Transcription
Hello. Um, good day to everyone. I am Dr. Lapira and I will be discussing a topic under chapter 10 which is the rythmical excitation of the heart. Okay.
So for the learning outcomes, at the end of this learning session, the future bedd must be able to first, uh, discuss the specialized excitatory and conductive system of the heart. Second, summarize transmission of the cardiac impulse through the human heart and understand the role of noduction and excitation of the heart.
So first, uh, we discuss this uh specialized excitatory and conductive system of the heart. So from this uh topic, um, we all know that the human heart has a special system, okay, which has the ability to perform rhythmic self-excitation. Okay, from the name, self-rhythmic. So may rhythm no yung contraction or beating nung heart, and the heart has the ability to be on its own, no, yung tinatawag na self-excitation. Okay, so aalamin natin kung paano yung nag-start no, and kung papaano siya nagiging spontaneous. Okay, so this self-excitation is uh repetitive, no, repetitive contraction approximately, according to Guyton, 100 times each day. Okay? Yung repetitive contraction ni heart, okay? And about 3 billion times, ano, in the average human lifetime. Okay? So imagine no, yung um workload nung heart ninyo no, which has to do rhythmic contraction throughout the day. Okay.
So first, ano ba, onong function ng uh conductive system natin? So when this system functions normally, so the atria no? So we all know the chambers of the heart. We have four chambers, right? Left and right atrium, and right and left ventricles. So, um, iyung function nitong mga to is to pump blood, okay, throughout the chambers, throughout the uh lungs, and throughout the systemic circulation. So ang function ng conductive system is para mag-contract ong mga chambers na to is to first generate electrical impulses. Okay? Pag naka-generate ka ng electrical impulses no, through the ability of the heart no, iyung tinatawag nating self-excitation, this will initiate now rhythmical contraction. Okay.
So this rhythmic contraction, it starts actually with the atria. Okay. So according to Guyton, yung atria daw natin contracts about 1/6. So remember that, the 1/6 of a second ahead of that of the ventricles. Okay. So again, your atria contracts about 1/6 of a second ahead of ventricular contractions. So para saan ba yun na nauunang mag-contract si atria? Okay. This is to allow filling of the ventricles. Okay? So imagine if sabay yan. Okay. So yung ifi-fill mo pa lang towards the ventricle is is na-pump na. Okay? Kung sabay sila. Okay. So kaya nas nauuna si atria ah compared kay ventricle, this will allowing of the ventricles before these ventricles pump blood towards the lungs and the systemic circulation. Okay.
Okay. So another function is again, conduct impulses rapidly through the heart. Okay. So hindi lang naman ang function ng ating heart is to pump blood on the peripheral circulation, but also to uh pump blood towards the coronaries. Okay. So siung si si blood mismo pagka-pump niyan no, during relaxation, diyan yung ah maximum uh blood flow no sa coronaries natin for our heart to be able to use no the nutrients and oxygen no na galing din sa lungs and systemic circulation. Okay.
So next. So this image or figure shows you no, an illustration showing the nodle system no, up to the perking fibers and yung mga ating mga bundle branches. Okay? On the right image shows you no, na dito evident yung contraction ni atria nauuna sa inyong ventricles. Okay? So spontaneous niyo siya no? And may rhythm. Okay.
So this again image shows the specialized excitatory and conductive system of the heart again, which controls cardiac contractions. So as you can see here, very visible si SA node no. You can found there. You can find there on the atria, right? Atrium, in which no sa sinus node or sinoatrial node natin, diyan po natin no nage-generate yung normal rhythm impulse no. Kaya nga siya tinawag na SA node is the pacemaker, kasi siya yung nagge-generate ng normal rhythmical impulse ng heart natin. So after the SA node, andiyan na yung ating internodal systems. When we say inter, means in between the two nodes, okay? The SA and the AV node. So that's the internodal pathway paste, which conducts impulses no from the SA node towards naman to the AV node. Okay.
So, um, we discuss now the SA node or your sinoatrial node. So it is a small, flattened, ellipsoidal strip of specialized cardiac muscles. So basically, your nodes are specialized cardiac muscles. A node is immediately located below and slightly lateral to the opening of the superior vena cava. Okay. So uh slightly lateral and opening of the superior vena cava and located on the superior posterolateral wall of the right atrium. Okay. And it connects directly with the atrial muscle fibers, so that any action potential that begins in the sinus node spreads immediately into the atrial muscle wall. Okay. So directly connected po siya sa mga muscle atrial muscle fiber, so that kapag itong node nag-generate ng impulse, and allows contraction of the right atrium spontaneously, pati atrium will also immediately contract. Okay?
For the automatic electric rhythmicity of the sinus fibers. So ito na yung tinatawag na self-excitation, no, the ability of these uh cardiac fibers to cause automatic rhythmical discharge and contraction. So this is uh capability is especially true of the heart's specialized conducting system. Okay. So including that of the sinus node. So self-excitation again is a process that can cause automatic rhythmical discharge and contraction. So yan yung special ability ng ng ating mga ah nodal fibers no, to generate impulse on their own. So alamin natin later on, paano ba nagge-generate ng impulses itong mga nodal systems natin. Okay?
So for this reason, the sinus node or SA node ordinarily controls the beat rate. Kaya nga tinawag na SA node is the pacemaker of the heart or the entire heart. Okay? So first, let's describe the automatic ethnicity.
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Now, we have here illustration no, which shows you the rhythmical discharge of the sinus nodal fiber, also the comparing it to the ventricular muscle fiber. Okay. So as you can see here no, meron tayong red arrow, so this shows you um the action potential. Okay. So the minimum action potential needed, the encircled area is actually the um atrial contraction. Okay. And the encircled area, no? Yung red circle, yan naman yung ventricular contraction. Okay. So note that the resting membrane potential of the sinus nodal fiber no, difference siya from the resting membrane potential of your ventricular muscle fiber. So from this illustration, makikita niyo yung x and y axis. So sa axis nandiyan yung millivolts. So for the atrial contraction to discharge, you'll be needing around -55 to -60 mV. No, in comparison to your ventricular muscle fiber, which is about -85 to -90 mV. Okay. So magkaiba siya. Yun pala.
And next, as you can see, um, the question here is, what is the cause of this lower negativity no, comparing your atrial from ventricular? Is that the cell membrane of the sinus fibers are naturally leaky to sodium and calcium ions, and positive charges of the entering sodium and calcium ions neutralize some of that intracellular negativity. Okay. So before we explain that, we have you have to recall no, kung papaano ba no yung um contraction ng ventricular fiber muscles no? Nandiyan yung four phases, if you will remember from your previous lectures. Then compare it to your atrial muscle fiber contractions. Okay. So ang laging tanong diyan, ano yung cause ng lower negativity no, seen on this sinus fibers, comparing it to the aventricular muscle fibers?
So right here, we review no, yyung phases ng inyong ventricular contraction. Okay? Ventricular muscle contraction, muscle fiber contraction. So first is phase zero. So that's basically your depolarization. So itong upstroke na nakikita niyo dito sa first illustration, that's the phase zero. That's depolarization. This is brought about by your fast sodium channels which opens. Okay. So opening of the fast sodium channel, yung cause ng upstroke. Next.
Sa phase 1 is what we call your initial repolarization. Ang cause naman nito is fast sodium channels closing. Okay. So opening of the fast sodium channels for a few 10,000 of a second is responsible for the rapid upstroke spike of the action potential seen in the ventricular contractions. Okay. So ang nangyayari kasi diyan, iyung rapid influx ng sodium no, na positive sodium ions goes inside of the fiber, causing depolarization.
Phase 2 is the plateau. No, anong nangyayari diyan is that calcium channels open fast. Okay. So the plateau of the ventricular action potential is uh primarily caused by slower opening of the slow sodium calcium channels, which last for about 0.3 seconds. No, kaya kung makikita niyo nag-plato lang siya ng um maikli no, before it undergo repolarization. Okay. So ang responsible naman sa repolarization is the opening of potassium channels, which allows diffusion of large amount of positive potassium ions in the outward direction. Okay. So yan yung cause ng inyong rapid repolarization. Okay. So, calcium channels close and slow potassium channels open.
And lastly, is phase 4, no? Balik na yan sa resting membrane potential. Okay. So, from this illustration, makikita niyo yung phases do sa taas. Okay. And they're corresponding [Music] um um inward and outward flow of your ions d sa baba. Okay. So first, again, review upstroke brought about by inward uh travel of your fast sodium channel, and then initial repo is closure naman ng sodium. Okay. And then the plateau, responsible naman yung calcium ions. And then itong rapid repolarization is potassium channel opens. Okay. And then balik na siya sa resting membrane potential. Okay.
So from the question earlier, so what maintains so bakit daw yyung atrial um muscle contraction is more negative? 'Di ba? It resting membrane potential is is a -5 no? Instead of the -90 dun sa ventricular muscle fiber. So ito iyung nakikita niyo dito no, na red arrow. So at this level, yung -55 mV, again, the fast sodium channels mainly have already become inactivated or blocked. Okay. So this is because uh anytime the membrane potential remains less negative than about less than -55 mV for more than a few milliseconds. Okay. And the inactivation gates on the inside of the cell membrane that close the fast sodium channels become closed and remain soap. Okay? So therefore, ang nangyayari diyan no, only the slow sodium calcium channels can open. Okay? Pag sinabing can open, sila lang yung magiging activated. So that's why it will cause no, the initiation of the action potential. Okay. As a result, atrial nodal action potential is slower, okay, to develop than the action potential of the ventricular muscle. So if you compare ba yung kanina illustration, yung nakabilog na dilaw is the atrial contraction, tapos yung nakabilog na red is the ventricular. Dito sa atrial, mabagal yung upstroke, okay, that's because yun nga yung leakiness ng na sinusodal fibers, comparing it dun sa ventricular na may depolarization, rapid repo, plateau, okay, initial repo, plateau, and rapid repo. So iba po yung sa atrial nodal action potential. Okay. So ito po yung sagot no, leakiness of sinusodal fibers. Okay.
So continuing no. So between heart beats no, kung makikita niyo yung mga red arrow na yan, the influx of positively charged sodium ions causes slow rising in the resting membrane potential. So as you can see dito no, may mabagal muna siyang rise before it reaches no, the threshold for this charge. Okay? So may slow rise muna sa resting membrane potential no, towards the positive direction. So because of the high sodium ion concentration in the extracellular fluid outside the nodal fiber, as well as moderate number of already open sodium channels. Positive ion from outside fibers normally tend to leak inside. No, itong itong leaky uh leakiness of the sinus nodal na to, yan yung tinatawag natin na funny currents. Okay no? So again, sodium ions from the outside fibers normally tend to leak no, to the inside of the nodal fibers, what we call funny currents. Okay. So the resting potential gradually rises. So as you can see there from the arrows, red arrows, and become more less negative no, kasi nga iyung sodium mo leaky no, pasok lang ng pasok towards the inside of the nodal fiber. That's why resting potential gradually rises no? Nagiging less negative siya no? As you can see between the two heart beats. And by the time no, the action potential reaches a threshold voltage of about, from this image, less than or -40 mV. What happens is that the L-type no, L-type calcium channel becomes activated. So pag na-activate na yon, na-reach na yung less than -40 mV, tsaka ka pa lang mag-a-action potential. So una, slow rise sa action potential. For example, less than -55. Tapos 'pag na-reach niya 'yung threshold na less than -40, ung responsible naman diyan is the L-type calcium channel. No, ma-activate, mag-o-open, causing now your action potential. So therefore, basically no, yung leakiness ng sinusodal fibers to both to both your sodium and calcium ions causes basically what we call yourself a excitation. Okay? So yan yung nagco-cause or nagge-generate ng impulse dun sa atrial muscle fiber contraction. Okay. So yan yung question ko kanina no. Ano bang nagco-cause nitong self-excitation or rhythmicity no, to generate impulse doon sa atrial walls?
So more questions is, why does this leakiness to sodium and calcium ions not cause the sinus nodal fibers to remain depolarized all the time? Okay. So next valid question is, why is this new state of hyperpolarization not maintained forever? So valid question no, since ah may leakiness nga no, into yung nodal fiber mo from the sodium and calcium, bakit daw hindi nagiging depolarized lang no? So depolarized lang siya, and nagra-rise lang at nagra-rise, hindi niyo ma-reach yung action potential. Okay. So, kabaliktaran no. Bakit naman hindi daw name-maintain yung high polarization on the other end? So, so the answer to this two questions uh can be shown in this illustration. So to answer question number one, no. Bakit daw hindi nagiging depolarized lang? Okay. So, two events occur during the course of the action potential to prevent such a constant state of depolarization. Okay. So ano onong events na to? So first, as you can see. So this illustration shows you an atrial action potential, atrial contraction. So very different from the the um waveform nung ventricular. So first, bakit daw nape-prevent ang constant state of depolarization is that your L-type calcium channels become inactivated. Okay? So as you can see here no, yung L-type no, calcium channels closes or become inactivated. Okay. So by the time na -40, nagco-close na siya dito sa taas. Okay. So within about 100 to 150 milliseconds after opening. So that's the first reason bakit hindi constant constant state of depolarization yung nangyayari. And the other answer to that question is that secondly, at about the same time na mag-close yung L-type calcium channel no, there is a greatly increased number of potassium channel that opens no, which allows now phase 3 repolarization. Okay. So the answer to that question is, kung bakit hindi daw nagiging constantly depolarized no, because of the leakiness of that sodium sodium ions is that spontaneously nagco-close si L-type calcium channel and at the same time potassium channels at a great number opens, which allows repolarization. Okay. So the answer to that question is nandito sa peak nung wave nung upstroke and repolarization. Okay.
So therefore no, in conclusion, influx of positive calcium and sodium ions through the this L-type calcium channel ceases or stops. Okay? So tigil yung influx ng positive calcium sodium ions mo kasi nga nagco-close itong calcium channel channels natin. Well, at the same time, a large quantity of potassium channel opens no, and diffuse out of the fiber, allowing repolarization. Okay? Furthermore, no, iyung potassium channels mo remain open for another few tens of a second, temporarily continuing movement of positive charges out of the cell with resultant excess negativity inside the fiber, which is known as the process called your hyperpolarization. So hindi siya laging upstroke na depolarization. Okay? So that's because again, sabay po na nangyari na nai-inactivate si L-type calcium channel. Tigil ang influx ng sodium at calcium. At the same time, potassium channels remains open. No, temporarily continuing kahit nag-close na po yung inyong L-type calcium channel, allowing hyperpolarization. Okay.
So, kailan ba titigil ong hyperpolarization? So, what's the answer to the second question? The hyperpolarization state initially carries the resting membrane potential down to about, babalik siya doon sa -55 to -60 mV no, at determination of the action potential. So hindi rin name-maintain no? Same as with the depolarization. Yung hyperpolarization hindi rin forever. The reason naman is that during the next few tens of a second after the action potential is over. Okay? So na-reach mo na action potential, pababa na siya, hyperpolarization na siya. So progressively more and more potassium channels will now close. Okay? So at this level, magco-close na ulit yung inyong potassium channels. Babalik naman tayo ngayon sa tinatawag natin na funny currents or the leakiness of those these nodal fibers to sodium sodium ions. Okay. So the inward leaking sodium funny currents and calcium ions now again no, over will balance out okay or balance out the outward flux of your potassium ions, which will now cause resting membrane potential again to drift upward slowly, and once more we reach the threshold for discharge, which is -40, and na, and the cycle continues. Okay. So 'yun po ang sagot kung bakit hindi forever ang depolarization, because of the leakiness of sodium and calcium ions, and hindi po forever or at a constant state nag-hyperpolarize yung inyong action potential. Okay.
Okay. So in summary again, the entire process begins again. So these process no, nodal contraction, ventricular contraction no, self-excitation, rhythmic contraction continues throughout a person's life. So from this illustration, so this shows you the difference between the SA node no, and iyung ventricular ah contraction. So as you can see here, magkaiba po ang phases ng atrial nodal fiber contraction from that of the ventricular. So ventricular kanina ba, phase zero no, 1, 2, 3, 4. So depo, initial repo, plateau, and then the rapid repo. Itong si SA node, may slow rise ka muna dito sa action potential. Pag na-reach niya yung -40, threshold for discharge, boom. Ano ulit no? Sodium influx. L-type, L-type calcium channel opens. If it reaches the peak, no, magco-close, magi-inactivate na L-type calcium channel, open naman si potassium channels. Hyperpolarization, and then baba ulit sa -55 to -60, which is the resting membrane potential. Again, the leakiness of sodium allows again the rise until it reaches another threshold for discharge. Okay. So this is the summary no, self-excitation causes the action potential, and then recovery from the action potential. So hyperpolarization until it reaches uh or it ceases the the ceases or inactivate the potassium channels, then balik na sa resting membrane potential, back to the threshold, and again re-excitement.
Next uh this images shows you the internodal and interaterial pathways no, and which transmits cardiac impulses through the atria. So this figures again shows your SA sa node again, where normal rhythmical impulses are generated and the internodal pathways. So coming from the SA node, kailangan iyung impulse umabot iyan sa AV node no, hanggang umabot sa sa AV bundle system, until it reaches their perking fibers. Okay? So that's the internodal system. So pagdating naman natin sa AV node, okay, tapos na tayo sa SA node no, which impulses uh came from, at usually delayed no. So sinabi natin kanina, mas una pong nagco-contract sa at 1/6 no, of a second from the ventricular, because that is because of the delay no, of impulse coming from the SA going to the AV node. Okay? Saan nangyari onong delay? Is bago po pumabot sa ventricles. Okay? Kasi meron tayong tinatawag diyan na AV bundle, okay? Atrioventricular bundle, which conducts impulses from the atria into the ventricles. So pagdating naman sa ventricles, okay, magdi-divide yan into left and right bundle branch. Now perking fiber, which conducts cardiac impulse to the rest or all parts of the ventricles. Okay. So there's a delay and impulse conducted from SA before it reaches to the AV. Okay. So ito yung tinatawag na internodes patte natin. This one is the AV node. T's meron pa tayo ditong atrioventricular fibrous tissue no, before it becomes your bundle branches no, right and left bundle branches. Okay? So AV, as you can see, kailangan niya munang ma-penetrate itong atrioventricular fibrous tissue. Okay? Before it will be divided into right and left bundle branches. Okay. So with this, your internodal interaterial pathways spreads through the entire muscle mass and eventually to the AV node. Okay. So the velocity of conduction in most atrial muscle is about 0.3 m per second. Okay. But conduction is more rapid no, about 1 m per second in several small bands of atrial fibers. Okay. So mas mabilis po no, yung impulse conduction no, dun sa small bands of the atrial fibers. Okay? Kaya spontaneous or simultaneous po yung contraction ng right atrium to the rest of the atrial wall. Okay. So one of this no, these bands no, maliliit, 1 m per second, is called your anterior interaterial band, also known as the Bachmann's bundle. Okay. So this Bachmann's bundle passes through the anterior walls of the atria to the left atrium. Okay? So kaya po halos sabay lang po ang impulse conduction ng inyong left and right atrium. It's because of these small bands of atrial fibers. No, your anterior interaterial band, also known as the Bachmann's bundle, going to the left atrium. As we all know, nasa right atrium yung ano 'ba, SA node. Okay. So yung impulse conduction is mas mabilis daw sa smaller bands. Okay? Kaya sabay po halos ang contraction nitong si left and right atrium. So the cause of more rapid velocity of conduction is that these bands no, in the presence of special conduction fibers, causes simultaneous atrial muscle fiber contraction. Okay.
So on the other hand, si perking fiber naman is come from the AV node no, through the AV bundle into the ventricles. So itong perking fibers no, very large fibers, even larger than the normal ventricular muscle fibers, and has a very high level of permeability of the gap junction at the intercalated disc. So with this no, si perking fibers, so since may permeability siya, the velocity of which is 1.5 to 4 m per second no? So ibig sabihin, mas mabilis siya no? A velocity of about six times that in the usual ventricular muscle and 150 times that in some of the AV nodal fibers. So the rapid transmission of action potentials by the perking fiber is believed to be caused by very high level permeability of the gap junctions at the intercalated disc. No, this intercalated disc can be can be found between those successive cells which makes up the perking fibers. Okay. So because of that, ions are transmitted easily from one cell to the next no, because of this gap junctions, enhancing the velocity of transmission. Okay? So normally, iyung AV bundle mo is a one-way conduction band. Okay? Or one-way conduction path. So one-way lang. Hindi pwedeng um may impulse ka sa sa AV bundle and then may sariling impulse generated from the perking fibers. Okay? So dapat manggaling sa SA, internodal, then AV, and then going to the bundle branches, going to your perking fibers. Okay. So these perking fibers actually allows instantaneous transmission of cardiac impulse throughout the entire remainder of the ventricular muscle. So pagkadating po natin sa AV node no, since um may high level of permeability po itong perking fibers natin, it allows rapid transmission of action potentials by the perking fibers throughout the remainder of the ventricles. Okay. Pero mas una pa rin po 'no 'yung atria na magkaroon ng contraction 'no, because of that Bachmann's bundle no, from the right atrium to the left atrium. Okay? So remember, the AV bundle is a one-way conduction path. Okay? Normally, dapat ganon. In special cases, no, if there's an inability or abnormal states, action potential may travel backwards. Okay? Kaya po tayo nagkakaroon ng tinatawag na arrhythmia or nagiging irregular or wala yung nawawalan ng rhythm yung contraction po ng ating chambers. Okay. For example, backward galing sa ventricles, yung impulse mo babalik siya sa node or sa atria. So this characteristic prevents reentry of cardiac impulses by this route from the from the ventricles to the atria, allowing only forward conduction from the atria to ventricles. So kaya tayo dito may naka-incircle na red area, which is the anong tawag diyan? Your fibrous tissue. Okay. So this prevents backward impulses from the AV node nodes or ventricles back to the atria. So this barrier actually allows as an insulator or acts as an insulator to prevent passage of cardiac impulse between atria and ventricle to any other route. Okay. So with this, after penetrating from that fibrous tissue between the atrial and ventricle muscles, the distal portion of the AV bundle passes downward in the ventricular septum. Okay? So dito, so after po niya doon sa fibrous tissue no, it will be it will pass through the ventricular septum, sa gitna po yan, will divide into your left and right bundle branch. Okay. So dapat yung impulse mo will spread downward towards the apex of the ventricles and will now core sideways around the ventricular wall towards the base of the heart. So the total elapsed time no, for this contraction, ventricular contraction is about 0.03 seconds from the time cardiac impulse enters the bundle branches. Okay. So therefore, once the cardiac impulse enters the perking uh conductive system, it spreads almost immediately to the entire ventricular muscle mass.
We're done with the excitation uh and conduction system. Ah, so yung normal. Now we proceed with how does the heart control this excitation and conduction. So as you all know, impulse normally arises in the SA node. Kaya nga siya tinawag na pacemaker or where the heartbeat starts or control of the heartbeat. However, other parts of the heart can also exhibit intrinsic rhythmical excitation. Kaya tayo may uh dito no, makikita niyo yung mga paces no, nung heartbeat depending on saang saang node nanggagaling. Okay? So there will be intrinsic rhythmical excitation not only seen on your sinus nodal fibers, particularly meron sa AV node and perking fiber. Kaya malalaman mo na kapag yung impulse generated no, makuha mo doun sa ah or na-analyze doun sa heart no, yung rhythmicity nung heart, kung saan saan pwede manggaling yung impulse na iyon. Kung 40 to 60, AV node. Per k, 15 to 40. Kapag sinus node, it's 70 to 80. So as as you can see from the uh numbers no, the discharge rate of the sinus node is faster, considerably faster than the natural self-excitator discharge rate of that of either the AV node and the perking fiber. Okay. So remember this um discharge rates. Okay. SA node, 70 to 80. AV node, 40 to 60. Perking fiber is 15 to 40 times per minute. Okay. So the sinus node discharges again before either of the AV node. So dapat one-way conduction system no? Paulit-ulit, mauna dapat si sinus node no? Before this AV node and perking fibers. Okay? So iyun ang normal. So sinus node discharges before or way ahead before these two other nodal systems can reach their thresholds for their own self-excitation. Okay.
The conclusion again, your SA node controls the beat of the heart okay because its rhythmical discharge is faster than any of that remaining nodes. Why the SA node is the normal pacemaker of the heart? So the question is, why then does the sinus node rather than the AV node or the perking fibers control the heart's rhythmicity? Again, the answer to that question is that mas mabilis ang discharge rate ni SA compared to AV and perking fiber, and your sinus node discharges again before either your AV or perking fiber reaches their threshold for self-excitation. So occasionally, merong nagiging abnormal no impulses no, na hindi po nanggagaling sa SA node or mas mabilis pa minsan sa SA node. Ito yung tinatawag nating ectopic pacemakers no? Some part of the heart develops rhythmical discharge rate which is rapid, more rapid than of than that of the SA node. Okay. So a pacemaker elsewhere than the SA node. So ang nangyayari, shift no? The heart shifts from the SA node to the AV node or to the excited perking fibers. Okay. So iba ngayon ang nagko-control no, nung rhythmicity nung heart mo, hindi yung SA node. And under rarer conditions, a place in the atrial or ventricular muscle develops excessive excitability and becomes the pacemaker. Kaya tayo nagkakaroon ng arrhythmias or irregular heartbeats. Okay. And this new pacemaker then uh usually occurs on the AV node or on the penetrating portion of the AV bundle going towards the ventricles. Okay. So cause of shift of pacemaker leading to blockage of transmission of the cardiac impulse from the sinus node. So as you can see here, nawalan no, ng connection dito sa mga sa bundle branch on the left no'. Kaya hindi magiging rhythmic excitation yung ventricular contraction mo. Okay. So this is a case of a bundle branch or heart block. Okay. So ang nangyayari diyan, may shift no, nung pacemaker. So may blockage ka dito no. May heart block, may left bundle branch block ka no? Nawawalan ng continuous transmission nung cardiac impulse coming from the SA. Okay.
So next is the parasympathetic nerve control of the heart. So for the parasympathetic, also known as the vagal stimulation of the heart, leads to slowing of the cardiac rhythm and conduction. So remember that the heart is supplied by both of the sympathetic and parasympathetic. Pag sinabi mong parasympathetic, vagal nerve or the vagus nerve are responsible to this. No, so this are distributed mainly sa SA node and to a lesser extent to the muscle of the two atria and very little directly to the ventricular ventricular muscle. So ang nangyayari dito sa parasympathetic is that there will be a release of acetylcholine from acetylcholine from the vagal endings, leading to decrease no, of the heart rate of the sinus node. So babagal po no, iung tibok no, iyung contraction ng heart, and then also leads to a decrease in excitability of the AV junctional fibers between the atrial musculature and the AV node. So pinag-aaralan na yan noon pa. No, kapag parasympathetic state ka, nangyayari no? Mas relax, and digest nga yan, 'di ba? Para simple. Hindi mo kailangan ng masyadong mataas na pressure or blood volume throughout the systemic circulation or towards the brain. Okay? So mas nagfo-focus yung ah blood systemic circulation mo sa digestive system. So this because of the release of acetylcholine, which uh leads to a decrease in the rhythm, a rate of rhythm on the sinus node, leading to a slower heartbeat. Okay. So again, so acetylcholine released at the vagal nerve endings greatly increases the permeability of the fiber membranes to potassium ion. So as you can remember, andito yung repolarization, 'di ba? Yung if you remember, potassium na yung bida dito sa repolarization. So increase permeability to potassium ions. Okay. This will now cause an increase negativity inside fiber, which we now call your hyperpolarization. So rapid leakage out of the conductive fiber, rapid repolarization. So ang nangyayari diyan no, mas mahaba yung repolarization mo, mas mabagal. Okay? Which again, which makes this excitable tissue less excitable, as explained. Okay? So longer to reach the threshold potential for excitation. Ibig sabihin, si acetylcholine ang ginagawa niya, increase permeabilities to potassium ions. Mas mahaba ngayon yung repolarization mo. Therefore, kung mas mahaba repolarization mo, okay, mas matagal, mas matagal ngayon yung rise no, for the other for the another action potential. So ibig sabihin, mas mabagal yung next impulse generation. Okay. So the initial rise of the sinus node membrane potential caused by inward sodium and calcium leakage requires much longer to reach the threshold potential for excitation. So yan po yung mechanism na mag-e-explain kung bakit si parasympathetic no, will cause a decrease in the rate of the rhythm of your heart contractions. Okay? It's because of the acetylcholine and potassium leakage or permeability, leading to longer repolarization, leading to longer reach for the threshold for the other action potential to begin. Okay. So, a moderate decrease simply delays conduction of the impulse, but a large decrease blocks conduction entirely. Okay. So, kaya nga minsan ba yung ginagamit sa lethal injection is potassium, if you remember, because it will slow down the heart and eventually at greater risk or higher levels, it will block the conduction entirely. Magka-cardiac arrest. Okay.
So on the other hand, ay nadoble yung doble yung videos. Sige. So for the sympathetic nerve control naman, so this is essentially opposite of that of what happens with the parasympathetic. Okay? So ang nangyayari dito, in short, your sympathetic stimulation increases the overall activity of the heart. No, 'di ba? Ito naman yung fight or flight response. So gusto mo kapag sympathetic, mas mabilis yung tibok ng puso no? To to allow more blood flow on the systemic circulation, sa lungs, sa brain. Okay? So maximal stimulation can almost triple the heartbeat frequency and can increase the strength of the heart contraction as much as two fold. So kabaliktaran lang po ang nangyayari sa parasympathetic. It increases the rate of the sinus nodal discharge, increases the rate of conduction, as well as the level of excitability at, and increases the force of contraction and of all cardiac musculature, both of the atria and that of the ventricle. Okay. So ano naman ang may kagagawa nito? So kung si parasympathetic is vagal stimulation, brought about by the release of your acetylcholine, ito naman pong sympathetic is brought about by the release of norepinephrine. So if you remember, on the SA node and AV bundles, there's increased sodium calcium permeability. So ito naman po no, kung kanina naka-focus tayo dito sa repolarization, which is crossed by potassium ions. Ito naman dito naman tayo mag-shift no, sa pacemaker potential. Okay. So ano ba, ano nga ulit ang nagco-cause nito 'di ba? Yung increase sodium calcium permeability. Yung tinatawag natin na funny currents. So gusto natin, since gusto natin mapabilis yung pagtibok ng puso, mapalakas, mapaikli, ah i-enhance natin ong funny currents na tinatawag. So so increase sodium calcium permeability. So makes it easier for the action potential to excite each succeeding portion of the conducting fiber bundles. So thereby, paiikliin mo ngayon yung threshold for action potential. So thereby, we decrease the conduction time from the atria to the ventricles. Okay. So anong nangyari dito? Um ah norepinephrine release no? This will then stimulate beta-1 adrenergic receptors. So which will then lead to an increase permeability to sodium and calcium ions. So ito yung funny currents natin. So more positive resting potential ang mangyayari until it reaches the threshold for discharge no? Pinapabilis natin or pinapaikli natin yung time for conduction. So accelerating self-excitation and increases eventually the heart rate. Okay.
So that's it for the um conduction and self-excitation system of the heart. So I hope no, marami kayong natutunan. So please read on this chapter no, chapter 10. Madali lang siyang intindihin. Um, just make sure you go back to the basics, no? Yung phases at iintindihin niyo kung anong nangyayari in each phases, na maiintindihan niyo ngayon kung paano ah nagkakaroon ng self-excitation. Pa bakit nagkakaroon ng um skip beats or ah delay in transmission, bakit nauuna si atrium, kay ventricles. So lahat po yan may purpose, and it's because of the ability of the heart to generate impulses on its own. Okay? Brought about by gradients nung inyong mga sodium, potassium, calcium ions. Okay? So focus on that concepts. I hope uh you all learn from this topic. If you have any questions or clarification, please feel free to message me on Canvas. Okay. So, and be ready for your post-test now after watching this topic. Thank you for listening. See you all around in the campus. Okay. And the lecture. So, with a healthy heart, the beat goes on. So, hopefully lahat kayo maka-survive on this week one of histology. So let the beat no, of your heart for the for that um dreams of of getting that MD goes on. Parang pagising lang yan sa umaga, you have to achieve that action potential, continue all throughout the day. Okay, see you all around and God bless on your medical journey.