High-Acuity Nursing, 6th Edition

Basic Cardiac Rhythm Interpretation Objectives: 1. Explain membrane permeability changes in cardiac cells and the relationship between membrane permeability and serum electrolyte levels. 2. Describe the cardiac conduction system, the normal electrocardiogram (ECG) complex, and nursing responsibilities for the patient who requires cardiac monitoring. 3. Interpret ECG patterns using a systematic approach. 4. Identify factors that place a person at risk for developing dysrhythmias. 5. Differentiate among common dysrhythmias arising from the sinoatrial (SA) node and their treatments. 6. Compare and contrast basic atrial dysrhythmias and their treatments. 7. Distinguish among common functional dysrhythmias and their treatments. 8. Differentiate among common ventricular dysrhythmias and their treatments. 9. Distinguish among the four conduction abnormalities, known as heart blocks, and their treatments. 10. Discuss pharmacologic and counter shock interventions and their nursing implications. 11. Identify indications for pacemaker and implantable cardio version /defibrillation therapy, types of devices, and nursing implications for the patient receiving these therapies. I. Cellular Membrane Permeability A. Resting cardiac cell 1. Cardiac function is dependent on myocardial cell permeability and is affected by concentrations of electrolytes. 2. During the resting state, the inside of the cell is more electrically negative relative to the outside of the cell due to the differences in ion concentrations. This negatively charged resting state is referred to as its polarized state. B. Active cardiac cell—action potential 1. Depolarization and repolarization a) The transmission of electrical conduction begins with a change in polarity called action potential, a five-phase cycle that produces changes in the myocardial cell membrane’s electrical charge, stimulating the cardiac cells extending across the myocardial muscle to produce contraction and relaxation. b) As the cardiac cell receives an electrical stimulus, electrolytes shift, resulting in cardiac depolarization and repolarization of the cardiac muscle. 2. Action potential phases a) Depolarization (Phase 0)—the cell is almost impermeable to sodium unless a stimulus occurs. b) Repolarization (Phases 1–3)—the process of repolarization takes place over phases 1, 2, and 3. c) Resting membrane potential (Phase 4)—during the resting membrane potential phase, repolarization is completed, the original electrochemical gradient is in place, and the cell is ready to be depolarized again. 3. Refractory and supranormal periods a) Absolute refractory period—the cell cannot respond to another stimulus regardless of the strength of the stimulus. b) Relative refractory period—the cell is relatively (but not completely) unresponsive. c) Supernormal period—a time in which a weaker than normal stimulus can produce depolarization. PowerPoint Slides 1. Cardiac Function Dependent on myocardial cell permeability. Cellular permeability is affected by electrolytes. Sodium and potassium main cations. Calcium main anion. 2. Resting Cardiac Cell Negatively charged or polarized. Potassium concentration is greater inside the cell. Sodium concentration is greater outside the cell. Calcium concentration is greater outside the cell. Produces intracellular electrical negativity. 3. Action Potential Initiates a change in myocardial cell polarity. Five-phase cycle 4. Refractory and Supernormal Periods Absolute refractory period Relative refractory period Supranormal period 5. Action Potential of a Cardiac Cell Produces changes in the cell’s membrane electrical charge. Depolarization Repolarization II. Cardiac Conduction and the Electrocardiogram 1. The cardiac cycle is maintained by an intrinsic electrical circuit in the myocardium, where specialized areas of myocardial cells influence the electrical conduction pathway. Understanding this cycle is essential for electrocardiographic interpretation. A. Electrical conduction of the heart 1. The primary pacemaker of the heart is the sinoatrial (SA) node, which controls the heart rate normally between 60 and 100 beats per minute (bpm). The impulse from the SA node is transmitted: a) From the atria b) To the ventricles c) Along a cardiac conduction pathway 2. The normal conduction pathway a) The impulse from the SA node is transmitted: (1) From the atria (2) To the ventricles (3) Along a cardiac conduction pathway b) Starting at the SA node, the conduction pathways continues: (1) To the atrial-ventricular (AV) node (2) To the bundle of His (3) Proceeding along the left and right bundle branches (4) Terminating at the Purkinje fibers (5) Leading to ventricular muscle cells B. The electrocardiogram 1. The Normal ECG Pattern. a) P wave and PR interval. b) QRS complex c) ST segment and T wave d) QT interval. C. Cardiac monitoring systems 1. Proper lead placement is essential for accurate cardiac monitoring, and lead placement is verified by the nurse at the beginning of each shift. Figure 8-7 shows placement of a five electrode lead system. D. Nursing care of a patient who requires cardiac monitoring 1. Electrode management. 2. Monitor alarms. 3. ECG strip analysis. E. Patient electrical safety 1. Always check for frayed wires or components before performing an ECG. F. Patient and family education 1. Patients need to know why they require ECG monitoring. PowerPoint Slides 1. Electrical Conduction of the Heart Intrinsic electrical circuit 2. Primary Pacemaker—Sinoatrial node (SA) 3. Cardiac Conduction Pathway 4. The Electrocardiogram (ECG) Represents electrical activity 5. Nursing Care of a Patient Who Requires Cardiac Monitoring Components of ECG monitoring Electrode placement III. Basic Interpretation Guidelines 1. The ECG is printed on graph paper, with each small block of the graph paper being equal to 1 mm or 0.04 seconds on the horizontal axis. The horizontal axis also represents time. The vertical axis of the graph paper represents voltage; each small block is equivalent to 1 mm (0.1 mV) on the vertical axis. For basic ECG interpretation, time is the most important factor to consider. Each small block equals 0.04 seconds; a large block, composed of five small blocks, equals 0.20 seconds. Five large blocks represent 1 second. 2. There are eight steps to follow when interpreting an ECG: get heart rate, observe R–R interval, examine the P wave, measure the PR interval, determine if each P wave is followed by a QRS complex, examine and measure the QRS complex, examine and measure the QT interval, and diagnose/interpret the rhythm. A. ECG graph paper B. Measure the heart rate C. Examine the R–R intervals D. Examine the P waves E. Measure the PR interval F. P waves precede each QRS G. Examine and measure the QRS complex H. Measure the QT interval I. Diagnose the rhythm J. Clinical significance PowerPoint Slides 1. ECG ECG paper 2. Eight steps for ECG Interpretation Measure heart rate IV. Risk Factors for Development of Dysrhythmias A. Electrolyte abnormalities 1. Dysrhythmias are abnormal heart rhythms that result from a variety of causes. They occur in both healthy hearts and diseased hearts. 2. A major complication associated with dysrhythmias is their negative impact on myocardial contractility. 3. Dysrhythmias are abnormal heart rhythms that result from a variety of causes. They occur in both healthy hearts and diseased hearts. 4. A major complication associated with dysrhythmias is their negative impact on myocardial contractility. 5. Potassium abnormalities. a) Hypokalemia b) Hyperkalemia 6. Calcium abnormalities a) Hypocalcemia. b) Hypercalcemia. 7. Magnesium abnormalities. a) Hypomagnesemia b) Hypermagnesemia B. Fluid volume abnormalities 1. Fluid volume deficit 2. Tachydysrhythmias 3. Fluid volume overload 4. Ventricular enlargement 5. Decreased contractility 6. Premature beats 7. Cardiac conduction blocks 8. Alteration in heart rate C. Hypoxemia 1. Decreased myocardial tissue perfusion 2. Affects action potentials 3. Increases cell excitability D. Altered body temperature 1. Hypothermia 2. Decreased electrical heart activity 3. Prolonged PR, QT intervals 4. Widened QRS complex 5. Increases electrical heart activity 6. Increases heart rate PowerPoint Slides 1. Dysrhythmias Abnormal heart rhythms Normal and abnormal cardiac events 2. Major Complication Associated with Dysrhythmias 3. High-Acuity patients with Electrolyte Abnormalities are Prone to the Development of Dysrhythmias. Fluid volume abnormalities Hypoxemia Altered body temperature Hyperthermia Increases electrical heart activity Increases heart rate V. Sinus Dysrhythmias A. Sinus bradycardia 1. Sinus bradycardia is defined as a heart rate less than 60 bpm; it originates in the SA node. It is evidenced by a regular P wave preceding each QRS complex. It is recognized as a normal rhythm in athletes as a result of stronger myocardial muscle contractions. 2. Symptomatic sinus bradycardia can result in lethal ventricular dysrhythmias and can be treated with medication that blocks the parasympathetic innervations to the SA node. B. Sinus tachycardia 1. Sinus tachycardia has a rapid rate, from 100 to 150, and is not associated with any abnormal characteristics in rhythm. Sinus tachycardia can produce angina if the cardiac output decreases to the point of reducing coronary circulation. Treatment for sinus tachycardia is aimed at relieving the cause of increased sympathetic stimulation and can include imagery, distraction, and drug therapy. 2. In cases of sinus node dysfunction, impulses originating in atria cells will result in a variety of atrial dysfunction, and can even require a pacemaker. PowerPoint Slides 1. Sinus Bradycardia Defined 2. Sinus Bradycardia Treatment: Atropine 3. Sinus Tachycardia Heart rate 100–150 Complications: angina Nursing measures Drug therapy 4. Sinus Node Dysfunction Impulses originate elsewhere in atria Decrease cardiac output Nursing assessment VI. Atrial Dysrhythmias 1. Atrial dysrhythmias originate from ectopic impulses within the atria. They may develop when the SA node is not working properly or when an irritable focus (or multiple foci) develops in the atria. A. Premature atrial contractions 1. Premature atrial contractions (PACs) are a common type of premature beat that originates from one or more (multifocal) ectopic pacemakers located in the atria B. Supraventricular tachycardia 1. Supraventricular tachycardia (SVT) has a rate between 150 and 250. The rhythm is regular; however, the P waves are not distinguishable, because they are buried in the preceding T wave. Normal QRS complex indicates that the ectopic pacemaker is located above the ventricles. 2. Treatment for SVT varies, from Valsalva’s maneuver to the use of calcium channel blocking agent’s antidysrhythmic agents such as adenosine, calcium channel blocking agents, beta adrenergic blocking agents, or digoxin. C. Atrial flutter 1. Atrial flutter has a faster rate than SVT has, with a rate greater than 250 bpm. The ventricular rate depends on the number of impulses that pass through the AV node. D. Atrial fibrillation 1. Atrial fibrillation (A Fib) is a condition in which the atria are contracting so fast—greater than 350 bpm—that they are unable to have adequate filling or contraction. PowerPoint Slides 1a. Atrial Dysrhythmias Characterized by a rapid atrial rate Rapid ventricular response results in symptoms. 1b. Atrial Fibrillation (AF) Most common sustained arrhythmia Atria contracting very rapidly, unable to empty, discharging greater than 400 bpm Unable to refill atrial chambers before contraction Inadequate ventricular filling Decreases stroke volume (SV) 25% Blood remaining in atria prone to form clots Increases risk of thrombotic stroke QRS complex normal, irregular Absent P waves Treatment 2. Superventricular Tachycardia 3. Supraventricular Tachycardia (SVT) Rate between 150 and 250 Regular rhythm Undistinguishable P wave QRS complex normal 4. Treatment Valsalva’s maneuver Calcium channel blocking agents 5. Atrial Flutter Atrial rate greater than 250 Ventricular rate regular or irregular Atrial oscillations appear as sawtooth or flutter waves Described by the number of atrial oscillations f waves 5a. Atrial Flutter 5b. Atrial Oscillations/Treatment Cardioversion Calcium channel blockers VII. Junctional Dysrhythmias 1. Junctional dysrhythmias occur because the SA node fails to fire, so the AV node initiates the impulses. The junctional area is located around the AV node. 2. Pacemaker cells around the AV node have an intrinsic rate of 40–60 bpm. 3. Once the pacemaker cell discharges, the impulse spreads upward to depolarize the atria and downward to depolarize the ventricles. 4. The QRS complex appears normal, the atria are depolarized in an abnormal manner; therefore, the P wave might be inverted. The timing of the P wave is abnormal; it precedes the QRS complex, and the PR interval is shorter than 0.12 seconds. The P wave also might be buried in the QRS complex, and might not be distinguishable, or might follow the QRS complex. 5. Junctional tachycardia refers to a junctional rhythm with a rate greater than 100 bpm. If the rate is between 60 and 100, it is called accelerated junctional rhythm. 6. Treatment is dependent on patient symptomology and can consist of drug therapy and/or the insertion of a pacemaker. PowerPoint Slides 1. Junctional Dysrhythmias SA node fails to fire 2. AV Node Becomes Pacemaker Junctional area around AV node Intrinsic rate 40–60 bpm 3. P Wave Timing 4. Junctional Tachycardia Junctional rhythm Possible precipitant Rate <100 bpm 5. Treatment VIII. Ventricular Dysrhythmias 1. Ventricular dysrhythmias are ectopic impulses that originate in the ventricle and can be life-threatening. 2. Ectopic impulses of ventricular origin alter hemodynamics. This results in a decrease in cardiac output from loss of the atrial kick from backwards depolarization and from pushing ventricular blood. A. Premature ventricular contractions 1. Premature ventricular contractions (PVCs) are ectopic impulses that originate in the ventricle and discharge before the next normal sinus beat is due. 2. During ECG interpretation, the nurse assesses and describes the patient’s underlying cardiac rhythm and the type of PVCs (unifocal versus multifocal). 3. A major responsibility of the nurse is to assess the patient for factors that contribute to the development of PVCs and the presence of specific PVC patterns (see Table 8-6) warrant high vigilance because they are associated with development of two life-threatening dysrhythmias, ventricular tachycardia (VT) and ventricular fibrillation (VF). Occasional PVCs do not require treatment. B. Ventricular tachycardia 1. Ventricular tachycardia (VT) is classified as three or more consecutive PVCs occurring at a rapid rate, usually greater than 100 bpm. 2. A danger of ventricular tachycardia is that it may deteriorate into ventricular fibrillation. 3. Support (ACLS) by trained interdisciplinary team members such as nurses, respiratory therapists, pharmacists, and physicians. C. Ventricular fibrillation 1. Ventricular fibrillation, a fatal rhythm, is the most common cause of sudden cardiac arrest. 2. Defibrillation is the treatment of choice (AHA, 2011). 3. Pharmacotherapy includes a bolus of epinephrine or vasopressin. If the patient remains pulseless, CPR and attempts at defibrillation continue per ACLS guidelines (AHA, 2011). D. Asystole 1. Asystole represents complete cessation of electrical impulses. The patient is unconscious and pulseless. 2. It is imperative that the nurse check that the rhythm is verified in two separate leads, as fine ventricular fibrillation can mimic asystole but requires different interventions. 3. Often, despite rigorous efforts, asystole is a terminal rhythm. PowerPoint Slides 1. Ventricular Dysrhythmias Life-threatening Inadequate ventricular ejection Insufficient stroke volume Decrease oxygen tissue perfusion. 2. Ventricular Contractions 3. Ventricular Tachycardia Classified as three or more consecutive PVCs occurring at a rapid rate, usually greater than 100 bpm Support (ACLS) by trained interdisciplinary team members May deteriorate into ventricular fibrillation. 4. Ventricular Contractions 5. Ventricular Fibrillation The most common cause of sudden cardiac arrest. Defibrillation is the treatment of choice (AHA, 2011). Pharmacotherapy includes a bolus of epinephrine or vasopressin. 6. Asystole Represents complete cessation of electrical impulses. Ventricular fibrillation can mimic asystole. Asytole is a terminal rhythm. IX. Conduction abnormalities 1. Cardiac impulse conduction can be inhibited anywhere along the conduction pathway. Factors that can slow conduction include cardiac ischemia, digitalis, antiarrhythmic agents, and increased parasympathetic activity. 2. When the delay occurs at the antrioventricular (AV) node area, it is called an AV block. Acute AV blocks are associated with myocardial infarction. Chronic AV blocks develop from coronary artery disease. AV blocks have three classifications, and are based on the relationship of the P wave to the QRS complex. A. First-degree atrioventricular block 1. First-degree atrioventricular block is denoted by a prolonged PR interval; there is a delay in conduction through the AV node; the remainder of the ECG is normal. Patients are usually asymptomatic; however, in the presence of acute MI or coronary artery disease, conduction delay can increase and can lead to second- or third-degree block. B. Second-degree atrioventricular block 1. Second-degree atrioventricular block indicates that an SA node impulse is conducted with a delay or a completely blocked AV nodal area. A P wave is present, but the PR interval is irregular or is not measurable, due to a missing QRS complex. There are two patterns of AV block, Mobitz I and Mobitz II. a) Mobitz Type I (Wenckebach) is a second-degree AV block (Wenckebach). b) Mobitz Type II second-degree AV block PR intervals are constant before dropping the QRS complex. Nursing management depends on the degree of block and symptoms indicative of hypoxia that are exhibited by the patient. c) Management of Second-Degree AV Block. C. Third-degree (complete) atrioventricular block 1. Third-degree (complete) atrioventricular block requires emergency treatment, because the atria and ventricles are contracting independently, resulting in inadequate filling of the ventricles. No impulses are conducted through the AV node. The atria and ventricles fire at a regular interval, but they do not function as a single unit. This form of block is usually associated with myocardial infarction. 2. P–P wave interval is regular, as is the R–R wave interval, but the PR intervals vary. There is no relationship between the P wave and the QRS complex, because the atria and the ventricles are paced by a separate pacemaker. The QRS complex is usually wide because of the ventricular origin of the stimulus. In rare cases, the ventricular rate is fast enough to maintain cardiac output; however, complete block can progress to ventricular fibrillation. Treatment for complete heart block is the same as for type II second-degree block. D. Bundle branch block 1. Bundle branch block (BBB) results from an impairment in conduction through the bundle of His branches. PowerPoint Slides 1. Conduction Abnormalities Inhibition of cardiac impulses along conduction pathway Factors Classification 2. First-Degree Atrioventricular Block PR interval >0.20 seconds Delayed conduction through AV node Rest of ECG normal Patient usually asymptomatic No treatment necessary Acute MI Coronary artery disease 3. Second-degree Atrioventricular Block SA node impulse conduction is delayed or completely blocked. Occurs in the AV nodal area. P wave is present. PR interval is irregular or not measurable. Two patterns of AV block. Associated with third-degree AV block and asystole. Management 4. Third-Degree (Complete) Atrioventricular Block Requires emergency treatment. Atria and ventricles are contracting independently. Cardiac output greatly diminished. Impulses are not conducted through the AV node. Atria and ventricles fire at regular rate, but not as a single unit. P–P and R–R wave interval are regular. PR interval varies. No relationship between the P wave and QRS complex. Wide QRS complex. Associated with myocardial infarction. Can progress to ventricular fibrillation. Treatment. 5. Bundle Branch Block (BBB) Impairment in conduction through the bundle of His branches. Conduction through right and left bundle branches can be impaired. Impulse travels slowly through the blocked side. 12-lead ECG necessary to determine type of block. Treatment not necessary. X. Pharmacologic and Countershock Interventions and Nursing Implications A. Antidysrhythmic agents 1. Antiarrhythmic agents are used in treating cardiac conduction disturbances. Antiarrhythmics have several subcategories, class I through class IV, and are classified according to their effects during the slow and fast action potentials. Each of these drugs is capable of producing new dysrhythmias or worsening current dysrhythmias (proarrhythmics). Therefore, constant ECG monitoring is required as these medications are initiated. Antiarrhythmic agents are summarized in the box called “Related Pharmacotherapy: Antiarrhythmic Agents.” 2. Class I agents a) Class I drugs are fast sodium channel blockers. By blocking these channels, these drugs slow impulse conduction through the atria, ventricles, and the bundle of His. There are three categories of class I drugs. (1) Class IA drugs suppress dysrhythmias by reducing automaticity and prolonging the refractory period of the heart. They are indicated in the treatment of supraventricular and ventricular dysrhythmias. (2) Class IB drugs decrease refractory periods but do not affect automaticity to a great extent, and are used chiefly in the treatment of ventricular dysrhythmias. (3) Class IC agents delay ventricular repolarization, and are used as a maintenance therapy for supraventricular dysrhythmias. 3. Class II agents  a) Class II agents block the effects of catecholamines (e.g., epinephrine). They decrease SA node automaticity and slow AV conduction velocity and myocardial contractility. Their exact effects depend on which catecholamine receptor they block. (1) Most of the class II agents used to treat dysrhythmias in this category are beta-blocking agents, and decrease cardiac stimulation, and can produce vasodilation and bronchoconstriction. Drugs in this category are used in treating tachydysrhythmias. (2) Class II drugs are not to be used in patients with severe congestive heart failure, significant bradycardia, and second-degree or higher heart blocks, because of decreased cardiac stimulation. They are contraindicated in asthma because of bronchoconstriction. Because class II drugs decrease the heart rate, the heart rate might be unable to increase to maintain CO in some situations, such as exercise. 4. Class III agents a) Class III agents block potassium channels, thereby delaying repolarization and prolonging the refractory period. They increase the fibrillation threshold (making the cell more resistant) and are indicated in the treatment of atrial and ventricular dysrhythmias. 5. Class IV agents a) Class IV agents are calcium channel blockers. These drugs block the entry of calcium through the cell membranes, thereby decreasing depolarization. Automaticity in the SA node is reduced, AV node conduction is slowed, and overall decrease in myocardial contractility is produced with class IV agents. Verapamil and Diltiazem are calcium channel blockers commonly used for treating supraventricular tachydysrhythmias. 6. Other agents  a) Adenosine and digoxin do not fit within the four major classes. Adenosine is classified as an antiarrhythmic and is first-line therapy to convert supraventricular tachycardia to normal sinus rhythm. It is administered rapidly IV push over a 1–3 second period (Diepenbrock, 2012). Digoxin is classified as a cardiac glycoside and inotropic agent. It can be used to treat supraventricular tachycardia, atrial fibrillation, and atrial flutter. 7. Nursing management of patients receiving antidysrhythmic agents a) Prior to administration of any antiarrhythmic agent, the nurse assesses the following baseline data: (1) Vital signs (2) ECG interpretation using the seven-step process b) Physical assessment of the cardiac, respiratory, and neurologic systems B. Countershock 1. Elective Cardioversion. Delivers electrical current that is synchronized with the patient’s heart rhythm. It is used to treat SVT that is resistant to medication, atrial fibrillation or atrial flutter, and ventricular tachycardia in an unstable patient. a) Nursing considerations. In preparation for the procedure, the nurse obtains informed consent and educates the patient as to the purpose of the cardioversion and what to expect during it. C. Defibrillation 1. Defibrillation is an emergency procedure used to treat ventricular tachycardia in an unresponsive patient and ventricular fibrillation. Defibrillation is an unsynchronized electric shock that usually administers a larger number of joules (up to 360 J) than cardioversion does, once again depending on the type of defibrillator used. PowerPoint Slides 1. Antiarrhythmic Agents Used in treating cardiac conduction disturbances Classifications 2. Class I Agents Fast sodium channel blockers Three categories 3. Class II Agents Block the effects of catecholamines. Decrease SA node automaticity. Slow AV conduction, velocity, and myocardial contractility. Four catecholamine receptors 4. Class III Block potassium channels. Delay repolarization. Prolong refractory period. Prolong QRS interval. Treat atrial and ventricular dysrhythmias. 5. Class IV Agents Calcium channel blockers Decrease depolarization Reduce automaticity in SA node AV node conduction delayed Decrease myocardial contractility Treatment for SVTs Nursing assessment Drug administration 6. Nurse Assessment of Baseline Data Vital signs ECG interpretation Physical assessment 7. Countershock Cardioversion Nurse’s responsibilities 8. Defibrillation An unsynchronized electric shock that usually administers a larger number of joules than cardioversion does XI. Electrical Therapy A. Pacemakers 1. A pacemaker is a pulse generator used to provide an electrical stimulus to the heart when the heart fails to conduct or generate impulses on its own at a rate that maintains cardiac output. a) The pulse generator is connected to leads (wires) that provide an electrical stimulus to the heart when necessary. b) Pacemakers are used in addition to drug therapy when one of three conditions exists: failure of the conduction system, failure to initiate an impulse spontaneously, or failure to maintain primary pacing control. (Spontaneous impulses might occur, but they are not synchronized.) c) There are three commonly used pacing mechanisms: external, epicardial, and endocardial. 2. External pacemakers a) External pacing is a temporary measure. It delivers electric impulses to the myocardium transthoracically through two electrode pads placed anteriorly and posteriorly on the chest. b) This type of pacing can be a painful experience for the patient, who should be medicated accordingly. c) The presence of an adequate pulse and blood pressure demonstrates mechanical capture. 3. Epicardial pacemakers a) Epicardial pacers are inserted during open heart surgery; electrodes are placed directly on the surface of the heart. b) Affixed to the epicardium, the pacing wires are brought through the skin (below the sternum) for access. 4. Transvenous pacemakers a) Temporary transvenous pacing is achieved through electrical stimulation of the right ventricular or right atrial endocardium by an electrode-tipped catheter. b) There are two approaches available for placing a pacing wire: by direct insertion of the pacing wire or by insertion of a special pulmonary artery catheter that has an embedded pacing port c) When the procedure is complete, a chest X-ray is required to assure proper placement of the lead wire in addition to assuring the patient did not experience complications from the central line placement (i.e., pneumothorax). d) Caring for the transvenous pacing wire and site is done with sterile technique as this line poses risks for blood stream infection. 5. Permanent Implanted Pacemakers. a) Permanent pacemakers use an internal pulse generator. This generator is typically located in a subcutaneous tissue pocket (above the muscles and ribs, below the clavicle) in the chest wall. b) The leads are passed transvenously into the heart and rest on the endocardium. c) The generator is a small, thin, sealed device that contains a battery and is programmed according to the needs of the patient (Fig. 8-38). B. Chambers paced 1. Ventricle— Pacemakers have the ability to pace the atrium, the ventricle, or both (called “dual” or “AV sequential”) chamber. 2. Atrium—The atria can also be paced and can be noted on the ECG rhythm strip as a spike that appears just before the wave. This method of pacing is used with sinus node disease. 3. Dual Chamber—Atrial-ventricular (AV) sequential or dual pacing is used to synchronize heart depolarization in order to maintain cardiac output. In this type of pacing, both the atria and the ventricles are paced (dual chamber). Spikes appear before the wave and the QRS complex on the ECG. C. Pacemaker sensing 1. Pacemakers have the capability of sensing intrinsic (heart generated) electrical activity and may be either set on demand or fixed pacing. a) In demand pacing b) Fixed pacing D. Pacemaker settings 1. As with many types of technology-based devices, desired settings need to be set into the device. Pacemakers have three major settings: sensitivity, output, and rate. E. Pacemaker modes 1. Pacemakers vary in how they respond to electrical events in the heart. There are three major modes: triggered, inhibited, and double. F. Pacing problems 1. The number of times the pacemaker fires is determined by the sensitivity setting of the pacemaker. If the sensitivity is too low, the pacemaker may not sense the patient’s own cardiac electrical activity and will pace more frequently. If the sensitivity is too high, the pacemaker is better able to sense the patient’s own cardiac electrical activity and is inhibited from firing. a) Failure to sense term b) Failure to capture c) Failure to fire. G. Pacemaker classification 1. Pacemakers are classified according to a uniform system that is universally used to describe how the device functions according to where the pacing leads are and the mode of pacing. H. Implantable cardioverter/defibrillator 1. An implantable cardioverter/defibrillator (ICD) is placed in patients who have had prior aborted sudden cardiac death or proven sustained ventricular tachycardia. a) It also may be placed prophylactically in high-risk groups, such as those with various forms of cardiomyopathy. b) The device is a fully implantable, battery-operated system designed to recognize and terminate ventricular tachyarrhythmias that can cause sudden death. c) Patients who need an ICD require extensive training. d) Patients must understand the difference between heart attack and cardiac arrest. e) The ICD does not prevent a myocardial infarction, but it does prevent cardiac arrest. 2. Patient education a) The patient is taught that the ICD can “reorganize” his heart rhythm as well as stimulate the heart. (Pacemaker action is available on most recent models.) b) Patients are encouraged to keep a diary of shocks received, activities before and after treatment, symptoms, and response after shock. c) They should contact their cardiologist when they receive a shock. I. Electrical Therapy Nursing Considerations 1. Caring for a patient with a pacemaker or ICD requires specialized nursing care, including preparing the patient for insertion of an endocardial pacemaker or applying and using an external pacing device correctly. PowerPoint Slides 1. Pacemakers A pulse generator to provide an electrical stimulus to the heart Used when myocardial conduction cannot maintain adequate cardiac output Pulse generator connected to wires that carry electrical stimulus to the myocardial cells Used in addition to drug therapy Pacing mechanism 2. External Pacing Temporary measure Electrical impulses to myocardium transthoracically Nursing intervention 3. Permanent Implanted Pacemakers Use internal pulse generator Location Epicardial pacing Endocardial pacing 4. Types of Pacing Programmed to pace different areas of the heart. Most common are designed to pace ventricles. Will produce a spike before QRS complex. Used when transmission of atrial impulses is blocked. Can be programmed to pace when an intrinsic beat is not sensed. Triggered mode. Initiates impulse on sensing electrical activity. Double function pacemaker. 5. Pacing Problems Low sensitivity High sensitivity Failure to sense Failure to capture 6. Pacemaker Classification Classified according to uniform, universal system Pacemaker code written using five-letter format DDD pacemaker DDDR pacemaker 7. Implantable cardioverter/defibrillator (ICD) Implanted for those who aborted sudden cardiac death Aborted proven sustained VT. Prophylactically in high cardiac risk groups Designed to recognize and terminate ventricular tachyarrhythmias Distinguish between VT and VF Provide backup bradycardia pacing. Storing cardiac events Implantation of ICD 8. Automatic External Defibrillator (AED) Used by both medical and non-medical personnel Taught to general public ECG pattern detected through large chest pads XII. Chapter Summary XIII. Clinical Reasoning Checkpoint XIV. Post-Test XV. References Suggestions for Classroom Activities Have the students practice identifying ECG wave forms, and identifying and measuring intervals and complexes associated with premature ventricular contractions using the seven steps in rhythm interpretation. Have students discuss patients they have cared for, past or present, who have had dysrhythmias. Ask if there were predisposing factors for the development of premature contractions. Discuss nursing diagnoses for patients experiencing cardiac dysrhythmias. Suggestions for Clinical Activities Have the students obtain ECG strips from several patients and practice wave form identification and interval and complex measurements. Discuss individual students’ strips specific to their assigned patients. Have students discuss patients they have cared for, past or present, who have had dysrhythmias. Ask if predisposing factors for the development of ventricular dysrhythmias were evident. Wagner et al., Instructor’s Resource Manual for High-Acuity Nursing, 6th Edition ©2014 by Education, Inc.