Nursing Interpretation of the Electrocardiogram
Kathleen Osborn Annita Watson


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.

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 body’s nervous systems. The heart’s 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 38–1 ). 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-



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


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 heart’s 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.

1076 UNIT 8

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 38–1 ). 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 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 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 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 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


Nursing Interpretation of the Electrocardiogram 1077

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 (0–4) of the action potential are shown in Figure 38–2 . 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 38–3 ). 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 38–2 ). 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



Closed Na channels

Closed K channel Cell interior


Anionic protein


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 38–2 ). The relative refractory period is a period when repolarization is almost complete (see Figure 38–2 ). 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


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 38–1 , 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.

Changes in the configuration of the waveforms or lengthening and/or shortening of time intervals may indicate an abnormality in the heart. It follows the T wave. and 43 . • P wave—The P wave represents contraction or depolarization of the atria. 42. and time intervals is obtained either with an electrocardiograph (ECG machine) or on a bedside cardiac monitor. 41. . • T wave—The T wave is ventricular recovery or repolarization. In other words. The ST segment signifies ventricular repolarization. These abnormalities are discussed in detail in Chapters 40. and there must always be a positive. The electrodes are connected to a cardiac monitor by lead wires. the electrical action potentials produced in the heart are widely conducted throughout the body via these tissues and fluids. specific equipment is needed including an electrode. it represents the beginning of the atrial contraction to the beginning of the ventricular contraction. represents the time it takes for the impulse to travel from the SA node down the intra-atrial pathways to the ventricles. as a connector from the electrode to the LA cardiac monitor. One complete cardiac cycle has five to six waveforms and time intervals. QRS. causing them to depolarize. and monitor or oscilloscope. These waveforms are referred to as P. sometimes referred to as the PRI or PR segment. represented on the ECG as an almost isoelectric line. are recorded. S. which represent the time it takes for the impulse to travel from one anatomical location in the heart to another. Both the right and left atria depolarize at the same time. described next. 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. As the electrical impulse travels through the cardiac conduction system. 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. a negative. and these colors assist the practitioner in attaching the lead wires to the appropriate electrode. • QRS complex—The QRS complex consists of the Q. Typically. • PR interval—The PR interval. To obtain an ECG tracing. R. An electrode is much like a camera in that it takes pictures of the electrical activity in the heart. a graphical representation of the signal referred to as a waveform is produced and recorded with monitoring equipment. These are described here and depicted in Figure 38–4 . the term also is used when discussing a view or picture of the heart from a particular angle or vantage point. but it is frequently seen in exercise. where they are converted into waveforms. and most frequently with low potassium levels. Q. The graphical depiction of these impulses. 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. Figure 38–5 shows the elecAV node trodes. The following sections discuss the method used to evaluate waveforms and time intervals. and QT.1078 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders diac cycle. These time intervals are called PR. The ground lead minimizes outside P ST QRS T U RBB LBB P QRS PR QT FIGURE 38–4 Waveform relationship to cardiac conduction system. and T. these wires are color coded according to machine manufacturer. In addition to using the term as just described. Both the absolute and the relative refractory periods are in place during the T wave. time intervals. • ST segment—The ST segment is a line extending from the S wave that gradually curves upward to the T wave. The impulses or action potentials can be detected from any point in the body.” LV 8 Lead Placement Body tissues and fluids surround the heart. waveforms. The rhythm strip gives the health care practitioner information about where the pathological processes are SA node occurring in the heart. and S waves. • J point—The point at which the QRS meets the ST segment is called the J point. Its etiology is unknown. Electrodes must be placed in certain positions on the body in order to obtain a clear picture of the electrical impulses in the heart. lead wire. waveforms characteristic of a given anatomical location are recorded. R. In this respect one can think of the lead as the “eye of the camera. and cardiac monitor. Cardiac Waveform and Time Intervals Measured on ECG When the electrical impulse leaves the SA node. and a ground electrode/lead. therefore. 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. 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. The printed version is called a rhythm strip or ECG strip. lead wire. Additionally. The term lead is used in different contexts when discussing ECGs. in drug toxicity. • U wave—The U wave is present only on some people’s ECG.

the lead or leads chosen depend on the desired view of the heart.10 0.0 -1. However.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1079 Device 1.50 1. For bedside monitoring it is not practical or necessary to have a 12-lead ECG or 12 continuous views of the heart. 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.70 2. The lead axis refers to the imaginary line drawn between the positive and negative electrodes. at the bedside typically only two simultaneous leads are used to view the heart with the five-electrode system. Think of the heart on a pedestal that one is able to move around while a camera takes pictures from various angles. Each electrode senses the flow of current in the heart in relation to the lead axis. This gives the practitioner 12 different views of the cardiac electrical activity.0 1.20 >180/min 0. Commonly the two leads that are run simultaneously are lead II and MCL1. view cardiac electrical conduction from different perspectives.0 0 25 50 75 100 125 150 175 200 Lead wire Gain Set mode Equalize Push/Reset FIGURE 38–5 Electrodes.5 0 Beats Thresh Limit # of samples 5300 Sample rate 5000 Set limit 1. as seen with a 12lead ECG.30 0. if more than one lead or picture of the heart is required.00 Channel 0 Chart 2. 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. If the axis is directed toward the negative lead.50 -1.010 f2 0. Multiple leads. there is an upward or positive deflection on the ECG tracing (above the isoelectric line).00 0.50 Electrode Max Peak 1.00 2.0 1. The specific dysrhythmia being monitored or anticipated may dictate the type of lead chosen. To obtain a single bedside ECG rhythm strip. However.5 f1 0.40 0. For example. and one ground. one negative. . lead II produces easily identifiable upright P waves and clear QRS Isoelectric line MCL 1 FIGURE 38–6 Lead II and MCL1 ECG configurations. Therefore.37 Time 0. Figure 38–6 shows a cardiac rhythm strip that has simultaneous lead II and MCL1 ECG views. The lead chosen is dependent on the unit policy and nurse and/or health care practitioner preference. No single monitoring lead is ideal for every patient. Therefore. lead wire.0 Below limit Beats/min <92/min 126.20 0.0 -2.0 Volts 0. These two leads provide different perspectives of the various normal and abnormal ECG configurations.5 1.31 Chirp output Chirp alarm parameters # Sam 700 amp 1 1.00 0. a minimum of three electrodes is required: one positive. If the axis is directed toward the positive lead. five electrodes are placed to increase the monitor’s capability beyond the three-electrode monitoring system.00 -5. there is a negative deflection on the ECG tracing (below the isoelectric line) Figure 38–6 .0 0. Either lead II or modified chest lead1 (MCL1) is commonly used for threeLead II electrode bedside monitoring.0 1. and cardiac monitor. The MCL1 is one of the V leads from the 12-lead ECG that is modified for bedside monitoring.17 Threshold 0. electrical interference.

FIGURE 38–7 Electrode placement for bedside cardiac monitoring. There are 3 bipolar and 9 unipolar leads in a 12-lead ECG. 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.1080 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders complexes. The color coding on the lead wire gives the nurse information about whether the lead is positive or negative. Placement of the electrodes depends on the lead being monitored and whether a three. Hudak. A bipolar lead has electrodes with opposite polarity. one positive and one negative. 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). to assess damage accurately requires viewing the area with more than one lead. Fontaine. Figure 38–7 shows the position of the electrodes for both lead II and MCL1. CHART 38–1 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. Typically the color black is negative. 2006). . depending on where a given lead is placed. An MCL1 lead is useful for evaluating abnormalities in the ventricles. Both bipolar and unipolar leads provide information in one direction only—between two points. A unipolar lead has only a positive polarity (Walraven. Figure 38–8 shows the horizontal plane and the frontal plane views. & Gallo. These added views provide a complete picture of the cardiac electrical system. 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. it provides – G Lead II: Positive electrode left abdomen Negative electrode right shoulder Ground electrode left shoulder + G – + MCL1: Positive electrode 4th ICS RSB Negative electrode left shoulder Ground electrode right shoulder MCL1 is modified chest lead 1. Frequently. It's like V1. In the five-lead system red and brown colors also are used and their polarity changes depending on the lead being monitored (Morton. and green is ground. whereas a 12-lead ECG provides 12 individual views or “snapshots” of the heart’s electrical patterns. necrosis. white is positive. Chart 38–1 provides the indications for a 12-lead ECG. 2005). A single-lead ECG rhythm strip gives one view of the electrical activity of the heart. Thus. 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.or five-lead system is being used.

• Palpate the intercostal spaces along the sternal border. • Record patient’s response to procedure. whereas the 6 chest (precordial) unipolar leads. and use of cardiac medications. For example. • Use 10 electrodes for the standard 12-lead ECG: 6 on the chest and 4 on the limbs. • Document patient’s height. lead V4 is over the cardiac apex. The standard bipolar leads and the augmented limb leads provide the 6 frontal plane leads of the 12-lead ECG. The limb leads are placed on the flat surfaces just above the wrists and ankles. and ST segment are used to evaluate the presence of damage. the nurse must have knowledge of the lead placement for each of the 12 leads. whereas others can record 3. The positive electrode is placed on 6 different sites across the chest as shown in the diagram in Figure 39–1 (p. Improper placement may result in inaccurate information and treatment. lead V1 evaluates the right ventricle. and the lead placement is used to identify the area of damage. 000) shows the correct placement of the electrodes. The Q wave. The type and sophistication of ECG machines varies. 000). T wave. or all 12 leads simultaneously. • After completing the ECG. Three more frontal plane. leads V2 and V3 span the interventricular septum. Patient Instructions Documentation • Explain the procedure and the rationale for the test prior to performing an ECG. or increase. until the fourth one is reached. remove electrodes and clean the skin as necessary. evaluate the horizontal plane of the heart. their size so they will show up on the ECG paper (Ellis. • Document reason for the ECG. 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. unipolar augmented limb leads can be created by using a central terminal.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1081 so named because they generate such small waveforms that the ECG machine must augment. Augmented leads are 8 CHART 38–2 12-Lead ECG Procedure • Bring the portable ECG machine to the patient’s bedside in any type of patient care setting. Frontal plane Horizontal plane FIGURE 38–8 Horizontal and frontal planes. unbroken contact with the skin. Chest hair may interfere with skin contact and. 2006). When performing an ECG. and leads V5 and V6 evaluate the lateral wall. some can record only one lead at a time. III—are applied to the right arm (RA). Electrical current flowing toward a positive electrode creates a positive deflection on the ECG paper. Chart 38–2 describes the procedure for obtaining a 12-lead ECG. and aVF. weight. 2002). • Leave the electrodes in place if the patient is going to have serial ECGs to ensure consistency of multiple readings. and left leg (LL). breathe normally. If there is an amputation. Figure 39–1 (p. The standard bipolar limb leads—I. and ST segment. aVL. should be shaved. 6. whereas electrical current flowing toward a negative electrode creates a negative deflection on the ECG paper (Walraven. The right leg electrode acts as a grounding electrode. II. T wave. and refrain from speaking while obtaining the ECG. . left arm (LA). • Adjust the ECG machine to obtain a clear picture of the cardiac electrical activity. • Place limb electrodes away from bony prominences and areas of significant muscle movement to prevent interference of other muscle activity. if any. Each lead records the following electrical conduction pattern: • Lead I records conduction from RA to LA. (need diagram rendered) a picture of the electrical activity from that vantage point within the heart. the lead is placed on the remaining stump. • Advise the patient to lie still. Chapter 40 discusses the myocardial damage associated with changes in the Q wave. These leads are aVR. • Lead II records conduction from RA to LL. if so. for placement of the first chest electrode. • Document current clinical manifestations if present and chief complaint. The electrodes must have firm. • Lead III records conduction from LA to LL. Electrode Placement Cable Connection and Machine operation • Connect the cable that is attached to each of the electrodes to the ECG machine. These chest leads provide the 6 horizontal leads of the 12-lead ECG. V1—V6.

patient education is essential. These signals. The patient keeps a diary of signs and symptoms and the associated activity performed. referred to as a Holter monitor. 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. 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.) and a diagram of where to place them. 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. This system. A signal averaged ECG also is used to evaluate His bundle activity. a signal averaged ECG is able to distinguish low-level signals not detected by the traditional ECG. Because it may be stressful and frightening for a patient to have his heart be continuously monitored. This method often is used as a follow-up evaluation for patients with cardiac pacemakers. are low-amplitude. Additional information on the Holter monitor is discussed in Chapter 39 . The ECG is recorded and evaluated at another location. The more familiar the nurse is with the patient and the monitoring system. which is typically at the nurses’ station. Hardwired systems have the capability to print a rhythm strip and provide visual and audible alarms when abnormalities in the heart rhythm occur. Nursing responsibility for monitored patients includes knowledge of the patient’s specific rhythm in order to assess for changes. It is necessary. Skin preparation. not controlled. referred to as late potentials. Precise lead placement is critical to accurate continuous cardiac monitoring. if present. With this type of monitoring. With the assistance of a computer. worn by the patient. electrode placement. Therefore. Another form of continuous ECG monitoring is typically done in the outpatient setting. the patient must be informed of its purpose and any necessary precautions. high-frequency spikes that occur at the end of the QRS complex and extend into the ST segment. The significance and severity of the individual rhythms are presented under each rhythm discussed throughout the chapter. presence of a left ventricular mass. where they are placed. or weakness. The nurse needs to be knowledgeable about electrode placement for the lead that has been designated for monitoring the patient. The nurse must stress that excessive movement will cause the alarm to go off frequently. Hardwired monitoring is done in critical care areas. Once a transient cardiac problem has occurred it is too late to change lead placement so that an accurate analysis can be performed. 8 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. whereas others produce them separately. The transmitter. dyspnea. 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 38–3).1082 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders mal activities of daily living. and surgical repair of congenital heart disease. that the patient report these conditions as they occur. V2. which is late into the QRS complex and ST segment. The electrode placement should be as comfortable as possible for the patient. effects of thrombolysis. the nurse needs to explain the procedure and why it is necessary. or when the heart is filling with blood. 8 Signal Averaged Electrocardiogram Certain abnormal impulses are conducted during diastole. Chapter 39 discusses pacemakers. This system allows the patient to ambulate about the unit while still being monitored. therefore. This system typically is able to monitor more than one lead simultaneously. The nurse must verify lead placement at the beginning of each shift. The hardwired system has an oscilloscope at the bedside and in a central location such as the nurses’ station. it can be accomplished by two methods. Some manufactures have the electrode and the lead wire attached. and monitor connection are described in Chart 38–3. Describe the electrodes. and depending on the lead used the system also is able to visualize ST segment depression and elevation. First. The patient needs to understand that this system does not report clinical manifestations such as angina. etc. can result in ventricular tachycardia and sudden cardiac death. by the equipment. These impulses may be present in a patient who has survived an acute myocardial infarction and. 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. 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 patient’s clinical response to the abnormalities. When continuous ECG monitoring is necessary. The nurse must be cognizant when obtaining an ECG about which rhythms require immediate notification of the health care practitioner for emergent treatment. These systems are computerized and therefore are able to interpret and store dysrhythmias in a memory bank. transmits the rhythms to a central bank of monitors. Documentation of the lead used needs to be included in the patient’s record. and how they are connected to the monitor. Transtelephonic monitoring is another method of outpatient ECG monitoring. the risk for lethal dysrhythmias can be assessed. Whichever system is being used. 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. Each ECG machine has its own method of identifying specific lead names (V1. the patient can be hardwired to a monitor whereby the leads are connected directly from the bedside monitor to the patient. The second method for continuously monitoring patients is with radio waves from a battery-operated transmitter. the quicker problems can be diagnosed . Nursing Management of the Monitored Patient Prior to placing the patient on ECG monitoring. It is essential that the patient understand that the heart is just being monitored.

negative. a dry washcloth. or a gauze pad. Assessment of patient tolerance of rhythm changes is the first nursing action. allow it to air dry. The problem could be as simple as the patient’s tapping the electrode. Alarm Setting Documentation • Document lead used. and appropriate action taken. unclear tracing. . These measurements help determine whether the rhythm falls within the time limits of normal cardiac activity. because these areas are prone to produce noncardiac waveforms and interference. for example. Abnormal measurements may indicate a malfunction of the cardiac conduction system and will be discussed later in conjunction with the various dysrhythmias. • Recognize that the alarms have upper and lower heart rate limits. Electrode Attachment Lead Wire and Cable Connection • Connect the electrode to the lead wire. For example. ectopic beats. to determine different alarm limits. • Position electrodes on the chest wall at prescribed locations depending on the lead or leads being monitored. • Attach the opposite end of the lead wire to the cable. and type of rhythm/dysrhythmia. Typically a snap attaches the lead wire to the electrode. They must be kept informed of when the patient needs to be off the monitor or of physical activities. • Set the alarm approximately 20 beats above and below the patient’s resting intrinsic heart rate. especially if it is a new abnormality. thick muscles. • Adjust the monitor to increase the size of the PQRST complex for more accurate interpretation. • Always leave the alarm on. • Follow institutional policy. it needs to be replaced. If the skin around the electrode becomes irritated the electrode must be removed and relocated.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1083 CHART 38–3 Procedure for Continuous ECG Monitoring • Choose an area to place the electrodes where there are no bony prominences. poor contact. be careful not to cause skin breakdown. which is approximately 16 inches long. neurological status. The skin will become reddened with the rubbing. • Wipe the skin with an alcohol sponge if skin is oily or a moist wipe. ECG Graph Paper ECG graph paper is specialized paper on which the ECG pattern is recorded. • Be aware that when the alarm sounds. Monitor Connection and Adjustment • Attach the cable to the monitor. the nurse then troubleshoots the equipment for problems such as a dry electrode or a disconnected wire. the first nursing responsibility is to check the patient. Communication with all personnel caring for the patient and observing the monitor is critical. When the electrode becomes dry or loose. and free of hair. and/or every 48 hours to avoid skin irritation. • Record ECG changes and patient’s response to changes. After determining patient status and stability. occurring that may sound the alarms. When abnormalities appear on a cardiac rhythm strip it is an essential nursing responsibility to assess the patient’s tolerance of the rhythm. Tolerance to the rhythm is assessed by obtaining and evaluating vital signs. • Change electrodes when wet. It may be necessary to shave the chest area of male patients. QRS width. It also is essential that the nurse is knowledgeable of which cardiac disturbances are reportable and/or life threatening. and no action would be necessary. • Make sure that the electrode pads are moistened with conducting gel prior to placing them on the chest to increase electrical conductivity. QT interval. • Remove dead skin cells to improve electrical conductivity by rubbing the skin with the rough patch on the back of the electrode. dry. such as bathing. A dry electrode is not effective for conducting the electrical activity. angina. and ground leads. • Recognize that movement by the patient may cause the alarm to sound falsely. • Read the operating instructions for the specific brand of monitor prior to use. The rhythm needs to be documented on the patient’s record. The paper is designed to allow the measurement of various calculations related to the electrical activity of the heart. The nurse needs to be knowledgeable about what changes need to be reported to the health care practitioner. The cable has individual color-coded receptacles or holes for each lead wire. It is standard nursing protocol to measure these calculations when a patient is on a cardiac monitor. that person must be informed of the patient’s leaving the floor and increased physical activities. • Prepare the skin for electrode placement by making sure that it is clean. prior to assessing for problems with the equipment. and the presence of signs and symptoms of decreased cardiac output. or skin folds. • The lead wires are color coded to represent positive. if there is a monitor technician. • Document PR interval. if present.

04 second in time. which is marked off in 3-second intervals with tick marks.5 boxes to 3 boxes. ECG Measurements When assessing either a rhythm strip or a 12-lead ECG. With a regular rhythm.12 sec QRS P T PR QRS QT 0. The normal HR is 60 to 100 beats per minute. Figure 38–11 demonstrates where each measurement begins and ends.43 sec Isoelectric line FIGURE 38–9 ECG graph paper FIGURE 38–11 ECG measurement. both the individual PQRST complexes need to be evaluated as well as the relationship of each individual complex to the overall rhythm. The shape of the QRS complex varies from individual to in- FIGURE 38–10 Calipers. • The large square equals 5 small squares.12 second or 1.34 to 0.43 second or 8. Count up the number of PQRST complexes that occur in 6 seconds and multiply that number by 10. 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. This measurement is rarely used because the size of the picture or millivolts can be adjusted at the monitoring station.12–. Both the amplitude and the voltage may be measured on the paper. For example. The normal range is from 0. • Five large squares represent 1 second.34–.20 second or 3 small boxes to 1 large box. The normal QT interval is 0. the distance between R waves is equal.06 to 0.20 sec QT . Two large squares on this axis equal 1 millivolt. • The large square is 5 mm in length and represents 0.20 sec 0. 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.20 second in time. This paper is standardized to allow for consistency in ECG measurement and strip analysis. • Heart rate—This is measured by using the very top of the ECG paper. The tick mark is a small straight line or hash mark above the tracing. QRS complexes are mostly positive in the lead II and mostly negative in the MCL1 lead (see Figure 38–6 ). The normal PR interval is from 0. thereby reducing the consistency of this measurement. • QT interval—This is measured from the Q wave to the end of the T wave. These squares are used to measure time intervals as follows: • The smallest square is 1 millimeter (mm) in length and represents 0. • QRS complex—The QRS complex is measured from the beginning of the Q wave to the end of the S wave. This method provides a general estimate of the heart rate. The vertical axis measures the amplitude and is stated in millivolts (mV). • Heart rhythm—This 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.04 sec 0. Calipers (Figure 38–10 ) are the instrument used to take all these measurements.12 to 0. The assessment of an ECG configuration includes the following: • P wave—There should be one P wave for every QRS complex.500.5 to 11 boxes.1084 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders dividual and also depends on the ECG lead being used. • PR interval—This is measured from the beginning of the P wave to the beginning of the QRS complex.04 sec . . The horizontal axis is divided into small squares. .06–. The ECG graph paper is arranged as a series of horizontal and vertical lines. Not everyone has a discernable Q wave. Figure 38–9 shows an example of ECG graph paper.

clammy skin.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1085 FIGURE 38–12 Artifact. Ectopic foci may affect cardiac output and must be assessed and documented carefully for their impact on the hemodynamic stability of the patient. the ST segment is isoelectric. Ventricular: how many R waves in 6 seconds times 10. such as poorly grounded beds and/or IV infusion pumps • Equipment failures. Any wave that has an upward deflection. Both methods work best when the rhythm is normal. QRS Complex QT Interval Rate Ectopic Focus Ectopic focus is a heartbeat originating from a site other than the primary cardiac pacemaker tissue. This is shown in Chart 38–4. These abnormalities are discussed at length throughout the remainder of the chapter.12 to 0. In a lead II the normal P wave has a positive deflection.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 10.20 second)? If the PR interval varies. When artifact is present. then there is a high probability of an ab- normality occurring in the conduction system. using a simple stepwise process provides a consistent method for rhythm strip evaluation. the S wave is negative. When the SA node fires. 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. the PR interval is isoelectric. which is above the isoelectric line. The terms dysrhythmia. This interference is due to several causes: • Malfunction of electrodes possibly due to dry conductive gel. or dense chest hair • Patient movement. 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. if so. it is difficult to diagnose cardiac abnormalities. A second method is to count the number of large boxes between two R waves and divide by 1500. Regularity (also called rhythm) Ectopic Beats ECG Rhythm Strip Evaluation and Documentation When evaluating an ECG rhythm strip. Depending on the lead. the R wave is positive. and any waveform that goes below the line is referred to as a negative deflection. the Q wave is the first negative deflection. which occurs when a patient is in contact with an outside source of electricity. is referred to as a positive deflection. the baseline or isoelectric line becomes fuzzy. If the rhythm strip falls out of the normal parameters. Figure 38–12 depicts artifact. the ECG waveform (the actual tracing on the graph paper) begins and moves away from the isoelectric line (see Figure 38–12 ). CHART 38–4 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. arrhythmia. and ectopic focus all mean the same thing and are used interchangeably. certain waves normally are positive and certain ones are negative. Isoelectric Line The isoelectric line marks the beginning and ending point of all waves. which precipitates a fluctuating isoelectric line that corrects itself when the patient lies still • Improper grounding. making it is necessary to correct the cause of the artifact. . which need to be exchanged for new equipment. and the T wave is positive. Because of this interference or artifact.06 to 0. What is the heart rate? Is it regular? Is it irregular? Are there any patterns to the irregularity? Are there any ectopic beats. such as broken wires or cables on the ECG equipment.

P Wave: Present 1 P wave/QRS complex. The most common dysrhythmias begin at the top of the heart with the SA node. QT Interval 0. The cardiac output decreases as the severity of the dysrhythmia increases. the severity is greater due to their impact on cardiac output. PR Interval: 0. and urine output. causing cardiac dysrhythmias to occur.” occurs when the SA node is firing at a rate of less than 60 beats per minute. and sinus arrest.34 and 0. Nursing Management When the patient is on a cardiac monitor. The final area of the heart where dysrhythmias may occur is in the ventricles. the date and time of rhythm strip collection. Ventricular: 90 bpm. QRS Complex: 0. QRS.12 and 0. level of consciousness. the nurse must begin the same process again: measure. not the dysrhythmia. • There is a 1:1 ratio of P wave to QRS complex. For exam3 seconds 6 seconds Sinus Dysrhythmias The four common dysrhythmias associated with the sinus area of the heart are sinus bradycardia. it becomes ischemic and irritable. which originate in different parts of the heart. there are not enough contractions per minute to pump the amount of blood needed for normal cardiac output. assess.18 second. often called “sinus brady. and the ECG lead used for the rhythm strip should be documented.43 second. Heart rhythms are categorized according to the cardiac structure in which they begin. or their site of origin. assessing. The next area in the heart where dysrhythmias may occur is in the intra-atrial pathways. the AV node or junction is where junctional dysrhythmias occur. because while there is adequate time for the heart to fill up with blood. There are a number of dysrhythmias. Rhythm: Regular. Whenever changes occur in the heart rhythm. Heart Rate: Atrial: 90 beats per minute (bpm).36 second. the electrical features of the rhythm should be documented including the presence of a P wave. P waves are present.06 and 0. Corresponding clinical manifestations associated with a given rhythm also need to be documented in the record. and document the patient’s rhythm strip at least every shift and more frequently depending on the patient’s condition and agency protocol. These ventricular dysrhythmias are considered to be the most dangerous because they precipitate the most profound decrease in the cardiac output. • Atrial and ventricular rate is between 60 and 100 beats per minute (beats/minute). This condition may lead to serious dysrhythmias and warrants careful monitoring. • QT interval is between 0. node.20 second. • QRS complex is between 0. pulse. Treatment is always based on the hemodynamic impact of the dysrhythmia.1086 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders ple. Sinus Bradycardia Sinus bradycardia. the heart rate. sinus tachycardia. When observing. sinus arrhythmia/dysrhythmia. Dysrhythmias When the cardiac muscle does not receive enough blood. and the presence of ectopy (ectopic focus). the PR interval. The following criteria must be present to be NSR: • P wave has a normal and consistent shape and appears before every QRS complex. .12 second. and treating dysrhythmias. As the dysrhythmias occur anatomically lower in the heart. Ectopic Beats: None FIGURE 38–13 Normal sinus rhythm. change in blood pressure. 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.06 second. An ECG strip showing sinus bradycardia is in Figure 38–14 . The nurse needs to understand when it is appropriate to report a change in the ECG to the health care practitioner. but because of this variable. A dysrhythmia is an abnormal disturbance of the electrical conduction system of the heart. the width of the QRS complex. most institutions require that a rhythm strip is attached to the patient’s chart once every shift and/or when a change in the rhythm occurs. • Atrial and ventricular rhythm is regular. The only difference between sinus bradycardia and normal sinus rhythm (NSR) is the heart rate. Sinus bradycardia may result in decreased cardiac output. assess. referred to as atrial dysrhythmias. The patient’s name. Moving anatomically down to the next area of the conduction system. QT) (Figure 38–13 ). it is critical for the nurse to remember that it is the patient being treated. Additionally. Sinus means the rhythm originated in the SA node. 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. sinus bradycardia is not normal. This chapter addresses dysrhythmias according to location in the heart. beginning at the top with the atrial dysrhythmias. therefore. or sinus. it is the nurse’s responsibility to measure. Nursing Documentation When documenting the heart rhythm in the patient’s record. These types of dysrhythmias are called sinus dysrhythmias due to their origin in the SA. and rhythm (regular verses irregular). the QT interval. • PR interval is between 0. and document the rhythm strip.

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. Ventricular: 40 bpm. Attempt to identify and treat the cause.CHAPTER 38 6 seconds Nursing Interpretation of the Electrocardiogram 1087 Sinus tachycardia results in increased oxygen consumption.08 second. Additionally. The rate of impulse formation and conduction varies with the respiratory cycle. • The QT interval tends to lengthen. If symptomatic. 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 athlete’s heart Physical Assessment Pulse: Less than 60 beats per minute and typically regular. Rhythm: Regular. the P to P and R to R intervals change with respiration. 1091). the following clinical manifestations may occur: • Angina • Syncope • Generalized weakness • Dizziness • Shortness of breath. P Wave: Present. Treatment Treat only if symptomatic. Treatment is typically instituted when syncope and/or alteration in consciousness occurs. The etiology. The heart rate increases during inspiration and decreases with expiration. physical assessment findings. Assess for changes in vital signs. This dysrhythmia is common in young children and tends to disappear as they grow older (Garcia & Miller. Significant ECG features of sinus bradycardia include: • Both atrial and ventricular rates are less than 60 beats per minute. although rare. QT Interval: 0. Ectopic Beats: None FIGURE 38–14 Sinus bradycardia. it is considered a variant of normal. Heart Rate: Atrial: 40 bpm. an acute myocardial infarction (AMI) may cause a decrease in the blood supply to the SA node. and some sedatives Toxins Vagal stimulation. and treatment for sinus tachycardia are outlined in Chart 38–5. it means there is a significant drop in cardiac output. 2004). it tends to disappear when the heart increases. physical assessment findings. However. • As the sinus rate accelerates. and decreased cardiac output. except for the slight irregularity in the heart rhythm. increased workload of the heart. with exercise. For example. It is called sinus tachycardia because there is a P wave present. both the PR interval and the QT interval tend to shorten slightly. Physical Assessment. PR Interval: . typical treatment includes: • Oxygen • IV access • Drug therapy (atropine) • Epinephrine or dopamine • Pacemaker evaluation. Blood pressure (BP): Lower than usual if for pathological conditions. and treatment for sinus bradycardia are outlined in Chart 38–5. • The rhythm may be slightly irregular as the rate begins to accelerate. Sinus Arrhythmia/Dysrhythmia Sinus arrhythmia/dysrhythmia resembles normal sinus rhythm. or anatomic changes Hypothermia Drugs. Whenever the heart rate increases. QRS Complex: 0. Altered mental state may be present. 1 P wave/QRS Complex. With poor perfusion. such as morphine. for example. The etiology. thus. CHART 38–5 Dysrhythmia Sinus bradycardia Sinus Dysrhythmias: Etiology.16 second. although it may be related to an abnormality of the SA node itself. more oxygen is required to nourish the muscle. referred to as fill time.32 second. Typically there is no clinical significance with this dysrhythmia. Decreased cardiac output occurs when the heart rate is fast enough to lose the period of time needed for blood to enter the heart. resulting in an abnormal response such as tachycardia. digoxin. and Treatment Etiology Decreased sympathetic tone. Observe for other dysrhythmias. If cardiac output is decreased. verapamil. but then becomes a rapid regular rhythm. resulting in increased work of the heart and increased oxygen consumption. (continued) . Significant ECG features of sinus tachycardia include: • Atrial and ventricular heart rates are over 100 beats per minute. An ECG strip showing sinus tachycardia is in Figure 38–15 (p.

Physical Assessment. e. Provide reassurance that this rhythm is not dangerous. If causes are identified and managed. Not treated unless the bradycardic phase causes clinical manifestations described under bradycardia. The etiology.1088 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders CHART 38–5 Dysrhythmia Sinus tachycardia Sinus Dysrhythmias: Etiology. Sinus arrest Pulse: irregular.g. BP: Lower than normal. the slow phase may drop below 60 beats per minute. Atropine for bradycardia. however. such as sick sinus syndrome and myocardial infarction Digoxin Factors that cause heart rate variability including exercise. • QT interval changes with the heart rate. Ascertain and treat cause. tight shirt collar Physical Assessment Pulse: Greater than 100 beats per minute. Treat only if patient is symptomatic and/or condition is complicated by other dysrhythmias. although rare. although rare. and presence of clinical manifestations. and Treatment—Continued Etiology Exercise Smoking Alcohol Caffeine Cocaine Fever Blood loss/anemia Hypovolemia Early sepsis Hypermetabolic state. diltiazem. Source: Adapted from American Heart Association. If cardiac output is decreased. such as beta-adrenergic blockers. with a variance of more than 0. If cardiac output is decreased. Sinus arrhythmia/ dysrhythmia Pulse: irregular. the following clinical manifestations may occur: • Angina • Syncope • Generalized weakness • Dizziness • Shortness of breath.. depending on the prognosis. physical assessment findings. Altered mental state may be present. becoming longer during the slow phase of the rhythm. 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. Significant ECG features of sinus arrhythmia/dysrhythmia include: • PR interval may change slightly as the heart rate changes. Treatment Treat only if symptomatic. if possible. Attempt to identify and treat the cause. Altered mental state may be present. Figure 38–16 shows an ECG strip of sinus arrhythmia/dysrhythmia. the following clinical manifestations may occur: • Angina • Syncope • Generalized weakness • Dizziness • Shortness of breath. and treatment for sinus arrhythmia/dysrhythmia are outlined in Chart 38–5. more susceptible to other dysrhythmias.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. Dallas. • Heart rhythm is regularly irregular. Typical treatment may include permanent or temporary artificial pacemaker for repeated episodes. e. Handbook of emergency cardiovascular care for healthcare providers. Treatment may include: • Drug therapy. Sinus Arrest Sinus arrest is a momentary cessation of sinus impulse formation (SA node failure). TX: Author. (2006).. • Heart rate is 60 to 100 beats per minute. mental stress.08 second in the acceleration and deceleration phases. and digoxin • Carotid massage/vagal maneuvers • Cardioversion • Anxiety medications • Fluid replacement. BP: Lower than normal depending on number of pauses per minute. generally the rhythm converts back to NSR. especially in children and young adults Pathological causes include underlying cardiac disease. • Ectopic beats may occur during the slow phase of the rhythm. but it needs to be evaluated to rule out more serious dysrhythmias. age. causing a pause in the cardiac rhythm . adenosine.

08 second. Ventricular: 80 bpm. and disorientation.40 second. • Underlying heart rhythm is regular except when the pauses occur. the patient may or may not be symptomatic.CHAPTER 38 6 seconds Nursing Interpretation of the Electrocardiogram 1089 P Wave: Present. followed by spontaneous resumption of electrical activity.14 second. Rhythm: Regular. Sinus arrest also is called sinus pause. such as angina.40 second. Depending on the type of dysrhythmia. The psychological impact of having a dysrhythmia also must be addressed. PR Interval: 0. 1092). Ectopic Beats None FIGURE 38–15 Sinus tachycardia. Ventricular: 90 bpm. Heart Rate: Atrial: 140 bpm.20 second. Ectopic Beats: None FIGURE 38–16 Sinus arrhythmia/dysrhythmia. if the abnormal rhythm results in a decreased cardiac output. Nursing Management for Sinus Dysrhythmias The nurse should first evaluate the patient’s response to and tolerance of any dysrhythmia. becoming longer during the slow phase of the rhythm. it is important to assess for the changes outlined on Chart 38–6 (p. QT Interval: 0. However. Rhythm: Irregular.08 second. 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. Heart Rate: Atrial: 80 bpm.36 second. QRS Complex: 0. • There may be marked bradycardia due to long sinus pauses. syncope. diaphoresis.18 second. 6 seconds P Wave: Present 1/QRS Complex. PR Interval: 0. • QT interval changes with the heart rate. . PR Interval: 0. Heart Rate: Atrial: 90 bpm. dizziness. QRS Complex: 0. Rhythm: Regular except for the pause. QT Interval: 0. Significant ECG features of sinus arrest include: • There is an absence of one entire PQRST complex. Ventricular: 140 bpm.10 second. With a sinus pause there will be an absence of the PQRST complex on the ECG strip and a loss of cardiac output. QT Interval: 0. and treatment for sinus arrest are outlined in Chart 38–5. It is frightening to most patients when they experience the clinical manifestations of cardiac dysrhythmias. Ectopic Beats: None Conclusion: Sinus arrest (pause) FIGURE 38–17 Sinus arrest (pause). Figure 38–17 shows an ECG strip of sinus arrest (pause). The etiology. physical assessment findings. 1/QRS Complex. QRS Complex: 0.

PR Interval: 0. Conclusion: One premature atrial contraction. The cause of the dysrhythmia. FIGURE 38–18 Premature atrial contraction. and sick sinus syndrome. When there are more than 5 to 6 PACs per minute. 2004). The etiology. Typically the patient is treated only if he becomes symptomatic and/or the condition is complicated by other more serious dysrhythmias. providing support. It frequently occurs when the underlying rhythm is normal sinus rhythm (NSR). • Heart rate and rhythm are typically within normal limits. Atrial flutter also causes a decreased cardiac output due to the loss of the atrial kick or Noncompensatory pause P Wave: Premature.1090 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders CHART 38–6 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. • PR interval may be shorter or longer than regular beats. such as talking with the patient. thereby limiting ventricular rate. QRS Complex: 0. If the patient is hemodynamically unstable. Ventricular: 70 bpm.40 second. Ectopic Beat PAC. physical assessment findings. which decreases the amount of blood pumped out of the heart.10 second. • P wave after the PAC falls earlier than expected because of the early electrical discharge. • P wave configuration (shape) may look different because electrical impulses do not come from the SA node. as outlined in Chart 38–5 (p. atrial fibrillation. but may be due to a variety of reasons not associated with a cardiac abnormality. except when the PAC occurs. the health care practitioner should be notified. This electrical impulse originates outside the SA node. and the only abnormality is the PAC. referred to as a noncompensatory pause. However. measures. When a dysrhythmia occurs. atrial rhythm with an atrial rate of 200 to 400 beats per minute (Garcia & Miller. must be evaluated and corrected. wandering atrial pacemaker. There is loss of SA node dominance. if the patient is anxious. . Rhythm: Regular except for premature beats. This makes the AV node the “gatekeeper” for the ventricles by prohibiting all of the atrial impulses from reaching the ventricles. they are termed frequent and have more clinical significance. which is the preferential pacemaker. Significant ECG features of PACs include: • P wave is present and is premature. the nurse needs to do an in-depth assessment of the patient to determine the clinical manifestations. pain and anxiety are two noncardiac causes of tachycardia. Atrial Flutter Atrial flutter is a rapid. Figure 38–18 is a rhythm strip showing premature atrial contractions. Most of the atrial beats fall during the AV node refractory period when the cardiac cell is unable to respond to any stimulus. Seven different atrial dysrhythmias are discussed next: premature atrial contraction.16 second. Only a fraction of the atrial impulses are conducted through the AV node to the ventricle. the P wave configuration of the ECG is different. and treatment of PACs are outlined in Chart 38–7. the cardiac output. 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. before the next expected SA node impulse. Chart 38–5 outlines the standard treatments for each of the sinus dysrhythmias. Therefore. A dysrhythmia may not always occur due to an abnormality in the heart. For example. causing depolarization and contraction of the cardiac muscle. Heart Rate: Atrial: 70 bpm. Lower than usual blood pressure Decreased or increased heart rate Syncope Generalized weakness Note: Clinical manifestations depend on the degree of decreased cardiac output. Supply the patient with a quiet environment and treatments to alleviate clinical manifestations. treatment may consist of pain medications or. the QRS complex is normal because the electrical impulse travels down the normal pathway from the AV node through the ventricle. 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. if the beats occur frequently cardiac output is decreased. • PACs are premature. supraventricular tachycardia. there is a loss of the time needed for blood to flow into the heart (fill time). thus preventing conduction of the impulse. 1089). Wolff-Parkinson-White syndrome. if possible. Whenever beats are premature. Because the electrical impulse does not come from the SA node. Also provide support by actively listening to the patient’s concerns and including family in the plan of care. QT interval: 0. Thus. regular. which then resets the SA node rhythm. atrial flutter. making the rhythm irregular.

If a rapid ventricular response control with drugs: digoxin is still the drug of choice. stress. 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) . and observe for decreased cardiac output (Chart 38–6).. betablockers (propranolol) and calcium channel blockers (verapamil. 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. i.g. moderate to heavy Idiopathic Physical Assessment Pulse: Irregular BP: If frequent PACs.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1091 CHART 38–7 Dysrhythmia Premature atrial contraction Atrial Dysrhythmias: Etiology.. i. digoxin is used to prevent reoccurrence. Drug therapy: adenosine is used to briefly terminate the rhythm for differential diagnosis. Treat the underlying cause.. although rare. Specific treatment may include: oxygen therapy and cardioversion.g. chronic or acute. Vagal maneuvers. although rare. If successful.. On rare occasions it may occur with normal healthy hearts. e. propranolol. may be decreased. Treatment Observe the frequency of the PACs. warfarin.g. or propranolol. e. 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. especially when hemodynamic instability is present. Frequent PAC’s or those that cause sustained tachycardia may require treatment with drugs that prolong atrial refractoriness.e. Physical Assessment. Pulse: Very fast. 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. hypokalemia. Prevent thromboembolic events with anticoagulant therapy. 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. 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: May be regular or irregular BP: Lower than normal if cardiac output is decreased. depending on the ventricular rate..e. bearing down. e. BP: Decreased if drop in cardiac output. digoxin Stress Anxiety Coronary atherosclerosis Valvular disease. Cardioversion is performed if drug therapy and vagal maneuvers are unsuccessful.g. 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. decreases heart rate. Cardioversion: Is used if new onset. diltiazem. and are the drug of choice when medically unstable. Drug therapy is used to reduce AV conduction: digitalis. verapamil. stress. Atrial flutter Cardioversion is a common intervention. Atrial fibrillation Control the ventricular response.. such as digoxin. If a chronic situation the patient may be placed on anticoagulants like warfarin. Verapamil is a calcium channel blocker. heart rate. Calcium channel blockers work the fastest. diltiazem). although rare. e. anxiety. and carotid artery massage. electrolyte imbalance. 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. coughing. It is necessary to find and treat the cause.

Anticoagulants are used because of blood stasis if atrial flutter/fibrillation is present. BP: May decrease due to decreased cardiac output.1092 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders CHART 38–7 Dysrhythmia Wolff-ParkinsonWhite (WPW) syndrome Atrial Dysrhythmias: Etiology. Physical Assessment. . BP: May be decreased due to fast heart rate. • PR intervals are not measurable. 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. resulting in a decreased cardiac output by as much as 30% (Shade & Wesley. Attempt to identify and treat the cause. Administer oxygen. • Atrial and ventricular rhythms typically are regular. normal atrial contraction. Physical Assessment Pulse: Rapid. Calcium channel blockers Frequently. Antihypertensive agents. Treatment Same as that for supraventricular tachycardia. and occurs in 0. Atrial kick forces more blood into the ventricle. intermittent and unpredictable. Atrial Fibrillation Atrial fibrillation. although rare. With atrial flutter the atria are just fluttering instead of contracting. 2007). and treatment of atrial flutter are outlined in Chart 38–7. leading to an increased incidence of clot formation. 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. physical assessment findings. although rare. creating a “sawtooth” baseline on the ECG strip. Wandering atrial pacemaker Frequently seen in normal individuals and is of no consequence. Digoxin toxicity Treat only if symptomatic. Additionally. Treatment typically is instituted when syncope and/or alteration in consciousness occurs. Figure 38–19 is a rhythm strip showing atrial flutter. which augments cardiac output. • QT interval is not measurable because the T waves are buried in the F waves. Significant ECG features of atrial flutter include: • P waves are not identifiable.1 to 0. although rare. and Treatment—Continued Etiology Congenital in origin: twice as common in males. which eventually leads to the development of hypoxia of the myocardial muscle and predisposes the left ventricular to fail. may occur in the absence of heart disease Myocardial infarction Inflammatory or degenerative processes Clinical manifestations and ECG findings determine treatment. 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. The only definitive treatment is a permanent pacemaker to replace the SA node. The etiology. but they may be irregular depending on how often the AV node allows impulses to travel to the ventricle.3% of the general population. The Evidence-Based Practice box outlines the genetic considerations of atrial fibrillation. blood stasis and pooling occur. Frequent episodes of palpitations.” is a common dysrhythmia. Pulse: 40–60 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. Finally. also referred to as “atrial fib” or “a-fib. referred to as brady-tachy syndrome. Radiofrequency ablation to terminate the accessory pathway. Pulse: Bradycardia that alternates with tachycardia. instead there are flutter waves (F waves). due to the rapid atrial rate myocardial oxygen consumption increases. with the loss of the atrial contraction.

Rhythm: Regular. Research Findings A new study conducted by the National Heart. R. Nurse Week: 23-24. It needs to be documented in the patient’s record that there is a family history of the disease. It is characterized by a disorganized. unexplained rapid heart rate. which causes many sites in the atria to become pacemakers and initiate electrical impulses. (2004). C. 2008 from http://www. A major emphasis needs to be placed on increasing public awareness of AF and its many causative factors.gov/new/press04-06-15. very rapid. JAMA: 291(23): 2852-2856. 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. Parise. When assessing a patient with new onset atrial fibrillation. National Heart. PR interval: None. With the loss of the atrial kick. Further research continues to determine which genes are involved and what steps are necessary to enhance early diagnosis and treatment. The rapid atrial firing also increases the workload on the heart.nhlbi. Atrial fibrillation causes three significant clinical manifestations: (1) loss of SA node pacemaker dominance. Retrieved August 8. When teaching a newly diagnosed patient how to live with AF.08 second. Ectopic Beats: Flutter waves.. which is the most reliable pacemaker.J. the hallmark feature. National Institutes of Health. depends on the rate that the AV node allows impulses to be conducted to the ventricles. Ventricular: 90 bpm. the risk tripled. blood stasis and pooling occur. 000). palpitations. This is especially essential if the patient has clinical manifestations and new onset irregular pulse. Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1093 P Wave: None. while it is present in 1 in 10 individuals at age 80 years and over. eventually causing hypoxia of the myocardial muscle. Genetic Considerations Clinical Problem A conservative estimate of the number of people who are affected by atrial fibrillation (AF) is approximately 2 million.. Seventy of the subjects developed AF within four years. and Blood Institute (2004) assessed the prevalence of AF in individuals who had it in their family history. The incidence of AF increases with age. (2004). D’Agostino. QRS Complex: 0. finds NHLBI’s Framingham Heart Study. It is important to specifically question the family history for the presence of AF. The study evaluated 2. Lung. H.htm . et al.. Heart Rate: Atrial: about 300 bpm. (2) decreased cardiac output due to loss of atrial kick. Treatment for AF is outlined on Chart 38–7 (p. The firing of these multiple sites causes the atria simply to quiver instead of contracting effectively. 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. Parental atrial fibrillation increases risk in offspring. The immediate concern for atrial fibrillation is the ventricular response because it determines cardiac output. referred to as the ventricular response.S. The cells in the atria have an increased irritability typically due to cardiac muscle hypoxia. with less than 1% of the population experiencing it before age 60 years. flutter waves. what types of questions would assist the nurse to determine if there is a risk for a genetic predisposition? 2. and Blood Institute (NHLBI). and irregular atrial rhythm resulting in an irregular ventricular rhythm. Heart failure Excessive alcohol consumption Previous myocardial infarction Diabetes Rheumatic heart disease Mitral valve disorders such as prolapse. Mom’s eyes and dad’s atrial fibrillation. leading to an increased incidence of clot formation. Elderly white men compose the largest group that is affected by AF. NIH News. The participants were at least 30 years of age and had no history of AF. FIGURE 38–19 Atrial flutter. Long-term hypoxia predisposes to left ventricular failure. Patients with a family history require more frequent and diligent testing. Therefore.B. Rapid or slow ventricular heart rate. and a sensation of “missed” beats. QT Interval: unable to obtain. and (3) increased myocardial oxygen consumption.nih. A heart rate that is too slow or too fast impacts cardiac output. Critical Thinking Questions 1. S. regurgitation. Figure 38–20 (p. Lung. 1096) is a rhythm strip showing atrial fibrillation. The nurse also must asses the presence of other risk factors for the development of AF including: Cardiomyopathy Hypertension Sources: Fox. If both parents had AF before 75 years of age.243 individuals whose parents were in the original Framingham Heart Study. It is the most common dysrhythmia that causes an irregular heart rate. 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. those individuals with atrial fibrillation are at high risk for a cardiovascular accident (CVA) and/or pulmonary emboli. (2005). Pavlovich-Dannis.

• Irregularly irregular rhythm occurs. Ectopic Beats: Depends on pacemaker site. • QT interval is not obtainable because the T waves are buried in the f waves. Atrial rate rapid. Heart Rate: Ventricular: 200 bpm. and treatment of atrial fibrillation are outlined in Chart 38–7. Normally people are born with only a single electrical pathway at the base of the right atrium where impulses travel to the AV node. FIGURE 38–21 Supraventricular tachycardia (SVT). This general term encompasses all fast (tachy) rhythms with normal QRS complexes and heart rates greater than 100 beats per minute. meaning that there is no pattern to the irregularity. it is buried in the QRS complex. • Heart rhythm may be regular or irregular due to varying conduction rates through the AV node. each with its own respective Supraventricular Tachycardia Supraventricular tachycardia (SVT) is a tachycardia that is generated somewhere above the ventricles. QRS complex is within normal limits unless distorted by the buried P waves. PR Interval: None. Rhythm: Irregular. occurring at 350 to 750 beats per minute. P wave is not seen. paroxysmal atrial tachycardia (PAT). Atrioventricular Nodal Reentry Tachycardia One phenomenon that can cause supraventricular tachycardia is atrioventricular nodal reentry tachycardia (AVNRT). depending on the pacemaker site. QT Interval: unable to obtain.10 second. If sustained. physical assessment findings. and paroxysmal junctional tachycardia (PJT). QRS Complex: 0. may result in a conversion to atrial flutter or fibrillation.1094 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders P Wave: None. Significant ECG features of atrial fibrillation include: • P waves are not identifiable due to the atrial quivering. PR Interval: None. Usually this rhythm is benign and is self-limiting when the cause is removed. QT Interval: unable to obtain. PR interval is not discernable. Rhythm: Regular. Heart Rate: Atrial: 80 bpm. Clinicians use the term supraventricular tachycardia when it is impossible to identify the source of the tachycardia. The etiology. loss of blood fill time (diastole) causes a drop in cardiac output. • f waves are ectopic beats. referred to as “f ” waves. some individuals are born with two separate electrical pathways leading to the AV node. • QT interval is not obtainable because the T waves are buried. • PR intervals are not measurable. Significant ECG features of supraventricular tachycardia include: • • • • Heart rate is 100 to 250 beats per minute. Eventually. QRS Complex: 0. FIGURE 38–20 Atrial fibrillation. • Ectopic beats may or may not be present. . physical assessment findings. Ectopic Beats: f waves. Rhythms included under the SVT umbrella include sinus tachycardia.10 second. signs and symptoms of congestive heart failure will be present. Prolonged episodes of supraventricular tachycardia increase myocardial oxygen demand and also P Wave: None. Figure 38–21 is a rhythm strip showing supraventricular tachycardia (SVT). However. and treatment of supraventricular tachycardia are outlined in Chart 38–7. The etiology.

the one in the fast track stimulates the AV node and bundle of His. The fast track impulse also travels retrograde (backward transmission) back through the slow track. they cancel each other out and the rhythm is normal. When the two impulses meet. causing ventricular depolarization and a normal-width QRS complex. If for any reason. These beats still are considered to be sinus complexes. because of its speed. then the slow track transmits the impulse. this is referred to as AVNRT (Garcia & Miller. The PR interval length differences are a result of the conduction alternating intermittently between the two functioning tracks. . The impulses are now able to continue to cycle the circuit or loop and initiate ventricular depolarization at a fast rate. When the impulse begins down these two pathways. one fast (beta) and one slow (alpha). the fast track will be unable to transmit the impulse. but the PR interval would be longer than the ones coming from the fast track. and can accept the impulse. meeting the impulse coming down the slow track.9% of the time. is no longer in a refractory state. The fast track has a long refractory period. 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. Each pathway has its own refractory period. the fast track is in refractory and therefore cannot accept the impulse. such as the presence of a refractory period in the fast track. The QRS complex would still be within normal limits. 99. An early impulse such as a PAC hits the two pathways. The AVNRT phenomenon occurs when a reentrant circuit or loop is created along the two pathways and the AV node (Figure 38–22 ). FIGURE 38–22 Reentrant circuit. (b) Micro re-entry at the cellular level in the AV node and Purkinje fibers. Impulses travel the two separate pathways simultaneously. to the AV node. causing depolarization of the ventricles. but the slow track can. and the slow track has a fast refractory period.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1095 properties. 2004). as opposed to coming from another atrial ectopic focus. This creates rhythm strips AVN that have identical QRS complexes but two different PR interval lengths. The impulse travels from the slow track. and then retrograde up the fast track because this track has recovered.

and carotid sinus massage. physical assessment findings. then the correct terminology is WPW syndrome. may occur with individuals of any age. 000). 2004). an atrial ectopic site. • Heart rate frequently tachycardic. Ventricular: 50 bpm. it takes longer for the impulse to travel through the ventricles. Heart Rate: Atrial: Approximately 60 bpm. Multifocal P waves. It is more predominant in women. When the patient does not exhibit any dysrhythmias.16 second. • Ectopic beats may be present due to the slow rhythm.16 second. PR Interval: 0. although AVNRT may cause angina or myocardial infarction in patients with coronary artery disease. the AV junction. stimulating gag reflex. • QT interval usually is normal. Treatment is aimed at breaking the reentrant cycle with the use of vagal maneuvers such as breath holding. Sick Sinus Syndrome Sick sinus syndrome (SSS) encompasses a broad range of abnormalities. The etiology. The hallmark feature on the ECG strip for the abnormal pathway is the presence of a delta wave. QRS Complex: 0. Clinical manifestations are the same as with any tachy dysrhythmia. Rhythm: Irregular. Ectopic Beats. These pacemaker sites may include the SA node. atrial fibrillation.04 second. is composed of an extra muscle bundle made up of working myocardial tissue. this is called WPW pattern. due to multiple atrial sites initiating the conduction. Because the conduction is outside the normal conduction system. Figure 38–23 is a rhythm strip showing Wolff-Parkinson-White dysrhythmia. Prognosis for patients without heart disease is usually good (Olshansky et al. and therefore could cause sudden cardiac death. When the patient becomes symptomatic or develops dysrhythmias. Rhythm: Regular Ectopic Beats: None. . and treatment of WPW syndrome are outlined in Chart 38–7 (p. which permits an atrial ectopic focus and junctional escape rhythms to “jump in” as atrial pacemakers.. Significant ECG features of Wolff-Parkinson-White syndrome include: • PR interval shortens to less than 0. Atrial flutter. FIGURE 38–24 Wandering atrial pacemaker. • Atrial rate and ventricular heart rate typically are slow. Wandering Atrial Pacemaker Wandering atrial pacemaker is a pacemaker from at least three different sites above the bundle of His acting as the heart’s pacemaker.12 second because the AV node is bypassed and delta waves appear just prior to the beginning of the R wave. • QT interval shortens if tachycardia occurs and lengthens with bradycardia. are common dysrhythmias in patients with WPW. physical assessment findings. it often occurs in patients with no structural heart disease. including disorders of impulse generation and conduction. 40-50 bpm. called the Kent bundle. Ventricular: 40-50 bpm. and a susceptibility to paroxysmal or P Wave: Multifocal. Significant ECG features of wandering atrial pacemaker include: • P waves have multiple shapes. failure of pacemakers. The abnormal pathway.1096 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders approximately several cases per thousand persons worldwide.12 second due to the delta waves. Figure 38–24 is a rhythm strip showing wandering atrial pacemaker. This abnormality occurs because of SA node slowing.52 second. bizarre QRS complex (Garcia & Miller. 2006). AVNRT is usually well tolerated. except during heart rate changes. The etiology. This extra muscle bundle forms a connection between the atria and the ventricles outside the normal conduction system. but has the delta wave. FIGURE 38–23 Wolff-Parkinson-White syndrome. This allows impulses coming from the atrium to bypass the normal AV connection. and/or any combination of these areas. • Heart rhythm is irregular due to changing pacemakers.12 second. but may be prolonged due to a slow heart rate. QRS Complex: 0. • Heart rhythm is regular. predisposing to heart failure. and supraventricular tachycardia that results in heart rates of greater than 250 beats per minute. and is common in young adults. The delta wave occurs when the impulse travels via the accessory pathway to the ventricles. An impulse leaving the atrium may travel down one or the other pathway without any specific pattern. QT Interval: 0. and treatment of wandering atrial pacemaker are outlined in Chart 38–7 (p. PR Interval: 0. QT Interval 0. 1093). referred to as an accessory pathway. Wolff-Parkinson-White Syndrome Wolff-Parkinson-White syndrome (WPW) is a genetic AV conduction disorder characterized by the presence of two AV conduction pathways. • QRS complex is greater than 0.06 second. a slurred upstroke at the beginning of the QRS complex (Figure 38–23 ). one normal and one abnormal. thus creating an abnormally wide. Delta Wave P Wave: Present and irregular. The increased heart rate increases the workload and oxygen consumption of the heart.

PR Interval: 0.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1097 110 110 110 50 50 50 P Wave: Present. and treatment of sick sinus syndrome are outlined in Chart 38–7. such as warfarin. Profound sinus bradycardia with SSS may progress to sinus pauses or arrest. The etiology. If these clots travel out of the atrium they tend to lodge in the brain.08 second. If the atrial flutter and/or atrial fibrillation are chronic conditions. especially if this is a new rhythm. AV junctional dysrhythmias have a distinctive pattern on ECG tracings because the impulse is not initiated in the SA node. and pulmonary embolus is discussed in Chapters 35 and 36 . chronic atrial tachycardia. The treatment may be narcotics for pain relief or an antianxiety medication for stress and increased anxiety. The atrial dysrhythmias do not have the impact on cardiac output that the more serious ventricular dysrhythmias do. and normal sinus rhythm cannot be reestablished. Atrial fibrillation also is seen in congenital heart disease. • PR interval varies due to changing P wave sites.14 second. Rhythm: Irregular. This treatment increases risk for myocardial infarction. thereby decreasing cardiac output. • Heart rhythm is irregular and highly variable. which is the delivery of electrical voltage in order to stop unwanted electrical activity and allow the SA node to resume the heart’s pacemaker. QRS Complex: 0. requires an in-depth assessment. on rare occasions in the lung. which increases the risk of clot formation. 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. QT Interval: 0. The impulse 8 8 8 8 8 8 8 8 . such as cardiac glycosides. Besides heart disease frequently there are other causes for atrial cardiac dysrhythmias that must be evaluated and treated. and pulmonary embolus. • Heart rate may be rapid or slow. stress. This is especially true if it is a new onset dysrhythmia and/or if the dysrhythmia causes a drop in the cardiac output. but variable configuration. The cause is a severely depressed nonreliable SA node due to heart disease or the side effect of certain cardiac drugs. and therefore. Nursing Management for Responsibilities for Atrial Dysrhythmias Nursing responsibility when any dysrhythmia occurs is to assess the patient’s response to the rhythm. Vital signs and clinical manifestations must be monitored frequently to assess tolerance of the rhythm. especially if it is sustained. but any change in cardiac output may cause clinical manifestations. calcium channel blockers. • QT interval varies due to rate changes. and. The patient is evaluated for the clinical manifestations of reduced cardiac output as outlined in Chart 38–6 (p. Significant ECG features of sick sinus syndrome include: • P waves may be present or absent depending on which dysrhythmia is occurring. FIGURE 38–25 Sick sinus syndrome. This treatment is indicated because a fluttering/fibrillating atrium creates blood stasis. The nurse needs to assess the patient post-cardioversion for clinical manifestations of these disorders. because medical intervention must be initiated to convert the rhythm back to normal sinus rhythm. and membrane active antiarrhythmic agents.40 second. 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. When the tachycardia occurs with SSS there is increased oxygen consumption and workload for the myocardium. 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.g. The health care practitioner needs to be notified. e. Ventricular: 60 bpm.. This disorder also is referred to as sinoatrial disease and sinoatrial dysfunction. Heart Rate: Atrial: 60 bpm. Treatment of atrial fibrillation/flutter may include cardioversion. 1092). beta-adrenergic blockers. sympatholytic antihypertensive agents. and anxiety. pain. Myocardial infarction is discussed in detail in Chapter 40 . or a combination of both. Atrial flutter and fibrillation may occur as a transient dysrhythmia in healthy young individuals. Cardioversion is discussed in detail in Chapter 39 . causing an alteration in normal function in these areas. The nurse may need only to sit and listen to the patient and provide emotional support. Ectopic Beats: May occur with slow rate. physical assessment findings. cerebral vascular accident (CVA). Cardiovascular accident (CVA) is discussed in Chapter 30 . • Ectopic beats may be present when a slow rate occurs. the patient often is placed on an anticoagulant. Figure 38–25 is a rhythm strip showing sick sinus syndrome.

and treatment of junctional escape rhythms are outlined in Chart 38–8. or buried in the QRS complex. and may occur before. the P wave is inverted or negatively deflected. respectively. or buried in QRS Complex. • QRS complex is normal in duration and shape. either fails to produce an impulse. or buried in. Heart Rate: Atrial: Not measurable. QRS Complex: 0. due to retrograde conduction. is initiated in the AV junctional tissue and must travel in a backward (retrograde) direction to activate the atria. If the rate is greater than 100 typically it is called junctional tachycardia. thus. • PR interval is dependent on the location of P wave. physical assessment findings.44 second. negatively deflected. the most important indicator of the clinical significance of any dysrhythmia is the patient’s response to or tolerance of the rhythm. • Entire rhythm is composed of ectopic beats because they all come from the AV junction instead of the SA node. and either occurs before. PR Interval: 0. The location of the P wave is. QT Interval: 0. and paroxysmal junctional tachycardia.40 second. QRS Complex: 0. therefore. or when the SA node’s rate of firing falls below the intrinsic rate of the AV node.1098 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders Figures 38–26 and 38–27 are ECG rhythm strips that show junctional escape rhythm and accelerated junctional rhythm.16 second. the QRS complex.14–0. 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. as compared to a series of beats that then is called a junctional rhythm. P Wave: Inverted and regular. the rate is between 38 and 60 beats per minute. Significant ECG features of junctional escape rhythms include: • P wave is inverted. after. Figure 38–28 (p. dependent on the speed with which the impulses travel in both chambers. This is not a dangerous dysrhythmia.10 second. Ventricular: 80 bpm. Ectopic Beats: None. It is prolonged with slow heart rate or shortened with increased heart rate. Premature Junctional Contraction A premature junctional contraction (PJC) originates as an ectopic beat that is initiated in the atrioventricular (AV) junction. Rhythm: Regular: Ectopic Beats: none. Therefore. If the rate is greater than 60 but less than 100 it is referred to as an accelerated junctional rhythm. the PR interval may or may not be present or normal. The three AV junctional dysrhythmias discussed in this chapter are: junctional escape rhythm. but as always. Junctional Escape Rhythm Junctional escape rhythm occurs when there is a problem with normal SA node function. The QRS complex configuration is normal in appearance because the impulse travels the normal pathway from the AV junctional node through the ventricles. due to this retrograde conduction. PR Interval: Not measurable. Heart Rate: Atrial: 80 bpm. premature junctional contractions. unless distorted by a buried P wave. It discharges before the next expected SA node impulse causing simultaneous atrial and ventricular contraction to occur. after. Rhythm: Regular.08 second: QT Interval: 0. . FIGURE 38–27 Accelerated junctional rhythm. When a rhythm is generated from the junction. AV junctional dysrhythmias are not considered lethal or life threatening. 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. Ventricular: 40 bpm. 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. Other ectopic beats may occur with slow heart rate. FIGURE 38–26 Junctional escape rhythm. • Heart rate is usually within normal range for a rhythm generated from the AV junction is 40 to 60 beats per minute. • QT interval is within normal range. The impulse simultaneously initiates both atrial and ventricular contractions. unless impacted by the heart rate. 1102) is P Wave: None. At this time the AV node will assume the role of the pacemaker. although it does indicate that some degree of cardiac ischemia is occurring. The etiology.

thus. 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. with patient experiencing a fluttering sensation. If occurring frequently. Oxygen Drug therapy initiated: includes: amiodarone or beta-adrenergic blockers. or buried in the QRS complex. Treatment Observe for other dysrhythmias if a slow rate is present. Generally this condition is asymptomatic. and shock. unless distorted by a buried P wave. . if possible. after. although rare. • Heart rhythm is irregular when PJCs are present. more than 5 times per minute. or it may be described as regular with premature beats. 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. heart failure. such as tachycardia. The etiology.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1099 CHART 38–8 Dysrhythmia Junctional escape rhythm Junctional Dysrhythmias: Etiology. and Treatment Etiology SA node disease Myocardial infarction Hypoxia and ischemia Heart failure Increased vagal tone Certain cardiac drugs: such as digoxin. Paroxysmal junctional tachycardia (PJT) Pulse: Rapid. • Ectopic beat is the PJC. a rhythm strip showing premature junctional contraction. the PR interval may or may not be present or normal. Find and treat the underlying cause. and digitalis may be discontinued. Physical Assessment. and treatment of PJCs are outlined in Chart 38–8. they can drop cardiac output. and predispose the patient to other dysrhythmias. physical assessment findings. contingent on the type of dysrhythmia. however. If it initiates a more serious dysrhythmia. Oxygen Drugs such as stimulants. typical treatment includes: Oxygen Drug therapy: (atropine. dopamine) Pacemaker Cardioversion Premature junctional contraction (PJC) Rarely causes symptoms. • QRS complex is normal in duration and shape. if symptomatic. Vagal maneuvers may be applied. thus typically not treated. therapy becomes more aggressive. Pulse: Irregular BP: Normal unless PJCs occur frequently enough to decrease cardiac output. Find and treat the cause as PJTs may be a predisposition to lethal dysrhythmias. 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. Significant ECG features of premature junction contractions include: • P wave is inverted and occurs before. BP: Lower than usual due to decreased cardiac output. sympathomimetics. • Heart rate is that of the underlying rhythm. • PR interval is dependent on the location of P wave. although rare. Cardioversion may be initiated if necessary. beta adrenergic blockers. • QT interval also is normal unless impacted by the heart rate.

This rhythm produces a junctional rate of over 60 beats per minute. Ventricular: 130 bpm. junctional dysrhythmias generally are not life threatening. therefore. • Heart rhythm is essentially regular. P Wave: Inverted and regular.1100 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders P Wave: Present and regular except for premature beat. 000). and treatment of PJTs are outlined in Chart 38–8. thus. The etiology. FIGURE 38–29 Paroxysmal junctional tachycardia. The health care practitioner needs to be notified. • PR interval is dependent on the location of P wave. and greater than 60 beats per minute. • P wave is inverted and occurs before. the PR interval may or may not be present or normal. be as low as 110 beats per minute or exceed 240 beats per minute. especially if it is a new onset dysrhythmia in order to determine cause and treatment. p. Ectopic Beats: None. physical assessment findings. Rhythm: Regular except for premature beats: Ectopic Beats: none FIGURE 38–28 Premature junctional contraction (PJC). Ventricular: 110 bpm. The term junctional tachycardia sometimes is used interchangeably with the term accelerated junctional rhythm. If it is a sustained rhythm. As always any significant rhythm change or the appearance of new onset dysrhythmias needs to be reported to the health care practitioner.08 second. after.g. It begins and ends abruptly. it may be referred to as junctional tachycardia. • Entire rhythm is composed of ectopic beats because they all come from the AV junction instead of the SA node. Therefore.08 second. It is essential that the nurse assist the health care practitioner in determining the cause and treatment of dysrhythmias. which is why it is called paroxysmal. 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. however. When rhythm is slow other ectopic foci may attempt to become the heart’s pacemaker. • QT interval shortens due to increased heart rate. the patient’s medical history should be reviewed to determine if the dysrhythmia is medication related. . digoxin. It may. Since some prescribed medications. It may become irregular as the rate increases. QRS Complex: 0. second. 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. QT Interval: 0. cause significant dysrhythmias.16 second. or buried in the QRS complex. initiating drug therapy. PR Interval: 0. the nurse must assess the rhythm for other aberrancies. treatment also may include applying vagal maneuvers. • QRS complex is normal in duration and shape. PR Interval: 0. Heart Rate: Atrial: 110 bpm. Nursing Management for Junctional Dysrhythmias Like atrial dysrhythmias.. Significant ECG features of paroxysmal junctional tachycardia include: • Heart rate usually is 160 to 240 beats per minute and constant. QRS Complex: 0.32 second. For symptomatic junctional tachycardia. Serum drug levels should be ordered as indicated. Rhythm: Regular. the decreased and/or increased heart rate does have an impact on cardiac output. However. the nurse must evaluate the patient for clinical manifestations of decreased cardiac output (Chart 38–6. Figure 38–29 is a rhythm strip showing paroxysmal junctional tachycardia. which was discussed previously.06 second. and completing cardioversion if necessary. e. unless distorted by a buried P wave. Heart Rate: Atrial: 130 bpm.

• QRS complexes are normal in shape and duration. PR Interval: 0. 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. Its presence only indicates a delay at the AV node. 000). and thus. physical assessment findings. Ventricular: 60 bpm.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1101 Due to the clinical manifestations of these dysrhythmias. Ectopic Beats: None. Mobitz II second-degree block. Conduction Block Dysrhythmias Cardiac conduction block dysrhythmias occur due to an interruption in the continuity of the cardiac electrical conduction system. rather than a definite block. QT Interval: 0. unless no QRS complex occurs. ventricular). the rate of the escape pacemaker (junctional vs. FIGURE 38–30 First-degree AV block. however when the block occurs. ventricular heart rate is less than that of the atrial rate. 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. • Atrial heart rate is normal and regular. Because of this consistent delay the PR interval is greater than 0. Rhythm: Regular. 1106) is a rhythm strip showing Mobitz I/Wenckebach dysrhythmia.20 second. Mobitz II Second Degree Block Mobitz II/second degree block results from an intermittent block of the AV node. • Heart rhythm is regular. . are used interchangeably to refer to the same abnormality. or bundle branches. An AV conduction ratio of 2 Ps for every 1 QRS. Mobitz I/Wenckebach/ Type I second-degree heart block. The etiology. Mobitz I/Wenckebach/Type I Second-Degree Heart Block The terms Mobitz I/Wenckebach/Type 1 second-eegree heart block. providing a calm environment. • QRS duration usually is normal. • QT interval is within normal limits. 2003).06 second. greater than 0. This dysrhythmia is characterized by progressive lengthening of the PR interval until a QRS complex fails to appear after a P wave (Beasley. the nurse also must assess and treat the anxiety by use of supportive measures. Significant ECG features of Mobitz I/Wenckebach dysrhythmia include: • P waves are present. QRS Complex: 0. Heart blocks are classified according to the degree of the block. • Atrial rhythm is regular. the bundle of His. Mobitz I/Wenckebach is one of the two types of second-degree block that occurs in the AV node. but are delayed at the AV node. 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. Figure 38–31 (p. and treatment of Mobitz I/Wenckebach/Type I second-degree heart block are outlined in Chart 38–9 (p. • PR interval progressively prolongs until there is a dropped QRS complex and then the progressive prolongation begins again. and medicating for anxiety and pain relief as appropriate. • QT interval is normal unless there is an abnormal rate. no ventricular contraction. either partial or complete obstruction of the electrical conduction pathway.24 second. and the patient’s response to that ventricular rate. and treatment of first-degree AV blocks are outlined in Chart 38–9 (p. First-degree AV block is not actually a dysrhythmia. and minor or significant. The etiology. with or without a bundle branch block P Wave: Present and regular. There is a prolongation or slowing of conduction rather than an actual block.40 second. • PR interval is prolonged. The clinical significance of an AV block depends on the degree (severity) of the block. the ventricular rhythm is irregular. • Heart rate is usually within normal range. 1104). offering reassurance. but constant. which prevents the sinus or atrial impulses from getting to the ventricles. and they precede the QRS complexes. Thus. Significant ECG features of first-degree AV block include: • P waves are present and normal in size and shape. These disorders may be either permanent or transient. and third-degree AV block (complete). such as listening to the patient’s concerns. or greater is common. making it abnormal. Heart Rate: Atrial: 60 bpm. This dysrhythmia occurs when this block causes an intermittent interruption in the electrical conduction system near or below the AV node. the P wave is not followed by a QRS complex. Figure 38–30 is a rhythm strip showing first-degree AV block. There are four types of heart block dysrhythmias discussed next: first degree AV block.20 second. 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. the patient and family may experience anxiety. 3Ps for every 1 QRS. physical assessment findings.

and may be followed by a permanent pacemaker. thus. and temporary cardiac pacing is required for symptomatic patients. If symptomatic. 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.1102 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders CHART 38–9 Dysrhythmia First-degree AV block AV Block Dysrhythmias: Etiology. especially for slow rates. 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. 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. If the QRS is narrow and the patient is symptomatic. This is often a transient rhythm and will revert to normal rhythm without treatment. Observe closely and place on an ECG monitor to detect additional signs and symptoms. especially in the presence of a myocardial infarction. 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. 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. May progress to a more advanced heart block. and is a result of medications. beta-blockers. If an AV junctional or ventricular escape pacemaker does not take over following a sudden onset of third-degree AV block. Physical Assessment. betablockers. initial management is atropine and/or transcutaneous pacing. betablockers. reaction to amiodarone. Often considered an emergent situation. transcutaneous pacing is started.g. 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. May progress to a third-degree AV block and ventricular asystole. occur. digoxin Septal wall necrosis Acute inferior or right ventricular MI Myocarditis Advanced coronary artery disease (general ischemia) Electrolyte imbalance Digitalis toxicity Reaction to amiodarone. When occurs in conjunction with acute myocardial infarction. Pulse: slow and typically irregular. 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. Clinical manifestations depend on the ventricular heart rate. angina.. asystole will occur. 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. shortness of breath. observe for increasing AV block. If the heart rate is slow and serious clinical manifestations such as low BP. a standby cardiac pacemaker is indicated for asymptomatic patients. For sustained permanent block. atropine or temporary pacing is considered. although rare. . If the QRS is wide and the patient is symptomatic. The health care practitioner should be notified at once. they should be withheld. a permanent pacemaker is inserted. Usually asymptomatic because the ventricular rate often remains nearly normal and cardiac output is not significantly affected. A temporary pacemaker is inserted.

they may be normal to prolonged when present. 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. In other words there are 2. or complete block. Therefore. This dysrhythmia also is referred to as AV dissociation because of the independent function of the atria and the ventricles. Thus.or second-degree AV block. especially in the setting of an acute MI if the block progresses to a complete AV block. • P waves are present and regular. or 4 P waves for every QRS complex.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1103 CHART 38–9 Dysrhythmia Bundle branch block (BBB) AV Block Dysrhythmias: Etiology. (Beasley. The SA node fires at regular intervals. 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. 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. • Ectopic beats may be present due to the slow heart rate. • PR intervals are constant with conducted beats. • QT intervals are within normal limits. Significant ECG features of Mobitz II/second-degree block include: • QRS complexes are intermittently absent. the top and bottom of the heart are not communicating. whereas. and they are usually prolonged due to bundle branch block. ventricular rhythm may be regular or irregular. causing a varying AV conduction ratio. rheumatic. or both. • Atrial rhythm is regular. Third-Degree AV Block (Complete) Third-degree AV block. they are beating independently. producing P waves at a normal rate of 60 to 100 beats per minute. is the independent excitation and contraction of the atria and ventricles due to the inability of any atrial impulses to reach the ventricles. Figure 38–32 (p. 3. physical assessment findings. with this dysrhythmia there may be enough dropped QRSs to significantly impact cardiac output. 1106) is a rhythm strip showing Mobitz II/second-degree block. and Treatment—Continued 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. The ventricular rhythm is irregular when the AV block is intermittent. • Atrial heart rate is usually normal. 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. Physical Assessment. The etiology. ventricular heart rate is less than the atrial rate. the ventricles are paced by either a pacemaker site in the ventricles themselves or in the junctional . thereby. and treatment of Mobitz II heart block are outlined in Chart 38–9. 2003). In other words.

FIGURE 38–31 Mobitz I/Wenckebach/second-degree heart block.60 second.degree heart block is referred to as a lethal dysrhythmia. Ectopic Beats: None. QT Interval: 0. Complete AV block associated with an inferior myocardial infarction is thought to be a block in the bundle of His.42–0. Ventricular 50 bpm. QRS Complex: 0. Ventricular: Irregular due to dropped beat. P P P P P P P P P P P Waves: Present and regular. third.10 second. Significant ECG features of third-degree heart block include: . 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. Conclusion: Mobitz I/Wenckeback Second-Degree Heart Block. However. Ventricular: Irregular due to dropped beat.1104 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders P P P P P P P P P P P P P Waves: Present and regular. Ectopic Beats: None. this is referred to as an idioventricular rhythm. If the QRS complex is narrow the pacemaker is in the junctional tissue with a rate of 40 to 60 beats per minute. and the slow ventricular heart rate results in decreased cardiac output. Since the ventricular rhythm may not be able to sustain adequate cardiac output. and often occurs after progression from first-degree AV block or second-degree AV block. QRS Complex: 0. PR Interval: 0. Heart Rate: Atrial: 70 bpm. FIGURE 38–32 Mobitz II/second-degree heart block. PR Interval: Progressively prolonged until one P wave is not conducted and the sequence begins again. Heart Rate: Atrial: 100 bpm. Rhythm: Atrial: Regular. tissue.24 second. Third-degree heart block is the most serious type of heart block because it may progress to asystole (a complete cessation of electrical activity).48 second. type I. Figure 38–33 is a rhythm strip showing third-degree or complete heart block.06 second. Ventricular 50 bpm. Rhythm: Atrial: Regular. QT Interval: 0.

• QRS complex may be narrow with a junctional rhythm. and treatment of bundle branch block are outlined in Chart 38–9.12 second if a complete bundle branch block is present. the nurse must observe the cardiac monitor for any changes in the rhythm indicating a progression to a more severe type of heart block. Atrial rhythm usually is regular. Bundle Branch Block Bundle branch block. therefore. physical assessment findings. FIGURE 38–33 Third-degree (complete) heart block. Atrial rhythm usually is regular.12 second is called an incomplete right or left bundle branch block. and ventricular rate is 20 to 40 beats per minute. patients are not symptomatic. and therefore. Ectopic Beats: None.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1105 P Waves: Present and regular. it is necessary to observe the axis of the complex to determine whether it is right or left bundle branch block. The etiology. 60 to 100 beats per minute. 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. Ventricular rhythm may be regular or irregular.12 second. It is necessary.40 second. • PR interval is 0. QRS Complex: 0. therefore. is a discontinuity of conduction. • Atrial and ventricular rhythms are independent of one another (dissociated).16 second. the ventricles depolarize asynchronously. • Atrial heart rate is regular. Ventricular: 90 bpm. tation to one ventricle. Heart Rate: Atrial: 90 bpm. Ventricular: Regular. or junctional rhythm. that the nurse frequently checks the monitor to identify potential changes. Bundle branch block is characterized by a delay of exci- P Wave: Normal sinus rhythm. Heart Rate: Atrial: 90 bpm. and treatment of Mobitz II heart block are outlined in Chart 38–9. The etiology. or wide with an idioventricular rhythm. • Ectopic beats usually are present due to slow rate. nodal rate is 40 to 60 beats per minute. in one branch of the bundle of His. complete or incomplete. but is not directly affected. which affects normal transmission of the impulse through the ventricles. Rhythm: Atrial: Regular. • PR interval is absent. Significant ECG features of bundle branch block include: • QRS complex is more than 0. depending on underlying sinus. With first-degree heart block. Nursing Management for Conduction Block Dysrhythmias The type of heart block determines the severity of the dysrhythmia. This delayed conduction causes a widening of the QRS complex to more than 0. . atrial.20 second. therefore. QT Interval: 0. QRS Complex: 0. • QRS measuring 0. P waves are present and regular.20 second. First-degree heart block and bundle branch block in isolation. • QT interval is within normal limits. Ectopic Beats: None. Mobitz I/Wenckebach often does not require treatment. however there is no relationship to QRS complexes. depending on underlying sinus. however. PR Interval: None. PR Interval: 0. Ventricular: 40–50 bpm. • P waves are present and regular.10 to 0. Figure 38–34 is a rhythm strip showing a bundle branch block. or junctional rhythm.12 to 0. Mobitz I/Wenckebach needs to be reported to the health care practitioner. nursing responsibilities. QT Interval: 0. an abnormal spread of electrical activity through the ventricles occurs. • Heart rhythm is regular. Ventricular rhythm may be regular or irregular. As with any new dysrhythmia. also referred to as intraventricular conduction defect. do not impact cardiac output. physical assessment findings. Rhythm: Regular.38 second. • Heart rate is 60 to 100 beats per minute. When one bundle is blocked. As with any dysrhythmia the patient’s tolerance to the rhythm must be evaluated when heart block develops. FIGURE 38–34 Bundle branch block. atrial.12 second. • QT interval may change with the rate change. When measuring the QRS complex. • Atrial and ventricular rhythms are independent of one another (dissociated).

not a rhythm. PR Interval: 0. QT Interval: 0. PVCs are followed by a full compensatory pause. AV block can be more ominous. The various types of ventricular dysrhythmias are discussed next: premature ventricular contraction. Figure 38–35 is a rhythm strip showing a premature ventricular contraction (PVCs) with a full compensatory pause. Ventricular: 80 bpm. ventricular tachycardia. following the PVC. measure the distance to the next beat. Premature ventricular contractions (PVCs) are individual beats.20 second.42 second. Ectopic Beats: One PVC. which generally is indicated for these types of dysrhythmias. there should not be a change in the cadence of the rhythm. Unifocal and Multifocal PVCs Premature ventricular contractions (PVCs) occur in various patterns. If untreated. meaning the SA node rate and rhythm are unaffected by the PVC. Each pattern differs in its severity and prognosis. Heart Rate: Atrial: 70 bpm.1106 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders pact on cardiac output. the health care practitioner should be notified at once. The nurse should prepare for a temporary pacemaker insertion (Chapter 39 ). atrial and junctional ectopic beats do not have a full compensatory pause. Because the activation begins outside the normal conduction system. Ventricular dysrhythmias are considered to be very serious dysrhythmias mainly due to their im- P Wave: Present and regular. At any indication of rhythm changes indicative of Mobitz II or complete heart block. A permanent pacemaker may be necessary if the block persists. the ventricles take over the pacing role. ventricular fibrillation. Premature Ventricular Contraction A premature ventricular contraction (PVC) is caused by an irritable focus within the ventricle that discharges before the next sinus impulse. First. stimulating the ventricle directly. QRS Complex: 0. A compensatory pause is measured by: • Measuring the two beats preceding the PVC • Moving the calipers along. In other words. In this situation. Mobitz II is described as a “treacherous and unpredictable” rhythm that can deteriorate to become a complete heart block. PVCs are more likely to occur during bradycardia when there is more time for them to emerge. and because it is an abnormal conduction pathway the QRS is wide and distorted. Typically. in certain circumstances. serve as the heart’s pacemaker. the full compensatory pause is present. Because the rhythm originates in the ventricle there is no P wave. The full compensatory pause is one of the factors used when evaluating and diagnosing PVCs. 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. the rate prior to the PVC resumes. pulseless electrical activity. they are said to be non-compensatory or partially compensatory. 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. thereby prolonging the QRS length. When the SA node fails or the impulse does not get through the AV node. The intrinsic ventricular rate is only 20 to 40 beats per minute. . Ventricular: Regular except for premature beat. these rhythms may progress to cardiac asystole and sudden death.12 second in length. Rhythm: Atrial: Regular.08 second. 8 8 FIGURE 38–35 Premature ventricular contractions (PVCs). it takes longer to travel the ventricular conduction pathways. especially when associated with wide and bizarre QRS complexes. and causing a contraction. except where absent (PVC). To distinguish PVCs from atrial and junctional ectopic beats. The onset of Mobitz II and complete heart block are emergent situations that require immediate intervention. Temporary cardiac pacemaker is required immediately for treatment of symptomatic third-degree block with wide QRS complexes. The pacemaker cells in the ventricles may. It is the nurse’s responsibility when working with monitored patients to be familiar with equipment location and operation. and asystole. torsade de pointes. meaning that there is a rhythm change following these dysrhythmias. Signs and symptoms of third-degree AV block are the same as those in symptomatic sinus bradycardia. therefore. 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. and marking where the next beat should have fallen • Then placing the calipers on the spot where the beat should have occurred. one ectopic beat. cardiac output is severely compromised. an electrical impulse may be instigated from both the bundle of His and the Purkinje network. causing further decrease in cardiac output. PVCs have a wide and bizarre QRS complex that is more than 0. if the atrium is not contracting there is no atrial kick. Also.

Figure 38–36 (p. These are referred to as unifocal PVCs. cardiopulmonary resuscitation (CPR) is initiated and help is requested. • PVC occurs prematurely.12 second or greater in width. and treatment of premature ventricular contractions are outlined in Chart 38–10 (p. The etiology. This is referred to as an R on T phenomenon. • Heart rhythm is irregular because the PVCs are premature. and treatment of ventricular tachycardia are outlined in Chart 38–10. with the T wave always occurring on the opposite side of the isoelectric line from the R wave. Ventricular tachycardia that is hemodynamically unstable and pulseless is treated using the ACLS guidelines for pulseless cardiac arrest (Appendix *** ) (AHA. but depends on underlying rhythm. • Ectopic beats are the PVCs. • P waves are not present or are buried in the PVCs. A sustained ventricular tachycardia is a rhythm that lasts longer than 30 seconds and usually requires termination by antiarrhythmic drugs. but the electrical activities do not affect one another. and occurrence every fourth beat is quadrigeminy. • QT interval is not measurable. If PVCs occur every third beat. These guidelines dictate that the nurse assess the patient for a pulse. causing PVCs to be initiated in more than one place in the ventricle. torsade de pointes. Ventricular tachycardia when sustained but hemodynamically stable (with pulse) is treated with pharmacologic agents such as lidocaine. procainamide or bretylium (AHA. The QT interval usually is more than 0. with the T wave occurring on the opposite side of the isoelectric line from the R wave. This dysrhythmia frequently begins rapidly. which is rare. is due to age. it is defined as ventricular tachycardia.” is a form of ventricular tachycardia that is usually accompanied by prolongation of the QT interval. usually wide and bizarre. the more serious the dysrhythmia. 1012) is a rhythm strip showing ventricular tachycardia. The name. Multifocal PVCs are more serious than unifocal PVCs because they indicate that there is more ischemia occurring in the myocardium. and is initiated by a PVC which then becomes the heart’s pacemaker.” The name characterizes the rhythm in that it resembles a turning about or twisting motion along the baseline or isoelectric line. if none is present.50 second in the beats preceding the onset of the rhythm. gender.12 second or greater. Ventricular tachycardia may be life threatening due to the severe drop in cardiac output. Vasopressors are administered when intravenous access has been established. and therefore. the dysrhythmia is coming from one irritable focus in the ventricle. frequently referred to as “torsades. and this occurrence may precipitate a run of ventricular tachycardia. drug toxicity. CPR and defibrillation cycles are repeated per ACLS guidelines until a viable rhythm is established or death occurs. 8 8 Ventricular Tachycardia Ventricular tachycardia (VT). is derived from the French term that signifies the “twisting of the points. 2006). physical assessment findings. The nurse must be prepared to shock the patient per AHA guideline joules. requiring urgent evaluation to assess cardiac output and the presence or absence of the pulse. measuring 0. 0. or electrical cardioversion. ventricular tachycardia affects the diseased heart. Significant ECG features with PVCs include: • QRS complex is premature. • Heart rhythm is essentially regular but may be irregular. 2006). At slower ventricular rates. As cardiac muscle ischemia increases the muscle becomes more irritable. Significant ECG features of ventricular tachycardia and ventricular fibrillation include: • QRS complexes are uniform in appearance.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1107 sistently. acting as the dominant pacemaker. Treatment is guided by published advanced cardiac support (ACLS) guidelines and varies based on the presence of a pulse. When multifocal. 1110). • Heart rate is greater than 100 beats per minute and usually not faster than 200 beats per minute. When there are three or more consecutive PVCs salvos. • PR interval is not discernable. and then rhythm is checked. If PVCs occur with every other beat the rhythm is referred to as bigeminy. niques. Ventricular tachycardia is an emergent situation. In general. The most serious or dangerous time for a PVC to occur is during the relative refractory period. the rhythm is called trigeminy. antitachycardia pacing tech- Torsade de Pointes Torsade de pointes. CPR is resumed for 5 cycles. 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. This form of VT. PVC Patterns When PVCs occur for two or more consecutive beats this is referred to as paired salvos. • Entire rhythm is ectopic beats. although it has been described in patients with apparently normal hearts. 2006). The more often the PVC occurs. This is referred to as multifocal PVCs. P waves may be recognized and may represent normal sinus node depolarization at a rate slower than VT. • PR interval-none. • QT interval is prolonged for the ectopic beat only. which is the top of the T wave on the ECG. the greater the drop in cardiac output. Oxygen is administered and the patient is placed on a monitor/defibrillator when available. or an idiosyncratic reaction to certain cardiac drugs such as . physical assessment findings. The patient is re-shocked if VT persists. the morphology (shape) of the QRSs varies. It is a rhythm that discharges repetitively. 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. 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. The etiology. 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. complexes are larger than the normal beats. • Heart rate usually is within normal range. • P waves in rapid VT are usually not recognizable. 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.

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. starting with confusion and restlessness. It is essential to identify and treat the underlying cause. they have no significance and require no treatment. When provoked by fast or slow heart rate. followed by a second attempt to produce the VT. procainamide.g.g.g. Treatment is directed at uncovering the etiology and providing adequate oxygenation. correcting the rate can abolish PVCs. burning the area or focus in the ventricle where the VT is coming from may also be considered. If hemodynamically unstable (pulseless) defibrillation and cardiopulmonary resuscitation (CPR) is indicated. amiodarone. Antidysrhythmic drugs such as amiodarone and lidocaine should be administered as ordered per frequency of occurrence. Presence and severity of the signs and symptoms depends on rhythm duration. hypokalemia. and rapid identification of causes. the drug is considered effective and continuous therapy is instituted. Conscious sensation of ineffective cardiac activity often accompanied by anxiety. Physical Assessment. Chapter 39 has a complete description of EPS and ablation. hypomagnesemia Acid/base imbalance Drug excess: e. then. lidocaine. If unable to reproduce the dysrhythmia. 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 depends on the cause and clinical manifestations. 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. hypercalcemia.. sympathomimetic amines. Treatment usually is not required. and lidocaiane. leading to unconsciousness. digitalis. amiodarone. 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. Radio-frequency ablation. Tricyclic antidepressants. Drugs used include: procainamide. 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. Usually.. drug intervention is appropriate e. The corresponding QRS complex may be detected on the monitor while contractions are felt as a peripheral pulse. Initial treatment is based on the presence or absence of a palpable pulse. 8 8 . with a pulse. BP: Normal or lower than usual due to decreased cardiac output leading to decreased perfusion.1108 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders CHART 38–10 Dysrhythmia Premature ventricular contraction (PVC) Ventricular Dysrhythmias: Etiology. Treatment PVCs may be isolated when there is no underlying heart condition. If hemodynamically stable. pain relief. e.

starting with confusion and restlessness. quinidine. overdrive ventricular pacing to keep the heart rate up and the QT interval within normal limits. if untreated Assess for pulse and blood pressure. e. e. e. 8 8 Asystole Pulse: None palpable BP: None Unconscious Death. and Treatment—Continued Physical Assessment Pulse: Rapid.g. hypomagnesemia Central nervous system lesions Tricyclic antidepressants Antidysrhythmic drugs. Clinical manifestations are related to the decreased cardiac output caused by the dysrhythmia. Drugs are modified or discontinued if QT interval is prolonged.. hypokalemia. initiate CPR protocol per ACLS guidelines (Appendix ** ). check the lead placement to make sure it has not fallen off. betablockers. which may be congenital or acquired Severe bradycardia Electrolyte imbalance. All agents that cause torsade de pointe are immediately discontinued. 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.g. amiodarone Antihistamines. agency protocol or doctor’s orders.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1109 CHART 38–10 Dysrhythmia Torsade de pointes (TdP) Ventricular Dysrhythmias: Etiology. Magnesium is the treatment of choice to shorten the QT interval. Seizures may be present with a prolonged rhythm. If unsuccessful. digoxin Metabolic abnormalities. Cardioversion and overdrive pacing are used to terminate torsades. Initiate CPR and ACLS protocols (Appendix ** ). e.g. if untreated Check the rhythm in two leads in order to rule out the possibility of fine ventricular fibrillation. palpitations felt. but only may be temporary.. if untreated Treatment Assessment of QT interval for prolongation. leading to unconsciousness..g. calcium channel blockers. digoxin Cardiac standstill from massive cardiac muscle damage Pulseless electrical activity Pulse: None palpable BP: None Unconscious Seizures may occur Death. e. hypokalemia..g. seldane Antibiotics. Pulse: None palpable and heart sounds usually absent BP: None Unconscious Seizures Apnea Death. Administer potassium intravenously if QT interval is abnormal.. Find cause and treat. e..g. tricyclics.. Also. 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. Physical Assessment.. e. Administer drugs per ACLS guidelines. procainamide. Initiate CPR and defibrillation per ACLS guidelines (Appendix*** ).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. 8 8 8 8 . Stress testing and Valsalva will prolong QT interval and can be used to diagnose congenital prolonged QT interval. e. Etiology Prolonged QT interval. psychotropics. severe pulmonary embolism Pericardial tamponade Myocardial rupture Massive cardiac trauma resulting in cardiac tamponade and/or tension pneumothorax Severe acidosis Hyperkalemia Hypothermia Drug overdose.g.

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. QRS complexes. Entire rhythm is ectopy. ted through the normal conduction pathway. Ventricular fibrillation (VF) is an ineffective quivering of the heart muscle that results in no blood delivery to tissues. Figure 38–37 is a rhythm strip showing torsade de pointes. just like atrial fibrillation. FIGURE 38–36 Ventricular tachycardia. There are no organized electrical impulses. • Heart rate is not discernable because there are no waves or complexes to measure. coarse VF typically progresses to fine VF unless treatment is initiated in a timely manner. It is. PR Interval: Not discernable. With this dysrhythmia multiple ventricular sites initiate electrical impulses that are not transmit- Significant ECG features of ventricular fibrillation include: • P waves. The myocardial cells appear to quiver rather than depolarize normally. therefore. Also. procainamide. or other agents that prolong the QT interval. distorted. broken ECG leads. Fine VF indicates that the rhythm has been present for an extended period of time. . ECG artifacts produced by loose or dry electrodes. disopyramide. essential to find and treat the underlying cause. QT is not measurable. FIGURE 38–37 Torsade de pointes.1110 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders P Wave: Two normal P waves present. The etiology. 2004). those that are less than 3 mm frequently are referred to as fine VF. or patient movements or muscle tremors. Rhythm: Both regular and irregular. and therefore. PR interval is not measurable. Ectopic Beats: PVCs. and QT intervals are all absent. There are no waveforms apparent on the ECG strip. PR Interval: Not discernable during dysrhythmia. QT Interval: not discernable. QRS Complex: Wide and distorted during dysrhythmia. Ventricular fibrillation may be classified further as coarse and fine. approximately 200 to 250 beats per minute. PR intervals. quinidine. rapid. and varying heights. Heart Rate: Atrial: Not discernable. thus. QRS Complex: Wide. Heart rate varies. Rate: Rapid. ventricular tachycardia/fibrillation. 1110). Significant ECG features of torsade de pointes include: • • • • • • • QRS complex height varies and undulates. • Entire rhythm is ectopy. torsade de pointes tends to recur repeatedly. In addition to being a life threatening dysrhythmia. • Heart rhythm is irregular. VF must be treated immediately. physical assessment findings. Electrolyte imbalance such as hypokalemia and hypomagnesemia also can initiate torsade de pointes (Garcia & Miller. Rhythm: Both regular and irregular. P Waves: Not discernable. Coarse VF responds better to treatment than does fine VF. Heart rhythm may be regular or irregular. often referred to as v-fib. is a dysrhythmia marked by rapid. QT Interval: Not discernable during dysrhythmia. P waves are not discernable. Ventricular Fibrillation Ventricular fibrillation (VF). Ectopic Beats: All. Ventricular: Rapid. no coordinated atrial or ventricular contraction or palpable pulse. and irregular with waves whose morphology varies greatly. Coarse waveforms are more easily visible and are greater than 3 mm. Figure 38–38 is a rhythm strip showing ventricular fibrillation. and treatment of torsade de pointes are outlined in Chart 38–10 (p. disorganized depolarization of the ventricles. The rhythm appears disorganized.

physical assessment findings. and treatment of ventricular fibrillation are outlined in Chart 38–10 (p. causing cardiac output and tissue perfusion to cease.g. Cardiac electrical activity is seen on the monitor. bradycardia. and clinical death to occur. PR Interval: Not discernable. and varying heights. QT Interval not discernable. physical assessment findings. and treatment of asystole are outlined in Chart 38–10 (p. Due to a variety of cardiac and noncardiac disorders such as acidosis. the heart muscle is unable to respond to the electrical stimuli. distorted. When PEA occurs biological death follows within minutes unless the cause is identified and treated (Beasley. Asystole Asystole is a complete termination of all cardiac electrical activity. The etiology. heart block). 2003). pulseless electrical activity was called electromechanical dissociation (EMD). physical assessment findings. the atria and ventricles do not contract causing immediate loss of oxygen supply to the brain and tissues. and cardiac rupture. Heart rate and rhythm are variable. FIGURE 38–38 Ventricular fibrillation. In hospital settings efforts are usually made to reestablish cardiac activity but. Ectopic beats may be present. (e. trauma. but the patient has no detectable pulse or blood pressure. Formerly. often are futile.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1111 P Waves: Not discernable. the muscle is unable to respond to the stimuli. QRS Complex: Wide. Without an electrical impulse. • PR intervals may or may not have a relationship to QRS complexes. Though the electrical activity is represented as an organized rhythm (other than VT or VF) on the cardiac monitor. The etiology. QT interval is variable. Figure 38–39 is a rhythm strip showing asystole. 1110). In asystole. Ectopic Beats: All. • • • • QRS complex may be narrow or wide. 1110). . the first nursing responsibility for ventricular dysrhythmias is to assess the patient’s response to the No measurable electrical activity FIGURE 38–39 Asystole. 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. Significant ECG features of pulseless electrical activity include: • P waves may or may not be present dependent on rhythm. no measurable electrical activity exists and the rhythm strip appears as a straight line on the ECG monitor. Heart Rate: Not discernable. 1110).. electrolyte imbalance. The etiology. Nursing Management for Ventricular Dysrhythmias As with any dysrhythmia. The clinical outcome usually is poor despite aggressive life support measures. usually bradycardia. and treatment of pulseless electrical activity are outlined in Chart 38–10 (p.

Ventricular dysrhythmias have the greatest impact on cardiac output and are. It also occurs with increased frequency in Asians. The seriousness and treatment of ventricular dysrhythmias depend on the duration and the impact on hemodynamic stability (blood pressure and cardiac output). the nurse needs to give a detailed description of the dysrhythmia pattern and the patient’s clinical response to the health care practitioner. Cultural awareness of populations that are at increased risk for ventricular dysrhythmias is discussed in the Cultural Considerations box (p. Depending on the variation in configuration and the frequency of occurrence. the leader of the resuscitation attempt may need to adapt application of the guidelines to unique circumstances. It occurs in patients with a structurally normal heart. 2003). 2004.com. Retrieved July 13.1112 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders of a loved one (Boyd. skill retention. Peberdy et al. 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 patient care plan detailed below outlines a systematic approach to assessing and providing . Continuous quality improvement issues focus on reducing time to CPR and shock delivery and improving the quality of CPR provided (Jacobs et al. clarify information. This syndrome occurs most often in young adults.10 second from the onset of the QRS complex or the bottom of the S wave. The National Guidelines box outlines the 2005 AHA national guidelines for selected CPR and emergency cardiovascular care. the most serious. http://www. therefore. and improving the effectiveness and efficiency of instruction. The nurse must be knowledgeable of the treatment regimens required for each of the ventricular dysrhythmias based on the standing orders. and agency specific protocols. and advocate for the patient. the guidelines also have streamlined the amount of information that rescuers need to learn and remember. 2003). 2005). They confirm the safety and effectiveness of many treatments and recommend new treatments that have undergone evidence evaluation. Nursing Management of Patients with Dysrhythmias Nursing responsibilities when caring for patients experiencing cardiac dysrhythmias have been discussed throughout this chapter. 000). The current guidelines contain recommendations designed to improve survival from sudden cardiac arrest and acute life-threatening cardiopulmonary disorders. Finally. for a family history of sudden cardiac death. 2000). and have clarified the most important skills that rescuers need to perform (American Heart Association. To assist the learner. Since the nurse is at the bedside it typically becomes a nursing responsibility to keep the family informed. Chapter 17 includes a complete description of end of life issues. It’s possible to have a Brugada sign without having Brugada syndrome. advanced cardiac life support (ACLS). Given that the guidelines do not apply to all situations. and a family history of sudden cardiac death. 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. Nurses need to complete a health history to assess the risk factors related to the occurrence of ventricular dysrhythmias that are outlined in Chart 38–10 (p. 2006. Generally. 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. and provide comfort (AHA 2005a). 000). act as a liaison. 8 CULTURAL CONSIDERATIONS The term Brugada sign is an abnormal finding on an electrocardiogram (ECG) that refers to distance of at least 0. so treatment is tailored to the specific dysrhythmia. and a reduction in barriers to action for basic and advanced life support providers (Chamberlain & Hazinski. to advanced life support treatments. and few or no coronary artery disease risk factor. to drug intervention.com/health/brugada-syndrome/AN00551. 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. If possible. 2005). These 2005 guidelines supersede the published 2000 guidelines for cardiovascular resuscitation and emergency cardiovascular care. Its presence may indicate Brugada syndrome which is an abnormality in the heart’s electrical system that causes lifethreatening heart rhythm disturbances such as ventricular fibrillation. Long-term treatment includes antidysrhythmic medication therapy and an implantable defibrillator. Source: Adapted from: Brugada Syndrome (2005). The cause isn’t clear. When reporting ventricular dysrhythmias. MayoClinic. It is imperative that the health care team offer this opportunity and be sensitive to the family during this crisis period. Future goals of the AHA are to continue to improve the guidelines based on new and evolving research and practice evidence. 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. basic cardiac life support (BCLS). 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. These guidelines are based on the most extensive evidence review of CPR yet published. ventricular dysrhythmias require a variety of interventions from simple observation. it is optimal to have a health care team member be assigned to the family to answer questions. in monitoring units the health care practitioners provide protocols or “standing orders” for treating each type of ventricular dysrhythmia. mayoclinic. specific abnormality. but it appears to be inherited in some cases. Foci will be placed on CPR education.

Health Promotion As with any disorder the primary focus is on prevention of the onset and progression of the disease. 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.americanheart. (2006). nursing care for these patients. (2006). the patient needs to be told to note if there is a pattern as to when the dysrhythmias occur. Nurses will assist in identifying whether or not the patient has a family history of dysrhythmias. All aspects of life including professional as well as personal relationships need to be examined. The nursing diagnosis is generated from the assessment data and guides the nurse toward desired patient outcomes and an intervention plan.jhtml?identifier=3022512. Retrieved June 30. 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. Chart 38–11 (p. To assist the nurse in the comprehensive assessment and interpretation of cardiac 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 . 2005 international consensus on CPR and ECC science with treatment recommendations. This in turn will aid in the early diagnosis. 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. Additionally. or prevention of the occurrence of life-threatening dysrhythmias. a mutation of gene ankyrin-B is now known to cause cardiac arrhythmia syndrome (Hamby. 1116) summarizes the characteristics of each type of dysrhythmia. 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. Mittal. Since the Human Genome Project ongoing research has focused on gaining a better understanding of how genetic disorders can predispose to dysrhythmias. Health teaching about risk factors and life style habits that cause the disorders that underlie the occurrence of cardiac dysrhythmias is essential for prevention. 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. & Stein.org/presenter. 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. what brings them on and what makes them go away. 2006. For example.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1113 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. treatment. For example. from http://www.

Irregular due to varying heart rates. Unable to obtain as T waves are buried. Varies with rhythm change T waves buried. 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 60–100 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. Irregular Fibrillation waves Supraventricular Tachycardia (SVT) Not seen –buried in QRS complex Not discernable Within normal limits. Atrial rate regular. Normal limits Changes with the heart rate.12–0. None Normal limits PAC Normal limits Unable to obtain as T waves are buried in F waves Depends on the AV conduction ratio. Normal if rate is normal. 60–100 bpm Possible during sinus pauses Premature Atrial Contraction (PAC) Atrial Flutter Present and Irregular When PAC occurs. Rapid ectopic focus takes over rhythm Paroxysmal Atrial Tachycardia (PAT) At onset of rhythm. Normal limits Normal 100–180 bpm May be slightly irregular as rate accelerates.1114 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders CHART 38–11 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. 100–250 beats/minute dependent on reference source.12 Normal QT Interval 0. then becomes a rapid regular rate. Underlying regular rhythm except where the sinus pauses occur.34–0. the PR interval tends to shorten slightly. Ectopic focus at onset of rapid rhythm . Within normal limits. shape of P waves different from sinus P waves. T waves are buried in the f waves. unless distorted by buried P waves. May change with PAC only. 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.06–0. 100–250 bpm Regular or irregular due to varying conduction through the AV node.08 seconds in the acceleration and deceleration phases. with a variance of more than 0. or there may be a fast ventricular response. unless distorted by buried P waves. Regular except for premature PAC which may reset rhythm. There may be a slow ventricular response.21 Normal limits QRS 0. There may be marked bradycardia due to long sinus pauses. No P wave f waves Normal limits. Regularly irregular. becoming longer during the slow phase of the rhythm.43 Lengthens to greater than normal Usually shortens Rate 60–100 bpm 40–60 bpm Rhythm Regular Regular Ectopic Beats None None As the sinus rate accelerates. so unable to obtain with fast rhythm.

10 seconds due to delta waves created by the abnormal conduction pathway. Variable Atrial rate within normal limits. None Usually none unless they occur during period when no QRS has occurred and there is a long pause. after.12 second if P wave occurs before QRS complex for the ectopic beat. Usually normal. Sick Sinus Syndrome Present or absent depending on which dysrhythmia is occurring. Appears regular. First Degree AV Block Mobitz I/Wenckeback Present and Regular Sinus P waves.12 second because the AV node is bypassed and contains presence of delta wave. except during heart rate changes. May occur before. Normal limits QT Interval Shortens with tachycardia and lengthens with bradycardia. PJC Junctional Tachycardia May occur before. ventricular is irregular. after. ventricular rate slower than atrial. bradycardic Ventricular: Slow. Atrial: Irregular Ventricular: Irregular Junctional Escape Rhythm Less than 0. May be prolonged d/t slow heart rate Atrial: Slow. or buried in. Ectopic Beats Delta waves: Occur just prior to R wave. may be normal (AV node) or prolonged when present. Atrial rate is regular. ventricular rate irregular and bradycardic Atrial is regular. All others normal. May occur due to slow rate. That of underlying rhythm. Greater than 100 beats per minute. the QRS complex Variable depending on the rhythm Normal limits Variable due to rate change. Regular May occur with slow rates Premature Junctional Contraction (PJC) Normal unless distorted by P wave for the ectopic beat. or buried in. Rate High incidence of tachydysrthrymias. May occur due to muscle irritability. Usually 40–60 (normal intrinsic rate for junctional tissue). Less than 0. Normal unless distorted by P wave. Normal Regular except for the premature beat. Progressively prolonged until one P wave is not conducted and the sequence begins. No specific change unless it is heart rate related. ECG Rhythm Wolff-Parkinson White Syndrome Wandering Atrial Pacemaker Present and Irregular Multiform Normal. ventricular rhythm is irregular. Normal Within normal limits. Within normal limits. All others normal. Rhythm Regular. (continued) .12 second if the P wave occurs before the QRS complex Less than 0. May be present due to the slow rhythm. the QRS complex May occur before. Normal unless impacted by rate. or buried in. after. Mobitz II/SecondDegree Block Present Not always followed by QRS Intermittently absent.20 second. bradycardic Bradycardia to tachycardia.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1115 CHART 38–11 ECG Measurements for Cardiac Rhythms—Continued P Wave Present and Regular PR Interval Less than 0. Normal Within normal limits. May be present with slow rate. Regular Atrial rhythm is regular. Greater than 0. the QRS complex Normal unless distorted by P wave for the ectopic beat. QRS Greater than 0. but may increase its rate.12 second if P wave occurs before QRS complex for the ectopic beat. Constant with conducted beats. Irregular due to changing pacemakers.

Torsade de Pointes Not discernable Not discernable Usually > 0. R and T waves opposite sides of isoelectric line Height undulates Within normal limits. All waves are ectopy Ventricular Fibrillation Pulseless Electrical Activity None None None Atrial: Absent Ventricular: Absent Variable. Rhythm Atrial is regular. May or may not have a relationship to QRS complexes None May be narrow or wide complex.12–0. Broad and premature and has increased amplitude. if notch higher on left. 0. Not discernible.12 second. R and T waves opposite sides of isoelectric line. (2007). Prolonged with PVC. If notch higher on right. Variable depends on rate. ventricular rate is 20–40 bpm. usually bradycardic. Essentially regular.50 seconds in the beats preceding the onset of the rhythm None Rates vary 200–250 beats/minute. 60–100 beats/minute. Ectopic Beats May occur due to slow rate. but not directly affected. 100–250 beats/minute. California State University. Variable. measuring > 0. . ECG Rhythm Third-Degree (Complete) Heart Block Bundle Branch Block Present and Regular sinus P waves Greater than 0. depends on rhythm. All waves are ectopy Ventricular Tachycardia None Visible Not discernible. Rate Atrial rate is regular. Sacramento. None Irregular All waves are ectopy May be present but none of the beats perfuse None May or may not be present. PVC more likely to occur during bradycardia when there is more time to emerge.1116 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders CHART 38–11 ECG Measurements for Cardiac Rhythms—Continued P Wave Present and Regular PR Interval P wave has no relationship to QRS complexes. Typically regular. None with PVC. indicates right bundle branch block. ventricular may be regular or irregular. Asystole None None None None Source: Megan Redeen. indicates left bundle branch block. Regular None Premature Ventricular Contraction (PVC) None with PVC.20 second. Wide and bizarre.12 seconds. QRS May be narrow (junctional rhythm). Underlying rate may be normal or abnormal. 60–100 bpm. or wide (idioventricular rhythm) QT Interval May be rate related. therefore no PR interval is present. nodal rate is 40–60 bpm. Irregular because PVC’s are premature.

000 premature junctional contraction (PJC) p.000 excitability p.000 isoelectric line p.000 unipolar lead p.000 ECG waveform p.000 12-lead ECG p.000 junctional escape rhythm p.000 anion p.000 atrial dysrhythmia p. Answers for review questions appear in Appendix 5 3.000 conductivity p.000 sinoatrial (SA) node p.000 irregularly-irregular rhythm p. Which of the following should be included in this patient’s plan of care? 1.000 graph paper p.000 action potential p.000 fill time p.000 torsade de pointes p.000 atrial flutter p. 3.CHAPTER 38 Nursing Interpretation of the Electrocardiogram 1117 NCLEX® REVIEW 1. 2. Implement ACLS protocols.000 QRS complex p. 4. 2.000 escape p. 0.000 supraventricular tachycardia (SVT) p.000 ST segment p.000 QT interval p.000 fascicles p. 4.000 ion p.12 second 0. 2.000 electrode p.000 dysrhythmia p. 4. 3.000 sinus arrhythmia/dysrhythmia p.000 quadrigeminy p.000 intra-atrial pathways p. 2.000 cardiac depolarization p.000 lead axis p.000 wandering atrial pacemaker p.000 positive deflection p.000 sinus tachycardia p.000 ventricular dysrhythmia p.000 artifact p.000 premature ventricular contraction (PVC) p.000 premature atrial contraction (PAC) p.000 cation p.15 second 4. Which of the following did the nurse assess on this patient’s ECG? 1.000 sick sinus syndrome (SSS) p.000 trigeminy p.000 bundle branch block p.000 junctional dysrhythmia p. Provide carotid artery massage. Prepare to administer magnesium.000 nodes (bundles) p.000 pulseless electrical activity (PEA) p.000 ventricular fibrillation (VF) p. the nurse believes the tracing is normal.000 automaticity p.06 second 0.000 relative refractory period p.000 J point p. Observe and treat the patient for anxiety.000 bigeminy p.000 atrial fibrillation p.000 Mobitz I/Wenckebach p. A patient is diagnosed with a junctional dysrhythmia.000 asystole p. Which of the following should be included in this patient’s plan of care? 1.000 cardiac repolarization p.000 millivolts p.000 bipolar lead p.03 second 0. Medicate with calcium channel blockers. 3.000 contractility p. 4. 3.000 Purkinje network fibers p. The electrocardiogram shows a normal heart rate with shorter PR intervals.000 U wave p.000 third-degree AV block (complete block) p.000 ventricular tachycardia (VT) p.000 refractory period p.000 atrial kick p.000 threshold p. 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. After reviewing the electrocardiogram of a patient.000 cardiac conduction system p.000 sinus arrest p. PR interval less than 0.50 seconds killed in an accident. Prepare to administer lidocaine. Plan for cardioversion.000 first-degree AV block p.000 pacemaker cell p.000 paroxysmal junctional tachycardia (PJT) p.000 .000 Bachmann bundle p.000 PR interval p.000 resting membrane potential p.000 bundle of His p. The complex spans 3 small boxes on the ECG paper.000 ectopic focus p.000 Wolff-Parkinson-White syndrome (WPW) p. Have a serum digoxin level drawn.000 Mobitz II/second-degree block p.000 normal sinus rhythm (NSR) p.000 P wave p.000 AV dissociation p.000 atrioventricular (AV) node p.000 T wave p. 2.000 negative deflection p.8 second QRS complex 0.10 second Absent PR interval QT interval greater and 0. The nurse is assessing the QRS complexes on a patient’s electrocardiogram.000 sinus bradycardia p. The nurse would identify this patient’s QRS complex to be: 1.

Philadelphia: Lippincott Williams & Wilkins.americanheart. 233–249. European Resuscitation Council. .. Porth. Boyd. 3(13).. B. Q & A review of EKG. Basic arrhythmias (6th ed.emedicine. K. Cardiopulmonary resuscitation of adult in the hospital: A report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation. (2006b). Australian Resuscitation Council.). Circulation. interAmerican Heart Foundation. Olshansky. & Stein. (2003).com/med/topic2955. 2575–2594. Atrioventricular nodal reentry tachycardia (AVNRT). S. cardioversion. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care: Part 2. (2005b). (2002a).com/ arrhythmia/arrhythmia8. (2002b). REFERENCES American Heart Association. & Wesley. Resuscitation. F. defibrillation. TX: Author. G.). R. M. Cardiac arrest and cardiopulmonary resuscitation outcome reports: Update and simplification of the Utstein templates resuscitation registries. M. Retrieved June 30.. Upper Saddle River. 112: III-I-III-136. A. jhtml?identifier=3022512 Beasley. L. (2004). IV-35–IV-46.cfm Holtschneider. (2003). Sudbury. M. eMedicine from WebMD. (2005a). M. & Miller G. (2004). 171–176. American Heart Association. (2004).htm Peberdy. Arrhythmia. C. (2003).. M. K. McBroom.. B. 2006. (2006). M. Handbook of emergency cardiovascular care for healthcare providers. Upper Saddle River. Fast and easy ECGs: A self-paced learning program. and pacing. Resuscitation Council of Southern Africa). Heart and Stroke Foundation of Canada. K. D. (2007). Witnessed resuscitation by relatives. et al. Education in resuscitation: An ILCOR symposium: Utstein Abbey: Stavanger. web links. American Heart Association. animations and videos. NJ: Prentice Hall Health. E. & Hazinski.org/presenter. A statement for health care professionals from a task force of the international liaison committee on resuscitation (AHA. Supplement to Circulation: Journal of the American Heart Association.com. MA: Jones and Bartlett. 2001. 2006. B. Retrieved July 17. Boston: McGraw-Hill.1118 UNIT 8 Nursing Management of Patients with Cardiovascular Disorders EXPLORE MyNursingKit is your one stop for online chapter review materials and resources. et al. Retrieved July 13. Understanding EKGs: A practical approach (2nd ed. American Heart Association. Ellis. 112. from http:// www. New Zealand Resuscitation Council. 108. T. ECG everywhere. Norway: June 22–24. Walraven. NJ: Prentice Hall Health. (2006). NJ: Prentice Hall. Prepare for success with additional NCLEX®-style practice questions. Shade. 20. American Heart Association. B. K. K. Advance for Nurses. M. 63. Garcia. (2006a). 112(24). IV-6–IV-11. Chamberlain. G. 297–308.. Mittal. from http:// heart. T. R. (2005c).. Dallas. interactive assignments and activities. 2006.mynursingkit. et al. A. Part 5: Electrical therapies: Automated external defibrillators. TX: Author.healthcentersonline. (2005). 58. (2000). & Patterson. Circulation: 2005. A. (2006). Hamby. 43. EKG plain and simple: From rhythm strips to 12leads. Ethical issues. Upper Saddle River. Resuscitation. International Liaison Committee on Resuscitation. Upper Saddle River. Dallas. I. 2005 International Consensus on CPR and ECC Science with Treatment Recommendations. Resuscitation. International consensus on cardiopulmonary resuscitation and emergency cardiovascular care since with treatment recommendations. M. Jacobs. Circulation.. Ellis. BLS guidelines for healthcare providers. and more! Register your access code from the front of your book at www. NJ: Prentice Hall Health. Arrhythmia recognition: The art of interruption. from http://www. (2006). Essentials of pathophysiology: Concepts of altered health states.