ECG

38Nursing Interpretation of the ElectrocardiogramKathleen Osborn Annita Watson

CHAPTER

Outcome-Based Learning ObjectivesAfter 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 importantand 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.1074

Anatomy of the HeartRecognition 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 SystemThe heart contains its own cardiac conduction system composed of specialized cell fibers called either nodes or bundles. These fibers enable the heart to generate and transmit action potentials without stimulation from the bodys nervous systems. The hearts conduction system is responsible for the electrical activity that controls each normal heartbeat. The special cells and fibers called nodes or bundles are located beneath the endocardium, or inner lining of the heart, in the cardiac conduction system. These are referred to as the sinoatrial (SA) node, the atrioventricular (AV) node, and the Purkinje network (Figure 381 ). Although the sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS) innervate the heart, these external neural impulses are not needed to maintain the cardiac cycle. The pacemaker cells are capable of initiating electrical activity automatically and act as a pacemaker; there-

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Nursing Interpretation of the Electrocardiogram 1075

Intra-Atrial PathwaysThe 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 JunctionThe atrioventricular (AV) node is located on the floor of the right atrium just above the tricuspid valve. Electrical activity at the AV node is delayed approximately 0.05 second to allow for atrial contraction, which increases the amount of blood reaching the ventricles. Atrial contraction, commonly referred to as atrial kick, augments the blood supply going to the ventricles and ultimately cardiac output. This delay also serves to stop the transmission for a very rapid succession of impulses that can occur under abnormal conditions. These abnormalities, called atrial flutter/fibrillation, are discussed later in the chapter. The AV junction contains fibers that can polarize spontaneously, forming an impulse that can spread through the heart chambers. This means that if the SA node fails or falls below its normal range, the AV node can take over, thus assuming the role of a secondary pacemaker. Under normal conditions the AV junction is the only pathway for the conduction of atrial impulses to the ventricles.

Right bundle

FIGURE 381

Electrical conduction system of the heart.

fore, the heart will beat in the absence of any nervous system connection. The SNS and the PSNS affect only the speed of the cardiac cycles and the diameter of the coronary arteries. It is essential to understand the hearts electrical conduction system in order to be able to understand an ECG strip interpretation. Each component of the system follows.

Bundle of His and Bundle BranchesThe 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) NodeThe 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 FibersPurkinje network fibers consist of a network of fibers that carry impulses directly to the ventricles. The rapid spread of the electrical impulse through the left and right bundle branches, the Purkinje network fibers, and the ventricular muscle initiates ventricular contraction. Purkinje fibers also may be pacemaker cells; they fire at an intrinsic rate of 20 to 40 beats per minute.

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Nursing Management of Patients with Cardiovascular Disorders the only mechanical function of the heart. Excitability, conductivity, and automaticity are electrical functions of the heart. Contractility may be thought of as the mechanical coordination of cardiac muscle contractions producing a heartbeat. In addition to these cell characteristics, normal cardiac function is dependent on maintaining electrolyte concentrations inside and outside the cell membrane. Specific electrolytes and their relationship to cardiac function are described next.

Cardiac CellsThere are two basic cardiac cell groups: the myocardial working cells and the specialized pacemaker cells of the electrical conduction system. The atria and the ventricles are constructed of myocardial working cells, which have an abundance of contractile filaments needed to generate cardiac muscle contraction. The cardiac muscle contraction is what actually pumps the blood through and out of the heart into the pulmonic and the systemic circulation. The myocardial working cells have the ability to contract in response to chemical, electrical, or mechanical stimuli. The second type of cardiac cell is the specialized pacemaker cell whose primary function is to generate and conduct electrical impulses (stimuli). These cells found in the heart wall and septum (membrane dividing the right and left sides of the heart) control the heart rate and rhythm by coordinating regular cardiac muscle depolarization (contraction) (see Figure 381 ). The myocardial contractions pump the blood through and out of the heart. The term threshold refers to the point at which an electrical stimulus produces a cell response. When a stimulus is strong enough for cardiac cells to reach this threshold, all of the cells will respond to the stimulus and cause a muscle contraction. This is called the all-or-none phenomenon; in other words, either all the cells respond, or none of the cells respond. This principle allows for a coordinated muscle contraction and greater efficiency in pumping blood. All cardiac cells possess four primary characteristics: automaticity, excitability, conductivity, and contractility. These characteristics are described next.

Electrolytes Affecting Cardiac FunctionAn 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.

AutomaticityAutomaticity 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.

ExcitabilityExcitability 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 RepolarizationWhen 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.

ConductivityConductivity 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.

ContractilityContractility is the ability of the cardiac cells to shorten and cause the muscle to contract in response to an electrical stimulus. This ability also is referred to as rhythmicity. Contractility is

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When a muscle cell receives a stimulus due to the Na-K pump exchange, a rapid change occurs in the Cell exterior resting membrane potential, known as the action potential, which is measured in millivolts (a unit of electrical voltage or potential difference equal to one-thousandth of a volt). Once the action potential occurs, the cell moves toward a positive charge. The four phases (04) of the action potential are shown in Figure 382 . Phase 0 is rapid depolarization, phase 1 is rapid repolarization, phase 2 is the plateau, phase 3 is final repolarization, and phase 4 is the resting state. To generate this action potential and the resulting muscle depolarization, the threshold potential must be reached, which is phase 0. To initiate phase 0, Na enters the cell causing a sharp positively charged rise of the intracellular ions. The cell moves from 90 millivolts (mV) in its resting state to a positive Open K channel 15 to 30 millivolts, causing myocardial depolarization to occur. When the threshold is reached, the cell will continue to depolarize with no further stimulation; this phenomenon is referred to as automaticity. During phase 1, the depolarized stage, the interior of the cell has a net positive charge. In this effort to continue to make the inside of the cell more positive, Ca enters; this is phase 2, the plateau phase. During phase 3 the calcium channels close, and Na is pulled from the cell by the Na-K pump; thus the cell is returning to its polarized negative resting membrane potential state (phase 4) (Figure 383 ). The first area of the cardiac muscle to be depolarized is the first area that is repolarized. For example, after the atria depolarize they repolarize while the ventricles are depolarizing. Thus, when the SA node fires again, the muscle will be ready to respond with a new action potential. Cardiac repolarization is the process whereby the depolarized cell is polarized, causing a return to the resting membrane potential (see Figure 382 ). Repolarization also is referred to as the recovery phase that every cardiac cell must go through in order to be ready to accept another stimulus. It is a slower process than that of depolarization. During repolarization the

Na

Cl

Closed Na channels

Closed K channel Cell interior

K

Anionic protein

FIGURE 383

Electrolyte movement during an action potential.

muscle is refractory (resistant) to stimulation. This refractory period consists of two stages; the absolute and the relative refractory periods. During the absolute refractory period, which is the majority of time for repolarization, the cardiac cell is unable to respond to any stimulus and thus cannot spontaneously depolarize (see Figure 382 ). The relative refractory period is a period when repolarization is almost complete (see Figure 382 ). This period is known as the vulnerable period of cardiac cell repolarization. If a stimulus is strong enough, it can cause depolarization that can be life threatening. These situations are discussed later in this chapter. The refractory periods play a major role in either causing or preventing cardiac dysrhythmias. Further discussion of their role is explained regarding the various dysrhythmias and throughout the chapter.

Summary of the Cardiac Conduction SystemECG Transmembrane potential (mV) 1 0 2 Action potential 0 3

4 100

4

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

Inside cell CELL MEMBRANE Outside cell

FIGURE 382

Action potential.

The electrical impulse begins in the SA node located in the upper right atrium, causing atrial contraction. The impulse then travels through the atria along intra-atrial pathways to the AV node located near the center of the heart. After leaving the AV node the impulse moves down into the bundle of His, through the right and left bundle branches, and into the Purkinje network fibers, causing ventricular contraction followed by repolarization (see Figure 381 , p. 1077). Then the cycle begins again. When caring for patients with actual or potential cardiac conduction abnormalities, it is essential that the nurse understand how the cardiac conduction system described here is graphically depicted on an electrocardiogram. Recognizing and interpreting these electrical impulses and their relationship to heart disease is an essential nursing responsibility. A discussion of how the electrical conduction system is depicted in an ECG follows.

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Nursing Management of Patients with Cardiovascular Disorders diac cycle. Both the absolute and the relative refractory periods are in place during the T wave. U waveThe U wave is present only on some peoples ECG. It follows the T wave. Its etiology is unknown, but it is frequently seen in exercise, in drug toxicity, and most frequently with low potassium levels. Changes in the configuration of the waveforms or lengthening and/or shortening of time intervals may indicate an abnormality in the heart. These abnormalities are discussed in detail in Chapters 40, 41, 42, and 43 . The following sections discuss the method used to evaluate waveforms and time intervals.

Cardiac Waveform and Time Intervals Measured on ECGWhen the electrical impulse leaves the SA node, a graphical representation of the signal referred to as a waveform is produced and recorded with monitoring equipment. As the electrical impulse travels through the cardiac conduction system, waveforms characteristic of a given anatomical location are recorded. These waveforms are referred to as P, Q, R, S, and T. Additionally, time intervals, which represent the time it takes for the impulse to travel from one anatomical location in the heart to another, are recorded. These time intervals are called PR, QRS, and QT. One complete cardiac cycle has five to six waveforms and time intervals. These are described here and depicted in Figure 384 . P waveThe P wave represents contraction or depolarization of the atria. Both the right and left atria depolarize at the same time. PR intervalThe PR interval, sometimes referred to as the PRI or PR segment, represents the time it takes for the impulse to travel from the SA node down the intra-atrial pathways to the ventricles. In other words, it represents the beginning of the atrial contraction to the beginning of the ventricular contraction. QRS complexThe QRS complex consists of the Q, R, and S waves, and represents the conduction of electrical impulses from the bundle of His near the AV junction to the Purkinje network fibers located in the ventricles, causing them to depolarize. J pointThe point at which the QRS meets the ST segment is called the J point. ST segmentThe ST segment is a line extending from the S wave that gradually curves upward to the T wave, represented on the ECG as an almost isoelectric line. The ST segment signifies ventricular repolarization. T waveThe T wave is ventricular recovery or repolarization. This is often referred to as the resting phase of the car-

ECG Monitoring Equipment

RA

Depolarization RV Repolarization

Electrocardiography detects cardiac electrical impulses at various points on the surface of the body. The graphical depiction of these impulses, waveforms, and time intervals is obtained either with an electrocardiograph (ECG machine) or on a bedside cardiac monitor. To obtain an ECG tracing, specific equipment is needed including an electrode, lead wire, and monitor or oscilloscope. An electrode is most commonly a round adhesive pad that is impregnated with conducting gel in the center and is attached to a lead wire. Electrodes are sensing devices that detect the electrical activity of the heart and conduct the electrical impulses from the skin surface back to the ECG machine, where they are converted into waveforms. An electrode is much like a camera in that it takes pictures of the electrical activity in the heart. The electrodes are connected to a cardiac monitor by lead wires. Typically, these wires are color coded according to machine manufacturer, and these colors assist the practitioner in attaching the lead wires to the appropriate electrode. The cardiac monitor records the electrical impulses and provides a real-time visual tracing of the waveforms on the screen and/or a printed version on specialized ECG graph paper, described next. The printed version is called a rhythm strip or ECG strip. The rhythm strip gives the health care practitioner information about where the pathological processes are SA node occurring in the heart. Figure 385 shows the elecAV node trodes, lead wire, and cardiac monitor. The term lead is used in different contexts when discussing ECGs. In addition to using the term as just described, as a connector from the electrode to the LA cardiac monitor, the term also is used when discussing a view or picture of the heart from a particular angle or vantage point. In this respect one can think of the lead as the eye of the camera.LV

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Lead PlacementBody tissues and fluids surround the heart; therefore, the electrical action potentials produced in the heart are widely conducted throughout the body via these tissues and fluids. The impulses or action potentials can be detected from any point in the body. Electrodes must be placed in certain positions on the body in order to obtain a clear picture of the electrical impulses in the heart, and there must always be a positive, a negative, and a ground electrode/lead. The ground lead minimizes outside

P

ST QRS

T

U

RBB

LBB

P QRS PR QT

FIGURE 384

Waveform relationship to cardiac conduction system.

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Device1.00

Channel 0 Chart 2.0 1.5 1.0 Volts 0.5 0 Beats Thresh Limit

# of samples

5300Sample rate

5000Set limit1.00 0.50 1.50

ElectrodeMax Peak 1.37 Time

0.00

2.00

-5.0 1.17Threshold0.20 0.10 0.00 0.30 0.40 0.50

-1.0

Below limit

Beats/min 180/min

0.31 Chirp output Chirp alarm parameters # Sam 700 amp 1 1.5 f1 0.010 f2 0.70 2.0 1.0 0.0 -1.0 -2.0 0 25 50 75 100 125 150 175 200

Lead wire

Gain Set mode Equalize Push/Reset

FIGURE 385

Electrodes, lead wire, and cardiac monitor.

electrical interference. Each electrode senses the flow of current in the heart in relation to the lead axis. The lead axis refers to the imaginary line drawn between the positive and negative electrodes. If the axis is directed toward the positive lead, there is an upward or positive deflection on the ECG tracing (above the isoelectric line). If the axis is directed toward the negative lead, there is a negative deflection on the ECG tracing (below the isoelectric line) Figure 386 . Multiple leads, as seen with a 12lead ECG, view cardiac electrical conduction from different perspectives. Think of the heart on a pedestal that one is able to move around while a camera takes pictures from various angles. This gives the practitioner 12 different views of the cardiac electrical activity. For bedside monitoring it is not practical or necessary to have a 12-lead ECG or 12 continuous views of the heart. Therefore, 1 or 2 of the 12 possible leads from the entire 12-lead ECG are chosen for constant bedside monitoring because they give a clear view of cardiac activity and abnormalities. To obtain a single bedside ECG rhythm strip, a minimum of three electrodes is required: one positive, one negative, and one ground. Either lead II or modified chest lead1 (MCL1) is commonly used for threeLead II

electrode bedside monitoring. The MCL1 is one of the V leads from the 12-lead ECG that is modified for bedside monitoring. The lead chosen is dependent on the unit policy and nurse and/or health care practitioner preference. The specific dysrhythmia being monitored or anticipated may dictate the type of lead chosen. No single monitoring lead is ideal for every patient. Therefore, if more than one lead or picture of the heart is required, five electrodes are placed to increase the monitors capability beyond the three-electrode monitoring system. The five-electrode monitoring system has an exploring chest electrode that allows one to obtain the same 12 views as a 12-lead ECG when needed. However, at the bedside typically only two simultaneous leads are used to view the heart with the five-electrode system. Commonly the two leads that are run simultaneously are lead II and MCL1. However, the lead or leads chosen depend on the desired view of the heart. Figure 386 shows a cardiac rhythm strip that has simultaneous lead II and MCL1 ECG views. These two leads provide different perspectives of the various normal and abnormal ECG configurations. For example, lead II produces easily identifiable upright P waves and clear QRS

Isoelectric line MCL 1

FIGURE 386

Lead II and MCL1 ECG configurations.

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complexes. An MCL1 lead is useful for evaluating abnormalities in the ventricles. Placement of the electrodes depends on the lead being monitored and whether a three- or five-lead system is being used. Figure 387 shows the position of the electrodes for both lead II and MCL1. The color coding on the lead wire gives the nurse information about whether the lead is positive or negative. Typically the color black is negative, white is positive, and green is ground. In the five-lead system red and brown colors also are used and their polarity changes depending on the lead being monitored (Morton, Fontaine, Hudak, & Gallo, 2005).

CHART 381Evaluation of: Axis deviation

Indications for a 12-Lead ECG

Cardiac valve disease Chamber dilation or hypertrophy Chest pain/angina Dysrhythmias Effect of cardiac drugs Electrolyte imbalance Hypothermia Myocardial ischemia Myocardial patterns of ischemia, necrosis, and infarction New versus old myocardial infarction Pericarditis Pulmonary embolism Bundle branch block

12-Lead Electrocardiogram (ECG)The rhythm strips that have been used to demonstrate dysrhythmias throughout this chapter have all been from a single lead. A single-lead ECG rhythm strip gives one view of the electrical activity of the heart, whereas a 12-lead ECG provides 12 individual views or snapshots of the hearts electrical patterns. These added views provide a complete picture of the cardiac electrical system, both top to bottom and front to back. A 12-lead ECG is useful in evaluating not only the presence of damage but also the location in the heart where that damage occurred. Frequently, to assess damage accurately requires viewing the area with more than one lead. Chart 381 provides the indications for a 12-lead ECG. There are 3 bipolar and 9 unipolar leads in a 12-lead ECG. A bipolar lead has electrodes with opposite polarity, one positive and one negative. A unipolar lead has only a positive polarity (Walraven, 2006). Both bipolar and unipolar leads provide information in one direction onlybetween two points. The two

dimensions on the chest in which leads can be placed are the frontal plane (up and down) and the horizontal plane (around the chest). Figure 388 shows the horizontal plane and the frontal plane views. The axis of a lead is the imaginary line drawn between the positive and the negative electrode in a bipolar lead and between the positive electrode and the zero reference point in a unipolar lead. Thus, depending on where a given lead is placed, it provides

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. It's like V1.

FIGURE 387

Electrode placement for bedside cardiac monitoring.

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so named because they generate such small waveforms that the ECG machine must augment, or increase, their size so they will show up on the ECG paper (Ellis, 2002). These leads are aVR, aVL, and aVF. Each lead records the following electrical conduction pattern: aVR: central terminal to right arm aVL: central terminal to left arm aVF: central terminal to left leg. The standard bipolar leads and the augmented limb leads provide the 6 frontal plane leads of the 12-lead ECG, whereas the 6 chest (precordial) unipolar leads, V1V6, evaluate the horizontal plane of the heart. The positive electrode is placed on 6 different sites across the chest as shown in the diagram in Figure 391 (p. 000). These chest leads provide the 6 horizontal leads of the 12-lead ECG. Chart 382 describes the procedure for obtaining a 12-lead ECG. For example, lead V1 evaluates the right ventricle; leads V2 and V3 span the interventricular septum; lead V4 is over the cardiac apex; and leads V5 and V6 evaluate the lateral wall. The Q wave, T wave, and ST segment are used to evaluate the presence of damage, and the lead placement is used to identify the area of damage. Chapter 40 discusses the myocardial damage associated with changes in the Q wave, T wave, and ST segment. When performing an ECG, the nurse must have knowledge of the lead placement for each of the 12 leads. Improper placement may result in inaccurate information and treatment. The electrodes must have firm, unbroken contact with the skin. The limb leads are placed on the flat surfaces just above the wrists and ankles. If there is an amputation, the lead is placed on the remaining stump. Chest hair may interfere with skin contact and, if so, should be shaved. The type and sophistication of ECG machines varies; some can record only one lead at a time, whereas others can record 3, 6, or all 12 leads simultaneously.

Frontal plane

Horizontal plane

FIGURE 388

Horizontal and frontal planes. (need diagram rendered)

a picture of the electrical activity from that vantage point within the heart. Electrical current flowing toward a positive electrode creates a positive deflection on the ECG paper, whereas electrical current flowing toward a negative electrode creates a negative deflection on the ECG paper (Walraven, 2006). The standard bipolar limb leadsI, II, IIIare applied to the right arm (RA), left arm (LA), and left leg (LL). Each lead records the following electrical conduction pattern: Lead I records conduction from RA to LA. Lead II records conduction from RA to LL. Lead III records conduction from LA to LL. The right leg electrode acts as a grounding electrode. Three more frontal plane, unipolar augmented limb leads can be created by using a central terminal. Augmented leads are

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CHART 382

12-Lead ECG Procedure Bring the portable ECG machine to the patients bedside in any type of patient care setting. Use 10 electrodes for the standard 12-lead ECG: 6 on the chest and 4 on the limbs. Figure 391 (p. 000) shows the correct placement of the electrodes. Place limb electrodes away from bony prominences and areas of significant muscle movement to prevent interference of other muscle activity. Palpate the intercostal spaces along the sternal border, until the fourth one is reached, for placement of the first chest electrode.

Electrode Placement

Cable Connection and Machine operation

Connect the cable that is attached to each of the electrodes to the ECG machine. Adjust the ECG machine to obtain a clear picture of the cardiac electrical activity. After completing the ECG, remove electrodes and clean the skin as necessary. Leave the electrodes in place if the patient is going to have serial ECGs to ensure consistency of multiple readings.

Patient Instructions Documentation

Explain the procedure and the rationale for the test prior to performing an ECG. Advise the patient to lie still, breathe normally, and refrain from speaking while obtaining the ECG. Document patients height, weight, and use of cardiac medications. Document current clinical manifestations if present and chief complaint. Document reason for the ECG. Record patients response to procedure, if any.

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Nursing Management of Patients with Cardiovascular Disorders mal activities of daily living. The patient keeps a diary of signs and symptoms and the associated activity performed. Additional information on the Holter monitor is discussed in Chapter 39 . Transtelephonic monitoring is another method of outpatient ECG monitoring. With this type of monitoring, a specific lead system is used for transmitting the signals and is accomplished by having the patient place a telephone mouthpiece over the transmitter box. The ECG is recorded and evaluated at another location. This method often is used as a follow-up evaluation for patients with cardiac pacemakers. Chapter 39 discusses pacemakers.

Each ECG machine has its own method of identifying specific lead names (V1, V2, etc.) and a diagram of where to place them. The nurse must be cognizant when obtaining an ECG about which rhythms require immediate notification of the health care practitioner for emergent treatment. The significance and severity of the individual rhythms are presented under each rhythm discussed throughout the chapter.

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

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

8

Cardiac Monitoring SystemsThe purpose of continuous ECG monitoring is to detect new and changing abnormal heart rhythms and to trend data relatively to frequency and duration of dysrhythmias. When continuous ECG monitoring is necessary, it can be accomplished by two methods. First, the patient can be hardwired to a monitor whereby the leads are connected directly from the bedside monitor to the patient. The hardwired system has an oscilloscope at the bedside and in a central location such as the nurses station. This system typically is able to monitor more than one lead simultaneously, and depending on the lead used the system also is able to visualize ST segment depression and elevation. Hardwired systems have the capability to print a rhythm strip and provide visual and audible alarms when abnormalities in the heart rhythm occur. These systems are computerized and therefore are able to interpret and store dysrhythmias in a memory bank. Hardwired monitoring is done in critical care areas. The second method for continuously monitoring patients is with radio waves from a battery-operated transmitter. The transmitter, worn by the patient, transmits the rhythms to a central bank of monitors, which is typically at the nurses station. This system allows the patient to ambulate about the unit while still being monitored. Whichever system is being used, the patient must be informed of its purpose and any necessary precautions. Because it may be stressful and frightening for a patient to have his heart be continuously monitored, patient education is essential. The patient needs to understand that this system does not report clinical manifestations such as angina, dyspnea, or weakness. It is necessary, therefore, that the patient report these conditions as they occur. Another form of continuous ECG monitoring is typically done in the outpatient setting. This system, referred to as a Holter monitor, records the heart electrical activity on a magnetic tape for 24 to 48 hours while the patient goes about nor-

All cardiac monitors have alarm systems built into them to alert the nurse when abnormalities occur. Alarm systems have both a high and a low setting so that the nurse is alerted when the heart rate goes above or below the set parameters. The nurse must ensure at the beginning of the shift that the monitor alarms are on and set with the appropriate parameters established for the patient (see Chart 383). The nurse needs to explain to the patient that these alarms may also go off with excessive movement or if the lead wire falls off. The patient needs to be told the nurse will respond to the alarm each time it goes off and must be reassured that it does not necessarily mean there is a problem with her heart. The nurse must stress that excessive movement will cause the alarm to go off frequently.When the monitor alarms it is essential that the nurse evaluates the clinical status of the patient prior to any other activities in order to assess for the presence of cardiac abnormalities and the patients clinical response to the abnormalities.

Nursing responsibility for monitored patients includes knowledge of the patients specific rhythm in order to assess for changes. The more familiar the nurse is with the patient and the monitoring system, the quicker problems can be diagnosed

CHAPTER 38


CHART 383

Procedure for Continuous ECG Monitoring Choose an area to place the electrodes where there are no bony prominences, thick muscles, or skin folds, because these areas are prone to produce noncardiac waveforms and interference. Prepare the skin for electrode placement by making sure that it is clean, dry, and free of hair. It may be necessary to shave the chest area of male patients. Remove dead skin cells to improve electrical conductivity by rubbing the skin with the rough patch on the back of the electrode, a dry washcloth, or a gauze pad. The skin will become reddened with the rubbing; be careful not to cause skin breakdown. Wipe the skin with an alcohol sponge if skin is oily or a moist wipe; allow it to air dry. Make sure that the electrode pads are moistened with conducting gel prior to placing them on the chest to increase electrical conductivity. A dry electrode is not effective for conducting the electrical activity. When the electrode becomes dry or loose, it needs to be replaced. If the skin around the electrode becomes irritated the electrode must be removed and relocated. Position electrodes on the chest wall at prescribed locations depending on the lead or leads being monitored. Change electrodes when wet, poor contact, unclear tracing, and/or every 48 hours to avoid skin irritation.

Electrode Attachment

Lead Wire and Cable Connection

Connect the electrode to the lead wire, which is approximately 16 inches long. Typically a snap attaches the lead wire to the electrode. The lead wires are color coded to represent positive, negative, and ground leads. Attach the opposite end of the lead wire to the cable. The cable has individual color-coded receptacles or holes for each lead wire.

Monitor Connection and Adjustment

Attach the cable to the monitor. Adjust the monitor to increase the size of the PQRST complex for more accurate interpretation. Read the operating instructions for the specific brand of monitor prior to use. Always leave the alarm on. Recognize that the alarms have upper and lower heart rate limits. Set the alarm approximately 20 beats above and below the patients resting intrinsic heart rate. Follow institutional policy, if present, to determine different alarm limits. Be aware that when the alarm sounds, the first nursing responsibility is to check the patient. Recognize that movement by the patient may cause the alarm to sound falsely.

Alarm Setting

Documentation

Document lead used. Document PR interval, QRS width, QT interval, ectopic beats, and type of rhythm/dysrhythmia. Record ECG changes and patients response to changes.

and appropriate action taken. Assessment of patient tolerance of rhythm changes is the first nursing action, prior to assessing for problems with the equipment.When abnormalities appear on a cardiac rhythm strip it is an essential nursing responsibility to assess the patients tolerance of the rhythm, especially if it is a new abnormality. The nurse needs to be knowledgeable about what changes need to be reported to the health care practitioner. The rhythm needs to be documented on the patients record.

Communication with all personnel caring for the patient and observing the monitor is critical. They must be kept informed of when the patient needs to be off the monitor or of physical activities, such as bathing, occurring that may sound the alarms. For example, if there is a monitor technician, that person must be informed of the patients leaving the floor and increased physical activities.

ECG Graph PaperECG graph paper is specialized paper on which the ECG pattern is recorded. The paper is designed to allow the measurement of various calculations related to the electrical activity of the heart. It is standard nursing protocol to measure these calculations when a patient is on a cardiac monitor. These measurements help determine whether the rhythm falls within the time limits of normal cardiac activity. Abnormal measurements may indicate a malfunction of the cardiac conduction system and will be discussed later in conjunction with the various dysrhythmias.

Tolerance to the rhythm is assessed by obtaining and evaluating vital signs, neurological status, and the presence of signs and symptoms of decreased cardiac output, for example, angina. After determining patient status and stability, the nurse then troubleshoots the equipment for problems such as a dry electrode or a disconnected wire. The problem could be as simple as the patients tapping the electrode, and no action would be necessary. It also is essential that the nurse is knowledgeable of which cardiac disturbances are reportable and/or life threatening.

1084 UNIT 8

Nursing Management of Patients with Cardiovascular Disorders dividual and also depends on the ECG lead being used. For example, QRS complexes are mostly positive in the lead II and mostly negative in the MCL1 lead (see Figure 386 ). Not everyone has a discernable Q wave. QT intervalThis is measured from the Q wave to the end of the T wave. The normal QT interval is 0.34 to 0.43 second or 8.5 to 11 boxes. Heart rateThis is measured by using the very top of the ECG paper, which is marked off in 3-second intervals with tick marks. The tick mark is a small straight line or hash mark above the tracing. Count up the number of PQRST complexes that occur in 6 seconds and multiply that number by 10. This method provides a general estimate of the heart rate. A more accurate method for measuring heart rate is to count the number of small squares between two R waves and divide the total into 1,500. The normal HR is 60 to 100 beats per minute. Heart rhythmThis is determined by measuring the distance between two R waves and then measuring each subsequent R wave to ensure it is the same distance apart as the previous ones. With a regular rhythm, the distance between R waves is equal. Calipers (Figure 3810 ) are the instrument used to take all these measurements. Figure 3811 demonstrates where each measurement begins and ends.

The ECG graph paper is arranged as a series of horizontal and vertical lines. This paper is standardized to allow for consistency in ECG measurement and strip analysis. Both the amplitude and the voltage may be measured on the paper. The vertical axis measures the amplitude and is stated in millivolts (mV). Two large squares on this axis equal 1 millivolt. This measurement is rarely used because the size of the picture or millivolts can be adjusted at the monitoring station, thereby reducing the consistency of this measurement. The horizontal axis is divided into small squares. The squares on the ECG paper are used to measure the length of time required for the electrical impulse to traverse a specific part of the heart. Figure 389 shows an example of ECG graph paper. These squares are used to measure time intervals as follows: The smallest square is 1 millimeter (mm) in length and represents 0.04 second in time. The large square is 5 mm in length and represents 0.20 second in time. The large square equals 5 small squares. Five large squares represent 1 second.

ECG MeasurementsWhen assessing either a rhythm strip or a 12-lead ECG, both the individual PQRST complexes need to be evaluated as well as the relationship of each individual complex to the overall rhythm. The assessment of an ECG configuration includes the following: P waveThere should be one P wave for every QRS complex. PR intervalThis is measured from the beginning of the P wave to the beginning of the QRS complex. The normal PR interval is from 0.12 to 0.20 second or 3 small boxes to 1 large box. QRS complexThe QRS complex is measured from the beginning of the Q wave to the end of the S wave. The normal range is from 0.06 to 0.12 second or 1.5 boxes to 3 boxes. The shape of the QRS complex varies from individual to in-

FIGURE 3810

Calipers.

.06.12 sec QRS

P

T

PR

QRS QT

0.04 sec 0.20 sec 0.04 sec .12.20 sec

QT .34.43 sec Isoelectric line

FIGURE 389

ECG graph paper

FIGURE 3811

ECG measurement.

CHAPTER 38


FIGURE 3812

Artifact.

Isoelectric LineThe isoelectric line marks the beginning and ending point of all waves. When the SA node fires, the ECG waveform (the actual tracing on the graph paper) begins and moves away from the isoelectric line (see Figure 3812 ). Any wave that has an upward deflection, which is above the isoelectric line, is referred to as a positive deflection, and any waveform that goes below the line is referred to as a negative deflection. Depending on the lead, certain waves normally are positive and certain ones are negative. In a lead II the normal P wave has a positive deflection, the PR interval is isoelectric, the Q wave is the first negative deflection, the R wave is positive, the S wave is negative, the ST segment is isoelectric, and the T wave is positive. CHART 384P Waves

Stepwise Process for ECG Strip EvaluationAre the P waves regular? Is there one P wave for every QRS and one QRS for every P wave? Is the P wave in front of the QRS or behind it? Is the P wave normal and upright in lead II? Do all the P waves look alike? Are the abnormal P waves associated with ectopic beats? Are all the PR intervals constant? Is the PR interval measurement within normal range (0.12 to 0.20 second)? If the PR interval varies, is there a pattern to the changing measurements? Are all the QRS complexes of equal duration? What is the measurement of the QRS complex size? Is the QRS complex measurement within normal limits (0.06 to 0.11 second)? Do all the QRS complexes look alike? Are the unusual QRS complexes associated with ectopic beats? What is the length of the QT interval? Is it normal or prolonged? Is the patient on a treatment that prolongs the interval? Atrial: how many P waves in 6 seconds times 10. Ventricular: how many R waves in 6 seconds times 10. A second method is to count the number of large boxes between two R waves and divide by 1500. Both methods work best when the rhythm is normal. What is the heart rate? Is it regular? Is it irregular? Are there any patterns to the irregularity? Are there any ectopic beats; if so, are they early or late? Are they present? What are they? How is the patient tolerating them? Do they require treatment?

PR Interval

ArtifactArtifact is defined as an ECG pattern caused by sources outside the heart creating a false and abnormal pattern on the ECG graph paper. This interference is due to several causes: Malfunction of electrodes possibly due to dry conductive gel, clammy skin, or dense chest hair Patient movement, which precipitates a fluctuating isoelectric line that corrects itself when the patient lies still Improper grounding, which occurs when a patient is in contact with an outside source of electricity, such as poorly grounded beds and/or IV infusion pumps Equipment failures, such as broken wires or cables on the ECG equipment, which need to be exchanged for new equipment. Because of this interference or artifact, the baseline or isoelectric line becomes fuzzy. When artifact is present, it is difficult to diagnose cardiac abnormalities, making it is necessary to correct the cause of the artifact. Figure 3812 depicts artifact.QRS Complex

QT Interval

Rate

Ectopic FocusEctopic focus is a heartbeat originating from a site other than the primary cardiac pacemaker tissue. Ectopic foci may affect cardiac output and must be assessed and documented carefully for their impact on the hemodynamic stability of the patient. The terms dysrhythmia, arrhythmia, and ectopic focus all mean the same thing and are used interchangeably.Regularity (also called rhythm)

Ectopic Beats

ECG Rhythm Strip Evaluation and DocumentationWhen evaluating an ECG rhythm strip, using a simple stepwise process provides a consistent method for rhythm strip evaluation. This is shown in Chart 384. If the rhythm strip falls out of the normal parameters, then there is a high probability of an ab-

normality occurring in the conduction system. These abnormalities are discussed at length throughout the remainder of the chapter.

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Nursing Management of Patients with Cardiovascular Disorders ple, change in blood pressure, pulse, level of consciousness, and urine output.

Normal Sinus RhythmNormal sinus rhythm (NSR) is a cardiac rhythm initiated from the SA or sinus node that has all the normal waveforms (PQRST) and normal time intervals (PR, QRS, QT) (Figure 3813 ). The following criteria must be present to be NSR: P wave has a normal and consistent shape and appears before every QRS complex. There is a 1:1 ratio of P wave to QRS complex. PR interval is between 0.12 and 0.20 second. QRS complex is between 0.06 and 0.12 second. QT interval is between 0.34 and 0.43 second. Atrial and ventricular rate is between 60 and 100 beats per minute (beats/minute). Atrial and ventricular rhythm is regular.

DysrhythmiasWhen the cardiac muscle does not receive enough blood, it becomes ischemic and irritable, causing cardiac dysrhythmias to occur. A dysrhythmia is an abnormal disturbance of the electrical conduction system of the heart. There are a number of dysrhythmias, which originate in different parts of the heart. This chapter addresses dysrhythmias according to location in the heart, beginning at the top with the atrial dysrhythmias. As the dysrhythmias occur anatomically lower in the heart, the severity is greater due to their impact on cardiac output. The cardiac output decreases as the severity of the dysrhythmia increases. Heart rhythms are categorized according to the cardiac structure in which they begin, or their site of origin. The most common dysrhythmias begin at the top of the heart with the SA node. These types of dysrhythmias are called sinus dysrhythmias due to their origin in the SA, or sinus, node. The next area in the heart where dysrhythmias may occur is in the intra-atrial pathways, referred to as atrial dysrhythmias. Moving anatomically down to the next area of the conduction system, the AV node or junction is where junctional dysrhythmias occur. The final area of the heart where dysrhythmias may occur is in the ventricles. These ventricular dysrhythmias are considered to be the most dangerous because they precipitate the most profound decrease in the cardiac output. When observing, assessing, and treating dysrhythmias, it is critical for the nurse to remember that it is the patient being treated, not the dysrhythmia. Treatment is always based on the hemodynamic impact of the dysrhythmia.

Nursing ManagementWhen the patient is on a cardiac monitor, it is the nurses responsibility to measure, assess, and document the patients rhythm strip at least every shift and more frequently depending on the patients condition and agency protocol. Whenever changes occur in the heart rhythm, the nurse must begin the same process again: measure, assess, and document the rhythm strip. The nurse needs to understand when it is appropriate to report a change in the ECG to the health care practitioner.

Nursing DocumentationWhen documenting the heart rhythm in the patients record, most institutions require that a rhythm strip is attached to the patients chart once every shift and/or when a change in the rhythm occurs. The patients name, the date and time of rhythm strip collection, and the ECG lead used for the rhythm strip should be documented. Additionally, the electrical features of the rhythm should be documented including the presence of a P wave, the PR interval, the width of the QRS complex, the QT interval, the heart rate, and rhythm (regular verses irregular), and the presence of ectopy (ectopic focus). Corresponding clinical manifestations associated with a given rhythm also need to be documented in the record. For exam3 seconds 6 seconds

Sinus DysrhythmiasThe four common dysrhythmias associated with the sinus area of the heart are sinus bradycardia, sinus tachycardia, sinus arrhythmia/dysrhythmia, and sinus arrest.

Sinus BradycardiaSinus bradycardia, often called sinus brady, occurs when the SA node is firing at a rate of less than 60 beats per minute. Sinus means the rhythm originated in the SA node; therefore, P waves are present. The only difference between sinus bradycardia and normal sinus rhythm (NSR) is the heart rate, but because of this variable, sinus bradycardia is not normal. Sinus bradycardia may result in decreased cardiac output, because while there is adequate time for the heart to fill up with blood, there are not enough contractions per minute to pump the amount of blood needed for normal cardiac output. Significant slowing of the heart rate predisposes the patient to an ectopic focus assuming the role of pacemaker in order to generate sufficient cardiac output. This condition may lead to serious dysrhythmias and warrants careful monitoring. An ECG strip showing sinus bradycardia is in Figure 3814 .

P Wave: Present 1 P wave/QRS complex; PR Interval: 0.18 second; QRS Complex: 0.06 second; QT Interval 0.36 second; Heart Rate: Atrial: 90 beats per minute (bpm); Ventricular: 90 bpm; Rhythm: Regular, Ectopic Beats: None

FIGURE 3813

Normal sinus rhythm.

CHAPTER 386 seconds


Sinus tachycardia results in increased oxygen consumption, increased workload of the heart, and decreased cardiac output. Whenever the heart rate increases, more oxygen is required to nourish the muscle, resulting in increased work of the heart and increased oxygen consumption. Decreased cardiac output occurs when the heart rate is fast enough to lose the period of time needed for blood to enter the heart, referred to as fill time. An ECG strip showing sinus tachycardia is in Figure 3815 (p. 1091). Significant ECG features of sinus tachycardia include: Atrial and ventricular heart rates are over 100 beats per minute. As the sinus rate accelerates, both the PR interval and the QT interval tend to shorten slightly. The rhythm may be slightly irregular as the rate begins to accelerate, but then becomes a rapid regular rhythm. The etiology, physical assessment findings, and treatment for sinus tachycardia are outlined in Chart 385.

P Wave: Present, 1 P wave/QRS Complex; PR Interval: .16 second; QRS Complex: 0.08 second; QT Interval: 0.32 second; Heart Rate: Atrial: 40 bpm; Ventricular: 40 bpm; Rhythm: Regular; Ectopic Beats: None

FIGURE 3814

Sinus bradycardia.

Significant ECG features of sinus bradycardia include: Both atrial and ventricular rates are less than 60 beats per minute. The QT interval tends to lengthen. The etiology, physical assessment findings, and treatment for sinus bradycardia are outlined in Chart 385.

Sinus Arrhythmia/DysrhythmiaSinus arrhythmia/dysrhythmia resembles normal sinus rhythm, except for the slight irregularity in the heart rhythm. The rate of impulse formation and conduction varies with the respiratory cycle; thus, the P to P and R to R intervals change with respiration. The heart rate increases during inspiration and decreases with expiration. This dysrhythmia is common in young children and tends to disappear as they grow older (Garcia & Miller, 2004). Additionally, it tends to disappear when the heart increases, for example, with exercise. Typically there is no clinical significance with this dysrhythmia; it is considered a variant of normal. However, the cyclic decreased heart rate may make the heart muscle

Sinus TachycardiaSinus tachycardia is defined as a firing of the (SA) node at a rate greater than 100 beats per minute. It is called sinus tachycardia because there is a P wave present, although it may be related to an abnormality of the SA node itself. For example, an acute myocardial infarction (AMI) may cause a decrease in the blood supply to the SA node, resulting in an abnormal response such as tachycardia.

CHART 385Dysrhythmia Sinus bradycardia

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

(continued)

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CHART 385Dysrhythmia Sinus tachycardia

Sinus Dysrhythmias: Etiology, Physical Assessment, and TreatmentContinuedEtiology Exercise Smoking Alcohol Caffeine Cocaine Fever Blood loss/anemia Hypovolemia Early sepsis Hypermetabolic state, e.g., burn injury Heart failure Allergic reactions Emotions Anxiety Pain Decreased PSNS Increased SNS stimulation Drug side effect of many over-the-counter cold drugs and drugs used to treat asthma and sinus conditions Compensatory response to a decreased cardiac output Common and normal finding, especially in children and young adults Pathological causes include underlying cardiac disease, such as sick sinus syndrome and myocardial infarction Digoxin Factors that cause heart rate variability including exercise, mental stress, and circadian rhythms Hypoxemia Cardiac muscle ischemia Damage to the SA node Digoxin Aspirin Abnormal potassium levels Myocardial infarction Vagal dominance Hypersensitive carotid sinus reflex, e.g., tight shirt collar Physical Assessment Pulse: Greater than 100 beats per minute. BP: Lower than normal. If cardiac output is decreased, the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath. Altered mental state may be present, although rare. Treatment Treat only if symptomatic. Attempt to identify and treat the cause. Treatment may include: Drug therapy, such as beta-adrenergic blockers, adenosine, diltiazem, and digoxin Carotid massage/vagal maneuvers Cardioversion Anxiety medications Fluid replacement. If causes are identified and managed, generally the rhythm converts back to NSR.

Sinus arrhythmia/ dysrhythmia

Pulse: irregular.

Not treated unless the bradycardic phase causes clinical manifestations described under bradycardia. Atropine for bradycardia. Provide reassurance that this rhythm is not dangerous, but it needs to be evaluated to rule out more serious dysrhythmias.

Sinus arrest

Pulse: irregular. BP: Lower than normal depending on number of pauses per minute. If cardiac output is decreased, the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath. Altered mental state may be present, although rare.

Treat only if patient is symptomatic and/or condition is complicated by other dysrhythmias. Ascertain and treat cause, if possible. Typical treatment may include permanent or temporary artificial pacemaker for repeated episodes, depending on the prognosis, age, and presence of clinical manifestations.

Source: Adapted from American Heart Association. (2006). Handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: Author.

more susceptible to other dysrhythmias. Figure 3816 shows an ECG strip of sinus arrhythmia/dysrhythmia. Significant ECG features of sinus arrhythmia/dysrhythmia include: PR interval may change slightly as the heart rate changes. QT interval changes with the heart rate, becoming longer during the slow phase of the rhythm. Heart rate is 60 to 100 beats per minute; however, the slow phase may drop below 60 beats per minute.

Heart rhythm is regularly irregular, with a variance of more than 0.08 second in the acceleration and deceleration phases. Ectopic beats may occur during the slow phase of the rhythm. The etiology, physical assessment findings, and treatment for sinus arrhythmia/dysrhythmia are outlined in Chart 385.

Sinus ArrestSinus arrest is a momentary cessation of sinus impulse formation (SA node failure), causing a pause in the cardiac rhythm

CHAPTER 386 seconds


P Wave: Present, 1/QRS Complex; PR Interval: 0.14 second; QRS Complex: 0.08 second; QT Interval: 0.36 second; Heart Rate: Atrial: 140 bpm, Ventricular: 140 bpm; Rhythm: Regular; Ectopic Beats None

FIGURE 3815

Sinus tachycardia.6 seconds

P Wave: Present 1/QRS Complex; PR Interval: 0.18 second; QRS Complex: 0.08 second; QT Interval: 0.40 second; Heart Rate: Atrial: 80 bpm, Ventricular: 80 bpm; Rhythm: Irregular; Ectopic Beats: None

FIGURE 3816

Sinus arrhythmia/dysrhythmia.

followed by spontaneous resumption of electrical activity. Sinus arrest also is called sinus pause. With a sinus pause there will be an absence of the PQRST complex on the ECG strip and a loss of cardiac output. Figure 3817 shows an ECG strip of sinus arrest (pause). Significant ECG features of sinus arrest include: There is an absence of one entire PQRST complex. QT interval changes with the heart rate, becoming longer during the slow phase of the rhythm. There may be marked bradycardia due to long sinus pauses. Underlying heart rhythm is regular except when the pauses occur. The etiology, physical assessment findings, and treatment for sinus arrest are outlined in Chart 385.

Nursing Management for Sinus DysrhythmiasThe nurse should first evaluate the patients response to and tolerance of any dysrhythmia. Depending on the type of dysrhythmia, the patient may or may not be symptomatic. However, if the abnormal rhythm results in a decreased cardiac output, it is important to assess for the changes outlined on Chart 386 (p. 1092). The psychological impact of having a dysrhythmia also must be addressed. It is frightening to most patients when they experience the clinical manifestations of cardiac dysrhythmias, such as angina, dizziness, syncope, diaphoresis, and disorientation. The nurse should reassure the patient that all appropriate treatment is being provided and offer comfortPause

6 seconds

P Wave: Present 1/QRS Complex; PR Interval: 0.20 second; QRS Complex: 0.10 second; QT Interval: 0.40 second; Heart Rate: Atrial: 90 bpm, Ventricular: 90 bpm; Rhythm: Regular except for the pause; Ectopic Beats: None Conclusion: Sinus arrest (pause)

FIGURE 3817

Sinus arrest (pause).

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CHART 386

Clinical Manifestations of Decreased Cardiac OutputExercise intolerance Dizziness Alteration in consciousness Angina

Premature Atrial ContractionPremature atrial contraction (PAC) is an ectopic focus in the atria that occurs early, before the next expected SA node impulse, causing depolarization and contraction of the cardiac muscle. This electrical impulse originates outside the SA node. It frequently occurs when the underlying rhythm is normal sinus rhythm (NSR), and the only abnormality is the PAC. When there are more than 5 to 6 PACs per minute, they are termed frequent and have more clinical significance. Whenever beats are premature, there is a loss of the time needed for blood to flow into the heart (fill time), which decreases the amount of blood pumped out of the heart, the cardiac output. Thus, if the beats occur frequently cardiac output is decreased. An increase in the frequency of the dysrhythmia also indicates irritability of the atrial muscle and becomes a cause for concern as it tends to increase the risk for other dysrhythmias occurring. Figure 3818 is a rhythm strip showing premature atrial contractions. Significant ECG features of PACs include: P wave is present and is premature. P wave configuration (shape) may look different because electrical impulses do not come from the SA node. PR interval may be shorter or longer than regular beats. PACs are premature, making the rhythm irregular. P wave after the PAC falls earlier than expected because of the early electrical discharge, which then resets the SA node rhythm, referred to as a noncompensatory pause. Heart rate and rhythm are typically within normal limits, except when the PAC occurs. The etiology, physical assessment findings, and treatment of PACs are outlined in Chart 387.

Lower than usual blood pressure Decreased or increased heart rate Syncope Generalized weakness

Note: Clinical manifestations depend on the degree of decreased cardiac output.

measures. Supply the patient with a quiet environment and treatments to alleviate clinical manifestations. Also provide support by actively listening to the patients concerns and including family in the plan of care. The cause of the dysrhythmia, as outlined in Chart 385 (p. 1089), must be evaluated and corrected, if possible. Typically the patient is treated only if he becomes symptomatic and/or the condition is complicated by other more serious dysrhythmias. When a dysrhythmia occurs, the nurse needs to do an in-depth assessment of the patient to determine the clinical manifestations. A dysrhythmia may not always occur due to an abnormality in the heart, but may be due to a variety of reasons not associated with a cardiac abnormality. For example, pain and anxiety are two noncardiac causes of tachycardia. Therefore, treatment may consist of pain medications or, if the patient is anxious, providing support, such as talking with the patient. If the patient is hemodynamically unstable, the health care practitioner should be notified. Chart 385 outlines the standard treatments for each of the sinus dysrhythmias.

Atrial DysrhythmiasAtrial dysrhythmias usually result from an irritable focus in the atria that initiates an electrical impulse before the SA node has fired in a normal fashion. Because the electrical impulse does not come from the SA node, the P wave configuration of the ECG is different. However, the QRS complex is normal because the electrical impulse travels down the normal pathway from the AV node through the ventricle. Seven different atrial dysrhythmias are discussed next: premature atrial contraction, atrial flutter, atrial fibrillation, supraventricular tachycardia, Wolff-Parkinson-White syndrome, wandering atrial pacemaker, and sick sinus syndrome.

Atrial FlutterAtrial flutter is a rapid, regular, atrial rhythm with an atrial rate of 200 to 400 beats per minute (Garcia & Miller, 2004). There is loss of SA node dominance, which is the preferential pacemaker. Only a fraction of the atrial impulses are conducted through the AV node to the ventricle. Most of the atrial beats fall during the AV node refractory period when the cardiac cell is unable to respond to any stimulus, thus preventing conduction of the impulse. This makes the AV node the gatekeeper for the ventricles by prohibiting all of the atrial impulses from reaching the ventricles, thereby limiting ventricular rate. Atrial flutter also causes a decreased cardiac output due to the loss of the atrial kick or

Noncompensatory pause

P Wave: Premature; PR Interval: 0.16 second; QRS Complex: 0.10 second; QT interval: 0.40 second; Heart Rate: Atrial: 70 bpm; Ventricular: 70 bpm; Rhythm: Regular except for premature beats. Ectopic Beat PAC. Conclusion: One premature atrial contraction.

FIGURE 3818

Premature atrial contraction.

CHAPTER 38


CHART 387Dysrhythmia Premature atrial contraction

Atrial Dysrhythmias: Etiology, Physical Assessment, and TreatmentEtiology Mitral stenosis Mitral valve prolapse Cor pulmonale Underlying cardiovascular disease including ischemia and myocardial infarction Hypoxia Infectious diseases Electrolyte imbalance Increased sympathetic tone Stimulants Drug toxicity, e.g., digoxin Stress Anxiety Coronary atherosclerosis Valvular disease; Cor pulmonale Pulmonary edema Myocardial infarction SA node disease Pulmonary embolism Digitalis toxicity ETOH abuse Postsurgical complication: one of the common dysrhythmias following open heart surgery. On rare occasions it may occur with normal healthy hearts. Acute myocardial infarction Left atrial stretch due to mitral stenosis and mitral regurgitation May be a chronic rhythm associated with heart failure Transient after open-heart surgery Long-standing hypertension Digoxin toxicity Alcohol intake, chronic or acute, moderate to heavy Idiopathic Physical Assessment Pulse: Irregular BP: If frequent PACs, may be decreased. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: May be regular or irregular BP: Lower than normal if cardiac output is decreased. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: Irregular (hallmark feature) BP: Lower than normal If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, depending on the ventricular rate. Pulse: Very fast. BP: Decreased if drop in cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Treatment Observe the frequency of the PACs, and observe for decreased cardiac output (Chart 386). Treat the underlying cause, e.g., stress, anxiety, electrolyte imbalance. Frequent PACs or those that cause sustained tachycardia may require treatment with drugs that prolong atrial refractoriness, such as digoxin, verapamil, or propranolol.

Atrial flutter

Cardioversion is a common intervention. Drug therapy is used to reduce AV conduction: digitalis, propranolol, diltiazem. If a chronic situation the patient may be placed on anticoagulants like warfarin.

Atrial fibrillation

Control the ventricular response, i.e., heart rate. If a rapid ventricular response control with drugs: digoxin is still the drug of choice; betablockers (propranolol) and calcium channel blockers (verapamil, diltiazem). Calcium channel blockers work the fastest, and are the drug of choice when medically unstable. Prevent thromboembolic events with anticoagulant therapy, e.g., warfarin, Cardioversion: Is used if new onset, especially when hemodynamic instability is present. If successful, digoxin is used to prevent reoccurrence. It is necessary to find and treat the cause, e.g., stress, hypokalemia. Vagal maneuvers, i.e., bearing down, coughing, and carotid artery massage. Specific treatment may include: oxygen therapy and cardioversion. Drug therapy: adenosine is used to briefly terminate the rhythm for differential diagnosis. Verapamil is a calcium channel blocker; decreases heart rate. Cardioversion is performed if drug therapy and vagal maneuvers are unsuccessful.

Supraventricular tachycardia includes paroxysmal Atrioventricular node reentry tachycardia AVNRT Atrial tachycardia

Heart disease Rheumatic heart disease Coronary artery disease (CAD) Hypoxia May be precipitated by a premature atrial contraction (PAC) May occur in healthy adults from a variety of causes: Overexertion Stress Excessive use of stimulants Smoking Hypokalemia

(continued)

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CHART 387Dysrhythmia Wolff-ParkinsonWhite (WPW) syndrome

Atrial Dysrhythmias: Etiology, Physical Assessment, and TreatmentContinuedEtiology Congenital in origin: twice as common in males, and occurs in 0.1 to 0.3% of the general population. Physical Assessment Pulse: Rapid. Frequent episodes of palpitations. BP: May be decreased due to fast heart rate. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: 4060 bpm BP: Lower than normal If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: Bradycardia that alternates with tachycardia, referred to as brady-tachy syndrome. BP: May decrease due to decreased cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Treatment Same as that for supraventricular tachycardia. Radiofrequency ablation to terminate the accessory pathway.

Wandering atrial pacemaker

Frequently seen in normal individuals and is of no consequence. Digoxin toxicity

Treat only if symptomatic. Treatment typically is instituted when syncope and/or alteration in consciousness occurs. Attempt to identify and treat the cause. Administer oxygen. Establish IV access Drug therapy: Atropine Evaluate for transcutaneous or permanent pacemaker depending on impact on cardiac output

Sick sinus syndrome

Coronary artery disease Drugs: Cardiac glycoside, Antihypertensive agents, Calcium channel blockers Frequently, intermittent and unpredictable, may occur in the absence of heart disease Myocardial infarction Inflammatory or degenerative processes

Clinical manifestations and ECG findings determine treatment. Anticoagulants are used because of blood stasis if atrial flutter/fibrillation is present. The only definitive treatment is a permanent pacemaker to replace the SA node.

normal atrial contraction. Atrial kick forces more blood into the ventricle, which augments cardiac output. With atrial flutter the atria are just fluttering instead of contracting, resulting in a decreased cardiac output by as much as 30% (Shade & Wesley, 2007). Additionally, with the loss of the atrial contraction, blood stasis and pooling occur, leading to an increased incidence of clot formation. Finally, due to the rapid atrial rate myocardial oxygen consumption increases, which eventually leads to the development of hypoxia of the myocardial muscle and predisposes the left ventricular to fail. Figure 3819 is a rhythm strip showing atrial flutter. Significant ECG features of atrial flutter include: P waves are not identifiable; instead there are flutter waves (F waves), creating a sawtooth baseline on the ECG strip.

PR intervals are not measurable. QT interval is not measurable because the T waves are buried in the F waves. Atrial and ventricular rhythms typically are regular, but they may be irregular depending on how often the AV node allows impulses to travel to the ventricle. The etiology, physical assessment findings, and treatment of atrial flutter are outlined in Chart 387.

Atrial FibrillationAtrial fibrillation, also referred to as atrial fib or a-fib, is a common dysrhythmia. The Evidence-Based Practice box outlines the genetic considerations of atrial fibrillation.

CHAPTER 38


P Wave: None, flutter waves; PR interval: None; QRS Complex: 0.08 second; QT Interval: unable to obtain; Heart Rate: Atrial: about 300 bpm, Ventricular: 90 bpm; Rhythm: Regular; Ectopic Beats: Flutter waves.

FIGURE 3819

Atrial flutter.

It is characterized by a disorganized, very rapid, and irregular atrial rhythm resulting in an irregular ventricular rhythm, the hallmark feature. Rapid or slow ventricular heart rate, referred to as the ventricular response, depends on the rate that the AV node allows impulses to be conducted to the ventricles. The cells in the atria have an increased irritability typically due to cardiac muscle hypoxia, which causes many sites in the atria to become pacemakers and initiate electrical impulses. The firing of these multiple sites causes the atria simply to quiver instead of contracting effectively. Atrial fibrillation causes three significant clinical manifestations: (1) loss of SA node pacemaker dominance, which is the most reliable pacemaker; (2) decreased cardiac output due to loss

of atrial kick; and (3) increased myocardial oxygen consumption. The immediate concern for atrial fibrillation is the ventricular response because it determines cardiac output. A heart rate that is too slow or too fast impacts cardiac output. With the loss of the atrial kick, blood stasis and pooling occur, leading to an increased incidence of clot formation. Therefore, those individuals with atrial fibrillation are at high risk for a cardiovascular accident (CVA) and/or pulmonary emboli. The rapid atrial firing also increases the workload on the heart, eventually causing hypoxia of the myocardial muscle. Long-term hypoxia predisposes to left ventricular failure. Figure 3820 (p. 1096) is a rhythm strip showing atrial fibrillation.

Genetic Considerations Clinical ProblemA conservative estimate of the number of people who are affected by atrial fibrillation (AF) is approximately 2 million. It is the most common dysrhythmia that causes an irregular heart rate, palpitations, unexplained rapid heart rate, and a sensation of missed beats. The incidence of AF increases with age, with less than 1% of the population experiencing it before age 60 years, while it is present in 1 in 10 individuals at age 80 years and over. Elderly white men compose the largest group that is affected by AF. Heart failure Excessive alcohol consumption Previous myocardial infarction Diabetes Rheumatic heart disease Mitral valve disorders such as prolapse, regurgitation, and annular calcification Smoking Caffeine The need for patient/family counseling about the increased risk for the development of AF is necessary along with instructions about the need for medical attention if clinical manifestations described above occur. A major emphasis needs to be placed on increasing public awareness of AF and its many causative factors. Patients with a family history require more frequent and diligent testing. Treatment for AF is outlined on Chart 387 (p. 000).

Research FindingsA new study conducted by the National Heart, Lung, and Blood Institute (2004) assessed the prevalence of AF in individuals who had it in their family history. The study evaluated 2,243 individuals whose parents were in the original Framingham Heart Study. The participants were at least 30 years of age and had no history of AF. Seventy of the subjects developed AF within four years. If individual participants had a history of one parent with AF they were twice as likely to develop the dysrhythmia as subjects who had no family history of AF. If both parents had AF before 75 years of age, the risk tripled. Further research continues to determine which genes are involved and what steps are necessary to enhance early diagnosis and treatment.

Critical Thinking Questions1. When assessing a patient with new onset atrial fibrillation, what types of questions would assist the nurse to determine if there is a risk for a genetic predisposition? 2. When teaching a newly diagnosed patient how to live with AF, in order of priority what must be included in the teaching plan?

Implications for Nursing PracticeImplications for nursing practice begin with the nursing assessment. It is important to specifically question the family history for the presence of AF. This is especially essential if the patient has clinical manifestations and new onset irregular pulse. It needs to be documented in the patients record that there is a family history of the disease. The nurse also must asses the presence of other risk factors for the development of AF including: Cardiomyopathy Hypertension

Sources: Fox, C.S., Parise, H., DAgostino, R.B., et al. (2004). Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring. JAMA: 291(23): 2852-2856; Pavlovich-Dannis, S.J. (2005). Moms eyes and dads atrial fibrillation. Nurse Week: 23-24. National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health. (2004). Parental atrial fibrillation increases risk in offspring, finds NHLBIs Framingham Heart Study. NIH News. Retrieved August 8, 2008 from http://www.nhlbi.nih.gov/new/press04-06-15.htm

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P Wave: None; PR Interval: None; QRS Complex: 0.10 second; QT Interval: unable to obtain; Heart Rate: Atrial: 80 bpm; Rhythm: Irregular; Ectopic Beats: f waves.

FIGURE 3820

Atrial fibrillation.

Significant ECG features of atrial fibrillation include: P waves are not identifiable due to the atrial quivering, referred to as f waves, occurring at 350 to 750 beats per minute. PR intervals are not measurable. QT interval is not obtainable because the T waves are buried in the f waves. Irregularly irregular rhythm occurs, meaning that there is no pattern to the irregularity. f waves are ectopic beats. The etiology, physical assessment findings, and treatment of atrial fibrillation are outlined in Chart 387.

may result in a conversion to atrial flutter or fibrillation. Eventually, signs and symptoms of congestive heart failure will be present. Figure 3821 is a rhythm strip showing supraventricular tachycardia (SVT). Significant ECG features of supraventricular tachycardia include: Heart rate is 100 to 250 beats per minute. P wave is not seen; it is buried in the QRS complex. PR interval is not discernable. QRS complex is within normal limits unless distorted by the buried P waves. QT interval is not obtainable because the T waves are buried. Heart rhythm may be regular or irregular due to varying conduction rates through the AV node. Ectopic beats may or may not be present, depending on the pacemaker site. The etiology, physical assessment findings, and treatment of supraventricular tachycardia are outlined in Chart 387. Atrioventricular Nodal Reentry Tachycardia One phenomenon that can cause supraventricular tachycardia is atrioventricular nodal reentry tachycardia (AVNRT). Normally people are born with only a single electrical pathway at the base of the right atrium w

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