Getting the books berne and levy cardiovascular physiology now is not type of . essential biology with physiology 4th edition pdf download, exercise. Cardiovascular Physiology, 10th Edition - Ebook download as PDF File .pdf), edition of Berne and Levy's classic monograph on cardiovascular physiology. BY MATTHEW N. LEVY. ROBERT M. (“BOB”) BERNE, an acclaimed authority in the field of cardiovascular physiology, died on October 4,. , at the age of

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cardiovascular physiology - berne & levy physiology, 6e, updated edition meded levy principles of physiology ebook pdf at our library. get berne levy. Overview of the CV system. • Purposes. – Distribute Venoconstriction raises ventricular filling, cardiac output . Berne and Levy, Cardiovascular. Physiology. Associate Professor of Medicine and Physiology. Office: VA room 2A Review of Cardiac Electrophysiology . Berne and Levy, Cardiovascular. Physiology.

These two features of the vagus nerves-brief latency and rapid decay of the response-permit them to exert beat-by-beat control of SA and AV nodal function.

In half of the trials, atropine was given first top curve ; in the other half, propranolol was given first bottom curve. Figure Changes in heart rate evoked by stimulation horizontal bars of the vagus A and sympathetic nerves B.

Figure Changes in heart rate when the vagus and cardiac sympathetic nerves are stimulated simultaneously. The sympathetic nerves are stimulated at 0, 2, and 4 Hz and the vagus nerves at 0, 4, and 8 Hz. Parasympathetic influences usually predominate over sympathetic effects at the SA node, as shown in Figure However, when the vagi are stimulated at 8 Hz, increasing the sympathetic stimulation frequency from 0 to 4 Hz has only a negligible influence on heart rate.

Sympathetic Pathways The cardiac sympathetic fibers originate in the intermediolateral columns of the upper five or six thoracic and lower one or two cervical segments of the spinal cord see Chapter These fibers emerge from the spinal column through the white communicating branches and enter the paravertebral chains of ganglia.

The preganglionic and postganglionic neurons synapse mainly in the stellate or middle cervical ganglia, depending on the species.

In the mediastinum, the postganglionic and preganglionic parasympathetic fibers join to form a complicated plexus of mixed efferent nerves to the heart. The postganglionic cardiac sympathetic fibers in this plexus approach the base of the heart along the adventitial surface of the great vessels. From the base of the heart, these fibers are distributed to the various chambers as an extensive epicardial plexus.

They then penetrate the myocardium, usually accompanying the coronary vessels. These processes are slow. Furthermore, the facilitatory effects of sympathetic stimulation on the heart attain steady-state values much more slowly than do the inhibitory effects of vagal stimulation. The onset of the cardiac response to sympathetic stimulation begins slowly for two main reasons. First, norepinephrine appears to be released slowly from the sympathetic nerve terminals.

Second, the cardiac effects of the neurally released norepinephrine are mediated mainly by a relatively slow second messenger system involving cAMP see Chapter 3.

Hence, sympathetic activity alters the heart rate and AV conduction much more slowly than vagal activity does. Although vagal activity can exert beat-by-beat control of cardiac function, sympathetic activity cannot.

Control by Higher Centers Stimulation of various brain regions can have significant effects on cardiac rate, rhythm, and contractility see Chapter In the cerebral cortex, centers that regulate cardiac function are located in the anterior half of the brain, principally in the frontal lobe, the orbital cortex, the motor and premotor cortex, the anterior portion of the temporal lobe, the insula, and the cingulate gyrus.

Stimulation of the midline, ventral, and medial nuclei of the thalamus elicits tachycardia. Stimulation of the posterior and posterolateral regions of the hypothalamus can also change the heart rate.

Stimuli applied to the H2 fields of Forel in the diencephalon evoke various cardiovascular responses, including tachycardia; these changes resemble those observed during muscular exercise. Undoubtedly, the cortical and diencephalic centers initiate the cardiac reactions that occur during excitement, anxiety, and other emotional states. The hypothalamic centers also initiate the cardiac response to alterations in environmental temperature. Experimentally induced temperature changes in the preoptic anterior hypothalamus alter the heart rate and peripheral resistance.

Stimulation of the parahypoglossal area of the medulla reciprocally activates cardiac sympathetic pathways and inhibits cardiac parasympathetic pathways. In certain dorsal regions of the medulla, distinct cardiac accelerator increase the heart rate and augmentor increase cardiac contractility sites have been detected in animals with transected vagi. The accelerator regions are more abundant on the right side, whereas the augmentor sites are more prevalent on the left.

A similar distribution also exists in the hypothalamus. Therefore, the sympathetic fibers mainly descend ipsilaterally through the brainstem. Baroreceptor Reflex Sudden changes in arterial blood pressure initiate a reflex that evokes an inverse change in heart rate Fig. Baroreceptors located in the aortic arch and carotid sinuses are responsible for this reflex. The inverse relationship between heart rate and arterial blood pressure is generally most pronounced over an intermediate range of arterial blood pressure.

Below this intermediate range, the heart rate maintains a constant, high value; above this pressure range, the heart rate maintains a constant, low value. Figure Heart rate as a function of mean arterial pressure. Figure Effects of changes in pressure in isolated carotid sinuses on neural activity in cardiac vagal and sympathetic efferent nerve fibers. The effects of these changes in carotid sinus pressure on activity in the cardiac autonomic nerves are presented in Figure , which shows that over an intermediate range of carotid sinus pressure to mm Hg , reciprocal changes are evoked in efferent vagal and sympathetic neural activity.

Below this range of carotid sinus pressure, sympathetic activity is intense and vagal activity is virtually absent. Conversely, above the intermediate range of carotid sinus pressure, vagal activity is intense and sympathetic activity is minimal. Bainbridge Reflex, Atrial Receptors, and Atrial Natriuretic Peptide page page Figure Intravenous infusions of blood or electrolyte solutions tend to increase the heart rate via the Bainbridge reflex and to decrease the heart rate via the baroreceptor reflex.

The actual change in heart rate induced by such infusions is the result of these two opposing effects. In , Bainbridge reported that infusing blood or saline into dogs accelerated their heart rate. This increase did not seem to be tied to arterial blood pressure because the heart rate rose regardless of whether arterial blood pressure did or did not change.

However, Bainbridge also noted that the heart rate increased whenever central venous pressure rose sufficiently to distend the right side of the heart. Bilateral transection of the vagi abolished this response. This is termed the Bainbridge reflex.

Many investigators have confirmed Bainbridge's observations and have noted that the magnitude and direction of the response depend on the prevailing heart rate. When the heart rate is slow, intravenous infusions usually accelerate the heart. At more rapid heart rates, however, infusions ordinarily slow the heart. What accounts for these different responses?

Increases in blood volume not only evoke the so-called Bainbridge reflex but also activate other reflexes notably the baroreceptor reflex.

These other reflexes tend to elicit opposite changes in heart rate. Therefore, changes in heart rate evoked by an alteration in blood volume are the result of these antagonistic reflex effects Fig. 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.

Robert M. Berne

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.

Berne & Levy Principles of Physiology

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.

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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. The duration is usually between 0. Abnormal prolongation may indicate a block in the normal conduction pathways through the ventricles such as a block of the left or right bundle branch.

A considerable fraction of this time involves passage of the impulse through the AV conduction system. These galvanometer connections were arbitrarily chosen so that the QRS complexes will be upright in all three standard limb leads in most normal individuals.

Its duration is about 0. Certain conventions dictate the manner in which these standard limb leads are connected to the galvanometer.

Therefore the ST segment lies on the isoelectric line. This so-called Einthoven triangle is oriented in the frontal plane of the body.

Hence only the projection of the resultant cardiac vector on the frontal plane is detected by this system of leads. If the vector in panel A of Figure is the result of the electrical events occurring during the peak of the QRS complex. For normal individuals. The arrow shows the sum of electrical forces as the cardiac vector obtained from the limb leads.

The white areas indicate the projection on the frontal plane of QRS waves in each limb lead. If the cardiac vector makes an angle. The positive direction of this axis is taken in the clockwise direction from the horizontal plane contrary to the usual mathematical convention.

The voltage of this central terminal remains at a theoretical zero potential throughout the cardiac cycle. B Sinus tachycardia. Altered Sinoatrial Rhythms The frequency of pacemaker discharge varies by the mechanisms described earlier in this chapter see Figure Other limb leads. With appreciable shift of the mean electrical axis to the right panel B of Figure Changes in the mean electrical axis may occur with alterations in the anatomical position of the heart or with changes in the relative preponderance of the right and left ventricles.

Disturbances of impulse initiation include those that arise from the SA node and those that originate from various ectopic foci. The other galvanometer terminal is usually connected to a central terminal. The principal disturbances of impulse propagation are conduction blocks and reentrant rhythms. The P. Sinus tachycardia.

Sinus bradycardia. With left axis shift panel C of Figure To obtain information concerning the projections of the cardiac vector on the sagittal and transverse planes of the body in scalar electrocardiography. C Sinus bradycardia. As is evident from this discussion. Such augmented lead systems are described in textbooks on electrocardiography and are not considered further here. Normal sinus rhythm. Examples of electrocardiograms of sinus tachycardia and sinus bradycardia are shown in Figure Changes in SA nodal discharge frequency are usually produced by cardiac autonomic nerves.

Most commonly. Electrocardiographic evidence of respiratory cardiac dysrhythmia is common and is manifested as a rhythmic variation in the P-P interval at the respiratory frequency see Figure They may originate in the atria.

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?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.

What accounts for these different responses? If the P a is maintained at its normal level under all circumstances. When a resting individual is given atropine, a muscarinic receptor antagonist that blocks parasympathetic effects, the heart rate generally increases substantially. This is a preview of subscription content, log in to check access.

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