BIOL- 2305 Cardiac Physiology - Anatomy Review

Cardiac Physiology

!nctions o" the #eart Generating blood pressure Routing blood Heart separates pulmonary and systemic circulations Ensuring one-way blood flow Regulating blood supply Changes in contraction rate and force match blood delivery to changing metabolic needs

Blood low $hro!gh and P!m% Action o" the #eart

Blood low $hro!gh #eart

Cardiac &!scle Cells &yocardial A!torhythmic Cells Membrane potential never rests pacema er potential! &yocardial Contractile Cells Have a different loo ing action potential due to calcium channels! Cardiac cell histology "ntercalated discs allow branching of the myocardium Gap #unctions $instead of synapses% fast Cell to cell signals Many mitochondria &arge ' tubes

'lectrical Activity o" #eart Heart beats rhythmically as result of action potentials it generates by itself $autorhythmicity% 'wo speciali(ed types of cardiac muscle cells Contractile cells ))* of cardiac muscle cells +o mechanical wor of pumping ,ormally do not initiate own action potentials A!torhythmic cells +o not contract -peciali(ed for initiating and conducting action potentials responsible for contraction of wor ing cells

Intrinsic Cardiac Cond!ction (ystem (A )ode *0-+0 ,%m -ets the pace of the heartbeat A- )ode .0-/0 ,%m +elays the transmission of action potentials P!r0in1e "i,ers 20-30 ,%m Can act as pacema ers under some conditions

"ntrinsic Conduction -ystem A!torhythmic cells. "nitiate action potentials Have drifting resting potentials called pacema er potentials /acema er potential - membrane slowly depolari(es drifts to threshold0 initiates action potential0 membrane repolari(es to -12 m3! 4se calcium influ5 $rather than sodium% for rising phase of the action potential

Pacema0er Potential 23 channels closed. +ecreased efflu5 of 67 Constant in"l!4 o" )a3. no voltage-gated ,a7 channels 5ri"ting de%olari6ation. 67 builds up and ,a7 flows inward -oltage-gated Ca23 $-channels o%en at 7 -55m-. -mall influ5 of Ca87 further depolari(es to threshold $-92 m3% via 'ransient Channels -oltage-gated Ca23 L-channels o%en at $hreshold8 sharp depolari(ation due to activation of Ca87 & channels allow large influ5 of Ca87 via &ong &asting Channels Pea0 at 7 320 m-8 Ca-& channels close0 voltage-gated 6 channels open0 repolari(ation due to normal 67 efflu5 23 channels close8 at -12m3

AP o" Contractile Cardiac cells Contractile cells Rapid depolari(ation

Rapid0 partial early repolari(ation0 prolonged period of slow repolari(ation which is plateau phase Rapid final repolari(ation phase :ction potentials of cardiac contractile cells e5hibit prolonged positive phase $%latea!% accompanied by prolonged period of contraction Ensures ade;uate e<ection time /lateau primarily due to activation of slow &-type Ca87 channels

9hy A Longer AP In Cardiac Contractile i,ers: :t no time would we want summation and tetanus in our myocardium =ecause long re"ractory %eriod occurs in con<unction with prolonged %latea! %hase0 summation and tetanus of cardiac muscle are impossible /lateau ensures alternate periods of contraction and rela5ation which are essential for pumping blood

Re"ractory %eriod

&em,rane Potentials in A!torhythmic and Contractile cells

Action Potentials

'4citation-Contraction Co!%ling in Cardiac Contractile Cells :ction potential from :utorhythmic cells is passed to contractile cells0 propagating down '-tubules0 causing a small influ5 of Ca87 via Ca87 &channels Ca87 entry through &-type channels in ' tubules triggers larger release of Ca87 from sarcoplasmic reticulum Ca87 induced Ca87 release leads to cross-bridge cycling and contraction

'lectrical (ignal low - Cond!ction Pathway Cardiac impulse originates at (A node :ction potential spreads throughout right and left atria "mpulse passes from atria into ventricles through A- node $only point of electrical contact between chambers% :ction potential briefly delayed at A- node $ensures atrial contraction precedes ventricular contraction to allow complete ventricular filling% "mpulse travels rapidly down interventricular septum by means of ,!ndle o" #is "mpulse rapidly disperses throughout myocardium by means of P!r0in1e "i,ers Rest of ventric!lar cells activated by cell-to-cell spread of impulse through gap <unctions

'lectrical Cond!ction in #eart :tria contract as single unit followed after brief delay by a synchroni(ed ventricular contraction

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'lectrocardiogram ;'C<= Record of overall spread of electrical activity through heart Represents. Recording part of electrical activity induced in body fluids by cardiac impulse that reaches body surface Recording of overall spread of activity throughout heart during depolari(ation and repolari(ation )ot direct recording of actual electrical activity of heart )ot a recording of a single action potential in a single cell at a single point in time Comparisons in voltage detected by electrodes at two different points on body surface0 not the actual potential +oes not record potential at all when ventricular muscle is either completely depolari(ed or completely repolari(ed 'lectrocardiogram ;'C<=

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'lectrocardiogram ;'C<=

'C< In"ormation <ained ,on-invasive Heart Rate -ignal conduction Heart tissue Conditions

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Intrinsic Cardiac Cond!ction (ystem

Cardiac Cycle - illing o" #eart Cham,ers Heart is two pumps that wor together0 right and left half Repetitive contraction $systole% and rela5ation $diastole% of heart chambers =lood moves through circulatory system from areas of higher to lower pressure! Contraction of heart ventricles produces the pressure

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Cardiac Cycle - &echanical 'vents

Cardiac Cycle - &echanical 'vents 2 Phases o" -entric!lar (ystole. Isovol!mic Contraction Phase8 >irst phase of ventricular contraction 3entricles begin to contract0 pushing :3 valves close0 -& valves still closed0 pressure in ventricles rises /ressure in ventricles is not enough to open semilunar valves 'herefore0 All -alves Are Closed -entric!lar '1ection Phase8 -econd $and last% phase of ventricular contraction /ressure in ventricles rises and forces semilunar valves open! =lood is e<ected into arteries! 3entricular pressure rises and e5ceeds pressure in the arteries0 the semil!nar valves o%en and ,lood is e1ected>

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9iggers 5iagram

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#eart (o!nds >irst heart sound or lubb :3 valves close and surrounding fluid vibrations at systole -econd heart sound or dupp Results from closure of aortic and pulmonary semilunar valves at diastole0 lasts longer

Le"t -entric!lar -ol!me '5- ? 7@35 mL 'he blood volume in the heart before ventricular e<ection0 about ?@A m&0 is called the end diastolic volume '(- ? 7 /5 mL 'he blood volume remaining in the heart after ventricular e<ection0 about 1A m&0 is called the end systolic volume

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Cardiac O!t%!t ;CO= and Reserve Cardiac O!t%!t ;CO= is the amount of blood pumped by each ventricle in one minute CB is the product of heart rate ;#R= and stro0e vol!me ;(-= HR is the number of heart beats per minute -3 is the amount of blood pumped out by a ventricle with each beat Cardiac reserve is the difference between resting and ma5imal CB Cardiac O!t%!t ? #eart Rate A (tro0e -ol!me Cardiac Butput C A litersDmin $resting0 on average% HR beatsDmin 5 -3 m&Dbeat E CB F2 beatsDmin 5 F2 m&Dbeat E 9)22 m&Dmin HR Rate. beats per minute -tro e 3olume. ml per beat -3 E E+3 G E-3s Residual $about A2*% orm!las8 CO ? #R A ((- ? '5- B '(actors A""ecting Cardiac O!t%!t Cardiac O!t%!t ;CO= ? #eart Rate ;#R= A (tro0e -ol!me ;(-= #eart rate :utonomic innervation Hormones - Epinephrine $E%0 norepinephrine$,E%0 and thyroid hormone $'@% Cardiac refle5es (tro0e vol!me -tarlings law 3enous return Cardiac refle5es actors In"l!encing Cardiac O!t%!t Intrinsic. results from normal functional characteristics of heart - contractility0 HR0 preload stretch '4trinsic. involves neural and hormonal control G :utonomic ,ervous system

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(tro0e -ol!me ;(-= +etermined by e5tent of venous return and by sympathetic activity "nfluenced by two types of controls "ntrinsic control E5trinsic control =oth controls increase stro e volume by increasing strength of heart contraction

Intrinsic actors A""ecting ( -tro e 3olume >actors. Contractility G cardiac cell contractile force due to factors other than E+3 /reload G amount ventricles are stretched by contained blood - E+3 3enous return - s eletal0 respiratory pumping :fterload G bac pressure e5erted by blood in the large arteries leaving the heart

ran0-(tarling Law /reload0 or degree of stretch0 of cardiac muscle cells before they contract is the critical factor controlling stro e volume

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ran0-(tarling Law -low heartbeat and e5ercise increase venous return to the heart0 increasing -3 =lood loss and e5tremely rapid heartbeat decrease -3

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'4trinsic actors In"l!encing ( Contractility is the increase in contractile strength $force of contraction%0 independent of stretch and E+3 "ncrease in contractility comes from "ncreased sympathetic stimuli Hormones - epinephrine and thyro5ine Ca87 and some drugs "ntra- and e5tracellular ion concentrations must be maintained for normal heart function Contractility and )ore%ine%hrine (ym%athetic stimulation releases nore%ine%hrine and initiates a cA&P second-messenger system

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&od!lation o" Cardiac Contractions

actors that A""ect Cardiac O!t%!t

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&ed!lla O,longata Centers A""ect A!tonomic Innervation Cardio-acceleratory center activates sym%athetic neurons Cardio-inhi,itory center controls %arasym%athetic neurons Receives input from higher centers0 monitoring blood pressure $,arorece%tors% and dissolved gas concentrations $chemorece%tors%

Re"le4 Control o" #eart Rate

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'sta,lishing )ormal #eart Rate -: node establishes baseline Modified by :, (ym%athetic stim!lation -upplied by cardiac ple5us0 stemming from the sym%athetic tr!n0 '%ine%hrine and nore%ine%hrine released /ositive chronotropic $HR% and inotropic $force% effect Parasym%athetic stim!lation - +ominates -upplied by cardiac ple5us0 stemming from vag!s nerve Acetylcholine secreted ,egative chronotropic $HR% and inotropic $force% effect

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Reg!lation o" Cardiac O!t%!t

Congestive #eart ail!re ;C# = Congestive heart failure $CH>% is caused by. Coronary atherosclerosis /ersistent high blood pressure Multiple myocardial infarcts +ilated cardiomyopathy $+CM%

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