PHYSIOLOGICAL PROPERTIES OF HEART
FORMATION OF
ELECTROCARDIOGRAPHY AS A METHOD OF OBSERVATION
Objectives for Students’ Independent Studies
You should prepare for the practical class using the existing textbooks and lectures. Special attention should be paid to the following:
List:
Physiological properties of heart
1. Morphology and functional organization of heart
2. Automaticity of the heart
3. Conductibility of the heart
4. Excitability of heart
5. Contractibility of the heart
6. Mechanism of contraction and relaxing of the heart muscle.
Formation of normal electrocardiogram
7. Separate myocardial cell electricity.
8. Electrogram and action potential of one myocardial cell.
9. Formation of EEG waves
10. ECG correspondence of heart depolarization
Electrocardiography as a method of observation
1. ECG leads
2. Algorithm of ECG registration:
3. ECG analysis
14. ECG analysis begins with estimation of control voltage and paper speed. Another analysis at usual performs in this order.
5. Investigation of conductive system in the heart
6. ECG registration
7. ECG analysis
PHYSIOLOGICAL PROPERTIES OF HEART
1. Morphology and functional organization of heart
a) Structure of heart.
The heart contains four chambers: two upper atria, which receive venous blood and two lower ventricles, which eject blood into arteries. The right ventricle pumps blood to the lungs, where the blood becomes oxygenated. The left ventricle pumps oxygenated blood to the entire body.
The right and left atria receive blood from the venous system. The right atrium and ventricle are separated from the left one by septum, which is the muscular wall. This septum normally prevents mixture oxygenated and not oxygenated blood.
Between the atria and ventricles there is a layer of dense connective tissue known as fibrous skeleton of the heart. The connective tissue of skeleton also forms rings, called annuli fibroses around two pairs of one-way valves.
b) Structure of myocardium.
Bundles of myocardial cells in the atria attach to the upper margin of this fibrous skeleton and form a myocardium. The myocardial cell bundles of the ventricles attach to the lower margin and form a different myocardium. As a result, the myocardium of the atria and ventricles are structurally and functionally separated from each other.
Weight of whole myocardium consist 250-300g. Atria myocardium has two layers of muscle cells – circular and
longitudinal. Circular cells layers surround mouth of vessels, which fall into atria and may cover again it in constriction.
Ventricles myocardium has three layers of muscle cells. External and internal layer have spiral form and are common for both ventricles. Middle layer has circular orientation and is separated in every ventricle.
c) Functional specialties of myocardial cells.
Myocardial cells contain actin and myosin filaments and contracts by means of the sliding filament mechanism. Myocardial cells are joined by gap junctions, due to which electrical impulses can spread to all cells in the mass. Sarcoplasmatic reticulum in myocardial cells is developed slightly. That is why some amount of calcium may enter the myocardial cell from the outside.
Besides contractive myocardial cells there are modified cells of the conduction system of the heart. They can generate and conduct impulses through myocardium.
d) Electrophysiological properties of the contractive myocardium.
The main electrophysiological properties of the contractive myocardium are automaticity, contractility, conductability and excitability.
Automaticity is property to contract replying to electrical impulses, originated in pacemaker cells of the conduction system of the heart.
Contractility is property to contract replying to irritation.
Conductibility is property to spread electrical impulses through the conduction system and contractive myocardium.
Excitability is property to reply the irritation.
2. Automaticity of the heart
a) Structure of conduction system.
Action potentials that originate in the sinoatrial node (SA-node) spread to adjacent myocardial cells of the right and left atria through the gap junction between these cells.
Since the myocardium of the atria is separated from the myocardium of ventricles by the fibroses skeleton of the heart, the impulse cannot be conducted directly from the atria to the ventricles. Besides that atria have to contract before ventricles to guarantee pumping of blood.
Once the impulses spreads through the atria, it passes to the atrio-ventricular node (AV-node), which is located on the inferior portion of the internal septum. From here, the impulse continues through the atrio-ventricular bundle, or bundle of His, beginning at the top of the interventricular septum. The atrio-ventricular bundle divides into right and left bundle branches, which are continues with Purkinje fibers within the ventricular walls.
Specialized excitatory and conductive system of the heart: consists of:
1. Sinus node “SA” node: also called sinoatrial node, located in the right atrium. It is concerned with the generation of rhythmical impulse; it is the pacemaker of the heart that initiates each heart beat. This automatic nature of the heart beat is referred to as automaticity.
2. Internodal pathways conduct the impulse generated in SA node to the AV node.
3. The AV node (atrioventricular node), located near the right AV valve at the lower end of the interatrial septum, in the posterior septal wall of the right atrium. At which impulse from the atria is delayed before passing into the ventricles.
4. The AV bundle (bundle of His) conducts the impulse from the atria into ventricles.
5. The left and right bundles of purkinje fibers, which conduct the cardiac impulse to all parts of the ventricles. The purkinje fibers distribute the electrical excitation to the myocytes of the ventricles.
Figure: The cardiac conduction system.
Figure: organization of the AV node.
The SA node as the pacemaker of the heart:
(Automaticity & rhythmicity)
Automaticity is the property of self-excitation (i.e. the ability of spontaneously generating action potentials independent of any extrinsic stimuli) while rhythmicity is the regular generation of these action potentials. In other words, the cardiac impulse normally arises in the SA node, which has the capability of originating action potentials and functioning as pacemaker. This action potential then spreads from the SA node throughout the atria and then into and throughout the ventricles.
The contractile cardiac muscle cells don’t normally generate action potentials but they can do in certain pathological conditions. This mean that all parts of the conduction system are able to generate a cardiac impulse; (autorhythmicity), but the normal primary pacemaker is the SA node, while the AV node is a secondary pacemaker and the Purkinje system is a tertiary (or latent) pacemaker. The AV node acts only if the SA node is damaged or blocked, while the tertiary pacemaker takes over only if impulse conduction via the AV node is completely blocked.
The SA node discharges at an intrinsic rhythmical rate of 100-110 times per minute (sinus rhythm). Under abnormal condition; the AV nodal fibers can exhibit rhythmical discharge and contraction at a rate of 40 to 60 times/minute. While those of purkinje fibers discharge at a rate between 15 and 40 times/minute.
Autorhythmicity is a myogenic property independent of cardiac innervation. This is evidenced by the following:
· Completely denervated heart continues beating rhythmically.
· Hearts removed from the body and placed in suitable solutions continue
· beating for relatively long periods.
· The transplanted heart (denervated heart) has no nerve supply but they beat regularly.
Self-excitation of SA node:
What causes the SA node to fire spontaneously?
Although the SA node discharges at an intrinsic rhythmical rate of 100-110 times per minute but the pulse rate averages 70 or 80 times per minute, this is because of the effect of vagal tone. SA node does not have a stable resting membrane potential which starts at about – 60 mV. This is due to the inherent leakiness of the SA nodal fibers to Na+ ions that causes this self-excitation (Na+ influx). in other words, because of the high Na+ ions concentration in the ECF as well as the negative electrical charge inside the resting sinus nodal fibers, the positive Na+ ions outside the fibers tend to leak to the inside, rising the membrane potential up to a threshed to fire an action potential.
Atrioventricular node (AV node):
The conductive system is organized, so that cardiac impulse will not travel from the atria into ventricles too rapidly. There is a delay of transmission of the cardiac impulse in the AV node to allow time for the atria to empty their blood into the ventricles before ventricular contraction begins.
b) Electrophisiological properties of conduction system.
The cells of SA-node do not keep a resting membrane potential in the manner of resting neurons or skeletal muscle cells. The membrane potential begins at about -60 mV and gradually depolarizes to -40 mV, which is the threshold for producing an action potential in these cells. This spontaneous depolarization is produced by the diffusion of Ca²+ through openings in membrane called slow calcium cannels. At the threshold level of depolarization, other channels, called fast calcium channels, open and calcium rapidly diffuses into the cells. The opening of voltage regulated sodium gates, and the inward diffusion of sodium that results, may also contribute to the upshot phase of the action potential in pacemaker cells.
The opening of potassium gates and outward diffusion of potassium, as in the other excitable tissues produce repolarization.
Once repolarization to -60 mV has been achieved, a new pacemaker potential begins, again culminating with a new action potential.
Action potential of SA node
The resting membrane potential of SA node is of -55 to -60 mV (millivolts). The cause of this reduced negativity “less negative” is that the cell membrane of the sinus fibers are naturally leaky to sodium ions “Na+ influx”. Therefore; Na+ influx causes a rising membrane potential “gradual depolarization” which when reaches a threshold voltage at about – 40 mV, the fast calcium and sodium channels opened, leading to a rapid entry of both Ca+2 and Na+ ions causing the action potential to about 0 mV (zero), to be followed by repolarization which is induced by K+ efflux out of the fiber because of the opening of K+ channels. This repolarization carries the resting membrane potential down to about -55 to -60 mV at the termination of action potential.
Figure: Action potentials of the SA node.
Action potential of ventricular cardiac muscle fiber
The membrane potential of cardiac ventricular muscle fiber cells is about -90 mV; the interior of the cell is electrically negative with respect to the exterior due to disposition; distribution of ions mainly Na+, K+ and Ca+2 ions across its membrane.
The action potential (AP) is an electrical signal or impulse produced by ionic redistribution that the potential changes into positive inside the cell (depolarization), to be followed by restoration of the ions; returning back to the resting potential (repolarization). Stimulation of cardiac muscle cells by SA produces a propagated action potential, that is responsible for muscle contraction i.e., excitation-contraction coupling. In other words, stimulation of cardiac muscle cells specifically those of the ventricles is performed by the propagated AP of the SA node from which the electrical impulses originating and propagated over the heart. According to the figure (a), the propagated AP of the SA node depolarized the ventricular muscle fiber cells rapidly with an overshoot (phase 0), followed by a plateau at around zero potential level (phase 2). This plateau is unique for the heart muscle; and is followed by phase 3 and 4; as final repolarization i.e., for the potential to return to baseline.
Ionic basis of the action potential of the cardiac ventricular muscle fiber cell:
The action potential of cardiac ventricular muscle fiber cell includes the following phases (a):
· Phase 0 (upstroke): initial rapid depolarization with an overshoot to about +20 mV are due to opening of the voltage-gated Na+ channels with rapid Na+ influx.
· Phase 1 (partial repolarization): initial rapid repolarization is due to K+ efflux (K+ outflow) followed the closure of Na+ channels when the voltage reaches at nearly +20 mV.
· Phase 2 (plateau): subsequent prolonged plateau is due to slower and prolonged opening of the voltage-gated Ca+2 channels with Ca+2 influx, Ca+2 enter through these channels prolong depolarization of the membrane.
· Phase 3 (rapid repolarization): final repolarization is due to opening of the voltage-gated K+ channels at zero voltage with rapid K+ outflow (K+ efflux) followed the closure of Ca+2 channels and, this restores the membrane to its resting potential.
· Phase 4 (complete repolarization): The membrane potential goes back to the resting level (-90 mV) i.e., restoration of the resting potential. This is achieved by the Na+-K+ pump that works to move the excess K+ in and the excess Na+ out.
Figure (a): The action potential of the ventricular muscle fiber.
Figure: Rhythmical action potentials from a purkinje and ventricular muscle fibers.
Figure: Rhythmical discharge of SA nodal fiber, compared with action potential of ventricular muscle fiber.
c) Function of pacemaker centers.
Some other regions of the heart, including the area around SA-node and the atrio-ventricular bundle can potentially produce pacemaker potentials. The rate of spontaneous depolarization of these cells however is slower, than that of SA-node.
As it determined SA-node produce 60-90 impulses per minute, AV-node – 40-50, bundle of His – 20-30 and Purkinje fibers 10-20 impulses per minute. The potential pacemaker cells are stimulated by action potential from SA-node before they can stimulate themselves through their own pacemaker potentials. If action potentials from the SA-node are prevented from reaching these areas (through blockade of conduction), they will generate pacemaker potentials at their own rate and save as sites for the origin of action as pacemakers.
A pacemaker other than SA-node is called as ectopic pacemaker or ectopic focus.
If the heart of a frog is removed from the body, and put in physiological solution, it will still continue to beat as long as the myocardial cells remained alive.
At a result of experiments with isolated myocardial cells and clinical experience with patients who have specific heart disorders, many regions within the heart have been shown to be capable of originating action potentials and functioning as pacemakers.
In a normal heart, however, only one region demonstrates spontaneous electrical activity and by this means functions as a pacemaker – SA-node.
3. Conductibility of the heart
a) Conduction of impulses in atria. After excitation of SA-node impulses conduct by bundle of Thorel, Venkenbuh and Buhman to AV-node.
Action potentials from SA-node spread at a rate of 0,8-1,0 m/s across the myocardial cells of both atria. At first the right atrium is excited and left is the second.
b) Peculiarities of conduction through AV-node. The conduction rate slows considerably as the impulse passes into the AV-node. Slow conduction of impulses (0,03-0,05 m/s) through the AV-node is caused by special form of AV-node and peculiarities of impulse development in cells of AV-node, as absence of rapid diffusion of ions. Slow conduction in AV-node is necessary for proper order of contracting atria and ventricles.
c) Excitation of ventricles. After the impulses spread through the AV-node, the conduction rate increases in the atrio-ventricular bundle and reaches 5 m/s in the Purkinje fibers. As a result of this rapid conduction of impulses, ventricular contraction begins 0,1-0,2 s after the contraction of atria.
High velocity of impulses in ventricles is caused by rapid Na+-gates.
At first middle part of septum is excited, than impulses spread to apex of heart, than to the right ventricle wall, to the left ventricle wall and to basal parts of ventricles myocardium.
4. Excitability of heart
a) Excitability changing during excitation.
Once contractive myocardial cell has been stimulated by action potentials origin in SA-node, it produces its own action potentials. The majority of myocardial cells have resting membrane potentials of about -90 mV. When stimulated by action potentials from a pacemaker region these cells become depolarized to threshold. At this point their voltage – regulated Na+-gates open.
The upshot phase of the action potential of no pacemaker cells is due to the inward diffusion of Na+. This period called depolarization.
Following the rapid reversal of the membrane polarity, the membrane potential quickly declines to about -15 mV. Opening K+ and Cl– gates and inward diffusion of K+ and Cl– causes it. This period called quickly initial repolarization.
Then this level potential maintained for 200-300 ms and cells plato phase. It’s due to opening of slow Ca2+ gates. Gradually slow Ca2+ diffusion stops and than diffusion of K+ increases. Rapid repolarization at the end of the plato is achieved by rapid outward diffusion of K+. During last phase of rest initial distribution of ions inwards and outwards is recovered by function of the sodium-potassium pumps. The heart normally cannot be stimulated until after it has relaxed from its previous contraction because myocardial cells have long refractory periods. It corresponds to the long duration of their action potentials. Summation of contractions is thus prevented and myocardium must relax after each contraction. The rhythmic pumping action of the heart is thus ensured.
Refractory period:
· Absolute refractory period (ARP), it is the interval during which no action potential can be produced, regardless of the stimulus intensity i.e., no stimulus however strong, can produce a propagated action potential. It lasts the upstroke plus plateau and initial repolarization till mid-repolarization at about -50 to -60 mV. It means that the cardiac muscle caot be exited during the whole period of systole and early part of diastole. This period prevents waves summation and tetanus.
· Relative refractory period (RRP), it is the interval during which a second action potential can be produced but at higher stimulus intensity i.e., the heart responds only to stronger stimuli. It lasts from the end of ARP (midrepolarization) and ends shortly before complete repolarization i.e., it lasts for a short period during diastole.
b) Excitability of the heart and skeletal muscles. Electrical impulses that originate at any point of myocardium can spread to all cells, according to ruler “all or nothing”. Because all cells in myocardium are electrically joined a myocardium behaves as a single functional unit. Unlike it, in skeletal muscle contraction depends oumber of excited neurons, which stimulate motor unit. Unlike skeletal muscles, cardiac muscle capable to produce action potentials by pacemaker cells. The rate of heartbeat is regulated by autonomic nervous system. In difference, skeletal muscles are regulated by somatic nervous system.
5. Contractibility of the heart
a) Mechanism of contraction and relaxing of the heart muscle.
Like skeletal muscle cells, cardiac muscle cells are striated. They contain actin and myosin filaments arranged in the form of sarcomeres. They contract by means of the sliding filament mechanism. Myocardial cells are short, branched and interconnected. Gap junctions join adjacent myocardial cells. That is why a myocardium contracts to its full extent each time and all of its cells contribute to the contraction. After opening Ca2+– gates contraction begins. The mechanism of contraction is similar to skeletal muscles. Sliding on thin filaments they produce shortening of the sarcomeres. In the process of contraction, the thin filaments slide deeper and deeper toward the center, producing increasing amounts of overlap with thick filaments. Sliding of the filaments is produced by the action of numerous cross brigs that extend out from the myosin toward the action. Before the cross brigs combine with actin the globular head function as myosin ATP-ase enzymes. Then cross brigs combine with actin and can attach to actin.
VIDEO
6. Mechanism of contraction and relaxing of the heart muscle.
b) Contractibility cardiac and skeletal muscles:
Contractility is the ability of the cardiac muscle to contract.
The effect of various factors on contractility is called inotropism; a positive (+ve) inotropic effect means an increase in myocardial contractility, whereas a negative (-ve) inotropic effect means a decrease in myocardial contractility.
– In skeletal muscles long fibrose cells are separated from each other functionally and structurally. But myocardial cells are short, branched and interconnected by gap junctions.
– Skeletal muscle produce contractions, which are graded depending on the number of cells stimulated. But a myocardium contracts as a single functional unit.
– Skeletal muscles require external stimulation by somatic motor nerves before they can produce action potentials and contract. But cardiac muscle is able to produce action potentials automaticity.
– Skeletal muscle capable to summation of contraction, but myocardial muscle pumps the blood by rhythmic contractions.
Excitation-Contraction coupling in the heart muscle:
As in skeletal muscles, the depolarization wave reaching via the T tubules causes the opening of Ca+2 channels in the sarcoplasmic reticulum adjacent to the T-tubules. The released Ca+2 from the cisternae of the sarcoplasmic reticulum (activator Ca+2; aCa+2) binds to troponin C, leading to cross bridge formation between actin and myosin, which results in contraction.
In cardiac muscle, the amount of this activator Ca+2 is often insufficient to initiate contraction, but it can be increased indirectly by the following mechanism:
The depolarization wave in the T-tubules opens the long-lasting Ca+2 channels in the T-tubule membrane, and sarcolemma, Ca+2 diffuses from the ECF through these channels into the cardiac muscle fibre cell causing a small increase in the cytosolic (fluid of the cytoplasm) calcium concentration in the region of the T-tubules and adjacent sarcoplasmic reticulum. This Ca+2 is called depolarizing Ca+2, and although its amount is normally very small, yet it is important because it acts as a signal for the release of large amount of activator Ca+2 from the cisternae of sarcoplasmic reticulum, it is mainly this cytosolic Ca+2 that causes the contraction, i.e. once Ca+2 is in the cytoplasm, it binds to troponin and stimulates contraction. As a result, myocardial cells contract when they are depolarized. The force of contraction is directly proportional to the amount of cytosolic Ca+2.
Contraction ends when the cytosolic Ca+2 concentration restored to its original level. In other words, relaxation of the cardiac muscle occurs as a result of release of the actin-myosin combination, this is achieved by decreasing the intracellular Ca+2 to its pre- contraction level, which occurs by:
1- Active re uptake of Ca+2 into the sarcoplasmic reticulum by Ca+2 pump (primary active transport of Ca+2).
2- Active pumping of excess Ca+2 outside the fibres by Na+– Ca+2 exchanger carrier protein (secondary active transport ; counter transport).
The heart normally cannot be stimulated again until after it has relaxed from its previous contraction because myocardial cells have long refractory periods that correspond the long duration of their action potentials. Summation of contractions and tetanus are thus prevented, and the myocardium must relax at each contraction to ensure the rhythmic pumping action of the heart.
Factors that affect cardiac contractility:
1) mechanical, 2) cardiac, 3) extracardiac
1). Mechanical factors:
* Preload (venous return)
* Afterload
The preload:
The preload is the load that determines the initial length of the resting muscle before contraction. The level of the preload is represented by the end-diastolic volume (EDV) i.e., by the venous return (VR). It affects the tension developed in the muscle. When the venous return (EDV), increases, the strength of ventricular contraction increases too, leading to an increase in the stroke volume (Frank-Starling law).
Frank-Starling’s law of the heart
This law describes the length-tension relationship in muscles; it states that the force of contraction of the ventricles depends on the initial length of ventricular muscle fibers. In such a way, that the force of myocardial contraction is directly proportional to the initial length of the cardiac muscle fibres (i.e. to the preload (VR) or EDV). This means that the greater the degree of stretching of the myocardium before contraction, the greater the force of contraction. In other words, Frank-Starling law reflects the relationship between ventricular end-diastolic volume (EDV) and stroke volume; when the blood returns to the heart during the filling phase, this blood will distend the ventricles so the ventricles will produce more powerful contraction to pump the increased volume of the blood.
The Significance of Frank-Starling’s law
The Starling’s law allows autoregulation of myocardial contractility (regulation of the contractility by changing the length of the muscle fibers), in the following conditions:
(1) In normal hearts. Starling’s law allows changes in the right ventricular output to match changes in the venous return (VR), and maintains equa outputs from both ventricles. For example, if the systemic VR increases, the EDV of the right ventricle increases, leading to a forceful contraction that increases its output to match the increased VR. At the same time, the increased right ventricular output increases the pulmonary VR to the leftventricle, which also increases its EDV, resulting in an increase of its output, which balances the increased right ventricular output.
(2) In denervated hearts (e.g. transplanted hearts); autoregulation of myocardial contractility becomes the main mechanism.
(3) In cases of rise of the arterial blood pressure: the stroke volume of the left ventricle would decrease. However, the retained blood in the left ventricle plus blood returning to it from the left atrium during the next diastole increase the EDV. This leads to a forceful contraction, thus the accumulated blood in the left ventricle will be ejected in spite of the increased arterial blood pressure.
The Afterload:
The afterload is the load that the muscle faces when it begins to contract. In the intact heart, the afterload is produced by the aortic impedance which is determined by:
· The aortic pressure (arterial systolic blood pressure).
· The arterial wall rigidity (arteriosclerosis).
· Blood viscosity (polycythemia).
2). Cardiac factors:
· The myocardial mass.
· The heart rate.
The myocardial mass:
A significant injury or loss of the functioning ventricular muscle (e.g. due to ischemia or necrosis) decreases the force of myocardial contractility. This also occurs in cases of heart failure.
The heart rate:
The force of cardiac contractility is affected by the frequency of stimulation. An increase in the frequency of stimulation (i.e. shortening the intervals between the stimuli) causes a proportional increase in the force of contraction.
Accordingly, tachycardia causes a positive inotropic effect while bradycardia exerts a negative inotropic action. The positive inotropic effect in tachycardia is due to the increase in the number of depolarization (which increases the intracellular Ca+2 content and its availability to the contractile proteins (troponin C).
3). Extra cardiac factors:
These factors affect the cardiac inotropic state and they include the following:
a). Neural
b). Physical
c). Chemical
a). Neural factors:
Sympathetic stimulation and noradrenaline exert a +ve inotropic effect by increasing;
· Cyclic-AMP in the cardiac muscle fibres (which leads to activation of the Ca+2 channels and more Ca+2 influx from the ECF).
· The heart rate.
Conversely, parasympathetic stimulation and acetylcholine exert a -ve inotropic effect (by opposite mechanism) but on the atrial muscle only (since the vagi nerves don’t supply the ventricles).
b). Physical factors:
A moderate rise of the body temperature strengthens cardiac contractility (by increasing the Ca+2 influx and ATP formation in the muscle) while an excessive rise of the body temperature (e.g. in fever) exhausts the metabolic substrates in the cardiac muscle and decreases its contractility. Hypothermia also decreases cardiac contractility.
c). Chemical factors:
(A) Hormones:
Catecholamines (epinephrine, norepinephrine and dopamine), glucagon and the thyroid hormones; all exert a +ve inotropic effect.
(B) Blood gases:
Moderate hypoxia (O2 lack) and hypercapnia (CO2 excess) increase the cardiac contractility, whereas severe hypoxia and hypercapnia directly depress the cardiac muscle and decrease its contractility.
(C) H + ion concentration (pH):
An increase of the blood [H+] i.e. drop of the blood pH (acidosis) produces a -ve inotropic effect, whereas a decrease of the blood [H+] i.e. rise of the blood pH (alkalosis) produces a + ve inotropic effect.
(D) Inorganic ions:
· Sodium: Hypernatraemia favors Na+ influx and Ca+2 efflux by the
· Na+-Ca+2 exchanger carrier, thus it has a -ve inotropic effect. On the other
· hand, hyponatraemia exerts a +ve inotropic effect by an opposite mechanism.
· Potassium: Hyperkalaemia has a -ve inotropic effect (weakens the myocardial contractility; flaccidity) and may stop the heart in diastole. This is because the excess K+ in the ECF decreases the resting membrane potential (more positive resting membrane potential; closer to the threshold)) in the cardiac muscle fibers, so the amplitude of the action potential is reduced leading to less influx of the depolarizing Ca+2 and in turn less release of activator Ca+2 from the sarcoplasmic reticulum. In addition, Hyperkalaemia increases excitation and decreases conduction leading to ectopics and dilated, flaccid heart. On the other hand, hypokalaemia produces a +ve inotropic effect by an opposite mechanism.
· Calcium: Hypercalcaemia exerts a +ve inotropic effect as a result of more cytosolic Ca+2. Whereas hypocalcaemia has a little (or no) -ve inotropic effect, since lowering of the serum Ca+2 level causes fatal tetany before affecting the heart. However, hypocalcaemia causes cardiac flaccidity like Hyperkalaemia.
(E) Toxins:
Several toxins (e.g. certain snake venoms and the toxin released by the diphtheria microorganisms) produce a-ve inotropic effect (mostly by a direct action on the contractile mechanism of the cardiac muscle).
(F) Drugs:
· Cardiac glycosides (e.g. digitalis; Digoxin): These drugs inhibit the Na+-K+ ATPase in the sarcolemma of the cardiac muscle fibres, so the intracellular Na+ concentration increases. This decrease the Na+ influx, thus Ca+2 efflux through the Na+-Ca+2 exchanger is also decreased. Accordingly, the intracellular Ca+2 concentration increases, producing a +ve inotropic effect. Digitalis also increases the slow Ca+2 influx during the action potential.
· Xanthines (e.g., caffeine and theophylline; bronchodilator): They exert a +ve inotropic effect.
· Ouinidine, barbiturates, procainamide (and other anesthetic drugs) as well as Ca+2 blocker drugs all have a -ve inotropic effect by decreasing Ca+2 influx into the cardiac muscle fibres.
7. Separate myocardial cell electricity.
Potential changes on cell membrane, which is recorded separately called electro gram. During resting potential membrane charge is positive. If two electrodes will dispose on membrane surface the voltage difference is absent and baseline is recorded. In irritation the cell membrane is depolarized some part firstly. The voltage between two electrodes increased and electro gram line deflects upward. The positive wave of electro gram is formed. After depolarizing all the membrane its surface charge becomes negative. The voltage under both electrodes temporarily becomes the same. Electro gram line returns downward to baseline level. Then repolarization begins from the same point as depolarization and in the same order. Polarity of cell membrane changes and electro gram deflects downward. The negative wave is formed. After depolarization of hole the membrane surface the voltage returns to rest potential level and baseline on electro gram record.
FORMATION OF
1. Electrogram and action potential of one myocardial cell.
An electrocardiograph is an instrument that measures and records the electrocardiogram (ECG), the electrical activity generated by the heart. Electrodes placed on various anatomical sites on the body help conduct the ECG to the electrocardiograph. The ECG alone is not sufficient to diagnose all abnormalities possible in the pacing or conduction system of the heart. The interpretation of the 12-lead ECG provides a differential diagnosis for many arrhythmias
During the depolarization phase the rapid Na+ gates open and inward diffusion of Na+ occur. This event corresponds to formation upward part of positive wave on electro gram line. The next fast initial repolarization begins with inward Cl– diffusion. Then electro gram returns to baseline level. When opening slow Ca2+ gates the potential difference temporarily isn’t essential and baseline continues. During the next phase outward K+ diffusion increases and external surface of membrane becomes positive. Voltage fluctuation leads to deflection of electro gram downward further returning to baseline level. In rest period all the membrane has positive charge on external surface and baseline is recorded. Through this period ion pumps restore initial distribution of ions.
2. Formation of EEG waves
Unexcited part of cell has already positive charge. Depolarized part has already negative charge. Between positive and negative charges the electrical power is recorded. Electrical power directs towards positive voltage. When changing polarity, electrical power of entire heart has different volume and direction in every moment of cardiac cycle.
To understand formation of ECG waves in different leads it is necessary to remember some rulers of this process:
– When electrical power directs towards positive pole of lead the upward wave is recorded;
– When electrical power directs towards negative lead pole, the downward wave occurs;
– If electrical power directs perpendicular to lead axis the baseline is recorded.
3. ECG as a representation of heart depolarization
Every cardiac cycle produces ECG waves designated as P, Q, R, S and T. These waves are not action potentials. They represent potentials between rested and depolarized or depolarized and repolarized parts of whole heart. Amplitude and duration of these waves correspond to electrical power fluctuation in entire heart.
After producing impulse in SA-node depolarization begins at first in cells of right atrium and ascend part of P wave is recorded. When depolarization spreads into left atrium, the ECG line returns to baseline level. Delay of depolarization in AV-node recorded as PQ-interval in baseline. Then impulse spreads into middle part of septum and heart apex. This event recorded as descend part of Q wave. Iext depolarization of right ventricle wall ECG line deflexed upward and formation of R wave begins. When impulse spreads into left ventricle wall, the ECG line returned in contrary side towards the lowest point of S wave. Depolarization of ventricles basis afterwards caused formation of S wave, which continues to baseline.
Repolarization of atria is failed to record in ECG because of greater depolarization of ventricles. Repolarization of ventricles develops firstly in right part of heart and then in left one. That is why ascend and descend parts of T wave are formed.
In diastole normally baseline is recorded but U wave may occur.
ELECTROCARDIOGRAPHY AS A METHOD OF OBSERVATION
1. ECG leads:
The electrical current generated by the heart is conducted through the pairs of electrodes and leads, and is amplified, recorded, and processed by the electrocardiograph. The wires connecting the pairs of electrodes on the surface of the body to the electrocardiograph are called leads. The different features and modules of a typical electrocardiograph include the protection circuitry, lead selector, calibration signal, preamplifier, isolation circuit, driver amplifier, memory system, microcomputer, and recorder or printer.
Twelve leads usually comprise a diagnostic ECG recording: six limb leads (three bipolar and three unipolar), and six unipolar precordial leads. The instantaneous cardiac scalar voltages resulting from the electrical activity in the heart is measured in each of the 12 leads. Since the cardiac vector varies in magnitude with time over a three-dimensional space, it is important to know its presentation (i.e. appearance or projection) in each of the 12 leads of the ECG.
a) Bipolar limb leads.
The bipolar limb leads record the voltage between electrodes placed on the wrists and legs. These leads were proposed by Einthoven in 1913.
I lead: left arm (+) – right arm (-);
II lead: left leg (+) – right arm (-);
III lead: left arm (+) – left leg (-).
For recording limb leads we put red electrode on right arm, yellow – on left arm, green – on left leg and black – on right leg. Black electrode has zero potential (ground).
b) The unipolar limb leads were proposed by Goldberger in 1942. They record voltage between single “exploratory electrode” fro one limb and zero joined electrode from two other limbs. So there are three leads AVR, AVL, AVF. In fact zero electrodes records middle voltage of two limbs. Bipolar limb leads and unipolar limb leads record electrical power in frontal projection.
c) The unipolar chest leads were suggested in 1934 by Vilson. One electrode, which is active, situated on the chest in six standard positions. They labeled V1 – V6. Joined zero electrode records middle potential of right arm, left arm and left leg. That is why every chest lead records voltage between active chest electrode and Vilson’s joined zero electrode.
These standard positions of active chest electrode are:
V1 – in crossing right IV right intercostal space and parasternal line;
V2 – in crossing left IV intercostal space and parasternal line;
V3 – between V2 and V4;
V4 – in crossing V left intercostal space and medioclavicular line;
V5 – in crossing V left intercostal space and anterior axilar line;
V6 – in crossing V left intercostal space and middle axilar line.
Unipolar chest leads records changes of heart polarity in horizontal projection.
RESUME:
Figure 1. shows the lead placement to acquire the 12-lead ECG. The leads can be categorized into the frontal leads (I, II, III, aVR, aVL, and aVF), and the transverse leads (V1, V2, V3, V4, V5, and V6).
The frontal leads measure the projection of the cardiac vector on the frontal plane of the body. The frontal plane is parallel to the floor when lying supine. The transverse or precordial leads measure the projection of the cardiac vector on the horizontal plane, (i.e. the plane that is parallel to the floor when standing).
Leads I, II, and III of the frontal plane are bipolar. They record the differences between two points on the body. Figure 1 shows that lead I is measured between an electrode on the left arm (the positive electrode) and an electrode on the right arm. The three-dimensional cardiac vector projects into each of the bipolar leads, indicating the strength and direction of the instantaneous cardiac vector.
Leads aVR (on the right arm), aVL (on the left arm), and aVF (on the foot) are unipolar leads. They measure the potential difference on the limbs with respect to a reference point formed by the two resistors between limb electrodes. For example, lead aVR is measured between an electrode on the right arm, and a reference point formed via a resistor to the left arm and another resistor to the left foot. These leads show the cardiac vector projection on the frontal plane and are amplified by about 50% (i.e. augmented) so that their amplitudes are comparable to those of the bipolar leads.
The six precordial leads, V1 to V6, are unipolar and measure the cardiac vector projection on the horizontal plane. These precordial leads are measured with respect to the Wilson central terminalwhich is formed by a three resistor network as shown in Figure 4.1. V1 and V2 are placed on the fourth intercostal space to the right and left, respectively, of the sternum. The V4 electrode is placed on the fifth intercostal space at the left midclavicular line. The V3 electrode lies between V2 and V4. Electrode V5 is placed to the left of V4 on the anterior axillary line, and V6 is placed on the same level as V5 on the midaxillary line. It is important to account for the position of these electrodes when interpreting the ECG on leads V1 through V6. The precordial leads measure the potential between each of V1 through V6 and the Wilson’s central terminal formed as shown in Figure 1.
The 12-lead ECG provides various viewpoints of the three-dimensional instantaneous cardiac vector that are somewhat redundant, and this is helpful in providing discriminatory information for diagnosing abnormalities in the pacing and conduction system of the heart.
The electrical activity due to the specialized cells in the heart results in an electric potential on the surface of the body. Each cell can be modeled by a dipole, and the superposition of the potentials from the dipoles for all of the cells in the myocardium results in a three-dimensional cardiac vector for the heart at each instant in time. The cardiac vector at each instant of time represents the net electrical activity in the heart.
Figure 2. Shows the Einthoven triangle superimposed on the locus of points formed in the frontal plane by a normal instantaneous cardiac vector, the vectorcardiographic loop during one cardiac cycle. The measured ECG on each lead is a projection of the instantaneous cardiac vector. The P wave corresponding to atrial contraction, projects onto leads I, II, and III as an upward deflected wave. However, the S wave is projected onto lead III remarkably more than in leads I and II. The instantaneous orientation of the cardiac vector, and the orientation of the lead determine whether there is a positive going or negative going waveform on the lead. Thus the different leads of the 12-lead ECG show various projections of the phases in the cardiac cycle.
Figure 3. the Einthoven triangle
Figure 3 shows the 6-axial reference system, which is used in the diagnosis of certain abnormalities. The 6-axial system shows the orientation of the frontal-plane leads. The various orientations of each lead result in a different projection of the cardiac vector onto that particular lead. A mean electrical axis as a function of time, during the depolarization and repolarization phases of a cardiac cycle can be calculated. For example, the electrical axis of ventricular depolarization, QRS, represents the average of the instantaneous cardiac vectors during ventricular depolarization. The QRS, usually lies between aVL and aVF in Figure 3. It is easy to diagnose left and right axis deviation, LAD and RAD respectively. In LAD, lead I is predominantly positive (i.e. R wave is positive) and both leads II and III are predominantly negative (i.e. R wave is small or absent) . Both II and III must be predominantly negative, i.e. if in lead II the S wave is smaller than the R wave, LAD is not present. If lead II is equiphasic (R and S waves have equal magnitudes), then there is borderline LAD. In RAD, lead I is predominantly negative and both II and III are predominantly positive (Bennett, 1989).
|
2. Algorithm of ECG registration:
Registration performs fare from electric motors and other electrical devices.
Tested person may have rest before registration in 10-15 minutes. This procedure needs 2-hour interval after eating or worm procedures.
For better contact between electrodes and skin use solution NaCl 5-10 % or special electrode past or electrode gel. Otherwise hindrances in ECG curve may occur. They will stand in the way of ECG analysis
ECG registration performs in quiet breathing in patients.
Registration begins from standard voltage 1 mV from the electrocardiograph for regulation of amplitude in ECG. Usually standard voltage amplitude is 10 mm. Then continue registration of bipolar limb leads, the next – unipolar limb leads and afterwards – unipolar chest leads.
3. ECG analysis:
In order to interpret the 12-lead ECG and use it to diagnose abnormalities, it is important to know the normal characteristics of the ECG, and understand the mechanisms underlying the generation of each segment of the ECG. Figure 1 shows the various fiducial points in the ECG, and typical values of the various intervals measured from the ECG.
Fig. 1. – Points various and intervals in the ECG
The main elements of ECG curve are:
– Waves P, Q, R, S and T. Sometimes U wave may occur;
– Segments – P-Q (from the end of P wave to beginning of Q wave), S-T (from the end of S wave until beginning of T wave);
– Intervals, which characterize certain time period of heart activity – P-Q (from the beginning of P wave to beginning of Q wave), Q-T (from beginning of Q wave to end of T wave);
– Complexes – atrial, which is presented by P wave, and ventricular -QRST.
a) P wave in healthy persons, is obligatory positive in I, II, AVF, V2-V6 leads. P wave may be negative in III, AVL and V1, either positive or biphasic. If it is diphasic, then the negative component comes after the positive component and is not excessively broad or deep. An absent P wave in the ECG may signify sinoatrial block, an abnormality in which the impulse from the SA node is not conducted to the AV node. Normally in II lead its amplitude is
The P wave is caused by atrial depolarization. The normal shape of the P wave does not include any notches or peaks.
b) P-Q interval reflects duration of AV-conduction, which is spreading of potential by AV node, His bundle and its branches. This interval lasts 0.12-0.20 s and depends on heartbeat rate.
c) QRST complex reflects spreading of excitation by ventricles. It hole amplitude is higher 5 mm of the waves are signed by capital letters. Otherwise it used little letters. ORS duration in II lead is not more than 0.1 s.
d) Q wave normally in II lead is less then 1/4 of R amplitude duration is 0.03 s. Normally in AVR deep and wide Q waves may be recorded. In V1, V2 – Q wave is particularly absent.
e) R-view usually is recorded in all leads; exalt AVR, which may be absent. In unipolar chest leads R amplitude gradually increases from V1 to V4 and some decreases in V5 and V6. So normally in unipolar chest leads both increasing R-amplitude and S-amplitude occurs. S-wave has amplitude not more than 20 mm, but it varies from lead to lead.
j) S-T –segment corresponds to excitation of both ventricles. Normally in bipolar and unipolar leads it lies on baseline and don’t move more than 0.5 mm. In V1-V3 deviation upward to 2 mm may occur.
h) T-wave normally is positive in I, II AVF, V2-V6, TI>TIII, TV6>TV1. T-wave has sloping ascend part and sleep descending part. In III, AVL, V1 T-wave may either be positive, negative or bipolar. In II lead T-amplitude is 5-6 mm, duration – 0.16-0.24 s.
i) Q-T interval is electrical systole of ventricles. Its duration directly depends on heartbeat rate. Proper duration may calculated by Buzett formula:h0
Q-T=K√¯R-R¯, where
K=0.37 in male or 0,40 in female
f) U-wave may be recorded in unipolar chest leads, which reflects excitation fare of excitability after electrical systole of ventricles myocardium. U-wave usually is positive and small.
4. ECG analysis begins with estimation of control voltage and paper speed. Another analysis at usual performs in this order.
1) Determining of impulse origin. Pay attention to proper order of waves in ECG. If P wave in II lead is positive and recorded before QRS complex is believed to determine pacemaker in SA node.
2) Heart rhythm evaluation by measuring of R-R duration. Normally adjacent R-R intervals duration may differ from each other not more 0.1 s. Usually II lead is examined.
3) Determining of heart rate. In proper rhythm 60 s is divided to R-R duration in seconds, which is calculated using paper speed.
4) Evaluation of ECG voltage. If in bipolar limb leads the lowest R wave is smaller than 5 mm and RI+RII+RIII less than 15 mm, the ECG voltage is decreased. Otherwise it is normal.
5) EMP direction determining.
– Visual method: needs measuring R amplitude in all bipolar limb leads. If true, that RII>RI>RIII, the EMP direction is near 30º-69º, that is normal;
– Graphic method use Baily co-ordinate. If in Einthoven’s triangle put through the center parallel to leads axes we’ll get Baily’s co-ordinate. Than in any two bipolar limbs leads it is necessary to determine summary amplitude of QRS waves. Upward waves have positive meaning and downward are negative. Summary amplitude put on corresponding axis with (+) or (-) sign. In this point lined perpendicular to lead axis. Next time determined cross point of two drown perpendiculars. When join this point to Baily’s co-ordinate center we’ll obtain the EMP direction outward the center.
6) ECG elements analysis. Pay attention to form, amplitude and duration of waves and intervals. Measure deviation from baseline if it occurs. Compare the results with normal rate.
Key words and phrases: myocardial cell electricity, cell membrane, electro gram, resting potential, membrane charge, voltage difference, depolarization, action potential, repolarization, electrical power, conductive system of the heart, ECG leads, bipolar limb leads, unipolar limb leads, unipolar chest leads, ECG registration, morphology and functional organization of heart, structure of heart atria, ventricles, fibrous skeleton of the heart, structure of myocardium, myocardial cells, filament mechanism, gap junctions, conduction system of the heart, automaticity, contractility, conductibility, excitability, sinoatrial node, atrio-ventricular node, atrio-ventricular bundle, bundle of His, Purkinje fibers, membrane potential, spontaneous depolarization, threshold level of depolarization, called fast calcium channels, voltage regulated sodium gates, pacemaker centers. ECG analysis, elements of ECG, waves P, Q, R, S and T, U wave, segments – P-Q, S-T, intervals, P-Q, Q-T, complexes – atrial, ventricular -QRST, AV-conduction, QRST complex, Buzett formula, determining of impulse origin, heart rhythm, ECG voltage, EMP duration.
Multiple Choice.
Choose the correct answer/statement:
1. In experimental animal delay in impulse transmission from atria to ventricles was revealed. What structure of the heart is responsible for this phenomenon?
A. AV bundle
B. SA-node
C. Internodal pathway
D. AV-node
E. Right and left branches of Purkinje fibers
2. In intact experimental animal delay in impulse transmission from atria to ventricles was revealed. What causes of delay?
A. Decrease Ca2+ in blood
B. Slow conduction
C. Increase K+ in blood
D. Cardiac flaccidity
E. Synchronous contraction of entire ventricles
3. On ECG contraction of ventricles is corresponding to:
A. Q-R interval
B. P-Q interval
C. Q-T interval
D. R wave
E. R-R interval
4. Time interval between onset of atria contraction and onset of ventricular one is recorded on ECG as:
A. R-wave
B. Q-T interval
C. QRS complex
D. P-Q interval
E. R-R interval
5. Time of one heartbeat is recorded on ECG as:
A. PQ-interval
B. Q-T interval
C. QRS complex
D. R-wave
E. R-R interval
6. What information is it necessary to obtain for calculation heartbeat rate from ECG:
A. R-R interval duration
B. Q-T interval duration
C. QRS complex duration
D. R wave amplitude
7. What information is it necessary to obtain for estimatioormal rhythmisity from ECG?
A. Total time period of ECG is 0.83 s
B. Order of waves PQRST
C. Adjacent cardio intervals difference less 0.1 s
D. Paper speed 50 mm/s
E. Q-T interval 0.35 s
8. What information is it necessary to obtain for estimatioormal direction of heart vector from ECG?
A. V2>V1>V3
B. RI>RII>RIII
C. V1>V2>V3
D. RII>RI>RIII
E. AVL>AVF>AVR
9. In ECG analysis for 35 aged man amplitude of Q wave is 1/6 comparing R wave was revealed. Duration of QRS complex was 0.08 s. What is your conclusion about function of ventricles?
A. Old myocardial infarction
B. Ventricular hypertrophy
C. Normal function
D. Dilation of ventricles
E. Distraction of cardiac muscle
Real-life situations to be solved:
1. A man comes for ECG registration. He has run through the stairs and his breathing was fast. Could the doctor to record ECG at this minute?
2. The nurse prepared patient for ECG registration and have put electrodes in such order: red electrode on right arm, yellow – on left arm, green – on left leg and black – on right leg. Could the doctor to record ECG?
3. In ECG analysis heartbeat rate 68 heartbeats/min was revealed. Could the doctor characterize the heart rhythm?
4. In ECG analysis order of waves P, Q, R, S, T was revealed. Could the doctor characterize the heart pacemaker?
5. Investigation of conductive system in the heart
After distraction brain in spinal cord by probe enter to thoracic cavity. Calculate rate of heartbeat in intact heart. Put the first Stannius’s ligature and calculate heartbeat upper and lover this one. Also put the II and III ligature. Every case calculate rate of heartbeat for venous sinus, atria and ventricles.
In the conclusion note would the automaticity gradient is characteristic for heart of frog. Describe, what is automaticity gradient.
6. ECG registration
Registration performs fare from electric motors and other electrical devices.
Tested person may have rest before registration in 10-15 minutes. This procedure needs 2-hour interval after eating or worm procedures.
For better contact between electrodes and skin use pieces of bandage, wet by solution NaCl 5-10 % or special electrode past or electrode gel. Otherwise hindrances in ECG curve may occur. They will stand in the way of ECG analysis
ECG registration performs in quiet breathing in patients.
Registration begins from standard voltage 1 mV from the electrocardiograph for regulation of amplitude in ECG.
Usually standard voltage amplitude is
VIDEO ECG 2
17. ECG analysis
1) Determining of impulse origin. Pay attention to proper order of waves in ECG. If P wave in II lead is positive and recorded before QRS complex is believed to determine pacemaker in SA node.
2) Heart rhythm evaluation by measuring of R-R duration. Normally adjacent R-R intervals duration may differ from each other not more 0.1 s. Usually II lead is examined.
3) Determining of heart rate. In proper rhythm 60 s is divided to R-R duration in seconds, which is calculated using paper speed.
4) Evaluation of ECG voltage. If in bipolar limb leads the lowest R wave is smaller than 5 mm and RI+RII+RIII less than 15 mm, the ECG voltage is decreased. Otherwise it is normal.
5) Electrical magnetic power (EMP) direction determining.
– Visual method: needs measuring R amplitude in all bipolar limb leads. If true, that RII>RI>RIII, the EMP direction is near 30º-69º, that is normal;
– Graphic method use Baily co-ordinate. If in Einthoven’s triangle put through the center parallel to leads axes we’ll get Baily’s co-ordinate. Than in any two bipolar limbs leads it is necessary to determine summary amplitude of QRS waves. Upward waves have positive meaning and downward are negative. Summary amplitude put on corresponding axis with (+) or (-) sign. In this point lined perpendicular to lead axis. Next time determined cross point of two drown perpendiculars. When join this point to Baily’s co-ordinate center we’ll obtain the EMP direction outward the center.
6) ECG elements analysis. Pay attention to form, amplitude and duration of waves and intervals. Measure deviation from baseline if it occurs. Compare the results with normal rate.
