Cardiac centers in medulla
o Cardioaccelerator% ce"ter increases cardiac output by increasing
sympathetic innervation
o Cardioi"#ibitor% ce"ter decreases cardiac output by increasing
parasympathetic innervation
+a!o&otor centers in medulla
o Co"trol of 2a!oco"!trictio"
<eurons innervating peripheral blood vessels release <A (adrenergic)
1timulation of receptor on smooth muscles in vessel walls of arterioles
vasoconstriction.
o Co"trol of 2a!odilatio"
<eurons innervating peripheral blood vessels release 2A11 <A
(decreased sympth. stimul.)
2ess stimulation of receptors on smooth muscles in vessel wall of
arterioles vasodilation
oth work together and sometimes independently of one another
See Fi$- )./66 a"d )./6<
Barorecetor Refle@
aroreceptors are speciali5ed receptors that monitor the degree of stretch in the walls of
distensible organs
The baroreceptors involved in cardiovascular regulation are located in the walls of the(
o Carotid !i"u!e! near the bases of the internal carotid arteries
o Aortic !i"u!e! in the walls of the ascending aorta
o Wall of the ri$#t atriu&
o See Fi$- )./6)
D
These receptors are components that ad@ust cardiac output and peripheral resistance to
maintain normal arterial pressure
See Fi$- )./66A Re!o"!e to i"crea!ed blood re!!ure
When - rises more stretch on barorecptors more stimulation send to &=
o 4ecrease in sympathetic output ) increase in parasympathetic output
=asodilation$ decreased force of contraction in ventricular myocardium$
decreased heart rate at 1% node decreased -0 and &B
0esults in decreased -
#t is a negative feedback loop
See Fi$- )./6<A Re!o"!e to decrea!ed blood re!!ure 'ort#o!tatic #%ote"!io"(
BP lowe!t with l%i"$ down due to equal forces of gravity all over body
o !eart does not have to work as hard to pump blood back up against gravity
BP #i$#e!t when !ta"di"$ due to blood having to overcome forces of gravity to get
blood back to heart via venous return
- increases when go from lying down$ to sitting$ to standing
When you stand up$ blood pools in lower e"tremities thus creating an instantaneous
decrease in venous return causing a decrease in -. This is called ort#o!tatic
#%ote"!io"
When - falls less stretch on baroreceptors less stimulation send to &=
o #ncrease in sympathetic output and decrease in parasympathetic output
=asoconstriction$ increased force of contraction in ventricular
myocardium$ increased heart rate at 1% node increased -0 and &B
0esults in increased - back to normal
o W#at would #ae" wit# t#e barorecetor refle@ a"d BP? if ela!ticit% i! lo!t i" t#e arterie! or
arteriole!B CH,NTA le!! ela!tic 9 le!! !tretc#D
o C#e&orecetor refle@e!
0esponds to changes in the &B6$ B6$ and p! levels in the blood and cerebrospinal fluid
&hemoreceptors involved are sensory neurons located in the carotid bodies in carotid sinus and
aortic bodies in aortic sinus
When chemoreceptors detect increase levels of &B6 or decrease in p! &= centers stimulated
results in an elevation in arterial pressure via stimulation of vasomotor center
1trong chemoreceptor stimulation (decrease in B6 levels) more widespread sympathetic
stimulation increasing !.0. and &.B.
o E"docri"e factor!
-rovides both long and short term regulation of cardiovascular performance
Apinephrine ) <orepinephrine from the adrenal medulla stimulate cardiac output ) peripheral
resistance
Bther hormones regulating &= function(
%ntidiuretic hormone (%4!) released in response to decrease in - or increase in
osmotic concentration of plasma
o 0esults in peripheral vasoconstriction increasing -
o %lso stimulates kidney8s to reabsorb water preventing a decrease in blood
volume further increases -
%ngiotension ## appears in blood following release of rennin in response to decrease in
renal - results in vasoconstriction and raises -
o 1timulates secretion of %4! and aldosterone (reabsorption of <aE in kidneys)
o 1timulates thirst additional water consumed w3 presence of %4! to retain
water elevates plasma volume increasing -
,