125 Introduction to Cardiovascular Physiology

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INTRODUCTION TO CARDIOVASCULARPHYSIOLOGYANAESTHESIA TUTORIAL OF THE WEEK 125

16TH

MARCH 2009

Toby Elkington, Specialist RegistrarCarl Gwinnutt, ConsultantDepartment of Anaesthesia, Salford Royal !S "oundationTrust, Salford, #$Correspondence to tobyelkington%hotmail&com

This tutorial is intended as a very basic introduction to cardiovascular physiology with particularreference 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 !etterappreciation 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 throughthe 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 !loodis 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 inprogressive 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. 4nthe 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 tissueswhile 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 thelow 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 thatoriginates in the sino8atrial -SA% node spreads through the atrial muscle crosses

the atrio8ventricular -A% node reaches the ventricles via the !undle of (is andsupplies 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 (isS 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 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 onlyindicates 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 toprevent !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%. Eventuallythe 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. Whenthe 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 pressurerises 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 thepressure 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. ndernormal 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 !yventricular 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.$+ sec. /iastole has !een reduced more than systole -3.*seccompared to 3.$+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 ininsufficient 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 heartrates 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 theproduct 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 allthe !lood would end up in either the systemic or pulmonary circulationH

Cardiac Output = Stroke Volume x Heart Rate

nder normal resting conditions this is appro0imately 63ml 0 63!eats;min I*


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Myocardial contractilityThis 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 propertyare 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 thesympathetic 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 inotropiceffect -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 thoseforces 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 !othventricles. 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 ofvasoconstriction -or dilatation% of the arteries and arterioles. The greater the

degree of constriction the smaller the vascular lumen and the greater theresistance 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 therelease 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 eitherdirectly 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 vagusnerve will decrease the heart rate -a negative chronotropic effect%. nder normal circumstances resting heart

rate is !elow $33 !eats;min and therefore there is dominance of vagal -parasympathetic% activity. :rovidingstroke 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 heartrates 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 iseventually 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 ratedrops !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? ventilationincreases 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%. Thereare 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 effectseceptor type Kocation Effects

Alpha8$ "lood vessels asoconstrictionAlpha8' "lood vessels asoconstriction

"eta8$ (eart 4ncrease heart rate4ncrease force of contraction

"eta8' "lood vesselsKungs

asodilatation"ronchodilatation

LOOD PRESSURE

So far we have concentrated on !lood flow from the heart -the cardiac output% however in day8to8day practicewe 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. Whenmeasuring 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 !eappro0imated to diastolic pressure plus one third of the pulse pressure and is

normally around


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maintains adeGuate organ perfusion. 4nitially S will increase to a greatere0tent 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 inducesfurther vasoconstriction.

6. As a result of decreased renal !lood flow and the sympathetic activity therenin8angiotensin8aldosterone 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 CLINICALLY

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 !evasoconstricted -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. rine output will decrease due to activation of the renin8angiotensin8aldosterone 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 isresuscitation 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 ANAESTHESIA

G%'%"a+ a'a%#%#&aAlmost all anaesthetic drugs have important actions on the cardiovascular system#

asodilators decreasing !oth preload and afterloadFegatively 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 reducedafterload 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 oncesurgery 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 torestore 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 thesystemic vascular resistance !y acting as agonists -stimulating% the alpha adrenergic receptors -ta!le '%. /rugsthat 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 areunavaila!le. 4t is an agonist at !oth alpha and !eta adrenergic receptors and the effects are dose8dependant? atlow 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 iscontri!uting to hypotension then it would !e sensi!le to use a drug with an

inotropic action. /o!utamine has !eta8$ agonist actions increasing contractilityand heart rate. /opamine the !iological precursor of noradrenaline has alpha and

!eta8$ agonist actions with the latter predominating at low doses and !oth effectsat higher doses.

Ta/+% 2.Drugs and their actions at adrenergic receptors/rug eceptor

Alpha8$ Alpha8' "eta8$ "eta8'

Adrenaline -low dose%

Adrenaline -high dose% Foradrenaline

:henylephrine

Betaraminol Ephedrine

/opamine -low dose% /opamine -high dose%

/o!utamine -%

R%(&!'a+ a'a%#%#&a #3&'a+ !" %3&4,"a+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 thesympathetic 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. 4naddition to adeGuate fluid volume to maintain preload atropine will !e reGuired -3.+mg iv%. Althoughmetaraminol 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 !olusdoses -$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 allowdistur!ances to !e treated in the safest and most effective manner with little potential for harm to the patient.

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125 Introduction to Cardiovascular Physiology