Physiology of heart

Anatomy and physiology

1. Mr.Binu Babu
Asst.Professor
Mrs.JincyEalias
Asst.Professor

2. Electrical Activity of the Heart
•Theheartbeatoriginatesinaspecialized
cardiacconductionsystem.
•Theheartbeatsnormallyinanorderly
sequence:Contractionoftheatria(atrial
systole)isfollowedbycontractionofthe
ventricles(ventricularsystole),andduring
diastoleallfourchambersarerelaxed.

3. CONDUCTION SYSTEM OF THE
HEART
•Action potentials (electrical impulses) in the heart
originate in specialized cardiac muscle cells, called
autorhythmiccells.
•These cells are self-excitable, able to generate an
action potential without external stimulation by
nerve cells.
•The autorhythmiccells serve as a pacemaker to
initiate the cardiac cycle (pumping cycle of the
heart) and provide a conduction system to
coordinate the contraction of muscle cells
throughout the heart.

4. •Theautorhythmiccellsareconcentratedin
thestructuresthatmakeuptheconduction
system
–thesinoatrialnode(SAnode)
–theinternodalatrialpathways
–theatrioventricularnode(AVnode)
–thebundleofHisanditsbranches
–thePurkinjesystem.

5. Sinoatrialnode
•Itisapartofthewallofrightatriumclosetothe
openingofsuperiorvenacava.Itgenerates
impulsesapproximatelyattherateof72
times/min.SAnodeiscalledthepacemaker
becauseitdepolarizesatafasterratethanany
othergroupofcellsintheheart,andimposesthat
fasterrateontheheartasawhole.
Atrioventricularnode
•Itisapartofthewallofrightatriumclosetothe
atrioventricularseptumandneartothetricuspid
valve.Itgeneratesimpulsesapproximatelyatthe
rateof60times/min.

6. BundleofHis
•Itisathickbandofmuscle
fibersstartingfromA.V
Node.Itrunsalongwithintra
ventricularseptum.Itdivides
intorightandleftbundle
branch.Itgeneratesimpulses
approximatelyattherateof
40times/min.
PurkinjeFibers
•Thesefibersarisefromthe
branchesofbundleofHis.
Thesefiberspierceintothe
ventricularmyocardium.

7. •Cardiacexcitationnormallybeginsinthesinoatrial(SA)
node,locatedintherightatrialwalljustinferiorand
lateraltotheopeningofthesuperiorvenacava.
•Thespontaneousdepolarizationisapacemaker
potential.(Thepacemakerpotentialisaslow,positive
increaseinvoltageacrossthecell'smembrane)
•Whenthepacemakerpotentialreachesthreshold,it
triggersanactionpotential.Eachactionpotentialfromthe
SAnodepropagatesbothatriaviagapjunctionsinthe
intercalateddiscsofatrialmusclefibersandcontractboth
atriaatthesametime.

9. •Byconductingalongatrialmusclefibers,the
actionpotentialreachestheatrioventricular
(AV)node,locatedintheinteratrialseptum,
justanteriortotheopeningofthecoronary
sinus.
•FromtheAVnode,theactionpotentialenters
theatrioventricular(AV)bundle(also
knownasthebundleofHis).Thisbundleis
theonlysitewhereactionpotentialscan
conductfromtheatriatotheventricles.

11. •AfterpropagatingalongtheAVbundle,the
actionpotentialentersboththerightandleft
bundlebranches.
•Finally,thelarge-diameterPurkinjefibers
rapidlyconducttheactionpotentialbeginning
attheapexoftheheartupwardtothe
remainderoftheventricularmyocardium.
Thentheventriclescontract,pushingtheblood
upwardtowardthesemilunarvalves.

12. Conduction Speeds in Cardiac Tissue
Tissue Conduction Rate (m/s)
SA node 0.05
Atrial pathways 0.1
AV node 0.05
Bundle of His 0.1
Purkinje system 0.4
Ventricular muscle 0.1

13. •SAnodeiscalledthepacemakeroftheheart.
IfforanyreasontheSAnodestopsbeating,the
AVnode,whichhasthenextfastestrateof
depolarization,wouldbecometheheart’s
pacemaker.IftheAVnodefailed,thebundleof
Hiswouldtakeover.Ifitfailed,thePerkinje
fiberswouldstarttheheartbeat,andifthey
failedaswell,agroupofcellssomewhereelse
intheheartwouldstartpulsing.Iffailed,
eventuallyitcannolongersustainlife.

14. The Electrocardiogram
•Thebodyfluidsaregood
conductors,fluctuationsin
potentialthatrepresentthe
algebraicsumoftheaction
potentialsofmyocardial
fiberscanberecorded
extracellularly.
•Therecordofthese
potential fluctuations
duringthecardiaccycleis
theelectrocardiogram
(ECG).

16. ECG Intervals.
Normal Durations
Intervals AverageRange
Events in the Heart during
Interval
PR interval
a
0.18
b
0.12–0.20
Atrial depolarization and
conduction through AV node
QRS duration 0.08 to 0.10
Ventricular depolarization
and atrial repolarization
QT interval 0.40 to 0.43
Ventriculardepolarization
plus ventricular
repolarization
ST interval (QT minus
QRS)
0.32 . . .
Ventricular repolarization
(during T wave)
a
Measuredfrom the beginning of the P wave to the beginning of the QRS
complex.
b
Shortensas heart rate increases from average of 0.18 s at a rate of 70
beats/min to 0.14 s at a rate of 130 beats/min.

17. Properties of cardiac muscles
•Excitability
•Conduction
•Contraction
•Refractory period
•Functional Syncytium
•Auto rhythmicity
•Staircase phenomenon

18. Excitation
•It is an electrical event. Calcium ion are responsible
for this event
Conduction
•Theactionpotentialispropagatedallalongthe
lengthofthemusclefiberthisphenomenonis
knownasconduction.
Contraction
•Itistheshorteningofmusclefibres.
Refractoryperiod
•Itistheperiodduringwhichthe2
nd
stimuluscannot
generateafreshactionpotential.Itisdividedinto
two
–Absoluterefractoryperiod(0.25sec)
–Relativerefractoryperiod(0.05sec)itmaygeneratean
actionpotential.

19. Functional Syncytium
•Cardiacmusclesactassingleunitthisphenomenon
iscalledFunctionalSyncytium.
Autorhythmicity
•Cardiacmusclecangeneratetheirownimpulse,this
propertyofheartiscalledtheautorhythmicity
Staircasephenomenon
•Whenaseriesofstimuliofthesameintensityare
sentintothemuscleafteracalmperiod,thefirstfew
contractionsoftheseriesshowasuccessiveincrease
inamplitude.

20. Cardiac Cycle
•Cardiaccycleisdefinedassequenceofcyclicalchanges
takingplaceintheheartfromonebeattothenext.
•Acardiaccycleconsistsofsystoleanddiastoleofthe
atriaplussystoleanddiastoleoftheventricles.
•Acardiaccycledurationis0.8sec.
ChangesduringCardiaccycle
1.Mechanicalchanges:contractionandrelaxationofatriaand
ventricles.
2.Electricalchanges
3.Volumechangeinsidetheheart
4.Pressurechangeinsidethechambers
5.Openingandclosingofvalves
6.Heartsounds

21. •Ineachcardiaccycle,theatriaand
ventriclesalternatelycontractandrelax,
forcingbloodfromareasofhigherpressure
toareasoflowerpressure.Asachamberof
theheartcontracts,bloodpressurewithinit
increases.

22. AtrialSystole
•DepolarizationoftheSAnodecausesatrialdepolarization
whichresultsatrialsystole.
•Duringatrialsystole,boththeatriacontractsatthesametime,
whereastheventriclesarerelaxed.
•Thecontractionofatrialmusclesnarrowsthevenacaval
orificesandpulmonaryveinorifices.
•Andexertapressureonthebloodatria,whichforcesbloodto
moveintoventriclesthroughtheopentricuspidandmitral
valves.
•Atrialsystolewhichlastsabout0.1sec.Theendofatrial
systoleisalsotheendofventriculardiastole(relaxation).
•Eachventriclecontainsabout130mLattheendofits
relaxationperiod(diastole).Thisbloodvolumeiscalledthe
end-diastolicvolume(EDV).

23. VentricularSystole
•Whentheventriclesarecontractingtheatria
arerelaxed(atrialdiastole).
•Ventriculardepolarizationcausesventricular
systole.Whenventricularsystolebegins,
pressurerisesinsidetheventriclesandpushes
bloodupagainsttheatrioventricular(AV)
valves,forcingthemshut.Forabout0.05
seconds,boththesemilunarandAVvalvesare
closed.Thisistheperiodofisovolumetric
contraction.

24. •Whenleftventricularpressureexceedsaorticpressure(80
mmHg)andrightventricularpressureexceedspressurein
thepulmonaryartery(20mmHg),bothsemilunarvalves
open.
•Atthispoint,ejectionofbloodfromtheventriclesbegins.
•Theleftventricleejectsabout70mLofbloodintotheaorta
andtherightventricleejectsthesamevolumeofbloodinto
thepulmonarytrunk.Thevolumeremainingineach
ventricleattheendofsystole,about60mL,istheend-
systolicvolume(ESV).
•Ventricularsystolelastsabout0.3sec.
•Strokevolume(SV)istheamountofbloodejectedbythe
leftventricleinonecontraction.
•SV=EDV-ESV(130-60=70ml)

25. RelaxationPeriod(diastole)
•Duringtherelaxationperiod,whichlastsabout0.4
sec,theatriaandtheventriclesarerelaxed.Blood
flowsintotheheartthroughoutdiastole,fillingthe
atriaandventricles.
•Oncetheatrialmusclesarerelaxedvenacaval
orificesandpulmonaryveinsopenandatriaisfilled
blood.
•Oncetheventricularmuscleisfullycontracted,the
ventricularpressuresdroprapidly.Andbloodinthe
aortaandpulmonarytrunkbeginstoflowbackward
towardtheregionsoflowerpressureinthe
ventricles.

26. •Astheventriclescontinuetorelax,thepressure
fallsquickly.Whenventricularpressuredrops
belowatrialpressure,theAVvalvesopen,and
ventricularfillingbegins.Bloodthathasbeen
flowingintoandbuildingupintheatriaduring
ventricularsystolethenrushesrapidlyintothe
ventricles.Attheendoftherelaxationperiod,
theventriclesareaboutthree-quartersfull.The
PwaveappearsintheECG,signalingthestart
ofanothercardiaccycle.

27. Cardiac Output
•Cardiacoutput(CO)isthevolumeofblood
ejectedfromtheheartineachminute.
•Cardiacoutputisexpressedinlitresperminute
(L/min).
•Cardiacoutputistheproductofheartrate(HR)
andstrokevolume(SV).
•CO=HRxSV
•Inaresting,supineman,itaveragesabout5
L/min(72beats/minx70mL).

28. Duringexercise,venousreturnincreasesand
stretchestheventricularmyocardium,which
inresponsecontractsmoreforcefully,andresultsin
increasestrokevolume.
Morebloodispumpedwitheachbeat,andat
thesametime,theheartrateincreases,causing
cardiacoutputtoincreasetoasmuchasfourtimes
therestinglevel,andevenmoreforathletes.

29. Factors affecting cardiac output
•Factors increases cardiac output
–Anxiety and excitement
–Eating
–Exercise
–High environmental temperature
–Pregnancy
•Factors decreases cardiac output
–Sitting or standing from lying position
–Rapid arrhythmias
–Heart disease

30. Regulation of cardiac output
•Changes in cardiac output can be produced
by changes in heart rate or stroke volume or
both.

31. Regulation of Heart Rate
•Theheartgeneratesitsownelectrical
impulse,whichbeginsattheSAnode.The
nervoussystemcanchangetheheartratein
responsetoenvironmentalcircumstances.
Inthebrain,themedullaoblongata
containsthecardiovascularcenters:the
acceleratorcenterandtheinhibitorycenter.

32. •Thecardiovascularcenterdirectsappropriate
outputbyincreasingordecreasingthe
frequencyofnerveimpulsesinboththe
sympatheticandparasympatheticbranchesof
theANS.
•Sympatheticimpulses—alongsympathetic
nervesfromthethoracicspinalcordtotheSA
node,AVnode,andmostofthemyocardium—
increaseheartrateandforceofcontraction.
•Parasympatheticimpulses—alongthevagus
nervetotheSAnode,AVnode,andatrial
myocardium—decreaseheartrate.

34. Medullary cardio vascular centerreceives information
necessaryfor changes in the heart rate from higher brain
centers(cerebral cortex, limbic system and hypothalamus)
and sensory receptors such as
–Proprioceptors
–Chemoreceptors
–Baroreceptors
located in the internal carotid arteries and the aortic arch.
•The baroreceptors detect changes in blood pressure.
•The chemoreceptors are cells specialized to detect changes
in the oxygen content of the blood (as well as changes in
carbon dioxide and hydrogen ion content).
•The Proprioceptors detect changes in position and
movement.

36. •In response to the information received by the
medullary cardiac center, either sympathetic
impulses or parasympathetic impulses gets
initiated.
•Sympathetic system response
Impulses in the cardiac accelerator nerves trigger
the release of norepinephrine (by adrenal
medulla), which binds to beta-1 (β1) receptors on
cardiac muscle fibers. This results,
–SA (and AV) node speeds the rate of spontaneous
depolarization so that they fire impulses more
rapidly and heart rate increases.
–Increased contraction of atria and ventricles thus
increases stroke volume.

37. •Parasympathetic system response,
They release acetylcholine, which ↓ HR by ↓
slow inflow of Na+ and Ca++ and by ↑the
subsequent outflow of potassium (K+).
–Decreased rate of spontaneous depolarization
of SA (and AV) node decreases heart rate.

38. Factors contribute to regulation of
heart rate
Chemical regulation
–Cardiac activity depressed by
•Hypoxia
•Acidosis
•Alkalosis
–Hormones
•Catecholaminesand thyroid hormones increase HR
and contractility
–Cations
•Alterations in balance of K
+
, Na
+
and Ca
2+
alter HR
and contractility

39. Age
Gender
•Female HR higher
Physical fitness
•Resting bradycardia
Body temperature
•Increase causes SA node to discharge more
rapidly

40. Regulation of Stroke Volume
•Strokevolumeisdeterminedbysympathetic
stimulimakingthemyocardialmusclefibers
contractwithgreaterstrengthand
parasympatheticstimulihavingtheopposite
effect.
•Thefactorsregulatestrokevolume
–Preload:thedegreeofstretchofheartmuscle
beforeitcontracts.
–Contractility:theforcefulnessofcontractionof
individualventricularmusclefibers.
–Afterload:theresistancetoejectionofbloodfrom
theventricle.

41. Preload
•Preload is defined as the force acting to stretch
the ventricular fibers at end-diastole.
•An increase in myocardial muscle fiber length
is associated with an increase in the force of
contraction and thus increases the stroke
volume and cardiac output.
•Higher the preload, the higher the stroke
volume will be.

42. Contractility
•Contractility refers to the force generated by
the contracting myocardium.
•Increased contractility results in increased
stroke volume.
•Contractility is enhanced by circulating
catecholamines, sympathetic neuronal activity,
and certain medications
•Contractility is depressed by hypoxemia,
acidosis, and certain medications (eg, beta-
adrenergic blocking agents)

43. Afterload
•Afterload is the resistance to ejection of blood from
the ventricle.
•Theejectionofbloodfromtheheartbeginswhen
pressureintherightventricleexceedsthepressure
inthepulmonarytrunk(about20mmHg),andwhen
thepressureintheleftventricleexceedsthe
pressureintheaorta(about80mmHg).Atthat
point,thehigherpressureintheventriclescauses
bloodtopushthesemilunarvalvesopen.The
pressurethatmustbeovercomebeforeasemilunar
valvecanopenistermedtheafterload.
•Anincreaseinafterloadcausesstrokevolumeto
decrease.