Conduction system of the heart -For skeletal muscle to contract, it has to be innervated by spinal nerves (there must be a neuromuscular junction). *The heart is innervated by autonomic nervous system (sympathetic and parasympathetic), if we cut the innervations (no nerve supply) the heart still contracts, even though we know that mechanical response does not occur unless there is an electrical response?? Then we conclude that the heart has an intrinsic system responsible for action potentials (electrical response) called The conduction system of the heart. So.. The cardiac muscle can contract autorythmically (automatically); without any stimulation of the nervous system but by the existence of the intrinsic system that cause the electrical response. That means if we remove the human s heart and put it in a beaker that is filled with a solution that contains calcium, the heart continues to contract. But if we did the same thing with a skeletal muscle, it won t contract because there is no innervation. And all of that is because the heart has a conduction system and that is our lecture. Slide 2: objectives Point out the regulation of the conduction system potential by Autonomic Nerves that means the innervation(the autonomic nervous system) responsible for regulation, not for initiation of the impulse and contraction. - A person with a heart transplant has no innervation. 1
Slide 3: Structures of the conduction system 1- SA node (sinoatrial node) is located in the posterior aspect of the right atrium, just below the entrance of the superior vena cava. All parts of the conduction system are modified cardiac muscle cells, they are not nerves. We will talk about how they are modified in terms of structure and function. 2- AV node (atrioventricular node) 3- Bundle that pierces the atrioventicular septum AV bundle / Bundle of His 4- The bundle branches into left bundle branch and right bundle branch 5- The branches subdivide into purkinje fibers sub-endocardially then these fibers go through up to almost 2/3 of the myocardium. So the myocardium of the ventricle receives their impulses at the end through purkinje fibers. Slide 4: electrical system of the heart Some believe that there are internodal fibers between the SA node and the AV node that run anterior, posterior and to all sides. -the Doctor believes that the impulse from SA node reaches the AV node through the atrial muscles not through internodal fibers. Slide 6: SA node (pacemaker of the heart) is able to produce intrinsic impulses with the rate of 60-80 beat-action potential-impulse/min. The AV node is able to produce intrinsic impulses with the rate of 40-60 impulse/min. The purkinje fibers (the last structure in the tract) are able to produce 15-40 impulse/min. - if the purkinje fibers are left alone (does not receive any stimulation from anywhere) it is able to produce impulses with the rate 15-40 impulse /min, BUT if it gets higher impulses it works with the higher one that it receives (the same thing with the AV node). 2
SO..Each has different speed, but all are connected together so what sets the speed is the one with the higher rate; the SA node (the pacemaker), BUT if the SA node is destroyed (e.g. because of ischemia), the AV node become the pacemaker BUT in an abnormal situation called Ectopic pacemaker. -Ectopic is a general term that means in an abnormal place e.g. ectopic pregnancy when the pregnancy happens in the tube or the abdomen while normally it should be in the uterus. *AV block- Heart block: When the AV node is destroyed there is NO connection between the SA node and the purkinje fibers, soo the ventricles will work on the rate of purkinje fibers and so is the heart rate (15-40 impulse/min). In this case the patient will need an artificial pacemaker?? We put it from the median cubital vein then in the axillary vein right subclavian v. brachiocephalic vein superior vena cava then we put it in the muscles of the right ventricle NOT atrium to overcome the damage in the AV node. Now the right ventricle will receive the rate of the artificial pacemaker that we set the left ventricle will receive the impulse through the muscles (as we said that the ventricles work as one syncitium,( so wherever the impulse is, it will reach both ventricles because of the gap junctions). -atrial rate depend on the SA node. Slide7: Autonomic innervation of the heart Sympathetic parasympathetic Comes from the cardiac plexus It supplies all parts of the heart: both atriums, the conduction system and both ventricles through the vagus nerve it supplies mainly the atria, AV node, SA node and( very little if nothing to the ventricles) 3
Slide 8: Conduction system as we said is modified cardiac muscle cells which are autorythmic and constitute about 1% of the cardiac muscle cells, the other part of the heart muscle called the contractile fibers in the ventricles and atriums. Slide 11: pathways of the heartbeat AV node act as a delay system: they delay the impulse to ensure that the atria contract and finish their contraction before the ventricles start to contract (we don t want the atria and the ventricles to contract together). - The AV node is the slowest conducting fibers (before we talked about impulse rate, which is different than conduction). 0.2 m/sec or even less 0.02 -the conduction rate of atrial and ventricular muscles is moderate. 0.5-1 m/sec -the fastest conduction is through the purkinje fibers, to ensure that the ventricles received the impulse almost at the same time (to contract as one unit) 4 m/sec Slide 15: Purkinje system They are wider and thicker than other cells. Slide 16: AV bundle Normally one-way conduction through the bundles, because of the refractory period. Slide 17: How does the conductive system intrinsically produce impulses (intrinsically active)? What is the mechanism? 4
*Anatomical modification: First we said that it is a modified cardiac muscle cells (In term of structure there is no contractile protein for contraction; very little if nothing actin and myosin). AV node s cells are very small that s why the conduction rate is very slow. (purkinjie fibers are very wide that means that the conduction is higher). *Physiological modification: the cells of the conduction system are leaky to sodium, means that normally the sodium permeability is very high.( there are sodium leaky channels) this is unlike other cells where Na permeability is low. Slides 17-21: *During phase 4 the membrane potential returns to -90, BUT if these cells are leaky to Na, the resting membrane potential will never reach -90 (it will be less negative -60 or -65). And since they are leaky to sodium there is slow depolarization phase until it reaches threshold slowly. -Recall: sodium channel has 2 gates: the activation gate (fast) and the inactivation gate (slow). Because we are reaching the threshold slowly; the inactivation gates close before the activation gates open (Na do not enter). So how is the upstroke produced (phase 0)?? Due to the opening of slow voltage gated calcium channels (NOT sodium). Sooo we have phase 4 followed by phase 0 then phase 3 and so on. (NO phase 1 or plateau) and this kind of response is called the slow response action potential. This action potential is autorythmic produced from SA node then through atrial muscles to the AV node, purkinje fibers to the ventricles. (In the AV node the same happens with lower rate). 5
Slide 20: Correction on the slide: in phase 0, slow Ca channels open NOT fast. *DVT (change in voltage over time) in phase 0 for cardiac muscle is much higher than the DVT in the slow response curve. Slide 23: Extrinsic Innervation of the Heart *Sympathetic stimulation through epinephrine and norepinephrine cause an increase in the permeability of the cardiac cell as a whole to Na and Ca. If there is increase in the permeability for Na the time to reach the threshold will be shortened increase in the rate of action potential(ap) change in the rate of heart rate is called the chronotropic effect (if it is +ve, there is an increase in the heart rate and if ve there is a decrease). The increase of the Ca permeability increase in the contractility of the cells change in the contractility is called inotropic effect. So.. The sympathetic causes a +ve inotropic and +ve chronotropic effects, because it increases the permeability of the cells to Na and Ca. *Parasympathetic system through its neurotransmitter acetylcholine, causes an increase in the permeability of these cells to potassium and chloride, and decrease in the permeability to Na and Ca. So there will be ve chronotropic effect and NO effect on inotropic effect because the parasympathetic does Not supply the ventricles. **BUT when we talk about acetylcholine itself, it has an effect on ventricles since there are receptors for it. 6
Slide 24: Pacemaker Function In the parasympathetic curve: the slow depolarization is slower ( K, Ca permeability) reach the threshold after more time rate decreases -ve chronotropic effect. In the sympathetic curve: permeability to Na the rate is faster +ve chronotropic effect. Slide 27: Ventricular Escape and Overdrive suppression- If we increase in the stimulation of the vagus nerve this lead to decrease in the heart rate and might lead to a stop in the heart for a while, after some time (15 to 30 seconds) there will be a slight increase in the heart rate (15-40 impulse/min) due to the purkinje fibers in the ventricles since they do NOT receive parasympathetic (so they are not suppressed). Purkinjie fibers need some time to work because in normal conditions they are already stimulated by higher rate (60-80) so their own rate is suppressed by the higher rate they receive this is what we call Overdrive suppression. Now if this higher rate stops they need 15-30 seconds to work so the ventricles escape the effect of the parasympathetic ventricular escape. That s what happens in Stokes-Adams syndrome, carotid abnormality that produces pressure on the vagus, thus vagal stimulation and inhibition of the SA node, so the person faints for a little while because there is no heart rate, then he wakes up because of the ventricular escape. Done by: Rayah Bani Kinanah Special thanx to: Aya, Dalia, Jamileh, Aseel and Dina. 7
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