Normal and pathologic ECG pattern. Dysrhythmias (sinus and atrial). Interventions for clients with sinus and atrial dysrhythmias

Normal and pathologic ECG pattern. Dysrhythmias (sinus and atrial).

Interventions for clients with sinus and atrial dysrhythmias.

 

Cardiac dysrhythmias are disturbances of cardiac electri­cal impulse formation, conduction, or both. Many diseases can affect the electrical activity of the heart, causing dys­rhythmias. Although more common in older adults, dys­rhythmias may occur in people of any age. Many dysrhyth­mias are benign; however, some cause cardiac dysfunction, and a few result in cardiac arrest.

To understand dysrhyth­mias and to interpret these disturbances correctly, an under­standing of cardiac electrophysiology, the conduction system of the heart, and the principles of electrocardiography is needed.

REVIEW OF CARDIAC ELECTROPHYSIOLOGY

Electrophysiologic Properties

The electrophysiologic properties of cardiac cells regulate heart rate and rhythm. Specialized cardiac muscle cells pos­sess unique properties: automaticity, excitability, conductiv­ity, and contractility.

AUTOMATICITY

Automaticity (spontaneous depolarization) is the ability of cardiac cells to generate an electrical impulse spontaneously and repetitively. Normally, only primary pacemaker cells possess this property. Under certain conditions, such as myocardial ischemia (decreased blood flow) and infarction (cell death), any cardiac cell may exhibit this property, generating electrical impulses independently and creating dysrhythmias.

EXCITABILITY

Excitability is the ability of nonpacemaker cardiac cells to re­spond to an electrical impulse generated from pacemaker cells and to depolarize. Depolarization occurs when the nor­mally negatively charged cells develop a positive charge.

CONDUCTIVITY

Conductivity is the ability to transmit an electrical stimulus from cell membrane to cell membrane. Consequently, ex­citable cells depolarize in rapid succession from cell to cell until all cells have depolarized. This wave of depolarization gives rise to the deflections of the electrocardiogram (ECG) waveforms that are recognized as the P wave and the QRS complex.

CONTRACTILITY

Contractility is the ability of atrial and ventricular muscle cells to shorten their fiber length in response to electrical stimulation, generating sufficient pressure to propel blood forward. This is the mechanical activity of the heart.

Action Potential

The cardiac cell membrane (sarcolemma) exhibits selective permeability to ions. An ion is an electrically charged particle. This creates an electrical imbalance, known as an action po­tential, across the cell membrane.

The cardiac cell at rest has an internal negative charge, whereas the charge outside the cell is positive. This state of electrical imbalance of the resting cell is called resting mem­brane potential.

CARDIAC CONDUCTION SYSTEM

The cardiac conduction system consists of specialized cells. It is responsible for the generation and con­duction of electrical impulses that cause atrial and ventricular depolarization. The conduction system consists of the sinoatrial node, atrioventricular junctional area, and bundle branch system

Sinoatrial Node

The conduction system begins with the sinoatrial (SA) node (also called the sinus node), located close to the epicardial surface of the right atrium near its junction with the superior vena cava. The SA node is the heart’s primary pacemaker. It can spontaneously and rhythmically generate electrical im­pulses at a rate of 60 to 100 beats/min, possessing the great­est degree of automaticity.

The SA node is richly supplied by the sympathetic and parasympathetic nervous systems, which accelerate and de­celerate the rate of discharge of the sinus node, respectively. This process results in changes in the heart rate.

Impulses from the sinus node move directly through atrial muscle without specialized pathways. The impulses lead to atrial depolarization and are reflected by a P wave on the ECG. Atrial muscle contraction should follow. Within the atrial muscle are slow and fast conduction pathways, leading to the atrioventricular node.

Atrioventricular Junctional Area

The atrioventricular (AV) junctional area consists of a transi­tional cell zone, the AV node itself, and the His bundle. The AV node lies just beneath the right atrial endocardium, between the tricuspid valve and the ostium of the coronary sinus. Here, T-cells (transitional cells) cause impulses to slow down or be delayed in the AV node before proceeding to the ventricles. This delay is reflected by the PR segment on the ECG.

This slow conduction provides a short delay, allowing the atria to contract. Blood can then fill the ventricle completely before ventricular contraction. This is known as the “atrial kick” and contributes 15% to 30% of additional blood volume for a greater cardiac output. The AV node is also controlled by both the sympathetic and the parasympathetic nervous systems. The His bundle connects with the distal portion of the AV node and continues on to perforate the interventricular septum

Bundle Branch System

The His bundle extends as a right bundle branch down the right side of the interventricular septum to the apex of the right ventricle. On the left side it extends as a left bundle branch, which further divides into two fascicles.

At the ends of both right and left bundle branch systems are the Purkinje fibers. These fibers are an interweaving network lo­cated on the endocardial surface of both ventricles, from apex to base. The fibers then partially penetrate into the myocardium.

Purkinje cells make up the His bundle, bundle branches, and terminal Purkinje fibers. These cells are responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and the sub­sequent ventricular muscle contraction. A few nodal cells in the ventricles may also occasionally demonstrate automaticity, giving rise to ventricular beats or rhythms.

ELECTROCARDIOGRAPHY

The electrocardiogram (ECG) provides a graphic represen­tation, or picture, of cardiac activity. The weak cardiac elec­trical currents are transmitted to the body surface. Electrodes, consisting of a conductive gel on an adhesive pad, are placed on specific sites on the body and attached to cables connected to an ECG machine or to a monitor. The cardiac electrical cur­rent is transmitted via the electrodes and through the lead wires to the machine or monitor, which displays the cardiac elec

trical activity.

A lead provides one view of the heart’s electrical activity. Multiple leads, or views, can be obtained. Electrode place­ment is the same for male and female clients.

Lead systems are made up of a positive pole and a negative pole. An imaginary line joining these two poles is called the lead axis. The direction of electrical current flow in the heart is the cardiac axis. The relationship between the cardiac axis and the lead axis is responsible for the deflections seen on the ECG pattern:

•  The baseline is the isoelectric line. It occurs when there  is no current flow in the heart after complete depolariza­  tion and also after complete repolarization. Positive de­  flections occur above this line, and negative deflections  occur below it. Deflections represent depolarization and  repolarization of cells.

•  If the direction of electrical current flow in the heart  (cardiac axis) is toward the positive pole, a positive deflection (above the baseline) is viewed (A).

•  If the direction of electrical current flow in the heart  (cardiac axis) is moving away from the positive pole to­  ward the negative pole, a negative deflection (below the  baseline) is viewed (B).

•  If the cardiac axis is moving neither toward nor away from the positive pole, a biphasic complex (both above and below baseline) will result (C).

Lead Systems

The standard 12-lead ECG consists of 12 leads (or views) of the heart’s electrical activity. Six of the leads are called limb leads because the electrodes are placed on the four limbs in the frontal plane. The remaining six leads are called chest (precordial) leads because the electrodes are placed on the chest in the horizontal plane.

LIMB LEADS

Standard bipolar limb leads consist of three leads that each measure the electrical activity between two points, and a fourth lead (right leg) that acts solely as a ground electrode. Of the three measuring leads, the right arm is always negative, the left leg is always positive, and the left arm can be either posi­tive or negative. Bipolar leads can be obtained by using a mon­itor with either three or five electrode cables or a 12-lead ECG machine. Leads I, II, and III are bipolar leads.

Unipolar limb leads consist of a positive electrode only. These leads can be obtained only by using a monitor with four or five electrode cables or a 12-lead ECG machine. The unipolar limb leads are aVR, aVL, and aVF, with a meaning augmented. V is a designation for a unipolar lead. The third letter denotes the positive electrode placement: R for right arm, L for left arm, and F for foot (left leg). The positive elec­trode is at one end of the lead axis. The other end is the cen­ter of the electrical field, at approximately the center of the heart.

CHEST LEADS

Chest (precordial) leads are also unipolar, or V, leads and therefore can be obtained only from a monitor with five elec­trode cables or a 12-lead ECG machine, which usually has 10 electrode cables. There are six chest leads, determined by the placement of the chest electrode. The four limb electrodes are placed on the extremities, as designated on each electrode (right arm, left arm, right leg, and left leg). The fifth (chest) electrode on a monitor system is the positive, or exploring, electrode and is placed in one of six designated positions to obtain the desired chest lead (see Table 34-1). With a 12-lead ECG, four leads are placed on the limbs and six are placed on the chest, eliminating the need to move any electrodes about the chest.

Positioning of the electrodes is crucial in obtaining an ac­curate ECG. Comparisons of ECGs taken at different times will be valid only when electrode placement is accurate and identical at each test. Positioning is particularly important when serving clients with chest deformities or large breasts. Clients may be asked to displace the breast to ensure proper electrode placement.

While obtaining a 12-lead ECG, the client should be as still as possible in a semireclined position, breathing nor­mally. Any repetitive movement will cause artifact and could lead to inaccurate interpretation of the ECG.

Often, nurses are responsible for obtaining 12-lead ECGs, but technicians are more commonly trained to take 12-lead ECGs in various health care settings. It is imperative that the technician bring any suspected abnormality to the attention of a nurse or physician. A nurse may direct a technician to take a 12-lead ECG on a client experiencing chest pain to observe for diagnostic changes, but it is ultimately the physician’s re­sponsibility to interpret the ECG.

Continuous Electrocardiographs Monitoring

For continuous electrocardiographic (ECG) monitoring, the electrodes are not placed on the limbs, because movement of the extremities causes “noise” or motion artifact, on the ECG signal. The nurse places the electrodes on the trunk, a more stable area, to minimize such artifacts and to obtain a clearer signal. If the monitoring system provides five electrode ca­bles, the nurse places the electrodes as follows:

■Right arm electrode just below the right clavicle

■Left arm electrode just below the left clavicle

■Right leg electrode on the lowest palpable rib, on the right midclavicular line

■Left leg electrode on the lowest palpable rib, on the left  midclavicular line

■Fifth electrode placed to obtain one of the six chest leads

With this placement, the monitor lead select control may be changed to provide lead I, II, III, aVR, aVL, or aVF or one chest lead. The monitor automatically alters the polarity of the electrodes to provide the lead selected.

If the monitoring system provides only three electrode ca­bles, the nurse places the right arm, the left arm, and the left leg electrodes as described. In this case, the lead selected pro­vides only lead I, II, or III.

The popular MCL, lead is a modified (M) bipolar chest (C) lead. It approximates the V₁ lead without requiring a five-electrode cable monitoring system because it is a bipolar lead system. To obtain MCL₁, the nurse places the negative elec­trode just below the left (L) midclavicle and the positive elec­trode in the V, position. The ground electrode may be placed anywhere but is usually placed under the right clavicle. The nurse uses this lead for bedside or telemetry monitoring to differentiate left from right electrical activity, such as left from right bundle branch block or left from right premature ventricular complexes, and to differentiate certain supraven-tricular beats from ventricular ectopic beats. The MCL, lead provides a right-sided view of cardiac electrical activity.

Another bipolar lead, MCL₆, is frequently used. It can be achieved by placing the negative and ground electrodes as for MCL, and moving the positive electrode to the V₆ position. This approximates the V₆ lead and provides a left-sided view of cardiac electrical activity. It is used for the same reasons as MCL₁.

The clarity of continuous ECG monitor recordings is af­fected by skin preparation and electrode quality. To ensure the best signal transmission, the nurse or assistive nursing per­sonnel decreases skin impedance by cleaning the skin with soap and water. The area is shaved if needed, and the elec­trode sites are wiped with an alcohol or other skin preparation pad and dried. The gel on each electrode must be moist and fresh. The nurse or assistive nursing personnel attaches the electrode to the lead cable, rubs the skin briskly with a gauze square or a washcloth until the skin is slightly reddened, and then applies the electrode onto the site for proper contact. This action rubs off surface cells and increases capillary blood flow to the area to improve transmission of electrical activity. The contact site should not have any lotion, tincture, or other substance on it that increases skin impedance. Electrodes can­not be placed on irritated skin or over scar tissue. The appli­cation of electrodes may be done by an assistive nursing per­sonnel, but the nurse must determine which lead to select. The nurse assesses the quality of the ECG rhythm transmission to the monitoring system and is responsible for assessment and management of the client.

ECG cables may be attached directly to a wall-mounted monitor (a hard-wired system) if the client’s activity is re­stricted to bedrest and sitting in a chair, as in a critical care unit. For an ambulatory client, the ECG cable is attached to a battery-operated transmitter (a telemetry system) held in a pouch worn by the client. The ECG is transmitted via anten­nae located in strategic places, usually in the ceiling, to a re­mote monitor. This device allows freedom of movement within a certain radius without losing transmission of the ECG.

Some acute care facilities employ monitor technicians who are educated in ECG rhythm interpretation and are responsi­ble for the following:

■ Watching a bank of monitors on a unit

■Printing ECG rhythm strips routinely and as needed

■Interpreting rhythms

■ Communicating with the nurse to report the client’s  rhythm and significant changes

This technical support is particularly helpful on a teleme­try unit that does not have monitors at the bedside. The nurse is reasonably assured that the ECG rhythm is being monitored “continuously,” although some rhythms will not be observed by technicians. The nurse remains ultimately responsible for accurate ECG rhythm interpretation, as well as client assess­ment and management.

Some units have full-disclosure monitors, which continu­ously store ECG rhythms in memory up to a maximum amount of time, allowing nurses and physicians to access and print them for more thorough assessment and management of clients with dysrhythmias. Routine strips, as well as any changes in rhythm, are printed and documented in the client’s record.

The physician is responsible for determining when moni­toring can be suspended, such as when the client is shower­ing. The health care provider also determines whether moni­toring is needed during transportation and off-unit testing procedures. The nurse collaborates with the physician in mak­ing these determinations.

Prehospital personnel, such as paramedics and EMTs with advanced training, frequently monitor a client’s ECG rhythm at the scene and en route to a health care facility. They func­tion under medical direction and protocols but may also be in communication with a nurse.

Electrocardiographic Paper

The electrocardiogram (ECG) strip is printed on graph paper, with each small block measuring 1 mm in height and width. ECG recorders and monitors are standard­ized at a speed of 25 mm/sec. Time is measured on the hori­zontal axis. At this speed, each small block represents 0.04 second. Five small blocks make up one large block, defined by darker bold lines and representing 0.20 second. Five large blocks represent 1 second, whereas 30 large blocks represent 6 seconds. Vertical lines in the top margin of the graph paper are usually 15 large blocks apart, representing 3-second segments.

Electrocardiographic Complexes, Segments, and Intervals

Complexes that make up a normal ECG consist of a P wave, a QRS complex, a T wave, and possibly a U wave. Segments include the PR segment, the ST segment, and the TP segment. Intervals include the PR interval, the QRS duration, and the QT interval.

P WAVE

The P wave is a deflection representing atrial depolarization. The shape of the P wave may be a positive, negative, or biphasic deflection, depending on the lead selected. When the elec­trical impulse is consistently generated from the sinoatrial (SA) node, the P waves have a consistent shape in a given lead. If an impulse is then generated from a different (ectopic) focus, such as atrial tissue, the shape of the P wave changes in that lead, indicating that an ectopic focus has fired.

 

PR SEGMENT

The PR segment is the isoelectric line from the end of the P wave to the beginning of the QRS complex, when the electrical impulse is traveling through the atrioventricular (AV) node, where it is delayed. It then travels through the ventric­ular conduction system to the Purkinje fibers.

 

PR INTERVAL

The PR interval is measured from the beginning of the P wave to the end of the PR segment. It represents the time required for atrial depolarization, as well as the impulse delay in the AV node and the travel time to the Purkinje fibers. It normally measures from 0.12 to 0.20 second

QRS COMPLEX

The QRS complex represents ventricular depolarization. The shape of the QRS complex depends on the lead selected.

The Q wave is the first negative deflection and is not present in all leads. When present, it is small and represents initial ventric­ular septal depolarization. The R wave is the first positive de­flection. It may be small, large, or absent, depending on the lead. The S wave is a negative deflection following the R wave and is not present in all leads.

■ QRS DURATION

The QRS duration represents the time required for depolar­ization of both ventricles. It is measured from the beginning of the QRS complex to the J-point (the junction where the QRS complex ends and the ST segment begins). It normally measures from 0.04 to 0.10 second.

■ ST SEGMENT

The ST segment is normally an isoelectric line and represents early ventricular repolarization. It occurs from the J-point to the beginning of the T wave. Its length varies with changes in the heart rate, the administration of medications, and elec­trolyte disturbances. It is normally not elevated more than 1 mm or depressed more than 0.5 mm from the isoelectric line. Its amplitude is measured at a point 1.5 to 2 mm after the J-point. ST elevation or depression can be caused by myocar-dial ischemia or infarction, conduction abnormalities, or the administration of medications.

■ T WAVE

The T wave follows the ST segment and represents ventricu­lar repolarization. It is usually positive, rounded, and slightly asymmetric. If an ectopic stimulus excites the ventricles dur­ing this time, it may cause ventricular irritability and possible cardiac arrest in the vulnerable heart. This is known as the R-on-T phenomenon. T waves may become tall and peaked, in­verted (negative), or flat as a result of myocardial ischemia, potassium or calcium imbalances, medications, or autonomic nervous system effects

■U WAVE

The U wave, when present, follows the T wave and may re­sult from slow repolarization of ventricular Purkinje fibers. It is of the same polarity as the T wave, although generally smaller. It is not normally seen in all leads and is more com­mon in lead V₃. Abnormal prominence of the U wave suggests an electrolyte abnormality (particularly hypokalemia) or other disturbance. Identifying it correctly is important so that it is not mistaken for a P wave.

■QT INTERVAL

The QT interval represents the total time required for ventric­ular depolarization and repolarization. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. This interval varies with the client’s age and sex and changes with the heart rate, lengthening with slower heart rates and shortening with faster rates. It may be prolonged by certain medications, electrolyte disturbances, Prinzmetal’s angina, or subarachnoid hemorrhage. A prolonged QT interval may lead to a unique type of ventricular tachycardia called Torsades de Pointes.

Determination of Heart Rate

The heart rate may be estimated by counting the number of P-P intervals (atrial rate) or R-R intervals (ventricular rate) in 6 seconds and multiplying that number by 10 to calculate the rate for a full minute. For ac­curacy, timing should begin with the P wave or the QRS complex and end exactly 30 large blocks (150 small blocks) later. The initial complex is the reference point and counts as zero. Subsequent complexes are counted until the end of 6 seconds, to include a fraction of the last interval; for ex­ample, if there are exactly seven R-R intervals, the heart rate is 70 beats/min; if there are 9.5 intervals, the heart rate is 95 beats/min. This method may be used for both regular and irregular rhythms. It is called the 6-second strip method.

Another method, which may be used only if the rhythm is regular, relies on either of the following mathematic calcula­tions:

Count the number of small blocks in a P-P or R-R inter­val and divide into 1500 (the number of small blocks in 1 minute). For example, 20 small blocks equals a heart rate of 75 beats/min (1500/20 = 75). Count the number of large blocks in an interval and di­vide into 300 (the number of large blocks in 1 minute). For example, three large blocks equals a heart rate of 100 beats/min (300/3 = 100).

Commercially prepared electrocardiogram (ECG) rate rulers are based on these calculations and may be used for regular rhythms. Current monitoring systems will display a continuous heart rate and print the heart rate on the ECG strip. The nurse must, however, use caution and confirm that the rate is correct by assessing the client’s heart rate directly. Many factors can incorrectly alter the rate displayed by the monitor.

Electrocardiographic Rhythm Analysis

Analysis of an ECG rhythm strip requires a systematic approach and is facilitated by the use of an ECG caliper:

1.Analyze the P waves. The nurse checks that the P-wave  shape is consistent throughout the strip, indicating that  atrial depolarization is occurring from impulses origi­  nating from one focus, normally the SA node. The  nurse determines whether there is one P wave occurring  before each QRS complex, establishing that a relation­  ship exists between the P wave and the QRS complex.  This relationship indicates that impulses from one focus  are responsible for both atrial and ventricular depolar­  ization. The nurse may observe more than one P wave  shape, more P waves than QRS complexes, absent P  waves, or P waves coming after the QRS, each indicat­  ing that a dysrhythmia exists.

2.Analyze the QRS complexes. The nurse checks that the  QRS complexes are consistent throughout the strip.  More than one QRS complex pattern or occasionally  missing QRS complexes may be observed, indicating a dysrhythmia.

3.Determine the atrial rhythm or regularity. The nurse  checks the regularity of the atrial rhythm by assessing  the P-P intervals, placing one caliper point on a P wave and the other point on the precise spot on the next P wave. Then the caliper is moved from P wave to P wave along the entire strip (“walking out” the P waves) to de­termine the regularity of the rhythm. P waves of a dif­ferent shape (ectopic waves), if present, create an irreg­ularity and do not walk out with the other P waves. A slight irregularity in the P-P intervals, varying no more than three small blocks, is considered essentially regu­lar if the P waves are all of the same shape.

4. Determine the ventricular rhythm or regularity. The  nurse checks the regularity of the ventricular rhythm by  assessing the R-R intervals, placing one caliper point on  a portion of the QRS complex (usually the most promi­  nent portion of the deflection) and the other point on the  precise spot of the next QRS complex. The caliper is  then moved from QRS complex to QRS complex along  the entire strip (walking out the QRS complexes) to de­  termine the regularity of the rhythm. QRS complexes of  a different shape (ectopic QRS complexes), if present,  create an irregularity and do not walk out with the other  QRS complexes. A slight irregularity of no more than  three small blocks between intervals is considered essentially regular if the QRS complexes are all of the  same shape.

5. Determine the heart rate. If the atrial and ventricular  rhythms are regular, the nurse may use any of the meth­  ods previously described to calculate the heart rate. If the  rhythms are irregular, the nurse must use the 6-second  strip method for accuracy.

6. Measure the PR interval. The nurse places one caliper  point at the beginning of the P wave and the other point  at the end of the PR segment. The PR interval normally measures between 0.12 and 0.20 second. The measure­ment should be constant throughout the strip. The PR interval is unable to be determined if there are no P waves or if P waves occur after the QRS complex.

7.Measure the  QRS duration.  The nurse places  one  caliper point at the beginning of the QRS complex and  the other at the J-point, where the QRS complex ends  and the ST segment begins. The QRS duratioormally  measures between 0.04 and 0.10 second. The measure­  ment should be constant throughout the entire strip.

8.Interpret the cardiac rhythm. Using accepted rules, the  nurse caow interpret the cardiac rhythm.

These steps can be reorganized and formatted as the basis for rules or criteria to differentiate normal and abnormal car­diac rhythms. The following format is used to describe ECG criteria:

•  Rhythm: Atrial and ventricular rhythms (regular or  irregular)

•  Rate: Atrial and ventricular rates

•  P waves: Presence, shape, and relationship to QRS com­  plexes

•  PR interval: Measurement and constancy

•  QRS duration: Measurement and constancy

 

NORMAL RHYTHMS

Normal Sinus Rhythm

Normal sinus rhythm (NSR) is the rhythm originating from the sinoatrial (SA) node (dominant pacemaker) that meets the following electrocardiographic (ECG) criteria:

•  Rhythm: Atrial and ventricular rhythms regular

•  Rate: Atrial and ventricular rates of 60 to 100 beats/min

•  P waves: Present, consistent configuration, one P wave  before each QRS complex

•  PR interval: 0.12 to 0.20 second and constant

•  QRS duration: 0.04 to 0.10 second and constant

Sinus Arrhythmia

Sinus arrhythmia is a variant of NSR. It results from changes in intrathoracic pressure during breathing. In this context the term arrhythmia does not denote an absence of rhythm, as the term suggests. Instead, the heart rate increases slightly during inspiration and decreases slightly during exhalation. This irregular rhythm is frequently observed in healthy children, as well as adults.

Sinus arrhythmia has all the characteristics of NSR, except for its irregularity. The P-P and R-R intervals vary, with the difference between the shortest and the longest intervals be­ing greater than 0.12 second (three small blocks):

Rhythm: Atrial and ventricular rhythms irregular, with the shortest P-P or R-R interval varying at least 0.12 sec­ond from the longest P-P or R-R interval

 Rate: Atrial and ventricular rates are between 60 and 100 beats/min

P waves: One P wave before each QRS complex; con­sistent configuration

PR interval: Normal, constant

QRS duration: Normal, constant Sinus arrhythmias may occasionally be due to nonrespira-tory causes, such as the administration of digitalis or mor­phine. These drugs enhance vagal tone and cause decreased heart rate and irregularity unrelated to the respiratory cycle.

OVERVIEW

Any disorder of the heartbeat is termed dysrhythmia. Histori­cally, the term arrhythmia has been used in the literature; however, it means an absence of cardiac rhythm. Although the terms are often used interchangeably, dysrhythmia, which means a disturbance in cardiac rhythm, is more accurate.

Dysrhythmias result from a disturbance in impulse forma­tion (either from an abnormal rate or from an ectopic focus), from a disturbance in impulse conduction (delays and blocks), or from both mechanisms. Although many dysrhyth­mias have no clinical manifestations, many others have seri­ous consequences. A summary of key features is provided in сhart

.

Dysrhythmia Terminology

TACHYDYSRHYTHIVIIAS

Tachydysrhythmias are heart rates greater than 100 beats/min.

These rhythms may have serious hemodynamic consequences in the adult client with coronary artery disease (CAD). Coronary artery blood flow occurs predominantly during diastole, when the aortic valve is closed, and is determined by diastolic time and blood pressure in the root of the aorta. The nurse must understand three important points to ap­preciate the seriousness of tachydysrhythmias:

•  Tachydysrhythmias shorten the diastolic time and there­fore the coronary perfusion time (the amount of time available for blood to flow through the coronary arteries  to the myocardium).

•  Tachydysrhythmias initially increase cardiac output and  blood pressure. However, a continued rise in heart rate  decreases the ventricular filling time because of a short­ened diastole, decreasing the stroke volume. Conse­quently, cardiac output and blood pressure will begin to decrease, reducing aortic pressure and therefore coronary perfusion pressure.

•  Tachydysrhythmias increase the work of the heart, in­creasing myocardial oxygen demand.

The client with a tachydysrhythmia may have palpitations; chest discomfort; pressure or pain from myocardial ischemia or infarction; restlessness; anxiety; pale, cool skin; and syn­cope from hypotension. Tachydysrhythmias may also lead to heart failure. Presenting symptoms may include dyspnea, orthopnea, pulmonary crackles, distended neck veins, fatigue, and weakness.

■   BRADYDYSRHYTHMIAS

Bradydysrhythmias are characterized by a heart rate less than 60 beats/min. These rhythms can also have serious hemodynamic consequences. The nurse considers the following three points:

•  Myocardial oxygen demand is reduced from the slow  heart rate, which is beneficial.

•  Coronary perfusion time is adequate because of a pro­ longed diastole, which is desirable.

•  Coronary perfusion pressure may decrease if the heart  rate is too slow to provide adequate cardiac output and  blood pressure; this is a serious consequence.

Therefore the client may tolerate the bradydysrhythmia well if the blood pressure is adequate. If the blood pressure is not adequate, symptomatic bradydysrhythmias may lead to myocardial ischemia or infarction, dysrhythmias, hypotension, and heart failure.

PREMATURE COMPLEXES

Premature complexes are early complexes. They occur when a cardiac cell or cell group, other than the sinoatrial (SA) node, becomes irritable and fires an impulse before the next sinus impulse is generated. This abnormal focus is called an ectopic focus and may be generated by atrial, junctional, or ventricular tissue. Following the premature complex, there is a pause before the next normal complex, creating an irregu­larity in the rhythm.

The client with premature complexes may be unaware of them or may feel palpitations or a “skip­ping” of the heartbeat. If premature complexes, especially those that are ventricular in nature, become more frequent, the client may experience symptoms of decreased cardiac output.

■   REPETITIVE RHYTHMS

Premature complexes may occur repetitively in a rhythmic fashion:

•  Bigeminy exists wheormal complexes and premature  complexes occur alternately in a repetitive two-beat pat­tern, with a pause occurring after each premature com­plex so that complexes occur in pairs.

•  Trigeminy is a repetitive three-beat pattern, usually oc­curring as two sequential normal complexes followed by  a premature complex and a pause, with the same pattern  repeating itself in triplets.

•  Quadrigeminy is a repetitive four-beat pattern, usually occurring as three sequential normal complexes fol­lowed by a premature complex and a pause, with the same pattern repeating itself in a four-beat pattern. Such patterns may occur with atrial, junctional, or ventric­ular premature complexes. Clients may be unaware of the premature beats or may feel palpitations.

 ESCAPE COMPLEXES AND RHYTHMS

Escape complexes or escape rhythms may occur when the SA node fails to discharge or is blocked or when a sinus impulse fails to depolarize the ventricles because of an atrioventricular (AV) nodal block. Escape complexes or rhythms serve as a secondary or escape pacemaker and are seen after a pause. Such impulses may originate from AV junctional or ventricu­lar tissue. They cease when the SA node or the AV node re­gains the ability to functioormally. If there are pauses fol­lowed by escape beats or rhythms, clients may feel lightheaded, dizzy, or faint during the pause.

Classification of Dysrhythmias

Dysrhythmias are classified according to their site of origin. The sites include the SA node, atrial tissue, AV node, junctional tissue, and ventricular tissue. Dysrhythmias may be caused by a disturbance in impulse formation or by conduction delays or blocks. The incidence and the prevalence of dysrhythmias are not precisely known, because they usually result from an un­derlying condition, such as heart disease.

The incidence of dys­rhythmias increases with age. A summary of the common dys­rhythmias and their treatment is provided in Table 34-2.

SINUS DYSRHYTHMIAS

The sinus node is the pacemaker in all sinus dysrhythmias. Sympathetic and parasympathetic nerve fibers are distributed to the SA node. Innervation from these two systems is nor­mally in balance to ensure a normal sinus rhythm (NSR). An imbalance increases or decreases the rate of SA node dis­charge either as a normal response to activity or physiologic changes or as a pathologic response to disease.

SINUS TACHYCARDIA

PATHOPHYSIOLOGY. Dominant sympathetic nervous system stimulation of the heart or vagal inhibition results in an increased rate of SA node discharge, which increases the heart rate (positive chronotropic effect).

When the rate of SA node discharge exceeds 100 beats/min, the rhythm is called sinus tachycardia. Sinus tachycardia, with heart rates of 200 to 220 beats/min, is nor­mal in infants and children. The rate gradually decreases until age 10 years. From age 10 years to adulthood, the heart rate normally does not exceed 100 beats/min except in response to activity and then usually does not exceed 160 beats/min. Rarely, the heart rate may reach 180 beats/min. Sinus tachy­cardia initially enhances cardiac output and blood pressure. However, sustained increases in heart rate decrease coronary perfusion time and coronary perfusion pressure, while increas­ing myocardial oxygen demand.

ETIOLOGY. Increased sympathetic stimulation is a nor­mal response to physical activity but may also be caused anxiety, pain, stress, fear, fever, anemia, hypoxemia, hyperthyroidism, and pulmonary embolism. Drugs such as catecholamines, atropine, caffeine, alcohol, nicotine, aminophylline, and thyroid medications may also increase the heart rate. In some cases, sinus tachycardia is a compensatory re­sponse to decreased cardiac output or blood pressure, as oc­curs in hypovolemia, shock, myocardial infarction, and heart failure.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. The client may be asymptomatic except for the in­creased pulse rate. However, if the rhythm is not well toler­ated, he or she may become symptomatic. The client is assessed for fatigue, weakness, shortness of breath, orthopnea, neck vein distention, decreased oxygen saturation, and de­creased blood pressure. The nurse also assesses for restless­ness and anxiety from decreased cerebral perfusion and for de­creased urine output from decreased renal perfusion. The adult client may experience anginal pain. The electrocardiographic (ECG) pattern may show T-wave inversion or ST-segment ele­vation or depression in response to myocardial ischemia.

INTERVENTIONS. The nurse and health care provider collaborate to identify the cause of sinus tachycardia and se­lect the appropriate treatment. The goal is to decrease the heart rate to normal levels by treating the underlying cause. For example, if the client has angina, the nurse administers oxygen, helps the client to rest, and administers nitroglycerin or morphine as prescribed. Diuretics and inotropic agents may be given for heart failure. The nurse initiates intravascular volume replacement for hypovolemia, administers an­tipyretics and antibiotics to the client with fever and infection, or provides comfort measures and administers analgesics or opioids to the client with noncardiac pain, as ordered.

The nurse collaborates with the respiratory therapist when indicated to oxygenate and suction the client with hypoxemia from excessive airway secretions. Beta-adrenergic blocking agents may be prescribed for the client with inap­propriate sympathetic nervous system stimulation. Emo­tional support and relevant teaching are important for the client and family.

SINUS BRADYCARDIA

PATHOPHYSIOLOGY. Dominance of the parasympathetic nervous system, with excessive vagal stimulation to the heart, causes a decreased rate of sinus node discharge. This slows the heart rate and decreases the speed of conduction through the AV node and conduction system.

When the rate of sinus node discharge is less than 60 beats/min in adults or below the nor­mal range in infants and children, the rhythm is called sinus bradycardia. Sinus bradycardia increases coronary perfusion time but may decrease coronary perfusion pressure. However, myocardial oxygen demand is decreased.

ETIOLOGY. Increased parasympathetic stimulation of the heart by the vagus nerve is a normal response to decreased physical activity. It also often occurs in well-conditioned ath­letes because the strong heart muscle is extremely efficient in providing an adequate stroke volume while not requiring a higher heart rate for a normal cardiac output. Excessive vagal stimulation may result from carotid sinus massage, vomiting, suctioning, Valsalva maneuvers (e.g., bearing down for a bowel movement or gagging), ocular pressure, or pain. Sinus bradycardia may also result from hypoxia, inferior wall myo­cardial infarction, and the administration of drugs such as beta-adrenergic blocking agents, calcium channel blockers, and digitalis.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. The client may be asymptomatic, except for the de­creased pulse rate. However, at times the rhythm may not be well tolerated. The nurse assesses the client for dizziness, weakness, syncope, confusion, hypotension, diaphoresis, shortness of breath, ventricular ectopy, and anginal pain. T-wave inversion or ST-segment elevation or depression may occur in response to myocardial ischemia.

INTERVENTIONS. If the client is symptomatic and the un­derlying cause cannot be determined, the treatment of choice is atropine administration, given as prescribed to increase the heart rate to approximately 60 beats/min. Oxygen should be applied. If the heart rate does not increase sufficiently, the nurse may apply an external pacemaker to increase the heart rate and notify the physician. However, if atropine administra­tion succeeds in achieving an adequate heart rate but the client remains hypotensive, the nurse initiates intravascular volume replacement, as ordered, rather than administering another dose of atropine. Excessive atropine may induce tachycardia. If a medication is determined to be the cause, the nurse with­holds the drug and notifies the physician for an order to dis­continue the drug temporarily or permanently.

 ■   ATRIAL DYSRHYTHMIAS

With atrial dysrhythmias, the focus of impulse generation has shifted away from the sinus node to the atrial tissue, which now acts as an ectopic pacemaker, for one or more beats. This shift changes the axis (direction) of atrial depolarization, re­sulting in a P-wave shape that differs from that of P waves with a sinus node origin. The most common atrial dysrhyth­mias are premature atrial complexes, supraventricular tachy­cardia, atrial flutter, and atrial fibrillation.

PREMATURE ATRIAL COMPLEXES

PATHOPHYSIOLOGY.   A premature atrial complex (PAC), or atrial premature complex (APC), occurs when atrial tissue becomes irritable, and this ectopic focus fires an impulse before the next sinus impulse is due, thus usurping the sinus pacemaker.

The premature P wave from the atrial focus is early and has a shape different from that of the P wave generated from the sinus node. The pre­mature P wave may not always be clearly visible, since it can be hidden in the preceding T wave. The T wave must be closely examined for any change in shape and compared with other T waves to reveal a hidden P wave. A PAC is usually followed by a pause.

ETIOLOGY. The causes of atrial irritability include stress; fatigue; anxiety; inflammation; infection; intake of caffeine, nicotine, or alcohol; and the administration of drugs such as catecholamines, sympathomimetics, amphetamines, digitalis, or anesthetic agents. PACs may also result from myocardial isch­emia, hypermetaboric states, electrolyte imbalance, or atrial stretch, as may occur with congestive heart failure, valvular dis­ease, and pulmonary hypertension with cor pulmonale.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. The client is usually asymptomatic, except for possi­ble heart palpitations, because PACs usually have no hemodynamic consequences.

INTERVENTIONS. No intervention is usually needed ex­cept to treat the cause, such as heart failure or valvular dis­ease. If PACs occur frequently, they may signal the onset of more serious atrial tachydysrhythmias and therefore may war­rant treatment. The nurse administers prescribed type IA antidysrhythmics, such as quinidine and procainamide (Pronestyl), or other drugs such as digitalis and propranolol (Inderal, Apo-Propranolol). Measures to reduce stress are also initiated, and the client is taught to avoid substances known to increase atrial irritability.

SUPRAVENTRICULAR TACHYCARDIA

PATHOPHYSIOLOGY.  

Supraventricular  tachycardia (SVT) involves the rapid stimulation of atrial tissue at a rate of 100 to 280 beats/min, with a mean of 170 beats/min in adults and 200 to 300 beats/min in children. SVT is most often due to a re-entry mechanism in which one impulse circulates repeatedly throughout the atrial pathway, restimulating the atrial tissue at a rapid rate. The term parox­ysmal supraventricular tachycardia (PSVT) is used when the rhythm is intermittent, initiated suddenly by a prematurcomplex such as a PAC, and terminated suddenly with or without intervention.

During SVT the P waves have a shape different from that of sinus P waves. The P waves may not be visible, especially if there is a 1:1 conduction with rapid rates, because the P waves are obscured in the preceding T wave.

ETIOLOGY. The causes of SVT are the same as those for PACs. SVT may occur in healthy young people without evi­dence of heart disease, usually women under 40 years of age. The condition commonly occurs in clients with a pre-excitation syndrome, such as Wolff-Parkinson-White (WPW) syndrome.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. The clinical manifestations depend on the duration of the SVT and the rate of the ventricular response. In clients with a sustained rapid ventricular response, the nurse assesses for palpitations, weakness, fatigue, shortness of breath, ner­vousness, anxiety, hypotension, and syncope. Hemodynamic deterioration may occur in the client with cardiac disease, causing angina, heart failure, and shock. With a nonsustained or slower ventricular response, the client may be asympto­matic except for transient palpitations.

INTERVENTIONS. If SVT occurs in a healthy person and terminates spontaneously, no intervention is necessary other than eliminating identified causative factors. If it is recurrent, the client should be studied in the electrophysiology labora­tory. The preferred treatment for recurrent SVT is radiofre-quency catheter ablation. In sustained SVT with a rapid ven­tricular response, the goals of treatment are to decrease the ventricular response, convert the dysrhythmia to a sinus rhythm, and treat the cause. Vagal stimulation (e.g., carotid massage) may be successful, but often only transiently, and must be performed only by a physician.

The nurse administers oxygen and prescribed antidysrhythmic drugs, which slow the ventricular rate by increasing the AV block (Chart 34-3). Some may also succeed in con­verting the dysrhythmia.

In the severely compromised client, the nurse may assist the physician in attempting atrial overdrive pacing or in de­livering a synchronized electrical shock (cardioversion) to re­establish an organized rhythm and regain cardiac stability.

 

 

ATRIAL FLUTTER

PATHOPHYSIOLOGY. Atrial flutter is rapid atrial depo­larization occurring at a rate of 250 to 350 times per minute. The most common rate is approximately 300 times per minute. An atrioventricular (AV) node blocks the number of impulses that reach the ventricles as a protective mechanism.

 When untreated, atrial flutter results in a 2:1 block.

 In general, when the ventricular rate is 150 beats/min, the nurse should suspect atrial flutter with 2:1 block and carefully scrutinize the electrocardiographic (ECG) baseline for evidence of atrial flutter waves

ETIOLOGY. Atrial flutter may be caused by rheumatic or ischemic heart disease, congestive heart failure, AV valve dis­ease, pre-excitation syndromes, septal defects, pulmonary emboli, thyrotoxicosis, alcoholism, or pericarditis. The dysrhythmia commonly occurs after cardiac surgery.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. The clinical manifestations depend on the rate of ventricular response. The nurse assesses the client for palpita­tions, weakness, fatigue, shortness of breath, nervousness, anxiety, syncope, angina, and evidence of heart failure and shock. Carotid sinus massage transiently decreases the ven­tricular rate to facilitate rhythm interpretation but can be per­formed only by the physician. The client with a normal ven­tricular rate is usually asymptomatic.

INTERVENTIONS. The treatment goals are the same as those for supraventricular tachycardia (SVT). The nurse admin­isters oxygen and prescribed drugs such as ibutilide (Covert), amiodarone (Cordarone), diltiazem (Cardizem), and verapamil (Calan, Isoptin) to slow the rapid ventricular response. Quini-dine or procainamide (Pronestyl) must not be administered un­less one of the above agents has slowed the ventricular response. Both drugs slow the atrial rate and may increase AV conduction, which could cause a 1:1 conduction with an increase in ventric­ular rate and hemodynamic deterioration.

The nurse helps the physician to attempt rapid atrial over­drive pacing or to achieve cardioversion if the client is hemodynamically compromised. If he or she fails to respond to these therapies, radiofrequency catheter ablation may be necessary

 

ATRIAL FIBRILLATION

PATHOPHYSIOLOGY. Atrial fibrillation (AF) is the most common dysrhythmia in the United States. Long-range epi-demiologic studies, such as the Framingham Heart Study, show a dramatic incidence of AF in the aging population. In fact, the incidence of AF increases more than 20 times between middle age (55 to 64 years of age) and older adulthood (85 to 94 years of age). It is estimated that millions of cases of intermittent or sustained AF occur each year in the United States. AF causes increased morbidity and mor­tality among those who experience it (Resnick, 1999).

 

Multiple, rapid impulses from many atrial foci, at a rate of 350 to 600 times per minute, depolarize the atria in a totally disorganized manner. The result is chaos, with no P waves, no atrial contractions, loss of the atrial kick, and an irregular ven­tricular response. The atria merely quiver in fibrillation (commonly called “A fib”), which may lead to the formation of mural thrombi (within the cardiac chambers) and potential embolic events.

ETIOLOGY. AF occurs most commonly in clients with systemic hypertension and is frequently seen in older adults (Resnick, 1999). It may also occur in clients with the follow­ing conditions:

•  Myocardial infarction

•  Rheumatic heart disease with mitral stenosis  Atrial septal defect

•  Congestive heart failure

•  Cardiomyopathy

•  Hyperthyroidism

•  Pulmonary emboli

•  Wolff-Parkinson-White (WPW) syndrome

•  Congenital heart disease

•  Chronic constrictive pericarditis

AF commonly occurs following cardiac surgery, in which case it is most often transient and usually responds well to treatment.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. AF may be intermittent or chronic. Symptoms de­pend on the ventricular rate. If the ventricular rate is rapid, the presenting symptoms may be as described for supraventricular tachycardia (SVT). Because of loss of the atrial kick, how­ever, the client in uncontrolled AF is at greater risk for an in­adequate cardiac output.

The nurse assesses the client for the presence of a pulse deficit, fatigue, weakness, shortness of breath, distended neck veins, dizziness, decreased exercise tolerance, anxiety, syncope, palpitations, chest discomfort or pain, and hypotension.

The client is also at risk for pulmonary embolism. Thrombi may accumulate within the right atrium and be transported through the right ventricle to the lungs. The nurse should as­sess for shortness of breath, chest pain, hemoptysis, and a feeling of impending doom.

In addition, the client is at risk for systemic emboli, par­ticularly an embolic stroke, which may cause severe neuro­logic impairment or death. Because approximately one third of clients with AF have thromboemboli, the nurse must be as­tute in assessing the client for evidence of embolic events. Changes in mentation, speech, sensory function, and motor function are particularly noted. The nurse also assesses pulses, urine output, back pain, and complaints of gastroin­testinal (GI) disturbances. Any of these symptoms should be reported to the health care provider immediately. Clients with AF who have valvular disease are particularly at risk for thromboemboli.

INTERVENTIONS. Treatment is the same as for atrial flutter. In addition, the nurse may administer anticoagu­lants, such as heparin, enoxaparin (Lovenox), and sodium warfarin, as prescribed by the physician for clients consid­ered to be at high risk for emboli. Before elective cardioversion, the nurse must initiate anticoagulation therapy for 4 to 5 weeks as prescribed to prevent a thromboembolic event if the rhythm is successfully converted. To assess for the presence of atrial clots, a contraindication for cardioversion in the compromised client, the physician may order a transesophageal echocardiogram (TEE) before at tempting emergency cardioversion. AF of greater than 12 months duration is not likely to respond to attempts at con­version to sinus rhythm by drug therapies and may fail to respond to cardioversion.

A class III antiarrhythmic, dofetilide (Tikosyn) is indicated for the conversion of AF and atrial flutter to normal sinus rhythm (NSR). It also is indicated for the maintenance of NSR in clients with AF/atrial flutter of more than 1 weeks’ duration who have been converted to NSR. Because it can prolong the QT interval, causing Torsades de Pointes, the client must be hospitalized for telemetry monitoring for at least 3 days during the initiation of therapy. In addition to car­diac rhythm and QT interval monitoring, the dose of Tikosyn must be adjusted to creatine clearance levels.

Clients with recurring, symptomatic AF resistant to med­ical therapies may be treated with radiofrequency catheter ab­lation to the His bundle to interrupt all conduction between the atria and the ventricles. However, this requires implanta­tion of a permanent ventricular pacemaker and does not stop the atria from fibrillating. The atrial kick is not restored, and clients remain at risk for embolic events.

Clients may benefit from the “maze” procedure, an open heart surgical technique. In this procedure the nurse first pre­pares the client for electrophysiologic mapping studies for confirmation of the diagnosis of AF. The nurse then prepares him or her for surgery. The surgeon places a maze of sutures in strategic places in the atrial myocardium to prevent electri­cal circuits from developing and perpetuating AF. Sinus im­pulses can then depolarize the atria before reaching the AV node and preserve the atrial kick.

■ JUNCTIONAL DYSRHYTHMIAS

Nodal cells in the atrioventricular (AV) junctional area can generate electrical impulses and are therefore secondary or latent pacemaker cells. They have a slower rate of discharge, usually 40 to 60 beats/min, and are usually suppressed. Occasionally, these cells do generate impulses as an escape pacemaker when the sinus node is excessively slow, or the cells may do so inappropriately as irritable rhythms. These rhythms are most commonly transient, and clients usually remain hemodynamically stable.

 

■ VENTRICULAR DYSRHYTHMIAS

The ventricles have the fewest number of nodal cells and are the slowest secondary pacemaker, generally being usurped by faster, higher pacemakers. However, irritable ventricular cells may generate electrical impulses and fire prematurely. Be­cause the impulse originates in and depolarizes one ventricle first, then spreads to depolarize the other, the resultant QRS complex is wide, usually measuring greater than 0.12 second. The QRS complex is bizarre or odd in shape, looking differ­ent from the normal QRS complexes. The repolarization se­quence is also different, so that the T wave is large and occurs in a direction opposite to the largest deflection of the QRS complex. The impulse most commonly is blocked in the AV node and cannot proceed further with retrograde conduction, so that the atria and the sinoatrial (SA) node are usually not affected by the ventricular impulse. The atrial rhythm typi­cally remains regular, unless the underlying rhythm is sinus arrhythmia.

IDIOVENTRICULAR    RHYTHM    (VENTRICULAR ESCAPE RHYTHM)

PATHOPHYSIOLOGY. During idioventricular rhythm (ventricular escape rhythm), the ventricular nodal cells pace the ventricles. Because their inherent rate of firing is slow, the rate is usually less than 40 beats/min (Figure 34-13). If P waves are seen, they are independent of the QRS complexes and not related (AV dissociation).

ETIOLOGY. Idioventricular rhythm is seen as a rhythm in the dying heart, where downward displacement of the pace­maker has occurred. It is sometimes referred to as an “agonal” rhythm. Pulseless electrical activity (PEA) is characterized by no palpable pulse and therefore no perfusion, although electrical activity is displayed on the monitor. The most common causes of PEA are hypovolemia, hypoxia, and cardiac tamponade.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. Because idioventricular pacemakers are unstable, un­reliable, and slow, the client is hypotensive and in shock or, most typically, is pulseless and therefore in cardiac arrest. The nurse assesses the client’s airway, breathing, circulation, level of consciousness, and pupillary response.

INTERVENTIONS. Usually, idioventricular rhythms re­quire immediate resuscitation measures, unless there is a donot-resuscitate (DNR) order. The nurse initiates cardiopul-monary resuscitation (CPR) and summons assistance. The team may initiate advanced cardiac life support (ACLS) meas­ures, including epinephrine administration, intravascular vol­ume replacement, and other measures. The physician may at­tempt pacemaker therapy or discontinue resuscitation efforts.

PREMATURE VENTRICULAR COMPLEXES

PATHOPHYSIOLOGY. Premature ventricular complexes (PVCs), also called ventricular premature beats (VPBs), result from increased irritability of ventricular cells. PVCs are early ventricular complexes, followed by a pause. When multiple PVCs are present, the QRS complexes may be unifocal or uni­form, meaning that they are of the same shape

 or multifocal or multiform, meaning that they are of differ­ent shapes.

 PVCs frequently occur in repeti­tive rhythms, such as bigeminy, trigeminy, and quadrigeminy. Two sequential PVCs are a pair, or couplet. Three or more suc­cessive PVCs are usually called nonsustained ventricular tachy­cardia (NSVT)

ETIOLOGY. PVCs are common, and their frequency in­creases with age. PVCs may be insignificant or may occur with myocardial ischemia or infarction, congestive heart fail­ure, chronic hypoxemia, chronic airway limitation (CAL), anemia, hypokalemia, or hypomagnesemia. The administra­tion of catecholamines, sympathomimetic drugs, and digi­talis, as well as acidosis, anesthesia, stress, nicotine intake, ingestion of caffeine and alcohol, infection, trauma, or surgery, can also cause PVCs.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. The client may be asymptomatic or may experience palpitations or chest discomfort caused by increased stroke volume of the normal beat after the pause. Peripheral pulses may be diminished or absent with the PVCs themselves be­cause the decreased stroke volume of the premature beats may decrease peripheral perfusion. Since other rhythms also cause widened QRS complexes, it is essential that the nurse assess whether the premature complexes perfuse. This is done by palpating the carotid, brachial, or femoral arteries while ob­serving the monitor for widened complexes, or auscultating for the apical heart sounds. With acute myocardial infarction, PVCs may be considered warning dysrhythmias, possibly heralding the onset of ventricular tachycardia (VT) or ventricular fibrillation (VF). For a client with chest discomfort or pain, the nurse reports to the physician whether PVCs in­crease in frequency, are multiform, are R-on-T phenomena, or occur in runs of VT.

INTERVENTIONS. If there is no underlying heart disease, PVCs are not usually treated other than by eliminating any contributing cause (e.g., caffeine, stress). With acute myocardial ischemia or infarction, the nurse treats significant PVCs by administering oxygen and lidocaine as prescribed. The nurse may administer other drugs as ordered, including pro-cainamide (Pronestyl), bretylium (Bretylol, Bretylate), mag­nesium sulfate, propranolol (Inderal, Apo-Propranolol), quinidine, and mexiletine (Mexitil). Potas­sium is administered as ordered for replacement therapy if hy-pokalemia is the cause.

VENTRICULAR TACHYCARDIA

PATHOPHYSIOLOGY.

Ventricular tachycardia (VT), sometimes referred to as “V tach,” occurs with repetitive fir­ing of an irritable ventricular ectopic focus, usually at a rate of 140 to 180 beats/min or more. VT may re­sult from increased automaticity or a re-entry mechanism. VT may be intermittent, as in three or more self-limiting beats (nonsustained VT), or sustained, lasting longer than 15 to 30 seconds. The sinus node continues to discharge independ­ently, depolarizing the atria but not the ventricles (atrioven-tricular [AV] dissociation), although P waves are seldom seen in sustained VT.

ETIOLOGY. VT may occur in clients with ischemic heart disease, myocardial infarction, cardiomyopathy, hypokalemia, hypomagnesemia, valvular heart disease, heart failure, drug toxicity, hypotension, or ventricular aneurysm. In clients who go into cardiac arrest, VT is commonly the initial rhythm be­fore deterioration into ventricular fibrillation (VF) as the ter­minal rhythm. VT is not common in infants and children un­less they have cardiac disease.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. Clinical manifestations of sustained VT partially de­pend on the ventricular rate. Slower rates are better tolerated. Clients may be hemodynamically compromised if the cardiac output decreases because of the shortened ventricular filling time and loss of the atrial kick. In some clients, VT causes car­diac arrest. The nurse assesses the client’s airway, breathing, circulation, level of consciousness, and pupillary response.

INTERVENTIONS. For the stable client with sustained VT, the nurse administers oxygen and confirms the rhythm via a 12-lead electrocardiogram (ECG). Amiodarone, procainamide, or magnesium sulfate may be given. Lidocaine, a long-established antidysrhythmic, has not been recommended for prophylaxis of ventricular dysrhythmias in acute myocar­dial infarction. Current advanced cardiac life support (ACLS) guidelines state that elective cardioversion is highly recom­mended for stable VT. Bretylium has been dropped from ACLS algorithms because of a severe shortage of the world’s natural sources of bretylium.

The physician may prescribe an oral antidysrhythmic agent, such as procainamide (Procan SR), mexiletine (Mexitil), or sotalol (Betapace, Sotacor).

For the client with unstable VT, the nurse assists the physi­cian in attempting emergency cardioversion followed by oxy­gen and antidysrhythmic therapy. The nurse may instruct the client to perform cough cardiopulmonary resusci­tation (CPR) if prescribed, telling him or her to inhale deeply and cough hard every 1 to 3 seconds. Cough CPR is some­times successful in either terminating the VT or at least briefly sustaining cerebral and coronary perfusion until other measures can be initiated. The physician may attempt rapid atrial or ventricular overdrive pacing if the VT is related to a significant bradydysrhythmia.

A precordial thump is sometimes successful in terminating VT, at least transiently. The physician or the ACLS-qualified nurse may administer a precordial thump to a client with un­stable VT only if a defibrillator and pacemaker are immedi­ately available.

With pulseless VT, the physician or ACLS-qualified nurse or other health care provider must immediately defibrillate the client or initiate CPR and defibrillate as soon as possible. A precordial thump may be administered initially, although it is frequently not successful in terminating VT. If the client re­mains pulseless, the nurse or other health care provider must resume CPR and full resuscitative measures following defib­rillation. This includes airway management and administra­tion of oxygen, epinephrine, and antidysrhythmic therapy with amiodarone, magnesium sulfate, and procainamide.

If the rhythm has been successfully converted, attention is given to treating reversible causes of VT, such as myocardial ischemia, hypokalemia, and hypomagnesemia. The nurse en­sures that oxygen therapy and antidysrhythmic agent admin­istration are continued, and the client is closely monitored for premature ventricular complexes (PVCs) and the recurrence of VT. The client with recurrent, medically refractory VT should be studied in the electrophysiology laboratory and may benefit from radiofrequency catheter ablation. Some forms of VT may require surgical intervention, such as coro­nary artery bypass graft (CABG) surgery, implantation of a cardioverter/defibrillator, aneurysmectomy, encircling endocardial ventriculotomy, cryosurgery, or endocardial resection.

VENTRICULAR FIBRILLATION

PATHOPHYSIOLOGY.   Ventricular  fibrillation  (VF), sometimes called “V fib,” is the result of electrical chaos in the ventricles. Impulses from many irritable foci fire in a to­tally disorganized manner so that ventricular contraction can­not occur. There are no recognizable deflections. Instead, there are irregular undulations of varying amplitudes, from coarse to fine.

The ventricles merely quiver, consuming a tremendous amount of oxygen. There is no car­diac output and therefore no cerebral, myocardial, or systemic perfusion. This rhythm is rapidly fatal if not successfully ter­minated within 3 to 5 minutes.

ETIOLOGY. VF may be the first manifestation of coronary artery disease (CAD). Clients with myocardial infarction are at great risk for VF. VF may also occur in clients with myocardial ischemia, hypokalemia, hypomagnesemia, hemor­rhage, antidysrhythmic therapy, rapid supraventricular tachydysrhythmias, shock, asynchronous pacing with competition, or severe metabolic disease. VF also occurs following surgery or trauma.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. On initiation of VF, the client becomes faint, imme­diately loses consciousness, and becomes pulseless and apneic. There is no blood pressure, and heart sounds are absent. Respiratory and metabolic acidosis develop. Seizures may oc­cur. Within minutes, the pupils become fixed and dilated, and the skin becomes cold and mottled. Death ensues without prompt restoration of an organized rhythm and cardiac output.

INTERVENTIONS. The goals of treatment are to termi­nate VF promptly and convert it to an organized rhythm. The physician or the ACLS nurse or other health care provider must immediately defibrillate the client to accomplish this goal. This is the management priority, and the ACLS algo­rithm for VF must be followed. If a defibrillator is not readily available, a precordial thump may be delivered. CPR must be continued until the defibrillator arrives.

If the VF does not terminate after three rapid successive shocks of increasing energy, the nurse and resuscitation team resume CPR and provide airway management. They also ad­minister oxygen and antidysrhythmic therapy with epineph-rine, amiodarone, procainamide (Pronestyl), lidocaine, and magnesium sulfate, along with attempting defibrillation frequently. If VF is successfully converted to an organized rhythm, the nurse continues supportive therapy and assists the physician in treating potential causes of VF and preventing its recurrence.

 VENTRICULAR ASYSTOLE

PATHOPHYSIOLOGY. Ventricular asystole, sometimes called ventricular standstill, is the complete absence of any ventricular rhythm. There are no electrical impulses in the ventricles and therefore no ventricular depolar­ization, no QRS complex, no contraction, no cardiac output, and no pulse, respirations, or blood pressure. The client is in full cardiac arrest. The sinoatrial (SA) node, in some cases, may continue to fire and depolarize the atria, with only P waves seen on the electrocardiogram (ECG), but the sinus impulses do not conduct to the ventricles, and QRS complexes remain absent.

In most cases, the entire conduction system is electrically silent, with no P waves seen on the ECG. There is only a mildly undulating line on the ECG. Fine ventricular fibrillation (VF) may resemble asystole in some leads. Because treatment of these two rhythms differs significantly, the nurse must assess two ECG leads for an accurate rhythm interpretation.

ETIOLOGY. Ventricular asystole usually results from my-ocardial hypoxia, which may be a consequence of advanced heart failure. It may also be caused by severe hyperkalemia and acidosis. If P waves are seen, asystole is likely because of severe ventricular conduction blocks. Rarely, excessive vagal stimulation may cause asystole.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. Clients are in full cardiac arrest with loss of con­sciousness and absence of pulse, respirations, and blood pres­sure. Ventricular asystole is often unresponsive to resuscitation measures and fatal.

INTERVENTIONS. The goal of treatment is to restore car­diac electrical activity. The nurse or other health care provider initiates CPR immediately and summons assistance. Another ECG lead is assessed to ensure that the rhythm is asystole and not fine VF, which warrants immediate defibrillation. When in doubt, the client should be defibrillated. The nurse and resus­citation team manage the airway and administer oxygen, epi-nephrine, and atropine. The nurse assists the physician with the initiation of noninvasive pacing or invasive transvenous or epicardial pacing, although pacemaker therapy is generally not effective. An isoproterenol infusion may also be tried. The prognosis for clients with asystole is poor.

ATRIOVENTRICULAR BLOCKS

Atrioventricular (AV) blocks exist when supraventricular impulses are excessively delayed or totally blocked in the AV node or intraventricular conduction system. Conduction may be transiently or permanently abnormal for a number of rea­sons. The SA node continues to functioormally, and atrial depolarizations and P waves occur regularly. Because of the conduction dysfunction, ventricular depolarizations and QRS complexes are either delayed or blocked.

There are different degrees of heart blocks, as follows:

•  In first-degree AV block, all sinus impulses eventually reach the ventricles.

•   In second-degree heart block, some sinus impulses reach the ventricles, but others do not because they are blocked.

•  In third-degree heart block (complete heart block), none of the sinus impulses reach the ventricles. The ventricles, therefore, are depolarized by a second, independent pacemaker. AV blocks are differentiated by their PR intervals.

FIRST-DEGREE ATRIOVENTRICULAR BLOCK

PATHOPHYSIOLOGY. First-degree AV block is actually a conduction delay rather than a block. AV node conduction is slow, prolonging the PR interval to greater than 0.20 second. However, all sinus impulses eventually reach the ventricles. The underlying rhythm must still be identified (e.g., sinus rhythm with first-degree AV block).

ETIOLOGY. First-degree AV block may be due to AV nodal ischemia from occlusion of the right coronary artery, as with an inferior or posterior myocardial infarction. It may also result from hypokalemia or hyperkalemia; the administration of digitalis, beta-adrenergic blockers, calcium channel blockers, or narcotics; excessive vagal stimulation; or degenerative AV nodal disease. It may also occur following cardiac surgery as a result of edema in the AV nodal area and usually resolves without treatment.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. First-degree AV block has no hemodynamic conse­quences and produces no symptoms. Any symptoms are the result of the underlying rhythm (e.g., sinus bradycardia). First-degree AV block may be insignificant and transient or may progress to more severe AV blocks.

INTERVENTIONS. In the stable client, no treatment is needed. If the PR interval is particularly long or is getting pro­gressively longer, the nurse must notify the physician. If the first-degree AV block is due to drug therapy, the nurse must withhold the offending drug and notify the physician. When first-degree AV block is associated with symptomatic brady­cardia, oxygen and atropine are administered as prescribed to accelerate AV conduction.

SECOND-DEGREE ATRIOVENTRICULAR BLOCK TYPE I (ATRIOVENTRICULAR WENCKEBACH OR MOBITZ TYPE I)

PATHOPHYSIOLOGY. In second-degree AV block type I, each successive sinus impulse takes a little longer to conduct through the impaired AV node, until one impulse is com­pletely blocked and fails to depolarize the ventricles. This block results in a nonconducted or dropped beat (missing QRS complex). There is progressive prolongation of the PR interval, followed by a dropped beat and a pause (a characteristic feature of this rhythm). The pause allows sufficient time for the AV node to recover so that the next beat is conducted with a shorter PR interval and the Wenckebach sequence is repeated. Although the atrial rhythm is usually regular, the ventricular rhythm is irregular, with an appearance of grouped beats separated by pauses. Group size (conduction ratios) may be constant or may vary. Because of the dropped QRS complex, each group normally has one more P wave than QRS complexes.

ETIOLOGY. The causes of AV Wenckebach block are the same as for first-degree AV block. It is often a transient rhythm and may revert to first-degree AV block or even a normal sinus rhythm (NSR). However, Mobitz I may progress to third-degree or complete heart block. Second-degree AVblock type I is also seen with rheumatic fever and digitalis ad­ministration.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. The client is usually asymptomatic if the frequency of dropped beats and the overall ventricular rate do not de­crease the cardiac output. If the ventricular rate is too slow, decreasing the cardiac output, the client will have symptoms of a symptomatic bradydysrhythmia. This rhythm is usually transient and terminates spontaneously.

INTERVENTIONS. No intervention is required in the sta­ble client, because this rhythm rarely progresses to a more se­vere block. In the symptomatic client, the nurse administers oxygen and atropine as prescribed. If atropine is not successful in speeding AV nodal conduction time and increasing the  heart rate, the nurse initiates pacemaker therapy as ordered  and notifies the physician.

SECOND-DEGREE HEART BLOCK TYPE II (MOBITZ TYPE II)

PATHOPHYSIOLOGY. In Mobitz type II block, the block is actually infranodal, occurring below the His bundle. It in­volves a constant block in one of the bundle branches, resulting in a wide QRS complex in conducted beats and an intermittent block in the other bundle branch, resulting in dropped beats be­cause both bundles are blocked (P waves are not followed by a QRS complex). Because the block is not in the AV node, sinus impulses that conduct to the ventricles always do so with a con­stant PR interval. Impulses may be blocked randomly, making the ventricular rhythm irregular. Alternatively, the impulses may be blocked at regular intervals, such as in 2:1 block, in which case the ventricular rhythm is regular.

ETIOLOGY. Second-degree AV block type II is less com­mon than type I. It may occur in the adult with an anterior wall myocardial infarction because of severe ischemic dam­age to the conduction system. It may also be caused by rheu­matic heart disease or degenerative disease of the conduction system. It is a serious block that may progress suddenly to a third-degree AV block (complete heart block) and an ominous prognosis.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. Symptoms depend on the frequency of dropped beats and the overall ventricular rate. If the cardiac output is inadequate, the client presents with a symptomatic bradydysrhythmia.

INTERVENTIONS. In the asymptomatic client, the nurse may assist the physician in initiating prophylactic pacing to avert the threat of sudden third-degree AV block. If slow ven­tricular rates are present, the nurse administers oxygen and at­ropine as prescribed. Atropine is usually ineffective because it does not reverse the infranodal block. An isoproterenol (Isuprel) infusion may be administered with caution but may be dangerous in adults with ischemic heart disease. Noninvasive (external) or invasive pacing is preferred. A permanent pace­maker may be required with recurrent Mobitz type II block.

THIRD-DEGREE HEART BLOCK (COMPLETE HEART BLOCK)

PATHOPHYSIOLOGY. In third-degree heart block, none of the sinus impulses conduct to the ventricles. The sinoatrial (SA) node is usually the pacemaker for the atria, producing P waves at a normal or even accelerated rate. A separate, independent pacemaker paces the ventricles. Thus AV dissociation exists. If the block is in the AV node, a junctional escape focus paces the ventricles, producing normal QRS complexes at a rate of 40 to 60 beats/min.

 If the block is below the His bundle (infranodal), a ventricular escape focus paces the ven­tricles, producing wide QRS complexes at a rate usually less than 40 beats/min. In either case, the atrial and ventricular rhythms are usually regular but independent of each other, with more P waves than QRS complexes.

Because the P waves and the QRS complexes are totally independent and bear no relationship to each other, the PR in­terval is not constant, which is the most characteristic feature of this rhythm. The ventricular escape pacemaker is the least dependable pacemaker. It may abruptly fail, causing ventric­ular asystole, or it may predispose to irritability in the form of premature ventricular complexes (PVCs), ventricular tachy­cardia (VT), or ventricular fibrillation (VF).

ETIOLOGY. Third-degree heart block in the adult may oc­cur from ischemic injury with coronary artery disease (CAD) or myocardial infarction, degenerative disease of the conduc­tion system, hypoxia, or calcific aortic stenosis. Third-degree heart block may occur with congenital heart disease, the ef­fects of drugs or electrolyte disturbances, or cardiac surgery.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. Clinical manifestations depend on the overall ventric­ular rate and cardiac output. Transient third-degree heart block may be well tolerated, particularly when the block is in the AV node. If the block is infranodal, it may have serious hemodynamic consequences. If cerebral perfusion is inadequate, clients may be confused and lightheaded or may experience episodes of syncope with or without seizures (Stokes-Adams attacks). Inadequate cardiac output may cause myocardial ischemia or infarction, heart failure, or hypotension. Third-degree heart block may predispose to cardiac arrest, causing VT, VF, or asystole. Therefore it is regarded as a dangerous rhythm.

INTERVENTIONS. Third-degree AV block with a junc­tional escape pacemaker is often transient and well tolerated. If the client is symptomatic, the nurse administers oxygen and atropine as prescribed. Clients with third-degree heart block with a ventricular escape pacemaker are frequently sympto­matic. The nurse administers oxygen and assists the physician in initiating pacing to avert the threat of cardiac arrest. At­ropine is usually not successful in infranodal blocks with wide QRS complexes. Cautious use of isoproterenol (Isuprel) infusions may be necessary as a temporary measure while awaiting pacemaker therapy but is dangerous in clients with acute myocardial infarction. Implantation of a permanent pacemaker may be required for clients with recurrent third-degree infranodal block.

 

BUNDLE BRANCH BLOCKS

PATHOPHYSIOLOGY. Bundle branch block is a conduc­tion delay or block within one of the two main bundle branches below the bifurcation of the His bundle. When one bundle branch is blocked, the supraventricular impulse is able to descend only down the unblocked bundle branch and to de­polarize that ventricle. The other ventricle is depolarized af­terward, as the wave of depolarization from the first ventricle proceeds from cell to cell to the other ventricle. Such slow de­polarization prolongs the QRS duration to 0.12 second or longer. The underlying rhythm is usually sinus in origin (e.g., sinus rhythm with bundle branch block).

ETIOLOGY. Bundle branch block may be a temporary or permanent conduction disorder. Right or left bundle branch blocks may occasionally be seen in clients with normal hearts. More commonly, they are seen in clients with cardiovascular disease, such as congenital heart disease, rheumatic heart dis­ease, ventricular hypertrophy, cardiomyopathy, severe aortic stenosis, chronic degenerative disease of the conduction sys­tem, or fibrotic scarring of the conduction system. Transient bundle branch block may be seen with acute conditions such as coronary insufficiency, myocardial infarction, or heart fail­ure; during right-sided heart catheterization; or with rapid supraventricular rates.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTA­TIONS. There are no clinical manifestations specifically re­lated to bundle branch block. The nurse must notify the ­physician when a new bundle branch block develops, especially in the client with an acute myocardial infarction. The conduction disorder may deteriorate to a more significant block requiring pacemaker therapy.

INTERVENTIONS. No interventions are specifically re­lated to bundle branch block. The client is assessed during al­terations in heart rate for symptoms of hemodynamic com­promise, which are reported to the physician. The nurse ensures that the client is resting and has adequate ventilation and oxygenation

 

■ COLLABORATIVE MANAGEMENT

COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

The following are the most commoursing diagnoses for clients with dysrhythmias:

1.Decreased Cardiac Output related to electrical and mechanical dysfunction

2.Ineffective Tissue Perfusion related to decreased cardiac output

ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS

In addition to the commoursing diagnoses, clients with dysrhythmias may have one or more of the following:

•  Impaired Gas Exchange related to altered oxygen supply

•  Ineffective Coping related to fear of death

•  Activity Intolerance related to fatigue from decreased  oxygen supply

•  Self-Care Deficit related to activity intolerance

An additional collaborative problem is Potential for Pul­monary Edema.

Planning and Implementation

DECREASED CARDIAC OUTPUT AND INEFFECTIVE TISSUE PERFUSION

PLANNING: EXPECTED OUTCOMES. The client with dysrhythmias is expected to demonstrate satisfactory cardiac output as evidenced by the following:

•  Normal, regular heart rate

•  No adventitious breath sounds

•  Cognitive status in expected range (IER)

•  Baseline skin color and temperature

•  Blood pressure IER

In addition, the client is expected to perform activities of daily living without dyspnea or excessive fatigue.

INTERVENTIONS. The nurse’s major role is to assess for complications and monitor the client for response to treat­ment. Interventions are specific to the type of dysrhythmia, the cause, the effect it has on cardiac output, and the risk it presents to the client.

CARDIAC CARE. The nurse or assistive nursing personnel monitors the client’s electrocardiographic (ECG) rhythm and/or assesses the client for signs and symptoms associated with dys­rhythmias, such as abnormal pulse rate and rhythm, palpitations, chest pain, syncope, decreased blood pressure, and dyspnea.

The nurse may assess the client’s apical and radial pulses for a full minute for any irregularity, which may occur with premature beats, escape beats, atrial fibrillation (AF), or sec­ond-degree heart blocks. If the apical pulse rate differs from the radial pulse rate, a pulse deficit exists and suggests that not all beats are perfusing.

In a critical care setting, if the client has a pulmonary ar­tery catheter and an arterial line, his or her hemodynamic profile is reviewed to determine the physiologic effects of the dysrhythmia. The nurse must also assess the psychosocial im­pact of dysrhythmias on clients and families and the effec­tiveness of their coping mechanisms.

Assessment of the client’s past and current history is es­sential because dysrhythmias are associated with both acute and chronic disorders and also with medical and surgical ther­apies. The nurse should also review the interpretation of the client’s 12-lead ECG and other ECG diagnostic tests, such as the Holter monitor, event monitor, or signal-averaged ECG.

NONSURGICAL MANAGEMENT. Nonsurgical manage­ment of dysrhythmias includes drug therapy, vagal maneu­vers, temporary pacing, cardioversion, cardiopulmonary re­suscitation (CPR), defibrillation, and catheter ablation.

DRUG THERAPY. Pharmacologic therapy administered for the control of dysrhythmias often includes drugs from one or more classes of antidysrhythmic agents. The Vaughn-Williams classification is commonly used to classify drugs according to their effects on the action poten­tial of cardiac cells. Other drugs also have antidysrhythmic ef­fects but do not fit the Vaughn-Williams classification.

Vaughn-Williams Classification. Class I antidysrhyth-mics are membrane-stabilizing agents, stabilizing phase 4 to decrease automaticity. There are three subclassifications in this group. Type IA drugs moderately slow conduction and prolong repolarization, prolonging the QT interval. These drugs are used to treat or to prevent supraventricular and ven­tricular premature beats and tachydysrhythmias. Examples in­clude  quinidine  sulfate  and procainamide  hydrochloride (Pronestyl). Type IB drugs shorten repolarization. These drugs are used to treat or prevent ventricular premature beats, ventricular tachycardia (VT), and ventricular fibrillation (VF). Examples include lidocaine and mexiletine hydrochlo-ride (Mexitil). Type IC drugs markedly slow conduction and widen the QRS complex. These drugs are used primarily to treat or to prevent recurrent, life-threatening ventricular pre­mature beats, VT, and VF. Examples include flecainide ac­etate (Tambocor) and propafenone hydrochloride (Rythmol).

Class II antidysrhythmics control dysrhythmias associated with excessive beta-adrenergic stimulation by competing for receptor sites and thereby decreasing heart rate and conduc­tion velocity. Beta-adrenergic blocking agents, such as pro-pranolol (Inderal, Apo-Propranolol) and esmolol hy­drochloride (Brevibloc), are class II drugs. They are used to treat or to prevent supraventricular and ventricular premature beats and tachydysrhythmias. Sotalol hydrochloride (Beta-pace, Sotacor) is an antidysrhythmic agent with both non-cardioselective beta-adrenergic blocking effects (class II) and action potential duration prolongation properties (class III). It is an oral agent recommended for the treatment of docu­mented ventricular dysrhythmias, such as VT, that are life threatening.

Class III antidysrhythmics lengthen the absolute refractory period and prolong repolarization and the action potential du­ration of ischemic cells. They decrease the disparity with nor­mal cells to prevent a re-entry response. Class III drugs include bretylium (Bretylol, Bretylate^O, amiodarone (Cordarone), and ibutilide (Covert) and are used to treat or prevent ventric­ular premature beats, VT, and VF.

Class IV antidysrhythmics impede the flow of calcium into the cell during depolarization, thereby depressing automaticity of the sinoatrial (SA) and atrioventricular (AV) nodes, de­creasing the heart rate, and prolonging the AV nodal refrac­tory period and conduction. Calcium channel blockers, such as verapamil hydrochloride (Calan, Isoptin^O and diltiazem hydrochloride (Cardizem), are class IV drugs. They are used to treat supraventricular tachycardia (SVT), atrial flutter, and atrial fibrillation (AF) to slow down the ventricular response.

Other Antidysrhythmic Drugs. Other drugs, such as digoxin, atropine, adenosine, and magnesium sulfate, are fre­quently used to treat dysrhythmias. Digoxin (Lanoxin, Novodigoxin) increases vagal tone, slowing AV nodal con­duction. It is useful in treating supraventricular tachydys­rhythmias, particularly chronic AF, by controlling the rate of ventricular response. Atropine is a parasympatholytic or vagolytic agent. It is used to treat vagally induced sympto­matic bradydysrhythmias. Adenosine is an endogenous nucle-oside that slows AV nodal conduction to interrupt re-entry pathways. It is effective in terminating paroxysmal SVT, a re­entrant tachydysrhythmia. Magnesium sulfate is an elec­trolyte administered to treat refractory VT or VF because these clients may be hypomagnesemic, with increased ven­tricular irritability.

Emergency Cardiac Drugs. In addition to antidys­rhythmics, several other drugs are used during cardiac arrest. Epinephrine (Adrenalin) is a first-line agent in all cardiac arrests. It is given predominantly for its alpha-adrenergic effects to increase vasomotor tone for myocardial and cerebral perfusion. Its beta-adrenergic effects may stim­ulate the heart and increase myocardial contractility to im­prove cardiac output. Dopamine hydrochloride (Intropin) isgenerally used for its beta-adrenergic effects after cardiac ar­rest but may be used for its alpha-adrenergic effects during resuscitation. Dobutamine hydrochloride (Dobutrex) is a beta-adrenergic agent used to improve myocardial contractil­ity and increase cardiac output.

Norepinephrine (Levophed) or phenylephrine hydrochlo­ride (Neo-Synephrine) may be used for its alpha-adrenergic ef­fects to increase vasomotor tone and increase perfusion pres­sure. Sodium bicarbonate is administered during cardiac arrest for clients who are hyperkalemic. It may also be used, if nec­essary, to treat a bicarbonate metabolic acidosis, as occurs in diabetic ketoacidosis or tricyclic antidepressant overdose. Iso-proterenol (Isuprel) is indicated to increase the heart rate in heart transplant clients, but pacing is preferred. Calcium chlo­ride, which increases myocardial contractility, is also rarely in­dicated. It is reserved for clients with hyperkalemia, hypocal-cemia, or calcium channel blocker toxicity because it may cause cell damage and cerebrovascular vasospasm.

 

VAGAL MANEUVERS. Vagal maneuvers induce vagal stimulation of the cardiac conduction system, specifically the SA and AV nodes. Vagal maneuvers are used to terminate supraventricular tachydysrhythmias. They include carotid si­nus massage and Valsalva maneuvers.

Carotid Sinus Massage. The physician massages over one carotid artery for a few seconds, observing for a change in cardiac rhythm. Massaging the carotid sinus causes vagal stimulation, slowing SA nodal and AV nodal conduction. The nurse prepares the client for this procedure, instructs him or her to turn the head slightly away from the side to be mas­saged, and observes the cardiac monitor for a change in rhythm. An electrocardiographic (ECG) rhythm strip is recorded before, during, and after the procedure. The nurse then assesses vital signs and the level of consciousness. Com­plications include bradydysrhythmias, asystole, VF, and cere­bral damage. Because of these risks, carotid massage is not commonly performed. A defibrillator and resuscitative equip­ment must be immediately available during the procedure.

Valsalva Maneuvers. To stimulate a vagal reflex, the health care provider instructs the client to bear down as if straining to have a bowel movement or induces the gag reflex. The nurse prepares the client for the procedure; assesses the heart rate, heart rhythm, and blood pressure; observes the car­diac monitor; and records an ECG rhythm strip before, dur­ing, and after the procedure to determine the effect of therapy. If gagging is induced and the client vomits, the nurse provides an emesis basin and oral hygiene and takes measures to pre­vent aspiration.

Unintended vagal stimulation may sometimes occur, and the nurse must be cautious when performing procedures that may inadvertently cause vagal stimulation. For example, tracheal suctioning, enema administration, and rectal tempera­ture checks can stimulate the vagus nerve and decrease the heart rate inappropriately. The nurse administers stool soften­ers as prescribed. The client is instructed not to strain during bowel movements and to avoid constipation through proper diet and exercise. He or she is also told to avoid inducing gag­ging during oral hygiene, which triggers a vagal response. The heart rate and rhythm of a client who is vomiting is mon­itored because a vagal reflex can result. Some clients experi­ence a vagal response when raising their arms above their head and must be instructed to avoid this movement

TEMPORARY PACING. Temporary pacing is a nonsurgical intervention that provides a timed electrical stimulus to the heart when either the impulse initiation or the intrinsic conduc­tion system of the heart is defective. The electrical stimulus then spreads throughout the heart to depolarize the cells, which should be followed by contraction and cardiac output. Electri­cal stimuli may be delivered to the right atrium or right ventri­cle (single-chamber pacemakers) or to both (dual-chamber pacemakers).

When a pacing stimulus is delivered to the heart, a spike (or pacemaker artifact) is seen on the monitor or ECG strip. The spike should be followed by evidence of depolarization (i.e., a P wave, indicating atrial depolarization, or a QRS com­plex, indicating ventricular depolarization). This pattern is re­ferred to as capture, indicating that the pacemaker success­fully depolarized, or captured, the chamber.

Temporary pacing is generally initiated in clients with symptomatic, atropine-refractory bradydysrhythmias, partic­ularly second-degree heart block type II and third-degree heart block, or in clients with asystole. Temporary pacing may also be initiated prophylactically in hemodynamically stable clients with left bundle branch block in certain situations, such as insertion of a pulmonary artery catheter.

A different type of pacing may be used to terminate symp­tomatic tachydysrhythmias. Occasionally, atrial overdrive pac­ing is attempted to terminate atrial tachydysrhythmias, such as atrial flutter or atrial fibrillation (AF). Overdrive pacing is ac­complished by rapidly pacing the atrium to capture the heart and control depolarization, followed by no pacing, in the hope that the sinus node will regain control of the heart. Ventricular overdrive pacing may be done to terminate ventricular tachy­dysrhythmias in much the same way. Overdrive pacing is usu­ally performed by the physician or the physician’s assistant. The nurse must have emergency equipment available in case the client becomes more unstable or goes into cardiac arrest.

Modes of Pacing. There are two basic modes of pacing: synchronous (demand) pacing and asynchronous (fixed-rate) pacing.

Synchronous (Demand) Pacing. Temporary pacing is most commonly done in the demand mode. The pacemaker’s sensitivity is set to sense the client’s own beats. When the client’s intrinsic rate is above the rate set on the pulse generator, the pacemaker is inhibited from firing. When the client’s rate is below that set on the generator, the pacemaker fires electrical impulses to stimulate depolarization

.

Asynchronous (Fixed-Rate) Pacing. The asynchronous mode is used when the client is asystolic or profoundly bradycardic, as may occur after open heart surgery. When the pulse generator is set in an asynchronous mode, it does not sense any intrinsic beats of the client. The pacemaker continues to fire at a fixed rate as set on the generator, regardless of the intrinsic rhythm. This continued firing is not a problem as long as the client remains asystolic or has a rate slower than the pacemaker rate, because all beats come from the pacemaker and there is no competition from the client’s beats.

 However, if the client’s rate increases and equals or exceeds the pace­maker rate, competition (undersensing) is noted. The danger is that a pacemaker stimulus may reach the heart during the vul­nerable period of repolarization (R-on-T phenomenon, with the pacer spike falling on the T wave) and possibly induce ventric­ular fibrillation (VF). The nurse must observe for pacemaker competition and set the pacemaker to a synchronous mode to avert potential problems.

Universal Pacemaker Code. In 1974 the Intersociety Commission for Heart Disease established a three-position pacemaker code (ICHD code) to standardize the description of pacemaker systems.

This code is used universally and makes it easier to quickly identify the primary functions of the pacemaker. AAI denotes an atrial demand pacemaker. AOO denotes an asynchronous atrial pacemaker. VVI denotes a ventricular demand pace­maker. VOO refers to an asynchronous ventricular pacemaker. DVI denotes a demand AV sequential pacemaker that can pace both chambers but senses only the ventricular chamber. DOO indicates an asynchronous dual-chamber pacemaker. DDD denotes a demand dual-chamber pacemaker that paces and senses both chambers and has a dual mode of response.

The code was expanded to five positions for standardization of multiprogrammable pacemakers and tachydysrhythmia functions, incorporating the original three-position code. This code was designed by the North American Society for Pacing and Eiectrophysioiogy (NASPE) and the British Pacing and Eiectrophysioiogy Group (BPEG). The code is referred to as the NASPE/BPEG generic (or NBG) code (Table 34-3).

There are two basic types of temporary pacing: noninvasive (external) temporary pacing and invasive temporary pacing.

Noninvasive Temporary Pacing. Noninvasive tempo­rary pacing (NTP) is accomplished through the application of two large patch electrodes. The electrodes are attached to an external pulse generator, which can operate on alternating current (AC) or battery power. The generator emits electrical pulses, which are transmitted through the cu­taneous patches and then transcutaneously to stimulate ven­tricular depolarization when the client’s heart rate is slower than the rate set on the pacemaker.

Electrical currents of 60 milliamperes (mA) or more are usually required to achieve ventricular depolarization. The current is applied for 20 to 40 milliseconds (msec), producing a pacing stimulus, or spike, that occupies 0.02 to 0.04 second on the electrocardiographic (ECG) paper.

NTP is used as an emergency measure to provide demand ventricular pacing in a profoundly bradycardic or asystolic client until invasive pacing can be instituted or the client’s in­trinsic rate returns to normal. It may be used prophylactically when performing procedures or transporting clients at risk for bradydysrhythmias. Prophylactic use of NTP may be costly because of the high cost of the external electrodes, and its use should therefore be carefully considered.

Procedure. The nurse explains NTP to the client and pre­pares the equipment. The skin is washed with soap and water To prevent skin abrasion, the skin must not be shaved. The nurse or assistive nursing personnel should not rub the skin or apply alcohol or tinctures on the skin, because electrical cur­rent flows from the patches through the skin and causes dis­comfort. The nurse then applies the large posterior electrode on the client’s back, between the spine and the left scapula, behind the heart. The electrode should not be placed higher over bone because bone is a poor conductor of electrical cur­rent. The anterior electrode is then applied on the chest, be­tween the V₂ and the V₅ positions, over the heart. The elec­trode cannot be placed over female breast tissue. The breast tissue is displaced to position the electrode underneath the breast.

The nurse sets the pacing rate as ordered and establishes the stimulation threshold, the lowest current that achieves capture with each pacing spike followed by a QRS complex. The QRS complex is wide because one ventricle depolarizes first, followed by the other. The electrical current is then set 10% above threshold levels.

The nurse palpates the right radial or carotid pulse and as­sesses the blood pressure using the client’s right arm, ensur­ing that each paced beat is perfused. Vital signs are not taken on the left side of the body because they may not be accurate, particularly if a high milliamperage is used.

Complications. Three complications may arise with NTP. The first is discomfort from cutaneous and muscle stimulation and skin irritation, as well as diaphoresis from the patch elec­trodes. The nurse ensures that the electrodes are in good con­tact with the skin and in the best location to achieve the low­est threshold for consistent capture. Analgesics or sedatives are given as prescribed to provide comfort.

The second problem is loss of capture, which occurs when the pacing spike is not followed by a QRS complex capture is regained; however, higher currents cause more discomfort.

The third problem is inappropriate pacing, which occurs when the pacemaker does not sense the client’s intrinsic QRS complex and therefore fires impulses at its preset rate, com­peting with the client’s rhythm. The nurse must assess elec­trode contact and the effect of the client’s position on pace­maker function. The client may need to avoid lying on the left side. If diaphoresis has caused poor contact and the electrodes must be replaced, the nurse must first turn the pacing function off to avoid receiving electrical shocks when touching the gel side of the electrodes.

Invasive Temporary Pacing. An invasive temporary pacemaker system consists of an external, battery-operated pulse generator and pacing electrodes, or lead wires. These wires attach to the generator on one end and are in contact with the heart on the other end. Electrical pulses, or stimuli, are emitted from the negative terminal of the generator, flow through a lead wire, and stimulate the cardiac cells to depo­larize. The current seeks ground by returning through the other lead wire to the positive terminal of the generator, thus completing a circuitous route. The intensity of electrical cur­rent is set by selecting the appropriate current output, meas­ured in milliamperes.

The client does not usually feel invasive pacemaker stim­uli; however, clients occasionally feel an uncomfortable sen­sation from the stimuli if strong electrical currents (high mil­liamperage) are delivered by the pacemaker. The discomfort may be alleviated by decreasing the current if possible.

The two types of invasive temporary pacing are transvenous pacing and epicardial pacing

Transvenous Pacing. Transvenous ventricular pacing in­volves the use of fluoroscopy to thread a sterile catheter, containing two lead wires, percutaneously through a vein to the right ventricle for temporary pacing. The catheter elec­trode tip (negative electrode) is in contact with the endocardial surface of the ventricle, where it fixates for stability.

 

 The positive electrode is located just proximal to the tip of the catheter. The bifurcated external end of the catheter is attached to the negative and positive terminals of a battery-operated pulse generator. The genera­tor provides the electrical current needed to stimulate the myocardial cells to depolarize. Some clients with a dysfunctional sinus node but an intact AV node may require only temporary atrial pacing.

 If the client needs the atrial kick from atrial con­tractions, a temporary dual-chamber pacemaker is used, with one catheter tip in the right atrium and the other in the right ventricle. This preserves the normal timing of atrial contraction preceding ventricular contraction.

Nursing management of the client after temporary transvenous pacemaker insertion includes continuous ECG monitor­ing, frequent assessment of vital signs and the pacemaker in­sertion site, restriction of the client’s movement to prevent lead wire displacement, and documentation of pacemaker set­tings. The qualified nurse or other health care provider must assess stimulation and sensitivity thresholds according to in­stitutional protocols.

Epicardial Pacing. Epicardial pacing is accomplished with separate lead wires loosely threaded on the epicardial surface of the heart after cardiac surgery. The other ends of the wires exit through the chest wall. They attach to the negative and positive terminals of a pulse generator. The electrical current flows from epicardium to endocardium, from right to left.

Complications. Complications of invasive temporary pac­ing may be serious and include the following:

•  Infection or hematoma at the pacemaker wire insertion  site

•  Ectopic complexes (usually premature ventricular com­plexes [PVCs]), caused by irritability from the pacing  wire in the ventricle, use of high current, or undersensing with pacemaker competition

•  Loss of capture, noted by the presence of a pacing stim­  ulus or spike but no QRS complex

•  Undersensing or pacemaker competition, noted when  pacing stimuli occur at a fixed rate in the presence of an  adequate intrinsic rhythm

•  Oversensing, noted when the pacemaker fails to fire in  the presence of an inadequate intrinsic rhythm

•  Electromagnetic interference, noted by altered generator  variables

•  Stimulation of the chest wall or diaphragm, noted by  rhythmic contraction of the chest wall muscles or hic­  cups with use of high current or from lead wire perfora­tion, which could cause cardiac tamponade

 Prevention of Microshock. When the metal external ends of lead wires are not attached to a pulse generator, the nurse must insulate the wire ends to prevent microshock. The fingertips of rubber gloves work well for this purpose, and the wire ends may then be looped and covered with nonconductive tape. All electrical equipment in the room must be prop­erly grounded, using a three-pronged plug. The nurse must re­port faulty electrical equipment, such as frayed or broken electrical wires, to the biomedical engineering department. Neither the client nor the bed should be in contact with such equipment. The risk is that ungrounded electrical current may conduct through the lead wire, stimulate the heart, and induce ventricular fibrillation (VF).

CARDIOVERSION. Cardioversion is a synchronized countershock that may be performed in emergencies for hemodynamically unstable ventricular or supraventricular tachydysrhythmias or electively for stable tachydysrhythmias that are resistant to medical therapies. If the client has been taking digitalis, the nurse withholds the drug for up to 48 hours preceding an elective cardioversion, as ordered. Digi­talis increases ventricular irritability and puts the client at risk for VF after the countershock.

The shock depolarizes a critical mass of myocardium si­multaneously during intrinsic depolarization. The shock is in­tended to stop the re-entry circuit and allow the sinus node to regain control of the heart. The physician and skilled person­nel must be in attendance during this procedure, with emer­gency equipment at hand. The physician explains the proce­dure to the client and assists him or her in signing a consent form unless the procedure is an emergency for a life-threaten­ing dysrhythmia. Because the client is usually conscious, the nurse administers IV sedation as ordered. An anesthesiologist may administer a short-acting anesthetic agent.

The defibrillator should be in the synchronized mode. This avoids discharging the shock during the vulnerable period (T wave), which may increase ventricular irritability, causing VF. The nurse charges the defibrillator to the energy ordered by the physician, usually starting at 50 to 100 Joules. The nurse en­sures that the oxygen delivery device has been removed and turned away from the client. Oxygen supports combustion, and a fire may result if there is arcing from the paddles. Arcing is usually due to improper paddle contact on the chest. At least 25 pounds of pressure should be applied to each paddle to pre­vent arcing. The nurse then loudly and clearly commands all personnel to clear contact with the client and the bed, as re­quired for electrical safety. The nurse ensures compliance of all personnel before delivering the shock. While the client is exhaling, both paddles are discharged simultaneously to de­liver the shock at end-expiration, when the heart is closer to the chest wall, so that more current flow can reach the heart for a better chance of success. This procedure may be performed by a qualified nurse, physician’s assistant, paramedic, or other qualified health care provider following medical protocols.

After cardioversion, the nurse assesses the client’s re­sponse and heart rhythm. Therapy is repeated as ordered, if necessary, until the desired result is obtained or alternative therapies are considered. If the client goes into VF after car­dioversion, the nurse must ensure that the synchronizer is turned off and then immediately defibrillate the client.

Nursing care after cardioversion includes the following:

§  Maintaining a patent airway

§  Administering oxygen

§  Assessing vital signs and the level of consciousness

§  Administering antidysrhythmic drug therapy

§  Monitoring for dysrhythmias

§  Assessing for chest burns from paddle edges that may not have been on the conductive pad

§  Providing emotional support

§  Documenting the results of cardioversion

 

CARDIOPULMONARY RESUSCITATION. Management of the client in cardiac arrest depends on prompt recognition and therapeutic interventions for successful reversal of a po­tentially fatal event.

When cardiac arrest occurs, cardiac output ceases. The un­derlying rhythm is usually ventricular tachycardia (VT), ven­tricular fibrillation (VF), or asystole. In rare instances, cardiac arrest occurs in the presence of an organized electrocardiographic (ECG) rhythm, but with no effectual mechanical re­sponse, a condition referred to as pulseless electrical activity (PEA). Without cardiac output, the client is pulseless and be­comes unconscious because of inadequate cerebral perfusion. Shortly after cardiac arrest, respiratory arrest occurs.

Cardiopulmonary resuscitation (CPR) must be initiated immediately to help prevent brain damage and death. The nurse, finding an unresponsive client, calls 911 or notifies the emergency response team before initiating CPR. The initial priorities are as follows:

•  Maintenance of a patent airway

•  Ventilation with a mouth-to-mask device 

•  Chest compressions

As soon as help arrives, a board is placed under the client who is not on a firm surface. To make room for the resuscita­tion team and the crash cart, the nurse commands that the area be cleared of movable items and unnecessary personnel.

Complications of CPR include rib fractures, fracture of the sternum, costochondral separation, lacerations of the liver and spleen, pneumothorax, hemothorax, cardiac tamponade, lung contusions, and fat emboli. The goal of resuscitation is the rapid return of a pulse, blood pressure, and consciousness. This is rarely achieved by CPR and basic measures alone. More definitive therapy must be initiated as soon as possible with advanced cardiac life support (ACLS) measures, includ­ing defibrillation, if warranted.

The goal is to be able to give a defibrillatory shock within 5 minutes of collapse outside of a hospital, and within 3 min­utes in a hospital. To help meet this goal, automated external defibrillators (AEDs) should be placed where there is a prob­ability of at least one sudden cardiac arrest every 5 years, such as on airplanes.

ADVANCED CARDIAC LIFE SUPPORT. When the crash cart arrives, the nurse applies ECG electrodes to the client’s chest and turns on the monitor, directing the team to continue CPR. If the client is found to be in VF or pulseless VT, the immediate priority is to defibrillate. Following defibrillation, CPR is resumed. An oropharyngeal airway is inserted to fa­cilitate proper ventilation. A manual resuscitation bag (MRB) with mask is attached to an oxygen flowmeter set at 10 to 15 L/min. The nurse directs that the person managing the airway now ventilate the lungs with the MRB, maintaining the proper head-tilt, chin-lift position of the client. Nurses initiate two large-bore IV lines if the client does not have any, infusing normal saline. These lines provide access for emergency drug administration. Suction equipment is also set up, with a tonsillar suction tube for suctioning vomitus and a suctioncatheter for endotracheal suctioning. Carotid or femoral pulse checks during chest compressions and without chest com­pressions, blood pressure measurements, and pupil assess­ments are done at frequent intervals. A nurse documents all assessments and findings, therapeutic measures, and the client’s responses throughout the resuscitation.

Additional measures include endotracheal intubation with ventilation and oxygenation, IV administration of emergency cardiac drugs, and occasionally, external pacing. Chest com­pressions are continued as long as the client remains pulseless or until a physician decides to terminate resuscitation attempts.

DEFIBRILLATION. Defibrillation, an asynchronous countershock, depolarizes a critical mass of myocardium simulta­neously to stop the re-entry circuit and to allow the sinus node to regain control of the heart. Early defibrillation is critical to terminate pulseless VT or VF. It must not be delayed for any reason after the equipment and skilled personnel are present. The earlier defibrillation is performed, the greater the chance of survival.

If a defibrillator is not immediately available, an ACLS-qualified nurse may deliver a precordial thump to a pulseless client in VF. There is a slight chance that it may succeed in terminating the VF. A precordial thump is performed by strik­ing the lower half of the sternum with a closed fist from a height of 8 to 12 inches (12 to 30 cm) above the sternum. If the client remains in VF, CPR is resumed and the nurse pre­pares the client’s chest for defibrillation. The nurse loudly and clearly commands all personnel to clear contact with the client and the bed and ensures their compliance before deliv­ering the shock.

AUTOMATIC EXTERNAL DEFIBRILLATION. The Amer­ican Heart Association promotes the use of automatic external defibrillators (AEDs) for use by laypersons and health care providers responding to cardiac arrest emergencies. The client in cardiac arrest must be on a firm, dry surface. The rescuer places two large adhesive patch electrodes on the client’s chest in the same positions as for defibrillator paddles. The rescuer stops CPR and commands anyone present to move away, ensuring that no one is touching the client. This meas­ure eliminates motion artifact when the machine analyzes the rhythm. The rescuer presses the “analyze” button on the ma­chine. After rhythm analysis, which may take up to 30 sec­onds, the machine either advises that a shock is necessary or advises that a shock is not indicated. Shocks are recom­mended for pulseless VF or VT only.

After issuing a command to clear all contact with the client, the rescuer charges the defibrillator and presses both discharge buttons on the machine simultaneously, delivering the first shock at 200 Joules. The shock is delivered through the patches, so it is hands-off defibrillation, which is safer for the rescuer. The rescuer then presses the analyze button again, repeating the sequence. With sustained VF or VT, two more shocks may be delivered, with the third at 360 Joules. If the client remains in cardiac arrest, CPR is performed for 1 minute, and then another series of three shocks may be deliv­ered, each at 360 Joules. It is imperative that ACLS be pro­vided as soon as possible. Use of automatic external defibril­lators (AEDs) results in earlier defibrillation of clients and therefore a greater chance of successful rhythm conversion and survival

RADIOFREQUENCY CATHETER ABLATION. Radiofrequency catheter ablation is an invasive procedure that may be used to abolish an irritable focus causing a supraventricular or ventricular tachydysrhythmia. The client must undergo electrophysiologic studies and mapping procedures to locate the focus. Then radiofrequency waves are delivered to abolish the irritable focus. When ablation is performed in the AV nodal or His bundle area, damage may also occur to the normal con­duction system, causing heart blocks and requiring implanta­tion of a permanent pacemaker.

SURGICAL MANAGEMENT. Clients who experience life-threatening dysrhythmias may require surgical treatment for long-term management. The type of treatment depends on the nature of the dysrhythmia. Procedures include permanent pacing, coronary artery bypass grafting, aneurysmectomy, in­sertion of an implantable cardioverter/defibrillator, and open-chest cardiac massage.

PERMANENT PACING. Permanent pacemaker insertion is performed for the resolution of conduction disorders that are not temporary, including complete heart block and sick si­nus syndrome. Permanent pacemakers are usually powered by a lithium battery and have an average life span of 10 years. After the battery power is depleted, the generator must be re­placed, a procedure done with the client under local anesthe­sia. Some pacemakers are nuclear powered and have a life span of 20 years or longer. Other pacemakers can be recharged externally.

Types of Pacemakers. Pacemakers may have a single chamber or dual chambers. With single-chamber pacemakers, a lead wire is positioned in the chamber to be paced, most commonly the right ventricle. Occasionally it is positioned in the right atrium for bradydysrhythmias originating from sinoatrial (SA) node disease with an intact atrioventricular (AV) conduction system.

Dual-chamber pacemakers have lead wires placed in the right atrium and the right ventricle for a more physiologic ef­fect, preserving the atrial kick. A programmed AV interval, which closely relates to the PR interval, ensures a ventricular response shortly after atrial depolarization.

 The DDD pacemaker is commonly implanted. It is able to sense both atrial and ventricular intrinsic activity and pace both the atrium and the ventricle. It allows sinus control of the ventricular rate to meet increased metabolic demands when the sinus node is functioning well. If the client’s sinus rate drops below the lower rate set, the generator paces both the atrium and the ventricle.

Another feature of many pacemakers is rate responsive­ness. To allow faster pacing rates to meet increased body de­mands, the generator changes the pacing rate in response to a detected change in a physiologic variable, such as muscle movement within the client with impaired sinus or atrial func­tion. Hysteresis, on the other hand, is a feature that allows the client’s rate to slow to 10 to 20 beats lower than the genera­tor’s preset rate before the generator paces the client. The slower pace allows for a more normal physiologic slowing re­sponse during rest or sleep.

Surgical Procedures. For both single-chamber and dual-chamber pacemakers, the surgeon most commonly im­plants the pulse generator in a surgically made subcuta­neous pocket at the shoulder in the right or left subclavicular area. The leads are introduced transvenously via the cephalic or the subclavian vein to the endocardium on the right side of the heart. After the procedure, the nurse mon­itors the client’s electrocardiographic (ECG) rhythm to en­sure that the pacemaker is functioning correctly. The im­plantation site is assessed for evidence of bleeding, swelling, redness, tenderness, or infection. The dressing over the site should remain clean and dry, and the client should be afebrile and have stable vital signs. The physician orders activity restrictions to enhance lead fixation. After 24 hours, activity is gradually increased. Complications of permanent pacemakers are similar to those for temporary invasive pacing.

Pacemaker checks are done on an ambulatory care basis at regular intervals. Reprogramming may be warranted if there are pacemaker problems. The pulse generator is interrogated using an electronic device to determine the pacemaker set­tings and battery life.

For clients who live far from the pacemaker clinic or physician’s office, pacemaker information can be sent via transtelephonic transmission of data. The client attaches ECG electrodes to the wrists and places the telephone receiver in a transmitting unit. The sound signals are relayed via telephone lines to the clinic or office, where they are converted and recorded as the client’s ECG rhythm strip and information about the pacemaker variables. The nurse stresses the need to keep clinic appointments for more detailed pacemaker checks and reprogramming, if necessary, as well as assessment.

CORONARY ARTERY BYPASS GRAFTING. Coronary artery bypass grafting (CABG) is performed if the cause of the dysrhythmia is coronary artery insufficiency that is unre­sponsive to medical therapy.

ANEURYSMECTOMY. Ventricular aneurysms are a com­plication of myocardial infarction and may be the source of in­tractable ventricular tachydysrhythmias. The surgeon resects the aneurysm, a dyskinetic or ballooning portion of the ven­tricular wall. Resection of the area eliminates the dangerous ir­ritable focus and thus the cause of the dysrhythmias. Care of the client is similar to that for CABG.

INSERTION OF IMPLANTABLE CARDIOVERTER/ DEFIBRILLATOR. The implantable cardioverter/defibrillator (ICD) is indicated for clients who have experienced one or more episodes of spontaneous sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) unrelated to a myocardial infarc­tion or other causes amenable to correction.

Clients undergo electrophysiologic studies to assess the inducibility of VTs and their response to medication. If the dys­rhythmias can be induced despite medical therapy, the client is considered a candidate for ICD implantation. The nurse collaborates with the physician and the electrophysiology nurse to prepare the client for an ICD. A psychologic profile is done to determine whether the client will be able to cope with the discomfort and fear associated with internal defibrillation from the ICD.

The leads are introduced percutaneously, and the generator is implanted in the left pectoral area, similar to a permanent pacemaker insertion procedure. This procedure is performed in the electrophysiology laboratory.

The electronic pulse generator is designed to monitor and to defibrillate for VT or VF. The generator is powered by a lithium battery and is connected to a transvenous endocardial lead. The ends of the lead are tunneled under the skin to at­tach to the generator. The sensing lead transmits electrical sig­nals from the heart to the generator, which continuously mon­itors the heart rhythm. If the client’s heart rate exceeds the generator’s programmed rate, such as with VT, the generator takes a few seconds to sense the cardiac electrical activity and then delivers a burst of antitachycardial pacing (ATP) to over­drive pace the rhythm. A programmed number of ATP thera­pies may be delivered. If the client’s rate continues to exceed the rate cutoff, the device can deliver a programmed number of low-energy and high-energy cardioversion shocks. In re­sponse to VF, the device delivers defibrillation shocks. Fol­lowing such therapy, the client may develop a transient bradycardia. Many ICD devices are capable of delivering bradycardial pacing (VVI or ventricular demand pacing). This tech­nology is rapidly changing.

If the ICD therapies are not successful and the client re­mains in VF or pulseless VT, the qualified nurse or health care provider must promptly externally defibrillate the client.

The generator may be activated or deactivated by the physician’s placing a magnet over the implantation site for a few moments. The client requires close monitoring in the postimplantation period for the occurrence of dysrhythmias and complications such as bleeding and cardiac tamponade. The nurse must know if the ICD is activated or deactivated. Care of the client is similar to that following implantation of a permanent pacemaker.

OPEN-CHEST CARDIAC MASSAGE. When external chest compressions and advanced cardiac life support meas­ures are unsuccessful in resuscitating a client in cardiac arrest, the physician may decide to perform open-chest cardiac mas­sage through a thoracotomy approach or through the median sternotomy incision in post-cardiac surgery clients. Internal defibrillation may also be performed. Open-chest cardiac massage is usually reserved for the client who goes into car­diac arrest during cardiac surgery, often because of cardiac tamponade. It may also be beneficial but is rarely indicated for hypothermia, crushing or penetrating chest injuries, pene­trating abdominal trauma, or chest deformities prohibiting ex­ternal chest compressions.

Community-Based Care

For many clients, dysrhythmias are a chronic disorder result­ing from chronic cardiac and pulmonary diseases. Clients may be cared for in a variety of settings, including the acute care hospital, subacute unit, traditional nursing home, or their own home. They are admitted to the hospital when they expe­rience life-threatening or potentially life-threatening dys­rhythmias, often associated with an acute disorder. Others can be managed with office or clinic visits or in other settings.

Clients discharged from the hospital may have consider­able needs, often more related to their underlying chronic dis­eases than to their dysrhythmias, which should be essentially controlled by drug or device therapy. A case manager or care coordinator can assess the need for health care resources and coordinate access to services.

HEALTH TEACHING

PREVENTION OF RECURRENCE. Clients who have experienced a dysrhythmia associated with an acute dis­order, such as electrolyte imbalance or ischemia related to a myocardial infarction, are instructed in the prevention, early recognition, and management of that disorder. The nurse teaches the client and family about lifestyle modifications de­signed to prevent, decrease, or control the occurrence of dys­rhythmias, as outlined in Chart 34-7. This teaching may be provided in the acute care setting, physician’s office, health care clinic, or home setting.

DRUG THERAPY. Clients and designated caregivers must have a thorough understanding of the prescribed med­ications, including antidysrhythmic agents. Pharmacies pro­vide written instructions with filled prescriptions. The nurse teaches clients and families the generic and trade names of their drugs, as well as the drugs’ purposes, using basic terms that are easily understood. Clear instructions regarding dosage schedules and common side effects are important. The nurse emphasizes the importance of report­ing these side effects and any dizziness, nausea, vomiting, chest discomfort, or shortness of breath to the health care provider. Chart 34-8 highlights special considerations for older adults receiving antidysrhythmic therapy.

PULSE CHECK. The nurse teaches all clients and their significant others or family members how to take a pulse. The nurse instructs them to report any signs of a change in heart rhythm, such as a significant decrease in pulse rate, a rate greater than 100 beats/min, or increased rhythm irregularity.

 

PACEMAKER. Clients who have a permanent pace­maker are given written and verbal information about the type and settings of their pacemaker. They are taught to report any pulse rate lower than that set on the pacemaker or lower than the hysteresis rate. The nurse also reviews the proper care of the pacemaker insertion site and the importance of reporting any fever or any redness, swelling, or drainage at the pace­maker insertion site. If the surgical incision is near either shoulder, the nurse teaches and demonstrates range-of-motion exercises to perform to prevent shoulder stiffness.

Clients with pacemakers are also instructed to keep hand­held cellular phones at least 6 inches away from the genera­tor, with the handset on the ear opposite the side of the generator. The nurse also teaches them to avoid sources of strong electromagnetic fields, such as magnets and telecommunica­tions transmitters. These may cause interference and could change the pacemaker settings, causing a malfunction. Mag­netic resonance imaging is contraindicated. The nurse in­structs clients to carry a pacemaker identification card and to wear a medical alert bracelet. Chart 34-9 outlines the major points for client and family teaching after the insertion of a permanent pacemaker.

IMPLANTABLE CARDIOVERTER/DEFIBRILLATOR. Clients with an implantable cardioverter/defibrillator (ICD) usually continue to receive antidysrhythmic drugs after discharge from the hospital. The nurse provides clear instruc­tions about the purposes of the medications, the dosage sched­ules, special instructions for taking the medications, and side effects to report. If clients experience an internal defibrillator shock, they must sit or lie down immediately and notify the physician. Some clients describe the experience of a shock as a quick thud or kick in the chest, whereas others relate severe pain similar to that of external defibrillation. The nurse in­forms family members that they may feel an electrical shock if they are touching the client during delivery of the shock but that it is not harmful. Information on how to access the emer­gency medical services (EMS) system in the community is provided. The nurse also recommends resources for the family to learn how to perform cardiopulmonary resuscitation (CPR).

The nurse teaches clients with an ICD to avoid sources of strong electromagnetic fields, such as large electrical genera­tors and radio or television transmitters. These may inhibit tachydysrhythmia detection and therapy or may cause inad­vertent antitachycardial pacing or shocks. Magnetic reso­nance imaging is contraindicated for clients with ICDs. Hand­held cellular phones must be at least 6 inches away from the generator, with the handset held to the ear opposite the side of the ICD. If the pulse generator emits a beeping sound or pro­vides some other indicator, the client must move away from the area as quickly as possible to prevent deactivation of the device. The client with an ICD should carry an ICD identifi­cation card and wear a medical alert bracelet. Chart 34-10 highlights the important points for teaching clients and fam­ily members and significant others.

■   HOME CARE MANAGEMENT

The focus of the home care nurse’s interventions is assessment and health teaching. Clients and families often fear recurrence of a life-threatening dysrhythmia. Clients with an ICD may dread or fear the activation of the ICD. The community-based nurse provides the client and family members with an oppor­tunity to verbalize their concerns and fears. The nurse provides emotional support, as well as information about support groups in the community, and makes appropriate referrals. The client is assessed for possible side effects of antidysrhythmic agents or complications from a pacemaker or ICD.

HEALTH CARE RESOURCES

The cardiac rehabilitatiourse typically provides written and oral information about dysrhythmias, antidysrhythmic drugs, pacemakers, and ICDs, as well as information about cardiac exercise programs, educational programs, and support groups. The office or clinic nurse may also provide information about resources. The nurse instructs the client on how to contact the local affiliate of the American Heart Association or the provincial affiliate of the Heart and Stroke Foundation in Canada for information about dysrhythmias, pacemakers, and CPR training Manufacturers of pacemakers and ICDs provide helpful booklets and videotapes to give clients and their families a better understanding of these therapies. Clients with pace­makers may have transtelephonic systems for transmission of their rhythms to a clinic or health care provider’s office. The nurse teaches clients how to use these systems. The impor­tance of keeping scheduled appointments for office visits with the cardiologist and pacemaker or ICD clinic is stressed. The nurse instructs clients with an ICD to contact the local ambu­lance or paramedic services and emergency facilities to in­form them that they have these devices implanted. The client and family are encouraged to attend pacemaker or ICD sup­port groups.

 Evaluation: Outcomes

 The nurse evaluates the care of the client with dysrhythmias on the basis of the identified nursing diagnoses and collabora­tive problems. The expected outcomes are that the client will:

§  Have vital signs in the expected range (IER)

§  Have cognitive status IER

§  Perform activities of daily living without dyspnea or fatigue

§  Be free of pulmonary edema