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The Electrocardiogram and Analysis of Cardiac DysrhythmiasELECTROCARDIOGRAMBody fluids are good conductors, making it possible to record the sum of the action potentials of myocardial fibers on thesurface of the body as the electrocardiogram (ECG).The normal ECG consists of a P-wave (atrial depolarization), a QRScomplex (ventricular depolarization), and a T-wave (ventricular repolarization) (Fig. 48-1). Ventricular repolarization isprolonged, explaining the low voltage of the T-wave compared with the QRS complex. The atrial T-wave, which reflectsrepolarization of the atria, is obscured on the ECG by the larger QRS complex. A U-wave, if present, may reflect slowrepolarization of the papillary muscles.FIGURE 48-1. The normal waves and intervals on the electrocardiograrn.

Recording the ElectrocardiogramPaper used for recording the ECG is designed such that each horizontal line corresponds to 0.1 mv and each vertical linecorresponds to 0.04 second, assuming proper calibration and paper speed of the recording device (Fig. 48-1). Electriccurrents generated by cardiac muscle during each cardiac cycle can change potentials and polarity in less than 0.01second. An oscilloscope display of the ECG, with or without the ability to provide a paper recording, is commonly used forclinical monitoring. Indeed, continuous monitoring of the ECG during anesthesia is considered to be a standard ofmonitoring for all patients under the anesthesiologist's care.The duration of events during conduction of the cardiac impulse can be calculated from a recording of the ECG (Table 48-1). The interval between the beginning of atrial contraction and the beginning of ventricular contraction is the P-R interval(actually the P-Q interval, but the Q-wave is frequently absent). The P-R interval is dependent on heart rate averaging 0.18second at a rate of 70 beats min -1 and 0.14 second at a rate of 130 beats min -1. The QRS complex reflects ventriculardepolarization, whereas the Q-T interval represents the time necessary for complete depolarization and repolarization ofthe ventricle. Like the P-R interval, the Q-T interval depends on heart rate. Using a small portable tape recorder (Holtermonitor), it is possible to record the ECG for prolonged periods in ambulatory individuals.

Scroll right to see more columns.Table 48-1 Intervals and Corresponding Events on the ElectrocardiogramAverage Range Event in HeartP-R interval* 0.18 sec 0.12-0.20 sec(Atrial depolarization and conduction through the atrioventricular node)QRS duration 0.08 sec 0.05-0.1 sec (Ventricular depolarization)Q-T interval* 0.40 sec 0.26-0.45 sec(Ventricular depolarization plus repolarization)S-T segment 0.32 sec (Ventricular repolarization )*Dependent on heart rate.

Electrocardiogram LeadsThe ECG is recorded using a unipolar lead (an exploring electrode connected to an indifferent electrode at zero potential) orbipolar leads (two active electrodes). Depolarization moving toward an active electrode produces a positive deflection,while depolarization moving in the 708 SECTION TWO: PHYSIOLOGY opposite direction produces a negative deflection.Electric current flow is normally from the base of the heart toward the apex during most of the depolarization phase with

the exception being at the extreme end of the wave. Therefore, an electrode nearer the base of the heart will record anegative potential with respect to an electrode placed nearer the apex of the heart. The usual 12-lead ECG consists ofthree bipolar standard limb leads, six unipolar chest leads, and three unipolar augmented limb leads.

Standard Limb LeadsStandard limb leads are placed on the left and right arms and the left leg (Fig. 48-2). These leads record the potentialdifference between two points on the body. Polarity is positive for the ECG recorded from these standard limb leads. Thelegs of the three standard limb leads form the arms of an equilateral (Einthoven's) triangle. The direction of depolarizationof the atria parallels lead II. For this reason, P-waves are prominent in this lead.

FIGURE 48-2. Standard limb leads of the electrocardiogram and typical recordings.

Chest LeadsPrecordial unipolar leads (V 1 through V 6) are recorded by placing an electrode on the anterior surface of the chest overone of six separate points (Table 48-2). Each chest lead records CHAPTER 48: The Electrocardiogram and Analysis ofCardiac Dysrhythmias 709 mainly the electrical potential of the cardiac muscle immediately beneath the electrode. Thenearness of the heart surface to the electrode means that relatively minute abnormalities in the ventricles, particularly in

the anterior ventricular wall, can produce marked changes in the corresponding ECG. In leads V 1 and V 2, the normal QRSrecordings are mainly negative because the chest electrode in these leads is nearer the base of the heart than the apex.Conversely, the QRS complexes in V 4 through V 6 are mainly positive because the chest electrode in these leads is nearerthe apex of the heart, which is the direction of electropositivity during depolarization.

Scroll right to see more columns.Table 48-2 Placement of Precordial LeadsV1 Fourth intercostal space at the right sternal borderV2 Fourth intercostal space at the left sternal borderV3 Equidistant between V2 and V4V4 Fifth intercostal space in the left midclavicular lineV5 Fifth intercostal space in the left anterior axillary lineV6 Fifth intercostal space in the left midaxillary line


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Augmented Limb LeadsAugmented unipolar limb leads are similar to the standard limb lead recordings except that the recording from the right-arm lead (aVR) is inverted. When the positive terminal is on the right arm, the lead is aVR; when on the left arm, the lead isaVL; and when on the left leg, the lead is a aVF

Interpretation of the ElectrocardiogramAbnormalities of the heart can be detected by analyzing the contours of the different waves in the various ECG leads. Theelectrical axis of the heart can be determined from the standard limb leads of Einthoven's triangle. In a normal heart, theaverage direction of the vector during spread of the depolarization wave is approximately 59 degrees (Fig. 48-3). When one

ventricle of the heart hypertrophies, the axis of the heart shifts toward the enlarged ventricle. The predominant direction ofthe vector through the heart during depolarization and repolarization of the ventricles is from base to apex. As a result, theT-waves and most of the QRS complexes in the normal ECG are positive. The vector of current flow during depolarization inthe atria is similar to that in the ventricles. As a result, the P-waves recorded from the three standard limb leads arepositive.

FIGURE 48-3. Electrical axis of the heart as determined from the standard limb leads of the electrocardiogram. In thenormal heart, the electrical axis is approximately 59 degrees (A) . Left axis deviation shifts the electrical axis to less than 0degrees (B) ; right axis deviation is associated with an electrical axis greater than 100 degrees. Abnormalities of the QRSComplexThe QRS complex is considered to be prolonged when it lasts more than 0.1 second. Hypertrophy of the ventricles prolongsthe duration of the QRS complex, reflecting the longer pathway the ventricular depolarization wave must travel. Blockadeof the Purkinje fibers necessary for conduction of the cardiac impulse greatly slows conduction and prolongs the duration ofthe QRS complex. Multiple peaks in an abnormally prolonged QRS complex most often reflect multiple local blocks inconduction of the cardiac impulse along Purkinje fibers as may occur from scar tissue formed at sites of myocardialinfarction.

Voltage of the QRS interval in the standard limb leads of the ECG varies between 0.5 and 2 mv with lead III usuallyrecording the lowest voltage and lead II the greatest. High-voltage QRS complexes are considered to be present when thesum of the voltages of all the QRS complexes of the three standard limb leads is more than 4 my. The most frequent causeof high voltage QRS complexes is ventricular hypertrophy. Decreased Voltage in the Standard Limb

LeadsCauses of decreased voltage on the ECG recorded from standard limb leads are (1) multiple small myocardial infarctionsthat prevent generation of large quantities of electrical currents, (2) rotation of the apex of the heart toward the anteriorchest wall, and (3) abnormal conditions around the heart so electric currents cannot be easily conducted from the heart tothe surface of the body. For example, pericardial fluid diminishes voltage recorded from standard limb leads due to theability of this fluid to rapidly conduct electric currents to multiple sites. Pulmonary emphysema is associated with reducedconduction of electric current through the lungs caused by the effects of excessive amounts of air in the lungs.

Current of InjuryA current of injury is due to the inability of damaged areas of the heart to undergo repolarization during diastole. Thecurrent of injury results when current flows between the pathologically depolarized (negative) and normally polarized(positive) areas. The most common cause of a current of injury is myocardial ischemia or infarction. Mechanical trauma tothe heart and infectious processes that damage cardiac muscle membranes (pericarditis or myocarditis) may also beresponsible for a current of injury. In these conditions, a current of injury occurs when the depolarization period of somecardiac muscle is so long that the muscle fails to repolarize completely before the next cardiac cycle begins.Specific leads of the ECG are more likely than other leads to reflect myocardial ischemia that develops in areas of themyocardium supplied by an individual coronary artery (Table 48-3). An estimated 80% to 90% of S-T segment informationcontained in a conventional 12-lead ECG is present on lead V 5. Lead II has special value in diagnosis of inferior wallmyocardial ischemia and the origin of cardiac dysrhythmias. Complete interruption of a coronary artery with infarction ofthe cardiac muscle results in a deep Q-wave in the ECG leads recording from the infarcted area. The Q-wave occursbecause there is no electrical activity in the infarcted area. A Q-wave whose amplitude is more than one third of thecorresponding R-wave and whose duration is more than 0.04 second is diagnostic of myocardial infarction. In the presenceof an old anterior myocardial infarction, a Q-wave develops in lead I because of loss of muscle mass in the anterior left wallof the left ventricle. Conversely, in posterior myocardial infarction, a Q-wave develops in lead III because of loss of cardiacmuscle in the posterior apical part of the ventricle.

Scroll right to see more columns.Table 48-3 Relationship of Electrocardiogram Lead Reflecting Myocardial Ischemia to Area of Myocardium Involved

Electrocardiogram Coronary Artery Responsible for Area of Myocardium Supplied by CoronaryLead IschemiaArtery

II, III, aVFRight coronary arteryRight atriumInteratrial septumRight ventricleSinoatrial nodeAtrioventricular nodeInferior wall of left ventricleV3-V5 Left anterior descending coronary arteryAnterior and lateral wall of left ventricleI, aVL Circumflex coronary artery


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Lateral wall of left ventricleSinoatrial nodeAtrioventricular node

Abnormalities of the T-waveThe T-wave is normally positive in the standard limb leads, reflecting repolarization of the apex of the heart before theendocardial surfaces of the ventricles. The direction in which repolarization spreads over the heart is backward to thedirection in which depolarization occurs. The T-wave becomes abnormal when the normal sequence of repolarization doesnot occur. For example, delay of conduction of the cardiac impulse through the ventricles (prolonged depolarization), asoccurs with left or right bundle branch block or ventricular premature contractions, results in a T-wave with a polarity

opposite the QRS complex.Myocardial ischemia is the most common cause of prolonged depolarization of cardiac muscle. When myocardial ischemiaoccurs in only one area of the heart, the duration of depolarization of this area increases disproportionately to that in otherareas, resulting in abnormalities (inversion or biphasic) of the T-wave. Myocardial ischemia also leads to elevation of the S-T segment on the ECG. To be clinically significant, the S-T elevation should be at least 1 mm above the base line.Artifactual S-T elevation or depression may be introduced by filters incorporated in some ECG monitors to eliminatebaseline drift due to movement such as that produced by breathing. For this reason, it is important to verify that themonitor is in the diagnostic mode before concluding that S-T changes represent myocardial ischemia. During exercise, thedevelopment of any change in T-waves or S-T segments is evidence that some portion of ventricular muscle has becomeischemic and is manifesting an increased period of depolarization out of proportion to the rest of the heart.

His Bundle ElectrogramThe His bundle electrogram is recorded from an electrode inserted through a vein and positioned near the tricuspid valve(Fig. 48-4) Ganong, 1987. The A deflection reflects activation of the atrioventricular node, the H spike is transmissionthrough the His bundle, and the V deflection occurs during ventricular depolarization. Using the standard ECG and Hisbundle electrogram, it is possible to accurately measure conduction time from the sinus node to the atrioventricular node

(AH interval), conduction time through the atrioventricular node, and conduction time through the bundle of His and bundlebranches (HV interval) (Fig. 48-4) Ganong, 1987. As such, the His bundle electrogram permits detailed analysis of the blocksite when there is a defect in the system for conduction of cardiac impulses through the heart.

FIGURE 48-4. A normal His bundle electrogram and the corresponding electrocardiogram (ECG). (From Ganong WF. Reviewof Medical Physiology. 13th ed. Norwalk, CT. Appleton and Lange. 1987; with permission.)

CARDIAC DYSRHYTHMIASMechanismsCardiac dysrhythmias may be caused by altered automaticity of pacemaker cardiac cells, altered excitability of myocardialcells, and altered conduction of cardiac impulses through the specialized conduction systems of the heart. Manifestationsof these alterations may be the appearance of an ectopic cardiac pacemaker, development of heart block, or appearanceof a reentry circuit. Cardiac dysrhythmias are observed to occur in 60% or more of patients undergoing anesthesia andsurgery when continuous methods of monitoring are used Atlee and Bosnjak, 1990.

AutomaticityAutomaticity depicts the ability of pacemaker cardiac cells to undergo spontaneous phase 4 depolarization. Under normalcircumstances, automaticity is exhibited by cells in the sinoatrial node, atrioventricular node, and specialized conductingfibers of the atria and ventricles.Activation of the sympathetic nervous system by events such as arterial hypoxemia, acidosis, or release of catecholaminesis the most common cause of enhanced automaticity. In addition, enhanced automaticity occurs when the thresholdpotential becomes more negative such that the difference between the threshold potential and resting transmembranepotential is less.Decreased automaticity is produced by increased parasympathetic nervous system activity, which reduces responsivenessof sinoatrial and atrioventricular node cells by increasing outward flux of potassium ions (K+) . This increased outwardmovement of K + evoked by acetylcholine hyperpolarizes cardiac cell membranes and prevents them from depolarizing.Vagal stimulation may decrease the vulnerability of the heart to develop ventricular fibrillation, especially in the presenceof sympathetic nervous system stimulation. Carotid sinus stimulation decreases the frequency of premature ventricularcontractions and can abolish ventricular tachycardia.

ECTOPIC PACEMAKERAn ectopic cardiac pacemaker (focus) manifests as a premature contraction of the heart that occurs between normal beats.A depolarization wave spreads outward from the ectopic pacemaker and initiates the premature contraction. The usual

cause of an ectopic pacemaker is an irritable area of cardiac muscle resulting from a local area of myocardial ischemia oruse of stimulants such as caffeine or nicotine. Sometimes an ectopic pacemaker becomes persistent and assumes the roleof pacemaker in place of the sinoatrial node. The most common point for development of an ectopic pacemaker is theatrioventricular node or atrioventricular bundle.

ExcitabilityExcitability is the ability of a cardiac cell to respond to a stimulus by depolarizing. A measure of excitability is the differencebetween the resting transmembrane potential and threshold potential of the cardiac cell membrane. The smaller thedifference between these potentials, the more excitable, or irritable, is the cell. Although epinephrine enhances excitability,this is somewhat offset by a concomitant small increase in the negativity of the resting transmembrane potential. Once acell depolarizes, it is no longer excitable, being refractory to all stimuli. After this absolute refractory period, cardiac cellsenter a relative refractory period during which greater than normal stimuli can cause cardiac cell membranes to depolarize.


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ConductionConduction of cardiac impulses proceeds through specialized conduction systems of the heart such that coordinatedcontractions occur (see Fig. 47-10). Abnormalities of conduction of cardiac impulses manifest as development of heartblock, reentry circuits, or preexcitation syndromes.HEART BLOCK The most frequent sites of heart block are the atrioventricular bundle or one of the bundle branches. Causesof heart block at these sites include (1) excessive parasympathetic nervous system stimulation, (2) drug-induced (digitalisor propranolol) depression of impulse conduction, (3) myocardial infarction, (4) pressure on the conduction system byatherosclerotic plaques, and (5) age-related degenerative process of the conduction system.REENTRY. Reentry (circus movements) implies re-excitation of cardiac tissue by return of the same cardiac impulse using acircuitous pathway (Fig. 48-5) Akhtar, 1982. This contrasts with automaticity, in which a new cardiac impulse is generated

each time to excite the heart. Reentry circuits can develop at any place in the heart where there is an imbalance betweenconduction and refractoriness. Causes of this imbalance include (1) elongation of the conduction pathway such as occurs indilated hearts (especially a dilated left atrium associated with mitral stenosis); (2) decreased velocity of conduction ofcardiac impulses as occurs with myocardial ischemia or hyperkalemia; and (3) a shortened refractory period of cardiacmuscle as produced by epinephrine or electric shock from an alternating current. Each of these conditions creates asituation in which the cardiac impulse conducted by a normal Purkinje fiber can return retrograde through the abnormalPurkinje fiber, which is not in a refractory state (a reentry circuit). A reentry circuit is the most likely mechanism forsupraventricular tachycardia, atrial flutter, atrial fibrillation, premature ventricular contractions, ventricular tachycardia,and ventricular fibrillation. Reentry circuits can be eliminated by speeding conduction through normal tissue so the cardiacimpulse reaches its initial site of origin when the fiber is still refractory, or by prolonging the refractory period of normalcells so the returning impulse cannot reenter.FIGURE 48-5. The essential requirement for initiation of a reentry circuit is a unilateral block that prevents uniformanterograde propagation of the initial cardiac impulse. This same cardiac impulse, under appropriate conditions, cantraverse the area of block in a retrograde direction and become a reentrant cardiac impulse. (From Akhtar M. Managementof ventricular tachyarrhythmias. JAMA 1982;247:671 4; with permission.)

PREEXCITATION SYNDROMESA preexcitation syndrome is present when the atrial impulse bypasses the atrioventricular node to produce early excitationof the ventricle. The most common accessory conduction pathway providing a direct connection of the atrium to theventricle is known as Kent's bundle (usually left atrium to left ventricle) (Table 48-4) Wellens et al, 1987. Conduction viathis accessory pathway produces the Wolff-Parkinson-White syndrome (P-R interval less than 0.12 second, QRS complexmore than 0.12 second, delta wave) most often manifesting as intermittent bouts of supraventricular tachydysrhythmias.Normally, the ventricles are protected from rapid atrial rhythms by the refractory period of the atrioventricular node.Propranolol has no specific effect on the accessory pathways, while digitalis preparations and verapamil may enhanceconduction through these pathways.

Table 48-4 Accessory Pathways and Preexcitation SyndromesConnections

Kent's Bundle Atrium to ventricleMahaim bundle Atrioventricular node to ventricleAtrio-Hissian fiberAtrium to His BundleJames fiber Atrium to atrioventricular node

AnesthesiaThe ability of halogenated anesthetics to evoke nodal rhythms and/or increase ventricular automaticity may be related toaltered K +, and Ca 2+ translocation dynamics across cell membranes Atlee and Bosnjak, 1990. Halothane, enflurane, andisoflurane slow the rate of sinoatrial node discharge and prolong His-Purkinje and ventricular conduction times. Changes inPaCO 2 dramatically alter autonomic nervous system effects on the sinoatrial and atrioventricular node depolarization aswell as reentry. Autonomic nervous system imbalance owing to drugs (anticholinergics, anticholinesterases, exogenouscatecholamines, or beta-antagonists) or light anesthesia may be responsible for the initiation of cardiac dysrhythmiasduring anesthesia and surgery.

Types of Cardiac DysrhythmiasSinus TachycardiaSinus tachycardia is usually defined as a heart rate more than 100 beats min -1. A common cause of sinus tachycardia issympathetic nervous system stimulation such as may occur during a noxious stimulus in the presence of lowconcentrations of anesthetic. Increased body temperature elevates heart rate approximately 18 beats min -1 for everydegree Celsius elevation. Fever causes tachycardia because increased temperature elevates the rate of metabolism in thesinoatrial node. Carotid sinus mediated reflex stimulation of the heart rate accompanies decreases in blood pressure as

produced by vasodilator drugs or acute hemorrhage.

Sinus BradycardiaSinus bradycardia is usually defined as a heart rate less than 60 beats min -1 . Heart-rate slowing accompaniesparasympathetic nervous system stimulation of the heart. Bradycardia that occurs in physically conditioned athletesreflects the ability of their hearts to eject a greater stroke volume with each contraction compared with the lessconditioned heart.

Sinus ArrhythmiaSinus arrhythmia is present during normal breathing with heart rate varying approximately 5% during various phases of thequiet breathing cycle (Fig. 48-6). This variation may increase to 30% during deep breathing. These variations in heart ratewith breathing most likely reflect baroreceptor reflex activity and changes in the negative intrapleural pressures that elicita waxing and waning Bainbridge reflex


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FIGURE 48-6. Sinus arrhythmia reflecting changes in sinoatrial pacemaker activity with the breathing cycle.

Atrioventricular Heart BlockFirst-degree atrioventricular heart block is considered to be present when the P-R interval is more than 0.2 second at anormal heart rate. Second-degree atrioventricular heart block is classified as the Wenckebach phenomenon (Type I) orMobitz (Type II) heart block. Wenckebach phenomenon is characterized by a progressive prolongation of the P-R intervaluntil conduction of the cardiac impulse is completely interrupted and a P-wave is recorded without a subsequent QRScomplex. After this dropped beat, the cycle is repeated. Mobitz Type II heart block is the occurrence of a nonconductedatrial impulse without a prior change in the P-R interval.Third-degree atrioventricular heart block occurs during complete block of the transmission of cardiac impulses from the

atria to the ventricles. The P-waves are dissociated from the QRS complexes and the heart rate depends on the intrinsicdischarge of the ectopic pacemaker beyond the site of conduction block. If the ectopic pacemaker is near theatrioventricular node, the QRS complexes appear normal and the heart rate is typically 40 to 60 beats min -1 (Fig. 48-7).When the site of block is infranodal, the escape ventricular pacemaker often has a discharge rate less than 40 beats min -1and the QRS complexes are wide, resembling a bundle branch block (Fig. 48-8). Patients may experience syncope (Stokes-Adams syndrome) at the onset of third-degree heart block, reflecting the 5- to 10-second period of asystole that mayprecede ventricular escape and appearance of an ectopic ventricular pacemaker. Occasionally, the interval of ventricularstandstill at the onset of third-degree heart block is so long that death occurs. Treatment of patients with third-degreeheart block is by insertion of a permanent artificial cardiac pacemaker. Temporary cardiac pacing may be provided withintravenous infusion of isoproterenol or a transvenous artificial cardiac pacemaker.FIGURE 48-7. Third-degree atrioventricular heart block occurring at the level of the atrioventricular node (QRS complexesare narrow). There is no relation between P-waves and QRS complexes.FIGURE 48-8. Third-degree atrioventricular heart block occurring at an infranodal level (QRS complexes are wide).

Premature Atrial ContractionsPremature atrial contractions are recognized by an abnormal P-wave and a shortened P-R interval (Fig. 48-9). The QRS

complex of the premature atrial contraction has a normal configuration. Also, the interval between the premature atrialcontraction and the next succeeding contraction is usually not prolonged. Premature atrial contractions are usually benignand often occur in persons without heart disease. FIGURE 48-9. Premature atrial contractions resulting in an irregularrhythm.

Premature Nodal ContractionsPremature nodal contractions are characterized by the absence of a P-wave preceding the QRS complex. The P-wave isobscured by the QRS complex of the premature contraction because the cardiac impulse travels retrograde into the atria atthe same time it travels forward into the ventricles.

Premature Ventricular ContractionsPremature ventricular contractions result from an ectopic pacemaker in the ventricles. The QRS complex of the ECG istypically prolonged because the cardiac impulse is conducted mainly through the slowly conducting muscle of the ventriclerather than Purkinje fibers (Fig. 48-10). The voltage of the QRS complex of the premature ventricular contraction isincreased, reflecting the absence of the usual neutralization that occurs when a normal cardiac impulse passes throughboth ventricles simultaneously. Following almost all premature ventricular contractions, the T-wave has an electricpotential opposite to that of the QRS complex. A compensatory pause following a premature ventricular contraction occursbecause the first impulse from the sinoatrial node reaches the ventricle during its refractory period. When a prematureventricular contraction occurs, the ventricle may not have filled adequately with blood and the stroke volume resultingfrom this contraction fails to produce a detectable pulse. The subsequent stroke volume, however, may be increased due toadded ventricular filling that occurs during the compensatory pause that typically follows a premature ventricularcontraction.FIGURE 48-10. Multifocal premature ventricular contractions.Premature ventricular contractions often reflect significant cardiac disease. For example, myocardial ischemia may beresponsible for initiation of a premature contraction from an irritable site in poorly oxygenated ventricular muscle.Treatment of premature ventricular contractions includes supplemental oxygen and intravenous administration oflidocaine.

Atrial Paroxysmal TachycardiaAtrial paroxysmal tachycardia, which often occurs in otherwise healthy young persons, is caused by rapid rhythmicdischarges of impulses from an ectopic atrial pacemaker. The rhythm on the ECG is perfectly regular and the P-waves areabnormal, often inverted, indicating a site of origin other than the sinoatrial node. The rapid discharge rate of this ectopicfocus causes it to become the pacemaker. Typically, the onset of atrial paroxysmal tachycardia is abrupt (a single beat)

and may end just as suddenly with the pacemaker shifting back to the sinoatrial node. Atrial paroxysmal tachycardia canbe terminated by producing parasympathetic nervous system stimulation at the heart with drugs or by unilateral externalpressure applied to the carotid sinus.

Nodal Paroxysmal TachycardiaNodal paroxysmal tachycardia resembles atrial paroxysmal tachycardia except P-waves are not identifiable on the ECG. P-waves are obscured by QRS complexes because the atrial impulse travels backward from the atrioventricular node at thesame time the ventricular impulse travels through the ventricles.

Ventricular TachycardiaVentricular tachycardia on the ECG resembles a series of ventricular premature contractions that occur at a rapid andregular rate without any normal supraventricular beats interspersed (Fig. 48-11). Stroke volume is often severelydepressed during ventricular tachycardia because the ventricles have insufficient time for cardiac filling. Sustained


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ventricular tachycardia may necessitate termination with electrical cardioversion. This cardiac dysrhythmia predisposes toventricular fibrillation. FIGURE 48-11. Ventricular tachycardia.

Atrial FlutterAtrial flutter on the ECG is characterized by 2:1, 3:1, or 4:1 conduction of atrial impulses to the ventricle (Fig. 48-12). Thisoccurs because the functional refractory period of Purkinje fibers and ventricular muscle is such that no more than 200impulses min -1 can be transmitted to the ventricles. P-waves have a characteristic saw-toothed appearance, especially inlead II.FIGURE 48-12. Atrial flutter.

Atrial FibrillationAtrial fibrillation is characterized by normal QRS complexes occurring at a rapid and irregular rate in the absence ofidentifiable P-waves (Fig. 48-13). The irregular ventricular response reflects arrival of atrial impulses at the atrioventricularnode at times that may or may not correspond to the refractory period of the node from a previous discharge. Strokevolume is reduced during atrial fibrillation because the ventricles do not have sufficient time to fill optimally betweencardiac cycles. A pulse deficit (heart rate by palpation less than that calculated from the ECG) reflects the inability of eachventricular contraction to eject a sufficient stroke volume to produce a detectable peripheral pulse. Treatment of atrialfibrillation is classically with digitalis, which prolongs the refractory period of the atrioventricular node. This prolongationdecreases the ventricular response, which improves stroke volume by permitting additional time for filling the ventriclesbetween cardiac cycles.FIGURE 48-13. Atrial fibrillation,

Ventricular FibrillationVentricular fibrillation on the ECG is characterized by an irregular wavy line with voltages that range from 0.25 to 0.5 mv(Fig. 48-14). There is total incoordination of contraction with cessation of any effective pumping activity and disappearanceof detectable blood pressure. Flutter or fibrillation is usually confined to either the atria or ventricles because the two

masses of muscle are electrically insulated from each other by the rings of fibrous tissue around the heart valves. Mostinstances of atrial or ventricular fibrillation are due to a reentry mechanism. The only effective treatment of ventricularfibrillation is the delivery of a direct electric current through the ventricles (defibrillation), which simultaneously depolarizesall ventricular muscle. This depolarization allows the reestablishment of a cardiac pacemaker at a site other than theirritable focus that was responsible for ventricular fibrillation.FIGURE 48-14. Ventricular fibrillation.

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