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WINDSOR UNIVERSITY SCHOOL OF MEDICINE
Cardio Vascular Physiology Electrical activity & Electrocardiography Dr.Vishal Surender.MD.
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Anatomy: Cardiac Muscle
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• Three features of the histology of cardiac muscle: 1. Nuclei
Cardiac Histology • Three features of the histology of cardiac muscle: 1. Nuclei 2. Intercalated Disks 3. Cardiac Myofibrils Cardiac Muscle Cells • There are two kinds of cell junctions on the intercalated disks. • The desmosomes are anchoring junctions that hold adjacent cells together. When the muscle cell contracts, they pull on each other. If it wasn't for the desmosomes, the heart would literally pull itself apart in doing its job. • The gap junctions allow the stimulating impulse to move across the heart from cell-to-cell so the heart beats as an entire unit. If each cardiac muscle cell were allowed to do its own thing the heart would be useless as a pump. desmosomes gap junctions intercalated disks.
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Cardiac muscle cells contract without Innervation
• The intrinsic conduction system sets the basic rhythm of the beating heart. • It consists of autorhythmic cardiac cells that initiate and distribute impulses (action potentials) throughout the heart.
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Intrinsic Conduction System
SA Node Internodal Pathway AV Node This diagram shows the location of the autorhythmic, or nodal cells of the intrinsic conduction system: SA Node Internodal Pathway AV Node AV Bundle Bundle Branches Purkinje Fibers AV Bundle Bundle Branches Purkinje Fibers
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Electrical Conduction in Myocardial Cells
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Electrical Conduction in Heart
THE CONDUCTING SYSTEM OF THE HEART SA node AV node Purkinje fibers Bundle branches A-V bundle Internodal pathways SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. Depolarization spreads more slowly across atria. Conduction slows through AV node. Depolarization moves rapidly through ventricular conducting system to the apex of the heart. Depolarization wave spreads upward from the apex. 1 4 5 3 2 Purple shading in steps 2–5 represents depolarization.
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Electrical Conduction
AV node Direction of electrical signals Delay the transmission of action potentials SA node Set the pace of the heartbeat at 70 bpm AV node (50 bpm) and Purkinje fibers (25-40 bpm) can act as pacemakers under some conditions
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Cardiac Muscle versus Skeletal Muscle
Smaller and have single nucleus per fiber Have intercalated disks Desmosomes allow force to be transferred Gap Junctions provide electrical connection T-tubules are larger and located at Z-lines. Sarcoplasmic reticulum is smaller Mitochondria occupy one-third of cell volume
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Cardiac Muscle Excitation-contraction coupling and relaxation in cardiac muscle Myosin Relaxation Contraction ATP 3 Na+ 2 K+ Sarcoplasmic reticulum (SR) ECF ICF Actin T-tubule Ca2+ spark Ca2+ signal SR Ryanodine receptor-channel stores Ca2+ ions bind to troponin to initiate contraction. Relaxation occurs when Ca2+ unbinds from troponin. Na+ gradient is maintained by the Na+-K+-ATPase. Voltage-gated Ca2+ channels open. Ca2+ enters cell. Ca2+ induces Ca2+ release through ryanodine receptor-channels (RyR). Local release causes Ca2+ spark. Ca2+ is pumped back into the sarcoplasmic reticulum for storage. Ca2+ is exchanged with Na+. Action potential enters from adjacent cell. Summed Ca2+ Sparks create a Ca2+ signal. 1 2 3 4 5 6 9 10 8 7
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• The coordinated contractions of the heart result from electrical changes that take place in cardiac cells. Intrinsic Conduction System • Cardiac autorhythmic cells in the intrinsic conduction system generate action potentials that spread in waves to all the cardiac contractile cells. This action causes a coordinated heart contraction. Gap Junctions • Action potentials generated by autorhythmic cells create waves of depolarization that spread to contractile cells via gap junctions. Gap Junctions autorhythmic cell contractile cells
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Autorhythmic Cell Anatomy
1. Sodium Channels - allow sodium ions to enter the cell 2. Calcium Channels - allow calcium ions to enter the cell. 3. Potassium Channels - allow potassium ions to leave the cell. . Sodium K+ Calcium Gap Junction
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Gap Junction
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Action Potentials in Cardiac Autorhythmic Cells(ex:-SA node)
Myocardial Autorhythmic Cells Generate action potentials spontaneously in the absence of input from the nervous system. This ability results from their unstable membrane potential, which starts at -60 mV and slowly drifts upward toward threshold. This unstable membrane potential is called a pacemaker potential rather than a resting membrane potential because it never "rests" at a constant value. Whenever a pacemaker potential depolarizes to threshold, the autorhythmic cell fires an action potential.
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Three ion channel mechanisms contribute to the pacemaker potential –
The first is a progressive reduction in potassium permeability. Second is presence of funny channels. Three ion channel mechanisms contribute to the pacemaker potential, which are shown in Figure . The first is a progressive reduction in potassium permeability. Potassium channels, which opened during the repolarization phase of the previous action potential, gradually close due to the return of the membrane to negative potentials. Second, pacemaker cells have a unique set of channels that, unlike most voltage-gated channels, open when the membrane potential is at negative values. These channels conduct an inward, depolarizing sodium current, which is designated the If current. (Do not confuse this type of sodium channel with the one that causes the action potential upstroke in neurons, skeletal muscle, and cardiac muscle cells.) The third pacemaker channel is a type of calcium channel that opens only briefly but contributes an inward calcium current and an important final depolarizing boost to the pacemaker potential. These channels are called T-type calcium channels (T transient). Once the pacemaker mechanisms have brought the nodal cell to threshold, an action potential occurs. The depolarizing phase is caused by calcium influx through the L-type calcium channels, and after a delay, the opening of potassium channels repolarizes the membrane. The return to negative potentials activates the pacemaker mechanisms once again, and the cycle continues. Thus, the pacemaker potential provides the SA node with automaticity, the capacity for spontaneous, rhythmical self-excitation. The slope of the pacemaker potential—that is, how quickly the membrane potential changes per unit time—determines how quickly threshold is reached and the next action potential elicited. The inherent rate of the SA node—the rate exhibited in the total absence of any neural or hormonal input to the node—is approximately 100 depolarizations per minute. Third is presence of T-type calcium channels (T transient).
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Upstroke of nodal action potential is due to L-type calcium channels
When the cell membrane poÂtential is -60 mV, If channels that are permeable to both K and Na+ open (Fig c). These channels are called It channels because they allow current (I) to flow and because of their unusual properties. The researchers who first deÂscribed the ion current through these channels initially did not understand its behavior and named it funny current— hence the subscript f. The If channels belong to the family of HCN channels, or hyperpolarization-activated cyclic nucleotide-gated channels. Other members of the HCN family are found in neurons. When If channels open at negative membrane potentials, Na+ influx exceeds K+ efflux (Fig b). (This is similar to what happens at the neuromuscular junction when nonspecific cation channels open . The net influx of positive charge slowly depolarizes the autorhythmic cell membrane potential becomes more positive, the If channels gradually close and some Ca2' channels open. The subsequent influx of Ca continues the depolarization, and the memÂbrane potential moves steadily toward threshold. When the membrane potential reaches threshold, addiÂtional Ca2+ channels open. Calcium rushes into the cell, creatÂing the steep depolarization phase of the action potential. Note that this process is different from that in other excitable cells, in which the depolarization phase is due to the opening of voltage-gated Na+ channels. When the Ca2+ channels close at the peak of the action potential, slow K' channels have opened. The repolarization phase of the autorhythmic action potential is due to the resulÂtant efflux of K+. This phase is similar to repolarization in other types of excitable cells. Upstroke of nodal action potential is due to L-type calcium channels (L-Longer acting).
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Regulation of the Heart Rate
HR is controlled by the ANS: both parasympathetic (PS) and sympathetic nerves. The speed with which pacemaker cells depolarize determines the rate at which the heart contracts (the heart rate),SA node-Pacemaker. The effects of the autonomic nervous system on heart rate are called chronotropic effects.
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Effects of Parasympathetic activity: ↓ HR -Bradycardia
PS fibres supplying the heart, are found in the right and left vagus nerves and the neurotransmitter released is acetylcholine. ACh binds to muscarinic (M2) receptors on the heart. ACh reduces the heart rate (negative chronotropic effect). Mechanism of bradycardia: Acetylcholine (ACh), released from parasympathetic nerve fibers, activates muscarinic (M2) receptors in the SA node. Activation of muscarinic receptors in the SA node has two effects that combine to produce a decrease in heart rate. First, these muscarinic receptors are coupled to a type of Gi protein called GK that inhibits adenylyl cyclase and produces a decrease in If. A decrease in If decreases the rate of phase 4 depolarization. Second, GK directly increases the conductance of a K+ channel called K+-ACh and increases an outward K+ current (similar to IK1) called IK-ACh. Enhancing this outward K+ current hyperpolarizes the maximum diastolic potential so that the SA nodal cells are further from threshold potential. In sum, the parasympathetic nervous system decreases heart rate through two major effects on the SA node: (1) slowing the rate of phase 4 depolarization, and (2) hyperpolarizing the maximum diastolic potential so that more inward current is required to reach threshold potential. As a result, the SA node is depolarized to threshold less frequently and fires fewer action potentials per unit time (i.e., decreased heart rate)
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Effects of sympathetic activity: ↑ HR (+ ve chronotropic effect)
↑ Force of contraction (+ve inotropic effect) Chronotropic Effect ↑ rate of pacemaker depolarization – threshold is reached sooner The interval between action potentials can be modified by altering the permeability of the autorhythmic cells to different ions. icrease ion flow through both If and Ca2+ channels. More rapid cation entry speeds up the rate of the pacemaker depolarizaÂtion, causing the cell to reach threshold faster and increasing the rate of action potential firing .When the pacemaker fires action potentials more rapidly, heart rate inÂcreases.
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Contractile Cell Anatomy
• The cardiac contractile cell relies on the autorhythmic cell to generate an action potential and pass the impulse down the line before the cell can contract. • Like the autorhythmic cell, it has ion transport channels, but they are slightly different. • Gap junctions link autorhythmic and contractile cells, and link contractile cells with each other. • Notice the sarcoplasmic reticulum (SR), which is a storage site for calcium. Channels within the SR membrane allow calcium ions to be released within the cell. • The myofilaments are the contractile units of the cardiac muscle cell. Fast Na+ K+ Slow Ca+ SR
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Myocardial Contractile Cells
Action potential of a cardiac contractile cell The action potentials of myocardial contractile cells are similar in several ways to those of neurons and skeletal muscle. The main difference between the action potential of the myocardial contractile cell and that of a skeletal muscle fiber or a neuron is that in the myocardial cell, there is a longer action potential due to Ca2+ entry. Phase Membrane channels PX = Permeability to ion X +20 -20 -40 -60 -80 -100 Membrane potential (mV) 100 200 300 Time (msec) PK and PCa PNa Na+ channels open Na+ channels close Ca2+ channels open; fast K+ channels close Ca2+ channels close; slow K+ channels open Resting potential 1 2 3 4
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Myocardial Contractile Cells
Phase 4: resting membrane potential. Myocardial contractile cells have a stable resting potential of about -90 mV. Phase 0: depolarization. When a wave of depolarization moves into a contractile cell the membrane potential becomes more positive. Voltage-gated Na+ channels open, Na+ enter the cell and rapidly depolarize it. The membrane potential reaches about +20 mV before the Na1 channels close. Phase Membrane channels PX = Permeability to ion X +20 -20 -40 -60 -80 -100 Membrane potential (mV) 100 200 300 Time (msec) PNa Na+ channels open Na+ channels close 1
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Myocardial Contractile Cells
Phase 1 Initial Rapid Repolarization The opening of the voltage gated K + channels causes K + to flow out of the cell through the outward rectifier channel. This outward current starts to repolarize the cell. The membrane potential is partially repolarized to just above zero. Phase Membrane channels PX = Permeability to ion X +20 -20 -40 -60 -80 -100 Membrane potential (mV) 100 200 300 Time (msec) PK and PCa PNa Na+ channels open Na+ channels close Ca2+ channels open; fast K+ channels close 1 2
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Myocardial Contractile Cells
Phase 2: the plateau. Due to result of two events: 1)a decrease in K+ permeability and 2)an increase in Ca2t permeability. The combination of Ca2+ influx and decreased K+ efflux causes the action potential to flatten out into a plateau Phase Membrane channels PX = Permeability to ion X +20 -20 -40 -60 -80 -100 Membrane potential (mV) 100 200 300 Time (msec) PK and PCa PNa Na+ channels open Na+ channels close Ca2+ channels open; fast K+ channels close Ca2+ channels close; slow K+ channels open 1 2 3
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Phase 3: rapid repolarization
Phase 3: rapid repolarization. The plateau ends when Ca2+ channels close and K+ permeability increases once more. The "slow" K1 channels responsible for this phase are similar to those in the neuron. When the slow K+ channels open, K+ exits rapidly, returning the cell to its resting potential (phase 4). Phase Membrane channels PX = Permeability to ion X +20 -20 -40 -60 -80 -100 Membrane potential (mV) 100 200 300 Time (msec) PK and PCa PNa Na+ channels open Na+ channels close Ca2+ channels open; fast K+ channels close Ca2+ channels close; slow K+ channels open Resting potential 1 2 3 4
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Cardiac Muscle Excitation-contraction coupling and relaxation in cardiac muscle Myosin Relaxation Contraction ATP 3 Na+ 2 K+ Sarcoplasmic reticulum (SR) ECF ICF Actin T-tubule Ca2+ spark Ca2+ signal SR Ryanodine receptor-channel stores Ca2+ ions bind to troponin to initiate contraction. Relaxation occurs when Ca2+ unbinds from troponin. Na+ gradient is maintained by the Na+-K+-ATPase. Voltage-gated Ca2+ channels open. Ca2+ enters cell. Ca2+ induces Ca2+ release through ryanodine receptor-channels (RyR). Local release causes Ca2+ spark. Ca2+ is pumped back into the sarcoplasmic reticulum for storage. Ca2+ is exchanged with Na+. Action potential enters from adjacent cell. Summed Ca2+ Sparks create a Ca2+ signal. 1 2 3 4 5 6 9 10 8 7 Figure 14-11
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The longer myocardial action potential helps preÂvent the sustained contraction called tetanus
The influx of Ca2' during phase 2 lengthens the total duraÂtion of a myocardial action potential. A typical action potential in a neuron or skeletal muscle fiber lasts between 1 and 5 msec. In a contractile myocardial cell, the action potential typically lasts 200 msec or more. The longer myocardial action potential helps preÂvent the sustained contraction called tetanus. Prevention of tetanus in the heart is important because cardiac muscles must relax between contractions so the ventricles can fill with blood. How does a longer action potential prevent tetanus? To understand this, compare the relationship between action poÂtentials, refractory periods and contraction in skeletal and cardiac muscle cells . As you may reÂcall from Chapter 8, the refractory period is the time following an action potential during which a normal stimulus cannot trigger a second action potential. In skeletal muscle, the action potential (red curve) and refractory period (yellow background) are ending as contraction (blue curve) begins. For this reason, a second action potential fired immediately after the refractory period causes summation of the contractions. If a series of acÂtion potentials occurs in rapid succession, the sustained conÂtraction known as tetanus results
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Electrical Conduction in Myocardial Cells
Electrical communication in the heart begins with an acÂtion potential in an autorhythmic cell. The depolarization spreads rapidly to adjacent cells through gap junctions in the intercalated disks (Fig •). The depolarization wave is folÂlowed by a wave of contraction that passes across the atria, then moves into the ventricles. Figure 14-17
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Electrical Conduction in Heart
THE CONDUCTING SYSTEM OF THE HEART SA node AV node Purkinje fibers Bundle branches A-V bundle Internodal pathways SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. Depolarization spreads more slowly across atria. Conduction slows through AV node. Depolarization moves rapidly through ventricular conducting system to the apex of the heart. Depolarization wave spreads upward from the apex. 1 4 5 3 2 Purple shading in steps 2–5 represents depolarization. Why is it necessary to direct the electrical signals through the AV node? Why not allow them to spread downward from the atria? The answer lies in the fact that blood is pumped out of the ventricles through openings at the top of the chambers . If electrical signals from the atria were conducted directly into the ventricles, the ventricles would start contracting at the top. Then blood would be squeezed downward and would become trapped in the bottom of the ventricles (think of squeezing a toothpaste tube at the top). The apex-to-base contraction squeezes blood toward the arterial openings at the base of the heart. Why is it necessary to direct the electrical signals through the AV node? Why not allow them to spread downward from the atria?
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Conduction of the Cardiac Action Potential
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FIBRILLATION If myocardial cells contract in a disorganized manner-fibrillation results. Atrial fibrillation –Not a immediate emergency condition. Ventricular fibrillation,- is an immediately life-threatening emergency.* Ventricular fibrillation,- is an immediately life-threatening emergency because withÂout coordinated contraction of the muscle fibers, the ventricles cannot pump enough blood to supply adequate oxygen to the brain. Treatement- electrical shock to the heart. The shock creates a depolarization that triggers action potentials in all cells simultaneously, coordinating them again.
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Electrical Conduction
AV node Direction of electrical signals Delay the transmission of action potentials SA node Set the pace of the heartbeat at 70 bpm AV node (50 bpm) and Purkinje fibers (25-40 bpm) can act as pacemakers under some conditions The ejection of blood from the ventricles is aided by the spiral arrangement of the muscles in the walls . As these muscles contract, they pull the apex and base of the heart closer together, squeezing blood out the openings at the top of the ventricles. A second function of the AV node is to delay the transmisÂsion of action potentials slightly, allowing the atria to complete their contraction before ventricular contraction begins. Why does the fastest pacemaker determine the pace of the heartbeat? Consider the following analogy. A group of people are playing "follow the leader" as they walk. Initially, everyone is walking at a different pace—some fast, some slow. When the game starts, everyone must match his or her pace to the pace of the person who is walking the fastest. The fastest person in the group is the SA node, walking at 70 steps per minute. Everyone else in the group (autorhythmic and contractile cells) sees that the SA node is fastest, and so they pick up their pace and follow the leader. In the heart, the cue to follow the leader is the electrical signal sent from the SA node to the other cells. Now suppose the SA node gets tired and drops out of the group. The role of leader defaults to the next fastest person, the AV node, who is walking at a rate of 50 steps per minute. The group slows to match the pace of the AV node, but everyÂone is still following the fastest walker. What happens if the group divides? Suppose that when they reach a corner, the AV node leader goes left but a renegade Purkinje fiber decides to go right. Those people who follow the AV node continue to walk at 50 steps per minute, but the peoÂple who follow the Purkinje fiber slow down to match his pace of 35 steps per minute. Now there are two leaders, each walkÂing at a different pace. In the heart, the SA node is the fastest pacemaker and norÂmally sets the heart rate. If this node is damaged and cannot function, one of the slower pacemakers in the heart takes over. Heart rate then matches the rate of the new pacemaker. It is even possible for different parts of the heart to follow different pacemakers, just as the walking group split at the corner.
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Complete heart block- The conduction of electrical signals from the atria to the ventricles through the AV node is disrupted. The SA node fires at its rate of 70 beats per minute, but those signals never reach the ventricles. So the ventricles coordinate with their fastest pacemaker. Because ventricular autorhythmic cells discharge only about 35 times a minute, the rate at which the ventricles contract is much slower than the rate at which the atria contract. If ventricular contraction is too slow to maintain adequate blood flow, it may be necessary for the heart's rhythm to be set artificially by a surgically implanted mechanical pacemaker. These battery-powered devices artificially stimulate the heart at a preÂdetermined rate.
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