CHAPTER 17 Patient Assessment: Cardiovascular System 245

Transcription

1 CHAPTER 17 Patient Assessment: Cardiovascular System 245 at any time to aid in diagnosis and to note trends in the patient s status Wireless communication devices carried by the nurse that provide data and alarms MONITORING LEAD SYSTEMS All cardiac monitors use lead systems to record the electrical activity generated by cardiac tissue. Each lead system is composed of a positive or recording electrode, a negative electrode, and a third electrode used as a ground. As the heart depolarizes, the waves of electrical activity move inferiorly, because the normal route of depolarization moves from the sinoatrial (SA) node and atria, downward through the AV node, His Purkinje system, and ventricles, and to the left because the muscle mass in the left side of the heart is greater than the muscle mass of the right side of the heart. Each lead system views these waves of depolarization from a different location on the chest wall and thus produces P waves and QRS complexes of varying configuration. The terminology used to describe lead systems can be confusing. The wires attached to the patient s chest are called leads, and the pictures produced by these wires are also called leads. A standard ECG uses 10 lead wires with electrodes at the ends (4 placed on the limbs and 6 placed on the chest) and produces 12 electrical views of the heart, known as 12 leads. Cardiac monitoring systems currently on the market vary from two- and three-electrode telemetry devices to three-, four-, and five-electrode hard-wire systems. The two- or three-electrode systems produce limited selections of leads I, II, or III with only a single lead viewed on the screen at one time (single-channel recording). Five-electrode systems allow the possibility of viewing any of the 12 ECG leads and permit the nurse to view two or more leads on the monitor screen simultaneously (multichannel recording). Three-Electrode Systems Monitors that require three electrodes use positive, negative, and ground electrodes that are placed in the right arm (RA), left arm (LA), and left leg (LL) positions on the chest as designated by markings on the monitor cable. When the electrodes are placed appropriately, the standard leads (leads I, II, III) may be obtained by moving the lead selector on the bedside monitor to the lead I, II, or III position (Fig ). The lead selector automatically adjusts which electrode is positive, which electrode is negative, and which electrode is ground to obtain an appropriate tracing. When lead I is selected, the LA is positive, the RA is negative, and the LL is ground. For a lead II configuration, the LL is positive, the RA is negative, and the LA is ground. To obtain a lead III, the LL is positive, the LA is negative, and the RA is ground. The configuration of leads I, II, and III, known as Einthoven s triangle, is illustrated in Figure To obtain a chest lead on the monitor that replicates the chest lead from the 12-lead ECG, a five-wire system is needed. (See Fig for a review of chest lead placement.) When only three wires are available, a modified version of any of the six chest leads may be obtained. To figure Three-electrode monitoring system. Leads placed in this position allow the nurse to monitor leads I, II, or III. The left leg electrode must be placed below the level of the heart. LA, left arm; LL, left leg; RA, right arm. configure a modified chest lead (MCL), the goal is to position the positive electrode in the designated chest position. For example, an MCL 1 would require the positive electrode to be placed in a V 1 position (fourth intercostal space, right sternal border). The negative electrode is always positioned under the left clavicle. The ground electrode can be positioned anywhere. figure Einthoven s triangle. Leads I, II, and III are known as the standard leads. When placed together over the chest, they form what is known as Einthoven s triangle. Lead I: Left arm is positive, and right arm is negative. Lead II: Left leg is positive, and right arm is negative. Lead III: Left leg is positive, and left arm is negative.

2 246 PART IV CARDIOVASCULAR SYSTEM To obtain an MCL 1 lead, the monitor is set to lead I (Box 17-10). By setting the monitor to lead I, the LA electrode is positive, the RA electrode is negative, and the leg wire is ground (Einthoven s triangle). The positive electrode (LA) is placed in a V 1 position (fourth intercostal space, right sternal border), and the negative electrode (RA) is positioned under the left clavicle. The ground electrode (LL) can be positioned anywhere, but if it is placed in a V 6 position, it is helpful when switching to an MCL 6 lead. To obtain an MCL 6 lead, the goal is to place a positive electrode in a V 6 position, a negative electrode under the left clavicle, and a ground wire anywhere. By setting the monitor to lead II, the LL electrode is positive, the RA electrode is negative, and the LA electrode is ground (Einthoven s triangle). The positive electrode (LL) is placed in the V 6 position (midaxillary line, same horizontal level as V 4 ), and the negative electrode (RA) is placed under the left clavicle. The ground wire can be placed anywhere, but if it is placed in a V 1 position, it will be helpful when switching to an MCL 1 lead. By arranging the electrodes as described, the nurse can monitor both MCL 1 and MCL 6 merely by switching the monitor from a lead I to a lead II without changing the electrode placement on the patient s chest. MCL 1 and MCL 6 are ideal leads for detecting bundle branch block rhythms and for differentiating supraventricular wide- QRS tachycardias from VT. Five-Electrode Systems The five-electrode system increases the monitor s capability beyond the three-electrode system. (The fourelectrode monitor requires a right leg electrode that is the ground for all leads described in the three-electrode system.) The five-electrode monitor adds an exploring chest electrode that allows one to obtain any one of the six chest leads and the six limb leads. In essence, a five-wire monitor system provides all the capabilities of the 12-lead ECG machine. The only difference is that the five-wire monitor has only one chest electrode, whereas the 12-lead ECG machine has six chest electrodes. Newer cardiac monitors now have all six chest electrodes and allow the nurse to view all 12 leads of the ECG simultaneously on the monitor screen. To monitor a patient with a five-wire system, the four limb electrodes are positioned on the body according to their designations. The fifth chest electrode is placed on the chest in the designated precordial position. For example, if the nurse wants to monitor V 1, the chest electrode is placed in the fourth intercostal space, right sternal border (Fig ). If the nurse wants to switch to a different chest lead for monitoring, the electrode must be repositioned on the patient s chest. A five-electrode monitor offers the additional advantage of allowing the nurse to view two or more different leads simultaneously on the monitor screen. 1 Lead Selection No single monitoring lead is ideal for every patient. Table 17-6 summarizes the use of various leads and the reasons for their use. Lead II is used commonly because it records clear upright P waves and QRS complexes that are helpful in determining the underlying rhythm. In addition to lead II, leads III, avf, and V 1 or MCL 1 show box Three-Electrode System To monitor MCL1 using a three-electrode monitor: 1. Select lead I on the monitor. 2. Refer to Einthoven s triangle to remember that LA is positive, RA is negative, and LL is ground for lead I. 3. Place the positive electrode (LA) in a V 1 position (fourth intercostal space, right sternal border). 4. Place the negative electrode (RA) under the left clavicle. 5. Place the ground wire (LL) in the V 6 position (fifth intercostal space, left midaxillary line). To monitor MCL 6 using a three-electrode monitor: 1. Select lead II on the monitor. 2. Refer to Einthoven s triangle to remember that LL is positive, RA is negative, and LA is ground for lead II. 3. Place the positive electrode (LL) in the V 6 position (fifth intercostal space, left midaxillary line). 4. Place the negative electrode (RA) under the left clavicle. 5. Place the ground wire (LA) in a V 1 position (fourth intercostal space, right sternal border). Note: The electrodes are in the same position on the chest for the MCL 1 lead and the MCL 6 lead. To view the two leads, the nurse merely switches the monitor from lead I to lead II. I II III MCL 1 RA LL LA

3 CHAPTER 17 Patient Assessment: Cardiovascular System 247 ing complex atrial arrhythmias, uncharacteristic-looking ventricular premature beats, and fascicular blocks. Another use of multilead monitoring is in assessment of myocardial ischemia, injury, and infarction. By continuously viewing one lead from each area of the heart, episodes of anginal pain or silent ischemia can be documented. As soon as possible, these changes should be confirmed by a full 12-lead ECG. figure Five-electrode monitoring system. Using a fiveelectrode system allows the nurse to monitor any of the 12 leads of the electrocardiogram. The chest electrode must be moved to the appropriate chest location when monitoring the precordial leads. well-formed P waves and therefore are helpful in identifying atrial arrhythmias. V 1 or MCL 1 is useful in recognizing RBBB and in differentiating ventricular ectopy from supraventricular rhythms with aberrancy. V 6 or MCL 6 is helpful in identifying LBBB and also is useful in differentiating ventricular ectopy from supraventricular rhythms with aberrancy. Lead I may be tried with the patient with respiratory disease who has much artifact on the tracing because there is less movement of the positive electrode in this lead than in a lead II or a V 1. As mentioned, there is no one ideal monitoring lead for every patient, and in several situations, multilead recording is desirable. Multilead ECG systems offer multiple views of the heart because they reflect a tracing from each of the major heart surfaces. One of the major uses of multilead monitoring is in the interpretation of complex cardiac arrhythmias, especially when differentiating aberrancy from ventricular ectopy and in identify- Procedure ELECTRODE APPLICATION Proper skin preparation and application of electrodes are imperative for good ECG monitoring. An adequate tracing should reflect (1) a narrow, stable baseline; (2) absence of distortion or noise ; (3) sufficient amplitude of the QRS complex to activate the rate meters and alarm systems properly; and (4) identification of P waves. The type of electrode currently used for ECG monitoring is a disposable silver- or nickel-plated electrode centered in a circle of adhesive paper or foam rubber. Most electrodes are pregelled by the manufacturer. They may have disposable wires attached to the electrodes or nondisposable wires that snap onto the electrodes. Electrodes should be comfortable for the patient. If not properly applied, undue artifact and false alarms may result. When applying electrodes, the following procedure should be followed: 1. Select a stable site. Avoid bony protuberances, joints, and folds in the skin. Areas in which muscle attaches to bone have the least motion artifact. 2. Shave excessive body hair from the site. 3. Rub the site briskly with a dry gauze pad to remove oils and cellular debris. Skin preparation with alcohol may be necessary if the skin is greasy; allow the alcohol to dry completely before applying the electrode. Follow the electrode table 17-6 Suggested Monitoring Lead Selection Lead II V 1 or MCL 1 V 6 or MCL 6 III, avf, V 1 I II, III, avf I, avl, V 5, V 6 V 1 through V 4 Rationale for Use Produces large, upright visible P waves and QRS complexes for determining underlying rhythm Helpful for detecting right bundle branch block and to differentiate ventricular ectopy from supraventricular rhythm aberrantly conducted in the ventricles Helpful lead for detecting left bundle branch block and to differentiate ventricular ectopy from supraventricular rhythm aberrantly conducted in the ventricles Produce visible P waves; useful in detecting atrial arrhythmias Useful in patients with respiratory distress Left arm and right arm electrodes involved and placements less affected by chest motion compared with other leads Helpful in detecting ischemia, injury, and infarction in the inferior wall Helpful in detecting ischemia, injury, and infarction in the lateral wall Helpful in detecting ischemia, injury, and infarction in the anterior wall

4 248 PART IV CARDIOVASCULAR SYSTEM manufacturer s directions because the chemical reaction between alcohol or other skinpreparation materials and the adhesives used in some electrodes may cause skin irritation or nonadhesion to the skin. 4. Remove the paper backing and apply each electrode firmly to the skin by smoothing with the finger in a circular motion. Attach each electrode to its corresponding ECG cable wire. Sometimes it is necessary to tape over the cable wire connection or make a stress loop with the cable wire for extra stability. 5. Change electrodes every 2 to 3 days, and monitor for skin irritation. While applying the electrodes, explain the purpose of the procedure to the patient. Reassure the patient that monitor alarm sounds do not necessarily indicate a problem with the patient s heart beat; alarms often occur when an electrode becomes loose or disconnected. MONITOR OBSERVATION Cardiac monitors are useful only if the information they provide is observed, either by computers with alarms for programmed parameters or by the human eye, and appropriately acted on by competent, responsible individuals. Some critical care units use monitor technicians whose main responsibilities are to observe monitors, obtain chart samples, and give appropriate information to the nurse about each patient s ECG status. Those observing the monitor should know the acceptable arrhythmia parameters for each patient and should be notified of any interruptions in monitoring, such as those caused by changing electrodes or by changing the patient to a portable monitor. The observer also should be aware of the presence of artifact from chest physical therapy or hiccups so that it may be considered in arrhythmia diagnosis. Regardless of the system used for monitor observation, certain practices always should be followed. If the monitor alarm sounds, the nurse evaluates the clinical status of the patient before doing anything else to see if the problem is an actual arrhythmia or a malfunction of the monitoring system. Asystole should not be mistaken for an unattached ECG wire, nor should a patient inadvertently tapping on an electrode be misread as VT. In addition, monitor alarms always should be in the functioning mode. Only when direct physical care is being given to the patient can the alarm system safely be put on standby. This ensures that no life-threatening arrhythmia goes unnoticed. If the change on the monitor is not caused by an artifact or a disconnected wire, a full 12-lead ECG should be recorded to evaluate the rhythm change further. Troubleshooting Electrocardiogram Monitor Problems Several problems may occur in monitoring the ECG, including baseline but no ECG trace, intermittent traces, wandering or irregular baseline, low-amplitude complexes, 60-cycle interference, excessive triggering of heart rate alarms, and skin irritation. 2 Box outlines the steps to follow when such problems occur. ARRHYTHMIAS AND THE 12- LEAD ELECTROCARDIOGRAM Arrhythmias and abnormalities of the 12-lead ECG commonly encountered in monitored patients can be recognized with a little practice. The types that occur most frequently are discussed in this chapter. Before presenting the individual arrhythmias and 12-lead ECG abnormalities, the method for evaluating a rhythm strip is addressed. To understand the causes, clinical significance, and treatment of arrhythmias, knowledge of the conduction system is essential. Chapter 16 provides a review of the essential elements of the cardiac conducting system. Evaluation of a Rhythm Strip ELECTROCARDIOGRAM PAPER An ECG tracing is a graphic recording of the heart s electrical activity. The paper consists of horizontal and vertical lines, each 1 mm apart. The horizontal lines denote time measurements. When the paper is run at a sweep speed of 25 mm/second, each small square measured horizontally is equal to 0.04 second, and a large square (five small squares) equals 0.2 second. Height or voltage is measured by counting the lines vertically. Each small square measured vertically is 1 mm, and the large square is 5 mm (Fig ). Most ECG paper also is marked by vertical slash marks across the top or bottom. The distance between two vertical markings represents 3 seconds. The distance between 6 seconds is used for rate calculation. WAVEFORMS AND INTERVALS During the cardiac cycle, the following waveforms and intervals are produced on the ECG surface tracing (see Fig ): P wave: The P wave is a small, usually upright and rounded deflection representing depolarization of the atria. It normally is seen before the QRS complex at a consistent interval. PR interval: The PR interval represents the time from the onset of atrial depolarization until the onset of ventricular depolarization. Included in the interval is the brief delay of the electrical signal at the AV node that allows time for the blood to move from the atria to the ventricles before the ventricles are depolarized. The interval is measured from the beginning of the P wave to the beginning of the QRS complex. A normal PR interval is 0.12 to 0.2 second. QRS complex: The QRS complex is a large waveform representing ventricular depolarization. Each component of the waveform has a specific connotation. The initial negative deflection is a Q wave, the initial positive deflection is an R wave, and the negative deflection after the R wave is an S wave. Not all QRS complexes have all three components, even though the complex is commonly called the QRS complex. A normal QRS complex is 0.06 to 0.11 second in width. Figure illustrates different kinds of QRS complexes.

5 CHAPTER 17 Patient Assessment: Cardiovascular System 249 box Troubleshooting: Electrocardiogram Monitor Problem Solving Excessive Triggering of Heart Rate Alarms Is the high low alarm set too close to the patient s heart rate? Is the monitor sensitivity level set too high or too low? Is the patient cable securely inserted into the monitor receptacle? Are the lead wires or connections damaged? Has the monitoring lead been properly selected? Were the electrodes applied properly? Are the R and T waves the same height, causing both waveforms to be sensed? Is the baseline unstable, or is there excessive cable or lead wire movement? Baseline But No Electrocardiogram (ECG) Trace Is the size (gain or sensitivity) control properly adjusted? Is an appropriate lead selector being used on the monitor? Is the patient cable fully inserted into the ECG receptacle? Are the electrode wires fully inserted into the patient cable? Are the electrode wires firmly attached to the electrodes? Are the electrode wires damaged? Is the patient cable damaged? Call for service if the trace is still absent. Is the battery dead (for telemetry system)? Intermittent Trace Is the patient cable fully inserted into the monitor receptacle? Are the electrode wires fully inserted into the patient cable? Are the electrode wires firmly attached to the electrodes? Are the electrode wire connectors loose or worn? Have the electrodes been applied properly? Are the electrodes properly located and in firm skin contact? Is the patient cable damaged? Wandering or Irregular Baseline Is there excessive cable movement? This can be reduced by clipping to the patient s clothing. Is the power cord on or near the monitor cable? Is there excessive movement by the patient? Are there muscle tremors from anxiety or shivering? Is site selection correct? Were proper skin preparation and application procedures followed? Are the electrodes still moist? Low-Amplitude Complexes Is size control adjusted properly? Were the electrodes applied properly? Is there dried gel on the electrodes? Change electrode sites. Check 12-lead ECG for lead with highest amplitude, and attempt to simulate that lead. If none of the preceding steps remedies the problem, the weak signal may be the patient s normal complex. Sixty-Cycle Interference Is the monitor size control set too high? Are there nearby electrical devices in use, especially poorly grounded ones? Were the electrodes applied properly? Is there dried gel on the electrodes? Are lead wires or connections damaged? figure Waveforms of the electrocardiogram. Schematic representation of the electrical impulse as it traverses the conduction system, resulting in depolarization and repolarization of the myocardium.

6 250 PART IV CARDIOVASCULAR SYSTEM figure Configurations of the QRS complex. A Q wave is a negative deflection before an R wave, an R wave is a positive deflection, and an S wave is a negative defection after an R wave. ST segment: The ST segment is the portion of the tracing from the end of the QRS complex to the beginning of the T wave. It represents the time from the end of ventricular depolarization to the beginning of ventricular repolarization. Normally, it is isoelectric. An isoelectric ST segment means the ST segment joins the QRS complex at the baseline. ST segments may be elevated or depressed in a variety of conditions. Elevated ST segments could indicate acute myocardial injury. Depressed ST segments may signify acute myocardial injury or myocardial ischemia. For a more detailed discussion of ST segment abnormalities, see Chapter 21. T wave: The T wave is the deflection representing ventricular repolarization or recovery. The T wave appears after the QRS complex. The atria also have a repolarization phase. However, there is no visible wave on the ECG to represent atrial repolarization because it occurs at the same time as the QRS complex. U wave: A U wave is a rarely seen, small, usually positive deflection after the T wave. Its significance is uncertain, but it typically is seen with hypokalemia. QT interval: The QT interval is the period from the beginning of ventricular depolarization to the end of ventricular repolarization. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Because the QT interval varies with heart rate, it is necessary to use a table in which QT intervals for various heart rates are listed. Tables are available for this purpose in most texts about arrhythmias (Table 17-7). If such a table is not available, a corrected QT interval (QT C ) can be calculated for comparison with normal values. Normal QT C usually does not exceed 0.42 second for men and 0.43 second for women. A quick method for obtaining a QT C is to use half of the preceding RR interval (described later). CALCULATION OF HEART RATE Although cardiac monitors and ECG strips can be used to calculate heart rate, the calculated rate is merely an estimate of the number of times per minute the heart has been electrically excited. In the normal heart, each excitation should be followed by cardiac contraction. However, in some situations, electrical activity can occur without contraction, resulting in a lack of perfusion. Therefore, the heart rate obtained from the cardiac monitor or ECG strip should never be substituted for the determination of heart rate by palpating the pulse. table 17-7 Approximate Normal Limits for QT Intervals in Seconds Heart Rate per Men and Minute Children Women

7 CHAPTER 17 Patient Assessment: Cardiovascular System 251 Both the atrial and the ventricular rates can be estimated by examining the ECG. To determine the ventricular rate, count the number of QRS complexes in a 6-second strip, and multiply by 10. To estimate the atrial rate, count the number of P waves in a 6-second strip and multiply by 10. In the normal patient, the atrial and the ventricular rates should be the same. This method of rate calculation provides an estimate of heart rate for regular and irregular rhythms. Another method of rate calculation can be used if the rhythm is regular. The ventricular heart rate is estimated by dividing 300 by the number of large boxes on the ECG paper between two R waves (the RR interval). The atrial rate is calculated by dividing 300 by the number of large boxes on ECG paper between two P waves (the PP interval). Another quick method for estimating rate involves the use of a series of numbers. To use this method for estimating ventricular rate, the nurse first finds a QRS complex that falls directly on a dark line of the ECG paper. This dark line is the reference point. The next six dark lines of the paper are labeled 300, 150, 100, 75, 60, and 50 (Fig ). Then, the nurse finds the next QRS complex immediately after the reference point and estimates the ventricular rate using the sequence of numbers. The same method can be used for estimating atrial rate by using the P waves. STEPS IN ASSESSING A RHYTHM STRIP The following analysis represents a systematic approach to assessment of a cardiac rhythm strip. Whether or not this method is used, it is important to take the time to complete each step because many arrhythmias are not as they first appear. 1. Determine the atrial and ventricular heart rates. Are they within normal limits? If not, is there a relationship between the two (i.e., one a multiple of the other)? 2. Examine the rhythm to see if it is regular. Is there an equal amount of time between each QRS complex (RR interval)? Is there an equal amount of time between each P wave (PP interval)? Are the PP and RR intervals the same? 3. Look for the P waves. Are they present? Is there one or more P wave for each QRS complex? Do all P waves have the same configuration? 4. Measure the PR interval. Is it normal? Is it the same throughout the strip, or does it vary? If it varies, is there a pattern to the variation? Reference 300 Reference then figure Method for estimating heart rate. Using this method, the heart rate is 85 beats/min.

8 252 PART IV CARDIOVASCULAR SYSTEM 5. Evaluate the QRS complex. Is it normal in width, or is it wide? Are all complexes of the same configuration? 6. Examine the ST segment. Is it isoelectric, elevated, or depressed? 7. Identify the rhythm and determine its clinical significance. Is the patient symptomatic? (Check skin, neurological status, renal function, coronary circulation, and hemodynamic status/blood pressure.) Is the arrhythmia life-threatening? What is the clinical context? Is the arrhythmia new or chronic? Normal Sinus Rhythm Normal sinus rhythm (Fig A) is the normal rhythm of the heart. The impulse is initiated at the sinus node in a regular rhythm at a rate of 60 to 100 beats/minute. A P wave appears before each QRS complex. The PR interval is within normal limits and of equal duration (0.12 to 0.2 second), and the QRS is narrow (<0.12 second) unless an intraventricular conduction defect is present. Arrhythmias Originating at the Sinus Node Table 17-8 summarizes and compares ECG characteristics of sinus rhythms. SINUS TACHYCARDIA In sinus tachycardia, the sinus node accelerates and initiates an impulse at a rate of 100 times/minute or more (see Fig B). The upper limits of sinus tachycardia extend to 160 to 180 beats/minute. All other ECG characteristics, except for heart rate, are the same as in normal sinus rhythm. Sinus tachycardia usually is caused by factors relating to an increase in sympathetic tone. Stress, exercise, and stimulants such as caffeine and nicotine can produce this arrhythmia. Sinus tachycardia also is associated with such clinical problems as fever, anemia, hyperthyroidism, hypoxemia, heart failure, and shock. Drugs such as atropine, which blocks vagal tone, and the catecholamines (e.g., epinephrine, dopamine) also can produce this rhythm. The cause of the sinus tachycardia and the underlying state of the myocardium determine the prognosis. Sinus tachycardia alone is not a lethal arrhythmia but often signals an underlying problem that should be pursued. In addition, the rapid rate of sinus tachycardia increases oxygen demands on the myocardium and decreases the filling time of the ventricles. In individuals who already have depleted cardiac reserve, ischemia, or heart failure, the persistence of a fast rate may worsen the underlying condition. Treatment for sinus tachycardia usually is directed at eliminating the underlying cause. Specific measures may include sedation, oxygen administration, digitalis, and diuretics if heart failure is present, or propranolol if the tachycardia is caused by thyrotoxicosis. SINUS BRADYCARDIA Sinus bradycardia is defined as a rhythm with impulses originating at the sinus node at a rate of less than 60 beats/ minute (see Fig C). The rhythm (RR interval) is regular and all other parameters are normal. Sinus bradycardia is common among individuals of all ages and may be normal in highly trained athletes. It is present in both healthy and diseased hearts. It may be associated with sleep, severe pain, inferior wall MI, acute spinal cord injury, and certain drugs (e.g., digitalis, beta-blockers, verapamil, diltiazem). Slow heart rates are tolerated well in individuals with healthy hearts. In those with severe heart disease, however, the heart may not be able to compensate for a slow rate by increasing the volume of blood ejected per beat. In this situation, sinus bradycardia leads to a low cardiac output. No treatment is indicated unless symptoms are present. If the pulse is very slow and the patient is symptomatic, A B C D figure Sinus rhythms. (A) Normal sinus rhythm. (Heart rate = beats/min.) (B) Sinus tachycardia. (Heart rate < 60 beats/min.) (C) Sinus bradycardia. (Difference between shortest and longest RR interval > 0.12 second.) (D) Sinus arrhythmia. (Heart rate = beats/min.)

9 CHAPTER 17 Patient Assessment: Cardiovascular System 253 table 17-8 A Comparison of the Electrocardiographic Characteristics of Sinus Rhythms Normal Sinus Sinus Sinus Sinus Rhythm Tachycardia Bradycardia Arrhythmia Rate beats/min >100 beats/min <60 beats/min beats/min Rhythm Regular Regular Regular Irregular P waves Present, one per QRS Present, one per QRS Present, one per QRS Present, one per QRS PR interval <0.20 s, equal <0.20 s, equal <0.20 s, equal <0.20 s, equal QRS complex <0.12 s <0.12 s <0.12 s <0.12 s appropriate measures include atropine (to block the vagal effect) or cardiac pacing. SINUS ARRHYTHMIA Sinus arrhythmia is a disorder of rhythm (see Fig D) that is said to be present if the RR intervals on the ECG, from the shortest RR interval to the longest, vary by more than 0.12 second. This arrhythmia is caused by an irregularity in sinus node discharge, often in association with phases of the respiratory cycle. The sinus node rate gradually increases with inspiration and gradually decreases with expiration. Sinus arrhythmia is a normal phenomenon, seen especially in young individuals in the setting of lower heart rates. It also occurs after enhancement of vagal tone (e.g., with digitalis or morphine). Because it is a normal finding, sinus arrhythmia does not imply the presence of underlying disease. Symptoms are uncommon unless there are excessively long pauses between heart beats, and usually no treatment is required. SINUS ARREST AND SINOATRIAL BLOCK Sinus arrest is a disorder of impulse formation. The sinus node fails to form a discharge, producing pauses of varying lengths because of the absence of atrial depolarization. The P wave is absent, and the resulting PP interval is not a multiple of the basic PP interval. The pause ends either when an escape pacemaker from the junction or ventricles takes over or sinus node function returns. An SA block often is difficult to differentiate from sinus arrest on a surface ECG tracing. In SA block, the sinus node fires, but the impulse is delayed or blocked from exiting the sinus node. If the block is complete, the duration of the pause is a multiple of the basic PP interval (Fig ). Both arrhythmias may result from disruption of the sinus node by infarction, degenerative fibrotic changes, drugs (digitalis, beta-blockers, calcium channel blockers), or excessive vagal stimulation. These rhythms usually are transient and insignificant unless a lower pacemaker fails to take over to pace the ventricles. Treatment is indicated if the patient is symptomatic. The goal is to increase the ventricular rate, which may require the use of atropine or, in the presence of serious hemodynamic compromise, a pacemaker. SICK SINUS SYNDROME Sick sinus syndrome refers to a chronic form of sinus node disease (Fig ). Patients exhibit severe degrees of sinus node depression, including marked sinus bradycardia, SA block, or sinus arrest. Often, rapid atrial arrhythmias, such as atrial flutter or fibrillation ( tachycardia bradycardia syndrome ), coexist and alternate with periods of sinus node depression. Management of sick sinus syndrome requires control of the rapid atrial arrhythmias with drug therapy and, in selected cases, control of very slow heart rates, often requiring implantation of a permanent pacemaker. figure Sinoatrial block. The pause is a multiple of the basic PP interval.

10 254 PART IV CARDIOVASCULAR SYSTEM figure Sick sinus syndrome. Atrial fibrillation is followed by atrial standstill. A sinus escape beat is seen at the end of the strip. Atrial Arrhythmias PREMATURE ATRIAL CONTRACTION A premature atrial contraction (PAC) occurs when an ectopic atrial impulse discharges prematurely and, in most cases, is conducted in a normal fashion through the AV conducting system to the ventricles (Fig ). On the ECG tracing, the P wave is premature and may even be buried in the preceding T wave; it often differs in configuration from the sinus P wave. The QRS complex usually is of normal configuration. However, because of timing, the QRS complex may appear wide and bizarre if conducted with some degree of delay (aberrant PAC) or may not appear at all if the atrial impulse is blocked from being conducted to the ventricles (blocked PAC). A short pause, usually less than compensatory, is present (see later definition of premature ventricular contraction). Individuals of all ages experience PACs. PACs may occur in healthy individuals as a result of various stimuli, such as emotions, tobacco, alcohol, and caffeine. PACs also may be associated with rheumatic heart disease, ischemic heart disease, mitral stenosis, heart failure, hypokalemia, hypomagnesemia, medications, and hyperthyroidism. Alternatively, PACs may be a precursor to an atrial tachycardia, atrial fibrillation, or atrial flutter, indicating an increasing atrial irritability. They also may indicate an underlying condition (e.g., heart failure). Patients may have the sensation of a pause or skip in rhythm when PACs are present. No treatment is necessary in many cases. The patient should be monitored and frequency of premature beats documented. In addition, the patient should be assessed for underlying conditions and treated. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA Paroxysmal supraventricular tachycardia (PSVT) describes a rapid atrial rhythm occurring at a rate of 150 to 250 beats/ minute (Fig ). The tachycardia begins abruptly, in most instances with a PAC, and it ends abruptly. P waves may precede the QRS complex, but also may be hidden in figure Premature atrial contraction. figure Paroxysmal supraventricular tachycardia, which begins with a premature atrial contraction. the QRS complex or precede the T wave at faster rates. (If some of the P waves are not followed by a QRS complex, this is referred to as PSVT with block and usually is caused by digitalis toxicity.) The P waves may be negative in leads II, III, and avf because of retrograde conduction from the AV node to the atria. The QRS complex usually is normal unless there is an underlying intraventricular conduction problem. The rhythm is regular and the paroxysms may last from a few seconds to several hours or even days. The term PSVT is used to identify rhythms previously called paroxysmal atrial tachycardia and paroxysmal nodal or junctional tachycardia, rhythms similar in all respects except in their sites of origin. PSVT also is known as AV nodal reentrant tachycardia because the mechanism most commonly responsible for this arrhythmia is a reentrant circuit or chaotic movement at the level of the AV node. PSVT must be differentiated from other narrow QRS complex (supraventricular) tachycardias. Table 17-9 is a guide to the differential diagnosis. The following points favor the diagnosis of PSVT versus a sinus tachycardia: An atrial premature beat often initiates the rhythm. The tachycardia begins and terminates abruptly. The rate often is faster than a sinus tachycardia and tends to be more regular from minute to minute. In response to a vagal maneuver, such as carotid sinus massage, the ectopic tachycardia either is unaffected or reverts to a normal sinus rhythm; sinus tachycardia, however, slows slightly in response to increased vagal tone. Like PACs, PSVTs often occur in adults with normal hearts for the same reasons (e.g., emotions, tobacco, alcohol, caffeine). When heart disease is present, such abnormalities as rheumatic heart disease, acute MI, and digitalis intoxication may serve as the background for a PVST. Often the patient has no underlying heart disease and may experience only palpitations and some lightheadedness, depending on the rate and duration of the PSVT. If the patient has underlying heart disease, dyspnea, angina pectoris, and heart failure may occur as ventricular filling time, and thus cardiac output, is decreased. Vagal stimulation often terminates the PSVT, either through carotid massage or the Valsalva maneuver. If vagal stimulation is unsuccessful, IV adenosine is given. If adenosine is not effective in treating the arrhythmia, IV procainamide may be used. Cardioversion or overdrive pacing may be required if drug therapy is unsuccessful. Long-term prophylactic therapy may be indicated.

11 CHAPTER 17 Patient Assessment: Cardiovascular System 255 table 17-9 Differential Diagnosis of Narrow QRS Tachycardia Response to Type of SVT Onset Atrial Rate Ventricular Rate RR Interval Carotid Massage Sinus tachycardia Gradual beats/min PSVT Abrupt beats/min Same as sinus rate Usually same as atrial; block seen with digitalis toxicity and AV node disease Occurs with 2:1, 3:1, 4:1, or varied ventricular response Depends on ability of AV node to conduct atrial impulse; decreased with drug therapy Regular Regular, except at onset and termination Gradual slowing May convert to normal sinus rhythm Atrial flutter Abrupt beats/min Regular or regularly irregular Abrupt slowing of ventricular response; flutter waves remain Abrupt slowing of ventricular response; fibrillation waves remain Atrial fibrillation Abrupt beats/min Irregularly irregular ATRIAL FLUTTER Atrial flutter is a rapid atrial ectopic rhythm in which the atria fire at rates of 250 to 350 beats/minute (Fig ). The AV node functions as a gatekeeper, preventing too many impulses from reaching the ventricle. If the ventricles are stimulated 250 to 350 times per minute, they are unable to respond with effective contractions, and cardiac output is insufficient to sustain life. The AV node may allow only every second, third, or fourth atrial stimulus to proceed to the ventricles, resulting in what is known as a 2:1, 3:1, or 4:1 flutter block. The rapid and regular atrial rate produces sawtooth or picket-fence P waves on the ECG. It is usual for a flutter wave to be partially concealed in the QRS complex or T wave. The QRS complex exhibits a normal configuration except when aberrant conduction is present. When the ventricular rate is rapid, the diagnosis of atrial flutter may be difficult. Vagal maneuvers, such as carotid sinus massage or the administration of adenosine, increase the degree of AV block and allow recognition of flutter waves. Atrial flutter often is seen in the presence of underlying cardiac disease, including coronary artery disease, cor pulmonale, and rheumatic heart disease. If atrial flutter occurs in conjunction with a rapid ventricular rate, the ventricular chambers cannot fill adequately, resulting in varying degrees of hemodynamic compromise. Likewise, if atrial flutter is accompanied by a very slow ventricular rate, cardiac output is diminished. The loss of atrial kick, figure Atrial flutter. (Atrial rate = beats/min. P wave shows characteristic sawtoothed pattern.) because atrial contraction is not occurring, is also a concern. The lack of atrial kick can compromise cardiac output. Finally, without atrial contractions, thrombi can form on the walls of the atria. If these thrombi break loose, the result could be pulmonary embolus, cerebral embolus, or MI. Treatment goals for atrial flutter are to reestablish sinus rhythm or to achieve ventricular rate control. When the ventricular rate is rapid, prompt treatment to control the rate or revert the rhythm to a sinus mechanism is indicated. Drugs may be selected to slow the conduction of the impulses through the AV node, including ibutilide, calcium channel blockers, digoxin, amiodarone, or betaadrenergic blockers. Ibutilide also may be used to achieve pharmacological conversion of the rhythm. If pharmacological conversion is not successful, electrical cardioversion can be used. Synchronized cardioversion is especially useful in the prompt treatment of atrial flutter. The patient should be NPO before the procedure and receive sedation. (For a more detailed discussion of cardioversion, see Chapter 18.) If the patient has been experiencing atrial flutter for more than about 72 hours, anticoagulation may be needed before pharmacological or electrical conversion of the rhythm is attempted. Other modes of therapy may be indicated for the long-term management of atrial flutter, such as ablation, pacing, and implantable devices. ATRIAL FIBRILLATION Atrial fibrillation is defined as a rapid atrial ectopic rhythm, occurring with atrial rates of 350 to 500 beats/minute (Fig ). It is characterized by chaotic atrial activity with the absence of definable P waves. Instead, the P waves appear as small, quivering fibrillatory waves. Like atrial flutter, the ventricular rate and rhythm depend on the ability of the AV junction to function as a gatekeeper. If too many atrial stimuli pass through the AV junction, the ventricular response is rapid. If too few atrial stimuli pass through the AV junction, the ventricular response is slow. The ventricular rhythm is characteristically irregular.

12 256 PART IV CARDIOVASCULAR SYSTEM figure Atrial fibrillation. (Atrial rate = beats/min with a variable ventricular response. Characteristic atrial fibrillatory waves seen.) Although atrial fibrillation may occur as a transient arrhythmia in healthy young individuals, the presence of chronic atrial fibrillation is usually associated with underlying heart disease. One or both of the following are present in patients with chronic atrial fibrillation: atrial muscle disease or atrial distension together with disease of the sinus node. This rhythm commonly occurs in the setting of heart failure, ischemic or rheumatic heart disease, pulmonary disease, and after open heart surgery. Atrial fibrillation also is seen in congenital heart disease. The immediate clinical concern in patients with atrial fibrillation is the rate of the ventricular response. If the ventricular rate is too fast, end-diastolic filling time is decreased and cardiac output is compromised. If the ventricular rate is too slow, cardiac output may again be decreased. As in atrial flutter, patients with atrial fibrillation have lost AV synchrony and atrial kick, resulting in a compromised cardiac output. Patients also are at risk for the formation of mural thrombi and embolic events, such as stroke, MI, and pulmonary embolus. The treatment principles for atrial fibrillation are the same as those for atrial flutter. The goal of therapy is to achieve rate control or to convert the rhythm to sinus. Drug therapy as described for atrial flutter may be used. If a patient has chronic atrial fibrillation, anticoagulant therapy is added to the drug regimen to prevent an embolic event. Cardioversion is indicated for rhythm control when drug therapy fails or in the setting of hemodynamic compromise. Ablation, pacing, and implantable devices are among the therapy options. 1,2 MULTIFOCAL ATRIAL TACHYCARDIA Multifocal atrial tachycardia is a rapid atrial rhythm with varying P-wave morphology, resulting from the firing of three or more atrial foci (Fig ). The atrial rate exceeds 100 beats/minute, and the rhythm usually is irregular. The P waves vary in shape because of the multiple foci. The PR intervals may vary also, depending on the proximity of the focus to the AV node. The QRS complexes are normal unless an impulse is conducted with aberrancy. figure Multifocal atrial tachycardia. (The atrial rate exceeds 100 beats/min with three or more different P-wave morphologies.) This rhythm characteristically occurs in patients with severe pulmonary disease. Such patients often exhibit hypoxemia, hypokalemia, alterations in serum ph, or pulmonary hypertension. They usually manifest symptoms associated with the underlying disease rather than with the arrhythmia itself. Treatment is directed at controlling the underlying pulmonary disease and slowing the ventricular rate if necessary. Junctional Arrhythmias JUNCTIONAL RHYTHM A junctional rhythm, also known as a nodal rhythm, is a rhythm originating in the AV node. When the SA node fails to fire, the AV node usually takes control, but the rate is slower. The rate of a junctional rhythm ranges between 50 and 70 beats/minute. The P wave in the arrhythmia can have one of three possible configurations. 1. The AV node fires and the wave of depolarization travels backward (retrograde conduction) into the atria. The impulse from the AV node then moves forward into the ventricle. When this sequence occurs, the P wave appears as an inverted wave before a normal QRS complex (Fig A). 2. The retrograde conduction into the atria occurs at the same time as the forward conduction into the ventricles. The resulting rhythm strip shows an absent P wave with a normal QRS complex. In reality, the P wave is not absent. Instead, it is buried inside the QRS complex (see Fig B). 3. Forward conduction of the ventricles precedes retrograde conduction of the atria. When this sequence occurs, a normal QRS complex is followed by an inverted P wave (see Fig C). A junctional rhythm may be the result of hypoxia, hyperkalemia, MI, heart failure, valvular disease, drugs (digoxin, beta-blockers, calcium channel blockers), or any cause of SA node dysfunction. Patients with a junctional rhythm may become symptomatic as a result of the slower rate. Hypotension, decreased cardiac output, and decreased perfusion may occur. The benefit of AV synchrony and atrial kick may be lost when the atria are stimulated with or after ventricular depolarization. Treatment should be directed at the underlying cause. Symptomatic patients may require immediate treatment. The heart rate can be increased through the use of atropine or cardiac pacing. Interventions are also directed toward improving cardiac output. PREMATURE JUNCTIONAL CONTRACTIONS A premature junctional contraction (PJC) is an ectopic impulse from a focus in the AV junction, occurring prematurely, before the next sinus impulse (Fig ). As in all rhythms originating in the AV junction, the QRS complex is narrow (<0.12 second), reflecting normal AV conduction. On rare occasions, the QRS complex may be wide if the impulse is conducted aberrantly. The atria are depolarized in a retrograde fashion before, during, or after ventricular excitation, producing inverted P waves that may occur before, during, or after the QRS complex. As with PACs,

13 CHAPTER 17 Patient Assessment: Cardiovascular System 257 A B C figure Junctional rhythm. (A) A junctional rhythm in which the inverted P wave appears before a normal QRS complex. (B) A junctional rhythm in which the inverted P wave is buried inside the QRS complex. (C) A junctional rhythm in which the inverted P wave follows the QRS complex. PJCs may occur in healthy individuals or in those with underlying heart disease. Ischemia or infarction may activate an ectopic focus in the AV junction, as may stimulants, such as nicotine or caffeine, or pharmacological agents (e.g., digitalis). Frequent PJCs may indicate increasing irritability and may be a precursor of a junctional rhythm. Although usually figure Premature junctional contraction. asymptomatic, patients may experience a skipped beat. Treatment for PJCs is not necessary. Ventricular Arrhythmias PREMATURE VENTRICULAR CONTRACTIONS A premature ventricular contraction (PVC) is an ectopic beat originating prematurely at the level of the ventricles (Fig A). The beat is ventricular in origin and results in no electrical activity in the atria. As a result, no P waves appear. The ventricular depolarization does not travel through the normal rapid ventricular conduction system. Instead, ventricular conduction spreads more slowly through the Purkinje system, resulting in a wide QRS complex with a T wave that is opposite in direction to the QRS complex. A compensatory pause often follows the premature beat as the heart awaits the next stimulus from the sinus node. The pause is considered fully compensatory if the cycles of the normal and premature beats equal the time of two normal heart cycles.