ECG/ DYSRHYTHMIAS Nancy Lin, RN, MSN

Reading Assignment Wong’s Lewis Adams & Urban: Pharmacology Cardiac dysrhythmias: pp. 1311-1313 Lewis EKG’s: CH 36 Adams & Urban: Pharmacology Antidysrhythmics CH 40

SLO’s Relate electrocardiogram changes to common cardiac problems. Discuss conduction system and electrocardiographic monitoring in pediatric and adult clients. Introduction to assessment of normal and abnormal cardiac rhythm and appropriate treatment in pediatric and adult clients. Compare and contrast nursing and collaborative management of pediatric and adult clients with common dysrhythmias. Discuss nursing management of pediatric and adult patients with central venous access.

Lecture Content EKG’s Cardiac Rhythms Pacemakers Defibrillation/Cardioversion Central Venous Access

Conduction System of the Heart http://highered.mcgraw-hill.com/sites/0072495855/student_view0/chapter22/animation__conducting_system_of_the_heart.html Self assessment: E A B

Electrocardiogram (ECG) Detects electrical activity of heart Components of an ECG waveform P wave P-R interval QRS complex ST segment QT interval T wave

P Wave P wave PR interval Begins with firing of SA node Depolarization of atria atrial contraction. PR interval time period for impulse to spread through atria, AV node, bundle of His & Purkinje fibers.

QRS Complex Depolarization from AV node throughout ventricles ventricular contraction QRS interval time it takes for depolarization

ST Segment Time between ventricular depolarization & repolarization

T wave Ventricle repolarization U wave may represent repolarization of Purkinje fibers or assoc. with _____________

Principle of ECG Formation

Calculating HR From ECG Count # of QRS complexes in 1 minute. Count # of R-R intervals in 6 seconds & multiply that # by 10.

The ECG Paper

Intrinsic Rates of Conduction System SA node AV node Bundle of His, Purkinje fibers

Rhythm analysis Basic rules that can be followed to identify a patient's heart rhythm. What is the rate? Is it regular or irregular? Are P waves present? Are QRS complexes present? Is there a 1:1 ratio between P waves and QRS complexes? Is the PR interval constant?

Questions to Consider 1. What is the dominant rhythm and/or dysrhythmia? 2. What is the clinical significance of the findings? 3. What is the treatment for the particular rhythm?

Self Assessment A QRS complex represents: a) Atrial depolarization b) Atrial repolarization c) Ventricular depolarization d) Ventricular repolarization

Pediatric ECG Normal pediatric ECG: an ECG that contains a P wave, a QRS complex normal for age and less than or equal to 0.08 second, and a T wave. Newborn: Resting (awake) 100-180; Resting (sleeping) 80-160; exercise (fever): <220 1wk-3mo: 100-220; 80-180; <220 3mo-2yr: 80-150; 70-120; <200 2yr-10yr: 70-110; 60-100; <180 10yr-adult: 55-90; 50-90; <180

Dysrhythmias Caused by disorders of impulse formation Cause of a dysrhythmia influences treatment of patient. Common causes: Cardiac conditions Other conditions

Dysrhythmias In children Occur with CHD Follow surgical repair of CHD Cardiomyopathy Cardiac tumors Metabolic & electrolyte imbalances Genetic etiology

Dysrhythmias Naming of most cardiac rhythms begin with the site that the impulse originated.

Normal Sinus Rhythm Originates in SA node Follows normal conduction pattern of cardiac cycles Rhythm: Regular Rate: 60-100 bpm QRS normal P Wave – visible before each QRS complex P-R interval: normal (<5 small squares)

Normal Sinus Rhythm 1, P wave 2, PR interval 3, QRS complex 4, ST segment 5, T wave 6, QT interval Isoelectric (flat) line

Sinus Bradycardia Conduction pathway same as in NSR SA node fires at a rate <60 beats/minute May be normal in Rhythm – Regular Rate – Less than 60 beats per minute QRS Duration – Normal P Wave – visible before each QRS complex P-R Interval – Normal Usually benign & often caused by pts on Beta blockers

Sinus Tachycardia Rate: >100 beats/minute QRS Duration – Normal P Wave – Visible before each QRS complex P-R Interval – Normal Impulse generating heart beats are nl, but are occurring at faster pace than nl. Seen during exercise.

Premature Atrial Contraction Contraction originating from an ectopic focus Ectopic signal originates in left or right atrium & travels across atria by an abnormal pathway, creating a distorted P wave. Clinical Associations ECG Characteristics Clinical Significance Treatment

Paroxysmal Supraventricular Tachycardia Dysrhythmia originating in an ectopic focus anywhere above bifurcation of bundle of His Paroxysmal: abrupt onset & termination Some degree of AV block may be present Can occur in presence of Wolff-Parkingson-White (WPW) syndrome Rhythm: Regular or sl irregular Rate – 100-300 beats per minute QRS Duration – usually normal P Wave – often buried in preceding T wave PR interval – may be shortened or nl

Atrial Flutter An atrial tachydysrhythmia Recurring, regular, sawtooth-shaped flutter waves Originates from a single ectopic focus in right atrium. Atrial Rate – about 250-300 beats per minute QRS Duration – usually normal P Wave – Replaced with multiple F (flutter) waves, usually 2:1, but sometimes 3:1 P-R interval: not measurable Atrial flutter with a 4:1 conduction (four flutter [F] waves to each QRS complex)

Atrial Fibrillation Total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction. May be chronic or intermittent Most common dysrhythmia in US Rhythm – irregularly irregular Atrial Rate – 350 to 600 beats/min, can be slower QRS duration – usually normal P Wave – not distinguishable as atria are firing off all over P-R interval – not measurable The atria fire electrical impulses in irregular fashion causing irregular heart rhythm

First-Degree AV Block Every impulse is conducted to ventricles but duration of AV conduction is prolonged. After impulse moves through AV node, it is usually conducted normally through ventricles. Rhythm – regular Rate – normal QRS Duration – normal P Wave – Ratio 1:1 P Wave Rate – Normal P-R interval – prolonged Z(>5 small squares) First-degree AV heart block with a PR interval of 0.40 seconds.

Premature Ventricular Contraction A contraction originating in an ectopic focus in the ventricles Premature occurrence of a QRS complex, which is wide & distorted in shape Multifocal PVCs: PVCs that are initiated from different foci appear different in shape from each other Unifocal PVCs: PVCs that appear to have same shape Ventricular bigeminy: when every other beat is a PVC Ventricular trigeminy: when every 3rd beat is a PVC Couplet: two consecutive PVCs Three or more PVCs: Ventricular tachycardia

Premature Ventricular Contractions Clinical Associations ECG Charcteristics Clinical Significance Treatment

Ventricular Tachycardia A run of three or more PVCs occur Different forms of VT exist, depending on QRS configuration Monomorphic VT Polymorphic VT May be sustained (lasts >30sec) or nonsustained (<30sec) Development of VT is an ominous sign A life threatening dysrhythmia

Ventricular Tachycardia Clinical Associations: ECG Characteristics: Ventricular rate 150-250 beats/min. Rhythm: reg or irregular. AV dissociation may be present, with P waves occurring independently of QRS complex P wave usually buried in QRS complex PR interval: not measurable QRS: distorted, duration >12 sec R-R interval: may be irregular or regular CNS: central nervous system

Ventricular Tachycardia Clinical Significance: Stable or unstable Sustained VT will cause severe dec. in CO Results: Dysrhythmia must be treated quickly Ventricular fibrillation may develop

Ventricular Tachycardia Treatment: - Identify & treat precipitating causes

Ventricular Tachycardia VT without a pulse is a life-threatening situation Treated in same manner as ventricular fibrillation CPR & defibrillation: 1st line of Rx, followed by administration of epinephrine if defib unsuccessful.

Ventricular Fibrillation A severe derangement of heart rhythm Irregular undulations of varying shapes & amplitude Firing of multiple ectopic foci in ventricle Mechanically ventricle is simple “quivering”, no effective contraction, no CO occurs. Clinical Associations: • ECG Characteristics: HR not measurable Rhythm irregular & chaotic P wave: not visible PR & QRS interval not measurable.

Ventricular Fibrillation Clinical Significance: results in an unresponsive, pulseless & apneic state Pt will die if not rapidly treated. • RX: Immediate CPR & ACLS measures w/use of defib & drug therapy. • This patient needs to be defibrillated!!! QUICKLY

Asystole Total absence of ventricular electrical activity No ventricular contraction Pts are unresponsive, pulseless & apneic Lethal dysrhythmia Requires immediate treatment Poor prognosis Rhythm – flat Rate – 0 beats per minute QRS Duration – none P Wave - none

Asystole Clinical Associations: Clinical Significance: Treatment: Carry out CPR!!! Intubation Transcutaneous pacing IV therapy with epinephrine & atropine

Pulseless Electrical Activity Electrical activity can be observed on ECG, but there is no mechanical activity of ventricles & patient has no pulse. Poor prognosis Most frequent causes: Treatment: correct underlying cause.

Defibrillation Most effective method of terminating VF & pulseless VT.

Defibrillation Monophasic: deliver energy in one direction Biphasic: deliver energy in two directions delivers successful shocks at lower energies & w/fewer post shock ECG abnormalities output measured in joules (watts/sec)

Synchronized Cardioversion

Implantable Cardioverter-Defibrillator

Pacemakers Indications Patient monitoring

ECG Changes Associated With Acute Coronary Syndrome ST segment, T wave, and Q wave changes associated with myocardial ischemia (A), injury (B), and infarction (C).

Resource ECG Simulator www.skillstat.com

Antidysrhythmics Used for Classifications Prevention & Rx of cardiac rhythm disorders Classifications Group I drugs Group II drugs Group III drugs Group IV drugs

Group I: Fast (Sodium) Channel Blockers Dec. fast sodium influx to cardiac cells Drug response Three groups: IA IB IC

Group I-A Drugs Procainamide Most widely used Reduces automaticity Slows electrical conduction & delays repolarization in atria, ventricles & Purkinje fibers Indicated for: ____________________________ Given IV or PO Side effects

Group I-B Drugs Lidocaine Major use in abolishing ventricular dysrhythmias Administered IV Contraindicated in _____________ Benefits Adverse effect

Group II: Beta-Blockers Decrease conduction velocity, automaticity & recovery time. Slows conduction through AV node Examples More frequently prescribed For vent. Dysrhythmias, Aflutter & afib.

Group III: Prolong Repolarization Used in emergency treatment of ventricular dysrhythmias when other antidysrhythmics are ineffective. Examples Increase refractory period & prolong action potential duration (delay repolarization) Can significantly prolong QT interval & pose risk for ventricular dysrhythmias

Group III Drugs Amiodarone Indicated for life-threatening VF & VT Most frequently used Dec. automaticity Prolongs AV conduction Given IV or PO Pregnancy safety category: D Has serious adverse effects Indicated for life-threatening VF & VT

Group IV: Calcium Channel Blockers Examples Slow (calcium) channel blocker that blocks calcium influx → ↓ excitability & contractility of myocardium. ↑ refractory period of AV node → ↓ ventricular response.

Group IV Drugs Diltiazem Indications Adverse effects

References Hockenberry, M.J. & Wilson, D. (2015). Wong’s Nursing care of infants and children (10th ed.). St. Louis, MO: Mosby. Lewis, S., Heitkemper, M. & Dirksen, S. (2014). Medical Surgical Nursing: Assessment and Management of Clinical Problems (9th ed.). St. Louis, MO: Mosby