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Acetylstrophanthidin was added to the bath. Learn how the microscopic and gross anatomy of the heart enables it to pump blood through the systemic and pulmonary circulations. Redrawn from Tomaselli G. Saravanan Thavamani Design Manager: In the slow response see Figure Action potentials evoked early in the relative refractory period are small. Because EADs may be initiated at either of two distinct levels of transmembrane potential.
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Volume 21 , Issue 4 April Pages Figures References Related Information. Email or Customer ID. Forgot password? Old Password. New Password.
Your password has been changed. Returning user. Request Username Can't sign in? Forgot your username? The Ionic Basis of the Resting Potential The various phases of the cardiac action potential are associated with changes in cell membrane permeability.
An experimental conversion from a fast to a slow response through the addition of tetrodotoxin. Some of these channels are controlled i. Vereecke J: Adrenaline and the plateau phase of the cardiac action potential. The action potential amplitude and the steepness of the upstroke are important determinants of propagation velocity.
The concentration of tetrodotoxin was 0 M in A. The action potentials in some of these cells may then be converted from fast to slow responses see Figure Changes in cell membrane permeability alter the rate of ion movement across the membrane..
Redrawn from Carmeliet E. Redrawn from Giles WR.. The term to the left. A chemical force. If the system comes into equilibrium. Therefore the electrostatic force is slightly weaker than the chemical diffusional force. This value is close to. ENa is about 70 mV see Table Positive values along the vertical axis represent outward currents. Baumgarten CM. The counterforce is electrostatic.
Singer DH: Prog Cardiovasc Dis If the transmembrane potential Vm were clamped at a level negative to EK. The Vm coordinate of the point of intersection open circle of the curve with the X axis is the reversal potential.
Imaizumi Y: Comparison of potassium currents in rabbit atrial and ventricular cells. J Physiol [Lond] In the resting cardiac cell. Biophysical considerations. The dependence of the transmembrane potential.
The characteristics of fast-response action potentials are shown in Figure A. The straight line represents the change in transmembrane potential predicted by the Nernst equation for EK. Redrawn from Page E: The electrical potential difference across the cell membrane of heart muscle.
If the pump is partially inhibited. Circulation With the cell at rest. Transmembrane segment 4 serves as a sensor whose conformation changes with applied voltage and is responsible for channel opening activation. Redrawn from Weidmann S: Elektrophysiologie der Herzmuskelfaser. The precise potential at which the m gates swing open is called the threshold potential.
The m gates are closed. Verlag Hans Huber. The chemical force. The other. One of these gates. Panel A in Figure represents the resting state phase 4 of a cardiac myocyte. The electrostatic force in Figure A is a potential difference of 90 mV. After depolarization. The extracellular portions of the loops that connect helices 5 and 6 in each domain form the pore region and participate in the determination of ion selectivity. The chemical force remains virtually constant.
Redrawn from Squire LR. Hence the lengths of the dark arrows in Figure remain constant at 60 mV. Roberts JL.
Spitzer NC. San Diego. When Vm becomes zero Figure C. Fundamental neuroscience. This reversal of the membrane polarity is the overshoot of the cardiac action potential.
The opening of the m gates occurs very rapidly. Transmembrane segment 4 is a voltage sensor whose conformation changes with applied voltage. The 4 domains are arranged around a central pore lined by the extracellular loops of transmembrane segments 5 and 6. Vm Figure B. Academic Press. A period of myocardial relaxation. The cell can begin to respond again to excitation Figure The h gates remain closed until the first half of repolarization. The electrostatic forces are represented by the white arrows.
During the second half of repolarization. Such channels are said to have recovered from inactivation. During phase 4. This mechanism prevents a sustained. When Vm reaches about 30 mV. The h gates remain closed until the cell has partially repolarized during phase 3 at about time d in Figure A. As Vm approaches 0.
The change in Vm also initiates the closure of inactivation h gates. From time c to time d.
Influx is negligible. This reduces the negative charge inside the cell. When Vm is positive by about 20 mV. About midway through phase 3 time d in Figure A. Redrawn from Rosen MR. Cellular electrophysiology of the mammalian heart. During the brief times that the two channels were open simultaneously.
At the arrow. Redrawn from Cachelin AB. Figure indicates that immediately after the membrane potential was made less negative. Wit AL. DePeyer JE. By time e in Figure A. Because the individual channels open and close randomly. The individual channels open and close repeatedly in a random manner. In the open state. It remained open for about 2 or 3 ms each time and closed for about 4 or 5 ms between openings.
As the stimulus is delivered progressively later during the course of phase 3. Hoffman BF: Electrophysiology and pharmacology of cardiac arrhythmias.
Kokubun S. Sodium channels in cultured cardiac cells. Am Heart J The clones and respective genes for the principal ionic currents are also tabulated. Electrophysiological remodeling in hypertrophy and heart failure. Outward currents are IK1. Redrawn from Tomaselli G. Genesis of the Plateau During the plateau phase 2 of the action potential. During phase 2 see Figure This interaction stimulates the membrane-bound enzyme. An increase in gCa by catecholamines. Some of their important characteristics are illustrated in Figure Upper panel.
Redrawn from Bean BP: Two kinds of calcium channels in canine atrial cells. Differences in kinetics. From Litovsky SH.
J Gen Physiol After the inward current reaches maximum in the downward direction. This change enhances the voltage-dependent activation. Antzelevitch C: Rate dependence of action potential duration and refractoriness in canine ventricular endocardium differs from that of epicardium: Hafner D: Effects of the calcium antagonist diltiazem on action potentials. This effect reduces the counterforce afterload that opposes the propulsion of blood from the ventricles into the arterial system.
Redrawn from Hirth C. An example of this relationship in an isolated ventricular myocyte is shown in Figure J Mol Cell Cardiol Borchard U. Hence vasodilator drugs. If gK1 were the same during the plateau as it is during phase 4.
Thus in this isolated ventricular cell. C 3 Force 10 30 mN 0. Thus when Vm equals or is negative to EK. The changes in gK1 during the different phases of the action potential may be appreciated through an examination of the current-voltage relationship for the IK1 channels the channels that mainly determine gK during phase 4.
The tracings were recorded under control conditions C and in the presence of diltiazem. Thus as Vm passes through this range of values less negative than EK. Hence the plateau of the action potential is much less pronounced in atrial than in ventricular myocytes Figure Such differences are induced. The transient outward current Ito not only accounts for the brief. Figure illustrates some of the differences that prevail in the epicardial and endocardial layers of the ventricle..
Figure shows that with increasing concentrations of diltiazem. The currents that activate more rapidly are designated IKr. During phase 4 of the cardiac cycle. Vm becomes progressively less positive. The distinction is based mainly on the speed of activation. Hence activation of these channels tends to increase IKr see next section slowly and slightly during phase 2. A given change in voltage causes only a small change in ionic current i.
In atrial cells. Therefore these outward IK currents tend to increase gradually throughout the plateau. These channels play only a minor role during phase 2. The action potentials recorded from myocytes in the endocardial. The effects of altering this balance are demonstrated by administration of diltiazem.
Mutations in KCNQ1. In the fast response. In the slow response see Figure Electrophysiology of the heart. Inherited LQTS is relatively rare. Note that the time calibration in B differs from that in A and C. Mutations in these genes alter the function of the corresponding cardiac ion channel proteins Kv4. From Hoffman BF. Molecular genetic studies show that mutations in genes encoding cardiac ion channels are linked to congenital LQTS.
New York. Gap junction channels are composed of proteins called connexins that form electrical connections between cells. In action potentials in panels B to E. These channels are rather nonselective in their permeability to ions and have a low electrical resistance that allows ionic current to pass from one cell to another.
For propagation of the impulse from one cell to another. Each cell synthesizes a hemichannel consisting of six connexons arranged like barrel staves. In the cell interior. When the wave of depolarization reaches the end of the cell. With elimination of the steep upstroke panel E. The sharp upstroke becomes progressively less prominent in action potentials in panels B to D. Certain cells in the heart.
Action potential A in Figure is a typical fast-response action potential. In electrolyte solutions. At the cell exterior. The electrical resistance of gap junctions is similar to that of cytoplasm. In Figure These ionic events closely resemble those that occur during the plateau of fast-response action potentials.
Gap junctions are preferentially located at the ends of the cell and are rather sparse along lateral cell borders. The hemichannel is transported to the gap junction locus on the cell membrane. Connexins vary in their composition and in their tissue distribution within the heart.
In the control tracing panel A. The magnitude of the local currents is proportional to this potential difference. Complex electrocardiography. The time from this artifact to the beginning of phase 0 is inversely proportional to the conduction velocity. Hence the amplitude of the action potential was mV. In general. The reason can be appreciated by referring again to Figure From Myerburg RJ.
The same process then begins at the new border. Lazzara R. At the end of phase 0. The amplitude of the action potential equals the difference in potential between the fully depolarized and the fully polarized regions of the cell interior see Figure The resting potential may vary for several reasons: The greater the potential difference between the depolarized and polarized regions i.
Thus the resting region adjacent to the active zone would be depolarized very slowly. Vm becomes progressively less negative during phase 4 see Figure B. The horizontal lines near the peaks of the action potentials denote 0 mV.
Because these local currents shift the potential of the resting zone toward the threshold value. FA Davis. The level of the resting membrane potential is also an important determinant of conduction velocity. In Fisch E. Period d to e is called the relative refractory period. At about this value of Vm. The action potentials in panels D and E are characteristic slow responses.
The fastresponse conduction velocities are about 0. Fast Response Once the fast response has been initiated. The nature of this voltage dependency is illustrated in Figure Such changes may lead to serious aberrations of cardiac rhythm and conduction. As a consequence of the greater amplitude and upstroke slope of the evoked response. When a fast response is evoked during the relative refractory period of a previous excitation.
The excitability characteristics of cardiac cells differ considerably. The conduction velocities of the slow responses in the SA and AV nodes are about 0. As a consequence. Still later in phase 4. The lengthy refractory periods also lead to conduction blocks. The recovery of full excitability is much slower than for the fast response. Impulses that arrive early in the relative refractory period are conducted much more slowly than those that arrive late in that period.
Ten Eick RE: Action potentials evoked early in the relative refractory period are small. Later in phase 4. Cellular electrophysiology of ventricular and other dysrhythmias: Slow Response The relative refractory period during the slow response extends well beyond phase 3 see Figure B. Even when slow responses recur at a low repetition rate.
Am J Cardiol This response. This characteristic. By the end of phase 3. Note that as the cycle length is diminished. Even after the cell has completely repolarized. The amplitudes and upstroke slopes gradually increase as action potentials are elicited later and later in the relative refractory period. The action potential is characterized by a large-amplitude.
Circ Arrhythmia Electrophysiol 2: Noble PJ. Science The action potential is characterized by a less negative resting potential. Zipes DP. Noble D. Circ Res The iKr current activates slowly.
He became weak. Cardiac ionic currents and acute ischemia: Hence the action potential duration diminishes. Jalife J: Cardiac electrophysiology: Priori SG: Am J Physiol Grant AO: Cardiac Ion Channels. Noble D: Modeling the heart—from genes to cells to the whole organ. An electrocardiogram indicated that the SA node was the source of. The effective refractory period begins at the upstroke of the action potential and persists until about midway through phase 3.
He called his physician. Sanguinetti MC: HERG1 channelopathies. A model for human ventricular tissue. The patient felt stronger and more comfortable almost immediately. Two hours after admission to the hospital.
The cardiologist found that the ventricles did not begin beating spontaneously until about 5 to 10 s after cessation of pacing. At other times. Describe the components of the electrocardiogram. Detailed mapping of the electrical potentials on the surface of the right atrium has revealed that two or three sites of automaticity.
All cardiac myocytes in the embryonic heart have pacemaker properties. Explain the basis of automaticity. Automaticity the ability of the heart to initiate its own beat and rhythmicity the regularity of pacemaking activity are properties intrinsic to cardiac tissue.
Ectopic pacemakers may serve as safety mechanisms when the normal pacemaking centers cease functioning. Explain various cardiac rhythm disturbances. Describe the conduction of excitation through the heart. The heart continues to beat even when it is completely removed from the body. At times. Others retain pacemaking ability and generate impulses spontaneously. Explain the basis of reentry. These dysrhythmias are discussed later in this chapter.
In humans it is about 8 mm long and 2 mm thick. The sinus node artery runs lengthwise through the center of the node. Ectopic foci may become pacemakers when 1 their own rhythmicity becomes enhanced. Redrawn from James TN: The sinus node. Sinoatrial Node The SA node is the phylogenetic remnant of the sinus venosus of lower vertebrate hearts. The SA node contains two principal cell types of: When the AV junction is unable to conduct the impulse from the atria to the ventricles.
Compared with the transmembrane potential recorded from a ventricular myocardial cell Figure A. It lies in the groove where the superior vena cava joins the right atrium Figure The round cells are probably the pacemaker cells.
A typical transmembrane action potential recorded from a cell in the SA node is depicted in Figure B. These are all characteristic of the slow response described in Chapter 2. When the SA node and the other components of the atrial pacemaker complex are excised or destroyed. Sinoatrial artery.
Depolarization proceeds at a steady rate until a threshold is attained. An increase in the maximum negativity at the end of repolarization from 3 to 4 also diminishes the frequency. In nonautomatic cells the potential remains constant during this phase. A change of the threshold potential. Kodama I: The sinoatrial node. Tetrodotoxin or local anesthetic drugs can block such channels and impede conduction from primary pacemaker cells to the atrium.
Honjo H. Redrawn from Boyett MR. A reduction in the slope of the pacemaker potential from 1 to 2 diminishes the frequency. Changes in autonomic neural activity often also induce a pacemaker shift. The discharge frequency of pacemaker cells may be varied by a change in either the rate of depolarization during phase 4 or the maximal diastolic potential Figure This current becomes activated toward the end of phase 4. Redrawn from van Ginneken AC.
If and ICa. The second current responsible for diastolic depolarization is the L-type calcium current. If exerts a greater role in pacemaking in subsidiary pacemaker. Increased sympathetic nervous activity.
This mechanism of increasing heart rate operates during physical exertion. The hyperpolarization-induced inward current. IK Figure The If current becomes activated during repolarization of the membrane. In SA node pacemaker cells. The more negative the membrane potential becomes at the end of repolarization.
FIGURE n Transmembrane potential changes top half tends to repolarize the cell after the upstroke of the action potential. The progressive diastolic depolarization mediated by the two inward currents. The thick bold line in the current trace indicates the magnitude and direction of estimated If. On the other hand. Giles W: Voltage clamp measurements of the hyperpolarization-activated inward current I f in single cells from rabbit sino-atrial node.
Increased vagal activity. The adrenergically mediated increase in the slope of diastolic depolarization indicates that the augmentations of If and ICa must exceed the enhancement of IK. The cardiac cycle lengths. Moe GK: Phasic effects of vagal stimulation on pacemaker activity of the isolated sinus node of the young cat.
Acetylcholine also depresses the If and ICa currents. This enhanced pump activity hyperpolarizes the cell through the net loss of cations from the cell interior. During each depolarization. Because of the hyperpolarization. Whether the hyperpolarization-induced inward current. In addition. Autonomic neurotransmitters affect automaticity by altering the ionic currents across the cell membranes.
In later studies a timing mechanism composed of ionic channels in the plasma membrane and the sarcoplasmic reticulum SR membrane has been proposed.
The hyperpolarization Figure induced by acetylcholine released at the vagus endings in the heart is 60 mV 2s FIGURE n Effect of a brief vagal stimulus arrow on the transmembrane potential recorded from a sinoatrial node pacemaker cell in an isolated cat atrium preparation. This phenomenon is known as overdrive suppression. The ionic basis for automaticity in the AV node pacemaker cells appears similar to that in the SA node cells.
Overdrive Suppression A period of excitation at a high frequency depresses automaticity of pacemaker cells. Three tracts. Some investigators assert that these pathways constitute the principal routes for conduction of the cardiac impulse from the SA node to the AV node. Compared with the potential recorded from a typical ventricular fiber see Figure A.
The resultant period of asystole cardiac standstill can cause loss of consciousness. Atrial Conduction From the SA node. The configuration of the atrial action potential is depicted in Figure C. In patients with the so-called sick sinus syndrome. A special pathway. In the N region.
The conduction times through the AN and N regions largely account for the delay between the onsets of the P wave the electrical manifestation of the spread of atrial excitation and the QRS complex spread of ventricular excitation in the electrocardiogram Figure The AV node is divided into three functional regions: The conduction velocity is actually less in the N region than in the AN region.
Millivolts 0 —25 25 ms C 0. The AV node contains the same two cell types as the SA node. The principal delay in the passage of the impulse from the atria to the ventricles occurs in the AN and N regions of the AV node. There is some anatomical evidence for this well-known observation. The node is situated posteriorly on the right side of the interatrial septum and is circumscribed by the ostium of the coronary sins.
The relative refractory period of the cells in the N region extends well beyond the period of complete.
This node is approximately 22 mm long. Cells in the inferior portion of the AV node serve as a subsidiary pacemaker. The existence of fast and slow conduction paths allows a substrate for reentrant circuits within the AV node. Conduction of the impulse from the atrium to the AV node has been described as consisting of fast and slow pathways. The shapes of the action potentials in the AN region are intermediate between those in the N region and the atria.
P-R interval is 0. P-R interval is As the repetition rate of atrial depolarizations is increased. Second-degree heart block 2: Stronger vagal activity may cause some or all of the impulses arriving from the atria to be blocked in the node. The autonomic nervous system regulates AV conduction.
This type of block may protect the ventricles from excessive contraction frequencies. Weak vagal activity may simply prolong the AV conduction time. First-degree heart block. The conduction pattern in which only a fraction of the atrial impulses are conducted to the ventricles is called second-degree AV block see Figure B. Third-degree heart block.
The conduction pattern in which none of the atrial impulses reach the ventricles over a substantial number of atrial depolarizations is called A P P P First-degree heart block. If the atria are depolarized at a high frequency. Retrograde conduction can occur through the AV node.
Most of the prolongation of AV conduction caused by an increase in repetition rate takes place in the N region. Impulses tend to be blocked in the AV node at stimulus frequencies that are easily conducted in other regions of the heart. Dreifus LS. Redrawn from Mazgalev T. AV block see Figure C. Vagally induced hyperpolarization in atrioventricular node.
Only a small. Michelson EL. This atrial impulse arrived at the AV node cell when its cell membrane was maximally A1 A2 A3 AV node fiber 50 mV Ventricular Conduction The bundle of His passes subendocardially down the right side of the interventricular septum for about 1 cm and then divides into the right and left bundle branches Figures and The atrial excitation A2 that arrived at the AV node when the cell was hyperpolarized failed to be conducted.
In the experiment shown in Figure The atrial excitations that preceded A1 and followed A3. They decrease AV conduction time and enhance the rhythmicity of the latent pacemakers in the AV junction. Cardiac sympathetic nerves. His bundle electrograms reveal that the most common sites of complete block are distal to the bundle of His.
Thirddegree AV block is most often caused by a degenerative process of unknown cause or by severe myocardial ischemia inadequate coronary blood supply. The right bundle branch is a direct continuation of the bundle of His and proceeds down the right side of the interventricular septum. On the subendocardial surface of the left side of the interventricular septum. The greater the hyperpolarization at the time of arrival of the atrial impulse.
Because of the slow ventricular rhythm 32 beats per minute in the example in Figure C. The norepinephrine released at the sympathetic nerve terminals increases the amplitude and slope of the upstroke of the AV nodal action potentials. The delayed conduction or block induced by vagal stimulation occurs largely in the N region of the node. Note that shortly after vagal stimulation.
The absence of a corresponding depolarization of the bundle of His H shows that the second atrial impulse was not conducted through the AV node. The left bundle branch. Conduction blocks in one or more of these pathways give rise to characteristic electrocardiographic patterns.
Block of either division of the left bundle branch is called left anterior hemiblock or left posterior hemiblock. Redrawn from DeWitt LM: Observations on the sino-ventricular connecting system of the mammalian heart. The small black arrows show conduction within the interventricular septum and the ventricular myocardium.
Anat Rec 3: Block of either of the main bundle branches is known as right or left bundle branch block. In certain mammalian species. The impulse that was conducted down branch L and through the connecting. The impulse from the left side cannot proceed further because the tissue beyond has just been depolarized from the other direction. Reentry may be ordered or random. The impulse cannot pass through bundle C from the right either.
Therefore at high heart rates. This phenomenon is called unidirectional block. The last portions of the ventricles to be excited are the posterior basal epicardial regions and a small zone in the basal portion of the interventricular septum.
A necessary condition for reentry is that at some point in the loop the impulse can pass in one direction but not in the other. This permits a rapid activation of the entire endocardial surface of the ventricles. Early contraction of the septum tends to make it more rigid and allows it to serve as an anchor point for the contraction of the remaining ventricular myocardium.
At slow heart rates. As the impulse reaches connecting link C. Therefore they fail to evoke a premature contraction of the ventricles. In each of the four panels. This phenomenon. The conditions necessary for reentry are illustrated in Figure Similar rate-dependent changes in the refractory period also occur in most of the other cells in the heart. Purkinje cells have abundant. In the ordered variety. Because the right ventricular wall is appreciably thinner than the left.
As shown in panel D. This function of protecting the ventricles against the effects of premature atrial depolarizations is especially pronounced at slow heart rates.
The wave of activation spreads into the septum from both its left and its right endocardial surfaces. The endocardial surfaces of both ventricles are activated rapidly. Bidirectional block exists in branch R.
The antegrade impulse is blocked blue square. Triggered activity is caused by afterdepolarizations. Slightly later. In panel D. The effective refractory period of the reentered region must also be less than the propagation time around the loop. The Wolff-Parkinson-White syndrome. It is easily detected in the electrocardiographic reading. Two types of afterdepolarizations are recognized: The depolarization wave enters the connecting branch C from both ends and is extinguished at the zone of collision.
EADs occur at the end of the plateau phase 2 of an action potential or about. Unidirectional block exists in branch R. The wave is blocked blue squares in the L and R branches C. Therefore the conditions that promote reentry are those that prolong conduction time or shorten the effective refractory period.
The antegrade impulse may be blocked simply because it arrives at the depressed region during its effective refractory period.
The antegrade impulse arrives at the depressed region in branch R earlier than the impulse that traverses a longer path and enters branch R from the opposite direction. Unidirectional block is a necessary condition for reentry. Such pathways often serve as a part of a reentry loop see Figure Some loops are very large and involve entire specialized conduction bundles.
Continuous circling around the loop leads to a very rapid rhythm supraventricular tachycardia. In the absence of pacing stimuli. When the cycle length was milliseconds ms panel A. This secondary activation. FIGURE n Effect of pacing at different cycle lengths Considerable information has been obtained about the mechanism responsible for those EADs that appear at the end of the plateau. The salient characteristics of DADs are shown in Figure When the cycle length was increased to 4 s.
EADs may be produced experimentally by interventions that prolong the action potential. Because EADs may be initiated at either of two distinct levels of transmembrane potential.
Triggered action potentials occur in salvos. Rosen M: Effects of pacing on triggered activity induced by early afterdepolarizations. Less information is available about the cellular mechanisms responsible for those EADs that appear midway through repolarization. The third EAD reaches threshold and triggers an action potential third arrow. EADs appeared. EADs that appear after each driven depolarization trigger an action potential.
DADs tend to appear when the heart rate is high. EADs occur and caused triggered automaticity. No afterdepolarizations were evident when the preparation was driven at a cycle length of 2 seconds s.
Early Afterdepolarizations EADs are more likely to occur when the prevailing heart rate is slow. In the electrocardiogram. Some EADs were subthreshold but eventually others reached threshold to trigger an action potential.
In each panel. EADs not evident. For those action potentials that trigger EADs. The more prolonged the action potential. As the action potential lengthens. The diverse electromotive forces that exist in the heart at any moment can be represented by a three-dimensional vector. Note that delayed afterpotentials occurred after the driven beats and that these afterpotentials reached threshold after the last driven beat in panels B to D but not in panel A.
The amplitudes of the DADs are increased Scalar Electrocardiography The systems of leads used to record routine electrocardiograms are oriented in certain planes of the body.
The science of electrocardiography is extensive and complex. From Ferrier GR. Components of vectors projected on such lines are not vectors but scalar quantities having magnitude but not direction.
Mendez C: A cellular mechanism for the generation of ventricular arrhythmias by acetylstrophanthidin. When the basic cycle length was diminished to ms panel B. This extrasystole was itself followed by a subthreshold afterpotential.
A system of recording leads oriented in a given plane detects the projection of the three-dimensional vector on that plane.
Slightly shorter basic cycle lengths or slightly greater concentrations of acetylstrophanthidin evoked a continuous sequence of nondriven beats. Acetylstrophanthidin was added to the bath.
Diminution of the basic cycle length to ms panel C evoked two extrasystoles after the last driven action potential. Hence in myocardial cells. Saunders JH. In his lead system the resultant cardiac vector the vector sum of all electrical activity occurring in the heart at any given moment was considered to lie in the center of a triangle assumed to be equilateral formed by the left and right shoulders and the pubic region Figure Any appreciable deviation from the isoelectric line is noteworthy and may indicate ischemic damage of the myocardium.
During the ST interval the entire ventricular myocardium is depolarized and there is negligible potential difference in the ventricle. Deviation of the T wave and QRS complex in the same direction from the isoelectric line indicates that the repolarization process proceeds in a direction counter to the depolarization process. The P-R interval or more precisely. For convenience.
Let the frontal projection of the resultant cardiac vector at some moment be represented by an arrow tail negative. Standard Limb Leads Einthoven devised the original electrocardiographic lead system. T waves that are abnormal in either direction or amplitude may indicate myocardial damage. The cardiac impulse progresses through the heart in a complex threedimensional pattern.