Arrhythmias / Dysrhythmias

Prepared & Reported by: Peter Arnold Tagimacruz Tubayan THE HEART Cardiac Conduction System consists of specialized cardiac cells that initiate or propagate electrical impulses throughout the myocardium as a precursor to cardiac muscle contraction. Electrical Pathways

1. The sinoatrial (SA) node, located at the junction of the right atrium and the

superior vena cava, functions as the pacemaker for the myocardium, initiating rhythmic electrical impulses at an intrinsic rate of 60 to 100 impulses per minute. 2. The Atrioventricular (AV) node, located in the septal wall of the right atrium, receives impulses from the SA node and relays them to the ventricles. 3. The Bundle of His, a bundle of specialized muscle fibers in the myocardial septum, conducts impulses from the AV node. The bundle of His divides into right and left branches.
a) The right bundle branch (RBB) conducts impulses down the right side

of the septum.
b) Left bundle branch (LBB) conducts impulses into right and left fascicles

that fan out into the left ventricular muscle.

c) The RBB and LBB terminate in the Purkinje fibers, which propagate

electrical impulses into the endocardium and on to the myocardium.

Electrical Impulse Activity Electrical impulses travelling through the cardiac conduction system can be measured and recorded by electrocardiography.

Waves, Complexes, and Intervals

P wave

Represents atrial depolarization (electrical stimulation and mechanical contraction) Amplitude: 2 to 3 mm Duration: 0.06 to 0.12 sec Deflection: positive or upright in leads I, II, aVF and V2 to V6, usually positive but may vary in leads III and aVL; negative or inverted in lead aVR,; biphasic or variable in lead I

PR interval

Represents the time from the beginning of atrial depolarization (P wave) to the beginning of the QRS complex. Duration: 0.12 to 0.20 sec

QRS Complex Represents ventricular depolarization (electrical stimulation and mechanical contraction) Amplitude: 5 to 30 mm, but differs for each lead used Duration: 0.06 to 0.10 sec Deflection: positive (with most of the complex above the baseline) in leads I, II, III aVL, aVF and V4 to V6; negative in leads aVR and V1 to V2; and biphasic in lead 3.

T wave

Represents ventricular repolarization (electrical relaxation and mechanical relaxation) Location: follows the ST segment Amplitude: 0.5 mm in leads I, II, III and up to 10 mm in the precordial leads. Configuration: typically rounded and smooth Deflection: usually positive or upright in leads I, II, and V2 to V6; inverted in lead aVR; variable in leads III and V1.

ST segment Location: extends from the S wave to the beginning of the T wave. Amplitude: may vary from -0.5 to +1 mm in some precordial leads

QT Interval Location: extends from the beginning of the QRS complex to the end of the T wave Duration: usually lasts from 0.36 to 0.44 sec U wave Activation of Purkinje fibers Location: follows the T wave Configuration: small wave, typically upright and round Deflection: upright, best seen in V3

Standard Placement of 12 Leads Electrocardiogram:

The electrodes for the chest leads MUST go in the standard positions:

V1 - Fourth intercostal space, right sternal border. V2 - Fourth intercostal space, left sternal border. V3 - Midway between V2 and V4. V4 - Fifth intercostal space, left midclavicular line. V5 - Level with V4, left anterior axillary line. V6 - Level with V4, left mid axillary line.

Additional 15 and 18 Leads ECG Placement: Although the 12-lead electrocardiogram (ECG) is certainly an important component, along with clinical presentation and serum markers, in evaluating patients with acute coronary ischemia, 12lead ECG has problems with its sensitivity and specificity. The primary usefulness of the 12-lead ECG is in the detection of infarctions of the inferior, anterior, and lateral walls of the left ventricle. Infarctions involving the right ventricle and/or posterior wall are not as easily seen on standard 12-lead ECGs. The importance of detection of right ventricular and posterior wall infarction is evident, as approximately 40% of patients with inferior wall infarctions have right ventricular and/or posterior wall involvement, which predisposes them to more complications and increased mortality. The addition of nonstandard ECG leads to increase both sensitivity and specificity in the detection of infarctions of the right ventricle and the posterior wall. These nonstandard leads are commonly identified as right precordial leads (V4R, V5R, V6R) and posterior leads (V7, V8, V9). By combining these leads, clinicians can produce a 15- or 18-lead ECG. Specialized equipment is available to obtain 15- and 18-lead ECGs, but it is not essential. Clinicians can easily obtain data from these additional leads with the standard 12-lead ECG machine by adding electrodes in specified locations and running the 12-lead a second time. Using a 15-lead ECG to increase sensitivity and the odds of detecting an injury pattern (STsegment elevation) to the right ventricle and posterior left ventricle. The 15-lead ECG adds V4R, V8, and V9. Using an 18-lead ECG because, it allows earlier identification and appropriate treatment in a larger portion of the MI population. Additional leads for the 18-lead ECG are the leads for the 15-lead ECG plus V5R, V6R, and V7. The clinician looks for ST-segment elevation in these leads as in the standard 12-lead ECG to detect injury. The procedure for obtaining a 15- or 18-lead ECG is simple. First, run a standard 12-lead ECG. Second, using the precordial leads (V1-V6), place additional electrodes in the appropriate locations and run a second 12-lead ECG. Some important hints: Dont forget to write in the label of the new leads because the machine does not know where the electrodes are located. Also,

patients must lie as still as possible to avoid artifact in the posterior leads. These leads are located as follows:

V4R: right midclavicular line, fifth intercostal space (use V3 lead) V5R: right anterior axillary line, straight line from V4R (use V2 lead) V6R: right midaxillary line, straight line from V5R (use V1 lead) V7: left posterior axillary line, straight line from V6 (use V4 lead) V8: left midscapular line, straight line from V7 (use V5 lead) V9: left paraspinal line, straight line from V8 (use V6 lead).

ANALYZING THE ELECTROCARDIOGRAM RHYTHM STRIP:

Steps in the Systematic ECG Rhythm Strip Interpretation:

Regularity? Is it regular or irregular? Rate? Is it slow or fast or normal? Rhythm? Is it sinus? Check the waveforms. Is there P wave followed by a QRST? Measure the intervals: PR, QRS, QT. Is there a rhythm abnormality?

Normal Sinus Rhythm

It occurs when the electrical impulse starts at a regular rate and rhythm in the sinus node and travels through the normal conduction pathway.

Rate: 60 to 100 bpm Rhythm: regular QRS: usually normal, but may be regularly abnormal P wave: normal and consistent shape; always in front of the QRS PR interval: between 0.12 to 0.20 sec. P: QRS ratio: 1:1

ARRHYTHMIAS / DYSRHYTHMIAS
Arrhythmias are disorders of the formation or conduction or both of the electrical impulse within the heart. These can cause disturbances of the heart rate, heart rhythm or both. Arrhythmias may initially be evidenced by the hemodynamic effect they cause (a change in conduction may change the pumping action of the heart and cause decreased blood pressure and heart rate) They are named according to the site of origin of the impulse and the mechanism of formation or conduction involved. Sites of Origin: Sinus (SA) Node Atria Atrioventricular (AV) Node or Junction Ventricles Mechanisms of Formation or Conduction:
Normal (idio) rhythm

Bradycardia Tachycardia Dysrhythmia Flutter Fibrillation

 Premature complexes Blocks Pathophysiology: Myocardial cells that have been injured or replaced with scar tissue do not have the ability to respond to SA node impulses. Even when the SA node is functioning properly, other cardiac cells can assume the pacemaker properties when myocardial cells are injured, oxygendeprived, or exposed to certain chemicals or drugs. When any other part of the heart except the SA node initiates the heart beat, an arrhythmia occurs.

TYPES OF ARRHYTHMIAS: Sinus Node Dysrhythmias: Sinus Bradycardia Sinus bradycardia occurs when the sinus node creates an impulse at a slower than normal rate. The following are characteristics of sinus bradycardia:

Rate: less than 60 bpm P wave: precedes each QRS complex PR interval: normal QRS complex: normal Conduction: normal Rhythm: regular Etiology: Lower metabolic needs (sleep, athletic training, hypothermia, hypothyroidism) Vagal stimulation (vomiting, suctioning, severe pain, extreme emotions) Medications (calcium channel blockers, amiodarone, beta-blockers) Increased intracranial pressure

Myocardial infarction, especially in inferior wall

Assessment Findings:

Often asymptomatic, but clinical manifestation may include fatigue, lightheadedness, and syncope.

Nursing Management: If the client is symptomatic, maintain adequate cardiac output through treating the underlying cause and administering the anticholinergic drug (Atropine) as prescribed. If appropriate, provide nursing care for the client who has and will receive a pacemaker. Sinus Tachycardia Sinus tachycardia occurs when the sinus node creates an impulse at a faster than normal rate. The following are characteristics of sinus tachycardia:

Rate: 100 to 180 bpm P wave: precedes each QRS complex PR interval: normal QRS complex: normal Conduction: normal Rhythm: regular Etiology: Exercise, anxiety, fever, drugs, anemia, heart failure, hypovolemia, shock Assessment Findings: Often asymptomatic, but the clinical manifestations may include occasional palpitations, hypotension, and angina with cardiovascular disease.

Nursing Management:

Administer prescribed treatment. Treatment is directed at the primary cause. Carotid sinus pressure or a beta-blocker agent may be used to reduce the heart rate quickly. Sinus Arrhythmia Sinus arrhythmia occurs when the sinus node creates an impulse at an irregular rhythm; the rate usually increases with inspiration and decreases with expiration. The following are characteristics of sinus arrhythmia:

Rate: 60 to 100 bpm P wave: precedes each QRS complex PR interval: consistent interval between 0.12 to 0.20 sec QRS: usually normal, but may be regularly abnormal Rhythm: irregular Etiology: Respiratory cause: inspiration and expiration Nonrespiratory cause: heart disease and valvular disease

Assessment Findings:

Asymptomatic, but symptoms may occur from the underlying disease

Nursing Management: Sinus arrhythmia does not cause any significant hemodynamic effect and usually is not treated. Monitoring is the primary focus of nursing care. Atrial Dysrhythmias Premature Atrial Complex or Contraction A premature atrial complex (PAC) is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node. PACs have the following characteristics:

Rate: depends on the underlying rhythm Rhythm: irregular due to early P waves, creating a PP interval that is shorter than the others. QRS: the QRS that follows the early P wave is usually normal, but it may be abnormal. P wave: an early and different P wave may be seen or may be hidden in the T wave; other P waves in the strip are consistent. PR interval: the early P wave has a shorter than normal PR interval, but still between 0.12 and 0.20 sec. Etiology: May be caused by caffeine, alcohol, stretched atrial myocardium (hypervolemia, anxiety, hypokalemia, or atrial ischemia, injury, or ischemia.

Assessment Findings: Asymptomatic, but symptoms may occur from the underlying disease

Nursing Management: If PACs are infrequent, no treatment is necessary. If they are frequent, this may herald a worsening disease state or the onset of more serious dysrhythmias. Treatment is directed toward the cause. Continuous monitoring is the primary nursing role. Atrial Flutter Atrial flutter occurs in the atrium and creates impulses at an atrial rate between 250 to 400 times per minute. Because the atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node.

Atrial rate: ranges between 250 to 400 bpm Ventricular rate: ranges from 75 to 150 bpm Rhythm: atrial rhythm is regular; the ventricular rhythm is usually regular but may be irregular because of change in the AV conduction. QRS: usually normal. But may be abnormal or may be absent. P wave: saw-toothed shape, referred as F waves. PR interval: multiple F waves may make it difficult to determine Etiology: Underlying cardiovascular disease

Assessment Findings: Serious signs and symptoms: chest pain, shortness of breath, low blood pressure.

Nursing Management: If patient is unstable, nurse initiate electrical cardioversion as ordered. If the patient is stable, administer medications as ordered (Diltiazem, Verapamil, beta-blockers, or digitalis) intravenously to slow ventricular rate and can slow conduction through the AV node. Administer anti arrhythmic drug intravenously as ordered to promote conversion to sinus rhythm. Once conversion has occurred, administer anti-arrhythmic drug as ordered to maintain sinus rhythm. Atrial Fibrillation Atrial fibrillation causes rapid, disorganized, and uncontrolled twitching of atrial musculature. Atrial fibrillation has the following characteristics:

Atrial rate: 300 to 600 bpm Ventricular rate: 120 to 100 bpm Rhythm: highly irregular QRS: may be normal, but may be abnormal. P wave: no discernible P waves; irregular undulating waves are seen, referred as fibrillatory waves or f waves. PR interval: cannot be measured.

Etiology: Valvular heart disease, coronary artery disease, hypertension, cardiomyopathy, hyperthyroidism, pulmonary disease, acute moderate to heavy ingestion of alcohol (Holiday heart syndrome), after open heart surgery.

Assessment Findings:

Atrial fibrillation may be asymptomatic, but clinical manifestations may include palpitations, dyspnea, pulmonary edema, and signs of cerebrovascular insufficiency.

Nursing Management: Administer prescribed treatment to decrease ventricular response, decrease atrial stability, and eliminate cause. Administer prescribed medication, which may include cardiac glycoside or calcium channel blocker. Assist with electrical cardioversion. For clients with chronic atrial fibrillation, implement anticoagulant therapy as appropriate to prevent thromboemboli from forming in the atria. Junction / Atrioventricular Node Dysrhythmias Premature Junctional Complex / Contraction A PJC is an impulse that starts in the AV nodal area before the next normal sinus impulse reaches the AV node. Premature junctional complexes are less common than PACs. PJCs has the following characteristics:

Rate: depends on the underlying rhythm P wave: may be absent, may follow the QRS or may occur before the QRS QRS: the QRS that follows the early P wave is usually normal, but it may be abnormal. PR interval: less than 0.12 sec

Etiology: Digitalis toxicity, congestive heart failure, coronary artery disease.

Assessment Findings: Asymptomatic

Nursing Management: Treatment is directed toward the cause. Continuous monitoring is the primary nursing role. Junctional Rhythm Junctional rhythm or idionodal rhythm occurs when the AV node , instead of the sinus node, becomes the pacemaker of the heart. When the sinus node slows or when the impulse cannot be conducted through the AV node, the AV node automatically discharges an impulse. Junctional rhythm has the following characteristics:

Ventricular and Atrial Rate: 40 to 60 bpm if P wave is discernible Rhythm: regular QRS: usually normal, but may be abnormal P wave: may be absent after or before the QRS; may be inverted. PR interval: if P wave is in front of the QRS, PR interval is less than 0.12 sec Etiology: Increased vagal tone, complete heart block

Assessment Findings: Often asymptomatic, but clinical manifestation may include fatigue, lightheadedness, and syncope.

Nursing Management: If the client is symptomatic, maintain adequate cardiac output through treating the underlying cause and administering the anticholinergic drug (Atropine) as prescribed. If appropriate, provide nursing care for the client who has and will receive a pacemaker. Ventricular Dysrhythmias Premature Ventricular Complexes / Contraction PVC is an impulse that starts in a ventricle and is conducted through the ventricles before the next normal sinus impulse. In the absence of disease, PVCs are not serious. In the patient with acute MI, PVCs may indicate the need for more aggressive therapy. PVCs may indicate the possibility of ensuing VT. PVCs have the following characteristics:

Rate: depends on the underlying rhythm Rhythm: irregular due to early QRS, creating one RR interval that is shorter than the others QRS: duration is 0.12 sec or longer; shape is bizarre and abnormal P wave: visibility of P wave depends on the timing of the PVC; may be absent PR interval: if the P wave is in front of the QRS, the PR interval is less than 0.12 sec Etiology: Causes of PVC includes use of caffeine, or alcohol; cardiac ischemia or infarction, increased cardiac workload (exercise, fever, hypervolemia, heart failure, tachycardia), digitalis toxicity, hypoxia, and electrolyte imbalances.

Assessment Findings: PVCs may be asymptomatic, but clinical manifestations may include palpitations, weakness and lightheadedness.

Nursing Management: Assess the cause of PVCs and treat.

Assess life-threatening PVCs (more than 6 PVCs per minute, mutifocal PVCs, bigeminy, trigeminy, quadrigeminy, R on T PVCs, cuplets). Administer anti arrhythmic medication as ordered.

Ventricular Tachycardia and Torsade de Pointes (polymorphic/irregular) Ventricular tachycardia is three or more consecutive PVCs. Ventricular tachycardia is considered a medical emergency because cardiac output cannot be maintained because of decreased diastolic filling. It may precede ventricular fibrillation. VT has the following characteristics:

Ventricular rate: 100 to 200 bpm Atrial rate: depends on the underlying rhythm Rhythm: usually regular QRS: duration is 0.12 sec or more; bizarre, abnormal shape P wave: very difficult to detect, so atrial rate and rhythm may be indeterminable. PR interval: very irregular, if P wave is seen Etiology: The cause of VT is linked to irritability of ventricular muscle ans is associated with coronary artery disaese.

Assessment Findings: Lightheadedness, weakness, dyspnea, unconsciousness, pulseless

Nursing Management:

Administer an anti arrhythmic medication intravenously as prescribed. If patient is conscious and if medication is unsuccessful, assist with cardioversion. If rhythm deteriorates to ventricular fibrillation or if the patient is pulseless, assist with defibrillation and use Advanced Cardiac Life Support (ACLS) algorithm for resuscitation. Assess underlying cause and possible treatment.

Ventricular Fibrillation Ventricular fibrillation is rapid but disorganized ventricular rhythm that causes ineffective quivering of the ventricles. There is no atrial activity seen in the ECG. VFib has the following characteristics:

Ventricular rate: greater than 300 per minute Rhythm: extremely irregular, without specific pattern QRS: irregular, undulating waves without recognizable QRS complexes Etiology:

The cause of VT is linked to irritability of ventricular muscle ans is associated with coronary artery disaese, myocardial infarction and ischemia. Untreated or unsuccessful treated VT Electrical shock; electrolyte imbalances Brugada syndrome / sudden death syndrome

Assessment Findings: Loss of consciousness Pulselessness Absence of audible heartbeat and respiration Loss of blood pressure; possible seizures

Nursing Management: Assist with defibrillation. Administer prescribed anti arrhythmic medications. Code is called and assists with defibrillation and use Advanced Cardiac Life Support (ACLS) algorithm for resuscitation. Assess underlying cause and possible treatment.

Asystole Asystole is described as a lack of RRS complexes, heartbeat, palpable pulse, and respiration. Without immediate intervention, asystole is fatal and it is commonly called flatline. Asystole has the following characteristics:

Rate: not present P wave: may be visible but does not conduct through the AV node and ventricles. QRS: not present Rhythm: not present Etiology: Causes may include any of the reasons for the previously described arrhythmias if medical treatment was not successful and if underlying cause is left untreated.

Assessment Findings: Loss of consciousness No respirations; pulselessness

Nursing Management: As indicated, call for code and assist with cardiopulmonary resuscitation. Administer medications as ordered such as atropine and epinephrine. Provide nursing care for the insertion of a transthoracic, transvenous, or external pacemaker.

Conduction Abnormalities

An AV block is a conduction defect within the AV junction that impairs conduction of atrial impulses to ventricular pathways. The nurse takes care first to identify the underlying rhythm. Then the PR interval is assessed for the possibility of an AV node block. AV blocks occur when the conduction of the impulse through the AV nodal area is decreased or stopped

Etiology:

Congenital, valvular and atherosclerotic heart disease Myocardial infarction and ischemia Medications such as digitalis, calcium channel blockers, beta-blockers

First Degree AV Block It occurs when all the atrial impulses are conducted through the AV node into the ventricles at a rate slower than normal. Conduction is delayed in the AV junction. First degree AV block has the following characteristic:

Rate: depends on the underlying rhythm Rhythm: depends on the underlying rhythm QRS: usually normal, but may be abnormal P wave: in front of the QRS complex, shows sinus rhythm; regular shape PR interval: greater than 0.20 sec: measurement is constant Assessment Findings: Asymptomatic

Nursing Management: No treatment is necessary. Discontinue causative drug if indicated. Monitoring is the primary nursing role.

Second Degree AV Block Mobitz I (Wenckebach) It occurs when all but one of the atrial impulses are conducted through the AV node into the ventricles. Each atrial impulse takes a longer time for conduction than the one before, until one impulse is fully blocked. Because the AV node is not depolarized by the Blocked atrial

impulse, the AV node has time to fully repolarize, so that the next atrial impulse can be conducted within the shortest amount of time. It has the following characteristics:

Rate: depends on the underlying rhythm Rhythm: atrial regular; ventricular irregular P waves: similar, more P waves than QRS PR interval: lengthens with each cycle until a P wave appears without a QRS. QRS: Usually normal but may be abnormal Assessment Findings:

Clinical manifestations include vertigo, weakness, and an irregular pulse, and heart rate is slowed.

Nursing Management: Assess underlying cause. Administer Atropine as ordered to increase heart rate. Monitoring is very important.

Second Degree AV Block Mobitz II It occurs when only some of the atrial impulses are conducted through the AV node into the ventricles. It has the following characteristics:

Rate: depends on the underlying rhythm Rhythm: atrial regular; ventricular irregular P waves: similar, more P waves than QRS

PR interval: may be normal or prolonged; remains constant QRS: may be absent after P waves Assessment Findings: Clinical manifestations include vertigo, weakness, and an irregular pulse, and heart rate is slowed.

Nursing Management: Assess underlying cause. Administer Atropine as ordered to increase heart rate. Monitoring is very important.

Third Degree AV Block / Complete Heart Block / AV Dissociation It occurs when no atrial impulse is conducted through the AV node into the ventricles. Two impulses stimulate the heart: one stimulates the ventricles represented by the QRS complex, and one stimulates the atria represented by the P wave. P waves may be seen, but the atrial electrical activity is not conducted down into the ventricles to cause the QRS complex, the ventricular electrical activity. No recognizable consistent or meaningful relationships between atrial and ventricular activity.

Rate: atrial is higher than ventricular rate which is slower between 30-60 bpm Rhythm: atrial and ventricular: no relationship between the two P wave: similar, more P waves than the QRS PR interval:atria and ventricles beat independently of each other QRS: may be narrow or wide depending on level of the block Assessment Findings: Clinical manifestations include hypotension, angina and heart failure

Nursing Management: Assess for the underlying cause.

Administer Atropine as ordered to support ventricular escape rhythm Prepare and assist with the pacemaker insertion which provides repetitive electrical stimuli to the heart muscle to control the heart rate.

NURSING PROCESS: Assessment: 1. Health History a. Elicit a description of present illness and chief complaint such as chest pain, palpitations, dyspnea, syncope, etc. b. Explore the clients health history for risk factors such as family history, age, gender, race, smoking, hypertension, obesity, sedentary lifestyle, etc. 2. Physical Examination a. Vital signs b. Inspection: i. general appearance for signs of distress, anxiety, altered level of consciousness and hypoxia. c. Palpation: pulses d. Auscultation: abnormal heart sounds 3. Laboratory and Diagnostic Studies: a. Electrocardiogram b. Holter monitoring c. Exercise ECG d. Echocardiogram e. Cardiac enzymes f. Lipid profile g. Cardiac catheterization Nursing Diagnoses: 1. 2. 3. 4. Decreased cardiac output Impaired gas exchange Anxiety Deficient knowledge

Planning and Goals: The major goals for the patient may include eradicating or decreasing the incidence of the arrhythmia by decreasing contributing factors to maintain cardiac output, minimizing anxiety, and acquiring knowledge about the arrhythmia and its treatment.

Implementation: 1. Assess cardiopulmonary status. a. Assess level of consciousness, heart rate and rhythm, heart sounds, blood pressure, pulses, skin color. b. Monitor electrocardiogram and attached to a cardiac monitor and admit patient in a critical care unit. c. Monitor arterial blood gases and pulse oximetry. 2. Enhance cardiac output a. Establish a patent intravenous line to administer fluids and medications. b. Assist in cardiopulmonary resuscitation as indicated, call for code. Apply Advanced Cardiac Life Support. 3. Promote gas exchange and patent airway a. Administer oxygen supplement as indicated. Assist in intubation if necessary. b. Maintain at semi-Fowlers position to decrease oxygen myocardial consumption. 4. Increase activity intolerance a. Balance periods of rest and exercise. Assist as needed with activities of daily living. 5. Promote comfort a. Assess the clients description of chest discomfort, including location, radiation, duration, and what precipitated pain. 6. Promote adequate sleep and rest a. Attempt to cluster nursing interventions to provide client with several hours of uninterrupted sleep. 7. Minimize anxiety a. Offer client opportunities to ventilate feelings, answer clients question, and develop a trusting and caring relationship with the client and clients family. 8. Provide client and family teaching. Evaluation / Expected Outcomes 1. Maintains cardiac output a. Demonstrates heart rate, blood pressure, respiratory rate, and level of consciousness within normal ranges. b. Demonstrates no or decreased episodes of arrhythmias. 2. Experiences reduced anxiety a. Expresses a positive attitude about living with the dysrhythmia b. Expresses confidence in ability to take appropriate actions in an emergency 3. Expresses understanding of the dysrhythmia and its treatment a. Explains the dysrhythmia and its effects b. Describes the medication regimen and its rationale c. Describes a plan to eradicate or limit factors that contribute to the occurrence of the dysrhythmia. d. States actions to take in the event of an emergency.

Adjunctive Modalities and Management: Pacemaker Therapy A cardiac pacemaker is a temporary or permanent electronic device that provides electrical stimuli to the heart muscle to initiate and maintain cardiac contractions when the hearts natural pacemakers are unable to do so. Pulses are generated from a batteryoperated pacer unit and transmitted to the heart through electrodes placed in direct contact with the heart muscle wall.

Cardioversion and Defibrillation Treatment for tachyarrhythmias They are used to deliver an electrical current to depolarize a critical mass of myocardial cells. When the cells repolarize, the sinus node is usually able to recapture its role as the hearts pacemaker.

Cardioversion Involves the delivery of a timed electrical current to terminate a tachyarrhythmia. In cardioversion, the defibrillator is set to as synchronize with the ECG on a cardiac monitor so that the electrical impulse discharges during ventricular depolarization (QRS complex) If cardioversion is elective: a. anticoagulation for a few weeks may be indicated before the cardioversion b. digoxin is usually withheld for 48 hours before cardioversion c. nothing per orem 8 hours before cardioversion. Amount of voltage used varies from 25 to 360 joules depending on the defibrillators technology and type of dysrhythmia Defibrillation Is used in emergency situations as the treatment of choice for ventricular fibrillation and pulseless ventricular tachycardia. Defibrillation depolarizes a critical mass of myocardial cells. When the cells repolarize, the sinus node is usually able to recapture its role as the hearts pacemaker.

 The electrical voltage required to defibrillate the heart is usually greater than the required cardioversion. Implantable Cardioverter Defibrillator (ICD) Standard Paddle Placement:

Electrophysiologic Studies
Is used to evaluate and treat various dysrhythmias that have cause cardiac arrest or

significant symptoms. It also indicated for patients with symptoms that suggest a dysrhythmia that has gone undetected and undiagnosed by other methods. An EP study is used to:

a. Identify the impulse formation and propagation through the cardiac electrical conduction system. b. Assess the function and dysfunction of the SA node and AV nodal areas. c. Identify the location (called mapping) and mechanism dysrhythmogenic foci. d. Assess the effectiveness of antiarrhythmic medication and devices for the patient with a dysrhythmia. e. Treat certain dysrhythmias through the destruction of the causatice cells (ablation) Cardiac Conduction Surgery Atrial tachycardias and ventricular tachycardias that do not respond to medications and are not suitable for antitachycardia pacing may be treated by methods other than medications and devices. Endocardial Isolation Endocardial isolation involves making an incision into the endocardium that separates the area where the dysrhythmia originates from the surrounding endocardium. The edges of the incision are then sutured together. The incision and its resulting scar tissue prevent the dysrhythmia from affecting the whole heart.

Catheter Ablation Therapy

Catheter ablation destroys specific cells that are the cause or central conduction method of a tachyarrhythmia. a. Radiofrequency ablation using sound waves; thermal injury b. Cryoablation using cooled temperature; freezing method c. Electrical ablation using shock 100 to 300 joules; burns tissue causing scarring.