Cardiac Conduction System PDF

CARDIAC CONDUCTION SYSTEM The heart's electrical conduction system initiates an impulse that stimulates the mechanical cells of the heart to contract (see Chapter 21, section "Cardiac Conduction Pathway and Cardiac Cycle"; Fig. 21.3). Electrical activity can be seen on a cardiac monitor or recorded...

CARDIAC CONDUCTION SYSTEM The heart's electrical conduction system initiates an impulse that stimulates the mechanical cells of the heart to contract (see Chapter 21, section "Cardiac Conduction Pathway and Cardiac Cycle"; Fig. 21.3). Electrical activity can be seen on a cardiac monitor or recorded on an electrocardiogram (ECG) tracing. Activity seen on an ECG is not proof that the mechanical cells of the heart have contracted in response to the electrical impulse seen. So how can you verify that the heart muscle contracts and perfusion occurs? With physical data collection! Obtain the patient's blood pressure and apical and peripheral pulses. These provide the evidence that cardiac contraction and perfusion occurred. Cardiac Cycle The electrical representation of the cardiac cycle (impulse that stimulates depolarization \[contraction\] and repolarization \[relaxation\] of the atria and ventricles) is a P wave, a QRS complex, and a T wave (Fig. 25.1).  ELECTROCARDIOGRAM The electrical activity of the heart can be seen with either an ECG or continuous cardiac monitoring. An ECG shows electrical activity during the moment the ECG is obtained. 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 activity. An 18-lead ECG shows 18 views. For continuous monitoring, one lead or two leads are viewed. Continuous 12-lead monitoring can also be done. By learning the characteristics of a normal heart rhythm and rules for common arrhythmias, you will be able to report rhythm changes to your supervisor or the health-care provider (HCP). WORD BUILDING arrhythmia: an---without or away + rhythm---rhythm + ia---condition FIGURE 25.1 Components of the cardiac cycle. Electrocardiogram Graph Paper Intervals of each of the components of a cardiac cycle tracing are measured in seconds of time on the ECG graph paper. The graph paper is calibrated within a grid. Small squares are divided into heavy lined blocks of 25 that are five squares wide and five squares high (Fig. 25.2). Each small square is 0.04 seconds wide. One-half of a square is 0.02 seconds wide. Nothing smaller than one-half of a square is used. There are five small squares horizontally between two heavy, vertical black lines. The waveforms are measured horizontally from left to right on the graph paper. The height of the 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 is called the isoelectric line (baseline). It occurs when there is no electrical current (e.g., when the ECG machine is turned on but not attached to a person) or when the positive and negative electrical activity is equal if attached to a person. The ECG graph paper displays a straight line when there are no positive (upward) or negative (downward) electrical wave deflections present. FIGURE 25.2 Electrocardiogram graph paper time intervals.  COMPONENTS OF A CARDIAC CYCLE P Wave The P wave is the first wave of the cardiac cycle. It represents atrial depolarization. When the SA node fires, the electrical impulse spreads from the right to left atrium. The normal P wave appears rounded. When compared with other waveforms, it looks like a small hill. Disorders that change atrial size cause alterations in P-wave shape and size. PR Interval The PR interval (PRI; duration) represents the time it takes for 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. To calculate the PRI, count the number of small squares horizontally that the interval covers. Then multiply by 0.04 to identify the length of the PRI (Fig. 25.3). The normal PRI is 0.12 to 0.20 seconds (three to five small horizontal squares). LEARNING TIP To remember the normal PR interval (PRI), use the R to recall normal respiratory rate and then add a decimal before each number. A normal respiratory rate is 12 to 20 breaths per minute, and a normal PRI is 0.12 to 0.20 seconds! FIGURE 25.3 PR interval. This PR interval covers four squares. Each square is 0.04 seconds: 4 × 0.04 = 0.16 seconds. LEARNING TIP To make identification and measuring of waves easier:   Identify the isoelectric line and place a straight-edged item exactly along the isoelectric line and let it lie below the line; note any positive waves that are above the isoelectric line. Then, lay the straight-edged item above the isoelectric line and note any negative waveforms that occur below the isoelectric line.   Find a wave that begins on a vertical line, if possible, to make it visually easier to double check the caliper measurement (see Fig. 25.3). FIGURE 25.4 (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 whether it is a Q or an S. QRS Complex The QRS complex represents ventricular depolarization. It is composed of three waves: Q, R, and S. The Q wave is the first downward deflection after the P wave. The R wave is the first upward deflection after the P wave. The S wave is the first negative deflection after the R wave (see Fig. 25.1). The S wave ends when it returns to the isoelectric line. (This is why locating the isoelectric line is helpful when first learning to identify waves.) It is very important to note that all three waves are not always present in every QRS complex. But even with absent waves, it is still referred to as the QRS complex and is considered normal (Fig. 25.4). The QRS complex is larger than the P wave because the ventricles are larger owing to more muscle mass. This makes the QRS complex look like the "mountain" when compared with other waveforms. 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 interval, count the number of squares from the wave that begins the QRS complex to the end of the wave that ends 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. 25.5). If there is only an R and an S present, measure from the beginning of the R to the end of the S. But when 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 to 2.5 boxes). FIGURE 25.5 QRS interval. This QRS interval covers two and a half squares. Each square is 0.04 seconds. One-half square is 0.02 seconds: 2.5 × 0.04 = 0.10 seconds. T Wave The T wave represents ventricular repolarization, which is the resting state of the heart when the ventricles are filling with blood and preparing to receive the next impulse. The T wave is a rounded wave. In size comparison with the other waves, it is a "medium-sized hill." In most leads, the normal T wave is an upward (positive) deflection. It follows the QRS complex (remember, depolarization must occur first!). The T wave ends with a return to the isoelectric line. An inverted (downward) T wave can indicate cardiac ischemia (Fig. 25.6). FIGURE 25.6 (A) T wave with positive deflection. (B) T wave with inverted, negative deflection, indicating ischemia. QT Interval The QT interval measures the time from the start of the Q wave to the end of the T wave (see Fig. 25.1). This represents the time for ventricular depolarization and repolarization. Normal ranges are 0.34 to 0.43 seconds. These vary depending on gender, heart rate, and age. A QT chart for identifying normal values is used. Prolonged or shortened QT intervals can lead to ventricular arrhythmias. Abnormal intervals may be due to genetic causes, heart conditions, electrolyte imbalances, or medications that prolong the QT interval. U Wave The U wave is small. It is often not seen. It occurs shortly after the T wave. It is most prominent in patients with hypokalemia (low serum potassium level; Fig. 25.7). FIGURE 25.7 Various locations where U waves may appear. 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 complex. It ends at the beginning of the T wave (Fig. 25.8A). The ST segment is checked when patients experience chest pain. If a patient has non-transmural (occurring across the entire wall of an organ) ischemia, the ST segment can become inverted or depressed (Fig. 25.8B). With transmural ischemia, the ST segment can rise from the isoelectric line (Fig. 25.8C). FIGURE 25.8 (A) ST segment. (B) ST segment inverted or depressed. (C) ST segment elevated.  INTERPRETATION OF CARDIAC RHYTHMS Six-Step Process for Arrhythmia Interpretation An orderly, systematic method for interpreting ECG rhythms should be used. This will increase understanding of the items to examine and ensure nothing is overlooked. Six steps are used (Table 25.1). The findings of the first five steps identify the ECG rhythm according to the five rules for each arrhythmia. Then, the QT interval is measured in the sixth step. A 6-second ECG tracing is used when interpreting rhythms (see Fig. 25.2). Step 1. Regularity of the Rhythm The regularity of the rhythm can be determined by looking at the R-to-R spacing on the ECG tracing (Fig. 25.9). The same spacing between each R to R, with a rare variation 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 wave. They should normally be the same number. A caliper (a two-sided, movable metal instrument with sharp points) can also be used to measure the R-to-R spacing. FIGURE 25.9 Normal cardiac waves are equal distances apart. (A) R-to-R waves. (B) P-to-P waves. Table 25.1 Six-Step Process for Arrhythmia Interpretation After answering these questions with the patient's electrocardiogram (ECG) data, you can name the patient's arrhythmia. Step Questions Step 1: Regularity of the rhythm Is the rhythm regular? Irregular? Is there a pattern to the irregularity? Step 2: Heart rate What is the heart rate? Step 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? Step 4: PR interval Is the PR interval normal and constant? Does the PR interval vary? Step 5: QRS interval Is the QRS duration normal and constant? Do the QRS complexes all look alike? Step 6: QT interval Is the QT interval normal? To use a caliper for measuring R waves, place one metal point on an R wave. Place the other point in the exact same location on the next R wave. Next, stabilize the caliper. Without changing the distance between the caliper points, move the caliper from R wave to R wave across the ECG tracing (also known as an ECG strip) to see if R waves are regularly (evenly) spaced. If the distance is always the same, the rhythm is regular. If the distance varies, the rhythm is irregular. An irregular rhythm can be regularly irregular or irregularly irregular. Regularly irregular means it has a predictable pattern of irregularity. Irregularly irregular means it has no pattern to the occurrence of the irregularity. LEARNING TIP If a caliper is not available, a mark can be made on a piece of paper at the peak of one R wave and another mark made at the peak of the following R wave. Then the marks on the paper can be moved along the R-to-R intervals on the tracing (just as caliper points are) to determine the rhythm's 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: Count the number of small (0.04-second) squares between two R waves. Divide that number into 1,500. This gives the bpm, because 1,500 small squares equal 1 minute (Fig. 25.10). This method is used only for regular rhythms. It is very accurate. A rate meter is a visual paper copy of this mathematical calculation for an entire 6-second ECG tracing. You view it to calculate a 1-minute heart rate. The 6-second method is used for irregular rhythms. It may also be used when a rapid estimate of a regular rhythm is needed. However, 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. 25.2). Count the number of R waves within 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 bpm (6 seconds × 10 = 60 seconds, or 1 minute; Fig. 25.11). FIGURE 25.10 Normal sinus rhythm, rhythm regular: Count the small squares between two of the R waves and divide into 1,500: 1,500/22 = 68 bpm. FIGURE 25.11 Rhythm irregular: Counting R waves in a 6-second strip. There are seven R waves in this 6-second strip. 7 × 10 = 70 bpm. Step 3. P Waves The P waves on the ECG tracing are examined to see whether (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. 25.9). 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 arrhythmia. Step 4. PR Interval All PRIs are measured to determine whether they are normal (0.12 to 0.20 seconds) and constant. If the PRI is found to vary, it is important to note whether there is a pattern to the variation. Step 5. QRS Interval The QRS complexes are measured to determine whether they are all within normal range (0.06 to 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. Abnormal intervals can lead to arrhythmias. They should be reported to the HCP. A prolonged QT could become life threatening if it slows the heart rate enough.  NORMAL SINUS RHYTHM Normal sinus rhythm (NSR) is the heart's normal rhythm (see Fig. 25.10). It originates in the SA node. NSR has complete, regular cardiac cycles at 60 to 100 bpm. Normal Sinus Rhythm Rules Rhythm: Regular Heart rate: 60 to 100 bpm P waves: Rounded, upright, precede each QRS complex, alike PRI: 0.12 to 0.20 seconds QRS interval: 0.06 to 0.10 seconds  ARRHYTHMIAS An arrhythmia, which is used interchangeably with the term dysrhythmia, is an abnormal rhythm of the heart. Several mechanisms can cause an arrhythmia. Examples of these mechanisms are disturbances in the formation of an impulse or in the conduction of the impulse. When impulse formation is disturbed, an impulse may arise from the atria, the AV node, or the ventricles instead of the SA node. This disturbance can result in an increased or decreased heart rate, early or late beats, or atrial or ventricular fibrillation. With a disturbance in conduction, the impulse becomes blocked within the electrical conduction system (as in heart blocks or right or left bundle branch block). See the American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) at www.heart.org. Systemic reviews and research trials have looked at safe performance of CPR during an airborne pandemic such as COVID-19 (Brown & Chan, 2020; Couper et al, 2020; Malysz et al, 2020). PRACTICE ANALYSIS TIP Linking NCLEX-PN® to Practice The LPN/LVN will:   Recognize and report basic abnormalities on a client cardiac monitor strip.   Respond and intervene to a client life-threatening situation (e.g., cardiopulmonary resuscitation). Arrhythmias 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. Arrhythmias arising from the SA node are rarely dangerous. People who cannot tolerate a rapid or slow heart rate, especially those with heart, lung, or kidney disease, may require treatment. LEARNING TIP The origin and the type of a problem are used to name an arrhythmia. Let's name a slow arrhythmia that originates in the sinoatrial (SA) node. The origin is sinus, and the type of problem (slow rate) is bradycardia. So, the arrhythmia's name is sinus bradycardia. The term normal is not used because there is an abnormality in the rate! What would a fast arrhythmia originating in the SA node be called? Sinus tachycardia, of course. It is easy to understand what is happening within an arrhythmia when you look at the name and what it conveys. Sinus Bradycardia Bradycardia is a rate slower than 60 bpm. It can be asymptomatic or symptomatic (usually when below 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. 25.12). Look to the name "sinus bradycardia," which tells us that the impulse is coming from the sinus node (sinus) but at a slower rate than normal (bradycardia). ETIOLOGY. Electrolyte imbalances, medications such as digoxin (Lanoxin), or myocardial infarction (MI) can cause bradycardia. Well-conditioned athletes, whose hearts work very efficiently, can also have slow heart rates. SINUS BRADYCARDIA RULES Rhythm: Regular Heart rate: Less than 60 bpm P waves: Rounded, upright, precede each QRS complex, alike PRI: 0.12 to 0.20 seconds QRS interval: 0.06 to 0.10 seconds SIGNS AND SYMPTOMS. With symptomatic bradycardia, decreased blood pressure, 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. The underlying cause must be identified for correction. For the symptomatic patient, begin treatment while the cause is corrected. Treatment can include IV atropine or infusions of dopamine or epinephrine. Transcutaneous pacing is used if atropine is ineffective (Table 25.2). Transvenous pacing can also be considered. Sinus Tachycardia Tachycardia is defined as a heart rate greater than 100 bpm. It originates from the SA node. Sinus tachycardia has the same components as NSR except the rate is faster (Fig. 25.13). WORD BUILDING dysrhythmia: dys---difficult or abnormal + rhythm---rhythm + ia---condition bradycardia: bradys---slow + kardia---heart FIGURE 25.12 Sinus bradycardia. Heart rate is 38. Table 25.2 Medications Used in Treatment of Arrhythmias Medication Class/Action Anticoagulant (Oral) Increases clotting time. Examples Reduces risk of blood clots in atrial fibrillation (AF). warfarin (Coumadin) Nursing Implications Monitor international normalized ratio regularly. Monitor for bruising and bleeding. Acetaminophen (Tylenol) should be used rather than aspirin for analgesia during therapy. Reversal agent is vitamin K. Reduces risk of blood clots in nonvalvular AF. apixaban (Eliquis) dabigatran (Pradaxa) edoxaban (Savaysa, Lixiana) rivaroxaban (Xarelto) No regular monitoring needed. No specific reversal agent available. Dosage adjustment may be required with reduced kidney function. Antiarrhythmics Examples In supraventricular tachycardia, slows conduction through AV node to restore normal sinus rhythm. adenosine (Adenocard) Nursing Implications Inform health-care provider (HCP) if female pregnant or nursing. Record rhythm strip during administration. Given via IV push fast (1--3 seconds), followed by normal saline flush fast. Inhibits AF, atrial flutter, and ventricular arrhythmias. amiodarone (IV: Nexterone; oral: Cordarone, Pacerone) dronedarone (Multaq) Contraindicated in atrioventricular (AV) block or pregnancy. Obtain baseline vital signs and electrocardiogram. Monitor for toxicity. Monitor for multiple medication interactions. Anticholinergic Increases heart rate to treat symptomatic bradycardia and asystole. Examples atropine sulfate Nursing Implications Contraindicated in angle-closure glaucoma. Beta Blockers Decrease myocardial contractility. Control rate in sinus tachycardia, premature atrial contraction, atrial flutter, AF, and premature ventricular contractions. Examples atenolol (Tenormin) esmolol (Brevibloc) metoprolol succinate (Lopressor, Toprol XL) Nursing Implications Check apical pulse and blood pressure (BP) before giving. If pulse is less than 60 bpm and BP less than 100 mm Hg systolic, notify HCP. Teach: Change positions slowly and do not stop drug abruptly. Calcium Channel Blocker Decreases myocardial contractility and depresses conduction system. Controls rate in sinus tachycardia, atrial flutter, and AF. Examples diltiazem (Cardizem) verapamil (Calan, Isoptin, Verelan) Nursing Implications IV route used for symptomatic arrhythmias. Monitor for bradycardia and hypotension. Inotrope---Cardiac Glycoside (Positive Inotrope and Negative Chronotrope) Slows heart rate. Maintains sinus rhythm for sinus tachycardia, atrial flutter, and AF. Examples digoxin (Lanoxicaps, Lanoxin) Nursing Implications Take apical pulse for 1 minute; if less than 60 bpm, notify HCP. Therapeutic digoxin levels: 0.5 to 2 mg/mL. Monitor drug level and electrolytes as hypokalemia, hypomagnesemia, and hypercalcemia increase toxicity. Vasopressors Examples For cardiac stimulation, vasoconstriction, and bronchodilation. Treats asystole, ventricular tachycardia, ventricular fibrillation, and symptomatic bradycardia. epinephrine/adrenalin norepinephrine Increases cardiac output and blood pressure; treats bradycardia. dopamine Nursing Implications Contraindicated with nonselective beta blockers. Monitor blood pressure and heart rate. FIGURE 25.13 Sinus tachycardia. Heart rate is 125. 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. It helps produce additional cardiac output to deliver oxygen to tissues. SINUS TACHYCARDIA RULES Rhythm: Regular Heart rate: 101 to 180 bpm P waves: Rounded, upright, precede each QRS complex, alike PRI: 0.12 to 0.20 seconds QRS interval: 0.06 to 0.10 seconds SIGNS AND SYMPTOMS. Sinus tachycardia can be asymptomatic. A very rapid rate (usually greater than 150 bpm) that is sustained for long periods may cause symptoms. The patient may have angina, dyspnea, syncope, or tachypnea. Older patients can become symptomatic more rapidly than younger patients (see "Gerontological Issues"). Patients with an MI may not tolerate a rapid heart rate. They can have more severe symptoms because cardiac workload is increased. THERAPEUTIC MEASURES. If the patient is stable, obtain an ECG and treat the cause. Medications such as adenosine (Adenocard), beta blockers, and calcium channel blockers are considered to slow the heart rate (when equal to or greater than 150 bpm; see Table 25.2). The treatment goal is to decrease the heart's workload and correct the cause. This usually resolves the tachycardia. For example, if the patient is hemorrhaging, immediate intervention is needed to stop bleeding and restore normal blood volume. Once normal blood volume is restored, the heart rate should return to normal. Gerontological Issues Arrhythmia Risk Factors that increase the risk of arrhythmias in older adults include:   Digitalis toxicity (most common)   Hypokalemia   Angina   Coronary insufficiency or cardiomyopathy (exercise, stress)   Sleep apnea   Hypothyroidism or hyperthyroidism Arrhythmias that occur most often in older adults include the following:   Atrial fibrillation (atria beating 400 to 700 times per minute)   Sick sinus syndrome (alternating episodes of bradycardia, normal sinus rhythm, tachycardia, and periods of long sinus pause)   Heart blocks (delayed or blocked impulses to the atria or ventricles) Some of the common age-related effects of arrhythmias include the following:   Bradycardia   Confusion   Dizziness   Dyspnea or shortness of breath   Fatigue   Hypotension   Palpitations   Syncope   Weakness Older adults have less ability to adapt to sudden changes or stressors. 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 in postoperative patients, patients with gastrointestinal bleeding or cancer, or trauma patients. Consider both external and internal bleeding. Apply pressure to a bleeding site. Report the tachycardia and any bleeding promptly for treatment. Arrhythmias Originating in the Atria As reviewed, all areas of the heart can initiate an impulse (see Chapter 21). If the atria begin to initiate impulses faster than the SA node, the primary pacemaker, the atria become the primary pacemaker. Atrial rhythms are usually faster than 100 bpm. They 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 of the SA node. This is an indicator that the SA node is not controlling the heart rate. When the atrial impulses travel to the ventricles, they initiate a normal-shaped QRS complex after each P wave. LEARNING TIP If a QRS complex measures 0.06 to 0.10 seconds and an arrhythmia is present, the problem originated above the ventricles. This is known as a supraventricular (above the ventricle) arrhythmia. Ventricular-originating arrhythmias produce wide QRS complexes that are greater than 0.10 seconds. 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 except where the early beat occurs. When looking at the ECG strip, a shortened R-to-R interval 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 next beat being regular (Fig. 25.14). FIGURE 25.14 Premature atrial contractions. ETIOLOGY. Causes of PACs include enlarged atria in valvular disorders, atrial fibrillation onset, cigarette smoking, electrolyte imbalances, heart failure, hypoxia, medications (such as digoxin), myocardial ischemia, and stress. PREMATURE ATRIAL CONTRACTIONS RULES Rhythm: Premature beat interrupts the underlying rhythm Heart rate: Depends on the underlying rhythm; if NSR, 60 to 100 bpm P waves: Early beat is abnormally shaped PRI: Normal if underlying rhythm normal; premature beat can have shortened or prolonged PRI QRS interval: 0.06 to 0.10 seconds (indicates normal conduction to ventricles) SIGNS AND SYMPTOMS. PACs can occur in healthy individuals as well as those with a diseased heart. No symptoms are usually present. If several PACs occur in succession, the patient may report feeling palpitations. THERAPEUTIC MEASURES. PACs are usually not serious. Often, no treatment is required other than correcting a cause. Frequent PACs indicate atrial irritability, which could worsen into other atrial arrhythmias. Beta blockers can be given for frequent PACs to slow the heart rate (see Table 25.2). Atrial Flutter In atrial flutter, the atria contract, or flutter, at a rate of 250 to 350 bpm. The very rapid P waves appear as flutter, or F waves, on the ECG. They appear in a sawtooth pattern. Some of the impulses travel through the AV node and reach the ventricles. This results in normal QRS complexes on the ECG. 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 will be regular (Fig. 25.15). The classic characteristics of atrial flutter are more than one P wave before a QRS complex, a sawtooth pattern of P waves, and an atrial rate of 250 to 350 bpm. FIGURE 25.15 Atrial flutter. ETIOLOGY. Causes of atrial flutter include heart failure, hypertension, rheumatic or ischemic heart diseases, pericarditis, pulmonary embolism, and postoperative coronary artery bypass surgery. Many medications can also cause this arrhythmia. ATRIAL FLUTTER RULES Rhythm: Atrial rhythm regular; ventricular rhythm regular or irregular depending on consistency of AV conduction of impulses Heart rate: Ventricular rate varies P waves: Flutter or F waves with sawtooth pattern PRI: None measurable QRS interval: 0.06 to 0.10 seconds SIGNS AND SYMPTOMS. The presence of symptoms in atrial flutter depends on the ventricular rate. If the ventricular 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 adequacy of cardiac output 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. Medications such as calcium channel blockers can be used to control the ventricular rate (see Table 25.2). Antiarrhythmic medications are used to convert atrial flutter. To terminate the atrial flutter in symptomatic patients, catheter ablation (usually in the right atrium) may be done. 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. Consequently, the ventricular rate is much lower than the atrial rate. There are no definable P waves. 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 few 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; permanent AF doubles the risk of death. Stroke risk is increased with AF because of the risk of thrombus formation in the atria from blood stasis caused by poor emptying of blood from the quivering atria (Fig. 25.16). ETIOLOGY. AF increases with age (65 and above), especially in those with heart disease. Causes include cardiac surgery, emphysema, heart failure, heart valve disease, hypertension, hyperthyroidism, MI, sleep apnea, and certain medications. Sometimes the cause is unknown. WORD BUILDING ablation: ab---away from + lat---carry ATRIAL FIBRILLATION RULES Rhythm: Irregularly irregular Heart rate: Atrial rate not measurable; ventricular rate under 100 bpm is controlled response; greater than 100 bpm is rapid ventricular response P waves: No identifiable P waves PRI: None can be measured because no P waves are seen QRS interval: 0.06 to 0.10 seconds LEARNING TIP Atrial fibrillation is easy to identify based on two classic characteristics on an ECG: lack of identifiable P waves and an irregularly irregular rhythm (R waves). FIGURE 25.16 Atrial fibrillation. SIGNS AND SYMPTOMS. With AF, most patients feel the irregular rhythm. Many describe it as palpitations, a racing heart, or a skipping heartbeat. They may feel shortness of breath, dizziness, or chest discomfort. 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 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 are used. These include beta blockers, calcium channel blockers, or sometimes digoxin (see Table 25.2). Anticoagulant therapy may be given to reduce thrombi and stroke risk. Pharmacological or electrical cardioversion can be used to attempt to convert the rhythm to NSR. This should be done after sufficient anticoagulation (3 to 4 weeks) to stabilize or resolve any existing blood clots in the atria. This prevents clots from being dislodged and causing a stroke. Rhythm control medications such as sodium or potassium channel blockers are used to restore and maintain NSR. If known, 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 stop impulses coming from the pulmonary veins (most AF impulses arise from pulmonary veins) or AV node, catheter ablation may be used. Intracardiac echocardiography maps the area of the heart requiring treatment. Then, released energy, such as cryothermy or radiofrequency energy, creates lesions either on all four pulmonary veins or near the AV node. The lesions heal and scar. This blocks those pathways for future impulses. Postprocedural care is similar to postangioplasty or postcardiac catheterization care (see Chapter 21). Surgery. The maze procedure creates multiple lines of scar tissue (a maze-like pattern) with cryothermy or radiofrequency energy to block reentry of the electrical impulses traveling to the AV node. Third-Degree Atrioventricular Block In third-degree AV block, SA node impulses are blocked and do not reach the ventricles to stimulate them to contract (Fig. 25.17). This is also known as complete heart block (CHB) or third-degree heart block. The escape pacemakers for the heart (junctional \[AV node\] or ventricular) must produce electrical impulses to cause the ventricles to contract, or else cardiac arrest will occur. Depending on the origin of the escape beat, the QRS complex will be either narrow (junctional) or wide (ventricular) on the ECG. Normal P waves march across the ECG strip at a constant P-to-P interval without any relationship to the regularly occurring but slower QRS complexes on the ECG. FIGURE 25.17 Third-degree atrioventricular block. ETIOLOGY. Cardiac ischemia or infarction, hyperkalemia (elevated serum potassium), infection, antiarrhythmic medications, or digoxin toxicity are some common causes of CHB. SIGNS AND SYMPTOMS. Typically, severe symptoms are seen. These include confusion, dyspnea, severe chest pain, hypotension, or syncope. With narrow QRS complex escape rhythms, fewer symptoms occur. They include dizziness, chest pain, and fatigue. THIRD-DEGREE ATRIOVENTRICULAR BLOCK RULES Rhythm: P-to-P interval regular; R-to-R interval regular; atria and ventricles controlled by separate electrical impulses from foci that are firing regularly Heart rate: Atrial 60 to 100 bpm; ventricular rate slower: 40 to 60 bpm is junctional foci; 20 to 35 bpm is ventricular foci P waves: Rounded, upright, alike; more P waves than QRS complexes; may occur within a QRS complex or upon a T wave PRI: No P waves conducted to the ventricles, so no relationship to the QRS complexes; therefore, there is no actual PRI (may appear as if the PRI varies) QRS interval: 0.06 to 0.10 seconds (junctional origin); greater than 0.10 (ventricular origin) THERAPEUTIC MEASURES. CHB is a medical emergency. Treatment is based on the level of the block in the heart. Atropine is considered. If the patient is symptomatic, transcutaneous pacing is needed immediately. Depending on the cause, a permanent pacemaker may be required for the rest of the patient's life. A temporary pacemaker may be used until the permanent pacemaker can be implanted. If medication toxicity is the cause, the CHB may be gone after the toxicity is resolved. A temporary pacemaker may be needed until this occurs. CUE RECOGNITION 25.1 You are caring for a patient who displays complete heart block with a wide QRS complex escape rhythm on the continuous ECG and reports dyspnea and severe chest pain. What action do you take? Suggested answers are at the end of the chapter. Ventricular Arrhythmias Premature ventricular contractions (PVCs) originate in the ventricles from an ectopic focus (a site other than the SA node). The irritable ventricles fire prematurely, before the SA node does. When the ventricles fire first, the impulses are not conducted normally through the electrical pathway. This results in a wide (greater than 0.10 seconds), bizarre QRS complex (Fig. 25.18). FIGURE 25.18 Premature ventricular contractions. (A) Unifocal PVCs arise from one foci (area) and look the same. (B) Multifocal PVCs arise from different foci and may look different. PVCs can occur in different shapes. Unifocal (one focus) PVCs all look the same. This is because they come from the same irritable ventricular area. Multifocal (multiple foci) PVCs do not all look the same because they are originating from several irritable areas in the ventricle. WORD BUILDING hyperkalemia: hyper---above + kalium---potassium + emia---blood There can be several repetitive cycles or patterns of PVCs:   Bigeminy occurs every other beat (a normal beat and then a PVC; Fig. 25.19).   Trigeminy occurs every third beat (two normal beats and then a PVC).   Quadrigeminy occurs every fourth beat (three normal beats and then a PVC).   When two PVCs occur together, they are referred to as a couplet (pair).   If three or more PVCs occur in a row, it is referred to as a run of PVCs, or ventricular tachycardia. FIGURE 25.19 Bigeminal premature ventricular contractions. ETIOLOGY. Anxiety, use of caffeine or alcohol, cardiomyopathy, hypokalemia, ischemia, and MI are common causes of PVCs. PREMATURE VENTRICULAR CONTRACTION RULES Rhythm: Depends on the underlying rhythm; PVC usually interrupts rhythm Heart rate: Depends on underlying rhythm P waves: Absent before the PVC QRS complex PRI: None for PVC QRS interval: In a 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. They are described as a skipped beat or palpitations. With frequent PVCs, cardiac output can be decreased. This leads to fatigue, dizziness, or more severe arrhythmias. 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, regularly occurring, multifocal, falling on the T wave (known as R-on-T phenomenon, which can trigger life-threatening arrhythmias), or caused by an acute MI, they can be dangerous. Typically, a beta blocker or sometimes a calcium channel blocker is used to treat PVC symptoms (see Table 25.2). Antiarrhythmic medications can be used if these are ineffective. CLINICAL JUDGMENT Mrs. Zhang, age 74, is 4 days postmyocardial infarction without complications. You assist her back to bed after she ambulates at 1400 hours. Her oxygen is on at 2 L/min via nasal cannula. Her vital signs are blood pressure 126/78 mm Hg, apical pulse 82 bpm, and respiratory rate 18 breaths per minute. She has no pain and says she feels good after walking. The cardiac monitor shows normal sinus rhythm. Five minutes later, you see that the monitor shows sinus rhythm with premature ventricular contractions of less than six per minute. Her vital signs are now blood pressure 132/84 mm Hg, apical pulse 92 bpm (regularly irregular), and respiratory rate 22 breaths per minute. She reports no pain but says, "I can feel my heart skipping. It takes my breath away." What do you do first? What do you do regarding the arrhythmia? As you collect data, what symptoms do you look for? What do you do if symptoms are present? What causes do you consider for this arrhythmia? With which health-care team members do you collaborate? How do you document your findings? What do you remain vigilant for? Suggested answers are at the end of the chapter. Ventricular Tachycardia The occurrence of three or more PVCs in a row is referred to as ventricular tachycardia (VT; Fig. 25.20). VT results from the continuous firing of an ectopic ventricular focus. During VT, the ventricles rather than the SA node become the pacemaker of the heart. The pathway of the ventricular impulses is different from the normal conduction pathway, so it produces a wide (greater than 0.10 seconds), bizarre QRS complex. FIGURE 25.20 Ventricular tachycardia. 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 Rhythm: Usually regular, may have some irregularity Heart rate: 150 to 250 ventricular bpm; slow VT is below 150 bpm P waves: Absent PRI: None QRS interval: Greater than 0.10 seconds SIGNS AND SYMPTOMS. Patients are aware of a sudden onset of rapid heart rate. They can experience dyspnea, palpitations, and lightheadedness. Angina commonly occurs. The seriousness of VT is determined by the duration of the arrhythmia. Sustained VT compromises cardiac output. It can become pulseless VT, a life-threatening rhythm. Evidence-Based Practice Clinical Question What is the best method for bystander CPR on an adult? Evidence A systematic review of 42 studies that included 32 randomized control trials identified interventions associated with improved quality of bystander CPR such as telephone-dispatcher assisted CPR with instructions, compression-only CPR, or heel of the hand only when the rescuer is tiring. Compression-only CPR had better CPR quality than conventional CPR because compression-only CPR provided more chest compressions, less hands-off time, and less time to first compression. Devices providing real-time feedback and mobile devices containing CPR applications or software were found to be beneficial, although they could cause a delay in CPR onset (Chen et al, 2019). Implications for Nursing Practice Encourage patients and their families to become certified in basic life support to be able to respond to an emergency. Reference: Chen, K., Ko, Y., Hsieh, M., Chiang, W., Ma, M., & Lin, S. (2019). Interventions to improve quality of bystander cardiopulmonary resuscitation: A systematic review. PloS One, 14(2), e0211792. https://doi.org/10.1371/journal.pone.0211792 THERAPEUTIC MEASURES. For a patient who is stable, antiarrhythmic medications are used. If the patient is pulseless or not breathing, cardiopulmonary resuscitation (CPR) and immediate defibrillation are required (see "Evidence-Based Practice"). Advanced cardiac life support (ACLS) protocols for pulseless VT treatment are used. Medications may include epinephrine and amiodarone (see Table 25.2). CRITICAL THINKING & CLINICAL JUDGMENT Mrs. Parker, age 76, is admitted to the long-term care unit where you are working. She has been transferred from the hospital after treatment for a recent MI and several episodes of ventricular tachycardia (VT). At 1600 hours, you find her unresponsive, with no palpable pulses and with shallow respirations. Vital signs are blood pressure 60/20 mm Hg, apical pulse 160 bpm, and respiratory rate 6 breaths per minute. Critical Thinking (The Why) Why are there no palpable pulses? What is happening to the heart when VT is occurring? Clinical Judgment (The Do) What action do you take? How do you document your findings? Suggested answers are at the end of the chapter. Ventricular Fibrillation Ventricular fibrillation (VF) occurs when many ectopic ventricular foci fire at the same time. Ventricular activity is chaotic. There are no discernible waves (Fig. 25.21). The ventricle quivers. It is unable to initiate a contraction. There is a complete loss of cardiac output. If this rhythm is not corrected immediately, death occurs. ETIOLOGY. Hyperkalemia, hypomagnesemia (low serum magnesium), electrocution, coronary artery disease, and MI are all possible causes of VF. Placement of intracardiac catheters and cardiac pacing wires can also lead to ventricular irritability and then VF. VENTRICULAR FIBRILLATION RULES Rhythm: Chaotic and extremely irregular Heart rate: Not measurable P waves: None PRI: None 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. Respiratory arrest, cyanosis, and pupil dilation occur. 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 provide quick access to easily used technology for defibrillation (see "Defibrillation" section). Endotracheal intubation with oxygen supports respiratory function. Medications are given according to ACLS protocols. They include epinephrine and amiodarone (see Table 25.2). WORD BUILDING hypomagnesemia: hypo---below + magnes---magnesium + emia---blood Asystole Asystole (the silent heart) is the absence of electrical activity within the cardiac muscle. It is referred to as cardiac arrest. A flat or straight line appears on an ECG strip (Fig. 25.22). ETIOLOGY. Hyperkalemia, VF, or a loss of a majority of functional cardiac muscle due to an MI are common causes of asystole. VF usually precedes asystole. VF must be reversed immediately to help prevent progression to asystole. ASYSTOLE RULES Rhythm: None Heart rate: None P waves: None PRI: None 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. Endotracheal intubation and oxygen support respiration. Epinephrine is administered per ACLS protocols (see Table 25.2). Reversible causes are treated. FIGURE 25.21 Ventricular fibrillation. FIGURE 25.22 Asystole.  CARDIAC PACEMAKERS Pacemakers are used to generate an electrical impulse when there is a problem with the heart's conduction system. Temporary Pacemaker Temporary pacemakers treat 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. The temporary pacemaker becomes the electrical conduction system. It stimulates the atria and ventricles to contract, which maintains cardiac output. Temporary pacemakers can be inserted during valve or open-heart surgery (epicardial). They can also be used in the cardiac catheterization laboratory or critical care unit (CCU; transvenous) for emergency treatment. They are kept in place until surgery can be scheduled to implant a permanent pacemaker. Transcutaneous pacemakers are used in emergency situations. They are quick and easy to apply. Impulses are delivered from the external generator via electrodes on the skin to the heart. The electrodes are placed on the chest and back. Permanent Pacemaker Permanent pacemakers are used for symptomatic bradycardia and third-degree AV block (complete dissociation between atrial and ventricular activity). Permanent pacemaker implantation is a procedure in which fluoroscopy, a screen that shows an image similar to a radiograph, is used. The pacemaker generator is implanted subcutaneously. It is attached to leads (insulated conducting wires) that are inserted via a vein into the heart. The lead then delivers an impulse directly to the heart wall. A single-lead pacemaker paces either the right atrium or right ventricle into which it is placed. Dual-chamber pacemakers have two leads (Fig. 25.23). One is in the right atrium, and the other is in the right ventricle. This allows pacing of both chambers. Activity-responsive pacemakers provide a rate range (e.g., 60 to 115 bpm). They allow rate changes in response to a person's activity level. This provides the patient with greater flexibility for increasing cardiac output when needed, such as during exercise. Leadless Pacemaker The leadless permanent pacemaker was approved in 2016 (visit www.medtronic.com). It is inserted via a leg vein, so no chest incision is needed for implantation into the right ventricle, without leads. Everything is contained within the pacemaker, which is about the size of a vitamin capsule. The battery lasts about 8 to 12 years. Few complications occur with this type of pacemaker. FIGURE 25.23 Dual-chamber permanent pacemaker. Pacemaker Activity 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. 25.24). Patients may have 100% paced beats, a mixture of their own beats and paced beats, or 100% their own beats. Pacemakers should not fire during a patients' own beat to prevent complications. Problems that can occur with pacemakers 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 (turn patient onto left side) FIGURE 25.24 ECG tracings. (A) Atrial-only pacemaker (yellow spike before P wave). (B) Ventricular-only pacemaker (green spike before QRS). (C) Dual-chamber pacemaker that paces both atrial and ventricular chambers (yellow spike before P and green spike before QRS). Nursing Care for Patients With Pacemakers Patients' heart rhythm, apical pulse, and incision are monitored after implantation of a pacemaker. 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 to the HCP immediately. The patient may have outpatient surgery or remain in the hospital overnight. Pacemaker teaching before discharge includes the following:   Care for an incision as instructed (e.g., dressing removal, keeping it clean and dry, resuming showers).   Maintain ordered activity restrictions (e.g., limit raising arm on pacemaker side, driving, returning to work).   Be aware of other devices:   Safe devices: microwaves, most cell phones if not held too closely to the cardiac device, Bluetooth headset, most common household devices.   Caution to be used with devices: antitheft systems, some cell phones with more magnets, security metal detectors (avoid having a hand wand passed over the pacemaker), MP3 player headphones, extracorporeal shock-wave lithotripsy.   Devices with possible risk: strong electromagnetic fields (magnetic resonance imaging with a cardiac device requires evaluation to determine if it is safe; newer pacing systems and cardiac devices are designed for use with MRI, such as the complete Revo MRI SureScan pacing system), welders above 130 amps, radio towers, or touching running car engines (information is available on the pacemaker manufacturer and AHA Web sites regarding various devices).   If you become lightheaded or dizzy near an electromagnetic device, move away from it.   Carry a pacemaker identification card to show to HCPs, airport security, or other security staff. Pacemaker metal may set off alarms, but the device is not harmed if one walks normally through the security device.   Report chest pain, dizziness, fainting, irregular heartbeats, palpitations, muscle twitching, or hiccups to the HCP.   Report signs of incision infection (e.g., redness, swelling, warmth, pain, fever, discharge) to the HCP.   Keep scheduled appointments with the HCP. Periodic pacemaker checks will be done by the HCP or remotely from home. The HCP can reprogram the pacemaker if needed. PRACTICE ANALYSIS TIP Linking NCLEX-PN® to Practice The LPN/LVN will assist in the care of a client with a pacing device. CRITICAL THINKING & CLINICAL JUDGMENT Mr. Treacher, age 58, underwent pacemaker placement 6 days ago and has a 100% paced rhythm. You are making patient rounds. You find his vital signs are blood pressure 138/72 mm Hg and apical pulse 72 bpm. Thirty minutes later, he says that he feels weak and tired. His vital signs are now blood pressure 100/60 mm Hg and apical pulse 60 bpm and irregular. Critical Thinking (The Why) What might be happening to Mr. Treacher? Clinical Judgment (The Do) What action do you take first? What actions do you take next? What interventions do you anticipate? Suggested answers are at the end of the chapter.  DEFIBRILLATION Defibrillation is a lifesaving procedure used for pulseless VT or VF. It delivers an electrical shock to attempt to reset the heart's rhythm. Self-adhesive pads (saline or with conductive jelly) are placed on the patient's chest. They prevent electrical burns and promote conduction of the electrical charge. The defibrillator is charged, then the paddles are pressed firmly and evenly against the chest wall to prevent burns or electrical arcing (Fig. 25.25). 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 defibrillating, should touch the bed or patient during this time to avoid being shocked. ACLS protocols specify guidelines for resuscitation. After successful defibrillation, the patient is checked for a pulse and adequate tissue perfusion. The patient is treated in the CCU after successful resuscitation. Emotional support for an alert patient who experiences 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. Then listen and allow them to express concerns. The patient is reassured that continuous cardiac monitoring will be done in the CCU. Families also require emotional support during resuscitation of a loved one. They may be present during the resuscitation per agency policy.  CARDIOVERSION Cardioversion is performed with a defibrillator set in the synchronized mode. In the synchronized mode, a mark is highlighted on the patient's R waves. The R wave must be recognized for a shock to be delivered. When the discharge button 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 safely is the same as for defibrillation. Synchronized cardioversion is used for VT with a pulse. Elective synchronized cardioversion is used for arrhythmias that are not responsive to medication therapy. These include AF, atrial flutter, and supraventricular tachycardia. The patient is given a sedative and monitored by anesthesia professionals during the procedure. If cardioversion is successful, there should be a return to NSR. If the rhythm does not immediately convert, additional cardioversion attempts can be made by the HCP. After the procedure, the patient is monitored for skin burns, rhythm disturbances and changes in the ST segment, vital sign changes and hypotension, and respiratory problems. WORD BUILDING defibrillation: de---from + fibrillation---quivering fibers FIGURE 25.25 Placement of defibrillator paddles on chest.  OTHER METHODS TO CORRECT ARRHYTHMIAS Automatic External Defibrillators An automatic external defibrillator (AED) is an external device that automatically analyzes rhythms. For VF or VT, it will either automatically deliver or prompt the operator to deliver an electrical shock for a shockable rhythm (Fig. 25.26). Minimally trained laypersons or hospital and rescue personnel can use these devices with little risk of injury to the patient because the AED, not the operator, analyzes the rhythm. The patient is connected to the AED with adhesive sternal-apex pads attached to cables coming from the device. This connection allows hands-free defibrillation. FIGURE 25.26 Automatic external defibrillator. AEDs are found in public places such as shopping malls, airports, stadiums, casinos, golf courses, and airplanes for immediate access. Defibrillation attempts must occur within minutes of cardiac arrest to increase chance of survival. AEDs are available for home use. They are recommended for people at high risk of sudden cardiac arrest. They are helpful for those at risk with rescue access that will take longer than 4 minutes, such as people living in rural areas, gated communities, or secured-access buildings. CUE RECOGNITION 25.2 You are caring for a resident who becomes unconscious and collapses onto the bed while standing. What action do you take? Suggested answers are at the end of the chapter. Cardioverter Defibrillator A wearable cardioverter defibrillator (WCD) vest next to the skin (see https://lifevest.zoll.com) or implantable cardioverter defibrillator (ICD) or a combination pacemaker/ICD is used for patients who are at risk for sudden cardiac death or experience rapid life-threatening arrhythmias. These devices have decreased the number of deaths from these arrhythmias by analyzing and treating these heart rhythms. When a rapid life-threatening rhythm is detected that could cause death (VF), the WCD/ICD automatically delivers an electrical shock. If the arrhythmia does not convert on the initial shock, more shocks are delivered sequentially. If a device detects VT, it can cardiovert the rhythm with lower energy. ICDs also have antitachycardia pacing ability if tachycardia rhythm is detected. ICD battery life depends on use. When battery life is low, the entire unit must be changed within a few months. Patients with these devices can be extremely anxious about receiving shocks from them. Defibrillator or cardioversion shocks may feel like a kick in the chest. Reinforcement of patient and family education is important. To prevent problems, those with these devices should take the same precautions as discussed earlier for those with pacemakers. Provide emotional support and answer questions.  NURSING PROCESS FOR THE PATIENT WITH ARRHYTHMIAS Data Collection Patients at risk for arrhythmias require careful monitoring. Obtaining apical and radial pulses at frequent intervals helps detect arrhythmias. Most arrhythmias are not life threatening. A patient's report of chest pain, dizziness, or palpitations should be investigated and reported to the HCP. Nursing Diagnoses, Planning, Implementation, and Evaluation See "Nursing Care Plan for the Patient With Arrhythmias." Assist the patient and family in understanding the plan of care and the reasons for the interventions. Allow them to express needs and fears. Family members are taught CPR or given information on local CPR classes, which gives them a sense of control and hope. If CPR is needed, the family can act instead of feeling helpless. The patient may feel more secure knowing that immediate help from family members is available until emergency medical help arrives. Nursing Care Plan for the Patient With Arrhythmias Nursing Diagnosis: Decreased Cardiac Output related to arrhythmias Expected Outcomes: The patient's cardiac status will be stabilized. Patient will be able to perform activities of daily living (ADLs). Evaluation of Outcomes: There is an absence of arrhythmias. The patient performs ADLs without tachycardia, chest pain, or weakness. Intervention Rationale Evaluation Monitor apical pulse, blood pressure, lung sounds, urinary output, and mental status with frequency based on stability. Identifies arrhythmias, heart failure, impending cardiac arrest, or shock. Dizziness, confusion, and restlessness may indicate decreased cerebral blood flow. Is patient free of arrhythmias with vital signs within normal limits? Ensure that patient receives assistance with ADLs as needed and does not exceed activity tolerance. Reduces dyspnea and decreases oxygen demand on the myocardium. Does patient tolerate activity without dyspnea or chest pain? Geriatric Administer antiarrhythmic medications as ordered and observe for adverse reactions. Older patients may have decreased kidney and liver function that may lead to rapid development of toxicity. Does patient have signs of medication toxicity? Nursing Diagnosis: Anxiety related to situational crisis Expected Outcomes: The patient will be able to effectively manage anxiety. The patient will report decreased anxiety. Evaluation of Outcomes: The patient uses effective coping mechanisms to manage anxiety. Patient expresses decreased anxiety. Intervention Rationale Evaluation Ask patient and family to identify anxiety and verbalize concerns. Helps correct and clarify their concerns. What are patient's feelings or concerns? Explain procedures to patient and family. Lack of knowledge increases anxiety. This knowledge will help with compliance of therapy. Does patient express understanding of therapy with decreased anxiety? Reinforce teaching of relaxation techniques such as guided imagery, muscle relaxation, and meditation. These measures can restore psychological and physical equilibrium and help decrease anxiety. Is patient successful in demonstrating relaxation techniques? Home Health Hints   Always have a pocket mask for cardiopulmonary resuscitation available.   Patients prone to arrhythmias should avoid straining with bowel movements. If the patient reports straining, request a laxative or stool softener order from the HCP.   Reinforce teaching if patient is on beta blockers and inotropic agents (e.g., digoxin) on how to take a radial pulse, because bradycardia is a major side effect. If pulse is below 60 bpm, inform the patient to call the HCP.   Reinforce teaching for patients with a new implanted pacemaker to wear loose tops for comfort. Women can wear a small pad over the pacemaker to cushion it from a bra strap.   Reinforce teaching for patients who are going to travel to refill medicines ahead of time. Key Points   The six-step process for arrhythmia interpretation includes checking regularity of the rhythm, heart rate, P waves, P-R interval, QRS interval, and QT-interval.   An arrhythmia (or dysrhythmia) is an abnormal rhythm of the heart. They occur from disturbances in the formation of an impulse or in the conduction of the impulse.   Treatment for bradycardia includes IV atropine; for tachycardia above 150 beats per minute includes adenosine, beta blockers, or calcium channel blockers; for atrial flutter in symptomatic patients, catheter ablation.   Treatment for AF includes rate control with beta blockers or calcium channel blockers, pharmacological or electrical rhythm conversion, and anticoagulant therapy to reduce thrombi and stroke risk.   CHB is a medical emergency. If the patient is symptomatic, transcutaneous pacing is needed immediately until a permanent pacemaker can be implanted.   PVCs are treated when there are more than six per minute; they are regularly occurring, multifocal, or falling on the T wave (which can trigger life-threatening arrhythmias); or are caused by an acute MI. A beta blocker, calcium channel blocker, or antiarrhythmic medication is prescribed if needed.   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.   For VF or VT, an AED analyzes the rhythm, and either automatically delivers or prompts the operator to deliver an electrical shock.   A WCD or ICD or a combination pacemaker/ICD is used for a patient who experiences life-threatening arrhythmias or is at risk for sudden cardiac death.