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INTRODUCTION TO CARDIOVASCULAR
PHYSIOLOGY
ANAESTHESIA TUTORIAL OF THE WEEK 125
16
TH
MARCH 2009
Toby Elkington, Specialist Registrar
Carl Gwinnutt, Consultant
Department of Anaesthesia, Salford Royal !S "oundation
Trust, Salford, #$
Correspondence to tobyelkington%hotmail&com
This tutorial is intended as a very basic introduction to cardiovascular physiology with particular
reference to anaesthesia. Once these basic principles have been mastered then it will be appropriate to
move on to the more detailed tutorials that are available.
Every anaesthetic given to a patient will have an impact on their physiology and in particular on the
cardiovascular system. Therefore understanding the physiology of the cardiovascular system allows a !etter
appreciation of the changes that occur when an anaesthetic is given and when and how !est to treat any adverse
events.
"efore reading this tutorial think a!out the following#
$% What events occur in the heart each time it !eats&
'% (ow much !lood does the heart pump out&
)% What factors affect the amount of !lood the heart pumps out&
*% (ow is !lood pressure related to !lood flow from the heart&
+% What are the normal cardiovascular responses to hypovolaemia&
,% (ow do anaesthetics affect the cardiovascular system&
ANATOMY
The heart is composed of four cham!ers left atrium and ventricle and right atrium and ventricle. The atria and
ventricles are separated !y the atrioventricular -A.% valves mitral on the left and tricuspid on the right.
/eo0ygenated !lood returns from the !ody via the great veins -superior and inferior vena cavae% to the right
atrium and then passes through the tricuspid valve into the right ventricle. 1rom here !lood is pumped through
the pulmonary valve into the pulmonary artery -the only artery which carries deo0ygenated !lood in an adult%
and on through the pulmonary capillaries in the lungs where it is o0ygenated -and car!on dio0ide removed%.
"lood returns to the left side of the heart via the pulmonary veins -the only veins to carry o0ygenated !lood in
the adult% into the left atrium then through the mitral valve into the left ventricle. 1rom the left ventricle !lood
is pumped through the aortic valve into the aorta and then via the systemic vascular tree to the !ody2s organs.
The vascular tree is comprised of arteries arterioles capillaries venules and veins conventionally descri!ed in
progressive order leaving from the left side of the heart and returning to the right. The arterial side of the
circulation carries o0ygenated !lood. "oth arteries and arterioles have thick muscular walls as they carry !lood
under relatively high pressure. The average adult has a circulating volume of appro0imately +333ml !lood. 4n
the normal resting state only a!out $+5 -6+3ml% of the circulating volume is within the arterial system. As
!lood traverses capillary !eds the pressure falls and the !lood gives up o0ygen and other nutrients to the tissues
while at the same time collecting car!on dio0ide and other waste products of meta!olism. The !lood now
relatively deo0ygenated starts its return 7ourney to the heart in the venules and veins -thin8walled !ecause of the
low pressure% finally entering the vena cavae. The venous system contains appro0imately ,35 -)333ml% of the
!lood volume and is often referred to as a capacitance system the volume of which can !e varied significantly
!y the sympathetic nervous system -see !elow%. The remaining '+5 -$'+3ml% of the !lood volume is in the
pulmonary circulation and heart.
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THE CARDIAC CYCLE
The cardiac cycle refers to the mechanical events that occur during the contraction
-systole% and rela0ation -diastole% of the ventricular muscle. 4t must !e
remem!ered that this activity is initiated !y the cardiac action potential that
originates in the sino8atrial -SA% node spreads through the atrial muscle crosses
the atrio8ventricular -A.% node reaches the ventricles via the !undle of (is and
supplies the :urkin7e fi!res which innervate the ventricles. The sum of these
action potentials is recorded as the E9>?
: wave atrial depolarisation
:@ interval spread of e0citation through the atria A. node and !undle of (is
A@S comple0 spread of e0citation through the ventricles
T wave ventricular repolarisation
There are two important points to remem!er#
$. Bechanical contraction occurs after depolarisation therefore systole starts at the end of the A@S
comple0 and ends during the T wave.
'. A cardiac action potential or E9> signal does not mean that the heart is pumping !lood it only
indicates electrical activity -remem!er the cardiac arrest patient with pulseless electrical activity
-:EA%.
Systole is the period of ventricular contraction. As contraction starts in !oth ventricles the A. valves close to
prevent !ack flow of !lood into the atria. .entricular contraction continues with a rapid increase in pressure !ut
no change in volume? this is called isovolumetric contraction -meaning literally Csame volumeD%. Eventually
the pressure within the left and right ventricles e0ceeds the pressures in the aorta and pulmonary arteries
respectively and at this point the aortic and pulmonary valves open and e7ection of !lood occurs. The amount of
!lood e7ected in one cycle is referred to as the stroke volume -S.% and this is around 63ml in an average adult at
rest. (owever the ventricles do not completely empty only si0ty to eighty percent of the !lood present in the
ventricle is e7ected -the e7ection fraction%. As the ventricles empty the pressure within them starts to fall. When
the pressure drops !elow that in the aorta and pulmonary artery the aortic and pulmonary valves respectively
close signalling the end of systole.
/iastole is the period of ventricular rela0ation. 4nitially there is a period of isovolumetric rela0ation -again
Csame volumeD% and all the valves are closed. As the atria fill with !lood returning to the heart the pressure
rises when it e0ceeds that in the ventricles the A. valves open and as a period of passive filling occurs the
volume of !lood in the ventricles starts to increase. This passive filling is initially rapid !ut slows as the
pressure gradient across the A. valves decreases. .entricular filling is completed !y contraction of the atria
contri!uting twenty to thirty percent of ventricular volume and signalling the end of diastole. The volume of
!lood in the ventricle at this point is often referred to as the end8diastolic volume -E/.% and is normally around
$'3ml.
4t is interesting to consider how long each of these components of the cycle takes as heart rate varies. Ender
normal resting conditions heart rate is appro0imately 63 !eats;min and each cardiac cycle therefore takes
appro0imately 3.=+ sec. Systole lasts 3.) sec and diastole lasts 3.++ sec most of the time !eing taken up !y
ventricular filling. Fow consider what happens when the heart rate is $=3 !eats;min? each cycle takes up 3.)
sec with diastole and systole !oth lasting 3.$+ sec. /iastole has !een reduced more than systole -3.*sec
compared to 3.$+sec% reducing the time for ventricular filling. Systole cannot !e reduced any more without
affecting the stroke volume. An increase in heart rate !eyond this rate reduces diastole further resulting in
insufficient time for ventricular filling and a reduction in the volume of !lood pumped out with each !eat.
Therefore for most adults the ma0imum heart rate is around $=3!eats;min. 4n addition perfusion of the muscles
of the ventricles -via the coronary arteries% occurs predominantly during diastole. /ue to this at very high heart
rates the duration of coronary !lood flow is reduced. This is the very time when the heart is working ma0imally
and so has a high o0ygen demand risking myocardial ischaemia -inadeGuate o0ygen supply to cardiac muscle%.
CARDIAC OUTPUT
So far we have defined the amount of !lood e7ected !y each heart !eat as the stroke volume. (owever it is the
constant flow of !lood that is more important and this is referred to as the Ccardiac outputD. 9ardiac output -9O%
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is defined as the volume of !lood e7ected !y each ventricle per minute and is the
product of the stroke volume -S.% and the heart rate -!eats;min% it is e0pressed in
litres;min. 9learly the output of !oth ventricles has to !e the same otherwise all
the !lood would end up in either the systemic or pulmonary circulationH
Cardiac Output = Stroke Volume x Heart Rate
Ender normal resting conditions this is appro0imately 63ml 0 63!eats;min I
*<33ml;min -around +l;min%. The stroke volume is conventionally only that of
one ventricle and hence cardiac output is also conventionally that of one ventricle.
The true volume of !lood passing through the !oth sides of the heart is however
dou!le this figure. /ue to fact that different siJed patients will have different
cardiac outputs to allow meaningful comparisons to !e made the cardiac inde0
-94% is often used. This relates 9O to !ody surface area and is e0pressed in
litres;min;m
'
. 4t is calculated !y dividing 9O !y !ody surface area.
Cardiac Index = Cardiac Output/Body surface area
FACTORS AFFECTING CARDIAC OUTPUT
1rom the formula a!ove it is o!vious that only two factors affect cardiac output?
$. Stroke volume
'. (eart rate
1. Fac!"# a$$%c&'( #"!)% *!+,-%
There are three principle determinants of stroke volume#
the degree of filling of the ventricle or CpreloadD
the contractility of the myocardium
the resistance against which the ventricle has to work or CafterloadD.
Preload
The more a muscle fi!re is stretched !efore !eing stimulated to contract the greater its force of contraction.
This property is however limited !y the internal molecular structure of muscle such that a!ove a critical
-optimal% point further lengthening reduces force of contraction. This property is often referred to as the 1rank8
Starling mechanism and applies eGually to cardiac muscle. "lood returning to the heart during diastole
stretches the ventricular muscle fi!res. The greater the volume in the ventricle the greater the force -or more
correctly velocity% of contraction. :reload is therefore directly related to the end diastolic volume -or end
diastolic pressure as the two vary together% and providing myocardial contractility and afterload remain
constant increasing preload will increase stroke volume. (owever as stated a!ove !eyond a certain point
contractility falls and the clinical state of cardiac failure occurs -1ig $.%
4n clinical practice it is difficult to measure end diastolic volume and so we estimate this? central venous
pressure -9.:% gives an estimate of the right ventricular E/. pulmonary artery occlusion pressure -:AO:
sometimes called the Cwedge pressureD% gives an estimate of the left ventricular E/. -clinically the side we are
more often interested in%.
1ig. $# 1rank8Starling 9urve
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Myocardial contractility
This refers to the intrinsic a!ility of the cardiac muscle fi!res to contract and is independent of the degree of
preload and afterload. This is often referred to as the degree of inotropy and su!stances affecting this property
are called inotropes? those increasing rate and force of contractility have a positive inotropic action those that
decrease contractility have a negative inotropic action. The most important determinant of contractility is the
sympathetic nervous system. 4t acts directly or via the release of catecholamines from the adrenal gland
stimulating adrenergic receptors -i.e. they respond to adrenaline see !elow% which results in a positive inotropic
effect -1ig '.%. Bany factors cause a decrease in contractility i.e. are negatively inotropic? e0amples would !e an
acidosis hypo0ia hypocalcaemia and many drugs -particularly anaesthetics and antiarrhythmic drugs%.
1ig '.
Afterload
At the end of diastole the ventricular muscle starts to contract. 4n order to achieve this it has to overcome those
forces that are preventing it namely the tension in the ventricular wall itself and the resistance offered to the
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e7ection of !lood from the ventricle. 9learly this will !e very different for !oth
ventricles. Beasurement of true afterload is difficult and usually appro0imated as
follows#
Keft ventricular afterload is the resistance offered !y the systemic circulation
and termed the systemic vascular resistance -S.@%.
@ight ventricular afterload is the resistance offered !y the pulmonary
circulation and termed the pulmonary vascular resistance -:.@%.
4n health afterload is determined predominantly !y vascular tone or the degree of
vasoconstriction -or dilatation% of the arteries and arterioles. The greater the
degree of constriction the smaller the vascular lumen and the greater the
resistance offered to e7ection of !lood from the ventricle. As a result for a given
preload and contractility less !lood will !e e7ected the end systolic volume is
increased and stroke volume falls. .ascular tone is controlled !y the sympathetic nervous system and !y the
release of catecholamines again acting on adrenergic receptors.
2. Fac!"# a$$%c&'( .% .%a" "a%
The heart has an intrinsic pacemaker the sinoatrial node which in the a!sence of any other influence discharges
at around $33 !eats;min. 9hanges in heart rate are !rought a!out !y the autonomic nervous system either
directly or via effects on the adrenal glands. >enerally speaking sympathetic stimulation will increase the heart
rate via adrenergic receptors -a positive chronotropic effect% and parasympathetic stimulation via the vagus
nerve will decrease the heart rate -a negative chronotropic effect%. Ender normal circumstances resting heart
rate is !elow $33 !eats;min and therefore there is dominance of vagal -parasympathetic% activity. :roviding
stroke volume is unchanged an increase in heart rate will cause a rise in cardiac output and vice versa -9OIS.
0 (@%. This is true in normal healthy individuals as the stroke volume is relatively unaffected !etween heart
rates of +38$+3;min. As e0plained a!ove at heart rates much greater than this stroke volume eventually falls
along with cardiac output. At lower heart rates ventricular filling can increase to compensate !ut the point is
eventually reached where filling -E/.% is ma0imal and with a further reduction in rate once again cardiac
output will fall. 1or e0ample if the ma0imal stroke volume is $'3ml cardiac output will fall once the heart rate
drops !elow *3!eats;min.
ADRENERGIC RECEPTORS AND THEIR ACTIONS
These receptors respond to stimulation !y the sympathetic nervous system and catecholamines from the adrenal
gland. Their primary function is to prepare the !ody for the primitive Cfight or flightD response? ventilation
increases along with !ronchodilation cardiac output is increased through an increase in rate and contractility
and !lood is diverted from non8vital organs -e.g. the gut% to vital organs -e.g. heart kidneys and muscle%. There
are two main types of adrenergic receptors alpha -L% and !eta -M% each of which is divided into two su!types L8
$ L8' and M8$ M8'. Their location and actions in the cardiovascular system when stimulated is shown in ta!le
$.
Ta/+% 1. Adrenergic receptors and their effects
@eceptor type Kocation Effects
Alpha8$ "lood vessels .asoconstriction
Alpha8' "lood vessels .asoconstriction
"eta8$ (eart 4ncrease heart rate
4ncrease force of contraction
"eta8' "lood vessels
Kungs
.asodilatation
"ronchodilatation
0LOOD PRESSURE
So far we have concentrated on !lood flow from the heart -the cardiac output% however in day8to8day practice
we rarely measure flow -it is technically difficult to measure flow accurately% !ut freGuently measure !lood
pressure. 4t is important to understand how the two are related as pressure does not eGuate to flow? patients can
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have a CnormalD !lood pressure with much reduced flow and vice versa. When
measuring systemic arterial pressure a num!er of different figures can !e
calculated.
Systolic pressure the ma0imum pressure generated normally around
$'3mm(g
/iastolic pressure the minimum pressure generated normally around
=3mm(g
:ulse pressure the difference !etween systolic and diastolic normally
*3mm(g
Bean pressure the average over each complete cardiac cycle. This can !e
appro0imated to diastolic pressure plus one third of the pulse pressure and is
normally around <38$33mm(g.
"lood pressure comes a!out as a result of the heart pumping !lood into the arterial system which is of
relatively small capacity containing only a!out $+5 of the circulating volume. 4f the volume of the arterial
system changes for a given cardiac output the pressure will change? a fall in volume of the arterial system
results in an increased pressure and vice versa. 4t is not possi!le to measure the volume of the arterial system
!ut it is related to the radius of the !lood vessels? as they constrict their radius and volume will decrease. As the
radius decreases the resistance to flow increases such that if the radius is halved resistance to flow increases
appro0imately $,8fold -strictly speaking this is only true of certain types of fluids flowing in a particular way
!ut it gives an indication of the magnitude of the effect%. Therefore as the volume of the arterial system
decreases the resistance to flow through it increases dramatically. As resistance can also !e e0pressed in terms
of pressure drop per unit flow -relating to Ohm2s law .I4@%#
Resistance of the circulation = blood pressure/cardiac output
Therefore#
Blood pressure = cardiac output CO! x systemic "ascular resistance SVR!
"y looking at this eGuation we can immediately see that in a patient with a very low cardiac output !lood
pressure can !e maintained simply !y the !ody increasing the S.@.
One might ask Cwhy do we need a !lood pressure&D. After all it is flow of !lood that is important and if the
S.@ was low the heart could pump !lood easily. The answer lies in the organs the !lood perfuses. The kidneys
reGuire an adeGuate pressure to ensure that the glomeruli can filter and all organs reGuire a pressure gradient
!etween the arteries and veins to ensure adeGuate flow through their vast capillary !eds. Kow or no pressure
would and does result in organ failureH
Ender normal circumstances !lood pressure is tightly controlled !y#
Sympathetic and parasympathetic nerves
(ormonal systems? adrenaline noradrenaline renin angiotensin antidiuretic hormone -A/( vasopressin%
aldosterone and atrial naturietic factor -AF1%.
Other factors can also influence !lood pressure initiating either a direct response or a response via the a!ove
mechanisms for e0ample sepsis and meta!olic acidosis.
These systems work to maintain an adeGuate perfusion pressure and !lood flow to the vital organs and tissues of
the !ody. 9onsider what happens in clinical practice a typical case might !e a patient who has lost $.+8'l
!lood as a result of trauma and is continuing to !leed.
$. The decrease in circulating volume will reduce venous return and preload. This causes a fall in E/. S.
9O and finally !lood pressure.
'. The fall in !lood pressure is sensed !y receptors -!aroreceptors% located in the carotid !ody the arch of the
aorta and within the heart that send impulses to the vasomotor centre in the medulla.
). 4n response the vasomotor centre increases sympathetic outflow to the heart !lood vessels and adrenal
gland and decreases parasympathetic outflow to the heart.
*. As a result heart rate and force of contraction increase to try and restore 9O the arterioles constrict to
increase the S.@ and the large veins constrict to divert !lood to the central circulation -remem!er ,35 of
!lood volume is normally within the veins%. The aim is to restore arterial !lood pressure to a value that
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maintains adeGuate organ perfusion. 4nitially S.@ will increase to a greater
e0tent than 9O hence we may have a CnormalD !lood pressure !ut reduced
9O.
+. The sympathetic activity will also constrict vessels of non8essential organs
e.g. the skin and gut to divert !lood to vital organs e.g. !rain and heart.
,. A/( is released from the pituitary which increases rea!sorption of water and
sodium in the kidneys to help maintain the circulating volume and induces
further vasoconstriction.
6. As a result of decreased renal !lood flow and the sympathetic activity the
renin8angiotensin8aldosterone system is activated further increasing retention
of water and electrolytes with angiotensin 44 acting as a vasoconstrictor.
=. 4f there is overshoot most of the a!ove systems have a negative feed!ack loop
and stretching of the atria will stimulate release of AF1 causing salt and
water loss via the kidneys.
HOW DOES THIS MANIFEST CLINICALLY1
Our hypovolaemic trauma patient will have a num!er of signs and symptoms as a result of the a!ove. The first
signs will !e as a result of the increase in sympathetic activity? the patient will have a tachycardia !e
vasoconstricted -cool pale peripheries increased capillary refill time slightly increased perspiration% and the
diastolic !lood pressure may !e elevated -increased S.@%. They may have an increased respiratory rate
-tachypnoea%. Eventually if untreated the tachycardia and tachypnoea will increase and as venous return falls
and the S.@ cannot compensate cardiac output falls the systolic !lood pressure will decrease. The diastolic
!lood pressure may not !e measura!le. Erine output will decrease due to activation of the renin8angiotensin8
aldosterone system stimulated !y a reduced !lood pressure across the renal capillary !ed. 1inally consciousness
is impaired as !lood flow to the !rain falls. Fot surprisingly the key principle in managing these patients is
resuscitation of the circulation to maintain an adeGuate !lood pressure -not necessarily normal% for organ
perfusion along with haemorrhage control.
HOW IS ALL THIS RELEVANT TO ANAESTHESIA1
G%'%"a+ a'a%#.%#&a
Almost all anaesthetic drugs have important actions on the cardiovascular system#
.asodilators decreasing !oth preload and afterload
Fegatively inotropic reducing cardiac contractility
Fot surprisingly induction and maintenance of anaesthesia is usually accompanied !y a fall in the patient2s
!lood pressure? cardiac output falls due to decreased preload and myocardial contractility and the reduced
afterload decreases systemic vascular resistance. The situation may !e worsened !y the fact that some drugs
also depress the !aroreceptor refle0 to a varying degree and so there may not !e a compensatory tachycardia.
1inally the anaesthetics also depress the medulla reducing the sympathetic response to the fall in !lood
pressure. 1ortunately most healthy adults will tolerate a fall in !lood pressure of appro0imately '35 and once
surgery starts this increases sympathetic activity and !lood pressure is restored. 4f the !lood pressure remains
low then treatment may !e reGuired. 1rom the information a!ove we can now formulate a logical method to
restore the !lood pressure and ensure an adeGuate !lood flow to the various organs.
Increase preload. 4n an emergency the patient2s legs can !e elevated to augment venous return and preload.
(owever it is more usual to give a !olus of fluid intravenously $3ml;kg initially and monitor the response.
4ncreasing preload increases cardiac output and in turn systemic !lood pressure. @emem!er continuing to give
fluid will eventually cause over8stretching of the myocardial muscles fi!res and reduce the force of contraction
-1ig $.% leading to cardiac failure -although in practice this is hard to achieve in young fit adults%.
Increase afterload. Once preload has !een addressed then vasopressor drugs can !e used. These increase the
systemic vascular resistance !y acting as agonists -stimulating% the alpha adrenergic receptors -ta!le '%. /rugs
that act in this way include phenylephrine metaraminol and noradrenaline -norepinephrine%. 9are must !e taken
as the !aroreceptor refle0 is preserved and profound !radycardia may occur. Ephedrine has weak alpha and
!eta8$ agonist effects. Adrenaline -epinephrine% is usually only used if other drugs have !een ineffective or are
unavaila!le. 4t is an agonist at !oth alpha and !eta adrenergic receptors and the effects are dose8dependant? at
low doses it is predominantly a !eta -$ N '% agonist and so whilst the increased heart rate and force of
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contraction -!eta8$ effect% may improve cardiac output S.@ may fall due to the
!eta8' effects. With increasing doses the alpha agonist effect dominates
peripherally and S.@ is increased.
Remember# increasin$ SVR alone may increase blood pressure# but at the expense
of a reduction in stroke "olume and cardiac output%
Increase contractility. 4f myocardial depression with reduced contractility is
contri!uting to hypotension then it would !e sensi!le to use a drug with an
inotropic action. /o!utamine has !eta8$ agonist actions increasing contractility
and heart rate. /opamine the !iological precursor of noradrenaline has alpha and
!eta8$ agonist actions with the latter predominating at low doses and !oth effects
at higher doses.
Ta/+% 2. Drugs and their actions at adrenergic receptors
/rug @eceptor
Alpha8$ Alpha8' "eta8$ "eta8'
Adrenaline -low dose% O O
Adrenaline -high dose% OO OO O O
Foradrenaline OOO OOO O
:henylephrine OO
Betaraminol OO
Ephedrine O O O
/opamine -low dose% O
/opamine -high dose% OO O
/o!utamine O -O%
R%(&!'a+ a'a%#.%#&a 2#3&'a+ !" %3&4,"a+5
These techniGues result in vasodilatation -reduced S.@% proportional to the height of the !lock. As the local
anaesthetic drug spreads cranially there is an increasing !lock of the sympathetic nerves leaving the spinal cord
-the sympathetic chain% that supply the vascular !eds. 4f cardiac output is maintained there will !e a slight fall in
!lood pressure -remem!er ":I9O 0 S.@%. 4f however the cardiac output also falls due to reduced preload
-failure to maintain an adeGuate venous return% then !lood pressure will fall significantly. This may !e
compounded further if the !lock e0tends to reach a!ove the level of T+ -anaesthesia a!ove the nipple% as the
sympathetic supply to the heart will !e reduced and result in a !radycardia -due to unopposed parasympathetic
activity% and profound hypotension.
Mild hypotension. >ive intravenous fluid !olus $38'3ml;kg to maintain preload and cardiac output.
Alternatively an alpha agonist could !e used to counteract the vasodilatation eg phenylephrine or metaraminol.
9are must !e taken if these drugs are used as the !aroreceptor refle0 is preserved and the increase in !lood
pressure may !e accompanied !y a !radycardia. (owever ephedrine is often used as the first line drug despite
the fact that its main effects are due to its !eta8$ agonist action increasing heart rate.
Although theoretically a head8down position will increase venous return -preload% it may also encourage the
spread of the !lock and cause further vasodilatation. 9are must !e taken if this techniGue is employed.
Moderate to severe hypotension. This is usually a result of a high !lock accompanied !y a !radycardia. 4n
addition to adeGuate fluid volume to maintain preload atropine will !e reGuired -3.+mg iv%. Although
metaraminol or phenylephrine will cause vasoconstriction the pro!lem of a refle0 !radycardia remains.
(ypotension and !radycardia that does not respond to the a!ove measures should !e treated with small !olus
doses -$3micrograms% of adrenaline.
CONCLUSION
The key to treating the changes that occur in a patient2s cardiovascular status as a result of giving them an
anaesthetic is understanding the underlying physiology and how this has !een distur!ed. This will then allow
distur!ances to !e treated in the safest and most effective manner with little potential for harm to the patient.
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