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CHAPTER
CHAPTER 38
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
Right bundle
FIGURE 381
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.
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Nursing Management of Patients with Cardiovascular Disorders the only mechanical function of the heart. Excitability, conductivity, and automaticity are electrical functions of the heart. Contractility may be thought of as the mechanical coordination of cardiac muscle contractions producing a heartbeat. In addition to these cell characteristics, normal cardiac function is dependent on maintaining electrolyte concentrations inside and outside the cell membrane. Specific electrolytes and their relationship to cardiac function are described next.
Cardiac Cells
There are two basic cardiac cell groups: the myocardial working cells and the specialized pacemaker cells of the electrical conduction system. The atria and the ventricles are constructed of myocardial working cells, which have an abundance of contractile filaments needed to generate cardiac muscle contraction. The cardiac muscle contraction is what actually pumps the blood through and out of the heart into the pulmonic and the systemic circulation. The myocardial working cells have the ability to contract in response to chemical, electrical, or mechanical stimuli. The second type of cardiac cell is the specialized pacemaker cell whose primary function is to generate and conduct electrical impulses (stimuli). These cells found in the heart wall and septum (membrane dividing the right and left sides of the heart) control the heart rate and rhythm by coordinating regular cardiac muscle depolarization (contraction) (see Figure 381 ). The myocardial contractions pump the blood through and out of the heart. The term threshold refers to the point at which an electrical stimulus produces a cell response. When a stimulus is strong enough for cardiac cells to reach this threshold, all of the cells will respond to the stimulus and cause a muscle contraction. This is called the all-or-none phenomenon; in other words, either all the cells respond, or none of the cells respond. This principle allows for a coordinated muscle contraction and greater efficiency in pumping blood. All cardiac cells possess four primary characteristics: automaticity, excitability, conductivity, and contractility. These characteristics are described next.
Automaticity
Automaticity is the ability of the pacemaker cells to generate their own electrical impulses without depending on nervous system stimulation external to the heart. This spontaneous activity is what produces regular depolarization of the cardiac muscle. This characteristic is specific to only certain pacemaker cell sites within the conduction system. These cell sites are the sinoatrial (SA) node, the atrioventricular (AV) node, and the Purkinje network fibers.
Excitability
Excitability is the ability of the electrical cell to respond to a stimulus. This ability also is referred to as irritability, and all electrical cardiac cells possess this property. When cardiac cells are highly irritable, a cell other than the normal pacemaker may cause a contraction. Cell irritability can be caused by a number of problems, including cardiac muscle ischemia due to hypoxia, or a lack of oxygen. This is the most common cause of cardiac dysrhythmias, the abnormal rhythms of the heart.
Conductivity
Conductivity is the ability of the cardiac cell to accept and then transmit a stimulus to other cardiac cells. All cardiac cells share this characteristic, thereby portraying the all-or-none property of the heart muscle; the cardiac cells function as a unit.
Contractility
Contractility is the ability of the cardiac cells to shorten and cause the muscle to contract in response to an electrical stimulus. This ability also is referred to as rhythmicity. Contractility is
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When a muscle cell receives a stimulus due to the Na-K pump exchange, a rapid change occurs in the Cell exterior resting membrane potential, known as the action potential, which is measured in millivolts (a unit of electrical voltage or potential difference equal to one-thousandth of a volt). Once the action potential occurs, the cell moves toward a positive charge. The four phases (04) of the action potential are shown in Figure 382 . Phase 0 is rapid depolarization, phase 1 is rapid repolarization, phase 2 is the plateau, phase 3 is final repolarization, and phase 4 is the resting state. To generate this action potential and the resulting muscle depolarization, the threshold potential must be reached, which is phase 0. To initiate phase 0, Na enters the cell causing a sharp positively charged rise of the intracellular ions. The cell moves from 90 millivolts (mV) in its resting state to a positive Open K channel 15 to 30 millivolts, causing myocardial depolarization to occur. When the threshold is reached, the cell will continue to depolarize with no further stimulation; this phenomenon is referred to as automaticity. During phase 1, the depolarized stage, the interior of the cell has a net positive charge. In this effort to continue to make the inside of the cell more positive, Ca enters; this is phase 2, the plateau phase. During phase 3 the calcium channels close, and Na is pulled from the cell by the Na-K pump; thus the cell is returning to its polarized negative resting membrane potential state (phase 4) (Figure 383 ). The first area of the cardiac muscle to be depolarized is the first area that is repolarized. For example, after the atria depolarize they repolarize while the ventricles are depolarizing. Thus, when the SA node fires again, the muscle will be ready to respond with a new action potential. Cardiac repolarization is the process whereby the depolarized cell is polarized, causing a return to the resting membrane potential (see Figure 382 ). Repolarization also is referred to as the recovery phase that every cardiac cell must go through in order to be ready to accept another stimulus. It is a slower process than that of depolarization. During repolarization the
Na
Cl
Closed Na channels
Anionic protein
FIGURE 383
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.
4 100
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.
RA
Depolarization RV Repolarization
Electrocardiography detects cardiac electrical impulses at various points on the surface of the body. The graphical depiction of these impulses, waveforms, and time intervals is obtained either with an electrocardiograph (ECG machine) or on a bedside cardiac monitor. To obtain an ECG tracing, specific equipment is needed including an electrode, lead wire, and monitor or oscilloscope. An electrode is most commonly a round adhesive pad that is impregnated with conducting gel in the center and is attached to a lead wire. Electrodes are sensing devices that detect the electrical activity of the heart and conduct the electrical impulses from the skin surface back to the ECG machine, where they are converted into waveforms. An electrode is much like a camera in that it takes pictures of the electrical activity in the heart. The electrodes are connected to a cardiac monitor by lead wires. Typically, these wires are color coded according to machine manufacturer, and these colors assist the practitioner in attaching the lead wires to the appropriate electrode. The cardiac monitor records the electrical impulses and provides a real-time visual tracing of the waveforms on the screen and/or a printed version on specialized ECG graph paper, described next. The printed version is called a rhythm strip or ECG strip. The rhythm strip gives the health care practitioner information about where the pathological processes are SA node occurring in the heart. Figure 385 shows the elecAV node trodes, lead wire, and cardiac monitor. The term lead is used in different contexts when discussing ECGs. In addition to using the term as just described, as a connector from the electrode to the LA cardiac monitor, the term also is used when discussing a view or picture of the heart from a particular angle or vantage point. In this respect one can think of the lead as the eye of the camera.
LV
Lead Placement
Body tissues and fluids surround the heart; therefore, the electrical action potentials produced in the heart are widely conducted throughout the body via these tissues and fluids. The impulses or action potentials can be detected from any point in the body. Electrodes must be placed in certain positions on the body in order to obtain a clear picture of the electrical impulses in the heart, and there must always be a positive, a negative, and a ground electrode/lead. The ground lead minimizes outside
ST QRS
RBB
LBB
P QRS PR QT
FIGURE 384
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Device
1.00
Channel 0 Chart 2.0 1.5 1.0 Volts 0.5 0 Beats Thresh Limit
# of samples
5300
Sample rate
5000
Set limit
1.00 0.50 1.50
Electrode
Max Peak 1.37 Time
0.00
2.00
-5.0 1.17
Threshold
0.20 0.10 0.00 0.30 0.40 0.50
-1.0
Below limit
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
FIGURE 385
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
FIGURE 386
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complexes. An MCL1 lead is useful for evaluating abnormalities in the ventricles. Placement of the electrodes depends on the lead being monitored and whether a three- or five-lead system is being used. Figure 387 shows the position of the electrodes for both lead II and MCL1. The color coding on the lead wire gives the nurse information about whether the lead is positive or negative. Typically the color black is negative, white is positive, and green is ground. In the five-lead system red and brown colors also are used and their polarity changes depending on the lead being monitored (Morton, Fontaine, Hudak, & Gallo, 2005).
CHART 381
Evaluation of: Axis deviation
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
dimensions on the chest in which leads can be placed are the frontal plane (up and down) and the horizontal plane (around the chest). Figure 388 shows the horizontal plane and the frontal plane views. The axis of a lead is the imaginary line drawn between the positive and the negative electrode in a bipolar lead and between the positive electrode and the zero reference point in a unipolar lead. Thus, depending on where a given lead is placed, it provides
Lead II: Positive electrode left abdomen Negative electrode right shoulder Ground electrode left shoulder +
MCL1: Positive electrode 4th ICS RSB Negative electrode left shoulder Ground electrode right shoulder
FIGURE 387
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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
a picture of the electrical activity from that vantage point within the heart. Electrical current flowing toward a positive electrode creates a positive deflection on the ECG paper, whereas electrical current flowing toward a negative electrode creates a negative deflection on the ECG paper (Walraven, 2006). The standard bipolar limb leadsI, II, IIIare applied to the right arm (RA), left arm (LA), and left leg (LL). Each lead records the following electrical conduction pattern: Lead I records conduction from RA to LA. Lead II records conduction from RA to LL. Lead III records conduction from LA to LL. The right leg electrode acts as a grounding electrode. Three more frontal plane, unipolar augmented limb leads can be created by using a central terminal. Augmented leads are
CHART 382
Electrode Placement
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.
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.
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
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CHART 383
Electrode Attachment
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.
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.
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.
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Nursing Management of Patients with Cardiovascular Disorders dividual and also depends on the ECG lead being used. For example, QRS complexes are mostly positive in the lead II and mostly negative in the MCL1 lead (see Figure 386 ). Not everyone has a discernable Q wave. QT intervalThis is measured from the Q wave to the end of the T wave. The normal QT interval is 0.34 to 0.43 second or 8.5 to 11 boxes. Heart rateThis is measured by using the very top of the ECG paper, which is marked off in 3-second intervals with tick marks. The tick mark is a small straight line or hash mark above the tracing. Count up the number of PQRST complexes that occur in 6 seconds and multiply that number by 10. This method provides a general estimate of the heart rate. A more accurate method for measuring heart rate is to count the number of small squares between two R waves and divide the total into 1,500. The normal HR is 60 to 100 beats per minute. Heart rhythmThis is determined by measuring the distance between two R waves and then measuring each subsequent R wave to ensure it is the same distance apart as the previous ones. With a regular rhythm, the distance between R waves is equal. Calipers (Figure 3810 ) are the instrument used to take all these measurements. Figure 3811 demonstrates where each measurement begins and ends.
The ECG graph paper is arranged as a series of horizontal and vertical lines. This paper is standardized to allow for consistency in ECG measurement and strip analysis. Both the amplitude and the voltage may be measured on the paper. The vertical axis measures the amplitude and is stated in millivolts (mV). Two large squares on this axis equal 1 millivolt. This measurement is rarely used because the size of the picture or millivolts can be adjusted at the monitoring station, thereby reducing the consistency of this measurement. The horizontal axis is divided into small squares. The squares on the ECG paper are used to measure the length of time required for the electrical impulse to traverse a specific part of the heart. Figure 389 shows an example of ECG graph paper. These squares are used to measure time intervals as follows: The smallest square is 1 millimeter (mm) in length and represents 0.04 second in time. The large square is 5 mm in length and represents 0.20 second in time. The large square equals 5 small squares. Five large squares represent 1 second.
ECG Measurements
When assessing either a rhythm strip or a 12-lead ECG, both the individual PQRST complexes need to be evaluated as well as the relationship of each individual complex to the overall rhythm. The assessment of an ECG configuration includes the following: P waveThere should be one P wave for every QRS complex. PR intervalThis is measured from the beginning of the P wave to the beginning of the QRS complex. The normal PR interval is from 0.12 to 0.20 second or 3 small boxes to 1 large box. QRS complexThe QRS complex is measured from the beginning of the Q wave to the end of the S wave. The normal range is from 0.06 to 0.12 second or 1.5 boxes to 3 boxes. The shape of the QRS complex varies from individual to in-
FIGURE 3810
Calipers.
PR
QRS QT
FIGURE 389
FIGURE 3811
ECG measurement.
CHAPTER 38
FIGURE 3812
Artifact.
Isoelectric Line
The isoelectric line marks the beginning and ending point of all waves. When the SA node fires, the ECG waveform (the actual tracing on the graph paper) begins and moves away from the isoelectric line (see Figure 3812 ). Any wave that has an upward deflection, which is above the isoelectric line, is referred to as a positive deflection, and any waveform that goes below the line is referred to as a negative deflection. Depending on the lead, certain waves normally are positive and certain ones are negative. In a lead II the normal P wave has a positive deflection, the PR interval is isoelectric, the Q wave is the first negative deflection, the R wave is positive, the S wave is negative, the ST segment is isoelectric, and the T wave is positive. CHART 384
P Waves
PR Interval
Artifact
Artifact is defined as an ECG pattern caused by sources outside the heart creating a false and abnormal pattern on the ECG graph paper. This interference is due to several causes: Malfunction of electrodes possibly due to dry conductive gel, clammy skin, or dense chest hair Patient movement, which precipitates a fluctuating isoelectric line that corrects itself when the patient lies still Improper grounding, which occurs when a patient is in contact with an outside source of electricity, such as poorly grounded beds and/or IV infusion pumps Equipment failures, such as broken wires or cables on the ECG equipment, which need to be exchanged for new equipment. Because of this interference or artifact, the baseline or isoelectric line becomes fuzzy. When artifact is present, it is difficult to diagnose cardiac abnormalities, making it is necessary to correct the cause of the artifact. Figure 3812 depicts artifact.
QRS Complex
QT Interval
Rate
Ectopic Focus
Ectopic focus is a heartbeat originating from a site other than the primary cardiac pacemaker tissue. Ectopic foci may affect cardiac output and must be assessed and documented carefully for their impact on the hemodynamic stability of the patient. The terms dysrhythmia, arrhythmia, and ectopic focus all mean the same thing and are used interchangeably.
Regularity (also called rhythm)
Ectopic Beats
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.
Dysrhythmias
When the cardiac muscle does not receive enough blood, it becomes ischemic and irritable, causing cardiac dysrhythmias to occur. A dysrhythmia is an abnormal disturbance of the electrical conduction system of the heart. There are a number of dysrhythmias, which originate in different parts of the heart. This chapter addresses dysrhythmias according to location in the heart, beginning at the top with the atrial dysrhythmias. As the dysrhythmias occur anatomically lower in the heart, the severity is greater due to their impact on cardiac output. The cardiac output decreases as the severity of the dysrhythmia increases. Heart rhythms are categorized according to the cardiac structure in which they begin, or their site of origin. The most common dysrhythmias begin at the top of the heart with the SA node. These types of dysrhythmias are called sinus dysrhythmias due to their origin in the SA, or sinus, node. The next area in the heart where dysrhythmias may occur is in the intra-atrial pathways, referred to as atrial dysrhythmias. Moving anatomically down to the next area of the conduction system, the AV node or junction is where junctional dysrhythmias occur. The final area of the heart where dysrhythmias may occur is in the ventricles. These ventricular dysrhythmias are considered to be the most dangerous because they precipitate the most profound decrease in the cardiac output. When observing, assessing, and treating dysrhythmias, it is critical for the nurse to remember that it is the patient being treated, not the dysrhythmia. Treatment is always based on the hemodynamic impact of the dysrhythmia.
Nursing Management
When the patient is on a cardiac monitor, it is the nurses responsibility to measure, assess, and document the patients rhythm strip at least every shift and more frequently depending on the patients condition and agency protocol. Whenever changes occur in the heart rhythm, the nurse must begin the same process again: measure, assess, and document the rhythm strip. The nurse needs to understand when it is appropriate to report a change in the ECG to the health care practitioner.
Nursing Documentation
When documenting the heart rhythm in the patients record, most institutions require that a rhythm strip is attached to the patients chart once every shift and/or when a change in the rhythm occurs. The patients name, the date and time of rhythm strip collection, and the ECG lead used for the rhythm strip should be documented. Additionally, the electrical features of the rhythm should be documented including the presence of a P wave, the PR interval, the width of the QRS complex, the QT interval, the heart rate, and rhythm (regular verses irregular), and the presence of ectopy (ectopic focus). Corresponding clinical manifestations associated with a given rhythm also need to be documented in the record. For exam3 seconds 6 seconds
Sinus Dysrhythmias
The four common dysrhythmias associated with the sinus area of the heart are sinus bradycardia, sinus tachycardia, sinus arrhythmia/dysrhythmia, and sinus arrest.
Sinus Bradycardia
Sinus bradycardia, often called sinus brady, occurs when the SA node is firing at a rate of less than 60 beats per minute. Sinus means the rhythm originated in the SA node; therefore, P waves are present. The only difference between sinus bradycardia and normal sinus rhythm (NSR) is the heart rate, but because of this variable, sinus bradycardia is not normal. Sinus bradycardia may result in decreased cardiac output, because while there is adequate time for the heart to fill up with blood, there are not enough contractions per minute to pump the amount of blood needed for normal cardiac output. Significant slowing of the heart rate predisposes the patient to an ectopic focus assuming the role of pacemaker in order to generate sufficient cardiac output. This condition may lead to serious dysrhythmias and warrants careful monitoring. An ECG strip showing sinus bradycardia is in Figure 3814 .
P Wave: Present 1 P wave/QRS complex; PR Interval: 0.18 second; QRS Complex: 0.06 second; QT Interval 0.36 second; Heart Rate: Atrial: 90 beats per minute (bpm); Ventricular: 90 bpm; Rhythm: Regular, Ectopic Beats: None
FIGURE 3813
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6 seconds
Sinus tachycardia results in increased oxygen consumption, increased workload of the heart, and decreased cardiac output. Whenever the heart rate increases, more oxygen is required to nourish the muscle, resulting in increased work of the heart and increased oxygen consumption. Decreased cardiac output occurs when the heart rate is fast enough to lose the period of time needed for blood to enter the heart, referred to as fill time. An ECG strip showing sinus tachycardia is in Figure 3815 (p. 1091). Significant ECG features of sinus tachycardia include: Atrial and ventricular heart rates are over 100 beats per minute. As the sinus rate accelerates, both the PR interval and the QT interval tend to shorten slightly. The rhythm may be slightly irregular as the rate begins to accelerate, but then becomes a rapid regular rhythm. The etiology, physical assessment findings, and treatment for sinus tachycardia are outlined in Chart 385.
P Wave: Present, 1 P wave/QRS Complex; PR Interval: .16 second; QRS Complex: 0.08 second; QT Interval: 0.32 second; Heart Rate: Atrial: 40 bpm; Ventricular: 40 bpm; Rhythm: Regular; Ectopic Beats: None
FIGURE 3814
Sinus bradycardia.
Significant ECG features of sinus bradycardia include: Both atrial and ventricular rates are less than 60 beats per minute. The QT interval tends to lengthen. The etiology, physical assessment findings, and treatment for sinus bradycardia are outlined in Chart 385.
Sinus Arrhythmia/Dysrhythmia
Sinus arrhythmia/dysrhythmia resembles normal sinus rhythm, except for the slight irregularity in the heart rhythm. The rate of impulse formation and conduction varies with the respiratory cycle; thus, the P to P and R to R intervals change with respiration. The heart rate increases during inspiration and decreases with expiration. This dysrhythmia is common in young children and tends to disappear as they grow older (Garcia & Miller, 2004). Additionally, it tends to disappear when the heart increases, for example, with exercise. Typically there is no clinical significance with this dysrhythmia; it is considered a variant of normal. However, the cyclic decreased heart rate may make the heart muscle
Sinus Tachycardia
Sinus tachycardia is defined as a firing of the (SA) node at a rate greater than 100 beats per minute. It is called sinus tachycardia because there is a P wave present, although it may be related to an abnormality of the SA node itself. For example, an acute myocardial infarction (AMI) may cause a decrease in the blood supply to the SA node, resulting in an abnormal response such as tachycardia.
CHART 385
Dysrhythmia Sinus bradycardia
(continued)
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CHART 385
Dysrhythmia Sinus tachycardia
Pulse: irregular.
Not treated unless the bradycardic phase causes clinical manifestations described under bradycardia. Atropine for bradycardia. Provide reassurance that this rhythm is not dangerous, but it needs to be evaluated to rule out more serious dysrhythmias.
Sinus arrest
Pulse: irregular. BP: Lower than normal depending on number of pauses per minute. If cardiac output is decreased, the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath. Altered mental state may be present, although rare.
Treat only if patient is symptomatic and/or condition is complicated by other dysrhythmias. Ascertain and treat cause, if possible. Typical treatment may include permanent or temporary artificial pacemaker for repeated episodes, depending on the prognosis, age, and presence of clinical manifestations.
Source: Adapted from American Heart Association. (2006). Handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: Author.
more susceptible to other dysrhythmias. Figure 3816 shows an ECG strip of sinus arrhythmia/dysrhythmia. Significant ECG features of sinus arrhythmia/dysrhythmia include: PR interval may change slightly as the heart rate changes. QT interval changes with the heart rate, becoming longer during the slow phase of the rhythm. Heart rate is 60 to 100 beats per minute; however, the slow phase may drop below 60 beats per minute.
Heart rhythm is regularly irregular, with a variance of more than 0.08 second in the acceleration and deceleration phases. Ectopic beats may occur during the slow phase of the rhythm. The etiology, physical assessment findings, and treatment for sinus arrhythmia/dysrhythmia are outlined in Chart 385.
Sinus Arrest
Sinus arrest is a momentary cessation of sinus impulse formation (SA node failure), causing a pause in the cardiac rhythm
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6 seconds
P Wave: Present, 1/QRS Complex; PR Interval: 0.14 second; QRS Complex: 0.08 second; QT Interval: 0.36 second; Heart Rate: Atrial: 140 bpm, Ventricular: 140 bpm; Rhythm: Regular; Ectopic Beats None
FIGURE 3815
Sinus tachycardia.
6 seconds
P Wave: Present 1/QRS Complex; PR Interval: 0.18 second; QRS Complex: 0.08 second; QT Interval: 0.40 second; Heart Rate: Atrial: 80 bpm, Ventricular: 80 bpm; Rhythm: Irregular; Ectopic Beats: None
FIGURE 3816
Sinus arrhythmia/dysrhythmia.
followed by spontaneous resumption of electrical activity. Sinus arrest also is called sinus pause. With a sinus pause there will be an absence of the PQRST complex on the ECG strip and a loss of cardiac output. Figure 3817 shows an ECG strip of sinus arrest (pause). Significant ECG features of sinus arrest include: There is an absence of one entire PQRST complex. QT interval changes with the heart rate, becoming longer during the slow phase of the rhythm. There may be marked bradycardia due to long sinus pauses. Underlying heart rhythm is regular except when the pauses occur. The etiology, physical assessment findings, and treatment for sinus arrest are outlined in Chart 385.
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
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CHART 386
Lower than usual blood pressure Decreased or increased heart rate Syncope Generalized weakness
measures. Supply the patient with a quiet environment and treatments to alleviate clinical manifestations. Also provide support by actively listening to the patients concerns and including family in the plan of care. The cause of the dysrhythmia, as outlined in Chart 385 (p. 1089), must be evaluated and corrected, if possible. Typically the patient is treated only if he becomes symptomatic and/or the condition is complicated by other more serious dysrhythmias. When a dysrhythmia occurs, the nurse needs to do an in-depth assessment of the patient to determine the clinical manifestations. A dysrhythmia may not always occur due to an abnormality in the heart, but may be due to a variety of reasons not associated with a cardiac abnormality. For example, pain and anxiety are two noncardiac causes of tachycardia. Therefore, treatment may consist of pain medications or, if the patient is anxious, providing support, such as talking with the patient. If the patient is hemodynamically unstable, the health care practitioner should be notified. Chart 385 outlines the standard treatments for each of the sinus dysrhythmias.
Atrial Dysrhythmias
Atrial dysrhythmias usually result from an irritable focus in the atria that initiates an electrical impulse before the SA node has fired in a normal fashion. Because the electrical impulse does not come from the SA node, the P wave configuration of the ECG is different. However, the QRS complex is normal because the electrical impulse travels down the normal pathway from the AV node through the ventricle. Seven different atrial dysrhythmias are discussed next: premature atrial contraction, atrial flutter, atrial fibrillation, supraventricular tachycardia, Wolff-Parkinson-White syndrome, wandering atrial pacemaker, and sick sinus syndrome.
Atrial Flutter
Atrial flutter is a rapid, regular, atrial rhythm with an atrial rate of 200 to 400 beats per minute (Garcia & Miller, 2004). There is loss of SA node dominance, which is the preferential pacemaker. Only a fraction of the atrial impulses are conducted through the AV node to the ventricle. Most of the atrial beats fall during the AV node refractory period when the cardiac cell is unable to respond to any stimulus, thus preventing conduction of the impulse. This makes the AV node the gatekeeper for the ventricles by prohibiting all of the atrial impulses from reaching the ventricles, thereby limiting ventricular rate. Atrial flutter also causes a decreased cardiac output due to the loss of the atrial kick or
Noncompensatory pause
P Wave: Premature; PR Interval: 0.16 second; QRS Complex: 0.10 second; QT interval: 0.40 second; Heart Rate: Atrial: 70 bpm; Ventricular: 70 bpm; Rhythm: Regular except for premature beats. Ectopic Beat PAC. Conclusion: One premature atrial contraction.
FIGURE 3818
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CHART 387
Dysrhythmia Premature atrial contraction
Atrial flutter
Cardioversion is a common intervention. Drug therapy is used to reduce AV conduction: digitalis, propranolol, diltiazem. If a chronic situation the patient may be placed on anticoagulants like warfarin.
Atrial fibrillation
Control the ventricular response, i.e., heart rate. If a rapid ventricular response control with drugs: digoxin is still the drug of choice; betablockers (propranolol) and calcium channel blockers (verapamil, diltiazem). Calcium channel blockers work the fastest, and are the drug of choice when medically unstable. Prevent thromboembolic events with anticoagulant therapy, e.g., warfarin, Cardioversion: Is used if new onset, especially when hemodynamic instability is present. If successful, digoxin is used to prevent reoccurrence. It is necessary to find and treat the cause, e.g., stress, hypokalemia. Vagal maneuvers, i.e., bearing down, coughing, and carotid artery massage. Specific treatment may include: oxygen therapy and cardioversion. Drug therapy: adenosine is used to briefly terminate the rhythm for differential diagnosis. Verapamil is a calcium channel blocker; decreases heart rate. Cardioversion is performed if drug therapy and vagal maneuvers are unsuccessful.
Supraventricular tachycardia includes paroxysmal Atrioventricular node reentry tachycardia AVNRT Atrial tachycardia
Heart disease Rheumatic heart disease Coronary artery disease (CAD) Hypoxia May be precipitated by a premature atrial contraction (PAC) May occur in healthy adults from a variety of causes: Overexertion Stress Excessive use of stimulants Smoking Hypokalemia
(continued)
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CHART 387
Dysrhythmia Wolff-ParkinsonWhite (WPW) syndrome
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
Coronary artery disease Drugs: Cardiac glycoside, Antihypertensive agents, Calcium channel blockers Frequently, intermittent and unpredictable, may occur in the absence of heart disease Myocardial infarction Inflammatory or degenerative processes
Clinical manifestations and ECG findings determine treatment. Anticoagulants are used because of blood stasis if atrial flutter/fibrillation is present. The only definitive treatment is a permanent pacemaker to replace the SA node.
normal atrial contraction. Atrial kick forces more blood into the ventricle, which augments cardiac output. With atrial flutter the atria are just fluttering instead of contracting, resulting in a decreased cardiac output by as much as 30% (Shade & Wesley, 2007). Additionally, with the loss of the atrial contraction, blood stasis and pooling occur, leading to an increased incidence of clot formation. Finally, due to the rapid atrial rate myocardial oxygen consumption increases, which eventually leads to the development of hypoxia of the myocardial muscle and predisposes the left ventricular to fail. Figure 3819 is a rhythm strip showing atrial flutter. Significant ECG features of atrial flutter include: P waves are not identifiable; instead there are flutter waves (F waves), creating a sawtooth baseline on the ECG strip.
PR intervals are not measurable. QT interval is not measurable because the T waves are buried in the F waves. Atrial and ventricular rhythms typically are regular, but they may be irregular depending on how often the AV node allows impulses to travel to the ventricle. The etiology, physical assessment findings, and treatment of atrial flutter are outlined in Chart 387.
Atrial Fibrillation
Atrial fibrillation, also referred to as atrial fib or a-fib, is a common dysrhythmia. The Evidence-Based Practice box outlines the genetic considerations of atrial fibrillation.
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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.
Research Findings
A new study conducted by the National Heart, Lung, and Blood Institute (2004) assessed the prevalence of AF in individuals who had it in their family history. The study evaluated 2,243 individuals whose parents were in the original Framingham Heart Study. The participants were at least 30 years of age and had no history of AF. Seventy of the subjects developed AF within four years. If individual participants had a history of one parent with AF they were twice as likely to develop the dysrhythmia as subjects who had no family history of AF. If both parents had AF before 75 years of age, the risk tripled. Further research continues to determine which genes are involved and what steps are necessary to enhance early diagnosis and treatment.
Sources: Fox, C.S., Parise, H., DAgostino, R.B., et al. (2004). Parental atrial fibrillation as a risk factor for atrial fibrillation in offspring. JAMA: 291(23): 2852-2856; Pavlovich-Dannis, S.J. (2005). Moms eyes and dads atrial fibrillation. Nurse Week: 23-24. National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health. (2004). Parental atrial fibrillation increases risk in offspring, finds NHLBIs Framingham Heart Study. NIH News. Retrieved August 8, 2008 from http://www.nhlbi.nih.gov/new/press04-06-15.htm
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P Wave: None; PR Interval: None; QRS Complex: 0.10 second; QT Interval: unable to obtain; Heart Rate: Atrial: 80 bpm; Rhythm: Irregular; Ectopic Beats: f waves.
FIGURE 3820
Atrial fibrillation.
Significant ECG features of atrial fibrillation include: P waves are not identifiable due to the atrial quivering, referred to as f waves, occurring at 350 to 750 beats per minute. PR intervals are not measurable. QT interval is not obtainable because the T waves are buried in the f waves. Irregularly irregular rhythm occurs, meaning that there is no pattern to the irregularity. f waves are ectopic beats. The etiology, physical assessment findings, and treatment of atrial fibrillation are outlined in Chart 387.
may result in a conversion to atrial flutter or fibrillation. Eventually, signs and symptoms of congestive heart failure will be present. Figure 3821 is a rhythm strip showing supraventricular tachycardia (SVT). Significant ECG features of supraventricular tachycardia include: Heart rate is 100 to 250 beats per minute. P wave is not seen; it is buried in the QRS complex. PR interval is not discernable. QRS complex is within normal limits unless distorted by the buried P waves. QT interval is not obtainable because the T waves are buried. Heart rhythm may be regular or irregular due to varying conduction rates through the AV node. Ectopic beats may or may not be present, depending on the pacemaker site. The etiology, physical assessment findings, and treatment of supraventricular tachycardia are outlined in Chart 387. Atrioventricular Nodal Reentry Tachycardia One phenomenon that can cause supraventricular tachycardia is atrioventricular nodal reentry tachycardia (AVNRT). Normally people are born with only a single electrical pathway at the base of the right atrium where impulses travel to the AV node. However, some individuals are born with two separate electrical pathways leading to the AV node, each with its own respective
Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is a tachycardia that is generated somewhere above the ventricles. This general term encompasses all fast (tachy) rhythms with normal QRS complexes and heart rates greater than 100 beats per minute. Rhythms included under the SVT umbrella include sinus tachycardia, paroxysmal atrial tachycardia (PAT), and paroxysmal junctional tachycardia (PJT). Clinicians use the term supraventricular tachycardia when it is impossible to identify the source of the tachycardia. Usually this rhythm is benign and is self-limiting when the cause is removed. If sustained, loss of blood fill time (diastole) causes a drop in cardiac output. Prolonged episodes of supraventricular tachycardia increase myocardial oxygen demand and also
P Wave: None; PR Interval: None; QRS Complex: 0.10 second; QT Interval: unable to obtain; Heart Rate: Ventricular: 200 bpm; Rhythm: Regular; Ectopic Beats: Depends on pacemaker site.
FIGURE 3821
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properties. Each pathway has its own refractory period, one fast (beta) and one slow (alpha). The fast track has a long refractory period, and the slow track has a fast refractory period. Impulses travel the two separate pathways simultaneously. When the impulse begins down these two pathways, because of its speed, the one in the fast track stimulates the AV node and bundle of His, causing ventricular depolarization and a normal-width QRS complex. The fast track impulse also travels retrograde (backward transmission) back through the slow track, meeting the impulse coming down the slow track. When the two impulses meet, 99.9% of the time, they cancel each other out and the rhythm is normal. If for any reason, such as the presence of a refractory period in the fast track, the fast track will be unable to transmit the impulse, then the slow track transmits the impulse, causing depolarization of the ventricles. The QRS complex would still be within normal limits, but the PR interval would be longer than the ones coming from the fast track. This creates rhythm strips
AVN
that have identical QRS complexes but two different PR interval lengths. These beats still are considered to be sinus complexes, as opposed to coming from another atrial ectopic focus. The PR interval length differences are a result of the conduction alternating intermittently between the two functioning tracks. The AVNRT phenomenon occurs when a reentrant circuit or loop is created along the two pathways and the AV node (Figure 3822 ). An early impulse such as a PAC hits the two pathways; the fast track is in refractory and therefore cannot accept the impulse, but the slow track can. The impulse travels from the slow track, to the AV node, and then retrograde up the fast track because this track has recovered, is no longer in a refractory state, and can accept the impulse. The impulses are now able to continue to cycle the circuit or loop and initiate ventricular depolarization at a fast rate; this is referred to as AVNRT (Garcia & Miller, 2004). It is estimated that AVNRT occurs in 60% of patients presenting with paroxysmal (sudden onset) SVT and occurs in
Purkinje
SAN AVN
SAN AVN
(a) Macro re-entry circut: antegrade through AV node and retrograde across an assessory pathway.
(b) Micro re-entry at the cellular level in the AV node and Purkinje fibers.
FIGURE 3822
Reentrant circuit.
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approximately several cases per thousand persons worldwide. It is more predominant in women, may occur with individuals of any age, and is common in young adults. AVNRT is usually well tolerated; it often occurs in patients with no structural heart disease. Clinical manifestations are the same as with any tachy dysrhythmia, although AVNRT may cause angina or myocardial infarction in patients with coronary artery disease. Prognosis for patients without heart disease is usually good (Olshansky et al., 2006). Treatment is aimed at breaking the reentrant cycle with the use of vagal maneuvers such as breath holding, stimulating gag reflex, and carotid sinus massage.
Delta Wave
P Wave: Present and irregular; PR Interval: 0.12 second; QRS Complex: 0.16 second. QT Interval 0.52 second, 40-50 bpm, Ventricular: 40-50 bpm; Rhythm: Regular Ectopic Beats: None.
FIGURE 3823
Wolff-Parkinson-White syndrome.
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White syndrome (WPW) is a genetic AV conduction disorder characterized by the presence of two AV conduction pathways, one normal and one abnormal. An impulse leaving the atrium may travel down one or the other pathway without any specific pattern. The abnormal pathway, called the Kent bundle, is composed of an extra muscle bundle made up of working myocardial tissue. This extra muscle bundle forms a connection between the atria and the ventricles outside the normal conduction system, referred to as an accessory pathway. This allows impulses coming from the atrium to bypass the normal AV connection. The hallmark feature on the ECG strip for the abnormal pathway is the presence of a delta wave, a slurred upstroke at the beginning of the QRS complex (Figure 3823 ). The delta wave occurs when the impulse travels via the accessory pathway to the ventricles. Because the conduction is outside the normal conduction system, it takes longer for the impulse to travel through the ventricles, thus creating an abnormally wide, bizarre QRS complex (Garcia & Miller, 2004). Atrial flutter, atrial fibrillation, and supraventricular tachycardia that results in heart rates of greater than 250 beats per minute, are common dysrhythmias in patients with WPW. The increased heart rate increases the workload and oxygen consumption of the heart, predisposing to heart failure, and therefore could cause sudden cardiac death. When the patient does not exhibit any dysrhythmias, but has the delta wave, this is called WPW pattern. When the patient becomes symptomatic or develops dysrhythmias, then the correct terminology is WPW syndrome. Figure 3823 is a rhythm strip showing Wolff-Parkinson-White dysrhythmia. Significant ECG features of Wolff-Parkinson-White syndrome include: PR interval shortens to less than 0.12 second because the AV node is bypassed and delta waves appear just prior to the beginning of the R wave.
QRS complex is greater than 0.12 second due to the delta waves. QT interval shortens if tachycardia occurs and lengthens with bradycardia. Heart rate frequently tachycardic. Heart rhythm is regular, except during heart rate changes. The etiology, physical assessment findings, and treatment of WPW syndrome are outlined in Chart 387 (p. 000).
P Wave: Multifocal; PR Interval: 0.16 second; QRS Complex: 0.06 second; QT Interval: 0.04 second; Heart Rate: Atrial: Approximately 60 bpm; Ventricular: 50 bpm; Rhythm: Irregular; Ectopic Beats; Multifocal P waves.
FIGURE 3824
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110
110
110
50
50
50
P Wave: Present, but variable configuration; PR Interval: 0.14 second; QRS Complex: 0.08 second; QT Interval: 0.40 second; Heart Rate: Atrial: 60 bpm, Ventricular: 60 bpm; Rhythm: Irregular; Ectopic Beats: May occur with slow rate.
FIGURE 3825
chronic atrial tachycardia. This disorder also is referred to as sinoatrial disease and sinoatrial dysfunction. The cause is a severely depressed nonreliable SA node due to heart disease or the side effect of certain cardiac drugs, such as cardiac glycosides, sympatholytic antihypertensive agents, beta-adrenergic blockers, calcium channel blockers, and membrane active antiarrhythmic agents. When the tachycardia occurs with SSS there is increased oxygen consumption and workload for the myocardium. Profound sinus bradycardia with SSS may progress to sinus pauses or arrest, thereby decreasing cardiac output. Figure 3825 is a rhythm strip showing sick sinus syndrome. Significant ECG features of sick sinus syndrome include: P waves may be present or absent depending on which dysrhythmia is occurring. PR interval varies due to changing P wave sites. QT interval varies due to rate changes. Heart rate may be rapid or slow, or a combination of both. Heart rhythm is irregular and highly variable. Ectopic beats may be present when a slow rate occurs. The etiology, physical assessment findings, and treatment of sick sinus syndrome are outlined in Chart 387.
Atrial flutter and fibrillation may occur as a transient dysrhythmia in healthy young individuals. If these conditions are chronic they are typically associated with heart disease including atrial muscle disease or atrial distention with disease of the sinus node. Atrial fibrillation also is seen in congenital heart disease. If the atrial flutter and/or atrial fibrillation are chronic conditions, and normal sinus rhythm cannot be reestablished, the patient often is placed on an anticoagulant, such as warfarin. This treatment is indicated because a fluttering/fibrillating atrium creates blood stasis, which increases the risk of clot formation. If these clots travel out of the atrium they tend to lodge in the brain, and, on rare occasions in the lung, causing an alteration in normal function in these areas. Treatment of atrial fibrillation/flutter may include cardioversion, which is the delivery of electrical voltage in order to stop unwanted electrical activity and allow the SA node to resume the hearts pacemaker. Cardioversion is discussed in detail in Chapter 39 . This treatment increases risk for myocardial infarction, cerebral vascular accident (CVA), and pulmonary embolus. The nurse needs to assess the patient post-cardioversion for clinical manifestations of these disorders. Myocardial infarction is discussed in detail in Chapter 40 . Cardiovascular accident (CVA) is discussed in Chapter 30 , and pulmonary embolus is discussed in Chapters 35 and 36 . Besides heart disease frequently there are other causes for atrial cardiac dysrhythmias that must be evaluated and treated, e.g., stress, pain, and anxiety. The treatment may be narcotics for pain relief or an antianxiety medication for stress and increased anxiety. The nurse may need only to sit and listen to the patient and provide emotional support.
Junctional Dysrhythmias
Junctional dysrhythmias also referred to as nodal rhythms result from either an irritable focus in the junctional tissue that discharges before the SA node has had a chance to or because the SA node has failed to fire and the junctional node becomes the secondary pacemaker. AV junctional dysrhythmias may occur if the impulse from the SA node is blocked as it exits the SA node or if it is not conducted through the atria. AV junctional dysrhythmias have a distinctive pattern on ECG tracings because the impulse is not initiated in the SA node. The impulse
8 8
8 8
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Nursing Management of Patients with Cardiovascular Disorders Figures 3826 and 3827 are ECG rhythm strips that show junctional escape rhythm and accelerated junctional rhythm, respectively. Significant ECG features of junctional escape rhythms include: P wave is inverted, negatively deflected, due to retrograde conduction, and either occurs before, after, or buried in the QRS complex. PR interval is dependent on the location of P wave; thus, the PR interval may or may not be present or normal. QRS complex is normal in duration and shape, unless distorted by a buried P wave. QT interval is within normal range, unless impacted by the heart rate. It is prolonged with slow heart rate or shortened with increased heart rate. Heart rate is usually within normal range for a rhythm generated from the AV junction is 40 to 60 beats per minute. For an accelerated junctional rhythm the rate is 60 to 100 beats per minute and for junctional tachycardia the heart rate is greater than 100 bpm. Heart rhythm is typically regular. Entire rhythm is composed of ectopic beats because they all come from the AV junction instead of the SA node. Other ectopic beats may occur with slow heart rate. The etiology, physical assessment findings, and treatment of junctional escape rhythms are outlined in Chart 388.
is initiated in the AV junctional tissue and must travel in a backward (retrograde) direction to activate the atria. Therefore, the P wave is inverted or negatively deflected, due to this retrograde conduction, and may occur before, after, or buried in, the QRS complex. Retrograde conduction means that the impulse originates in the AV junction so it stimulates the atria from the bottom up instead of the top down. The impulse simultaneously initiates both atrial and ventricular contractions. The location of the P wave is, therefore, dependent on the speed with which the impulses travel in both chambers. The QRS complex configuration is normal in appearance because the impulse travels the normal pathway from the AV junctional node through the ventricles. AV junctional dysrhythmias are not considered lethal or life threatening, but as always, the most important indicator of the clinical significance of any dysrhythmia is the patients response to or tolerance of the rhythm. The three AV junctional dysrhythmias discussed in this chapter are: junctional escape rhythm, premature junctional contractions, and paroxysmal junctional tachycardia.
P Wave: None, or buried in QRS Complex; PR Interval: Not measurable; QRS Complex: 0.10 second; QT Interval: 0.40 second; Heart Rate: Atrial: Not measurable, Ventricular: 40 bpm; Rhythm: Regular; Ectopic Beats: None.
FIGURE 3826
P Wave: Inverted and regular; PR Interval: 0.140.16 second; QRS Complex: 0.08 second: QT Interval: 0.44 second; Heart Rate: Atrial: 80 bpm, Ventricular: 80 bpm; Rhythm: Regular: Ectopic Beats: none.
FIGURE 3827
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CHART 388
Dysrhythmia Junctional escape rhythm
Rarely causes symptoms, thus typically not treated. Find and treat the underlying cause, if possible. If it initiates a more serious dysrhythmia, such as tachycardia, therapy becomes more aggressive, contingent on the type of dysrhythmia. If occurring frequently, more than 5 times per minute, they can drop cardiac output, and predispose the patient to other dysrhythmias. Oxygen Drugs such as stimulants, sympathomimetics, and digitalis may be discontinued.
Pulse: Rapid, with patient experiencing a fluttering sensation. BP: Lower than usual due to decreased cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare.
Find and treat the cause as PJTs may be a predisposition to lethal dysrhythmias, heart failure, and shock. Vagal maneuvers may be applied. Oxygen Drug therapy initiated: includes: amiodarone or beta-adrenergic blockers. Cardioversion may be initiated if necessary.
a rhythm strip showing premature junctional contraction. Significant ECG features of premature junction contractions include: P wave is inverted and occurs before, after, or buried in the QRS complex. PR interval is dependent on the location of P wave; thus, the PR interval may or may not be present or normal. QRS complex is normal in duration and shape, unless distorted by a buried P wave.
QT interval also is normal unless impacted by the heart rate. Heart rate is that of the underlying rhythm. Heart rhythm is irregular when PJCs are present; or it may be described as regular with premature beats. Ectopic beat is the PJC. The etiology, physical assessment findings, and treatment of PJCs are outlined in Chart 388.
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P Wave: Present and regular except for premature beat; PR Interval: 0.16 second; QRS Complex: 0.08 second; second; Heart Rate: Atrial: 110 bpm, Ventricular: 110 bpm; Rhythm: Regular except for premature beats: Ectopic Beats: none
FIGURE 3828
The etiology, physical assessment findings, and treatment of PJTs are outlined in Chart 388.
P Wave: Inverted and regular; PR Interval: 0.08 second; QRS Complex: 0.06 second; QT Interval: 0.32 second; Heart Rate: Atrial: 130 bpm, Ventricular: 130 bpm. Rhythm: Regular; Ectopic Beats: None.
FIGURE 3829
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Due to the clinical manifestations of these dysrhythmias, the patient and family may experience anxiety. Thus, the nurse also must assess and treat the anxiety by use of supportive measures, such as listening to the patients concerns, offering reassurance, providing a calm environment, and medicating for anxiety and pain relief as appropriate.
The etiology, physical assessment findings, and treatment of first-degree AV blocks are outlined in Chart 389 (p. 1104).
First-Degree AV Block
First-degree AV block represents a conduction disturbance in which electrical impulses flow normally from the SA node through the atria, but are delayed at the AV node. There is a prolongation or slowing of conduction rather than an actual block. Because of this consistent delay the PR interval is greater than 0.20 second, making it abnormal. First-degree AV block is not actually a dysrhythmia. Its presence only indicates a delay at the AV node, rather than a definite block. Figure 3830 is a rhythm strip showing first-degree AV block. Significant ECG features of first-degree AV block include: P waves are present and normal in size and shape. PR interval is prolonged, greater than 0.20 second, but constant. QRS duration usually is normal. QT interval is normal unless there is an abnormal rate. Heart rate is usually within normal range. Heart rhythm is regular.
P Wave: Present and regular; PR Interval: 0.24 second; QRS Complex: 0.06 second; QT Interval: 0.40 second; Heart Rate: Atrial: 60 bpm, Ventricular: 60 bpm; Rhythm: Regular; Ectopic Beats: None.
FIGURE 3830
First-degree AV block.
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CHART 389
Dysrhythmia First-degree AV block
Pulse: Irregular BP: May be decreased with frequently dropped beats due to decreased cardiac output. If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present, although rare. Pulse: slow and typically irregular, depending on ventricular response BP: Decreased due to low cardiac output If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present. Pulse: Slow and usually irregular BP: Lower than usual If cardiac output is decreased the following clinical manifestations may occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Altered mental state may be present.
This is often a transient rhythm and will revert to normal rhythm without treatment. Usually asymptomatic because the ventricular rate often remains nearly normal and cardiac output is not significantly affected. If symptomatic, and is a result of medications, they should be withheld. If the heart rate is slow and serious clinical manifestations such as low BP, angina, shortness of breath, occur, atropine or temporary pacing is considered. When occurs in conjunction with acute myocardial infarction, observe for increasing AV block. Often considered an emergent situation. The health care practitioner should be notified at once. May progress to a third-degree AV block and ventricular asystole, thus, a standby cardiac pacemaker is indicated for asymptomatic patients, and temporary cardiac pacing is required for symptomatic patients. For sustained permanent block, a permanent pacemaker is inserted.
Mobitz II second-degree AV
Ischemic damage Septal wall necrosis Acute inferior or right ventricular MI due to the effect of vagal tone and ischemia on the AV node Acute anterior MI Myocarditis Coronary artery disease Cardiomyopathies Cardiac muscle diseases Rheumatic heart disease Drug toxicity, reaction to amiodarone, beta-blockers, or calcium channel blockers Electrolyte imbalance Rheumatic heart disease Congenital condition usually located at the level of the AV junction
Treatment is essential as third-degree block is potentially lethal. If an AV junctional or ventricular escape pacemaker does not take over following a sudden onset of third-degree AV block, asystole will occur. Clinical manifestations depend on the ventricular heart rate, especially for slow rates. If the QRS is narrow and the patient is symptomatic, initial management is atropine and/or transcutaneous pacing. If the QRS is wide and the patient is symptomatic, transcutaneous pacing is started. A temporary pacemaker is inserted, and may be followed by a permanent pacemaker.
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CHART 389
Dysrhythmia Bundle branch block (BBB)
(Beasley, 2003). In other words there are 2, 3, or 4 P waves for every QRS complex. Thus, with this dysrhythmia there may be enough dropped QRSs to significantly impact cardiac output. Therefore, Mobitz II is a more serious dysrhythmia than either first-degree AV block or Mobitz I (Wenckebach/ Type I seconddegree heart block) because of the impact on the cardiac output and an increased risk of progression to third degree block or complete heart block. Figure 3832 (p. 1106) is a rhythm strip showing Mobitz II/second-degree block. Significant ECG features of Mobitz II/second-degree block include: QRS complexes are intermittently absent; they may be normal to prolonged when present; and they are usually prolonged due to bundle branch block. P waves are present and regular. PR intervals are constant with conducted beats. QT intervals are within normal limits. Atrial heart rate is usually normal; ventricular heart rate is less than the atrial rate.
Atrial rhythm is regular; ventricular rhythm may be regular or irregular. The ventricular rhythm is irregular when the AV block is intermittent; thereby, causing a varying AV conduction ratio. Ectopic beats may be present due to the slow heart rate. The etiology, physical assessment findings, and treatment of Mobitz II heart block are outlined in Chart 389.
1104 UNIT 8
P Waves: Present and regular; PR Interval: Progressively prolonged until one P wave is not conducted and the sequence begins again; QRS Complex: 0.10 second; QT Interval: 0.420.60 second; Heart Rate: Atrial: 70 bpm, Ventricular 50 bpm; Rhythm: Atrial: Regular, Ventricular: Irregular due to dropped beat; Ectopic Beats: None. Conclusion: Mobitz I/Wenckeback Second-Degree Heart Block.
FIGURE 3831
P Waves: Present and regular; PR Interval: 0.24 second; QRS Complex: 0.06 second; QT Interval: 0.48 second; Heart Rate: Atrial: 100 bpm, Ventricular 50 bpm; Rhythm: Atrial: Regular, Ventricular: Irregular due to dropped beat; Ectopic Beats: None.
FIGURE 3832
tissue. If the QRS complex is narrow the pacemaker is in the junctional tissue with a rate of 40 to 60 beats per minute. However, if the QRS complex is wide the pacemaker is in the Purkinje network and the heart rate ranges from 20 to 40 beats per minute; this is referred to as an idioventricular rhythm. Complete AV block associated with an inferior myocardial infarction is thought to be a block in the bundle of His, and often occurs after progression from first-degree AV block or second-degree AV
block, type I. Third-degree heart block is the most serious type of heart block because it may progress to asystole (a complete cessation of electrical activity), and the slow ventricular heart rate results in decreased cardiac output. Since the ventricular rhythm may not be able to sustain adequate cardiac output, third- degree heart block is referred to as a lethal dysrhythmia. Figure 3833 is a rhythm strip showing third-degree or complete heart block. Significant ECG features of third-degree heart block include:
CHAPTER 38
P Waves: Present and regular; PR Interval: None; QRS Complex: 0.12 second; QT Interval: 0.38 second; Heart Rate: Atrial: 90 bpm, Ventricular: 4050 bpm; Rhythm: Regular; Ectopic Beats: None.
tation to one ventricle; therefore, an abnormal spread of electrical activity through the ventricles occurs. This delayed conduction causes a widening of the QRS complex to more than 0.12 second. When measuring the QRS complex, it is necessary to observe the axis of the complex to determine whether it is right or left bundle branch block. Figure 3834 is a rhythm strip showing a bundle branch block. Significant ECG features of bundle branch block include: QRS complex is more than 0.12 second if a complete bundle branch block is present. P waves are present and regular. PR interval is 0.12 to 0.20 second. QRS measuring 0.10 to 0.12 second is called an incomplete right or left bundle branch block. QT interval is within normal limits. Heart rate is 60 to 100 beats per minute. Heart rhythm is regular. The etiology, physical assessment findings, and treatment of bundle branch block are outlined in Chart 389.
FIGURE 3833
Atrial and ventricular rhythms are independent of one another (dissociated). Atrial rhythm usually is regular, depending on underlying sinus, atrial, or junctional rhythm. Ventricular rhythm may be regular or irregular. P waves are present and regular; however there is no relationship to QRS complexes. PR interval is absent. QRS complex may be narrow with a junctional rhythm, or wide with an idioventricular rhythm. QT interval may change with the rate change, but is not directly affected. Atrial heart rate is regular, 60 to 100 beats per minute; nodal rate is 40 to 60 beats per minute; and ventricular rate is 20 to 40 beats per minute. Atrial and ventricular rhythms are independent of one another (dissociated). Atrial rhythm usually is regular, depending on underlying sinus, atrial, or junctional rhythm. Ventricular rhythm may be regular or irregular. Ectopic beats usually are present due to slow rate. The etiology, physical assessment findings, and treatment of Mobitz II heart block are outlined in Chart 389.
P Wave: Normal sinus rhythm; PR Interval: 0.16 second; QRS Complex: 0.20 second; QT Interval: 0.40 second. Heart Rate: Atrial: 90 bpm, Ventricular: 90 bpm; Rhythm: Atrial: Regular, Ventricular: Regular; Ectopic Beats: None.
FIGURE 3834
1106 UNIT 8
Nursing Management of Patients with Cardiovascular Disorders pact on cardiac output. The various types of ventricular dysrhythmias are discussed next: premature ventricular contraction, ventricular tachycardia, torsade de pointes, ventricular fibrillation, pulseless electrical activity, and asystole.
The onset of Mobitz II and complete heart block are emergent situations that require immediate intervention. Mobitz II is described as a treacherous and unpredictable rhythm that can deteriorate to become a complete heart block. If untreated, these rhythms may progress to cardiac asystole and sudden death. At any indication of rhythm changes indicative of Mobitz II or complete heart block, the health care practitioner should be notified at once. The nurse should prepare for a temporary pacemaker insertion (Chapter 39 ), which generally is indicated for these types of dysrhythmias. A permanent pacemaker may be necessary if the block persists. It is the nurses responsibility when working with monitored patients to be familiar with equipment location and operation.
Signs and symptoms of third-degree AV block are the same as those in symptomatic sinus bradycardia. AV block can be more ominous, especially when associated with wide and bizarre QRS complexes. If an AV junctional or ventricular escape pacemaker does not take over the pacing of the heart following a sudden onset of third-degree AV block or ventricular asystole will occur. Temporary cardiac pacemaker is required immediately for treatment of symptomatic third-degree block with wide QRS complexes. The nurse must report this rhythm immediately to the health care provider in order to initiate treatment before a significant drop in cardiac output occurs.
Ventricular Dysrhythmias
Ventricular dysrhythmias are caused by ectopic or irritable foci in the walls of the ventricles. The pacemaker cells in the ventricles may, in certain circumstances, serve as the hearts pacemaker. When the SA node fails or the impulse does not get through the AV node, the ventricles take over the pacing role. In this situation, an electrical impulse may be instigated from both the bundle of His and the Purkinje network. The intrinsic ventricular rate is only 20 to 40 beats per minute; therefore, cardiac output is severely compromised. Also, if the atrium is not contracting there is no atrial kick, causing further decrease in cardiac output. Because the rhythm originates in the ventricle there is no P wave, and because it is an abnormal conduction pathway the QRS is wide and distorted. Ventricular dysrhythmias are considered to be very serious dysrhythmias mainly due to their im-
P Wave: Present and regular, except where absent (PVC); PR Interval: 0.20 second; QRS Complex: 0.08 second; QT Interval: 0.42 second; Heart Rate: Atrial: 70 bpm, Ventricular: 80 bpm; Rhythm: Atrial: Regular, Ventricular: Regular except for premature beat; Ectopic Beats: One PVC.
8 8
FIGURE 3835
CHAPTER 38
sistently, the dysrhythmia is coming from one irritable focus in the ventricle. These are referred to as unifocal PVCs. If PVCs occur with every other beat the rhythm is referred to as bigeminy. If PVCs occur every third beat, the rhythm is called trigeminy, and occurrence every fourth beat is quadrigeminy. The more often the PVC occurs, the greater the drop in cardiac output, and therefore, the more serious the dysrhythmia. The drop in cardiac output is due to the premature occurrence of the rhythm which does not allow for sufficient diastole or ventricle filling time. As cardiac muscle ischemia increases the muscle becomes more irritable, causing PVCs to be initiated in more than one place in the ventricle. This is referred to as multifocal PVCs. When multifocal, the morphology (shape) of the QRSs varies. Multifocal PVCs are more serious than unifocal PVCs because they indicate that there is more ischemia occurring in the myocardium. PVC Patterns When PVCs occur for two or more consecutive beats this is referred to as paired salvos. When there are three or more consecutive PVCs salvos, it is defined as ventricular tachycardia. Ventricular tachycardia may be life threatening due to the severe drop in cardiac output. The most serious or dangerous time for a PVC to occur is during the relative refractory period, which is the top of the T wave on the ECG. This is referred to as an R on T phenomenon, and this occurrence may precipitate a run of ventricular tachycardia. Significant ECG features with PVCs include: QRS complex is premature, 0.12 second or greater in width, complexes are larger than the normal beats, with the T wave always occurring on the opposite side of the isoelectric line from the R wave. P waves are not present or are buried in the PVCs. PR interval-none. QT interval is prolonged for the ectopic beat only. PVC occurs prematurely. Heart rate usually is within normal range, but depends on underlying rhythm. Heart rhythm is irregular because the PVCs are premature. Ectopic beats are the PVCs. The etiology, physical assessment findings, and treatment of premature ventricular contractions are outlined in Chart 3810 (p. 1110).
niques, or electrical cardioversion. If the rhythm lasts less than 30 seconds it is a non-sustained rhythm or simply a run of ventricular tachycardia (three beats or longer) that terminates spontaneously. Ventricular tachycardia is an emergent situation, requiring urgent evaluation to assess cardiac output and the presence or absence of the pulse. Treatment is guided by published advanced cardiac support (ACLS) guidelines and varies based on the presence of a pulse. Ventricular tachycardia when sustained but hemodynamically stable (with pulse) is treated with pharmacologic agents such as lidocaine, procainamide or bretylium (AHA, 2006). Ventricular tachycardia that is hemodynamically unstable and pulseless is treated using the ACLS guidelines for pulseless cardiac arrest (Appendix *** ) (AHA, 2006). These guidelines dictate that the nurse assess the patient for a pulse, if none is present, cardiopulmonary resuscitation (CPR) is initiated and help is requested. Oxygen is administered and the patient is placed on a monitor/defibrillator when available. The nurse must be prepared to shock the patient per AHA guideline joules, CPR is resumed for 5 cycles, and then rhythm is checked. The patient is re-shocked if VT persists. Vasopressors are administered when intravenous access has been established. CPR and defibrillation cycles are repeated per ACLS guidelines until a viable rhythm is established or death occurs. Figure 3836 (p. 1012) is a rhythm strip showing ventricular tachycardia. Significant ECG features of ventricular tachycardia and ventricular fibrillation include: QRS complexes are uniform in appearance, usually wide and bizarre, measuring 0.12 second or greater, with the T wave occurring on the opposite side of the isoelectric line from the R wave. P waves in rapid VT are usually not recognizable. At slower ventricular rates, P waves may be recognized and may represent normal sinus node depolarization at a rate slower than VT, but the electrical activities do not affect one another. PR interval is not discernable. QT interval is not measurable. Heart rate is greater than 100 beats per minute and usually not faster than 200 beats per minute. Heart rhythm is essentially regular but may be irregular. Entire rhythm is ectopic beats. The etiology, physical assessment findings, and treatment of ventricular tachycardia are outlined in Chart 3810.
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Ventricular Tachycardia
Ventricular tachycardia (VT), often referred to as v-tach is a life threatening ventricular rhythm arising from an excitable ventricular focus in the tissue distal to the bifurcation of the bundle of His. In general, ventricular tachycardia affects the diseased heart, although it has been described in patients with apparently normal hearts. It is a rhythm that discharges repetitively, acting as the dominant pacemaker. It is present when three or more PVCs occur in a row at a rate of greater than 100 beats per minute (American Heart Association, 2006). This dysrhythmia frequently begins rapidly, and is initiated by a PVC which then becomes the hearts pacemaker. A sustained ventricular tachycardia is a rhythm that lasts longer than 30 seconds and usually requires termination by antiarrhythmic drugs, antitachycardia pacing tech-
Torsade de Pointes
Torsade de pointes, frequently referred to as torsades, is a form of ventricular tachycardia that is usually accompanied by prolongation of the QT interval. The QT interval usually is more than 0.50 second in the beats preceding the onset of the rhythm. Once the rhythm has occurred the QRS complexes have varying morphology or shape and width that usually begin after a pause in the rhythm or bradycardia. The name, torsade de pointes, is derived from the French term that signifies the twisting of the points. The name characterizes the rhythm in that it resembles a turning about or twisting motion along the baseline or isoelectric line. This form of VT, which is rare, is due to age, gender, drug toxicity, or an idiosyncratic reaction to certain cardiac drugs such as
1108 UNIT 8
CHART 3810
Dysrhythmia Premature ventricular contraction (PVC)
Pulse: Rapid and weak BP: Hypotensive Cardiac output is decreased therefore the following clinical manifestations occur: Angina Syncope Generalized weakness Dizziness Shortness of breath Changes in mental status, starting with confusion and restlessness, leading to unconsciousness. Conscious sensation of ineffective cardiac activity often accompanied by anxiety. Presence and severity of the signs and symptoms depends on rhythm duration.
Initial treatment is based on the presence or absence of a palpable pulse. If hemodynamically stable, with a pulse, drug intervention is appropriate e.g., procainamide, amiodarone, lidocaine. If hemodynamically unstable (pulseless) defibrillation and cardiopulmonary resuscitation (CPR) is indicated. After initial stabilization other treatments which may be considered include: Implantable cardioverter defibrillator Electrophysiology Studies (EPS): ventricles are stimulated to produce VT: then antiarrhythmic drugs are administered, followed by a second attempt to produce the VT. If unable to reproduce the dysrhythmia, the drug is considered effective and continuous therapy is instituted. Drugs used include: procainamide, amiodarone, and lidocaiane. Radio-frequency ablation, burning the area or focus in the ventricle where the VT is coming from may also be considered. Chapter 39 has a complete description of EPS and ablation.
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CHAPTER 38
CHART 3810
Dysrhythmia Torsade de pointes (TdP)
Etiology Prolonged QT interval, which may be congenital or acquired Severe bradycardia Electrolyte imbalance, e.g., hypokalemia, hypomagnesemia Central nervous system lesions Tricyclic antidepressants Antidysrhythmic drugs, e.g., quinidine, procainamide, amiodarone Antihistamines, e.g., seldane Antibiotics, e.g., erythromycin Diuretics Liquid protein diets Starvation Or any combination of the above
Severe myocardial ischemia Coronary heart disease Myocardial infarction Advanced heart block Abnormal repolarization Vagal stimulation Drug toxicity, e.g., psychotropics, digoxin Metabolic abnormalities, e.g., hypokalemia, hypomagnesemia Hypoxia Trauma Terminal event in many disease states Electrical shock Profound hypovolemia Massive myocardial damage Excessive vagal tone due to loss of sympathetic tone Obstruction of blood flow to or from the heart, e.g., severe pulmonary embolism Pericardial tamponade Myocardial rupture Massive cardiac trauma resulting in cardiac tamponade and/or tension pneumothorax Severe acidosis Hyperkalemia Hypothermia Drug overdose, e.g., tricyclics, betablockers, calcium channel blockers, digoxin Cardiac standstill from massive cardiac muscle damage
Pulse: None palpable BP: None Unconscious Seizures may occur Death, if untreated
Assess for pulse and blood pressure; initiate CPR protocol per ACLS guidelines (Appendix ** ). Find cause and treat.
8 8
Asystole
Check the rhythm in two leads in order to rule out the possibility of fine ventricular fibrillation. Also, check the lead placement to make sure it has not fallen off. Initiate CPR and ACLS protocols (Appendix ** ). Administer drugs per ACLS guidelines, agency protocol or doctors orders.
8 8 8 8
1110 UNIT 8
P Wave: Two normal P waves present; PR Interval: Not discernable during dysrhythmia; QRS Complex: Wide and distorted during dysrhythmia; QT Interval: Not discernable during dysrhythmia; Heart Rate: Atrial: Not discernable, Ventricular: Rapid; Rhythm: Both regular and irregular; Ectopic Beats: PVCs, ventricular tachycardia/fibrillation.
FIGURE 3836
Ventricular tachycardia.
quinidine, procainamide, disopyramide, or other agents that prolong the QT interval. Electrolyte imbalance such as hypokalemia and hypomagnesemia also can initiate torsade de pointes (Garcia & Miller, 2004). In addition to being a life threatening dysrhythmia, torsade de pointes tends to recur repeatedly. It is, therefore, essential to find and treat the underlying cause. Figure 3837 is a rhythm strip showing torsade de pointes. Significant ECG features of torsade de pointes include: QRS complex height varies and undulates. P waves are not discernable. PR interval is not measurable. QT is not measurable. Heart rate varies; approximately 200 to 250 beats per minute. Heart rhythm may be regular or irregular. Entire rhythm is ectopy.
ted through the normal conduction pathway. There are no waveforms apparent on the ECG strip. The rhythm appears disorganized, rapid, and irregular with waves whose morphology varies greatly. Ventricular fibrillation may be classified further as coarse and fine, just like atrial fibrillation. Coarse waveforms are more easily visible and are greater than 3 mm; those that are less than 3 mm frequently are referred to as fine VF. Coarse VF responds better to treatment than does fine VF. Also, coarse VF typically progresses to fine VF unless treatment is initiated in a timely manner. Fine VF indicates that the rhythm has been present for an extended period of time. Figure 3838 is a rhythm strip showing ventricular fibrillation.
Ventricular fibrillation (VF) is an ineffective quivering of the heart muscle that results in no blood delivery to tissues, thus, VF must be treated immediately. Detection of VF on a monitor requires immediate patient evaluation by the nurse to begin prompt treatment and to rule out equipment malfunctions that mimic VF such as, ECG artifacts produced by loose or dry electrodes, broken ECG leads, or patient movements or muscle tremors.
The etiology, physical assessment findings, and treatment of torsade de pointes are outlined in Chart 3810 (p. 1110).
Ventricular Fibrillation
Ventricular fibrillation (VF), often referred to as v-fib, is a dysrhythmia marked by rapid, disorganized depolarization of the ventricles. There are no organized electrical impulses, and therefore, no coordinated atrial or ventricular contraction or palpable pulse. The myocardial cells appear to quiver rather than depolarize normally. With this dysrhythmia multiple ventricular sites initiate electrical impulses that are not transmit-
Significant ECG features of ventricular fibrillation include: P waves, PR intervals, QRS complexes, and QT intervals are all absent. Heart rate is not discernable because there are no waves or complexes to measure. Heart rhythm is irregular. Entire rhythm is ectopy.
P Waves: Not discernable; PR Interval: Not discernable; QRS Complex: Wide, distorted, and varying heights; QT Interval: not discernable; Rate: Rapid; Rhythm: Both regular and irregular; Ectopic Beats: All.
FIGURE 3837
Torsade de pointes.
CHAPTER 38
P Waves: Not discernable; PR Interval: Not discernable; QRS Complex: Wide, distorted, and varying heights; QT Interval not discernable; Heart Rate: Not discernable; Ectopic Beats: All.
FIGURE 3838
Ventricular fibrillation.
The etiology, physical assessment findings, and treatment of ventricular fibrillation are outlined in Chart 3810 (p. 1110).
QRS complex may be narrow or wide. QT interval is variable. Heart rate and rhythm are variable, usually bradycardia. Ectopic beats may be present.
The etiology, physical assessment findings, and treatment of pulseless electrical activity are outlined in Chart 3810 (p. 1110).
Asystole
Asystole is a complete termination of all cardiac electrical activity. Without an electrical impulse, the atria and ventricles do not contract causing immediate loss of oxygen supply to the brain and tissues. In hospital settings efforts are usually made to reestablish cardiac activity but, often are futile. Figure 3839 is a rhythm strip showing asystole. In asystole, no measurable electrical activity exists and the rhythm strip appears as a straight line on the ECG monitor. The etiology, physical assessment findings, and treatment of asystole are outlined in Chart 3810 (p. 1110).
FIGURE 3839
Asystole.
1112 UNIT 8
Nursing Management of Patients with Cardiovascular Disorders of a loved one (Boyd, 2000). The research concluded that even family members with no medical background found it comforting to be with their loved one during the final moments of life. It is imperative that the health care team offer this opportunity and be sensitive to the family during this crisis period. If possible, it is optimal to have a health care team member be assigned to the family to answer questions, clarify information, and provide comfort (AHA 2005a). Since the nurse is at the bedside it typically becomes a nursing responsibility to keep the family informed, act as a liaison, and advocate for the patient. Chapter 17 includes a complete description of end of life issues.
specific abnormality. Nurses need to complete a health history to assess the risk factors related to the occurrence of ventricular dysrhythmias that are outlined in Chart 3810 (p. 000). Cultural awareness of populations that are at increased risk for ventricular dysrhythmias is discussed in the Cultural Considerations box (p. 000). Ventricular dysrhythmias have the greatest impact on cardiac output and are, therefore, the most serious. Depending on the variation in configuration and the frequency of occurrence, ventricular dysrhythmias require a variety of interventions from simple observation, to drug intervention, to advanced life support treatments. Generally, in monitoring units the health care practitioners provide protocols or standing orders for treating each type of ventricular dysrhythmia. The nurse must be knowledgeable of the treatment regimens required for each of the ventricular dysrhythmias based on the standing orders, basic cardiac life support (BCLS), advanced cardiac life support (ACLS), and agency specific protocols. When reporting ventricular dysrhythmias, the nurse needs to give a detailed description of the dysrhythmia pattern and the patients clinical response to the health care practitioner, so treatment is tailored to the specific dysrhythmia. The seriousness and treatment of ventricular dysrhythmias depend on the duration and the impact on hemodynamic stability (blood pressure and cardiac output). If the resuscitation efforts are initiated it is imperative that family and significant others be kept informed and be allowed to participate in the decision-making process. Research in the United States and the United Kingdom revealed that most family members wished to be present during the attempted resuscitation
CULTURAL CONSIDERATIONS
The term Brugada sign is an abnormal finding on an electrocardiogram (ECG) that refers to distance of at least 0.10 second from the onset of the QRS complex or the bottom of the S wave. Its presence may indicate Brugada syndrome which is an abnormality in the hearts electrical system that causes lifethreatening heart rhythm disturbances such as ventricular fibrillation. It occurs in patients with a structurally normal heart, and few or no coronary artery disease risk factor, and a family history of sudden cardiac death. Its possible to have a Brugada sign without having Brugada syndrome. This syndrome occurs most often in young adults. It also occurs with increased frequency in Asians. The cause isnt clear, but it appears to be inherited in some cases. Nursing implications are to assess young patients and patients of Asian decent who are having ventricular dysrhythmias with little to no risk of heart disease, for a family history of sudden cardiac death. Those considered at risk have: A family history of sudden cardiac death in young relatives A personal history of serious heart rhythm problems A personal history of severe fainting spells Immediate treatment for ventricular fibrillation is outlined on the American Heart Association ACLS guidelines for 2005. Long-term treatment includes antidysrhythmic medication therapy and an implantable defibrillator.
Source: Adapted from: Brugada Syndrome (2005). MayoClinic.com. http://www. mayoclinic.com/health/brugada-syndrome/AN00551. Retrieved July 13, 2006.
CHAPTER 38
disease the best way to prevent dysrhythmias is to have the patient closely follow a treatment plan and make the necessary life style habit changes. Life style habits most closely associated with heart disease and the occurrence of dysrhythmias include: Smoking Alcohol use Caffeine intake Sedentary life style Stress Overweight/obesity Diet.
nursing care for these patients. Beginning with the assessment the nurse needs to identify what type of information is necessary to help find the risk factors and causes that precipitate the occurrence or progression of cardiac dysrhythmias. The nursing diagnosis is generated from the assessment data and guides the nurse toward desired patient outcomes and an intervention plan. To assist the nurse in the comprehensive assessment and interpretation of cardiac dysrhythmias, Chart 3811 (p. 1116) summarizes the characteristics of each type of dysrhythmia.
Health Promotion
As with any disorder the primary focus is on prevention of the onset and progression of the disease. Health teaching about risk factors and life style habits that cause the disorders that underlie the occurrence of cardiac dysrhythmias is essential for prevention. Once an individual has been diagnosed with heart
The nurse needs to develop a teaching plan that will effectively assist the patient in reducing or eliminating these risk factors. Additionally, the patient needs to be told to note if there is a pattern as to when the dysrhythmias occur, what brings them on and what makes them go away. For example, does it take a long time for the heart rate to return to normal after exercise or exertion? Instruct the patient to identify high-stress situations that bring on the dysrhythmias and examine with the patient how to diminish or avoid them as much as possible. All aspects of life including professional as well as personal relationships need to be examined. Since the Human Genome Project ongoing research has focused on gaining a better understanding of how genetic disorders can predispose to dysrhythmias. For example, a mutation of gene ankyrin-B is now known to cause cardiac arrhythmia syndrome (Hamby, Mittal, & Stein, (2006). The goal is to use gene-based therapies in the future to better treat dysrhythmias as well as identifying those individuals who are susceptible to dysrhythmias. Nurses will assist in identifying whether or not the patient has a family history of dysrhythmias. This in turn will aid in the early diagnosis, treatment, or prevention of the occurrence of life-threatening dysrhythmias.
1114 UNIT 8
CHART 3811
ECG Rhythm Normal Sinus Rhythm Sinus Bradycardia Sinus Tachycardia
As the sinus rate accelerates, the PR interval tends to shorten slightly. Normal limits
Normal
100180 bpm
May be slightly irregular as rate accelerates; then becomes a rapid regular rate. Regularly irregular, with a variance of more than 0.08 seconds in the acceleration and deceleration phases. Underlying regular rhythm except where the sinus pauses occur. Regular except for premature PAC which may reset rhythm. Atrial rate regular. Ventricular rate may be regular or irregular
None
Sinus Arrhythmia
Normal limits
Changes with the heart rate becoming longer during the slow phase of the rhythm
60100 bpm
Normal limits
Changes with the heart rate, becoming longer during the slow phase of the rhythm. Normal if rate is normal.
There may be marked bradycardia due to long sinus pauses. 60100 bpm
Normal limits
PAC
Normal limits
Depends on the AV conduction ratio. There may be a slow ventricular response, or there may be a fast ventricular response. T waves are buried in the f waves.
Flutter waves
Atrial Fibrillation
No P wave f waves
None
Normal limits
Unable to obtain because the T waves are buried in the f waves. Unable to obtain as T waves are buried.
Irregular
Fibrillation waves
Not discernable
Within normal limits, unless distorted by buried P waves. Within normal limits, unless distorted by buried P waves.
100250 bpm
Regular or irregular due to varying conduction through the AV node. Irregular due to varying heart rates.
CHAPTER 38
CHART 3811
May be present due to the slow rhythm. May be present with slow rate.
Present or absent depending on which dysrhythmia is occurring. May occur before, after, or buried in, the QRS complex May occur before, after, or buried in, the QRS complex
Normal limits
Less than 0.12 second if the P wave occurs before the QRS complex Less than 0.12 second if P wave occurs before QRS complex for the ectopic beat. All others normal. Less than 0.12 second if P wave occurs before QRS complex for the ectopic beat. Greater than 0.20 second. Progressively prolonged until one P wave is not conducted and the sequence begins. Constant with conducted beats.
Usually 4060 (normal intrinsic rate for junctional tissue). That of underlying rhythm.
Regular
Normal unless distorted by P wave for the ectopic beat. All others normal.
Normal
PJC
Junctional Tachycardia
Variable Atrial rate within normal limits; ventricular rate slower than atrial.
None Usually none unless they occur during period when no QRS has occurred and there is a long pause. May occur due to slow rate.
(continued)
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CHART 3811
Greater than 0.12 second. If notch higher on right, indicates right bundle branch block; if notch higher on left, indicates left bundle branch block. Broad and premature and has increased amplitude. R and T waves opposite sides of isoelectric line. Wide and bizarre, measuring > 0.12 seconds. R and T waves opposite sides of isoelectric line Height undulates
60100 beats/minute.
Regular
None
PVC more likely to occur during bradycardia when there is more time to emerge. All waves are ectopy
Ventricular Tachycardia
None Visible
Not discernible.
Not discernible.
100250 beats/minute.
Essentially regular.
Torsade de Pointes
Not discernable
Not discernable
Usually > 0.50 seconds in the beats preceding the onset of the rhythm None
Typically regular.
None
None
None
Atrial: Absent Ventricular: Absent Variable, depends on rhythm; usually bradycardic. None
Irregular
All waves are ectopy May be present but none of the beats perfuse None
Variable.
Asystole
None
None
None
None
CHAPTER 38
NCLEX REVIEW
1. After reviewing the electrocardiogram of a patient, the nurse believes the tracing is normal. Which of the following did the nurse assess on this patients ECG?
1. 2. 3. 4. PR interval less than 0.8 second QRS complex 0.10 second Absent PR interval QT interval greater and 0.50 seconds
killed in an accident. The electrocardiogram shows a normal heart rate with shorter PR intervals. Which of the following should be included in this patients plan of care?
1. 2. 3. 4. Plan for cardioversion. Observe and treat the patient for anxiety. Medicate with calcium channel blockers. Provide carotid artery massage.
2. The nurse is assessing the QRS complexes on a patients electrocardiogram. The complex spans 3 small boxes on the ECG paper. The nurse would identify this patients QRS complex to be:
1. 2. 3. 4. 0.03 second 0.06 second 0.12 second 0.15 second
4. A patient is diagnosed with a junctional dysrhythmia. Which of the following should be included in this patients plan of care?
1. 2. 3. 4. Have a serum digoxin level drawn. Implement ACLS protocols. Prepare to administer magnesium. Prepare to administer lidocaine.
Answers for review questions appear in Appendix 5
3. A patient comes into the emergency department to be seen for chest pain that started after learning that his brother was
KEY TERMS
absolute refractory period p.000 action potential p.000 anion p.000 artifact p.000 asystole p.000 atrial dysrhythmia p.000 atrial fibrillation p.000 atrial flutter p.000 atrial kick p.000 atrioventricular (AV) node p.000 automaticity p.000 AV dissociation p.000 Bachmann bundle p.000 bigeminy p.000 bipolar lead p.000 bundle branch block p.000 bundle of His p.000 cardiac conduction system p.000 cardiac depolarization p.000 cardiac repolarization p.000 cation p.000 conductivity p.000 contractility p.000 dysrhythmia p.000 ECG waveform p.000 escape p.000 ectopic focus p.000 electrode p.000 excitability p.000 fascicles p.000 fill time p.000 first-degree AV block p.000 graph paper p.000 intra-atrial pathways p.000 ion p.000 irregularly-irregular rhythm p.000 isoelectric line p.000 J point p.000 junctional dysrhythmia p.000 junctional escape rhythm p.000 lead axis p.000 millivolts p.000 Mobitz I/Wenckebach p.000 Mobitz II/second-degree block p.000 negative deflection p.000 nodes (bundles) p.000 normal sinus rhythm (NSR) p.000 P wave p.000 pacemaker cell p.000 paroxysmal junctional tachycardia (PJT) p.000 positive deflection p.000 PR interval p.000 premature atrial contraction (PAC) p.000 premature junctional contraction (PJC) p.000 premature ventricular contraction (PVC) p.000 pulseless electrical activity (PEA) p.000 Purkinje network fibers p.000 QRS complex p.000 QT interval p.000 quadrigeminy p.000 refractory period p.000 relative refractory period p.000 resting membrane potential p.000 sick sinus syndrome (SSS) p.000 sinoatrial (SA) node p.000 sinus arrest p.000 sinus arrhythmia/dysrhythmia p.000 sinus bradycardia p.000 sinus tachycardia p.000 ST segment p.000 supraventricular tachycardia (SVT) p.000 T wave p.000 third-degree AV block (complete block) p.000 threshold p.000 torsade de pointes p.000 trigeminy p.000 12-lead ECG p.000 U wave p.000 unipolar lead p.000 ventricular dysrhythmia p.000 ventricular fibrillation (VF) p.000 ventricular tachycardia (VT) p.000 wandering atrial pacemaker p.000 Wolff-Parkinson-White syndrome (WPW) p.000
1118 UNIT 8
EXPLORE
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REFERENCES
American Heart Association. (2005a). Handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: Author. American Heart Association. (2005b). Part 5: Electrical therapies: Automated external defibrillators, defibrillation, cardioversion, and pacing. Supplement to Circulation: Journal of the American Heart Association, 112(24), IV-35IV-46. American Heart Association. (2005c). 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care: Part 2. Ethical issues. Circulation, 112, IV-6IV-11. American Heart Association. (2006a). BLS guidelines for healthcare providers. Dallas, TX: Author. American Heart Association. (2006b). 2005 International Consensus on CPR and ECC Science with Treatment Recommendations. Retrieved June 30, 2006, from http://www.americanheart.org/presenter. jhtml?identifier=3022512 Beasley, B. M. (2003). Understanding EKGs: A practical approach (2nd ed.). Upper Saddle River, NJ: Prentice Hall. Boyd, R. (2000). Witnessed resuscitation by relatives. Resuscitation, 43, 171176. Chamberlain, D. A., & Hazinski, M. F. (2003). Education in resuscitation: An ILCOR symposium: Utstein Abbey: Stavanger, Norway: June 2224, 2001. Circulation, 108, 25752594. Ellis, K. M. (2002a). EKG plain and simple: From rhythm strips to 12leads. Upper Saddle River, NJ: Prentice Hall Health. Ellis, K. M. (2002b). Q & A review of EKG. Upper Saddle River, NJ: Prentice Hall Health. Garcia, T. B., & Miller G. T. (2004). Arrhythmia recognition: The art of interruption. Sudbury, MA: Jones and Bartlett. Hamby, R. L., Mittal, S., & Stein, K. M. (2006). Arrhythmia. Retrieved July 17, 2006, from http:// heart.healthcentersonline.com/ arrhythmia/arrhythmia8.cfm Holtschneider, M. E., McBroom, K. G., & Patterson, A. (2006). ECG everywhere. Advance for Nurses, 3(13), 20. International Liaison Committee on Resuscitation. (2005). International consensus on cardiopulmonary resuscitation and emergency cardiovascular care since with treatment recommendations. Circulation: 2005; 112: III-I-III-136. Jacobs, I., et al. (2004). Cardiac arrest and cardiopulmonary resuscitation outcome reports: Update and simplification of the Utstein templates resuscitation registries. A statement for health care professionals from a task force of the international liaison committee on resuscitation (AHA, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, interAmerican Heart Foundation, Resuscitation Council of Southern Africa). Resuscitation, 63, 233249. Olshansky, B. et al. (2006). Atrioventricular nodal reentry tachycardia (AVNRT). eMedicine from WebMD. Retrieved July 13, 2006, from http:// www.emedicine.com/med/topic2955.htm Peberdy, M. A. et al. (2003). Cardiopulmonary resuscitation of adult in the hospital: A report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation. Resuscitation, 58, 297308. Porth, C. M. (2004). Essentials of pathophysiology: Concepts of altered health states. Philadelphia: Lippincott Williams & Wilkins. Shade, B., & Wesley, K. (2007). Fast and easy ECGs: A self-paced learning program. Boston: McGraw-Hill. Walraven, G. (2006). Basic arrhythmias (6th ed.). Upper Saddle River, NJ: Prentice Hall Health.