Copy of ECG Dysrhythmia Recognition Fall 2010 for VISTA (1)

ECG & Dysrhythmia RecognitionSusan S. Sammons, PhD (c), RN, CEN : 

ECG & Dysrhythmia RecognitionSusan S. Sammons, PhD (c), RN, CEN

What Makes Your Heart Special : 

What Makes Your Heart Special Automaticity: Ability to initiate an impulse spontaneously and continuously Excitability: Ability to be electrically stimulated Conductivity: Ability to transmit an impulse along a membrane in an orderly manner Contractility: Ability to respond mechanically to an impulse

Conduction Pathways : 

Conduction Pathways

Pacemakers & Rates : 

Pacemakers & Rates SA Node Primary pacemaker Fastest intrinsic rate 60-100 AV Node (Gatekeeper) Delays impulse to allow atria to contract and empty Intrinsic rate 40-60 Bundle of His Conducts impulses to the Right & Left Bundle Branches Bundle Branches Conduct impulses to the Purkinje Fibers Conduction through the Bundle of His  Bundle branches  Purkinje fibers = Full Ventricular Contraction Ventricular cells of the heart have the lowest intrinsic rate 20-40

Classification for Dysrhythmias : 

Classification for Dysrhythmias Site of origin SA node Atria AV node Ventricle Effect on Heart Bradycardia Tachycardia Heart block Premature beats Flutter Fibrillation Asystole

Common Causes of Dysrhythmias : 

Common Causes of Dysrhythmias Cardiac Valve disease Myocardial infarction Myocardial cell degeneration Heart failure Conduction defects Cardiomyopathy Accessory pathways Non-Cardiac Acid-base imbalance Drug effects or toxicity Alcohol Caffeine Tobacco Herbal supplements Electric shock Electrolyte imbalances Hypoxia Metabolic conditions Near drowning Poisoning

Cardiac Monitoring : 

Cardiac Monitoring 12 Lead 3 or 5 Lead (continuous monitoring)

Time & Voltage for ECG : 

Time & Voltage for ECG

Parts of the ECG : 

Parts of the ECG

P Waves & PR Interval : 

P Waves & PR Interval P Wave represents atrial contraction Duration 0.06-0.12 sec Disturbances noted here stem from conduction in the atria PR Interval Measured at the beginning of the P wave to the start of the QRS complex Duration 0.12-0.20 sec Disturbances noted here stem from conduction in the AV node, Bundle of His, Bundle Branches or the atria

QRS Complex : 

QRS Complex QRS Complex Ventricular depolarization Duration 0.04-0.12 sec Disturbances noted here result from conduction abnormalities in the bundle branches or ventricles

T Wave & ST Segment : 

T Wave & ST Segment T Wave represents the repolarization (relaxation) of the heart Duration 0.16 sec Disturbances are caused by: Ischemia and/or infarction Electrolyte imbalances ST Segment The time between ventricular repolarization & depolarization (contraction) Duration 0.12 sec Disturbances are caused by: Ischemia and/or infarction

5 Steps to Analyzing a Rhythm Strip : 

5 Steps to Analyzing a Rhythm Strip Determine Regularity of the R waves Calculate the Heart Rate Identify and examine P Waves Measure the PR Interval Measure the QRS Complex

Calculating Rate : 

Calculating Rate Six Second Strip Method 30 large boxes = 6 seconds Measure a six seconds strip Count the number of complexes Multiply number by 10 1500 Method Count the small boxes between two consecutive P waves (atrial rate/P-P interval) or two consecutive R waves (ventricular rate/R-R interval) Divide 1500 by the number of boxes counted

What is the heart rate? : 

What is the heart rate?

Normal Sinus Rhythm : 

Normal Sinus Rhythm Normal configuration of the P wave, QRS complex and T wave Normal rate: 60-100 bpm P wave is always present and followed by the QRS complex PR interval is no longer than 0.20 sec Benchmark to compare other rhythms

Sinus Bradycardia : 

Sinus Bradycardia Sinus rhythm with a heart rate < 60 bpm May be normal in aerobically trained athletes and during sleep Response to valsalva maneuver & increased vagal tone

Sinus Bradycardia : 

Sinus Bradycardia Clinical Associations Carotid sinus massage Valsalva maneuver Hypothermia Increased vagal tone Hypothyroidism Increased intracranial pressure Inferior wall MI Parasympathomimetic drugs Clinical Manifestations Dizziness/Syncope Dyspnea Weakness Angina Hypotension Confusion/Disorientation Pale, cool skin Treatment Anticholinergic drugs (Atropine) Pacemaker therapy We only treat SYMPTOMATIC patients

Sinus Tachycardia : 

Sinus Tachycardia Sinus rhythm with heart rate > 100 bpm

Sinus Tachycardia : 

Sinus Tachycardia Clinical Associations Exercise Fever Pain Hypotension Hypovolemia/anemia Hypoglycemia MI & HF Hyperthyroidism Fear/anxiety Medications Clinical Significance Dizziness Dyspnea Hypotension Treatment Treat underlying cause Adenosine Beta-Blocker

Paroxysmal Supraventricular Tachycardia : 

Paroxysmal Supraventricular Tachycardia Origination above the bifurcation of the bundle branches Re-excitation of the atria Has an abrupt onset and termination HR is 100-300 bpm

PSVT : 

PSVT Clinical Associations Overexertion Emotional stress Deep inspiration Stimulants Rheumatic heart disease Digitalis toxicity Cor pulmonale Wolff-Parkinson-White Syndrome Clinical Significance Hypotension Angina Dyspnea Prolonged HR >180 may lead to decreased CO Treatment Vagal stimulation Adenosine 1st line treatment Beta-blockers Digitalis Amiodarone Direct current cardioversion

Premature Atrial Contraction (PAC) : 

Premature Atrial Contraction (PAC) Underlying rhythm is usually regular P wave is premature and abnormal in shape, size or direction PR interval may be normal or prolonged QRS complex is normal

PAC : 

PAC Clinical Associations Emotional stress Ingestion of alcohol, caffeine, tobacco Electrolyte disturbances Hypoxia Hyperthyroidism COPD CAD & MI Digitalis toxicity Dilated or hypertrophied atria Sympathomimetic drugs Isolated PACs are not significant Frequent PACs may lead into more serious dysrhythmias (PSVT) Treatment Decrease ingestion of caffeine and alcohol and use of tobacco Beta-blocker

Atrial Flutter : 

Atrial Flutter Atrial tachydysrhythmia Recurring, regular, sawtooth-shaped P waves Originate from ectopic focus in right atria T wave is partially or completely obstructed QRS complexes are usually normal

Atrial Flutter : 

Atrial Flutter Clinical Associations CAD Hypertension Mitral valve disorders Pulmonary embolus Chronic lung disease Cor pulmonale Cardiomyopathies Hyperthyroidism Digoxin Epinephrine Clinical Significance Decreased CO HF Thrombus formation Treatment Slow ventricular rate Ca+ Channel Blockers Beta Blockers Electrical Cardioversion Antiarrhythmics: amiodarone Radiofrequency Ablation

Atrial Fibrillation : 

Atrial Fibrillation Arises from multiple ectopic pacemakers in the atria, complete disorganization Impulse so rapid atria quivers vs. contract Ventricular rate is grossly irregular

Atrial Fibrillation : 

Atrial Fibrillation Controlled Atrial Fibrillation: when the ventricular rate is < 100 bpm Atrial Fibrillation with a Rapid Ventricular Response: when the ventricular rate is >100 bpm Most common next to sinus rhythm May be seen in a healthy or diseased heart Common following heart surgery

Atrial Fibrillation : 

Atrial Fibrillation Temporary A-Fib Last only a few hours/days Associated with emotional stress Associated with excessive alcohol or caffeine ingestion May be idopathic Chronic A-Fib Associated with valve disease (especially mitral valve stenosis and regurgitation) Hypertension Coronary heart disease Cardiomyopathies Myocarditis & Pericarditis Heart Failure Hyperthyroidism Pulmonary disease Congenital heart disease

Atrial Fibrillation : 

Atrial Fibrillation Clinical Significance Decreased CO Thrombus formation Embolization: MI, PE, CVA Dyspnea Dizziness/syncope Hypotension Treatment Goal: decrease ventricular response <100 bpm or conversion Ca+ Channel Blockers: diltiazem Beta Blockers Digoxin Antidysrhythmics: amiodarone Direct current cardioversion Anticoagulation therapy Radiofrequency ablation

Heart (AV) Blocks : 

Heart (AV) Blocks Arrhythmias in which there is a delayed or failed conduction through the AV node 1st Degree Heart (AV) Block 2nd Degree Heart (AV) Block Mobitz type I or Wenckebach Mobitz type II 3rd Degree Heart (AV) or complete Block

1st Degree Heart (AV) Block : 

1st Degree Heart (AV) Block Sinus impulse is conducted normally but is delayed at the AV node Rhythm is regular P wave is normal PR interval is >0.20 sec but is constant QRS complex is normal

1st Degree Heart (AV) Block : 

1st Degree Heart (AV) Block Clinical Associations CAD MI Rheumatic Fever Hyperthyroidism Vagal stimulation Digoxin Beta Blockers Calcium Channel Blockers May be a precursor of a higher degree block Patients are usually asymptomatic No treatment Modification of medications if they are the cause Careful monitoring for changes in rhythm

2nd Degree Heart (AV) Block- Type 1 : 

2nd Degree Heart (AV) Block- Type 1 Failure of some of the sinus impulses to be conducted to the ventricles Regular atrial rhythm & irregular ventricle rhythm Rate is based on the underlying rhythm P waves are normal PR interval gets progressively longer until it occurs without the QRS complex QRS complex is normal

2nd Degree Heart (AV) Block- Type 1 : 

2nd Degree Heart (AV) Block- Type 1 Clinical Associations Beta Blockers Digoxin CAD Myocardial ischemia or infarct Clinical Significance Generally transient Generally well tolerated In patients following an MI it may signal a serious AV conduction disturbance Treatment if Symptomatic Atropine Temporary pacemaker

2nd Degree Heart (AV) Block-Type 2 : 

2nd Degree Heart (AV) Block-Type 2 More than one P wave before each QRS complex Rhythm of the atria are regular, ventricles may vary depending on the conduction ratio Rate is based on the underlying rhythm P waves are normal PR interval may be normal or prolonged but is constant QRS complex is normal or wide

2nd Degree Heart (AV) Block-Type 2 : 

2nd Degree Heart (AV) Block-Type 2 Clinical Associations Rheumatic heart disease CAD Anterior MI Digitalis toxicity Clinical Significance Often progresses to complete block Decreased HR  Decreased CO Hypotension Myocardial ischemia Treatment Temporary Pacemaker (emergent) Permanent Pacemaker (long term) Symptomatic management of hypotension, angina

3rd Degree Heart (AV) Block : 

3rd Degree Heart (AV) Block Regular atrial & ventricular rhythm Rate: Atrial based on underlying rhythm, ventricular 20-60 bpm P waves are normal but without relationship to QRS complex PR interval varies QRS complex is normal or wide

3rd Degree Heart (AV) Block : 

3rd Degree Heart (AV) Block Clinical Associations Severe Heart Disease CAD MI Myocarditis Cardiomyopathy Systemic diseases Digitalis Beta Blockers Calcium Channel Blockers Clinical Significance Decreased CO Myocardial ischemia Heart Failure Shock Syncope Treatment Temporary pacemaker (emergent) Permanent pacemaker (long term) Atropine Symptom management

Premature Ventricular Contraction (PVC) : 

Premature Ventricular Contraction (PVC) Premature, ectopic impulse originating from the ventricle Rhythm is usually regular Rate based on the underlying rhythm P wave not associated with PVC PR interval is not measurable QRS complex is premature and wide (>0.12) A run of >3 PVC complexes is ventricular tachycardia

PVCs : 

PVCs Unifocal PVC: identical in size, shape and direction Multifocal PVC: differ in size, shape and direction

PVC Patterns : 

PVC Patterns Bigeminy Trigeminy Couplets

PVC : 

PVC Clinical Associations Caffeine Alcohol Nicotine Epinephrine Electrolyte imbalances Hypoxia Fever Exercise Emotional stress CAD & MI Mitral valve prolapse HF Clinical Significance Usually benign (healthy heart) Depending on the frequency; decrease CO Angina HF Treatment Treat the cause Beta Blockers Antiarrhythmic

Ventricular Tachycardia (VT) : 

Ventricular Tachycardia (VT) Arrhythmia originating in an ectopic focus in the ventricles Lethal arrhythmia if sustained!!! Rhythm is regular P wave: usually hidden in QRS PR interval is not measurable QRS complex is wide >0.12 sec

Ventricular Tachycardia : 

Ventricular Tachycardia Monomorphic Polymorphic

Ventricular Tachycardia: Torsades de Pointes : 

Ventricular Tachycardia: Torsades de Pointes

Ventricular Tachycardia : 

Ventricular Tachycardia Clinical Associations MI CAD Significant electrolyte imbalance Cardiomyopathy Mitral valve prolapse Long QT syndrome Digitalis toxicity CNS disorders Clinical Significance Sustained  significant decreased CO Hypotension Pulmonary edema Decreased cerebral blood flow Cardiopulmonary arrest

Treatment of Torsades de Pointes : 

Treatment of Torsades de Pointes Patient becomes hemodynamically unstable quickly Commonly a forerunner of V-Fib Identify the causative factor: drugs, electrolye imbalance, bradycardia Magnesium loading dose & maintenance infusion *Rapid Mg+ administration  hypotension & asystole If precipitated by bradycardia temporary pacemaker may be used Drug therapy with isoproterenol, phenytoin or lidocaine may be used

Ventricular Fibrillation (V-Fib) : 

Ventricular Fibrillation (V-Fib) Disorganized, chaotic electrical focus in the ventricles Rhythm is irregular & chaotic Rate: 0 P waves are absent PR interval is not measurable QRS complex is absent

Ventricular Fibrillation : 

Ventricular Fibrillation Clinical Associations Acute MI Myocardial ischemia CAD Cardiomyopathy During cardiac pacing During cardiac catheterization Accidental electric shock Hyperkalemia Hypoxemia Acidosis Drug toxicity Clinical Significance Pulselessness  no CO Apneic state Death

Treatment of Ventricular Fibrillation & Pulseless Ventricular Tachycardia: SCREAM : 

Treatment of Ventricular Fibrillation & Pulseless Ventricular Tachycardia: SCREAM Shock: 360 J CPR: begin immediate chest compressions & respirations Primary ABC: airway, breathing, circulation Secondary ABCD: advanced airway, breathing (ventilation w/ O2), circulation (IV access), differential diagnosis (PATCH 4 MDS or 5Hs & 5Ts) Rhythm: check the rhythm after 2 mins of CPR; shock again if indicated Epinephrine: 1mg every 2-5 min Antiarrhythmic Medications: Consider Any Legitimate Medication (Amiodarone, Lidocaine, Magnesium)

Defibrillation : 

Defibrillation Most effective method of terminating a ventricular arrhythmia (V-fib & VT) Monophasic: delivers energy in one direction Biphasic: deliver energy in two directions; can deliver effective shock with less energy Synchronized cardioversion: delivers a shock on the R wave of the QRS complex Implantable Cardioverter Defibrillator Survived SCD Have spontaneous sustained VT Syncope w/ VT or V-fib High risk for future lethal arrhythmias

Monophasic vs. Biphasic : 

Monophasic vs. Biphasic

PATCH 4 MDS or 5H’s & 5T’s : 

PATCH 4 MDS or 5H’s & 5T’s Pulmonary embolus Acidosis Tension Pneumothorax Cardiac Tamponade Hyperkalemia Hypokalemia Hypovolemia Hypoxia Myocardial infarction Drugs Shivering Thrombus: MI Thrombus: PE Tension Pneumothorax Tamponade Tablets Hydrogen ions Hyperkalemia Hypokalemia Hypovolememia Hypoxia Hypothermia

Asystole : 

Asystole Total absence of ventricular electrical activity Rhythm: 0 Rate: 0 P waves: may be present PR interval: not measurable QRS complex: absent

PEA (pulseless electrical activity) : 

PEA (pulseless electrical activity) Treatment…. Check another lead CPR Problem search (differential diagnosis) Epinephrine 1mg every 3-5 min Atropine 1mg every 3-5 mins (3mg max dose)

Pacemakers : 

Pacemakers Used to pace the heart when normal conduction pathways are damaged or diseased Pace the atria and one or both ventricles Permanent Pacemaker: implanted Temporary Pacemaker: transvenous or transcutaneous

Implantable Pacemaker : 

Implantable Pacemaker

Pacemakers: Indication : 

Pacemakers: Indication Acquired AV Block Second degree Third degree Bundle Branch Block Cardiomyopathy Heart Failure Sick Sinus Syndrome Tachydysrhythmias (overdrive pacing)