ECG

38
Nursing Interpretation of the Electrocardiogram

Kathleen Osborn Annita Watson
CHAPTER
Outcome-Based Learning Objectives

After studying this chapter, the learner will be able to: 1. Describe the configuration of the normal electrocardiogram (ECG). 2. Identify and calculate heart rate, rhythm, PR interval, QRS complex, and QT interval for normal and abnormal cardiac rhythms. 3. Discuss the etiology and significant ECG features of the following dysrhythmia classifications: sinus, atrial, junctional, block, ventricular, and asystole. 4. Interpret the significance of each of the dysrhythmias and formulate nursing responsibilities for each dysrhythmia.
THE ELECTROCARDIOGRAM (ECG) is the most important

and definitive noninvasive diagnostic procedure that shows a graphic depiction of the electrical activity of the heart. It is used to assist the health care team in diagnosing and monitoring cardiac electrical system function. The ECG was first used less than a century ago, in the early 1900s. Initially the equipment was large and cumbersome and had limited use. As equipment improved, ECG bedside monitoring became possible in the 1960s. Today, due to increased patient acuity levels, the use of ECGs has become widespread, moving outside the traditional critical and emergent care settings. Thus, so has the expectation for nurses to have the knowledge and understanding of ECG interpretation. Nurses are expected to read and interpret ECGs when planning, providing, and evaluating patient care (Holtschneider, McBroom, & Patterson, 2006). In order to orient the learner to the cardiac conduction system, this chapter provides a brief overview of the anatomy and electrophysiology of the heart. This review is followed by information on how to obtain the graphic representation of the electrical activity of the heart, the ECG (also referred to as EKG). The equipment and skills needed to obtain an ECG are described. The learner is guided in the necessary steps for interpretation of both normal and abnormal cardiac rhythms. This is followed by a description of the appropriate nursing interventions and evaluation criteria.
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Anatomy of the Heart

Recognition of common cardiac rhythms measured by an electrocardiogram requires a basic understanding of cardiac anatomy and physiology. A complete description of the cardiac anatomy is outlined in Chapter 37 . Knowledge of the cardiac conduction system needed for ECG interpretation is presented here.
Cardiac Conduction System

The heart contains its own cardiac conduction system composed of specialized cell fibers called either nodes or bundles. These fibers enable the heart to generate and transmit action potentials without stimulation from the bodys nervous systems. The hearts conduction system is responsible for the electrical activity that controls each normal heartbeat. The special cells and fibers called nodes or bundles are located beneath the endocardium, or inner lining of the heart, in the cardiac conduction system. These are referred to as the sinoatrial (SA) node, the atrioventricular (AV) node, and the Purkinje network (Figure 381 ). Although the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS) innervate the heart, these external neural impulses are not needed to maintain the cardiac cycle. The pacemaker cells are capable of initiating electrical activity automatically and act as a pacemaker; there-
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Nursing Interpretation of the Electrocardiogram 1075
Intra-Atrial Pathways
The intra-atrial pathways, located in the atria, transport impulses from the SA node to the AV node. There are three pathways: the anterior, middle, and posterior intranodal or intra-atrial pathways, and Bachmann bundle. Bachmann bundle, which is a part of the anterior pathway, is a group of fibers contained in the left atrium. All of the intranodal pathways and Bachmann bundle receive electrical impulses as they exit the SA node, distribute these impulses throughout the atria, and transmit them to the AV node (Beasley, 2003).
SA node
AV node Bundle of His Purkinje fibers Left bundle branch
Atrioventricular (AV) Node and AV Junction

The atrioventricular (AV) node is located on the floor of the right atrium just above the tricuspid valve. Electrical activity at the AV node is delayed approximately 0.05 second to allow for atrial contraction, which increases the amount of blood reaching the ventricles. Atrial contraction, commonly referred to as atrial kick, augments the blood supply going to the ventricles and ultimately cardiac output. This delay also serves to stop the transmission for a very rapid succession of impulses that can occur under abnormal conditions. These abnormalities, called atrial flutter/fibrillation, are discussed later in the chapter. The AV junction contains fibers that can polarize spontaneously, forming an impulse that can spread through the heart chambers. This means that if the SA node fails or falls below its normal range, the AV node can take over, thus assuming the role of a secondary pacemaker. Under normal conditions the AV junction is the only pathway for the conduction of atrial impulses to the ventricles.
Right bundle
FIGURE 381
Electrical conduction system of the heart.
fore, the heart will beat in the absence of any nervous system connection. The SNS and the PSNS affect only the speed of the cardiac cycles and the diameter of the coronary arteries. It is essential to understand the hearts electrical conduction system in order to be able to understand an ECG strip interpretation. Each component of the system follows.
Bundle of His and Bundle Branches

The bundle of His is approximately 15 millimeters long and lies on top of the interventricular septum, between the right and left ventricles. This area, also referred to as the common bundle, contains pacemaker cells that have the ability to self-initiate electrical activity at a rate of 38 to 60 beats per minute. At the top of the interventricular septum, the bundle of His divides into two bundle branches, the right and left bundles. The right bundle, a long, thin structure that lies beneath the endocardium, runs down the right side of the interventricular septum and terminates at the papillary muscles in the right atrium. The left bundle is shorter than the right bundle and divides into pathways that spread from the left side of the interventricular septum throughout the left ventricle. The two pathways of the left bundle branch are called fascicles, one being anterior and the other posterior. The anterior fascicle carries electrical impulses to the anterior wall of the left ventricle. The posterior fascicle spreads electrical impulses to the posterior ventricular wall. The bundle branches continue to divide until they finally terminate in the Purkinje network fibers.
Sinoatrial (SA) Node

The sinoatrial (SA) node is located in the upper posterior portion of the right atrial wall, near the opening of the superior vena cava. The node is made up of hundreds of cells that compose a knot of modified heart muscle. The SA node is capable of generating impulses that travel throughout the muscle fibers of both atria, resulting in atrial depolarization. The SA node is commonly called the primary pacemaker of the heart because under normal conditions it depolarizes more consistently, frequently, and reliably than other normal pacemaker cells. The normal firing rate of the SA node is 60 to 100 beats per minute. Depolarization of the atria occurs as the impulse leaves the SA node and travels in a downward or waterfall fashion through the conduction pathways. If the SA node (pacemaker) fails to fire due to some abnormality, other pacemaker cells are able to take over, that is, the AV node or the Purkinje network. The emergence of a pacemaker that is lower in the heart, which sustains a heart rate when the SA node fails, is referred to as an escape mechanism or rhythm. During an escape rhythm, the heart rate is slower than the dominant pacemaker. If the rhythm originates in the junctional tissue, it is referred to as a junctional escape rhythm. If the rhythm originates in the ventricle, it is referred to as a ventricular escape rhythm.
Purkinje Network Fibers

Purkinje network fibers consist of a network of fibers that carry impulses directly to the ventricles. The rapid spread of the electrical impulse through the left and right bundle branches, the Purkinje network fibers, and the ventricular muscle initiates ventricular contraction. Purkinje fibers also may be pacemaker cells; they fire at an intrinsic rate of 20 to 40 beats per minute.
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Nursing Management of Patients with Cardiovascular Disorders the only mechanical function of the heart. Excitability, conductivity, and automaticity are electrical functions of the heart. Contractility may be thought of as the mechanical coordination of cardiac muscle contractions producing a heartbeat. In addition to these cell characteristics, normal cardiac function is dependent on maintaining electrolyte concentrations inside and outside the cell membrane. Specific electrolytes and their relationship to cardiac function are described next.
Cardiac Cells
There are two basic cardiac cell groups: the myocardial working cells and the specialized pacemaker cells of the electrical conduction system. The atria and the ventricles are constructed of myocardial working cells, which have an abundance of contractile filaments needed to generate cardiac muscle contraction. The cardiac muscle contraction is what actually pumps the blood through and out of the heart into the pulmonic and the systemic circulation. The myocardial working cells have the ability to contract in response to chemical, electrical, or mechanical stimuli. The second type of cardiac cell is the specialized pacemaker cell whose primary function is to generate and conduct electrical impulses (stimuli). These cells found in the heart wall and septum (membrane dividing the right and left sides of the heart) control the heart rate and rhythm by coordinating regular cardiac muscle depolarization (contraction) (see Figure 381 ). The myocardial contractions pump the blood through and out of the heart. The term threshold refers to the point at which an electrical stimulus produces a cell response. When a stimulus is strong enough for cardiac cells to reach this threshold, all of the cells will respond to the stimulus and cause a muscle contraction. This is called the all-or-none phenomenon; in other words, either all the cells respond, or none of the cells respond. This principle allows for a coordinated muscle contraction and greater efficiency in pumping blood. All cardiac cells possess four primary characteristics: automaticity, excitability, conductivity, and contractility. These characteristics are described next.
Electrolytes Affecting Cardiac Function

An electrolyte is a substance or compound whose molecules dissociate into charged components, or ions, when placed in water, producing positively and negatively charged ions. A positively charged ion is called a cation. A negatively charged ion is called an anion. Myocardial cells are bathed in electrolyte solutions; thus, both the mechanical and the electrical cardiac functions are influenced by electrolytes. The major cations that affect cardiac function are potassium (K), sodium (Na), and calcium (Ca). Magnesium (Mg) also is an important cation, but is not as influential as K, Na, and Ca with regard to stimulating the action potential discussed here. Magnesium, potassium, and calcium are intracellular cations, meaning they reside within the cell; whereas Na is an extracellular cation, residing outside the cell. Chloride (Cl) is a major anion in electrocardiac function. Chloride provides electroneutrality in relation to Na. Transport of chloride is passive and follows the active transport of sodium (Na). Abnormally high or low levels of electrolytes, especially K, can potentiate very serious, life-threatening ventricular dysrhythmias. Therefore, monitoring and maintaining normal electrolyte values is essential. Nurses have a responsibility to report immediately any significant abnormal values to the health care practitioner.
Assessing laboratory values is an essential nursing responsibility. Each time laboratory results are completed on a patient the nurse needs to compare the new results with reference normal values and previous findings, if applicable, and report significant changes and/or trends.
Automaticity
Automaticity is the ability of the pacemaker cells to generate their own electrical impulses without depending on nervous system stimulation external to the heart. This spontaneous activity is what produces regular depolarization of the cardiac muscle. This characteristic is specific to only certain pacemaker cell sites within the conduction system. These cell sites are the sinoatrial (SA) node, the atrioventricular (AV) node, and the Purkinje network fibers.
Excitability
Excitability is the ability of the electrical cell to respond to a stimulus. This ability also is referred to as irritability, and all electrical cardiac cells possess this property. When cardiac cells are highly irritable, a cell other than the normal pacemaker may cause a contraction. Cell irritability can be caused by a number of problems, including cardiac muscle ischemia due to hypoxia, or a lack of oxygen. This is the most common cause of cardiac dysrhythmias, the abnormal rhythms of the heart.
Cardiac Depolarization and Repolarization

When impulses travel through the myocardial muscle, they cause changes in the muscle fibers referred to as depolarization and repolarization. Cardiac depolarization refers to cardiac muscle contraction resulting from an electrolyte exchange in the cardiac cells, which then changes the electrical charge. As with all cells of the body, cardiac cells are electrically charged, with the inside of the cell more negative than the outside. To move Na and K across the cell membrane requires active transport by a mechanism referred to as the sodium-potassium adenosine triphosphatase (ATP) pump (Na-K pump). The Na-K pump is an energy-driven mechanism by which 3 Na ions are pumped out for every 2 K ions. Two enzymes, adenosine triphosphate (ATP) and adenosine triphosphatase (ATPase), are involved in the energy production for the pump (Porth, 2004). Prior to depolarization the cells must be in a resting state, referred to as the resting membrane potential. In this state the myocardial cell is negatively charged to 90 millivolts (mV). This negative state is maintained until depolarization occurs.
Conductivity
Conductivity is the ability of the cardiac cell to accept and then transmit a stimulus to other cardiac cells. All cardiac cells share this characteristic, thereby portraying the all-or-none property of the heart muscle; the cardiac cells function as a unit.
Contractility
Contractility is the ability of the cardiac cells to shorten and cause the muscle to contract in response to an electrical stimulus. This ability also is referred to as rhythmicity. Contractility is
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When a muscle cell receives a stimulus due to the Na-K pump exchange, a rapid change occurs in the Cell exterior resting membrane potential, known as the action potential, which is measured in millivolts (a unit of electrical voltage or potential difference equal to one-thousandth of a volt). Once the action potential occurs, the cell moves toward a positive charge. The four phases (04) of the action potential are shown in Figure 382 . Phase 0 is rapid depolarization, phase 1 is rapid repolarization, phase 2 is the plateau, phase 3 is final repolarization, and phase 4 is the resting state. To generate this action potential and the resulting muscle depolarization, the threshold potential must be reached, which is phase 0. To initiate phase 0, Na enters the cell causing a sharp positively charged rise of the intracellular ions. The cell moves from 90 millivolts (mV) in its resting state to a positive Open K channel 15 to 30 millivolts, causing myocardial depolarization to occur. When the threshold is reached, the cell will continue to depolarize with no further stimulation; this phenomenon is referred to as automaticity. During phase 1, the depolarized stage, the interior of the cell has a net positive charge. In this effort to continue to make the inside of the cell more positive, Ca enters; this is phase 2, the plateau phase. During phase 3 the calcium channels close, and Na is pulled from the cell by the Na-K pump; thus the cell is returning to its polarized negative resting membrane potential state (phase 4) (Figure 383 ). The first area of the cardiac muscle to be depolarized is the first area that is repolarized. For example, after the atria depolarize they repolarize while the ventricles are depolarizing. Thus, when the SA node fires again, the muscle will be ready to respond with a new action potential. Cardiac repolarization is the process whereby the depolarized cell is polarized, causing a return to the resting membrane potential (see Figure 382 ). Repolarization also is referred to as the recovery phase that every cardiac cell must go through in order to be ready to accept another stimulus. It is a slower process than that of depolarization. During repolarization the
Na
Cl
Closed Na channels
Closed K channel Cell interior
Anionic protein
FIGURE 383
Electrolyte movement during an action potential.
muscle is refractory (resistant) to stimulation. This refractory period consists of two stages; the absolute and the relative refractory periods. During the absolute refractory period, which is the majority of time for repolarization, the cardiac cell is unable to respond to any stimulus and thus cannot spontaneously depolarize (see Figure 382 ). The relative refractory period is a period when repolarization is almost complete (see Figure 382 ). This period is known as the vulnerable period of cardiac cell repolarization. If a stimulus is strong enough, it can cause depolarization that can be life threatening. These situations are discussed later in this chapter. The refractory periods play a major role in either causing or preventing cardiac dysrhythmias. Further discussion of their role is explained regarding the various dysrhythmias and throughout the chapter.
Summary of the Cardiac Conduction System

ECG Transmembrane potential (mV) 1 0 2 Action potential 0 3
4 100
Na+ ATP K+ Na+ Ca+ K+ K+ K+
Inside cell CELL MEMBRANE Outside cell
FIGURE 382
Action potential.
The electrical impulse begins in the SA node located in the upper right atrium, causing atrial contraction. The impulse then travels through the atria along intra-atrial pathways to the AV node located near the center of the heart. After leaving the AV node the impulse moves down into the bundle of His, through the right and left bundle branches, and into the Purkinje network fibers, causing ventricular contraction followed by repolarization (see Figure 381 , p. 1077). Then the cycle begins again. When caring for patients with actual or potential cardiac conduction abnormalities, it is essential that the nurse understand how the cardiac conduction system described here is graphically depicted on an electrocardiogram. Recognizing and interpreting these electrical impulses and their relationship to heart disease is an essential nursing responsibility. A discussion of how the electrical conduction system is depicted in an ECG follows.
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Nursing Management of Patients with Cardiovascular Disorders diac cycle. Both the absolute and the relative refractory periods are in place during the T wave. U waveThe U wave is present only on some peoples ECG. It follows the T wave. Its etiology is unknown, but it is frequently seen in exercise, in drug toxicity, and most frequently with low potassium levels. Changes in the configuration of the waveforms or lengthening and/or shortening of time intervals may indicate an abnormality in the heart. These abnormalities are discussed in detail in Chapters 40, 41, 42, and 43 . The following sections discuss the method used to evaluate waveforms and time intervals.
Cardiac Waveform and Time Intervals Measured on ECG

When the electrical impulse leaves the SA node, a graphical representation of the signal referred to as a waveform is produced and recorded with monitoring equipment. As the electrical impulse travels through the cardiac conduction system, waveforms characteristic of a given anatomical location are recorded. These waveforms are referred to as P, Q, R, S, and T. Additionally, time intervals, which represent the time it takes for the impulse to travel from one anatomical location in the heart to another, are recorded. These time intervals are called PR, QRS, and QT. One complete cardiac cycle has five to six waveforms and time intervals. These are described here and depicted in Figure 384 . P waveThe P wave represents contraction or depolarization of the atria. Both the right and left atria depolarize at the same time. PR intervalThe PR interval, sometimes referred to as the PRI or PR segment, represents the time it takes for the impulse to travel from the SA node down the intra-atrial pathways to the ventricles. In other words, it represents the beginning of the atrial contraction to the beginning of the ventricular contraction. QRS complexThe QRS complex consists of the Q, R, and S waves, and represents the conduction of electrical impulses from the bundle of His near the AV junction to the Purkinje network fibers located in the ventricles, causing them to depolarize. J pointThe point at which the QRS meets the ST segment is called the J point. ST segmentThe ST segment is a line extending from the S wave that gradually curves upward to the T wave, represented on the ECG as an almost isoelectric line. The ST segment signifies ventricular repolarization. T waveThe T wave is ventricular recovery or repolarization. This is often referred to as the resting phase of the car-
ECG Monitoring Equipment
RA
Depolarization RV Repolarization
Electrocardiography detects cardiac electrical impulses at various points on the surface of the body. The graphical depiction of these impulses, waveforms, and time intervals is obtained either with an electrocardiograph (ECG machine) or on a bedside cardiac monitor. To obtain an ECG tracing, specific equipment is needed including an electrode, lead wire, and monitor or oscilloscope. An electrode is most commonly a round adhesive pad that is impregnated with conducting gel in the center and is attached to a lead wire. Electrodes are sensing devices that detect the electrical activity of the heart and conduct the electrical impulses from the skin surface back to the ECG machine, where they are converted into waveforms. An electrode is much like a camera in that it takes pictures of the electrical activity in the heart. The electrodes are connected to a cardiac monitor by lead wires. Typically, these wires are color coded according to machine manufacturer, and these colors assist the practitioner in attaching the lead wires to the appropriate electrode. The cardiac monitor records the electrical impulses and provides a real-time visual tracing of the waveforms on the screen and/or a printed version on specialized ECG graph paper, described next. The printed version is called a rhythm strip or ECG strip. The rhythm strip gives the health care practitioner information about where the pathological processes are SA node occurring in the heart. Figure 385 shows the elecAV node trodes, lead wire, and cardiac monitor. The term lead is used in different contexts when discussing ECGs. In addition to using the term as just described, as a connector from the electrode to the LA cardiac monitor, the term also is used when discussing a view or picture of the heart from a particular angle or vantage point. In this respect one can think of the lead as the eye of the camera.
LV
Lead Placement
Body tissues and fluids surround the heart; therefore, the electrical action potentials produced in the heart are widely conducted throughout the body via these tissues and fluids. The impulses or action potentials can be detected from any point in the body. Electrodes must be placed in certain positions on the body in order to obtain a clear picture of the electrical impulses in the heart, and there must always be a positive, a negative, and a ground electrode/lead. The ground lead minimizes outside
ST QRS
RBB
LBB
P QRS PR QT
FIGURE 384
Waveform relationship to cardiac conduction system.
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Device
1.00
Channel 0 Chart 2.0 1.5 1.0 Volts 0.5 0 Beats Thresh Limit
# of samples
5300
Sample rate
5000
Set limit
1.00 0.50 1.50
Electrode
Max Peak 1.37 Time
0.00
2.00
-5.0 1.17
Threshold
0.20 0.10 0.00 0.30 0.40 0.50
-1.0
Below limit
Beats/min <92/min 126.20 >180/min
0.31 Chirp output Chirp alarm parameters # Sam 700 amp 1 1.5 f1 0.010 f2 0.70 2.0 1.0 0.0 -1.0 -2.0 0 25 50 75 100 125 150 175 200
Lead wire
Gain Set mode Equalize Push/Reset
FIGURE 385
Electrodes, lead wire, and cardiac monitor.
electrical interference. Each electrode senses the flow of current in the heart in relation to the lead axis. The lead axis refers to the imaginary line drawn between the positive and negative electrodes. If the axis is directed toward the positive lead, there is an upward or positive deflection on the ECG tracing (above the isoelectric line). If the axis is directed toward the negative lead, there is a negative deflection on the ECG tracing (below the isoelectric line) Figure 386 . Multiple leads, as seen with a 12lead ECG, view cardiac electrical conduction from different perspectives. Think of the heart on a pedestal that one is able to move around while a camera takes pictures from various angles. This gives the practitioner 12 different views of the cardiac electrical activity. For bedside monitoring it is not practical or necessary to have a 12-lead ECG or 12 continuous views of the heart. Therefore, 1 or 2 of the 12 possible leads from the entire 12-lead ECG are chosen for constant bedside monitoring because they give a clear view of cardiac activity and abnormalities. To obtain a single bedside ECG rhythm strip, a minimum of three electrodes is required: one positive, one negative, and one ground. Either lead II or modified chest lead1 (MCL1) is commonly used for threeLead II
electrode bedside monitoring. The MCL1 is one of the V leads from the 12-lead ECG that is modified for bedside monitoring. The lead chosen is dependent on the unit policy and nurse and/or health care practitioner preference. The specific dysrhythmia being monitored or anticipated may dictate the type of lead chosen. No single monitoring lead is ideal for every patient. Therefore, if more than one lead or picture of the heart is required, five electrodes are placed to increase the monitors capability beyond the three-electrode monitoring system. The five-electrode monitoring system has an exploring chest electrode that allows one to obtain the same 12 views as a 12-lead ECG when needed. However, at the bedside typically only two simultaneous leads are used to view the heart with the five-electrode system. Commonly the two leads that are run simultaneously are lead II and MCL1. However, the lead or leads chosen depend on the desired view of the heart. Figure 386 shows a cardiac rhythm strip that has simultaneous lead II and MCL1 ECG views. These two leads provide different perspectives of the various normal and abnormal ECG configurations. For example, lead II produces easily identifiable upright P waves and clear QRS
Isoelectric line MCL 1
FIGURE 386
Lead II and MCL1 ECG configurations.
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complexes. An MCL1 lead is useful for evaluating abnormalities in the ventricles. Placement of the electrodes depends on the lead being monitored and whether a three- or five-lead system is being used. Figure 387 shows the position of the electrodes for both lead II and MCL1. The color coding on the lead wire gives the nurse information about whether the lead is positive or negative. Typically the color black is negative, white is positive, and green is ground. In the five-lead system red and brown colors also are used and their polarity changes depending on the lead being monitored (Morton, Fontaine, Hudak, & Gallo, 2005).
CHART 381
Evaluation of: Axis deviation
Indications for a 12-Lead ECG
Cardiac valve disease Chamber dilation or hypertrophy Chest pain/angina Dysrhythmias Effect of cardiac drugs Electrolyte imbalance Hypothermia Myocardial ischemia Myocardial patterns of ischemia, necrosis, and infarction New versus old myocardial infarction Pericarditis Pulmonary embolism Bundle branch block
12-Lead Electrocardiogram (ECG)

The rhythm strips that have been used to demonstrate dysrhythmias throughout this chapter have all been from a single lead. A single-lead ECG rhythm strip gives one view of the electrical activity of the heart, whereas a 12-lead ECG provides 12 individual views or snapshots of the hearts electrical patterns. These added views provide a complete picture of the cardiac electrical system, both top to bottom and front to back. A 12-lead ECG is useful in evaluating not only the presence of damage but also the location in the heart where that damage occurred. Frequently, to assess damage accurately requires viewing the area with more than one lead. Chart 381 provides the indications for a 12-lead ECG. There are 3 bipolar and 9 unipolar leads in a 12-lead ECG. A bipolar lead has electrodes with opposite polarity, one positive and one negative. A unipolar lead has only a positive polarity (Walraven, 2006). Both bipolar and unipolar leads provide information in one direction onlybetween two points. The two
dimensions on the chest in which leads can be placed are the frontal plane (up and down) and the horizontal plane (around the chest). Figure 388 shows the horizontal plane and the frontal plane views. The axis of a lead is the imaginary line drawn between the positive and the negative electrode in a bipolar lead and between the positive electrode and the zero reference point in a unipolar lead. Thus, depending on where a given lead is placed, it provides
Lead II: Positive electrode left abdomen Negative electrode right shoulder Ground electrode left shoulder +
MCL1: Positive electrode 4th ICS RSB Negative electrode left shoulder Ground electrode right shoulder
MCL1 is modified chest lead 1. It's like V1.
FIGURE 387
Electrode placement for bedside cardiac monitoring.
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so named because they generate such small waveforms that the ECG machine must augment, or increase, their size so they will show up on the ECG paper (Ellis, 2002). These leads are aVR, aVL, and aVF. Each lead records the following electrical conduction pattern: aVR: central terminal to right arm aVL: central terminal to left arm aVF: central terminal to left leg. The standard bipolar leads and the augmented limb leads provide the 6 frontal plane leads of the 12-lead ECG, whereas the 6 chest (precordial) unipolar leads, V1V6, evaluate the horizontal plane of the heart. The positive electrode is placed on 6 different sites across the chest as shown in the diagram in Figure 391 (p. 000). These chest leads provide the 6 horizontal leads of the 12-lead ECG. Chart 382 describes the procedure for obtaining a 12-lead ECG. For example, lead V1 evaluates the right ventricle; leads V2 and V3 span the interventricular septum; lead V4 is over the cardiac apex; and leads V5 and V6 evaluate the lateral wall. The Q wave, T wave, and ST segment are used to evaluate the presence of damage, and the lead placement is used to identify the area of damage. Chapter 40 discusses the myocardial damage associated with changes in the Q wave, T wave, and ST segment. When performing an ECG, the nurse must have knowledge of the lead placement for each of the 12 leads. Improper placement may result in inaccurate information and treatment. The electrodes must have firm, unbroken contact with the skin. The limb leads are placed on the flat surfaces just above the wrists and ankles. If there is an amputation, the lead is placed on the remaining stump. Chest hair may interfere with skin contact and, if so, should be shaved. The type and sophistication of ECG machines varies; some can record only one lead at a time, whereas others can record 3, 6, or all 12 leads simultaneously.
Frontal plane
Horizontal plane
FIGURE 388
Horizontal and frontal planes. (need diagram rendered)
a picture of the electrical activity from that vantage point within the heart. Electrical current flowing toward a positive electrode creates a positive deflection on the ECG paper, whereas electrical current flowing toward a negative electrode creates a negative deflection on the ECG paper (Walraven, 2006). The standard bipolar limb leadsI, II, IIIare applied to the right arm (RA), left arm (LA), and left leg (LL). Each lead records the following electrical conduction pattern: Lead I records conduction from RA to LA. Lead II records conduction from RA to LL. Lead III records conduction from LA to LL. The right leg electrode acts as a grounding electrode. Three more frontal plane, unipolar augmented limb leads can be created by using a central terminal. Augmented leads are
CHART 382
12-Lead ECG Procedure

Bring the portable ECG machine to the patients bedside in any type of patient care setting. Use 10 electrodes for the standard 12-lead ECG: 6 on the chest and 4 on the limbs. Figure 391 (p. 000) shows the correct placement of the electrodes. Place limb electrodes away from bony prominences and areas of significant muscle movement to prevent interference of other muscle activity. Palpate the intercostal spaces along the sternal border, until the fourth one is reached, for placement of the first chest electrode.
Electrode Placement
Cable Connection and Machine operation
Connect the cable that is attached to each of the electrodes to the ECG machine. Adjust the ECG machine to obtain a clear picture of the cardiac electrical activity. After completing the ECG, remove electrodes and clean the skin as necessary. Leave the electrodes in place if the patient is going to have serial ECGs to ensure consistency of multiple readings.
Patient Instructions Documentation
Explain the procedure and the rationale for the test prior to performing an ECG. Advise the patient to lie still, breathe normally, and refrain from speaking while obtaining the ECG. Document patients height, weight, and use of cardiac medications. Document current clinical manifestations if present and chief complaint. Document reason for the ECG. Record patients response to procedure, if any.
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Nursing Management of Patients with Cardiovascular Disorders mal activities of daily living. The patient keeps a diary of signs and symptoms and the associated activity performed. Additional information on the Holter monitor is discussed in Chapter 39 . Transtelephonic monitoring is another method of outpatient ECG monitoring. With this type of monitoring, a specific lead system is used for transmitting the signals and is accomplished by having the patient place a telephone mouthpiece over the transmitter box. The ECG is recorded and evaluated at another location. This method often is used as a follow-up evaluation for patients with cardiac pacemakers. Chapter 39 discusses pacemakers.
Each ECG machine has its own method of identifying specific lead names (V1, V2, etc.) and a diagram of where to place them. The nurse must be cognizant when obtaining an ECG about which rhythms require immediate notification of the health care practitioner for emergent treatment. The significance and severity of the individual rhythms are presented under each rhythm discussed throughout the chapter.
Signal Averaged Electrocardiogram

Certain abnormal impulses are conducted during diastole, or when the heart is filling with blood, which is late into the QRS complex and ST segment. These impulses may be present in a patient who has survived an acute myocardial infarction and, if present, can result in ventricular tachycardia and sudden cardiac death. These signals, referred to as late potentials, are low-amplitude, high-frequency spikes that occur at the end of the QRS complex and extend into the ST segment. With the assistance of a computer, a signal averaged ECG is able to distinguish low-level signals not detected by the traditional ECG. Therefore, the risk for lethal dysrhythmias can be assessed. A signal averaged ECG also is used to evaluate His bundle activity, presence of a left ventricular mass, effects of thrombolysis, and surgical repair of congenital heart disease.
Nursing Management of the Monitored Patient

Prior to placing the patient on ECG monitoring, the nurse needs to explain the procedure and why it is necessary. It is essential that the patient understand that the heart is just being monitored, not controlled, by the equipment. Describe the electrodes, where they are placed, and how they are connected to the monitor. Skin preparation, electrode placement, and monitor connection are described in Chart 383. The nurse needs to be knowledgeable about electrode placement for the lead that has been designated for monitoring the patient. Some manufactures have the electrode and the lead wire attached, whereas others produce them separately. The electrode placement should be as comfortable as possible for the patient. Documentation of the lead used needs to be included in the patients record.
Precise lead placement is critical to accurate continuous cardiac monitoring. The nurse must verify lead placement at the beginning of each shift. Once a transient cardiac problem has occurred it is too late to change lead placement so that an accurate analysis can be performed.
Cardiac Monitoring Systems

The purpose of continuous ECG monitoring is to detect new and changing abnormal heart rhythms and to trend data relatively to frequency and duration of dysrhythmias. When continuous ECG monitoring is necessary, it can be accomplished by two methods. First, the patient can be hardwired to a monitor whereby the leads are connected directly from the bedside monitor to the patient. The hardwired system has an oscilloscope at the bedside and in a central location such as the nurses station. This system typically is able to monitor more than one lead simultaneously, and depending on the lead used the system also is able to visualize ST segment depression and elevation. Hardwired systems have the capability to print a rhythm strip and provide visual and audible alarms when abnormalities in the heart rhythm occur. These systems are computerized and therefore are able to interpret and store dysrhythmias in a memory bank. Hardwired monitoring is done in critical care areas. The second method for continuously monitoring patients is with radio waves from a battery-operated transmitter. The transmitter, worn by the patient, transmits the rhythms to a central bank of monitors, which is typically at the nurses station. This system allows the patient to ambulate about the unit while still being monitored. Whichever system is being used, the patient must be informed of its purpose and any necessary precautions. Because it may be stressful and frightening for a patient to have his heart be continuously monitored, patient education is essential. The patient needs to understand that this system does not report clinical manifestations such as angina, dyspnea, or weakness. It is necessary, therefore, that the patient report these conditions as they occur. Another form of continuous ECG monitoring is typically done in the outpatient setting. This system, referred to as a Holter monitor, records the heart electrical activity on a magnetic tape for 24 to 48 hours while the patient goes about nor-
All cardiac monitors have alarm systems built into them to alert the nurse when abnormalities occur. Alarm systems have both a high and a low setting so that the nurse is alerted when the heart rate goes above or below the set parameters. The nurse must ensure at the beginning of the shift that the monitor alarms are on and set with the appropriate parameters established for the patient (see Chart 383). The nurse needs to explain to the patient that these alarms may also go off with excessive movement or if the lead wire falls off. The patient needs to be told the nurse will respond to the alarm each time it goes off and must be reassured that it does not necessarily mean there is a problem with her heart. The nurse must stress that excessive movement will cause the alarm to go off frequently.
When the monitor alarms it is essential that the nurse evaluates the clinical status of the patient prior to any other activities in order to assess for the presence of cardiac abnormalities and the patients clinical response to the abnormalities.
Nursing responsibility for monitored patients includes knowledge of the patients specific rhythm in order to assess for changes. The more familiar the nurse is with the patient and the monitoring system, the quicker problems can be diagnosed
CHAPTER 38
CHART 383
Procedure for Continuous ECG Monitoring

Choose an area to place the electrodes where there are no bony prominences, thick muscles, or skin folds, because these areas are prone to produce noncardiac waveforms and interference. Prepare the skin for electrode placement by making sure that it is clean, dry, and free of hair. It may be necessary to shave the chest area of male patients. Remove dead skin cells to improve electrical conductivity by rubbing the skin with the rough patch on the back of the electrode, a dry washcloth, or a gauze pad. The skin will become reddened with the rubbing; be careful not to cause skin breakdown. Wipe the skin with an alcohol sponge if skin is oily or a moist wipe; allow it to air dry. Make sure that the electrode pads are moistened with conducting gel prior to placing them on the chest to increase electrical conductivity. A dry electrode is not effective for conducting the electrical activity. When the electrode becomes dry or loose, it needs to be replaced. If the skin around the electrode becomes irritated the electrode must be removed and relocated. Position electrodes on the chest wall at prescribed locations depending on the lead or leads being monitored. Change electrodes when wet, poor contact, unclear tracing, and/or every 48 hours to avoid skin irritation.
Electrode Attachment
Lead Wire and Cable Connection
Connect the electrode to the lead wire, which is approximately 16 inches long. Typically a snap attaches the lead wire to the electrode. The lead wires are color coded to represent positive, negative, and ground leads. Attach the opposite end of the lead wire to the cable. The cable has individual color-coded receptacles or holes for each lead wire.
Monitor Connection and Adjustment
Attach the cable to the monitor. Adjust the monitor to increase the size of the PQRST complex for more accurate interpretation. Read the operating instructions for the specific brand of monitor prior to use. Always leave the alarm on. Recognize that the alarms have upper and lower heart rate limits. Set the alarm approximately 20 beats above and below the patients resting intrinsic heart rate. Follow institutional policy, if present, to determine different alarm limits. Be aware that when the alarm sounds, the first nursing responsibility is to check the patient. Recognize that movement by the patient may cause the alarm to sound falsely.
Alarm Setting
Documentation
Document lead used. Document PR interval, QRS width, QT interval, ectopic beats, and type of rhythm/dysrhythmia. Record ECG changes and patients response to changes.
and appropriate action taken. Assessment of patient tolerance of rhythm changes is the first nursing action, prior to assessing for problems with the equipment.
When abnormalities appear on a cardiac rhythm strip it is an essential nursing responsibility to assess the patients tolerance of the rhythm, especially if it is a new abnormality. The nurse needs to be knowledgeable about what changes need to be reported to the health care practitioner. The rhythm needs to be documented on the patients record.
Communication with all personnel caring for the patient and observing the monitor is critical. They must be kept informed of when the patient needs to be off the monitor or of physical activities, such as bathing, occurring that may sound the alarms. For example, if there is a monitor technician, that person must be informed of the patients leaving the floor and increased physical activities.
ECG Graph Paper

ECG graph paper is specialized paper on which the ECG pattern is recorded. The paper is designed to allow the measurement of various calculations related to the electrical activity of the heart. It is standard nursing protocol to measure these calculations when a patient is on a cardiac monitor. These measurements help determine whether the rhythm falls within the time limits of normal cardiac activity. Abnormal measurements may indicate a malfunction of the cardiac conduction system and will be discussed later in conjunction with the various dysrhythmias.
Tolerance to the rhythm is assessed by obtaining and evaluating vital signs, neurological status, and the presence of signs and symptoms of decreased cardiac output, for example, angina. After determining patient status and stability, the nurse then troubleshoots the equipment for problems such as a dry electrode or a disconnected wire. The problem could be as simple as the patients tapping the electrode, and no action would be necessary. It also is essential that the nurse is knowledgeable of which cardiac disturbances are reportable and/or life threatening.
1084 UNIT 8
Nursing Management of Patients with Cardiovascular Disorders dividual and also depends on the ECG lead being used. For example, QRS complexes are mostly positive in the lead II and mostly negative in the MCL1 lead (see Figure 386 ). Not everyone has a discernable Q wave. QT intervalThis is measured from the Q wave to the end of the T wave. The normal QT interval is 0.34 to 0.43 second or 8.5 to 11 boxes. Heart rateThis is measured by using the very top of the ECG paper, which is marked off in 3-second intervals with tick marks. The tick mark is a small straight line or hash mark above the tracing. Count up the number of PQRST complexes that occur in 6 seconds and multiply that number by 10. This method provides a general estimate of the heart rate. A more accurate method for measuring heart rate is to count the number of small squares between two R waves and divide the total into 1,500. The normal HR is 60 to 100 beats per minute. Heart rhythmThis is determined by measuring the distance between two R waves and then measuring each subsequent R wave to ensure it is the same distance apart as the previous ones. With a regular rhythm, the distance between R waves is equal. Calipers (Figure 3810 ) are the instrument used to take all these measurements. Figure 3811 demonstrates where each measurement begins and ends.
The ECG graph paper is arranged as a series of horizontal and vertical lines. This paper is standardized to allow for consistency in ECG measurement and strip analysis. Both the amplitude and the voltage may be measured on the paper. The vertical axis measures the amplitude and is stated in millivolts (mV). Two large squares on this axis equal 1 millivolt. This measurement is rarely used because the size of the picture or millivolts can be adjusted at the monitoring station, thereby reducing the consistency of this measurement. The horizontal axis is divided into small squares. The squares on the ECG paper are used to measure the length of time required for the electrical impulse to traverse a specific part of the heart. Figure 389 shows an example of ECG graph paper. These squares are used to measure time intervals as follows: The smallest square is 1 millimeter (mm) in length and represents 0.04 second in time. The large square is 5 mm in length and represents 0.20 second in time. The large square equals 5 small squares. Five large squares represent 1 second.
ECG Measurements
When assessing either a rhythm strip or a 12-lead ECG, both the individual PQRST complexes need to be evaluated as well as the relationship of each individual complex to the overall rhythm. The assessment of an ECG configuration includes the following: P waveThere should be one P wave for every QRS complex. PR intervalThis is measured from the beginning of the P wave to the beginning of the QRS complex. The normal PR interval is from 0.12 to 0.20 second or 3 small boxes to 1 large box. QRS complexThe QRS complex is measured from the beginning of the Q wave to the end of the S wave. The normal range is from 0.06 to 0.12 second or 1.5 boxes to 3 boxes. The shape of the QRS complex varies from individual to in-
FIGURE 3810
Calipers.
.06.12 sec QRS
PR
QRS QT
0.04 sec 0.20 sec 0.04 sec .12.20 sec
QT .34.43 sec Isoelectric line
FIGURE 389
ECG graph paper
FIGURE 3811
ECG measurement.
CHAPTER 38
FIGURE 3812
Artifact.
Isoelectric Line
The isoelectric line marks the beginning and ending point of all waves. When the SA node fires, the ECG waveform (the actual tracing on the graph paper) begins and moves away from the isoelectric line (see Figure 3812 ). Any wave that has an upward deflection, which is above the isoelectric line, is referred to as a positive deflection, and any waveform that goes below the line is referred to as a negative deflection. Depending on the lead, certain waves normally are positive and certain ones are negative. In a lead II the normal P wave has a positive deflection, the PR interval is isoelectric, the Q wave is the first negative deflection, the R wave is positive, the S wave is negative, the ST segment is isoelectric, and the T wave is positive. CHART 384
P Waves
Stepwise Process for ECG Strip Evaluation

Are the P waves regular? Is there one P wave for every QRS and one QRS for every P wave? Is the P wave in front of the QRS or behind it? Is the P wave normal and upright in lead II? Do all the P waves look alike? Are the abnormal P waves associated with ectopic beats? Are all the PR intervals constant? Is the PR interval measurement within normal range (0.12 to 0.20 second)? If the PR interval varies, is there a pattern to the changing measurements? Are all the QRS complexes of equal duration? What is the measurement of the QRS complex size? Is the QRS complex measurement within normal limits (0.06 to 0.11 second)? Do all the QRS complexes look alike? Are the unusual QRS complexes associated with ectopic beats? What is the length of the QT interval? Is it normal or prolonged? Is the patient on a treatment that prolongs the interval? Atrial: how many P waves in 6 seconds times 10. Ventricular: how many R waves in 6 seconds times 10. A second method is to count the number of large boxes between two R waves and divide by 1500. Both methods work best when the rhythm is normal. What is the heart rate? Is it regular? Is it irregular? Are there any patterns to the irregularity? Are there any ectopic beats; if so, are they early or late? Are they present? What are they? How is the patient tolerating them? Do they require treatment?
PR Interval
Artifact
Artifact is defined as an ECG pattern caused by sources outside the heart creating a false and abnormal pattern on the ECG graph paper. This interference is due to several causes: Malfunction of electrodes possibly due to dry conductive gel, clammy skin, or dense chest hair Patient movement, which precipitates a fluctuating isoelectric line that corrects itself when the patient lies still Improper grounding, which occurs when a patient is in contact with an outside source of electricity, such as poorly grounded beds and/or IV infusion pumps Equipment failures, such as broken wires or cables on the ECG equipment, which need to be exchanged for new equipment. Because of this interference or artifact, the baseline or isoelectric line becomes fuzzy. When artifact is present, it is difficult to diagnose cardiac abnormalities, making it is necessary to correct the cause of the artifact. Figure 3812 depicts artifact.
QRS Complex
QT Interval
Rate
Ectopic Focus
Ectopic focus is a heartbeat originating from a site other than the primary cardiac pacemaker tissue. Ectopic foci may affect cardiac output and must be assessed and documented carefully for their impact on the hemodynamic stability of the patient. The terms dysrhythmia, arrhythmia, and ectopic focus all mean the same thing and are used interchangeably.
Regularity (also called rhythm)
Ectopic Beats
ECG Rhythm Strip Evaluation and Documentation

When evaluating an ECG rhythm strip, using a simple stepwise process provides a consistent method for rhythm strip evaluation. This is shown in Chart 384. If the rhythm strip falls out of the normal parameters, then there is a high probability of an ab-
normality occurring in the conduction system. These abnormalities are discussed at length throughout the remainder of the chapter.
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Nursing Management of Patients with Cardiovascular Disorders ple, change in blood pressure, pulse, level of consciousness, and urine output.
Normal Sinus Rhythm

Normal sinus rhythm (NSR) is a cardiac rhythm initiated from the SA or sinus node that has all the normal waveforms (PQRST) and normal time intervals (PR, QRS, QT) (Figure 3813 ). The following criteria must be present to be NSR: P wave has a normal and consistent shape and appears before every QRS complex. There is a 1:1 ratio of P wave to QRS complex. PR interval is between 0.12 and 0.20 second. QRS complex is between 0.06 and 0.12 second. QT interval is between 0.34 and 0.43 second. Atrial and ventricular rate is between 60 and 100 beats per minute (beats/minute). Atrial and ventricular rhythm is regular.
Dysrhythmias
When the cardiac muscle does not receive enough blood, it becomes ischemic and irritable, causing cardiac dysrhythmias to occur. A dysrhythmia is an abnormal disturbance of the electrical conduction system of the heart. There are a number of dysrhythmias, which originate in different parts of the heart. This chapter addresses dysrhythmias according to location in the heart, beginning at the top with the atrial dysrhythmias. As the dysrhythmias occur anatomically lower in the heart, the severity is greater due to their impact on cardiac output. The cardiac output decreases as the severity of the dysrhythmia increases. Heart rhythms are categorized according to the cardiac structure in which they begin, or their site of origin. The most common dysrhythmias begin at the top of the heart with the SA node. These types of dysrhythmias are called sinus dysrhythmias due to their origin in the SA, or sinus, node. The next area in the heart where dysrhythmias may occur is in the intra-atrial pathways, referred to as atrial dysrhythmias. Moving anatomically down to the next area of the conduction system, the AV node or junction is where junctional dysrhythmias occur. The final area of the heart where dysrhythmias may occur is in the ventricles. These ventricular dysrhythmias are considered to be the most dangerous because they precipitate the most profound decrease in the cardiac output. When observing, assessing, and treating dysrhythmias, it is critical for the nurse to remember that it is the patient being treated, not the dysrhythmia. Treatment is always based on the hemodynamic impact of the dysrhythmia.
Nursing Management
When the patient is on a cardiac monitor, it is the nurses responsibility to measure, assess, and document the patients rhythm strip at least every shift and more frequently depending on the patients condition and agency protocol. Whenever changes occur in the heart rhythm, the nurse must begin the same process again: measure, assess, and document the rhythm strip. The nurse needs to understand when it is appropriate to report a change in the ECG to the health care practitioner.
Nursing Documentation
When documenting the heart rhythm in the patients record, most institutions require that a rhythm strip is attached to the patients chart once every shift and/or when a change in the rhythm occurs. The patients name, the date and time of rhythm strip collection, and the ECG lead used for the rhythm strip should be documented. Additionally, the electrical features of the rhythm should be documented including the presence of a P wave, the PR interval, the width of the QRS complex, the QT interval, the heart rate, and rhythm (regular verses irregular), and the presence of ectopy (ectopic focus). Corresponding clinical manifestations associated with a given rhythm also need to be documented in the record. For exam3 seconds 6 seconds
Sinus Dysrhythmias
The four common dysrhythmias associated with the sinus area of the heart are sinus bradycardia, sinus tachycardia, sinus arrhythmia/dysrhythmia, and sinus arrest.
Sinus Bradycardia
Sinus bradycardia, often called sinus brady, occurs when the SA node is firing at a rate of less than 60 beats per minute. Sinus means the rhythm originated in the SA node; therefore, P waves are present. The only difference between sinus bradycardia and normal sinus rhythm (NSR) is the heart rate, but because of this variable, sinus bradycardia is not normal. Sinus bradycardia may result in decreased cardiac output, because while there is adequate time for the heart to fill up with blood, there are not enough contractions per minute to pump the amount of blood needed for normal cardiac output. Significant slowing of the heart rate predisposes the patient to an ectopic focus assuming the role of pacemaker in order to generate sufficient cardiac output. This condition may lead to serious dysrhythmias and warrants careful monitoring. An ECG strip showing sinus bradycardia is in Figure 3814 .
P Wave: Present 1 P wave/QRS complex; PR Interval: 0.18 second; QRS Complex: 0.06 second; QT Interval 0.36 second; Heart Rate: Atrial: 90 beats per minute (bpm); Ventricular: 90 bpm; Rhythm: Regular, Ectopic Beats: None
FIGURE 3813
Normal sinus rhythm.
CHAPTER 38
6 seconds
Sinus tachycardia results in increased oxygen consumption, increased workload of the heart, and decreased cardiac output. Whenever the heart rate increases, more oxygen is required to nourish the muscle, resulting in increased work of the heart and increased oxygen consumption. Decreased cardiac output occurs when the heart rate is fast enough to lose the period of time needed for blood to enter the heart, referred to as fill time. An ECG strip showing sinus tachycardia is in Figure 3815 (p. 1091). Significant ECG features of sinus tachycardia include: Atrial and ventricular heart rates are over 100 beats per minute. As the sinus rate accelerates, both the PR interval and the QT interval tend to shorten slightly. The rhythm may be slightly irregular as the rate begins to accelerate, but then becomes a rapid regular rhythm. The etiology, physical assessment findings, and treatment for sinus tachycardia are outlined in Chart 385.
P Wave: Present, 1 P wave/QRS Complex; PR Interval: .16 second; QRS Complex: 0.08 second; QT Interval: 0.32 second; Heart Rate: Atrial: 40 bpm; Ventricular: 40 bpm; Rhythm: Regular; Ectopic Beats: None
FIGURE 3814
Sinus bradycardia.
Significant ECG features of sinus bradycardia include: Both atrial and ventricular rates are less than 60 beats per minute. The QT interval tends to lengthen. The etiology, physical assessment findings, and treatment for sinus bradycardia are outlined in Chart 385.
Sinus Arrhythmia/Dysrhythmia
Sinus arrhythmia/dysrhythmia resembles normal sinus rhythm, except for the slight irregularity in the heart rhythm. The rate of impulse formation and conduction varies with the respiratory cycle; thus, the P to P and R to R intervals change with respiration. The heart rate increases during inspiration and decreases with expiration. This dysrhythmia is common in young children and tends to disappear as they grow older (Garcia & Miller, 2004). Additionally, it tends to disappear when the heart increases, for example, with exercise. Typically there is no clinical significance with this dysrhythmia; it is considered a variant of normal. However, the cyclic decreased heart rate may make the heart muscle
Sinus Tachycardia
Sinus tachycardia is defined as a firing of the (SA) node at a rate greater than 100 beats per minute. It is called sinus tachycardia because there is a P wave present, although it may be related to an abnormality of the SA node itself. For example, an acute myocardial infarction (AMI) may cause a decrease in the blood supply to the SA node, resulting in an abnormal response such as tachycardia.
CHART 385
Dysrhythmia Sinus bradycardia
Sinus Dysrhythmias: Etiology, Physical Assessment, and Treatment

Etiology Decreased sympathetic tone, or anatomic changes Hypothermia Drugs, such as morphine, digoxin, verapamil, and some sedatives Toxins Vagal stimulation, as with vomiting or Valsalva maneuver Hypothyroidism Infectious diseases Acidosis Hypovolemia Hypo/hyperkalemia Hypoglycemia Cardiac tamponade Tension pneumothorax Thrombosis: coronary and/or pulmonary Trauma Increased intracranial pressure Normal conditions: sleeping and a wellconditioned athletes heart Physical Assessment Pulse: Less than 60 beats per minute and typically regular. Blood pressure (BP): Lower than usual if for pathological conditions. If cardiac output is decreased, the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath. Altered mental state may be present, although rare. Treatment Treat only if symptomatic. Treatment is typically instituted when syncope and/or alteration in consciousness occurs. If symptomatic, it means there is a significant drop in cardiac output. Attempt to identify and treat the cause. Assess for changes in vital signs. Observe for other dysrhythmias. With poor perfusion, typical treatment includes: Oxygen IV access Drug therapy (atropine) Epinephrine or dopamine Pacemaker evaluation.
(continued)
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CHART 385
Dysrhythmia Sinus tachycardia
Sinus Dysrhythmias: Etiology, Physical Assessment, and TreatmentContinued

Etiology Exercise Smoking Alcohol Caffeine Cocaine Fever Blood loss/anemia Hypovolemia Early sepsis Hypermetabolic state, e.g., burn injury Heart failure Allergic reactions Emotions Anxiety Pain Decreased PSNS Increased SNS stimulation Drug side effect of many over-the-counter cold drugs and drugs used to treat asthma and sinus conditions Compensatory response to a decreased cardiac output Common and normal finding, especially in children and young adults Pathological causes include underlying cardiac disease, such as sick sinus syndrome and myocardial infarction Digoxin Factors that cause heart rate variability including exercise, mental stress, and circadian rhythms Hypoxemia Cardiac muscle ischemia Damage to the SA node Digoxin Aspirin Abnormal potassium levels Myocardial infarction Vagal dominance Hypersensitive carotid sinus reflex, e.g., tight shirt collar Physical Assessment Pulse: Greater than 100 beats per minute. BP: Lower than normal. If cardiac output is decreased, the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath. Altered mental state may be present, although rare. Treatment Treat only if symptomatic. Attempt to identify and treat the cause. Treatment may include: Drug therapy, such as beta-adrenergic blockers, adenosine, diltiazem, and digoxin Carotid massage/vagal maneuvers Cardioversion Anxiety medications Fluid replacement. If causes are identified and managed, generally the rhythm converts back to NSR.
Sinus arrhythmia/ dysrhythmia
Pulse: irregular.
Not treated unless the bradycardic phase causes clinical manifestations described under bradycardia. Atropine for bradycardia. Provide reassurance that this rhythm is not dangerous, but it needs to be evaluated to rule out more serious dysrhythmias.
Sinus arrest
Pulse: irregular. BP: Lower than normal depending on number of pauses per minute. If cardiac output is decreased, the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath. Altered mental state may be present, although rare.
Treat only if patient is symptomatic and/or condition is complicated by other dysrhythmias. Ascertain and treat cause, if possible. Typical treatment may include permanent or temporary artificial pacemaker for repeated episodes, depending on the prognosis, age, and presence of clinical manifestations.
Source: Adapted from American Heart Association. (2006). Handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: Author.
more susceptible to other dysrhythmias. Figure 3816 shows an ECG strip of sinus arrhythmia/dysrhythmia. Significant ECG features of sinus arrhythmia/dysrhythmia include: PR interval may change slightly as the heart rate changes. QT interval changes with the heart rate, becoming longer during the slow phase of the rhythm. Heart rate is 60 to 100 beats per minute; however, the slow phase may drop below 60 beats per minute.
Heart rhythm is regularly irregular, with a variance of more than 0.08 second in the acceleration and deceleration phases. Ectopic beats may occur during the slow phase of the rhythm. The etiology, physical assessment findings, and treatment for sinus arrhythmia/dysrhythmia are outlined in Chart 385.
Sinus Arrest
Sinus arrest is a momentary cessation of sinus impulse formation (SA node failure), causing a pause in the cardiac rhythm
CHAPTER 38
6 seconds
P Wave: Present, 1/QRS Complex; PR Interval: 0.14 second; QRS Complex: 0.08 second; QT Interval: 0.36 second; Heart Rate: Atrial: 140 bpm, Ventricular: 140 bpm; Rhythm: Regular; Ectopic Beats None
FIGURE 3815
Sinus tachycardia.
6 seconds
P Wave: Present 1/QRS Complex; PR Interval: 0.18 second; QRS Complex: 0.08 second; QT Interval: 0.40 second; Heart Rate: Atrial: 80 bpm, Ventricular: 80 bpm; Rhythm: Irregular; Ectopic Beats: None
FIGURE 3816
Sinus arrhythmia/dysrhythmia.
followed by spontaneous resumption of electrical activity. Sinus arrest also is called sinus pause. With a sinus pause there will be an absence of the PQRST complex on the ECG strip and a loss of cardiac output. Figure 3817 shows an ECG strip of sinus arrest (pause). Significant ECG features of sinus arrest include: There is an absence of one entire PQRST complex. QT interval changes with the heart rate, becoming longer during the slow phase of the rhythm. There may be marked bradycardia due to long sinus pauses. Underlying heart rhythm is regular except when the pauses occur. The etiology, physical assessment findings, and treatment for sinus arrest are outlined in Chart 385.
Nursing Management for Sinus Dysrhythmias

The nurse should first evaluate the patients response to and tolerance of any dysrhythmia. Depending on the type of dysrhythmia, the patient may or may not be symptomatic. However, if the abnormal rhythm results in a decreased cardiac output, it is important to assess for the changes outlined on Chart 386 (p. 1092). The psychological impact of having a dysrhythmia also must be addressed. It is frightening to most patients when they experience the clinical manifestations of cardiac dysrhythmias, such as angina, dizziness, syncope, diaphoresis, and disorientation. The nurse should reassure the patient that all appropriate treatment is being provided and offer comfort
Pause
6 seconds
P Wave: Present 1/QRS Complex; PR Interval: 0.20 second; QRS Complex: 0.10 second; QT Interval: 0.40 second; Heart Rate: Atrial: 90 bpm, Ventricular: 90 bpm; Rhythm: Regular except for the pause; Ectopic Beats: None Conclusion: Sinus arrest (pause)
FIGURE 3817
Sinus arrest (pause).
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CHART 386
Clinical Manifestations of Decreased Cardiac Output

Exercise intolerance Dizziness Alteration in consciousness Angina
Premature Atrial Contraction

Premature atrial contraction (PAC) is an ectopic focus in the atria that occurs early, before the next expected SA node impulse, causing depolarization and contraction of the cardiac muscle. This electrical impulse originates outside the SA node. It frequently occurs when the underlying rhythm is normal sinus rhythm (NSR), and the only abnormality is the PAC. When there are more than 5 to 6 PACs per minute, they are termed frequent and have more clinical significance. Whenever beats are premature, there is a loss of the time needed for blood to flow into the heart (fill time), which decreases the amount of blood pumped out of the heart, the cardiac output. Thus, if the beats occur frequently cardiac output is decreased. An increase in the frequency of the dysrhythmia also indicates irritability of the atrial muscle and becomes a cause for concern as it tends to increase the risk for other dysrhythmias occurring. Figure 3818 is a rhythm strip showing premature atrial contractions. Significant ECG features of PACs include: P wave is present and is premature. P wave configuration (shape) may look different because electrical impulses do not come from the SA node. PR interval may be shorter or longer than regular beats. PACs are premature, making the rhythm irregular. P wave after the PAC falls earlier than expected because of the early electrical discharge, which then resets the SA node rhythm, referred to as a noncompensatory pause. Heart rate and rhythm are typically within normal limits, except when the PAC occurs. The etiology, physical assessment findings, and treatment of PACs are outlined in Chart 387.
Lower than usual blood pressure Decreased or increased heart rate Syncope Generalized weakness
Note: Clinical manifestations depend on the degree of decreased cardiac output.
measures. Supply the patient with a quiet environment and treatments to alleviate clinical manifestations. Also provide support by actively listening to the patients concerns and including family in the plan of care. The cause of the dysrhythmia, as outlined in Chart 385 (p. 1089), must be evaluated and corrected, if possible. Typically the patient is treated only if he becomes symptomatic and/or the condition is complicated by other more serious dysrhythmias. When a dysrhythmia occurs, the nurse needs to do an in-depth assessment of the patient to determine the clinical manifestations. A dysrhythmia may not always occur due to an abnormality in the heart, but may be due to a variety of reasons not associated with a cardiac abnormality. For example, pain and anxiety are two noncardiac causes of tachycardia. Therefore, treatment may consist of pain medications or, if the patient is anxious, providing support, such as talking with the patient. If the patient is hemodynamically unstable, the health care practitioner should be notified. Chart 385 outlines the standard treatments for each of the sinus dysrhythmias.
Atrial Dysrhythmias
Atrial dysrhythmias usually result from an irritable focus in the atria that initiates an electrical impulse before the SA node has fired in a normal fashion. Because the electrical impulse does not come from the SA node, the P wave configuration of the ECG is different. However, the QRS complex is normal because the electrical impulse travels down the normal pathway from the AV node through the ventricle. Seven different atrial dysrhythmias are discussed next: premature atrial contraction, atrial flutter, atrial fibrillation, supraventricular tachycardia, Wolff-Parkinson-White syndrome, wandering atrial pacemaker, and sick sinus syndrome.
Atrial Flutter
Atrial flutter is a rapid, regular, atrial rhythm with an atrial rate of 200 to 400 beats per minute (Garcia & Miller, 2004). There is loss of SA node dominance, which is the preferential pacemaker. Only a fraction of the atrial impulses are conducted through the AV node to the ventricle. Most of the atrial beats fall during the AV node refractory period when the cardiac cell is unable to respond to any stimulus, thus preventing conduction of the impulse. This makes the AV node the gatekeeper for the ventricles by prohibiting all of the atrial impulses from reaching the ventricles, thereby limiting ventricular rate. Atrial flutter also causes a decreased cardiac output due to the loss of the atrial kick or
Noncompensatory pause
P Wave: Premature; PR Interval: 0.16 second; QRS Complex: 0.10 second; QT interval: 0.40 second; Heart Rate: Atrial: 70 bpm; Ventricular: 70 bpm; Rhythm: Regular except for premature beats. Ectopic Beat PAC. Conclusion: One premature atrial contraction.
FIGURE 3818
Premature atrial contraction.
CHAPTER 38
CHART 387
Dysrhythmia Premature atrial contraction
Atrial Dysrhythmias: Etiology, Physical Assessment, and Treatment

Etiology Mitral stenosis Mitral valve prolapse Cor pulmonale Underlying cardiovascular disease including ischemia and myocardial infarction Hypoxia Infectious diseases Electrolyte imbalance Increased sympathetic tone Stimulants Drug toxicity, e.g., digoxin Stress Anxiety Coronary atherosclerosis Valvular disease; Cor pulmonale Pulmonary edema Myocardial infarction SA node disease Pulmonary embolism Digitalis toxicity ETOH abuse Postsurgical complication: one of the common dysrhythmias following open heart surgery. On rare occasions it may occur with normal healthy hearts. Acute myocardial infarction Left atrial stretch due to mitral stenosis and mitral regurgitation May be a chronic rhythm associated with heart failure Transient after open-heart surgery Long-standing hypertension Digoxin toxicity Alcohol intake, chronic or acute, moderate to heavy Idiopathic Physical Assessment Pulse: Irregular BP: If frequent PACs, may be decreased. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: May be regular or irregular BP: Lower than normal if cardiac output is decreased. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: Irregular (hallmark feature) BP: Lower than normal If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, depending on the ventricular rate. Pulse: Very fast. BP: Decreased if drop in cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Treatment Observe the frequency of the PACs, and observe for decreased cardiac output (Chart 386). Treat the underlying cause, e.g., stress, anxiety, electrolyte imbalance. Frequent PACs or those that cause sustained tachycardia may require treatment with drugs that prolong atrial refractoriness, such as digoxin, verapamil, or propranolol.
Atrial flutter
Cardioversion is a common intervention. Drug therapy is used to reduce AV conduction: digitalis, propranolol, diltiazem. If a chronic situation the patient may be placed on anticoagulants like warfarin.
Atrial fibrillation
Control the ventricular response, i.e., heart rate. If a rapid ventricular response control with drugs: digoxin is still the drug of choice; betablockers (propranolol) and calcium channel blockers (verapamil, diltiazem). Calcium channel blockers work the fastest, and are the drug of choice when medically unstable. Prevent thromboembolic events with anticoagulant therapy, e.g., warfarin, Cardioversion: Is used if new onset, especially when hemodynamic instability is present. If successful, digoxin is used to prevent reoccurrence. It is necessary to find and treat the cause, e.g., stress, hypokalemia. Vagal maneuvers, i.e., bearing down, coughing, and carotid artery massage. Specific treatment may include: oxygen therapy and cardioversion. Drug therapy: adenosine is used to briefly terminate the rhythm for differential diagnosis. Verapamil is a calcium channel blocker; decreases heart rate. Cardioversion is performed if drug therapy and vagal maneuvers are unsuccessful.
Supraventricular tachycardia includes paroxysmal Atrioventricular node reentry tachycardia AVNRT Atrial tachycardia
Heart disease Rheumatic heart disease Coronary artery disease (CAD) Hypoxia May be precipitated by a premature atrial contraction (PAC) May occur in healthy adults from a variety of causes: Overexertion Stress Excessive use of stimulants Smoking Hypokalemia
(continued)
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CHART 387
Dysrhythmia Wolff-ParkinsonWhite (WPW) syndrome
Atrial Dysrhythmias: Etiology, Physical Assessment, and TreatmentContinued

Etiology Congenital in origin: twice as common in males, and occurs in 0.1 to 0.3% of the general population. Physical Assessment Pulse: Rapid. Frequent episodes of palpitations. BP: May be decreased due to fast heart rate. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: 4060 bpm BP: Lower than normal If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: Bradycardia that alternates with tachycardia, referred to as brady-tachy syndrome. BP: May decrease due to decreased cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Treatment Same as that for supraventricular tachycardia. Radiofrequency ablation to terminate the accessory pathway.
Wandering atrial pacemaker
Frequently seen in normal individuals and is of no consequence. Digoxin toxicity
Treat only if symptomatic. Treatment typically is instituted when syncope and/or alteration in consciousness occurs. Attempt to identify and treat the cause. Administer oxygen. Establish IV access Drug therapy: Atropine Evaluate for transcutaneous or permanent pacemaker depending on impact on cardiac output
Sick sinus syndrome
Coronary artery disease Drugs: Cardiac glycoside, Antihypertensive agents, Calcium channel blockers Frequently, intermittent and unpredictable, may occur in the absence of heart disease Myocardial infarction Inflammatory or degenerative processes
Clinical manifestations and ECG findings determine treatment. Anticoagulants are used because of blood stasis if atrial flutter/fibrillation is present. The only definitive treatment is a permanent pacemaker to replace the SA node.
normal atrial contraction. Atrial kick forces more blood into the ventricle, which augments cardiac output. With atrial flutter the atria are just fluttering instead of contracting, resulting in a decreased cardiac output by as much as 30% (Shade & Wesley, 2007). Additionally, with the loss of the atrial contraction, blood stasis and pooling occur, leading to an increased incidence of clot formation. Finally, due to the rapid atrial rate myocardial oxygen consumption increases, which eventually leads to the development of hypoxia of the myocardial muscle and predisposes the left ventricular to fail. Figure 3819 is a rhythm strip showing atrial flutter. Significant ECG features of atrial flutter include: P waves are not identifiable; instead there are flutter waves (F waves), creating a sawtooth baseline on the ECG strip.
PR intervals are not measurable. QT interval is not measurable because the T waves are buried in the F waves. Atrial and ventricular rhythms typically are regular, but they may be irregular depending on how often the AV node allows impulses to travel to the ventricle. The etiology, physical assessment findings, and treatment of atrial flutter are outlined in Chart 387.
Atrial Fibrillation
Atrial fibrillation, also referred to as atrial fib or a-fib, is a common dysrhythmia. The Evidence-Based Practice box outlines the genetic considerations of atrial fibrillation.
CHAPTER 38
P Wave: None, flutter waves; PR interval: None; QRS Complex: 0.08 second; QT Interval: unable to obtain; Heart Rate: Atrial: about 300 bpm, Ventricular: 90 bpm; Rhythm: Regular; Ectopic Beats: Flutter waves.
FIGURE 3819
Atrial flutter.
It is characterized by a disorganized, very rapid, and irregular atrial rhythm resulting in an irregular ventricular rhythm, the hallmark feature. Rapid or slow ventricular heart rate, referred to as the ventricular response, depends on the rate that the AV node allows impulses to be conducted to the ventricles. The cells in the atria have an increased irritability typically due to cardiac muscle hypoxia, which causes many sites in the atria to become pacemakers and initiate electrical impulses. The firing of these multiple sites causes the atria simply to quiver instead of contracting effectively. Atrial fibrillation causes three significant clinical manifestations: (1) loss of SA node pacemaker dominance, which is the most reliable pacemaker; (2) decreased cardiac output due to loss
of atrial kick; and (3) increased myocardial oxygen consumption. The immediate concern for atrial fibrillation is the ventricular response because it determines cardiac output. A heart rate that is too slow or too fast impacts cardiac output. With the loss of the atrial kick, blood stasis and pooling occur, leading to an increased incidence of clot formation. Therefore, those individuals with atrial fibrillation are at high risk for a cardiovascular accident (CVA) and/or pulmonary emboli. The rapid atrial firing also increases the workload on the heart, eventually causing hypoxia of the myocardial muscle. Long-term hypoxia predisposes to left ventricular failure. Figure 3820 (p. 1096) is a rhythm strip showing atrial fibrillation.
Genetic Considerations Clinical Problem

A conservative estimate of the number of people who are affected by atrial fibrillation (AF) is approximately 2 million. It is the most common dysrhythmia that causes an irregular heart rate, palpitations, unexplained rapid heart rate, and a sensation of missed beats. The incidence of AF increases with age, with less than 1% of the population experiencing it before age 60 years, while it is present in 1 in 10 individuals at age 80 years and over. Elderly white men compose the largest group that is affected by AF. Heart failure Excessive alcohol consumption Previous myocardial infarction Diabetes Rheumatic heart disease Mitral valve disorders such as prolapse, regurgitation, and annular calcification Smoking Caffeine The need for patient/family counseling about the increased risk for the development of AF is necessary along with instructions about the need for medical attention if clinical manifestations described above occur. A major emphasis needs to be placed on increasing public awareness of AF and its many causative factors. Patients with a family history require more frequent and diligent testing. Treatment for AF is outlined on Chart 387 (p. 000).
Research Findings
A new study conducted by the National Heart, Lung, and Blood Institute (2004) assessed the prevalence of AF in individuals who had it in their family history. The study evaluated 2,243 individuals whose parents were in the original Framingham Heart Study. The participants were at least 30 years of age and had no history of AF. Seventy of the subjects developed AF within four years. If individual participants had a history of one parent with AF they were twice as likely to develop the dysrhythmia as subjects who had no family history of AF. If both parents had AF before 75 years of age, the risk tripled. Further research continues to determine which genes are involved and what steps are necessary to enhance early diagnosis and treatment.
Critical Thinking Questions

1. When assessing a patient with new onset atrial fibrillation, what types of questions would assist the nurse to determine if there is a risk for a genetic predisposition? 2. When teaching a newly diagnosed patient how to live with AF, in order of priority what must be included in the teaching plan?
Implications for Nursing Practice

Implications for nursing practice begin with the nursing assessment. It is important to specifically question the family history for the presence of AF. This is especially essential if the patient has clinical manifestations and new onset irregular pulse. It needs to be documented in the patients record that there is a family history of the disease. The nurse also must asses the presence of other risk factors for the development of AF including: Cardiomyopathy Hypertension
Sources: Fox, C.S., Parise, H., DAgostino, R.B., et al. (2004). Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring. JAMA: 291(23): 2852-2856; Pavlovich-Dannis, S.J. (2005). Moms eyes and dads atrial fibrillation. Nurse Week: 23-24. National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health. (2004). Parental atrial fibrillation increases risk in offspring, finds NHLBIs Framingham Heart Study. NIH News. Retrieved August 8, 2008 from http://www.nhlbi.nih.gov/new/press04-06-15.htm
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P Wave: None; PR Interval: None; QRS Complex: 0.10 second; QT Interval: unable to obtain; Heart Rate: Atrial: 80 bpm; Rhythm: Irregular; Ectopic Beats: f waves.
FIGURE 3820
Atrial fibrillation.
Significant ECG features of atrial fibrillation include: P waves are not identifiable due to the atrial quivering, referred to as f waves, occurring at 350 to 750 beats per minute. PR intervals are not measurable. QT interval is not obtainable because the T waves are buried in the f waves. Irregularly irregular rhythm occurs, meaning that there is no pattern to the irregularity. f waves are ectopic beats. The etiology, physical assessment findings, and treatment of atrial fibrillation are outlined in Chart 387.
may result in a conversion to atrial flutter or fibrillation. Eventually, signs and symptoms of congestive heart failure will be present. Figure 3821 is a rhythm strip showing supraventricular tachycardia (SVT). Significant ECG features of supraventricular tachycardia include: Heart rate is 100 to 250 beats per minute. P wave is not seen; it is buried in the QRS complex. PR interval is not discernable. QRS complex is within normal limits unless distorted by the buried P waves. QT interval is not obtainable because the T waves are buried. Heart rhythm may be regular or irregular due to varying conduction rates through the AV node. Ectopic beats may or may not be present, depending on the pacemaker site. The etiology, physical assessment findings, and treatment of supraventricular tachycardia are outlined in Chart 387. Atrioventricular Nodal Reentry Tachycardia One phenomenon that can cause supraventricular tachycardia is atrioventricular nodal reentry tachycardia (AVNRT). Normally people are born with only a single electrical pathway at the base of the right atrium where impulses travel to the AV node. However, some individuals are born with two separate electrical pathways leading to the AV node, each with its own respective
Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is a tachycardia that is generated somewhere above the ventricles. This general term encompasses all fast (tachy) rhythms with normal QRS complexes and heart rates greater than 100 beats per minute. Rhythms included under the SVT umbrella include sinus tachycardia, paroxysmal atrial tachycardia (PAT), and paroxysmal junctional tachycardia (PJT). Clinicians use the term supraventricular tachycardia when it is impossible to identify the source of the tachycardia. Usually this rhythm is benign and is self-limiting when the cause is removed. If sustained, loss of blood fill time (diastole) causes a drop in cardiac output. Prolonged episodes of supraventricular tachycardia increase myocardial oxygen demand and also
P Wave: None; PR Interval: None; QRS Complex: 0.10 second; QT Interval: unable to obtain; Heart Rate: Ventricular: 200 bpm; Rhythm: Regular; Ectopic Beats: Depends on pacemaker site.
Atrial rate rapid,
FIGURE 3821
Supraventricular tachycardia (SVT).
CHAPTER 38
properties. Each pathway has its own refractory period, one fast (beta) and one slow (alpha). The fast track has a long refractory period, and the slow track has a fast refractory period. Impulses travel the two separate pathways simultaneously. When the impulse begins down these two pathways, because of its speed, the one in the fast track stimulates the AV node and bundle of His, causing ventricular depolarization and a normal-width QRS complex. The fast track impulse also travels retrograde (backward transmission) back through the slow track, meeting the impulse coming down the slow track. When the two impulses meet, 99.9% of the time, they cancel each other out and the rhythm is normal. If for any reason, such as the presence of a refractory period in the fast track, the fast track will be unable to transmit the impulse, then the slow track transmits the impulse, causing depolarization of the ventricles. The QRS complex would still be within normal limits, but the PR interval would be longer than the ones coming from the fast track. This creates rhythm strips
AVN
that have identical QRS complexes but two different PR interval lengths. These beats still are considered to be sinus complexes, as opposed to coming from another atrial ectopic focus. The PR interval length differences are a result of the conduction alternating intermittently between the two functioning tracks. The AVNRT phenomenon occurs when a reentrant circuit or loop is created along the two pathways and the AV node (Figure 3822 ). An early impulse such as a PAC hits the two pathways; the fast track is in refractory and therefore cannot accept the impulse, but the slow track can. The impulse travels from the slow track, to the AV node, and then retrograde up the fast track because this track has recovered, is no longer in a refractory state, and can accept the impulse. The impulses are now able to continue to cycle the circuit or loop and initiate ventricular depolarization at a fast rate; this is referred to as AVNRT (Garcia & Miller, 2004). It is estimated that AVNRT occurs in 60% of patients presenting with paroxysmal (sudden onset) SVT and occurs in
Purkinje
SAN AVN
SAN AVN
(a) Macro re-entry circut: antegrade through AV node and retrograde across an assessory pathway.
(b) Micro re-entry at the cellular level in the AV node and Purkinje fibers.
FIGURE 3822
Reentrant circuit.
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approximately several cases per thousand persons worldwide. It is more predominant in women, may occur with individuals of any age, and is common in young adults. AVNRT is usually well tolerated; it often occurs in patients with no structural heart disease. Clinical manifestations are the same as with any tachy dysrhythmia, although AVNRT may cause angina or myocardial infarction in patients with coronary artery disease. Prognosis for patients without heart disease is usually good (Olshansky et al., 2006). Treatment is aimed at breaking the reentrant cycle with the use of vagal maneuvers such as breath holding, stimulating gag reflex, and carotid sinus massage.
Delta Wave
P Wave: Present and irregular; PR Interval: 0.12 second; QRS Complex: 0.16 second. QT Interval 0.52 second, 40-50 bpm, Ventricular: 40-50 bpm; Rhythm: Regular Ectopic Beats: None.
FIGURE 3823
Wolff-Parkinson-White syndrome.
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White syndrome (WPW) is a genetic AV conduction disorder characterized by the presence of two AV conduction pathways, one normal and one abnormal. An impulse leaving the atrium may travel down one or the other pathway without any specific pattern. The abnormal pathway, called the Kent bundle, is composed of an extra muscle bundle made up of working myocardial tissue. This extra muscle bundle forms a connection between the atria and the ventricles outside the normal conduction system, referred to as an accessory pathway. This allows impulses coming from the atrium to bypass the normal AV connection. The hallmark feature on the ECG strip for the abnormal pathway is the presence of a delta wave, a slurred upstroke at the beginning of the QRS complex (Figure 3823 ). The delta wave occurs when the impulse travels via the accessory pathway to the ventricles. Because the conduction is outside the normal conduction system, it takes longer for the impulse to travel through the ventricles, thus creating an abnormally wide, bizarre QRS complex (Garcia & Miller, 2004). Atrial flutter, atrial fibrillation, and supraventricular tachycardia that results in heart rates of greater than 250 beats per minute, are common dysrhythmias in patients with WPW. The increased heart rate increases the workload and oxygen consumption of the heart, predisposing to heart failure, and therefore could cause sudden cardiac death. When the patient does not exhibit any dysrhythmias, but has the delta wave, this is called WPW pattern. When the patient becomes symptomatic or develops dysrhythmias, then the correct terminology is WPW syndrome. Figure 3823 is a rhythm strip showing Wolff-Parkinson-White dysrhythmia. Significant ECG features of Wolff-Parkinson-White syndrome include: PR interval shortens to less than 0.12 second because the AV node is bypassed and delta waves appear just prior to the beginning of the R wave.
QRS complex is greater than 0.12 second due to the delta waves. QT interval shortens if tachycardia occurs and lengthens with bradycardia. Heart rate frequently tachycardic. Heart rhythm is regular, except during heart rate changes. The etiology, physical assessment findings, and treatment of WPW syndrome are outlined in Chart 387 (p. 000).
Wandering Atrial Pacemaker

Wandering atrial pacemaker is a pacemaker from at least three different sites above the bundle of His acting as the hearts pacemaker. These pacemaker sites may include the SA node, the AV junction, an atrial ectopic site, and/or any combination of these areas. This abnormality occurs because of SA node slowing, which permits an atrial ectopic focus and junctional escape rhythms to jump in as atrial pacemakers. Figure 3824 is a rhythm strip showing wandering atrial pacemaker. Significant ECG features of wandering atrial pacemaker include: P waves have multiple shapes, due to multiple atrial sites initiating the conduction. QT interval usually is normal, but may be prolonged due to a slow heart rate. Heart rhythm is irregular due to changing pacemakers. Atrial rate and ventricular heart rate typically are slow. Ectopic beats may be present due to the slow rhythm. The etiology, physical assessment findings, and treatment of wandering atrial pacemaker are outlined in Chart 387 (p. 1093).
Sick Sinus Syndrome

Sick sinus syndrome (SSS) encompasses a broad range of abnormalities, including disorders of impulse generation and conduction, failure of pacemakers, and a susceptibility to paroxysmal or
P Wave: Multifocal; PR Interval: 0.16 second; QRS Complex: 0.06 second; QT Interval: 0.04 second; Heart Rate: Atrial: Approximately 60 bpm; Ventricular: 50 bpm; Rhythm: Irregular; Ectopic Beats; Multifocal P waves.
FIGURE 3824
Wandering atrial pacemaker.
CHAPTER 38
110
110
110
50
50
50
P Wave: Present, but variable configuration; PR Interval: 0.14 second; QRS Complex: 0.08 second; QT Interval: 0.40 second; Heart Rate: Atrial: 60 bpm, Ventricular: 60 bpm; Rhythm: Irregular; Ectopic Beats: May occur with slow rate.
FIGURE 3825
Sick sinus syndrome.
chronic atrial tachycardia. This disorder also is referred to as sinoatrial disease and sinoatrial dysfunction. The cause is a severely depressed nonreliable SA node due to heart disease or the side effect of certain cardiac drugs, such as cardiac glycosides, sympatholytic antihypertensive agents, beta-adrenergic blockers, calcium channel blockers, and membrane active antiarrhythmic agents. When the tachycardia occurs with SSS there is increased oxygen consumption and workload for the myocardium. Profound sinus bradycardia with SSS may progress to sinus pauses or arrest, thereby decreasing cardiac output. Figure 3825 is a rhythm strip showing sick sinus syndrome. Significant ECG features of sick sinus syndrome include: P waves may be present or absent depending on which dysrhythmia is occurring. PR interval varies due to changing P wave sites. QT interval varies due to rate changes. Heart rate may be rapid or slow, or a combination of both. Heart rhythm is irregular and highly variable. Ectopic beats may be present when a slow rate occurs. The etiology, physical assessment findings, and treatment of sick sinus syndrome are outlined in Chart 387.
Nursing Management for Responsibilities for Atrial Dysrhythmias

Nursing responsibility when any dysrhythmia occurs is to assess the patients response to the rhythm. This is especially true if it is a new onset dysrhythmia and/or if the dysrhythmia causes a drop in the cardiac output. The atrial dysrhythmias do not have the impact on cardiac output that the more serious ventricular dysrhythmias do, but any change in cardiac output may cause clinical manifestations, and therefore, requires an in-depth assessment. The patient is evaluated for the clinical manifestations of reduced cardiac output as outlined in Chart 386 (p. 1092). Vital signs and clinical manifestations must be monitored frequently to assess tolerance of the rhythm, especially if it is sustained. The health care practitioner needs to be notified, especially if this is a new rhythm, because medical intervention must be initiated to convert the rhythm back to normal sinus rhythm.
Atrial flutter and fibrillation may occur as a transient dysrhythmia in healthy young individuals. If these conditions are chronic they are typically associated with heart disease including atrial muscle disease or atrial distention with disease of the sinus node. Atrial fibrillation also is seen in congenital heart disease. If the atrial flutter and/or atrial fibrillation are chronic conditions, and normal sinus rhythm cannot be reestablished, the patient often is placed on an anticoagulant, such as warfarin. This treatment is indicated because a fluttering/fibrillating atrium creates blood stasis, which increases the risk of clot formation. If these clots travel out of the atrium they tend to lodge in the brain, and, on rare occasions in the lung, causing an alteration in normal function in these areas. Treatment of atrial fibrillation/flutter may include cardioversion, which is the delivery of electrical voltage in order to stop unwanted electrical activity and allow the SA node to resume the hearts pacemaker. Cardioversion is discussed in detail in Chapter 39 . This treatment increases risk for myocardial infarction, cerebral vascular accident (CVA), and pulmonary embolus. The nurse needs to assess the patient post-cardioversion for clinical manifestations of these disorders. Myocardial infarction is discussed in detail in Chapter 40 . Cardiovascular accident (CVA) is discussed in Chapter 30 , and pulmonary embolus is discussed in Chapters 35 and 36 . Besides heart disease frequently there are other causes for atrial cardiac dysrhythmias that must be evaluated and treated, e.g., stress, pain, and anxiety. The treatment may be narcotics for pain relief or an antianxiety medication for stress and increased anxiety. The nurse may need only to sit and listen to the patient and provide emotional support.
Junctional Dysrhythmias
Junctional dysrhythmias also referred to as nodal rhythms result from either an irritable focus in the junctional tissue that discharges before the SA node has had a chance to or because the SA node has failed to fire and the junctional node becomes the secondary pacemaker. AV junctional dysrhythmias may occur if the impulse from the SA node is blocked as it exits the SA node or if it is not conducted through the atria. AV junctional dysrhythmias have a distinctive pattern on ECG tracings because the impulse is not initiated in the SA node. The impulse
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Nursing Management of Patients with Cardiovascular Disorders Figures 3826 and 3827 are ECG rhythm strips that show junctional escape rhythm and accelerated junctional rhythm, respectively. Significant ECG features of junctional escape rhythms include: P wave is inverted, negatively deflected, due to retrograde conduction, and either occurs before, after, or buried in the QRS complex. PR interval is dependent on the location of P wave; thus, the PR interval may or may not be present or normal. QRS complex is normal in duration and shape, unless distorted by a buried P wave. QT interval is within normal range, unless impacted by the heart rate. It is prolonged with slow heart rate or shortened with increased heart rate. Heart rate is usually within normal range for a rhythm generated from the AV junction is 40 to 60 beats per minute. For an accelerated junctional rhythm the rate is 60 to 100 beats per minute and for junctional tachycardia the heart rate is greater than 100 bpm. Heart rhythm is typically regular. Entire rhythm is composed of ectopic beats because they all come from the AV junction instead of the SA node. Other ectopic beats may occur with slow heart rate. The etiology, physical assessment findings, and treatment of junctional escape rhythms are outlined in Chart 388.
is initiated in the AV junctional tissue and must travel in a backward (retrograde) direction to activate the atria. Therefore, the P wave is inverted or negatively deflected, due to this retrograde conduction, and may occur before, after, or buried in, the QRS complex. Retrograde conduction means that the impulse originates in the AV junction so it stimulates the atria from the bottom up instead of the top down. The impulse simultaneously initiates both atrial and ventricular contractions. The location of the P wave is, therefore, dependent on the speed with which the impulses travel in both chambers. The QRS complex configuration is normal in appearance because the impulse travels the normal pathway from the AV junctional node through the ventricles. AV junctional dysrhythmias are not considered lethal or life threatening, but as always, the most important indicator of the clinical significance of any dysrhythmia is the patients response to or tolerance of the rhythm. The three AV junctional dysrhythmias discussed in this chapter are: junctional escape rhythm, premature junctional contractions, and paroxysmal junctional tachycardia.
Junctional Escape Rhythm

Junctional escape rhythm occurs when there is a problem with normal SA node function, either fails to produce an impulse, or when the SA nodes rate of firing falls below the intrinsic rate of the AV node. At this time the AV node will assume the role of the pacemaker. The ability of the AV node to assume this role is a safety measure in that it becomes the pacemaker for the heart when the SA node fails to do so. When an isolated beat from the AV junction occurs it is called a junctional escape beat or complex, as compared to a series of beats that then is called a junctional rhythm. When a rhythm is generated from the junction, the rate is between 38 and 60 beats per minute. If the rate is greater than 60 but less than 100 it is referred to as an accelerated junctional rhythm. If the rate is greater than 100 typically it is called junctional tachycardia.
Premature Junctional Contraction

A premature junctional contraction (PJC) originates as an ectopic beat that is initiated in the atrioventricular (AV) junction. It discharges before the next expected SA node impulse causing simultaneous atrial and ventricular contraction to occur. This is not a dangerous dysrhythmia, although it does indicate that some degree of cardiac ischemia is occurring. Figure 3828 (p. 1102) is
P Wave: None, or buried in QRS Complex; PR Interval: Not measurable; QRS Complex: 0.10 second; QT Interval: 0.40 second; Heart Rate: Atrial: Not measurable, Ventricular: 40 bpm; Rhythm: Regular; Ectopic Beats: None.
FIGURE 3826
Junctional escape rhythm.
P Wave: Inverted and regular; PR Interval: 0.140.16 second; QRS Complex: 0.08 second: QT Interval: 0.44 second; Heart Rate: Atrial: 80 bpm, Ventricular: 80 bpm; Rhythm: Regular: Ectopic Beats: none.
FIGURE 3827
Accelerated junctional rhythm.
CHAPTER 38
CHART 388
Dysrhythmia Junctional escape rhythm
Junctional Dysrhythmias: Etiology, Physical Assessment, and Treatment

Etiology SA node disease Myocardial infarction Hypoxia and ischemia Heart failure Increased vagal tone Certain cardiac drugs: such as digoxin, beta adrenergic blockers, and calcium channel blockers Sinus bradycardia Digoxin toxicity Hyperkalemia Valve disease Irritability of the AV junctional tissue caused by: SA node disease Myocardial infarction Sinus bradycardia Mitral stenosis Mitral valve prolapse Cor pulmonale Hypoxia Ischemia Infectious diseases Increased vagal tone Increased sympathetic tone Electrolyte imbalances Digoxin Stimulants Stress Anxiety May precede AV block May occur at any age with no prior history of underlying heart disease. Digoxin toxicity (most common cause) Inferior wall myocardial infarction Myocarditis Ischemia Untoward response to open heart surgery Frequent ingestion of stimulants Anxiety Increased catecholamine secretion Physical Assessment Pulse: rhythm is regular with a usual rate of 40 60 bpm unless it is an accelerated rhythm of > 100 bpm If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: Irregular BP: Normal unless PJCs occur frequently enough to decrease cardiac output. Treatment Observe for other dysrhythmias if a slow rate is present. Generally this condition is asymptomatic; however, if symptomatic, typical treatment includes: Oxygen Drug therapy: (atropine, dopamine) Pacemaker Cardioversion
Premature junctional contraction (PJC)
Rarely causes symptoms, thus typically not treated. Find and treat the underlying cause, if possible. If it initiates a more serious dysrhythmia, such as tachycardia, therapy becomes more aggressive, contingent on the type of dysrhythmia. If occurring frequently, more than 5 times per minute, they can drop cardiac output, and predispose the patient to other dysrhythmias. Oxygen Drugs such as stimulants, sympathomimetics, and digitalis may be discontinued.
Paroxysmal junctional tachycardia (PJT)
Pulse: Rapid, with patient experiencing a fluttering sensation. BP: Lower than usual due to decreased cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare.
Find and treat the cause as PJTs may be a predisposition to lethal dysrhythmias, heart failure, and shock. Vagal maneuvers may be applied. Oxygen Drug therapy initiated: includes: amiodarone or beta-adrenergic blockers. Cardioversion may be initiated if necessary.
a rhythm strip showing premature junctional contraction. Significant ECG features of premature junction contractions include: P wave is inverted and occurs before, after, or buried in the QRS complex. PR interval is dependent on the location of P wave; thus, the PR interval may or may not be present or normal. QRS complex is normal in duration and shape, unless distorted by a buried P wave.
QT interval also is normal unless impacted by the heart rate. Heart rate is that of the underlying rhythm. Heart rhythm is irregular when PJCs are present; or it may be described as regular with premature beats. Ectopic beat is the PJC. The etiology, physical assessment findings, and treatment of PJCs are outlined in Chart 388.
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P Wave: Present and regular except for premature beat; PR Interval: 0.16 second; QRS Complex: 0.08 second; second; Heart Rate: Atrial: 110 bpm, Ventricular: 110 bpm; Rhythm: Regular except for premature beats: Ectopic Beats: none
FIGURE 3828
Premature junctional contraction (PJC).
Paroxysmal Junctional Tachycardia

The paroxysmal junctional tachycardia (PJT) rhythm is defined as an irritable focus in the AV junction that assumes the pacemaker role by discharging impulses more rapidly than the SA node. It begins and ends abruptly, which is why it is called paroxysmal. If it is a sustained rhythm, and greater than 60 beats per minute, it may be referred to as junctional tachycardia. The term junctional tachycardia sometimes is used interchangeably with the term accelerated junctional rhythm, which was discussed previously. This rhythm produces a junctional rate of over 60 beats per minute. Figure 3829 is a rhythm strip showing paroxysmal junctional tachycardia. Significant ECG features of paroxysmal junctional tachycardia include: Heart rate usually is 160 to 240 beats per minute and constant. It may, however, be as low as 110 beats per minute or exceed 240 beats per minute. P wave is inverted and occurs before, after, or buried in the QRS complex. PR interval is dependent on the location of P wave; thus, the PR interval may or may not be present or normal. QRS complex is normal in duration and shape, unless distorted by a buried P wave. QT interval shortens due to increased heart rate. Heart rhythm is essentially regular. It may become irregular as the rate increases. Entire rhythm is composed of ectopic beats because they all come from the AV junction instead of the SA node.
The etiology, physical assessment findings, and treatment of PJTs are outlined in Chart 388.
Nursing Management for Junctional Dysrhythmias

Like atrial dysrhythmias, junctional dysrhythmias generally are not life threatening. However, the decreased and/or increased heart rate does have an impact on cardiac output. This is especially true in the presence of heart disease when the heart is unable to significantly increase the force of the muscle contraction to compensate for the rate changes. Therefore, the nurse must evaluate the patient for clinical manifestations of decreased cardiac output (Chart 386, p. 000). When rhythm is slow other ectopic foci may attempt to become the hearts pacemaker, therefore, the nurse must assess the rhythm for other aberrancies. The health care practitioner needs to be notified, especially if it is a new onset dysrhythmia in order to determine cause and treatment. It is essential that the nurse assist the health care practitioner in determining the cause and treatment of dysrhythmias. Since some prescribed medications, e.g., digoxin, cause significant dysrhythmias, the patients medical history should be reviewed to determine if the dysrhythmia is medication related. Serum drug levels should be ordered as indicated. For symptomatic junctional tachycardia, treatment also may include applying vagal maneuvers, initiating drug therapy, and completing cardioversion if necessary. As always any significant rhythm change or the appearance of new onset dysrhythmias needs to be reported to the health care practitioner.
P Wave: Inverted and regular; PR Interval: 0.08 second; QRS Complex: 0.06 second; QT Interval: 0.32 second; Heart Rate: Atrial: 130 bpm, Ventricular: 130 bpm. Rhythm: Regular; Ectopic Beats: None.
FIGURE 3829
Paroxysmal junctional tachycardia.
CHAPTER 38
Due to the clinical manifestations of these dysrhythmias, the patient and family may experience anxiety. Thus, the nurse also must assess and treat the anxiety by use of supportive measures, such as listening to the patients concerns, offering reassurance, providing a calm environment, and medicating for anxiety and pain relief as appropriate.
The etiology, physical assessment findings, and treatment of first-degree AV blocks are outlined in Chart 389 (p. 1104).
Mobitz I/Wenckebach/Type I Second-Degree Heart Block

The terms Mobitz I/Wenckebach/Type 1 second-eegree heart block, are used interchangeably to refer to the same abnormality. This abnormality is depicted as a progressive prolongation of the electrical impulse delay in the AV node until there is a complete loss of the QRS complex, and thus, no ventricular contraction. This dysrhythmia is characterized by progressive lengthening of the PR interval until a QRS complex fails to appear after a P wave (Beasley, 2003). Mobitz I/Wenckebach is one of the two types of second-degree block that occurs in the AV node. Figure 3831 (p. 1106) is a rhythm strip showing Mobitz I/Wenckebach dysrhythmia. Significant ECG features of Mobitz I/Wenckebach dysrhythmia include: P waves are present, and they precede the QRS complexes. PR interval progressively prolongs until there is a dropped QRS complex and then the progressive prolongation begins again. QRS complexes are normal in shape and duration. QT interval is within normal limits, unless no QRS complex occurs. Atrial heart rate is normal and regular; ventricular heart rate is less than that of the atrial rate. Atrial rhythm is regular; the ventricular rhythm is irregular. The etiology, physical assessment findings, and treatment of Mobitz I/Wenckebach/Type I second-degree heart block are outlined in Chart 389 (p. 000).
Conduction Block Dysrhythmias

Cardiac conduction block dysrhythmias occur due to an interruption in the continuity of the cardiac electrical conduction system. This discontinuity is caused by a loss of blood supply to the conduction system as a result of ischemic heart disease or coronary artery disease. Heart blocks are classified according to the degree of the block, either partial or complete obstruction of the electrical conduction pathway. These disorders may be either permanent or transient, and minor or significant. The clinical significance of an AV block depends on the degree (severity) of the block, the rate of the escape pacemaker (junctional vs. ventricular), and the patients response to that ventricular rate. There are four types of heart block dysrhythmias discussed next: first degree AV block; Mobitz I/Wenckebach/ Type I second-degree heart block; Mobitz II second-degree block; and third-degree AV block (complete).
First-Degree AV Block
First-degree AV block represents a conduction disturbance in which electrical impulses flow normally from the SA node through the atria, but are delayed at the AV node. There is a prolongation or slowing of conduction rather than an actual block. Because of this consistent delay the PR interval is greater than 0.20 second, making it abnormal. First-degree AV block is not actually a dysrhythmia. Its presence only indicates a delay at the AV node, rather than a definite block. Figure 3830 is a rhythm strip showing first-degree AV block. Significant ECG features of first-degree AV block include: P waves are present and normal in size and shape. PR interval is prolonged, greater than 0.20 second, but constant. QRS duration usually is normal. QT interval is normal unless there is an abnormal rate. Heart rate is usually within normal range. Heart rhythm is regular.
Mobitz II Second Degree Block

Mobitz II/second degree block results from an intermittent block of the AV node, the bundle of His, or bundle branches. This dysrhythmia occurs when this block causes an intermittent interruption in the electrical conduction system near or below the AV node, which prevents the sinus or atrial impulses from getting to the ventricles. On the ECG strip the P wave (atrial contraction) is present at regular intervals because the SA node is generating impulses in a normal manner; however when the block occurs, the P wave is not followed by a QRS complex. An AV conduction ratio of 2 Ps for every 1 QRS; 3Ps for every 1 QRS, or greater is common, with or without a bundle branch block
P Wave: Present and regular; PR Interval: 0.24 second; QRS Complex: 0.06 second; QT Interval: 0.40 second; Heart Rate: Atrial: 60 bpm, Ventricular: 60 bpm; Rhythm: Regular; Ectopic Beats: None.
FIGURE 3830
First-degree AV block.
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CHART 389
Dysrhythmia First-degree AV block
AV Block Dysrhythmias: Etiology, Physical Assessment, and Treatment

Etiology May occur without any underlying heart disease May occur in athletes Occurs in about 13% of the population Drug reactions to digoxin, betablockers, and CA channel blockers Cardiac related causes include: Ischemia Myocardial infarction Rheumatic heart disease Coronary artery disease Conduction delay within the AV node Most commonly associated with AV nodal ischemia secondary to occlusion of the right coronary artery Other causes may be: Myocardial infarction Inferior/right ventricular structural heart disease or an anatomical abnormality Myocarditis Transient side effect of open heart surgery Increased vagal activity Drug toxicity, e.g., digoxin Septal wall necrosis Acute inferior or right ventricular MI Myocarditis Advanced coronary artery disease (general ischemia) Electrolyte imbalance Digitalis toxicity Reaction to amiodarone, betablockers, or calcium channel blockers Physical Assessment Pulse: Within normal limits BP: Within normal limits Treatment This is not a dangerous rhythm in itself and usually is asymptomatic. May progress to a more advanced heart block, especially in the presence of a myocardial infarction. Observe closely and place on an ECG monitor to detect additional signs and symptoms.
Mobitz I / Wenckebach/ Type I seconddegree heart block
Pulse: Irregular BP: May be decreased with frequently dropped beats due to decreased cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: slow and typically irregular, depending on ventricular response BP: Decreased due to low cardiac output If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present. Pulse: Slow and usually irregular BP: Lower than usual If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present.
This is often a transient rhythm and will revert to normal rhythm without treatment. Usually asymptomatic because the ventricular rate often remains nearly normal and cardiac output is not significantly affected. If symptomatic, and is a result of medications, they should be withheld. If the heart rate is slow and serious clinical manifestations such as low BP, angina, shortness of breath, occur, atropine or temporary pacing is considered. When occurs in conjunction with acute myocardial infarction, observe for increasing AV block. Often considered an emergent situation. The health care practitioner should be notified at once. May progress to a third-degree AV block and ventricular asystole, thus, a standby cardiac pacemaker is indicated for asymptomatic patients, and temporary cardiac pacing is required for symptomatic patients. For sustained permanent block, a permanent pacemaker is inserted.
Mobitz II second-degree AV
Third-degree AV block (complete)
Ischemic damage Septal wall necrosis Acute inferior or right ventricular MI due to the effect of vagal tone and ischemia on the AV node Acute anterior MI Myocarditis Coronary artery disease Cardiomyopathies Cardiac muscle diseases Rheumatic heart disease Drug toxicity, reaction to amiodarone, beta-blockers, or calcium channel blockers Electrolyte imbalance Rheumatic heart disease Congenital condition usually located at the level of the AV junction
Treatment is essential as third-degree block is potentially lethal. If an AV junctional or ventricular escape pacemaker does not take over following a sudden onset of third-degree AV block, asystole will occur. Clinical manifestations depend on the ventricular heart rate, especially for slow rates. If the QRS is narrow and the patient is symptomatic, initial management is atropine and/or transcutaneous pacing. If the QRS is wide and the patient is symptomatic, transcutaneous pacing is started. A temporary pacemaker is inserted, and may be followed by a permanent pacemaker.
CHAPTER 38
CHART 389
Dysrhythmia Bundle branch block (BBB)
AV Block Dysrhythmias: Etiology, Physical Assessment, and TreatmentContinued

Etiology Causes vary depending on whether it is the right or left BBB Right BBB may be present in healthy individuals with apparently normal hearts without any apparent underlying cause Common pathological causes include: Coronary artery disease Cardiac tumors Cardiomyopathy Myocarditis Atrial septal defect Cardiac surgery Congenital RBBB Acute anterioseptal MI Acute pulmonary embolism or infarction Acute heart failure Unlike RBBB, LBBB always indicates a diseased heart and generally is more common in individuals with diseased hearts Common causes include: Hypertensive heart disease Cardiomyopathy Myocarditis Syphilitic, rheumatic, and congenital heart disease Cardiac tumors Idiopathic degenerative disease of the electrical conduction system Aberrant ventricular conduction associated with supraventricular premature contractions and tachycardia Physical Assessment Pulse: Within normal limits BP: Within normal limits Treatment Specific treatment usually is not indicted if it is present alone and is not the result of an acute MI. Temporary cardiac pacing is indicated for the treatment of a right or left bundle branch block under the following conditions: results from an acute MI is complicated by a first- or second-degree AV block, or both, especially in the setting of an acute MI if the block progresses to a complete AV block.
(Beasley, 2003). In other words there are 2, 3, or 4 P waves for every QRS complex. Thus, with this dysrhythmia there may be enough dropped QRSs to significantly impact cardiac output. Therefore, Mobitz II is a more serious dysrhythmia than either first-degree AV block or Mobitz I (Wenckebach/ Type I seconddegree heart block) because of the impact on the cardiac output and an increased risk of progression to third degree block or complete heart block. Figure 3832 (p. 1106) is a rhythm strip showing Mobitz II/second-degree block. Significant ECG features of Mobitz II/second-degree block include: QRS complexes are intermittently absent; they may be normal to prolonged when present; and they are usually prolonged due to bundle branch block. P waves are present and regular. PR intervals are constant with conducted beats. QT intervals are within normal limits. Atrial heart rate is usually normal; ventricular heart rate is less than the atrial rate.
Atrial rhythm is regular; ventricular rhythm may be regular or irregular. The ventricular rhythm is irregular when the AV block is intermittent; thereby, causing a varying AV conduction ratio. Ectopic beats may be present due to the slow heart rate. The etiology, physical assessment findings, and treatment of Mobitz II heart block are outlined in Chart 389.
Third-Degree AV Block (Complete)

Third-degree AV block, or complete block, is the independent excitation and contraction of the atria and ventricles due to the inability of any atrial impulses to reach the ventricles. In other words, the top and bottom of the heart are not communicating; they are beating independently. This dysrhythmia also is referred to as AV dissociation because of the independent function of the atria and the ventricles. The SA node fires at regular intervals, producing P waves at a normal rate of 60 to 100 beats per minute; whereas, the ventricles are paced by either a pacemaker site in the ventricles themselves or in the junctional
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P Waves: Present and regular; PR Interval: Progressively prolonged until one P wave is not conducted and the sequence begins again; QRS Complex: 0.10 second; QT Interval: 0.420.60 second; Heart Rate: Atrial: 70 bpm, Ventricular 50 bpm; Rhythm: Atrial: Regular, Ventricular: Irregular due to dropped beat; Ectopic Beats: None. Conclusion: Mobitz I/Wenckeback Second-Degree Heart Block.
FIGURE 3831
Mobitz I/Wenckebach/second-degree heart block.
P Waves: Present and regular; PR Interval: 0.24 second; QRS Complex: 0.06 second; QT Interval: 0.48 second; Heart Rate: Atrial: 100 bpm, Ventricular 50 bpm; Rhythm: Atrial: Regular, Ventricular: Irregular due to dropped beat; Ectopic Beats: None.
FIGURE 3832
Mobitz II/second-degree heart block.
tissue. If the QRS complex is narrow the pacemaker is in the junctional tissue with a rate of 40 to 60 beats per minute. However, if the QRS complex is wide the pacemaker is in the Purkinje network and the heart rate ranges from 20 to 40 beats per minute; this is referred to as an idioventricular rhythm. Complete AV block associated with an inferior myocardial infarction is thought to be a block in the bundle of His, and often occurs after progression from first-degree AV block or second-degree AV
block, type I. Third-degree heart block is the most serious type of heart block because it may progress to asystole (a complete cessation of electrical activity), and the slow ventricular heart rate results in decreased cardiac output. Since the ventricular rhythm may not be able to sustain adequate cardiac output, third- degree heart block is referred to as a lethal dysrhythmia. Figure 3833 is a rhythm strip showing third-degree or complete heart block. Significant ECG features of third-degree heart block include:
CHAPTER 38
P Waves: Present and regular; PR Interval: None; QRS Complex: 0.12 second; QT Interval: 0.38 second; Heart Rate: Atrial: 90 bpm, Ventricular: 4050 bpm; Rhythm: Regular; Ectopic Beats: None.
tation to one ventricle; therefore, an abnormal spread of electrical activity through the ventricles occurs. This delayed conduction causes a widening of the QRS complex to more than 0.12 second. When measuring the QRS complex, it is necessary to observe the axis of the complex to determine whether it is right or left bundle branch block. Figure 3834 is a rhythm strip showing a bundle branch block. Significant ECG features of bundle branch block include: QRS complex is more than 0.12 second if a complete bundle branch block is present. P waves are present and regular. PR interval is 0.12 to 0.20 second. QRS measuring 0.10 to 0.12 second is called an incomplete right or left bundle branch block. QT interval is within normal limits. Heart rate is 60 to 100 beats per minute. Heart rhythm is regular. The etiology, physical assessment findings, and treatment of bundle branch block are outlined in Chart 389.
FIGURE 3833
Third-degree (complete) heart block.
Atrial and ventricular rhythms are independent of one another (dissociated). Atrial rhythm usually is regular, depending on underlying sinus, atrial, or junctional rhythm. Ventricular rhythm may be regular or irregular. P waves are present and regular; however there is no relationship to QRS complexes. PR interval is absent. QRS complex may be narrow with a junctional rhythm, or wide with an idioventricular rhythm. QT interval may change with the rate change, but is not directly affected. Atrial heart rate is regular, 60 to 100 beats per minute; nodal rate is 40 to 60 beats per minute; and ventricular rate is 20 to 40 beats per minute. Atrial and ventricular rhythms are independent of one another (dissociated). Atrial rhythm usually is regular, depending on underlying sinus, atrial, or junctional rhythm. Ventricular rhythm may be regular or irregular. Ectopic beats usually are present due to slow rate. The etiology, physical assessment findings, and treatment of Mobitz II heart block are outlined in Chart 389.
Nursing Management for Conduction Block Dysrhythmias

The type of heart block determines the severity of the dysrhythmia, and therefore, nursing responsibilities. As with any dysrhythmia the patients tolerance to the rhythm must be evaluated when heart block develops. First-degree heart block and bundle branch block in isolation, do not impact cardiac output, therefore, patients are not symptomatic. With first-degree heart block, the nurse must observe the cardiac monitor for any changes in the rhythm indicating a progression to a more severe type of heart block. Mobitz I/Wenckebach often does not require treatment, however, the ECG monitoring and patient assessment are necessary because this type of block may lead to a more serious Mobitz II or complete heart block. It is necessary, therefore, that the nurse frequently checks the monitor to identify potential changes. As with any new dysrhythmia, Mobitz I/Wenckebach needs to be reported to the health care practitioner.
Bundle Branch Block

Bundle branch block, also referred to as intraventricular conduction defect, is a discontinuity of conduction, complete or incomplete, in one branch of the bundle of His, which affects normal transmission of the impulse through the ventricles. When one bundle is blocked, the ventricles depolarize asynchronously. Bundle branch block is characterized by a delay of exci-
P Wave: Normal sinus rhythm; PR Interval: 0.16 second; QRS Complex: 0.20 second; QT Interval: 0.40 second. Heart Rate: Atrial: 90 bpm, Ventricular: 90 bpm; Rhythm: Atrial: Regular, Ventricular: Regular; Ectopic Beats: None.
FIGURE 3834
Bundle branch block.
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Nursing Management of Patients with Cardiovascular Disorders pact on cardiac output. The various types of ventricular dysrhythmias are discussed next: premature ventricular contraction, ventricular tachycardia, torsade de pointes, ventricular fibrillation, pulseless electrical activity, and asystole.
The onset of Mobitz II and complete heart block are emergent situations that require immediate intervention. Mobitz II is described as a treacherous and unpredictable rhythm that can deteriorate to become a complete heart block. If untreated, these rhythms may progress to cardiac asystole and sudden death. At any indication of rhythm changes indicative of Mobitz II or complete heart block, the health care practitioner should be notified at once. The nurse should prepare for a temporary pacemaker insertion (Chapter 39 ), which generally is indicated for these types of dysrhythmias. A permanent pacemaker may be necessary if the block persists. It is the nurses responsibility when working with monitored patients to be familiar with equipment location and operation.
Signs and symptoms of third-degree AV block are the same as those in symptomatic sinus bradycardia. AV block can be more ominous, especially when associated with wide and bizarre QRS complexes. If an AV junctional or ventricular escape pacemaker does not take over the pacing of the heart following a sudden onset of third-degree AV block or ventricular asystole will occur. Temporary cardiac pacemaker is required immediately for treatment of symptomatic third-degree block with wide QRS complexes. The nurse must report this rhythm immediately to the health care provider in order to initiate treatment before a significant drop in cardiac output occurs.
Premature Ventricular Contraction

A premature ventricular contraction (PVC) is caused by an irritable focus within the ventricle that discharges before the next sinus impulse, stimulating the ventricle directly, and causing a contraction. PVCs are more likely to occur during bradycardia when there is more time for them to emerge. Premature ventricular contractions (PVCs) are individual beats, one ectopic beat, not a rhythm. PVCs have a wide and bizarre QRS complex that is more than 0.12 second in length. Because the activation begins outside the normal conduction system, it takes longer to travel the ventricular conduction pathways, thereby prolonging the QRS length. PVCs are followed by a full compensatory pause, meaning the SA node rate and rhythm are unaffected by the PVC. In other words, the rate prior to the PVC resumes, following the PVC. A compensatory pause is measured by: Measuring the two beats preceding the PVC Moving the calipers along, and marking where the next beat should have fallen Then placing the calipers on the spot where the beat should have occurred, measure the distance to the next beat, there should not be a change in the cadence of the rhythm. The full compensatory pause is one of the factors used when evaluating and diagnosing PVCs. To distinguish PVCs from atrial and junctional ectopic beats, the full compensatory pause is present. Typically, atrial and junctional ectopic beats do not have a full compensatory pause, they are said to be non-compensatory or partially compensatory, meaning that there is a rhythm change following these dysrhythmias. Figure 3835 is a rhythm strip showing a premature ventricular contraction (PVCs) with a full compensatory pause. Unifocal and Multifocal PVCs Premature ventricular contractions (PVCs) occur in various patterns. Each pattern differs in its severity and prognosis. First, if the PVC configuration (size and shape) remains the same con-
Ventricular Dysrhythmias
Ventricular dysrhythmias are caused by ectopic or irritable foci in the walls of the ventricles. The pacemaker cells in the ventricles may, in certain circumstances, serve as the hearts pacemaker. When the SA node fails or the impulse does not get through the AV node, the ventricles take over the pacing role. In this situation, an electrical impulse may be instigated from both the bundle of His and the Purkinje network. The intrinsic ventricular rate is only 20 to 40 beats per minute; therefore, cardiac output is severely compromised. Also, if the atrium is not contracting there is no atrial kick, causing further decrease in cardiac output. Because the rhythm originates in the ventricle there is no P wave, and because it is an abnormal conduction pathway the QRS is wide and distorted. Ventricular dysrhythmias are considered to be very serious dysrhythmias mainly due to their im-
P Wave: Present and regular, except where absent (PVC); PR Interval: 0.20 second; QRS Complex: 0.08 second; QT Interval: 0.42 second; Heart Rate: Atrial: 70 bpm, Ventricular: 80 bpm; Rhythm: Atrial: Regular, Ventricular: Regular except for premature beat; Ectopic Beats: One PVC.
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FIGURE 3835
Premature ventricular contractions (PVCs).
CHAPTER 38
sistently, the dysrhythmia is coming from one irritable focus in the ventricle. These are referred to as unifocal PVCs. If PVCs occur with every other beat the rhythm is referred to as bigeminy. If PVCs occur every third beat, the rhythm is called trigeminy, and occurrence every fourth beat is quadrigeminy. The more often the PVC occurs, the greater the drop in cardiac output, and therefore, the more serious the dysrhythmia. The drop in cardiac output is due to the premature occurrence of the rhythm which does not allow for sufficient diastole or ventricle filling time. As cardiac muscle ischemia increases the muscle becomes more irritable, causing PVCs to be initiated in more than one place in the ventricle. This is referred to as multifocal PVCs. When multifocal, the morphology (shape) of the QRSs varies. Multifocal PVCs are more serious than unifocal PVCs because they indicate that there is more ischemia occurring in the myocardium. PVC Patterns When PVCs occur for two or more consecutive beats this is referred to as paired salvos. When there are three or more consecutive PVCs salvos, it is defined as ventricular tachycardia. Ventricular tachycardia may be life threatening due to the severe drop in cardiac output. The most serious or dangerous time for a PVC to occur is during the relative refractory period, which is the top of the T wave on the ECG. This is referred to as an R on T phenomenon, and this occurrence may precipitate a run of ventricular tachycardia. Significant ECG features with PVCs include: QRS complex is premature, 0.12 second or greater in width, complexes are larger than the normal beats, with the T wave always occurring on the opposite side of the isoelectric line from the R wave. P waves are not present or are buried in the PVCs. PR interval-none. QT interval is prolonged for the ectopic beat only. PVC occurs prematurely. Heart rate usually is within normal range, but depends on underlying rhythm. Heart rhythm is irregular because the PVCs are premature. Ectopic beats are the PVCs. The etiology, physical assessment findings, and treatment of premature ventricular contractions are outlined in Chart 3810 (p. 1110).
niques, or electrical cardioversion. If the rhythm lasts less than 30 seconds it is a non-sustained rhythm or simply a run of ventricular tachycardia (three beats or longer) that terminates spontaneously. Ventricular tachycardia is an emergent situation, requiring urgent evaluation to assess cardiac output and the presence or absence of the pulse. Treatment is guided by published advanced cardiac support (ACLS) guidelines and varies based on the presence of a pulse. Ventricular tachycardia when sustained but hemodynamically stable (with pulse) is treated with pharmacologic agents such as lidocaine, procainamide or bretylium (AHA, 2006). Ventricular tachycardia that is hemodynamically unstable and pulseless is treated using the ACLS guidelines for pulseless cardiac arrest (Appendix *** ) (AHA, 2006). These guidelines dictate that the nurse assess the patient for a pulse, if none is present, cardiopulmonary resuscitation (CPR) is initiated and help is requested. Oxygen is administered and the patient is placed on a monitor/defibrillator when available. The nurse must be prepared to shock the patient per AHA guideline joules, CPR is resumed for 5 cycles, and then rhythm is checked. The patient is re-shocked if VT persists. Vasopressors are administered when intravenous access has been established. CPR and defibrillation cycles are repeated per ACLS guidelines until a viable rhythm is established or death occurs. Figure 3836 (p. 1012) is a rhythm strip showing ventricular tachycardia. Significant ECG features of ventricular tachycardia and ventricular fibrillation include: QRS complexes are uniform in appearance, usually wide and bizarre, measuring 0.12 second or greater, with the T wave occurring on the opposite side of the isoelectric line from the R wave. P waves in rapid VT are usually not recognizable. At slower ventricular rates, P waves may be recognized and may represent normal sinus node depolarization at a rate slower than VT, but the electrical activities do not affect one another. PR interval is not discernable. QT interval is not measurable. Heart rate is greater than 100 beats per minute and usually not faster than 200 beats per minute. Heart rhythm is essentially regular but may be irregular. Entire rhythm is ectopic beats. The etiology, physical assessment findings, and treatment of ventricular tachycardia are outlined in Chart 3810.
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Ventricular Tachycardia
Ventricular tachycardia (VT), often referred to as v-tach is a life threatening ventricular rhythm arising from an excitable ventricular focus in the tissue distal to the bifurcation of the bundle of His. In general, ventricular tachycardia affects the diseased heart, although it has been described in patients with apparently normal hearts. It is a rhythm that discharges repetitively, acting as the dominant pacemaker. It is present when three or more PVCs occur in a row at a rate of greater than 100 beats per minute (American Heart Association, 2006). This dysrhythmia frequently begins rapidly, and is initiated by a PVC which then becomes the hearts pacemaker. A sustained ventricular tachycardia is a rhythm that lasts longer than 30 seconds and usually requires termination by antiarrhythmic drugs, antitachycardia pacing tech-
Torsade de Pointes
Torsade de pointes, frequently referred to as torsades, is a form of ventricular tachycardia that is usually accompanied by prolongation of the QT interval. The QT interval usually is more than 0.50 second in the beats preceding the onset of the rhythm. Once the rhythm has occurred the QRS complexes have varying morphology or shape and width that usually begin after a pause in the rhythm or bradycardia. The name, torsade de pointes, is derived from the French term that signifies the twisting of the points. The name characterizes the rhythm in that it resembles a turning about or twisting motion along the baseline or isoelectric line. This form of VT, which is rare, is due to age, gender, drug toxicity, or an idiosyncratic reaction to certain cardiac drugs such as
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CHART 3810
Dysrhythmia Premature ventricular contraction (PVC)
Ventricular Dysrhythmias: Etiology, Physical Assessment, and Treatment

Etiology Organic heart disease Coronary artery disease Myocardial ischemia/irritability and infarction Cardiac valve disease Mitral valve prolapse Heart failure Primary electrical instability Fever Fluid volume deficit Electrolyte imbalance, e.g., hypokalemia, hypercalcemia, hypomagnesemia Acid/base imbalance Drug excess: e.g.; Tricyclic antidepressants; digitalis, sympathomimetic amines, and antiarrhythmic agents Moderate to excessive alcohol intake Increase in catecholamine release and sympathetic tone as in emotional stress Sarcoidosis Change in posture Exercise Emotional excitement Vagal stimulation Normal variation that increases with age Precipitated by the same conditions as premature ventricular contractions (see above) Physical Assessment Pulse: May be irregular due to asynchronous firing of the ventricles. The corresponding QRS complex may be detected on the monitor while contractions are felt as a peripheral pulse. BP: Normal or lower than usual due to decreased cardiac output leading to decreased perfusion. Thumping sensation in chest/throat Palpitations If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present. Treatment PVCs may be isolated when there is no underlying heart condition. Usually, then, they have no significance and require no treatment. Treatment depends on the cause and clinical manifestations. It is essential to identify and treat the underlying cause. When provoked by fast or slow heart rate, correcting the rate can abolish PVCs. Treatment usually is not required. Treatment is directed at uncovering the etiology and providing adequate oxygenation, pain relief, and rapid identification of causes. Antidysrhythmic drugs such as amiodarone and lidocaine should be administered as ordered per frequency of occurrence.
Ventricular tachycardia (VT)
Pulse: Rapid and weak BP: Hypotensive Cardiac output is decreased therefore the following clinical manifestations occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Changes in mental status, starting with confusion and restlessness, leading to unconsciousness. Conscious sensation of ineffective cardiac activity often accompanied by anxiety. Presence and severity of the signs and symptoms depends on rhythm duration.
Initial treatment is based on the presence or absence of a palpable pulse. If hemodynamically stable, with a pulse, drug intervention is appropriate e.g., procainamide, amiodarone, lidocaine. If hemodynamically unstable (pulseless) defibrillation and cardiopulmonary resuscitation (CPR) is indicated. After initial stabilization other treatments which may be considered include: Implantable cardioverter defibrillator Electrophysiology Studies (EPS): ventricles are stimulated to produce VT: then antiarrhythmic drugs are administered, followed by a second attempt to produce the VT. If unable to reproduce the dysrhythmia, the drug is considered effective and continuous therapy is instituted. Drugs used include: procainamide, amiodarone, and lidocaiane. Radio-frequency ablation, burning the area or focus in the ventricle where the VT is coming from may also be considered. Chapter 39 has a complete description of EPS and ablation.
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CHAPTER 38
CHART 3810
Dysrhythmia Torsade de pointes (TdP)
Ventricular Dysrhythmias: Etiology, Physical Assessment, and TreatmentContinued

Physical Assessment Pulse: Rapid, palpitations felt, often the first symptom BP: Low due to decreased cardiac output If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Changes in mental status, starting with confusion and restlessness, leading to unconsciousness. Seizures may be present with a prolonged rhythm. Clinical manifestations are related to the decreased cardiac output caused by the dysrhythmia. Pulse: None palpable and heart sounds usually absent BP: None Unconscious Seizures Apnea Death, if untreated Treatment Assessment of QT interval for prolongation. Magnesium is the treatment of choice to shorten the QT interval. If unsuccessful, overdrive ventricular pacing to keep the heart rate up and the QT interval within normal limits. Stress testing and Valsalva will prolong QT interval and can be used to diagnose congenital prolonged QT interval. All agents that cause torsade de pointe are immediately discontinued. Administer potassium intravenously if QT interval is abnormal. Cardioversion and overdrive pacing are used to terminate torsades, but only may be temporary. Drugs are modified or discontinued if QT interval is prolonged. Initiate CPR and defibrillation per ACLS guidelines (Appendix*** ).
Etiology Prolonged QT interval, which may be congenital or acquired Severe bradycardia Electrolyte imbalance, e.g., hypokalemia, hypomagnesemia Central nervous system lesions Tricyclic antidepressants Antidysrhythmic drugs, e.g., quinidine, procainamide, amiodarone Antihistamines, e.g., seldane Antibiotics, e.g., erythromycin Diuretics Liquid protein diets Starvation Or any combination of the above
Ventricular fibrillation (VF)
Severe myocardial ischemia Coronary heart disease Myocardial infarction Advanced heart block Abnormal repolarization Vagal stimulation Drug toxicity, e.g., psychotropics, digoxin Metabolic abnormalities, e.g., hypokalemia, hypomagnesemia Hypoxia Trauma Terminal event in many disease states Electrical shock Profound hypovolemia Massive myocardial damage Excessive vagal tone due to loss of sympathetic tone Obstruction of blood flow to or from the heart, e.g., severe pulmonary embolism Pericardial tamponade Myocardial rupture Massive cardiac trauma resulting in cardiac tamponade and/or tension pneumothorax Severe acidosis Hyperkalemia Hypothermia Drug overdose, e.g., tricyclics, betablockers, calcium channel blockers, digoxin Cardiac standstill from massive cardiac muscle damage
Pulseless electrical activity
Pulse: None palpable BP: None Unconscious Seizures may occur Death, if untreated
Assess for pulse and blood pressure; initiate CPR protocol per ACLS guidelines (Appendix ** ). Find cause and treat.
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Asystole
Pulse: None palpable BP: None Unconscious Death, if untreated
Check the rhythm in two leads in order to rule out the possibility of fine ventricular fibrillation. Also, check the lead placement to make sure it has not fallen off. Initiate CPR and ACLS protocols (Appendix ** ). Administer drugs per ACLS guidelines, agency protocol or doctors orders.
8 8 8 8
1110 UNIT 8
P Wave: Two normal P waves present; PR Interval: Not discernable during dysrhythmia; QRS Complex: Wide and distorted during dysrhythmia; QT Interval: Not discernable during dysrhythmia; Heart Rate: Atrial: Not discernable, Ventricular: Rapid; Rhythm: Both regular and irregular; Ectopic Beats: PVCs, ventricular tachycardia/fibrillation.
FIGURE 3836
Ventricular tachycardia.
quinidine, procainamide, disopyramide, or other agents that prolong the QT interval. Electrolyte imbalance such as hypokalemia and hypomagnesemia also can initiate torsade de pointes (Garcia & Miller, 2004). In addition to being a life threatening dysrhythmia, torsade de pointes tends to recur repeatedly. It is, therefore, essential to find and treat the underlying cause. Figure 3837 is a rhythm strip showing torsade de pointes. Significant ECG features of torsade de pointes include: QRS complex height varies and undulates. P waves are not discernable. PR interval is not measurable. QT is not measurable. Heart rate varies; approximately 200 to 250 beats per minute. Heart rhythm may be regular or irregular. Entire rhythm is ectopy.
ted through the normal conduction pathway. There are no waveforms apparent on the ECG strip. The rhythm appears disorganized, rapid, and irregular with waves whose morphology varies greatly. Ventricular fibrillation may be classified further as coarse and fine, just like atrial fibrillation. Coarse waveforms are more easily visible and are greater than 3 mm; those that are less than 3 mm frequently are referred to as fine VF. Coarse VF responds better to treatment than does fine VF. Also, coarse VF typically progresses to fine VF unless treatment is initiated in a timely manner. Fine VF indicates that the rhythm has been present for an extended period of time. Figure 3838 is a rhythm strip showing ventricular fibrillation.
Ventricular fibrillation (VF) is an ineffective quivering of the heart muscle that results in no blood delivery to tissues, thus, VF must be treated immediately. Detection of VF on a monitor requires immediate patient evaluation by the nurse to begin prompt treatment and to rule out equipment malfunctions that mimic VF such as, ECG artifacts produced by loose or dry electrodes, broken ECG leads, or patient movements or muscle tremors.
The etiology, physical assessment findings, and treatment of torsade de pointes are outlined in Chart 3810 (p. 1110).
Ventricular Fibrillation
Ventricular fibrillation (VF), often referred to as v-fib, is a dysrhythmia marked by rapid, disorganized depolarization of the ventricles. There are no organized electrical impulses, and therefore, no coordinated atrial or ventricular contraction or palpable pulse. The myocardial cells appear to quiver rather than depolarize normally. With this dysrhythmia multiple ventricular sites initiate electrical impulses that are not transmit-
Significant ECG features of ventricular fibrillation include: P waves, PR intervals, QRS complexes, and QT intervals are all absent. Heart rate is not discernable because there are no waves or complexes to measure. Heart rhythm is irregular. Entire rhythm is ectopy.
P Waves: Not discernable; PR Interval: Not discernable; QRS Complex: Wide, distorted, and varying heights; QT Interval: not discernable; Rate: Rapid; Rhythm: Both regular and irregular; Ectopic Beats: All.
FIGURE 3837
Torsade de pointes.
CHAPTER 38
P Waves: Not discernable; PR Interval: Not discernable; QRS Complex: Wide, distorted, and varying heights; QT Interval not discernable; Heart Rate: Not discernable; Ectopic Beats: All.
FIGURE 3838
Ventricular fibrillation.
The etiology, physical assessment findings, and treatment of ventricular fibrillation are outlined in Chart 3810 (p. 1110).
Pulseless Electrical Activity

Pulseless electrical activity (PEA) is a clinical phenomenon that occurs when the heart muscle loses its ability to contract even though cardiac electrical activity is present. Cardiac electrical activity is seen on the monitor, but the patient has no detectable pulse or blood pressure. Though the electrical activity is represented as an organized rhythm (other than VT or VF) on the cardiac monitor, (e.g., bradycardia, heart block), the heart muscle is unable to respond to the electrical stimuli. Due to a variety of cardiac and noncardiac disorders such as acidosis, electrolyte imbalance, trauma, and cardiac rupture, the muscle is unable to respond to the stimuli, causing cardiac output and tissue perfusion to cease, and clinical death to occur. When PEA occurs biological death follows within minutes unless the cause is identified and treated (Beasley, 2003). Formerly, pulseless electrical activity was called electromechanical dissociation (EMD). The clinical outcome usually is poor despite aggressive life support measures. Significant ECG features of pulseless electrical activity include: P waves may or may not be present dependent on rhythm. PR intervals may or may not have a relationship to QRS complexes.
QRS complex may be narrow or wide. QT interval is variable. Heart rate and rhythm are variable, usually bradycardia. Ectopic beats may be present.
The etiology, physical assessment findings, and treatment of pulseless electrical activity are outlined in Chart 3810 (p. 1110).
Asystole
Asystole is a complete termination of all cardiac electrical activity. Without an electrical impulse, the atria and ventricles do not contract causing immediate loss of oxygen supply to the brain and tissues. In hospital settings efforts are usually made to reestablish cardiac activity but, often are futile. Figure 3839 is a rhythm strip showing asystole. In asystole, no measurable electrical activity exists and the rhythm strip appears as a straight line on the ECG monitor. The etiology, physical assessment findings, and treatment of asystole are outlined in Chart 3810 (p. 1110).
Nursing Management for Ventricular Dysrhythmias

As with any dysrhythmia, the first nursing responsibility for ventricular dysrhythmias is to assess the patients response to the
No measurable electrical activity
FIGURE 3839
Asystole.
1112 UNIT 8
Nursing Management of Patients with Cardiovascular Disorders of a loved one (Boyd, 2000). The research concluded that even family members with no medical background found it comforting to be with their loved one during the final moments of life. It is imperative that the health care team offer this opportunity and be sensitive to the family during this crisis period. If possible, it is optimal to have a health care team member be assigned to the family to answer questions, clarify information, and provide comfort (AHA 2005a). Since the nurse is at the bedside it typically becomes a nursing responsibility to keep the family informed, act as a liaison, and advocate for the patient. Chapter 17 includes a complete description of end of life issues.
specific abnormality. Nurses need to complete a health history to assess the risk factors related to the occurrence of ventricular dysrhythmias that are outlined in Chart 3810 (p. 000). Cultural awareness of populations that are at increased risk for ventricular dysrhythmias is discussed in the Cultural Considerations box (p. 000). Ventricular dysrhythmias have the greatest impact on cardiac output and are, therefore, the most serious. Depending on the variation in configuration and the frequency of occurrence, ventricular dysrhythmias require a variety of interventions from simple observation, to drug intervention, to advanced life support treatments. Generally, in monitoring units the health care practitioners provide protocols or standing orders for treating each type of ventricular dysrhythmia. The nurse must be knowledgeable of the treatment regimens required for each of the ventricular dysrhythmias based on the standing orders, basic cardiac life support (BCLS), advanced cardiac life support (ACLS), and agency specific protocols. When reporting ventricular dysrhythmias, the nurse needs to give a detailed description of the dysrhythmia pattern and the patients clinical response to the health care practitioner, so treatment is tailored to the specific dysrhythmia. The seriousness and treatment of ventricular dysrhythmias depend on the duration and the impact on hemodynamic stability (blood pressure and cardiac output). If the resuscitation efforts are initiated it is imperative that family and significant others be kept informed and be allowed to participate in the decision-making process. Research in the United States and the United Kingdom revealed that most family members wished to be present during the attempted resuscitation
National Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Since 1974 the American Heart Association has been publishing guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. The guidelines were most recently updated in 2005 and are based on evidenced evaluation from the 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care with Treatment Recommendations (International Liaison Committee on Resuscitation, 2005). These 2005 guidelines supersede the published 2000 guidelines for cardiovascular resuscitation and emergency cardiovascular care. The current guidelines contain recommendations designed to improve survival from sudden cardiac arrest and acute life-threatening cardiopulmonary disorders. These guidelines are based on the most extensive evidence review of CPR yet published. They confirm the safety and effectiveness of many treatments and recommend new treatments that have undergone evidence evaluation. Given that the guidelines do not apply to all situations, the leader of the resuscitation attempt may need to adapt application of the guidelines to unique circumstances. Finally, the guidelines also have streamlined the amount of information that rescuers need to learn and remember, and have clarified the most important skills that rescuers need to perform (American Heart Association, 2005). Future goals of the AHA are to continue to improve the guidelines based on new and evolving research and practice evidence. Foci will be placed on CPR education, and improving the effectiveness and efficiency of instruction, skill retention, and a reduction in barriers to action for basic and advanced life support providers (Chamberlain & Hazinski, 2003). Continuous quality improvement issues focus on reducing time to CPR and shock delivery and improving the quality of CPR provided (Jacobs et al, 2004; Peberdy et al, 2003). The National Guidelines box outlines the 2005 AHA national guidelines for selected CPR and emergency cardiovascular care.
CULTURAL CONSIDERATIONS
The term Brugada sign is an abnormal finding on an electrocardiogram (ECG) that refers to distance of at least 0.10 second from the onset of the QRS complex or the bottom of the S wave. Its presence may indicate Brugada syndrome which is an abnormality in the hearts electrical system that causes lifethreatening heart rhythm disturbances such as ventricular fibrillation. It occurs in patients with a structurally normal heart, and few or no coronary artery disease risk factor, and a family history of sudden cardiac death. Its possible to have a Brugada sign without having Brugada syndrome. This syndrome occurs most often in young adults. It also occurs with increased frequency in Asians. The cause isnt clear, but it appears to be inherited in some cases. Nursing implications are to assess young patients and patients of Asian decent who are having ventricular dysrhythmias with little to no risk of heart disease, for a family history of sudden cardiac death. Those considered at risk have: A family history of sudden cardiac death in young relatives A personal history of serious heart rhythm problems A personal history of severe fainting spells Immediate treatment for ventricular fibrillation is outlined on the American Heart Association ACLS guidelines for 2005. Long-term treatment includes antidysrhythmic medication therapy and an implantable defibrillator.
Source: Adapted from: Brugada Syndrome (2005). MayoClinic.com. http://www. mayoclinic.com/health/brugada-syndrome/AN00551. Retrieved July 13, 2006.
Nursing Management of Patients with Dysrhythmias

Nursing responsibilities when caring for patients experiencing cardiac dysrhythmias have been discussed throughout this chapter. To assist the learner, the patient care plan detailed below outlines a systematic approach to assessing and providing
CHAPTER 38
NATIONAL GUIDELINES for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Adult basic life support Advanced cardiac life support Electrical therapies CPR techniques and devices Adjuncts for airway control and ventilation Management of cardiac arrest Management of symptomatic bradycardia and tachycardia Monitoring and medications Post-resuscitation support Stabilizing of the patient with acute coronary syndromes
Source: Adapted from American Heart Association. (2006). 2005 international consensus on CPR and ECC science with treatment recommendations. Retrieved June 30, 2006, from http://www.americanheart.org/presenter.jhtml?identifier=3022512.
disease the best way to prevent dysrhythmias is to have the patient closely follow a treatment plan and make the necessary life style habit changes. Life style habits most closely associated with heart disease and the occurrence of dysrhythmias include: Smoking Alcohol use Caffeine intake Sedentary life style Stress Overweight/obesity Diet.
nursing care for these patients. Beginning with the assessment the nurse needs to identify what type of information is necessary to help find the risk factors and causes that precipitate the occurrence or progression of cardiac dysrhythmias. The nursing diagnosis is generated from the assessment data and guides the nurse toward desired patient outcomes and an intervention plan. To assist the nurse in the comprehensive assessment and interpretation of cardiac dysrhythmias, Chart 3811 (p. 1116) summarizes the characteristics of each type of dysrhythmia.
Health Promotion
As with any disorder the primary focus is on prevention of the onset and progression of the disease. Health teaching about risk factors and life style habits that cause the disorders that underlie the occurrence of cardiac dysrhythmias is essential for prevention. Once an individual has been diagnosed with heart
The nurse needs to develop a teaching plan that will effectively assist the patient in reducing or eliminating these risk factors. Additionally, the patient needs to be told to note if there is a pattern as to when the dysrhythmias occur, what brings them on and what makes them go away. For example, does it take a long time for the heart rate to return to normal after exercise or exertion? Instruct the patient to identify high-stress situations that bring on the dysrhythmias and examine with the patient how to diminish or avoid them as much as possible. All aspects of life including professional as well as personal relationships need to be examined. Since the Human Genome Project ongoing research has focused on gaining a better understanding of how genetic disorders can predispose to dysrhythmias. For example, a mutation of gene ankyrin-B is now known to cause cardiac arrhythmia syndrome (Hamby, Mittal, & Stein, (2006). The goal is to use gene-based therapies in the future to better treat dysrhythmias as well as identifying those individuals who are susceptible to dysrhythmias. Nurses will assist in identifying whether or not the patient has a family history of dysrhythmias. This in turn will aid in the early diagnosis, treatment, or prevention of the occurrence of life-threatening dysrhythmias.
NURSING PROCESS: Patient Care Plan for Dysrhythmias

Assessment Health history Social Habits Psychosocial assessment Physical assessment Coexisting conditions: Heart disease Chronic obstructive pulmonary disease Prescription and over-thecounter medications Clinical manifestations: Syncope Dizziness Fatigue Chest discomfort Nursing Diagnosis Alteration in tissue perfusion Altered cardiac output Anxiety related to fear of the unknown Knowledge deficit related to dysrhythmias and their treatment Expected Outcomes/Evaluation Maintain adequate cardiac output Free of clinical manifestations Reduced anxiety Verbalizes understanding of disorder and treatments Interventions Monitoring and managing the dysrhythmia Finding the cause Reducing risk factors through patient teaching Controlling incidence Minimizing anxiety Promoting home and communitybased care
1114 UNIT 8
CHART 3811
ECG Rhythm Normal Sinus Rhythm Sinus Bradycardia Sinus Tachycardia
ECG Measurements for Cardiac Rhythms

P Wave Present and Regular Present and Regular Present and Regular PR Interval 0.120.21 Normal limits QRS 0.060.12 Normal QT Interval 0.340.43 Lengthens to greater than normal Usually shortens Rate 60100 bpm 4060 bpm Rhythm Regular Regular Ectopic Beats None None
As the sinus rate accelerates, the PR interval tends to shorten slightly. Normal limits
Normal
100180 bpm
May be slightly irregular as rate accelerates; then becomes a rapid regular rate. Regularly irregular, with a variance of more than 0.08 seconds in the acceleration and deceleration phases. Underlying regular rhythm except where the sinus pauses occur. Regular except for premature PAC which may reset rhythm. Atrial rate regular. Ventricular rate may be regular or irregular
None
Sinus Arrhythmia
Present and Irregular
Normal limits
Changes with the heart rate becoming longer during the slow phase of the rhythm
60100 bpm
May occur during the slow phase of the rhythm
Sinus Arrest (Pause)
Present and Irregular
May be the same before and after sinus pauses.
Normal limits
Changes with the heart rate, becoming longer during the slow phase of the rhythm. Normal if rate is normal.
There may be marked bradycardia due to long sinus pauses. 60100 bpm
Possible during sinus pauses
Premature Atrial Contraction (PAC) Atrial Flutter
Present and Irregular When PAC occurs. No P wave f waves
Normal limits. May change with PAC only. None
Normal limits
PAC
Normal limits
Unable to obtain as T waves are buried in F waves
Depends on the AV conduction ratio. There may be a slow ventricular response, or there may be a fast ventricular response. T waves are buried in the f waves.
Flutter waves
Atrial Fibrillation
No P wave f waves
None
Normal limits
Unable to obtain because the T waves are buried in the f waves. Unable to obtain as T waves are buried.
Irregular
Fibrillation waves
Supraventricular Tachycardia (SVT)
Not seen buried in QRS complex
Not discernable
Within normal limits, unless distorted by buried P waves. Within normal limits, unless distorted by buried P waves.
100250 bpm
Regular or irregular due to varying conduction through the AV node. Irregular due to varying heart rates.
Rapid ectopic focus takes over rhythm
Paroxysmal Atrial Tachycardia (PAT)
At onset of rhythm, shape of P waves different from sinus P waves.
Varies with rhythm change
T waves buried, so unable to obtain with fast rhythm.
100250 beats/minute dependent on reference source.
Ectopic focus at onset of rapid rhythm
CHAPTER 38
CHART 3811
ECG Measurements for Cardiac RhythmsContinued

P Wave Present and Regular PR Interval Less than 0.12 second because the AV node is bypassed and contains presence of delta wave. Usually normal. QRS Greater than 0.10 seconds due to delta waves created by the abnormal conduction pathway. Normal limits QT Interval Shortens with tachycardia and lengthens with bradycardia. Rate High incidence of tachydysrthrymias. Rhythm Regular, except during heart rate changes. Ectopic Beats Delta waves: Occur just prior to R wave.
ECG Rhythm Wolff-Parkinson White Syndrome
Wandering Atrial Pacemaker
Present and Irregular Multiform
Normal. May be prolonged d/t slow heart rate
Atrial: Slow, bradycardic Ventricular: Slow, bradycardic Bradycardia to tachycardia.
Irregular due to changing pacemakers.
May be present due to the slow rhythm. May be present with slow rate.
Sick Sinus Syndrome
Present or absent depending on which dysrhythmia is occurring. May occur before, after, or buried in, the QRS complex May occur before, after, or buried in, the QRS complex
Variable depending on the rhythm
Normal limits
Variable due to rate change.
Atrial: Irregular Ventricular: Irregular
Junctional Escape Rhythm
Less than 0.12 second if the P wave occurs before the QRS complex Less than 0.12 second if P wave occurs before QRS complex for the ectopic beat. All others normal. Less than 0.12 second if P wave occurs before QRS complex for the ectopic beat. Greater than 0.20 second. Progressively prolonged until one P wave is not conducted and the sequence begins. Constant with conducted beats.
Normal unless distorted by P wave.
Normal unless impacted by rate.
Usually 4060 (normal intrinsic rate for junctional tissue). That of underlying rhythm.
Regular
May occur with slow rates
Premature Junctional Contraction (PJC)
Normal unless distorted by P wave for the ectopic beat. All others normal.
Normal
Regular except for the premature beat.
PJC
Junctional Tachycardia
May occur before, after, or buried in, the QRS complex
Normal unless distorted by P wave for the ectopic beat.
No specific change unless it is heart rate related.
Greater than 100 beats per minute.
Appears regular, but may increase its rate.
May occur due to muscle irritability.
First Degree AV Block Mobitz I/Wenckeback
Present and Regular Sinus P waves.
Normal Within normal limits.
Normal Within normal limits.
Variable Atrial rate within normal limits; ventricular rate slower than atrial.
Regular Atrial rhythm is regular; ventricular rhythm is irregular.
None Usually none unless they occur during period when no QRS has occurred and there is a long pause. May occur due to slow rate.
Mobitz II/SecondDegree Block
Present Not always followed by QRS
Intermittently absent; may be normal (AV node) or prolonged when present.
Within normal limits.
Atrial rate is regular; ventricular rate irregular and bradycardic
Atrial is regular; ventricular is irregular.
(continued)
1116 UNIT 8
CHART 3811
ECG Measurements for Cardiac RhythmsContinued

P Wave Present and Regular PR Interval P wave has no relationship to QRS complexes; therefore no PR interval is present. 0.120.20 second. QRS May be narrow (junctional rhythm), or wide (idioventricular rhythm) QT Interval May be rate related, but not directly affected. Rate Atrial rate is regular, 60100 bpm; nodal rate is 4060 bpm; ventricular rate is 2040 bpm. Rhythm Atrial is regular; ventricular may be regular or irregular. Ectopic Beats May occur due to slow rate.
ECG Rhythm Third-Degree (Complete) Heart Block
Bundle Branch Block
Present and Regular sinus P waves
Greater than 0.12 second. If notch higher on right, indicates right bundle branch block; if notch higher on left, indicates left bundle branch block. Broad and premature and has increased amplitude. R and T waves opposite sides of isoelectric line. Wide and bizarre, measuring > 0.12 seconds. R and T waves opposite sides of isoelectric line Height undulates
Within normal limits.
60100 beats/minute.
Regular
None
Premature Ventricular Contraction (PVC)
None with PVC.
None with PVC.
Prolonged with PVC.
Underlying rate may be normal or abnormal.
Irregular because PVCs are premature.
PVC more likely to occur during bradycardia when there is more time to emerge. All waves are ectopy
Ventricular Tachycardia
None Visible
Not discernible.
Not discernible.
100250 beats/minute.
Essentially regular.
Torsade de Pointes
Not discernable
Not discernable
Usually > 0.50 seconds in the beats preceding the onset of the rhythm None
Rates vary 200250 beats/minute.
Typically regular.
All waves are ectopy
Ventricular Fibrillation Pulseless Electrical Activity
None
None
None
Atrial: Absent Ventricular: Absent Variable, depends on rhythm; usually bradycardic. None
Irregular
All waves are ectopy May be present but none of the beats perfuse None
May or may not be present.
May or may not have a relationship to QRS complexes None
May be narrow or wide complex.
Variable.
Variable depends on rate.
Asystole
None
None
None
None
Source: Megan Redeen, (2007). California State University, Sacramento.
CHAPTER 38
NCLEX REVIEW
1. After reviewing the electrocardiogram of a patient, the nurse believes the tracing is normal. Which of the following did the nurse assess on this patients ECG?
1. 2. 3. 4. PR interval less than 0.8 second QRS complex 0.10 second Absent PR interval QT interval greater and 0.50 seconds
killed in an accident. The electrocardiogram shows a normal heart rate with shorter PR intervals. Which of the following should be included in this patients plan of care?
1. 2. 3. 4. Plan for cardioversion. Observe and treat the patient for anxiety. Medicate with calcium channel blockers. Provide carotid artery massage.
2. The nurse is assessing the QRS complexes on a patients electrocardiogram. The complex spans 3 small boxes on the ECG paper. The nurse would identify this patients QRS complex to be:
1. 2. 3. 4. 0.03 second 0.06 second 0.12 second 0.15 second
4. A patient is diagnosed with a junctional dysrhythmia. Which of the following should be included in this patients plan of care?
1. 2. 3. 4. Have a serum digoxin level drawn. Implement ACLS protocols. Prepare to administer magnesium. Prepare to administer lidocaine.
Answers for review questions appear in Appendix 5
3. A patient comes into the emergency department to be seen for chest pain that started after learning that his brother was
KEY TERMS
absolute refractory period p.000 action potential p.000 anion p.000 artifact p.000 asystole p.000 atrial dysrhythmia p.000 atrial fibrillation p.000 atrial flutter p.000 atrial kick p.000 atrioventricular (AV) node p.000 automaticity p.000 AV dissociation p.000 Bachmann bundle p.000 bigeminy p.000 bipolar lead p.000 bundle branch block p.000 bundle of His p.000 cardiac conduction system p.000 cardiac depolarization p.000 cardiac repolarization p.000 cation p.000 conductivity p.000 contractility p.000 dysrhythmia p.000 ECG waveform p.000 escape p.000 ectopic focus p.000 electrode p.000 excitability p.000 fascicles p.000 fill time p.000 first-degree AV block p.000 graph paper p.000 intra-atrial pathways p.000 ion p.000 irregularly-irregular rhythm p.000 isoelectric line p.000 J point p.000 junctional dysrhythmia p.000 junctional escape rhythm p.000 lead axis p.000 millivolts p.000 Mobitz I/Wenckebach p.000 Mobitz II/second-degree block p.000 negative deflection p.000 nodes (bundles) p.000 normal sinus rhythm (NSR) p.000 P wave p.000 pacemaker cell p.000 paroxysmal junctional tachycardia (PJT) p.000 positive deflection p.000 PR interval p.000 premature atrial contraction (PAC) p.000 premature junctional contraction (PJC) p.000 premature ventricular contraction (PVC) p.000 pulseless electrical activity (PEA) p.000 Purkinje network fibers p.000 QRS complex p.000 QT interval p.000 quadrigeminy p.000 refractory period p.000 relative refractory period p.000 resting membrane potential p.000 sick sinus syndrome (SSS) p.000 sinoatrial (SA) node p.000 sinus arrest p.000 sinus arrhythmia/dysrhythmia p.000 sinus bradycardia p.000 sinus tachycardia p.000 ST segment p.000 supraventricular tachycardia (SVT) p.000 T wave p.000 third-degree AV block (complete block) p.000 threshold p.000 torsade de pointes p.000 trigeminy p.000 12-lead ECG p.000 U wave p.000 unipolar lead p.000 ventricular dysrhythmia p.000 ventricular fibrillation (VF) p.000 ventricular tachycardia (VT) p.000 wandering atrial pacemaker p.000 Wolff-Parkinson-White syndrome (WPW) p.000
1118 UNIT 8
EXPLORE
MyNursingKit is your one stop for online chapter review materials and resources. Prepare for success with additional NCLEX-style practice questions, interactive assignments and activities, web links, animations and videos, and more! Register your access code from the front of your book at www.mynursingkit.com.
REFERENCES
American Heart Association. (2005a). Handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: Author. American Heart Association. (2005b). Part 5: Electrical therapies: Automated external defibrillators, defibrillation, cardioversion, and pacing. Supplement to Circulation: Journal of the American Heart Association, 112(24), IV-35IV-46. American Heart Association. (2005c). 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care: Part 2. Ethical issues. Circulation, 112, IV-6IV-11. American Heart Association. (2006a). BLS guidelines for healthcare providers. Dallas, TX: Author. American Heart Association. (2006b). 2005 International Consensus on CPR and ECC Science with Treatment Recommendations. Retrieved June 30, 2006, from http://www.americanheart.org/presenter. jhtml?identifier=3022512 Beasley, B. M. (2003). Understanding EKGs: A practical approach (2nd ed.). Upper Saddle River, NJ: Prentice Hall. Boyd, R. (2000). Witnessed resuscitation by relatives. Resuscitation, 43, 171176. Chamberlain, D. A., & Hazinski, M. F. (2003). Education in resuscitation: An ILCOR symposium: Utstein Abbey: Stavanger, Norway: June 2224, 2001. Circulation, 108, 25752594. Ellis, K. M. (2002a). EKG plain and simple: From rhythm strips to 12leads. Upper Saddle River, NJ: Prentice Hall Health. Ellis, K. M. (2002b). Q & A review of EKG. Upper Saddle River, NJ: Prentice Hall Health. Garcia, T. B., & Miller G. T. (2004). Arrhythmia recognition: The art of interruption. Sudbury, MA: Jones and Bartlett. Hamby, R. L., Mittal, S., & Stein, K. M. (2006). Arrhythmia. Retrieved July 17, 2006, from http:// heart.healthcentersonline.com/ arrhythmia/arrhythmia8.cfm Holtschneider, M. E., McBroom, K. G., & Patterson, A. (2006). ECG everywhere. Advance for Nurses, 3(13), 20. International Liaison Committee on Resuscitation. (2005). International consensus on cardiopulmonary resuscitation and emergency cardiovascular care since with treatment recommendations. Circulation: 2005; 112: III-I-III-136. Jacobs, I., et al. (2004). Cardiac arrest and cardiopulmonary resuscitation outcome reports: Update and simplification of the Utstein templates resuscitation registries. A statement for health care professionals from a task force of the international liaison committee on resuscitation (AHA, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, interAmerican Heart Foundation, Resuscitation Council of Southern Africa). Resuscitation, 63, 233249. Olshansky, B. et al. (2006). Atrioventricular nodal reentry tachycardia (AVNRT). eMedicine from WebMD. Retrieved July 13, 2006, from http:// www.emedicine.com/med/topic2955.htm Peberdy, M. A. et al. (2003). Cardiopulmonary resuscitation of adult in the hospital: A report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation. Resuscitation, 58, 297308. Porth, C. M. (2004). Essentials of pathophysiology: Concepts of altered health states. Philadelphia: Lippincott Williams & Wilkins. Shade, B., & Wesley, K. (2007). Fast and easy ECGs: A self-paced learning program. Boston: McGraw-Hill. Walraven, G. (2006). Basic arrhythmias (6th ed.). Upper Saddle River, NJ: Prentice Hall Health.

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38

Nursing Interpretation of the Electrocardiogram

Outcome-Based Learning Objectives

THE ELECTROCARDIOGRAM (ECG) is the most important

Anatomy of the Heart

Cardiac Conduction System

Nursing Interpretation of the Electrocardiogram 1075

AV node Bundle of His Purkinje fibers Left bundle branch

Atrioventricular (AV) Node and AV Junction

Electrical conduction system of the heart.

Bundle of His and Bundle Branches

Sinoatrial (SA) Node

Purkinje Network Fibers

Electrolytes Affecting Cardiac Function

Cardiac Depolarization and Repolarization

Nursing Interpretation of the Electrocardiogram 1077

Closed K channel Cell interior

Electrolyte movement during an action potential.

Summary of the Cardiac Conduction System

Na+ ATP K+ Na+ Ca+ K+ K+ K+

Inside cell CELL MEMBRANE Outside cell

Cardiac Waveform and Time Intervals Measured on ECG

ECG Monitoring Equipment

Waveform relationship to cardiac conduction system.

Nursing Interpretation of the Electrocardiogram 1079

Beats/min <92/min 126.20 >180/min

Gain Set mode Equalize Push/Reset

Electrodes, lead wire, and cardiac monitor.

Isoelectric line MCL 1

Lead II and MCL1 ECG configurations.

Nursing Management of Patients with Cardiovascular Disorders

Indications for a 12-Lead ECG

12-Lead Electrocardiogram (ECG)

MCL1 is modified chest lead 1. It's like V1.

Electrode placement for bedside cardiac monitoring.

Nursing Interpretation of the Electrocardiogram 1081

Horizontal and frontal planes. (need diagram rendered)

12-Lead ECG Procedure

Cable Connection and Machine operation

Patient Instructions Documentation

Signal Averaged Electrocardiogram

Nursing Management of the Monitored Patient

Cardiac Monitoring Systems

Nursing Interpretation of the Electrocardiogram 1083

Procedure for Continuous ECG Monitoring

Lead Wire and Cable Connection

Monitor Connection and Adjustment

ECG Graph Paper

.06.12 sec QRS

0.04 sec 0.20 sec 0.04 sec .12.20 sec

QT .34.43 sec Isoelectric line

ECG graph paper

Nursing Interpretation of the Electrocardiogram 1085

Stepwise Process for ECG Strip Evaluation

ECG Rhythm Strip Evaluation and Documentation

Normal Sinus Rhythm

Normal sinus rhythm.

Nursing Interpretation of the Electrocardiogram 1087

Sinus Dysrhythmias: Etiology, Physical Assessment, and Treatment

Nursing Management of Patients with Cardiovascular Disorders

Sinus Dysrhythmias: Etiology, Physical Assessment, and TreatmentContinued

Sinus arrhythmia/ dysrhythmia

Nursing Interpretation of the Electrocardiogram 1089