Nursing Care of Patients with Cardiac Dysrhythmias PDF

4068_Ch25_499-520 15/11/14 1:34 PM Page 499 25 Nursing Care of Patients With Cardiac Dysrhythmias LINDA S. WILLIAMS LEARNING OUTCOMES 1. Describe how electrical activity flows through the heart. 2. List the six steps used for dysrhythmia interpretation. 3. Explain current medical treatments for ea...

4068_Ch25_499-520 15/11/14 1:34 PM Page 499 25 Nursing Care of Patients With Cardiac Dysrhythmias LINDA S. WILLIAMS LEARNING OUTCOMES 1. Describe how electrical activity flows through the heart. 2. List the six steps used for dysrhythmia interpretation. 3. Explain current medical treatments for each type of cardiac dysrhythmias. 4. Identify types of cardiac pacemakers and implantable cardioverter defibrillators and their uses. 5. Plan nursing care for patients with a dysrhythmia. 6. Plan nursing care for patients with an implanted device. KEY TERMS ablation (uh-BLAY-shun) atrial depolarization (AE-tree-uhl DEE-poh-lur-ih-ZAYshun) atrial systole (AE-tree-uhl SISS-tuh-lee) atrioventricular node (AE-tree-oh-ven-TRICK-yoo-lur NOHD) bigeminy (bye-JEM-ih-nee) bradycardia (BRAY-dih-KAR-dee-yah) bundle of His (BUN-duhl of HISS) cardioversion (KAR-dee-oh-VER-zhun) defibrillation (dee-FIB-ri-lay-shun) dysrhythmia (dis-RITH-mee-yah) electrocardiogram (ee-LECK-troh-KAR-dee-oh-GRAM) fluoroscopy (fluh-RAHS-kuh-pee) hyperkalemia (HIGH-per-kuh-LEE-mee-ah) hypomagnesemia (HIGH-poh-MAG-nuh-ZEE-mee-ah) isoelectric line (EYE-so-e-LECK-trick LINE) multifocal (MUHL-tee-FOH-kuhl) sinoatrial node (SIGH-noh-AY-tree-al NOHD) trigeminy (try-JEM-i-nee) unifocal (YOO-ni-FOH-cull) ventricular diastole (ven-TRICK-yoo-lar dye-AS-tuh-lee) ventricular repolarization (ven-TRICK-yoo-lar RE-pollahr-i-ZAY-shun) ventricular systole (ven-TRICK-yoo-lar SIS-tuh-lee) ventricular tachycardia (ven-TRICK-yoo-lar TACK-eeKAR-dee-yah) 499 4068_Ch25_499-520 15/11/14 1:34 PM Page 500 UNIT FIVE 500 Understanding the Cardiovascular System CARDIAC CONDUCTION SYSTEM The heart’s electrical conduction system initiates an impulse whose purpose is to stimulate the mechanical cells of the heart to contract (Fig. 25.1). Electrical activity can be viewed on a cardiac monitor or recorded on an electrocardiogram (ECG) tracing. The activity seen on an ECG does not necessarily mean that the mechanical cells of the heart ha ve contracted in response to the electrical impulse. So how can you verify heart muscle contraction and subsequent pumping of blood? By assessing the patient’s blood pressure and apical and peripheral pulses, you will have evidence to determine if cardiac contraction occurred. Do you recall what area of the conduction system is referred to as the normal pacemaker of the heart? Located in the upper posterior wall of the right atrium is the sinoatrial (SA) node. The SA node is the primary pacemaker of the heart because its inherent (built-in) rate is faster than those of the other conduction sites in the atrioventricular (AV) node or ventricles. It normally fires at a rate of 60 to 100 beats per minute (bpm). As a protective mechanism if the SA node slo ws or fails, other areas of the heart can initiate impulses to keep the heart beating. This mechanism is referred to as escape. The AV node has an inherent rate of 40 to 60 bpm. The body can usually function adequately with this rate. If the AV node is unable to initiate an impulse, then the ventricles can take over at 20 to 40 bpm. However, the ventricular rate of 20 to 40 bpm is not adequate to meet the body’s oxygen needs, so the patient begins to show signs of inadequate cardiac output such as dyspnea, abnormal vital signs, and changes in level of consciousness. Treatment is usually needed to reestablish a normal heart rate as soon as possible. After the SA node fires, the impulse spreads through the atria conduction system to the AV node, stimulating the atria to contract. This is known as atrial systole. The atrial contraction propels blood out of the atria and into the relaxed ventricles during ventricular diastole. At the AV node, the impulse is briefly delayed. Next the impulse travels down the bundle of His, which divides into right and left bundle branches through the Purkinje fibers. This stimulates both ventricles to contract upward from the apex of the heart, pushing blood to ward the arteries. This contraction is known as ventricular systole. Cardiac Cycle A cardiac cycle is the period from the beginning of one heartbeat to the be ginning of the ne xt. The cardiac cycle is the electrical representation of the impulse that stimulates contraction and relaxation of the atria and ventricles. Within the normal cardiac cycle, there is a P wave, a QRS complex, and a T wave (Fig. 25.2). ELECTROCARDIOGRAM The electrical activity of the heart is seen either with an ECG that shows the activity for that moment when the ECG is obtained or with continuous cardiac monitoring. Electrodes placed on the patient’s skin allow various views of the heart’s electrical activity to be seen. Each view of the heart is referred to as a lead. A 12-lead ECG provides 12 different views of the heart’s electrical acti vity, whereas an 18-lead ECG sho ws 18 views. For continuous monitoring of cardiac electrical activity, one lead providing a good view may be used, although R T wave Left atrium P wave SA node Right atrium AV node Right ventricle AV bundle (Bundle of His) Q Purkinje fibers S Left ventricle Left bundle branch Right bundle branch FIGURE 25.1 Conduction pathway of the heart. From Scanlon, V., & Sanders, T. (2015). Essentials of anatomy and physiology (7th ed.). Philadelphia: F.A. Davis, with permission. P-R Interval QRS ST Complex Segment QT FIGURE 25.2 Components of the cardiac cycle. From Scanlon, V., & Sanders, T. (2015). Essentials of anatomy and physiology (7th ed.). Philadelphia: F.A. Davis, with permission. 4068_Ch25_499-520 15/11/14 1:34 PM Page 501 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias with a five-electrode system, two views can be displayed at the same time. Continuous 12-lead monitoring can also be done. Specialized training, usually obtained by physicians, is required to interpret ECGs for normal and abnormal heart rhythms. By learning the characteristics of a normal heart rhythm and rules for common dysrhythmias, you will be able to report rhythm changes to your supervisor or the health care provider (HCP). LEARNING TIP Think of a 12- or 18-lead ECG as if you had a camera that you were using to take pictures (views) of an object such as an apple. To obtain views that showed you all of the areas of the apple—front, side, back, side—you would take a picture and then move the camera a little to get the view next to the one you had just taken. You would continue moving the camera until you had worked your way around the entire apple. This would then give you a view of the entire apple. This is what a 12- or 18-lead ECG does to allow viewing of the entire conduction system of the heart. 501 heavy vertical black lines (see Fig. 25.3). You will measure the waveforms horizontally from left to right on the graph paper . The height of waveforms (amplitude) is measured vertically. You have probably seen a heart monitor, perhaps on television, with a straight line displayed on it.This straight line, called the isoelectric line (baseline), occurs when there is no electrical current, or the positive and negative electrical activity is equal. The isoelectric line is seen when there are no positive or negative electrical wave deflections. When cardiac cycle electrical impulses (seen as waveforms) occur, they are either upward (positive) or downward (negative) from the isoelectric line. COMPONENTS OF A CARDIAC CYCLE P Wave The P wave is the first wave of the cardiac cycle and represents atrial depolarization. When the SA node f ires, the electrical impulse spreads from the right to left atrium. The normal P wave appears rounded. When compared with other waveforms, it looks lik e a small hill. Disorders that change atrial size cause alterations in P-wave shape and size. LEARNING TIP To make measuring waves easier: Electrocardiogram Graph Paper The intervals of each of the components of a cardiac c ycle can be measured in seconds of time on the ECG graph paper on which the heart rhythm is recorded. The graph paper is calibrated in a grid with small squares di vided into heavy lined blocks of 25, five squares wide and f ive squares high (Fig. 25.3). Each small square is 0.04 seconds wide. There are five small squares, which equal 0.20 seconds of time, horizontally between tw o 6 second strip 3 seconds 3 seconds • Identify the isoelectric line as you measure waveform tracings to help you determine the presence and type of wave. Place a straight edge along the isoelectric line so that it lays below this line, to then see any positive waves above the line; then lay the straight edge above the line to see any waves that fall below the line. • If possible, find a wave that begins on a line to make it visually easier to see the interval being measured (Fig. 25.4). • If the wave starts or ends in the middle of a small square, count it as one-half of a square, which is 0.02 seconds. Do not go smaller than one-half of a square. PR Interval 0.04 sec. 0.04 0.04 0.04 0.04 0.04 ⫽ 0.20 0.20 seconds FIGURE 25.3 Electrocardiogram recording paper time intervals. The PR interval (PRI) represents the time it takes the electrical impulse to travel from the SA node to the AV node. The PRI starts at the beginning of the P wave and ends at the beginning of the QRS complex. Counting the number of small squares horizontally that the interval covers and then multiplying by 0.04 determines the length of the PRI (see Fig. 25.4).The normal PRI is 0.12 to 0.20 seconds (three to five small squares). • WORD • BUILDING • dysrhythmia: dys—difficult or abnormal + rhythm—rhythm 4068_Ch25_499-520 15/11/14 1:34 PM Page 502 502 UNIT FIVE Understanding the Cardiovascular System QRS Interval The QRS interval represents the time it takes for the electrical impulse to travel from the AV node rapidly through the ventricles. To measure the QRS interv al, count the number of squares from the wave that starts the QRS complex to the end of the wave that completes the QRS complex. For example, when a Q, R, and S are present, measure from the beginning of the Q wave to the end of the S wave (Fig. 25.6). If there is an R and an S present, measure from the beginning of the R to the end of the S. But if there is only an R present, measure from the beginning of the R to the end of the R. The normal QRS interval is 0.06 to 0.10 seconds (1.5–2.5 boxes). T Wave PR interval FIGURE 25.4 PR interval. This PR interval covers four squares. Each square is 0.04 seconds; 4 × 0.04 = 0.16 seconds. LEARNING TIP To remember a normal PRI, you can use the “R” to think of normal respiratory rate and then add a decimal in front. A normal respiratory rate is 12 to 20 per minute, and a normal PRI is 0.12 to 0.20 seconds. The T wave represents ventricular repolarization, the resting state of the heart, when the v entricles are filling with blood and preparing to receive the next impulse. It is a nicely rounded w ave, and, in our size comparisons of other waves, it is a medium-size hill. In most leads, the T wave is an upw ard (positive) deflection, after the QRS complex, and ends with a return to the isoelectric line. An inverted (downward) T wave can indicate coronary ischemia (Fig. 25.7). QT Interval The QT interval measures the time from the start of the Q wave to the end of the T wave (see Fig. 25.2). This represents the time for v entricular depolarization and QRS Complex The QRS complex represents ventricular depolarization and is composed of three waves: Q, R, and S. The Q wave is the first downward deflection after the P w ave. The R w ave is the first upward deflection after the P wave. The S wave is the first negative deflection after the R wave (see Fig. 25.2). The S wave ends when it returns to the isoelectric line (this is why locating the isoelectric line is helpful when f irst learning to identify waves). It is important to note that all three w aves are not always present in e very QRS comple x. Even with absent waves, the QRS is still referred to as the QRS complex and can be considered normal (Fig. 25.5). The QRS complex is larger than the P wave because the ventricles have more muscle mass, so it looks like a mountain compared with the size of other waveforms. R QRS R FIGURE 25.6 QRS interval. This QRS interval covers two and one-half squares. Each square is 0.04 seconds. One-half square is 0.02 seconds; 2.5 × 0.04 = 0.10 seconds. A Q S B S R C D QS FIGURE 25.5 (A) QRS complex with a Q wave. (B) QRS complex without a Q wave. (C) QRS complex without a Q or an S wave. (D) QRS complex with no R wave. The wave present is called a QS because it is not known if it is a Q or an S. A B FIGURE 25.7 (A) T wave with positive deflection. (B) T wave with inverted, negative deflection, indicating ischemia. 4068_Ch25_499-520 15/11/14 1:34 PM Page 503 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias repolarization. Normal ranges, 0.34 to 0.43 seconds, v ary based on gender, heart rate, and age (a QT chart for identifying normal values is used). Prolonged or shortened QT intervals can lead to v entricular dysrhythmias. Abnormal intervals may be due to genetic causes, heart conditions, electrolyte imbalances, or medications that can prolong the QT interval. U Wave The U wave is small and often not seen. It occurs shortly after the T wave. It is most prominent in patients with hypokalemia (low serum potassium level; Fig. 25.8). ST Segment The ST segment reflects the time from completion of a contraction (depolarization) to recovery (repolarization) of myocardial muscle for the next impulse. The ST segment starts at the end of the QRS and ends at the beginning of the T wave (Fig. 25.9A). The ST segment is examined when patients experience chest pain. If a patient has nontransmural ischemia, the ST se gment can become inverted or depressed (Fig. 25.9B). With transmural ischemia, the ST segment can elevate from the isoelectric line (Fig. 25.9C). TABLE 25.1 SIX-STEP PROCESS FOR DYSRHYTHMIA INTERPRETATION After answering the questions listed here, you should be able to name the patient’s dysrhythmia. Step Topic Questions 1 Regularity of Is the rhythm regular? rhythm Irregular? Is there a pattern to the irregularity? 2 Heart rate What is the heart rate? 3 P waves Is there one P wave in front of every QRS complex? Is the atrial rate the same as the ventricular rate? Are the P waves smooth, rounded, and upright? 4 PR interval Is the PR interval normal and constant? Does the PR interval vary? 5 QRS interval Is the QRS interval normal and constant? Do the QRS complexes all look alike? 6 QT interval Is the QT interval normal? INTERPRETATION OF CARDIAC RHYTHMS Six-Step Process for Dysrhythmia Interpretation An orderly, systematic method for interpreting ECG rhythms should be used to increase understanding of items to examine and ensure nothing is overlooked. Six steps are examined in this process (Table 25.1). Use the findings of the first five steps to identify the ECG rhythm according to the five rules for each dysrhythmia. Then measure the QT 503 interval so that abnormalities can be reported to the HCP . A 6-second ECG tracing is used when interpreting rhythms (see Fig. 25.3). Step 1. Regularity of the Rhythm FIGURE 25.8 Various locations where U waves may appear. A ST B C FIGURE 25.9 (A) ST segment. (B) ST segment inverted or depressed. (C) ST segment elevated. The regularity of the rhythm can be determined by looking at the R-to-R spacing on the ECG (Fig. 25.10). The same spacing between each R to R, with a rare v ariation of no greater than two small squares, is seen in a normal rhythm. To determine the regularity of a rhythm, count the number of small squares between each R w ave, which normally should remain the same, or use a caliper (two-sided, movable metal instrument with sharp points) to measure the R-to-R spacing. To use a caliper for measuring R w aves, one point is placed on an R w ave, and the other point is placed in the same spot on the next R wave. Then, without changing the distance between the caliper points, move the caliper from R wave to R wave across the ECG tracing (also kno wn as an ECG strip) to see if R waves are regularly spaced. If the distance is the same, the rhythm is re gular. If the distance varies, the rhythm is irregular. This can be further described by these fun terms: an irre gular rhythm can be re gularly irregular, which means it has a predictable pattern of irregularity, or irre gularly irregular, without an y pattern of irregularity. 4068_Ch25_499-520 15/11/14 1:34 PM Page 504 UNIT FIVE 504 Understanding the Cardiovascular System A FIGURE 25.10 Normal cardiac waves are equal distances apart. (A) R to R waves. (B) P to P waves. B calculate the 1-minute heart rate. It is readily available in locations where these calculations are routinely done. 2. Six-second method: the 6-second method is used for irregular rhythms. It may also be used when a rapid estimate of a regular rhythm is needed, although it is not the most accurate method for regular rhythms. At the top of ECG graph paper are vertical marks at 3-second intervals (see Fig. 25.3). Count the number of R waves in a 6-second strip (three vertical marks) and multiply the total by 10 (the number of 6-second time periods in a minute) to obtain the beats per minute (6 seconds × 10 = 60 seconds or 1 minute; Fig. 25.12). LEARNING TIP If a caliper is not available, a piece of paper can be placed on the ECG tracing. A mark can be made on the paper at the top of one R wave and another mark made on the paper at the top of the next R wave. The marks on the paper can then be moved across the R-to-R intervals on the tracing ( just as caliper points would be) to determine the rhythm regularity. Step 2. Heart Rate After rhythm regularity is determined, a 1-minute heart rate is calculated. One of the two following methods is used: 1. Count the number of small (0.04-second) squares between two R waves and divide that number into 1500. This gives the beats per minute, because 1500 small squares equals 1 minute (Fig. 25.11). This method is used only for regular rhythms and is very accurate. A rate meter is a visual paper copy of this mathematical calculation for an entire 6-second ECG tracing that the nurse can view to Step 3. P Waves The P w aves on the ECG tracing are e xamined to see if (1) there is one P wave in front of every QRS, (2) the P waves are regularly occurring, and (3) the P waves all look alike (see Fig. 25.10). If all of the P waves meet these criteria, they are considered normal. If they do not, further examination of the tracing is necessary to determine the dysrhythmia. Step 4. PR Interval All PR intervals are measured to determine whether they are normal (0.12–0.20 seconds) and constant. If the PRI is found FIGURE 25.11 Rhythm regular: Count the small squares between two of the R waves and divide into 1500: 1500/25 = 60 beats per minute. Alternatively, count the large squares between two of the R waves and divide into 300: 300/5 = 60 beats per minute. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. 1 2 3 4 5 6 7 FIGURE 25.12 Rhythm irregular: Counting R waves in a 6-second strip. There are six R waves in this 6-second strip, and 6 × 10 = 60 beats per minute. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. 4068_Ch25_499-520 15/11/14 1:34 PM Page 505 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias to vary, it is important to note whether there is a pattern to the variation. Step 5. QRS Interval The QRS intervals are measured to determine whether the y are all within normal range (0.06–0.10 seconds). Abnormal QRS complexes require further examination. Step 6. QT Interval Finally, the QT interval is measured to ensure that it is not shortened or prolonged, which can lead to dysrhythmias. Abnormal QT intervals should be reported to the HCP. NORMAL SINUS RHYTHM 505 system, resulting in abnormal conduction (as in heart block or b undle branch blocks). See www.heart.org for American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. Dysrhythmias Originating in the Sinoatrial Node Rhythms arising from the SA node are referred to as sinus rhythms. Disturbances in conduction from the SA node can cause irregular rhythms or abnormal heart rates. Dysrhythmias arising from the SA node are rarely dangerous. Patients, especially those with heart, lung, or kidne y disease, who cannot tolerate a rapid or slow heart rate, can require treatment. Description Normal sinus rhythm (NSR) is the heart’ s normal rhythm (Fig. 25.13). It originates in the SA node and has complete, regular cardiac cycles at 60 to 100 bpm. NORMAL SINUS RHYTHM RULES 1. Rhythm: regular 2. Heart rate: 60 to 100 bpm 3. P waves: rounded, upright, precede each QRS complex, alike 4. PR interval: 0.12 to 0.20 seconds 5. QRS interval: less than or equal to 0.10 seconds. LEARNING TIP The origin and the type of a problem are used to name a dysrhythmia. Let’s name a slow dysrhythmia that originates in the sinoatrial node. The origin is sinus and the type of problem (slow rate) is bradycardia = sinus bradycardia. The term normal is not used because there is a problem. So what would a fast dysrhythmia originating in the SA node be called? Yes! Sinus tachycardia. DYSRHYTHMIAS Two terms are used for rhythm disturbances: arrhythmia (irregularity or loss of rhythm of the heartbeat) and dysrhythmia (abnormal, disordered, or disturbed rhythm). These two terms are used interchangeably, but dysrhythmia is the most accurate term for the discussion of most abnormal rhythms. Several mechanisms can cause a dysrhythmia. Examples of these mechanisms are a disturbance in the formation of an impulse and a disturbance in the conduction of the impulse. When impulse formation is disturbed, the impulse may arise from the atria, the AV node, or the v entricles rather than the SA node. This disturbance can be seen as an increased or decreased heart rate, early or late beats, or atrial or v entricular fibrillation. With a disturbance in conduction, there may be normal formation of the impulse, but it becomes block ed within the electrical conduction FIGURE 25.13 Normal sinus rhythm. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. Sinus Bradycardia Bradycardia is a rate slower than 60 bpm that can be asymptomatic or symptomatic (usually belo w 50 bpm). Sinus bradycardia has the same cardiac cycle components as NSR. The only difference between the two is a slower rate caused by fewer impulses originating from the SA node (Fig. 25.14). Do you see that the term sinus bradycardia tells you this difference? The name says the impulse is coming from the sinus node (sinus) but at a slower rate than normal (bradycardia). See, it is easy to understand what is happening in the dysrhythmia when you look at what the name is telling you. • WORD • BUILDING • bradycardia: bradys—slow + kardia—heart 4068_Ch25_499-520 15/11/14 1:34 PM Page 506 506 UNIT FIVE Understanding the Cardiovascular System FIGURE 25.14 Sinus bradycardia. Heart rate is 56. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. ETIOLOGY. Medications such as digoxin (Lanoxin) as well as myocardial infarction (MI) and electrolyte imbalances can cause bradycardia. Well-conditioned athletes can also ha ve slower heart rates because their hearts work efficiently. SINUS BRADYCARDIA RULES. 1. Rhythm: regular 2. Heart rate: less than 60 bpm 3. P waves: smoothly rounded, precede each QRS complex, alike 4. PR interval: 0.12 to 0.20 seconds 5. QRS interval: less than or equal to 0.10 seconds. SIGNS AND SYMPTOMS. With symptomatic bradycardia decreased BP, respiratory distress, diminished or absent peripheral pulses, fatigue, or syncope can occur. THERAPEUTIC MEASURES. Asymptomatic bradycardia does not require treatment. Observe the patient for symptom development, while the underlying cause is identified for correction. For the symptomatic patient, treatment is begun as the cause is corrected. Treatment can include intra venous (IV) atropine, or infusions of dopamine or epinephrine or transcutaneous pacing if atropine is ineffective (Table 25.2). Transvenous pacing can be considered, if needed. Sinus Tachycardia Tachycardia is defined as a heart rate greater than 100 bpm that originates from the SA node. Sinus tachycardia has the same components as NSR e xcept the rate is f aster (Fig. 25.15). ETIOLOGY. Sinus tachycardia causes include physical activity; hemorrhage; shock; medications such as epinephrine, atropine, or nitrates; dehydration; fever; MI; electrolyte imbalance; fear; and anxiety. Tachycardia occurs as a compensatory mechanism for hypoxia when additional cardiac output is needed to deliver oxygen to tissues. SINUS TACHYCARDIA RULES. 1. Rhythm: regular 2. Heart rate: 101 to 180 bpm 3. P waves: rounded, precede each QRS complex, alike 4. PR interval: 0.12 to 0.20 seconds 5. QRS interval: less than or equal to 0.10 seconds. TABLE 25.2 MEDICATIONS USED TO TREAT DYSRHYTHMIAS Medication Class/Action Examples Nursing Implications Anticoagulant Increases clotting time. Reduces risk of blood clots in AF. warfarin (Coumadin) Monitor INR regularly. Monitor for bruising and bleeding. Acetaminophen (Tylenol) used instead of aspirin during therapy. Antidote: vitamin K. No regular monitoring. apixaban (Eliquis), dabigatran (Pradaxa), rivaroxaban (Xaletro) Antidysrhythmics Inhibit ventricular dysrhythmias, atrial fibrillation, atrial flutter. Inhibits atrial fibrillation, atrial flutter. amiodarone (Cordarone, Pacerone) Contraindicated in AV block or pregnancy. Obtain baseline vital signs and ECG. Monitor for toxicity. Avoid grapefruit juice with oral form. dronedarone (Multaq) Less toxicity than amiodarone. Contraindicated in heart failure. 4068_Ch25_499-520 15/11/14 1:34 PM Page 507 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias 507 TABLE 25.2 MEDICATIONS USED TO TREAT DYSRHYTHMIAS—cont’d Medication Class/Action Anticholinergic Increases heart rate. Treats symptomatic bradycardia, asystole. Beta Blockers Decrease myocardial contractility. Controls rate in sinus tachycardia, PAC, atrial flutter, atrial fibrillation, PVC. Calcium Channel Blocker Decreases myocardial contractility and depresses conduction system. Controls rate in sinus tachycardia, atrial flutter, and atrial fibrillation. Examples Nursing Implications atropine Contraindicated in angle closure glaucoma. atenolol (Tenormin), metoprolol succinate (Lopressor, Toprol XL) Check apical pulse and BP before giving. If pulse <60 bpm, BP less than 100 mm Hg systolic, notify HCP. Instruct patient to rise slowly and not stop drug abruptly. amlodipine (Norvasc) Assess apical pulse and blood pressure. If BP <90 mm Hg systolic or apical rate less than 60 bpm, notify HCP. Administer before meals and at bedtime. Inotrope—Cardiac Glycoside (Positive Inotrope and Negative Chronotrope) Take apical pulse for 1 minute; if less than Slows heart rate. Digoxin (Lanoxicaps, 60 bpm, notify HCP. Maintains sinus rhythm for Lanoxin) Therapeutic digoxin levels: 0.5–2 mg/mL. sinus tachycardia, atrial Monitor drug level and electrolytes (hypokalemia, flutter, atrial fibrillation. hypomagnesemia, hypercalcemia increase toxicity). Vasopressors Cardiac stimulation, vasoconstriction, bronchodilation. Treats asystole, ventricular tachycardia, ventricular fibrillation, symptomatic bradycardia. epinephrine (Adrenalin) Contraindicated with nonselective beta blockers. Vasoconstricts. Reduces urine volume. Single dose may replace dose of epinephrine. Treats pulseless ventricular tachycardia, ventricular fibrillation, asystole. vasopressin (Pitressin) Avoid IV site extravasation because of risk of necrosis and gangrene. Increases cardiac output and blood pressure. Treats bradycardia. dopamine Monitor blood pressure. Note. INR = international normalized ratio; PAC = premature atrial contraction; PVC = premature ventricular contractions. SIGNS AND SYMPTOMS. Sinus tachycardia can be asymptomatic. But if the rate is v ery rapid (usually >150 bpm) and sustained for long periods, the patient may experience angina, dyspnea, syncope, or tachypnea. Older patients can become symptomatic more rapidly than younger patients (“Gerontological Issues—Dysrhythmia Risk”). Patients with MI might not tolerate a rapid heart rate and have more severe symptoms because cardiac workload is increased. 4068_Ch25_499-520 15/11/14 1:34 PM Page 508 508 UNIT FIVE Understanding the Cardiovascular System FIGURE 25.15 Sinus tachycardia. Heart rate is 115. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. THERAPEUTIC MEASURES. If stable, obtain an ECG and treat the cause. Medications such as adenosine, calcium channel blockers, or beta block ers can be used to slo w the heart rate (when ≥150 bpm; see Table 25.2). The treatment goal is to decrease the heart’s workload and resolve the cause, which then usually corrects the tachycardia. For example, if the patient is hemorrhaging, immediate intervention is needed to stop the bleeding and restore normal blood volume. Once normal blood volume is restored, the heart rate should return to normal. Gerontological Issues Dysrhythmia Risk Factors that increase the risk of dysrhythmias in older adults include the following: • Digitalis toxicity (most common) • Hypokalemia • Acute infection • Hemorrhage • Angina • Coronary insufficiency or cardiomyopathy (exercise, stress) • Thickness of the heart tissue • Sleep apnea • Hypothyroidism or hyperthyroidism. Dysrhythmias that occur most often in older adults include the following: • Atrial fibrillation (atria beating 400–700 times per minute) • Sick sinus syndrome (alternating episodes of bradycardia, NSR, tachycardia, and periods of long sinus pause) • Heart block (delayed or blocked impulses to the atria or ventricles) Age-related effects of dysrhythmias include the following: • Weakness • Fatigue • Forgetfulness • Palpitations • Dizziness • Hypotension • Bradycardia • Syncope • Dyspnea or shortness of breath • Delayed capillary refill • Diaphoresis • Anxiety and fear • Nausea and vomiting • Stroke Older adults are especially sensiti ve to changes in heart rate that increase the heart’s workload. Whenever the heart works harder, as in tachycardia, the cardiac cells require more oxygen to function properly . Older adults have less ability to adapt to sudden changes or stressors, and they may not be able to tolerate tachycardia for very long. Any new-onset tachycardia in an older patient should be reported promptly. LEARNING TIP Tachycardia is often the first sign of hemorrhage. It is a compensatory mechanism to maintain cardiac output. If a patient develops sudden tachycardia, consider whether hemorrhage could be the cause, such as in postoperative patients, patients with gastrointestinal bleeding or cancer, or trauma patients. The bleeding may be external, or it may be internal and therefore not visible. Apply pressure to the site if the bleeding is obvious. Monitor the patient and report the tachycardia and any obvious bleeding promptly. Dysrhythmias Originating in the Atria As previously discussed, all areas of the heart can initiate an impulse. The SA node is the primary pacemak er, but if the atria initiate impulses faster than the SA node, they become the primary pacemak er. Atrial rhythms are usually faster than 100 bpm and can exceed 200 bpm. When an impulse originates outside the SA node, the P waves produced look different (flatter, notched, or peaked) from the rounded P waves from the SA node. This indicates that the SA node is not controlling the heart rate. These atrial impulses travel to the ventricles to initiate a normal QRS complex after each P wave. 4068_Ch25_499-520 15/11/14 1:34 PM Page 509 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias 509 SIGNS AND SYMPTOMS. Premature atrial contractions can LEARNING TIP • If a QRS complex measures less than or equal to 0.10 seconds and a dysrhythmia is present, the problem originated above the ventricles. This is known as a supraventricular (above the ventricle) dysrhythmia. • Ventricular originating dysrhythmias produce wide QRS complexes that are greater than 0.10 seconds. occur in healthy individuals, as well as in the patient with a diseased heart. No symptoms are usually present. If man y PACs occur in succession, the patient may report the sensation of palpitations. THERAPEUTIC MEASURES. PACs are usually not dangerous, and often no treatment is required other than correcting the cause. Frequent PACs indicate atrial irritability, which may worsen into other atrial dysrhythmias. Beta block ers can be given to a patient having frequent PACs to slow the heart rate (see Table 25.2). Atrial Flutter Premature Atrial Contractions The term premature refers to an “early” beat. When the atria fire an impulse before the SA node fires, a premature beat results. If the underlying rhythm is NSR, the distance between R waves is the same e xcept where the early beat occurs. When looking at the ECG strip, a shortened R-to-R interv al is seen where the premature beat occurs.The R wave preceding the premature atrial contraction (PAC) and the PAC’s R wave are close together, followed by a pause, with the ne xt beat being regular (Fig. 25.16). ETIOLOGY. Causes of PACs include hypoxia, cigarette smok- ing, stress, myocardial ischemia, enlar ged atria in valvular disorders, medications (such as digoxin), electrolyte imbalances, atrial fibrillation onset, and heart failure. PREMATURE ATRIAL CONTRACTIONS RULES. 1. Rhythm: premature beat interrupts underlying rhythm where it occurs 2. Heart rate: depends on the underlying rhythm; if NSR, 60 to 100 bpm 3. P waves: early beat is abnormally shaped 4. PR interval: usually appears normal, but premature beat could have shortened or prolonged PR interval 5. QRS interval: less than or equal to 0.10 seconds (indicates normal conduction to ventricles). FIGURE 25.16 Premature atrial contractions (PACs). In atrial flutter, the atria contract, or flutter, at a rate of 250 to 350 bpm. The very rapid P w aves appear as flutter, or F waves, on ECG and appear in a sawtoothed pattern. Some of the impulses get through the AV node and reach the ventricles, resulting in normal QRS comple xes. There can be from two to four F waves between QRS complexes. If impulses pass through the AV node at a consistent rate, the rhythm is regular (Fig. 25.17). The classic characteristics of atrial flutter are more than one P wave before a QRS complex, a sawtoothed pattern of P waves, and an atrial rate of 250 to 350 bpm. ETIOLOGY. Causes of atrial flutter include rheumatic or ischemic heart diseases, congestive heart failure (CHF), hypertension, pericarditis, pulmonary embolism, and postoperative coronary artery bypass surgery. Many medications can also cause this dysrhythmia. ATRIAL FLUTTER RULES. 1. Rhythm: atrial rhythm regular; ventricular rhythm regular or irregular depending on consistency of AV conduction of impulses 2. Heart rate: ventricular rate varies 3. P waves: flutter or F waves with sawtoothed pattern 4. PR interval: none measurable 5. QRS interval: less than or equal to 0.10 seconds. PAC PAC Flutter waves FIGURE 25.17 Atrial flutter. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. 4:1 4068_Ch25_499-520 15/11/14 1:34 PM Page 510 510 UNIT FIVE Understanding the Cardiovascular System SIGNS AND SYMPTOMS. The presence of symptoms in atrial flutter depends on the v entricular rate. If the v entricular rate is normal, usually no symptoms are present. If the rate is rapid, the patient may experience palpitations, angina, or dyspnea. THERAPEUTIC MEASURES. The ventricular rate and cardiac out- put guide treatment. The goal is to control the ventricular rate with conversion to NSR. For an unstable patient with a rapid ventricular rate, synchronized cardioversion (electrical shock) is used. Rapid atrial pacing may also stop the atrial flutter . Medications can be used to control the ventricular rate such as calcium channel blockers (see Table 25.2). Antiarrhythmic medications are used to convert atrial flutter. To terminate the atrial flutter in symptomatic patients, a radiofrequency catheter ablation (usually in the right atrium) may be done. LEARNING TIP AF is easy to identify based on its two classic characteristics: a lack of identifiable P waves and an irregularly irregular rhythm (R waves). SIGNS AND SYMPTOMS. With AF, most patients feel the ir- regular rhythm. Many describe it as palpitations or a skipping heartbeat. A patient’s radial pulse may be faint because of a decreased stroke volume (volume of blood ejected with each contraction). If the ventricular rhythm is rapid and sustained, the patient can go into left-sided heart failure. THERAPEUTIC MEASURES. The focus of AF treatment is to Atrial Fibrillation In atrial fibrillation (AF), the atrial rate is extremely rapid and chaotic. An atrial rate of 350 to 600 bpm can occur. However, the AV node blocks most of the impulses, so the v entricular rate is much lower than the atrial rate. There are no definable P waves because the atria are fibrillating, or quivering, rather than beating effectively. No P waves can be seen or measured. A wavy pattern is produced on the ECG. Because the atrial rate is so irregular and only a fe w of the atrial impulses are allowed to pass through the AV node, the R waves are irregular. The ventricular rate varies from normal to rapid. AF can be self-limiting, persistent, or permanent, which doubles the risk of death. Strok e risk is increased due to thrombus formation in the atria from blood stasis caused by poor emptying of blood from the quivering atria (Fig. 25.18). ETIOLOGY. Causes of AF include aging (increases after age 60 and is the most common sustained dysrhythmia), history of cigarette smoking, rheumatic or ischemic heart diseases, heart failure, hypertension, pericarditis, pulmonary embolism, and postoperative coronary artery bypass surgery and some medications. ATRIAL FIBRILLATION RULES. 1. Rhythm: irregularly irregular 2. Heart rate: atrial rate not measurable; ventricular rate under 100 is controlled response; greater than 100 is rapid ventricular response 3. P waves: no identifiable P waves 4. PR interval: none can be measured because no P waves are seen 5. QRS interval: less than or equal to 0.10 seconds. control rate, prevent thromboembolism, and restore normal rhythm. If the patient is unstable, synchronized cardioversion is done immediately to try to return the heart to NSR. For the patient who is stable, medications to control the ventricular rate such as beta block ers, calcium channel blockers, or digoxin are used (see Table 25.2). Anticoagulant therapy is given to reduce thrombi, which can cause a stroke. Pharmacological or electrical cardioversion may be performed to convert the rhythm after sufficient anticoagulation (about 3 weeks). Rhythm control medications such as sodium or potassium channel blockers are used to restore and maintain NSR. If kno wn, the underlying cause of AF is treated. For patients with AF who do not respond to medications or electrical cardioversion other therapies can be used. Catheter Ablation. To isolate impulses coming from the pul- monary veins (most AF impulses arise from pulmonary veins) or AV node, catheter ablation may be used to cure AF. Intracardiac echocardiography maps the area of the heart requiring treatment. Then released ener gy such as radiofrequency waves create lesions either on all four pulmonary veins or near the AV node that heal and scar to block pathways for future impulses. Postprocedural care is similar to postangioplasty or postcardiac catheterization care (see Chapter 21). Surgery. The MAZE procedure is often done as minimally invasive robotic-guided surgery. Incisions are made in the • WORD • BUILDING • ablation: ab—away from + lat—carry Irregular R-R intervals FIGURE 25.18 Atrial fibrillation. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. 4068_Ch25_499-520 15/11/14 1:34 PM Page 511 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias atria that create a “maze,” or route, for electrical impulses to travel to the AV node. These impulses cannot go of f course because scar tissue surrounds the incision sites. Premature ventricular contractions (PVCs) originate in the ventricles from an ectopic focus (a site other than the SA node). The ventricles are irritable and fire prematurely, before the SA node does. When the ventricles fire first, the impulses are not conducted normally through the electrical pathw ay. This results in a wide (>0.10 seconds), bizarre QRS complex on an ECG (Fig. 25.19). PVCs can occur in different shapes. The shape of the PVC is referred to as unifocal (one focus) if all the PVCs look the same because they come from the same irritable v entricular area. Multifocal PVCs do not all look the same because they are originating from several irritable areas in the v entricle. There can be several repetitive cycles or patterns of PVCs: • Bigeminy is a PVC that occurs every other beat (a normal beat and then a PVC; Fig. 25.20). • Trigeminy is a PVC that occurs every third beat (two normal beats and then a PVC). • Quadrigeminy is a PVC that occurs every fourth beat (three normal beats and then a PVC). • When two PVCs occur together, they are referred to as a couplet (pair). ETIOLOGY. Use of caffeine or alcohol, anxiety, hypokalemia, B PREMATURE VENTRICULAR CONTRACTION RULES. 1. Rhythm: depends on the underlying rhythm; PVC usually interrupts rhythm 2. Heart rate: depends on underlying rhythm 3. P waves: absent before PVC QRS complex 4. PR interval: none for PVC 5. QRS interval: if PVC, is greater than 0.10 seconds; T wave is in the opposite direction of QRS complex (i.e., QRS upright, T downward; or QRS downward, T upright). SIGNS AND SYMPTOMS. PVCs may be felt by the patient and are described as a skipped beat or palpitations.With frequent PVCs, cardiac output can be decreased, leading to f atigue, dizziness, or more severe dysrhythmias. THERAPEUTIC MEASURES. Treatment depends on the type and number of PVCs and whether symptoms are produced. Occasional PVCs do not usually require treatment. However, if the PVCs are more than six per minute, re gularly occurring, multifocal, falling on the T wave (known as “R-on-T phenomenon,” which can trigger life-threatening dysrhythmias), or caused by an acute MI, they can be dangerous. Antidysrhythmic PVC A PVC • If three or more PVCs occur in a row, it is referred to as a run of PVCs or ventricular tachycardia. cardiomyopathy, ischemia, and MI are common causes of PVCs. Ventricular Dysrhythmias FIGURE 25.19 Premature ventricular contractions. (A) Unifocal PVCs arise from one area and look the same. (B) Multifocal PVCs arise from different foci and may look different. Modified from Jones, S. A. (2008). ECG success: Exercises in ECG interpretation. Philadelphia: F.A. Davis, with permission. 511 PVC PVC PVC PVC PVC PVC PVC FIGURE 25.20 Bigeminal premature ventricular contractions. PVC 4068_Ch25_499-520 15/11/14 1:34 PM Page 512 512 UNIT FIVE Understanding the Cardiovascular System drugs that depress myocardial acti vity are used to treat PVCs such as amiodarone and beta blockers (see Table 25.2). CRITICAL THINKING Ventricular Tachycardia Mrs. Mae The occurrence of three or more PVCs in a row is referred to as ventricular tachycardia (VT) (Fig. 25.21). VT results from the continuous firing of an ectopic v entricular focus. During VT, the ventricles rather than the SA node become the pacemaker of the heart. The pathway of the v entricular impulses is different from normal conduction, producing a wide (>0.10 seconds), bizarre QRS complex. ETIOLOGY. Myocardial irritability, MI, and cardiomyopathy are common causes of VT. Respiratory acidosis, hypokalemia, digoxin toxicity, cardiac catheters, and pacing wires can also produce VT. VENTRICULAR TACHYCARDIA RULES. 1. Rhythm: usually regular, may have some irregularity 2. Heart rate: 150 to 250 ventricular bpm; slow VT is below 150 bpm 3. P waves: absent 4. PR interval: none 5. QRS interval: greater than 0.10 seconds. SIGNS AND SYMPTOMS. The seriousness of VI is determined by the duration of the dysrhythmia. Sustained VT compromises cardiac output. Patients are aware of a sudden onset of rapid heart rate and can experience dyspnea, palpitations, and lightheadedness. Angina commonly occurs. The severity of symptoms can increase rapidly if the left v entricle fails and complete cardiac arrest results. THERAPEUTIC MEASURES. If the patient is pulseless or not breathing, cardiopulmonary resuscitation (CPR) and immediate defibrillation are required. Advanced cardiac life support (ACLS) protocols for pulseless VT treatment should be followed. Medications may include epinephrine, vasopressin, and amiodarone (see Table 25.2). If the patient is stable, medications are tried f irst, such as amiodarone. Magnesium can be used to help stabilize ventricular muscle excitability if the patient’s magnesium level is low. Ventricular Fibrillation Ventricular fibrillation (VF) occurs when many ectopic ventricular foci f ire at the same time. Ventricular activity is chaotic with no discernible waves (Fig. 25.22). The ventricle VT starts FIGURE 25.21 Ventricular tachycardia. Mrs. Mae, age 70, is 5 days post-MI without complications. You assist her back to bed at 1400 hours after she ambulates. Her oxygen is on at 2 L/min via nasal cannula. Her vital signs are BP 126/78 mm Hg, apical pulse 82 bpm, R 18 per minute. She has no pain and says she feels good after walking. The cardiac monitor shows normal sinus rhythm. Fi ve minutes later, you see that the monitor shows sinus rhythm with PVCs of less than six per minute. Her vital signs are no w BP 132/84 mm Hg, apical pulse 92 bpm, irre gular, and R 22 per minute. She reports no pain but says, “I can feel my heart skipping. It tak es my breath a way.” You call the registered nurse (RN) while staying with the patient to provide reassurance. ■ 1. What should you do first? 2. What should you do regarding the dysrhythmia? 3. What might be some of the causes for this dysrhythmia? 4. What symptoms, if any, would you expect to be present? 5. What would you do if symptoms were present? 6. With which health care team members might you collaborate? 7. What type of orders would you anticipate from the HCP? 8. How would you document your findings? Suggested answers are at the end of the chapter. quivers and is unable to initiate a contraction.There is a complete loss of cardiac output. If this rhythm is not terminated immediately, death ensues. ETIOLOGY. Hyperkalemia (elevated serum potassium), hypo- magnesemia (low serum magnesium), electrocution, coronary • WORD • BUILDING • hyperkalemia: hyper—above + kalium—potassium + emia— blood hypomagnesemia: hypo—below + magnes—magnesium + emia—blood VT ends 4068_Ch25_499-520 15/11/14 1:34 PM Page 513 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias CRITICAL THINKING Mrs. Parker You are caring for Mrs. Parker, age 66, on the cardiac medical unit. She had an MI and several episodes of VT while she was in the intensive care unit before transferring to your unit. At 1600 hours, you find her unresponsive, with no palpable pulses and shallo w respirations and in VT on the ECG. Vital signs are BP 80/40 mm Hg, P 150 bpm, R 6 per minute. ■ 1. 2. 3. 4. Why are there no palpable pulses? What is happening to the heart when VT is occurring? What action should you take? How will you document your findings? Suggested answers are at the end of the chapter. artery disease, and MI are all possible causes ofVF. Placement of intracardiac catheters and cardiac pacing wires can also lead to ventricular irritability and then VF. VENTRICULAR FIBRILLATION RULES. 1. Rhythm: chaotic and extremely irregular 2. Heart rate: not measurable 3. P waves: none 4. PR interval: none 5. QRS complex: none. SIGNS AND SYMPTOMS. Patients experiencing VF lose consciousness immediately. There are no heart sounds, peripheral pulses, or blood pressure readings. These are all indicative of circulatory collapse. Additionally, respiratory arrest, cyanosis, and pupil dilation occur. FIGURE 25.22 Ventricular fibrillation. FIGURE 25.23 Asystole. 513 THERAPEUTIC MEASURES. Immediate defibrillation is the best treatment for terminating VF. Each minute that passes without defibrillation reduces survival. CPR is started until the defibrillator is available. Automatic external defibrillators (AEDs) provide quick access to easily used technology for defibrillation (see the later “Def ibrillation” section). Endotracheal intubation and v entilation support respiratory function. Medications are gi ven according to ACLS protocols and may include epinephrine, vasopressin, amiodarone, and magnesium (see Table 25.2). Asystole Asystole (the silent heart) is the absence of electrical activity in the cardiac muscle. It is referred to as cardiac arrest. A straight line appears on an ECG strip (Fig. 25.23). ETIOLOGY. VF and a loss of a majority of functional cardiac muscle due to an MI are common causes of asystole.VF usually precedes this rhythm and must be reversed immediately to help prevent asystole. Hyperkalemia is another cause of asystole. ASYSTOLE RULES. 1. Rhythm: none 2. Heart rate: none 3. P waves: none 4. PR interval: none 5. QRS interval: none. SIGNS AND SYMPTOMS. Patients in asystole are unconscious and unresponsive. There are no heart sounds, peripheral pulses, blood pressure readings, or respirations. THERAPEUTIC MEASURES. CPR is started immediately. Endo- tracheal intubation to support respirations is performed. Epinephrine or v asopressin can be administered per ACLS protocols (see Table 25.2). 4068_Ch25_499-520 15/11/14 1:34 PM Page 514 514 UNIT FIVE Understanding the Cardiovascular System CARDIAC PACEMAKERS Pacemakers can be temporary (epicardial, transcutaneous, transvenous) or permanent (Fig. 25.24). They are used to generate an electrical impulse when there is a problem with the heart’s conduction system. Temporary pacemakers are used for bradycardia or tachycardia (overdrive pacing) that does not respond to medications or synchronized cardioversion. They may also be used after an MI to allow the heart time to heal when the diseased myocardium is unable to respond to or is not receiving electrical impulses because of damage within the conduction system. The temporary pacemak er becomes the electrical conduction system and stimulates the atria and v entricles to contract to maintain cardiac output. Temporary pacemakers can be inserted during v alve or open heart sur gery (epicardial), or in the cardiac catheterization lab or critical care unit (transvenous) as emergency treatment until sur gery can be scheduled to implant a permanent pacemaker. Transcutaneous pacemakers are used in emer gency situations because the y are quick and easy to apply . Impulses are deli vered to the heart through the skin from the e xternal generator via electrodes that are attached to the chest and back. CRITICAL THINKING Mr. Peet You are making rounds. When you enter Mr. Peet’s room, you note that he is having difficulty breathing and is unresponsive. ■ 1. What are your initial actions? 2. What should you do after assessing and finding no pulse or respirations? 3. What is your responsibility during a cardiac/ respiratory arrest code? Suggested answers are at the end of the chapter. Permanent Pacemaker Implantation Permanent pacemaker implantation is a procedure in which fluoroscopy, a screen that sho ws an image similar to a radiograph, is used. The pacemaker generator is implanted subcutaneously and attached to leads (insulated conducting wires) that are inserted via a v ein into the heart. The lead then delivers the impulse directly to the heart wall. A singlelead pacemaker paces either the right atrium or right v entricle depending on its chamber placement. Dual-chamber pacemakers have two leads, with one in the right atrium and the other in the right v entricle. This allows pacing of both chambers. Activity-responsive pacemakers provide a rate range (e.g., 60–115 bpm) in response to a person’s activity level. This provides the patient with greater flexibility FIGURE 25.24 Dual-chamber permanent pacemaker. for increasing cardiac output when needed, such as during exercise. When a patient is in a paced rhythm, a small spike (vertical line) is seen on the ECG at the start of the paced beat. This spike is the electrical stimulus. It can precede the P wave, QRS complex, or both depending on what is being paced (Fig. 25.25). P atients may have 100% paced beats, a mixture of their own beats and paced beats, or all of their own beats. Pacemakers should not f ire on patients’ own beats. Problems that can occur with pacemak ers include the following: • Failure to sense a patient’s own beat • Failure to pace because of a malfunction of the pulse generator • Failure to capture, which is the heart’s lack of depolarization Nursing Care for Patients With Pacemakers Patients’ heart rhythm, apical pulse, and incision are monitored after implantation of a pacemak er. Irregular heart rhythms or a rate slower than the pacemaker’s set rate can indicate pacemaker malfunction. Any change in heart rhythm, reports of chest pain, or changes in vital signs are reported immediately. The patient may remain in the hospital overnight. Pacemaker care teaching before dischar ge includes the following: • Report signs of incision infection (redness, swelling, warmth, pain, fever, or discharge) to the HCP. • Care for incision as instructed (dressing removal, keep clean and dry, resuming showers). • Report chest pain, dizziness, fainting, irregular heartbeats, palpitations, muscle twitching, or hiccups. • Maintain ordered activity restrictions (limiting raising arm on pacemaker side, driving, return to work). 4068_Ch25_499-520 15/11/14 1:34 PM Page 515 Chapter 25 Nursing Care of Patients With Cardiac Dysrhythmias 515 Atrial pacemaker spike A Ventricular pacemaker spike B FIGURE 25.25 ECG tracings. (A) Atrialonly pacemaker (yellow spike before P wave). (B) Ventricular-only pacemaker (green spike before QRS). (C) AV sequential pacemaker that paces both atrial and ventricular chambers (yellow spike before P and green spike before QRS). C • Carry your pacemaker ID card to show to HCPs, airport security, or other security staff. Pacemaker metal may set off alarms but is not harmed if one walks normally through the security device. Avoid having a hand wand passed over the pacemaker. • Understand electromagnetic restrictions to follow. Information is available on pacemaker manufacturer websites regarding various devices. Avoid strong electromagnetic fields (such as magnetic resonance imaging [MRI] unless it is the complete Revo MRI SureScan pacing system designed for use with MRI, welders above 130 amps, radio towers, or touching running car engines). • Microwaves and most common household devices may be used. • Keep cell phone of 3 watts or less 6 inches from your generator and on opposite side. • If become lightheaded or dizzy near an electromagnetic device, move away from it. • Keep scheduled appointments with the HCP. Periodic pacemaker checks will be done either by the HCP or remotely from home. The HCP can reprogram the pacemaker if needed. CRITICAL THINKING Mr. Treacher ■ Mr. Treacher, age 58, underwent pacemak er placement 6 days ago and is being transferred to the medical floor. After transfer, his vital signs are BP 138/72 mm Hg, apical pulse 72 bpm, and 100% paced rhythm. Thirty minutes later, he says that he feels weak and tired. His vital signs are now BP 100/60 mm Hg, apical pulse 60 bpm, and irregular. 1. 2. 3. 4. What is your first action? What actions should be taken next? What might be happening to Mr. Treacher? What interventions should you anticipate next? Suggested answers are at the end of the chapter. DEFIBRILLATION Defibrillation is a lifesaving procedure used for pulseless VT or VF. It deli vers an electrical shock to reset the heart’ s rhythm. Self-adhesive pads, conductive jelly, or saline pads are placed on the patient’ s chest to prevent electrical burns and promote conduction of the electrical charge. After the defibrillator is char ged, the paddles are pressed f irmly and evenly against the chest w all to prevent burns or electrical arcing (Fig. 25.26). For safety, the person who is defibrillating must announce “Clear.” The phrase “One. I’m clear. Two. You’re clear. Three. All clear” is suggested. No one, including the person def ibrillating, should touch the bed or patient during this time to avoid also being shocked. ACLS protocols specify the guidelines for resuscitation. • WORD • BUILDING • defibrillation: de—from + fibrillation—quivering fibers 4068_Ch25_499-520 15/11/14 1:34 PM Page 516 516 UNIT FIVE Understanding the Cardiovascular System After the procedure, the patient is monitored for skin b urns, rhythm disturbances, vital sign changes, respiratory problems, hypotension, and changes in the ST segment. OTHER METHODS TO CORRECT DYSRHYTHMIAS Automatic External Defibrillators FIGURE 25.26 Placement of defibrillator paddles on chest. After successful defibrillation, the patient is assessed for a pulse and adequate tissue perfusion. The patient is treated in the critical care unit (CCU) after successful resuscitation. Emotional support for an alert patient having experienced cardiac arrest and defibrillation is an important aspect of nursing care. This can be an extremely frightening event for the patient. It is important to explain to the patient what happened and to listen and allo w him or her to e xpress concerns. The patient is reassured that continuous cardiac monitoring is done in the CCU. F amilies also require emotional support during resuscitation of a loved one and might be present during it per agency policy. CARDIOVERSION Cardioversion is performed with a def ibrillator set in the synchronized mode. When the defibrillator is in the synchronized mode, it marks a highlighted area on the patient’s R waves, which must be recognized to deli ver a shock. When the discharge trigger is pressed, the shock is released when the machine senses it is safe to do so. The number of joules delivered with each shock usually ranges from 25 to 50. The procedure for delivering the shock is the same as for defibrillation. Synchronized cardioversion is used for ventricular tachycardia with a pulse. Electi ve synchronized cardioversion is used for dysrhythmias such as AF, atrial flutter, and supraventricular tachycardia that are not responsi ve to drug therap y. The patient is given a sedative and monitored by anesthesia personnel during the procedure. If cardioversion is successful, there should be a return to NSR. If the rhythm does not immediately convert, more cardioversion attempts can be made as determi