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Transcript
Wandering Atrial Pacemaker Multifocal Atrial Tachycardia Atrial Tachycardia Premature Atrial Contractions Paroxysmal Supraventricular Tachycardia Atrial Flutter Atrial Fibrillation Rules of Interpretation Wandering Pacemaker Rate Rhythm Pacemaker Site P Waves Usually normal Slightly Irregular Varies Changes from beat to beat PRI Normal QRS Normal Wandering Etiology Transfer of pacemaker sites from the sinus node to other latent pacemaker sites in the atria and AV junction A variant of sinus dysrhythmia, a normal phenomenon in the very young or the aged, Ischemic heart disease, atrial dilation Clinical significance Pacemaker Usually has no detrimental effects Precursor of other atrial dysrhythmias such as atrial fibrillation Treatment If the patient is symptomatic, consider adenosine or verapamil Rules of Interpretation Multifocal Atrial Tachycardia Rate Rhythm More than 100 Irregular Pacemaker Site Ectopic sites in atria P Waves Organized, nonsinus P waves; at least 3 forms PRI Varies depending on source of impulse QRS Variable Multifocal Etiology Often seen in acutely ill patients May result from pulmonary disease, metabolic disorders, ischemic heart disease, or recent surgery Clinical Significance Atrial Tachycardia Presence of multifocal atrial tachycardia often indicates a serious underlying illness Treatment Treat the underlying illness Rules of Interpretation Premature Atrial Contractions Rate Rhythm Pacemaker Site P Waves PRI QRS Depends on underlying rhythm Usually regular except for the PAC Ectopic sites in atria Occurs earlier than expected Varies dependent on foci of impulse Usually normal Premature Etiology Single electrical impulse originating outside the SA node May result from use of caffeine, tobacco, or alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic Clinical Significance Atrial Contractions None. Presence of PACs may be a precursor to other atrial dysrhythmias. Treatment None if asymptomatic. Treat symptomatic patients by administering high-flow, high-concentration oxygen and establishing IV access. Rules of Interpretation Paroxysmal Supraventricular Tachycardia Rate Rhythm Pacemaker Site P Waves 150–250 Regular Atrial (outside SA Node) Often buried in preceding T wave PRI Usually normal QRS Usually normal Paroxysmal Etiology Supraventricular Tachycardia Rapid atrial depolarization overrides the SA node May be precipitated by stress, overexertion, smoking, caffeine Clinical Significance May be tolerated well by healthy patients for short periods Marked reduction in cardiac output can precipitate angina, hypotension, or congestive heart failure Paroxysmal Supraventricular Tachycardia Treatment Vagal Maneuvers Pharmacological Therapy Adenosine Electrical Therapy Consider if patient symptomatic with HR >150. Synchronized cardioversion starting at 50-100 J (or biphasic equivalent Rules of Interpretation Supraventricular Tachycardia Rate Rhythm Pacemaker Site P Waves PRI QRS 150-250 bpm Regular In the atria Difficult to see Usually normal Normal Supraventricular Etiology Refers to tachycardias that originate above the ventricles Use of caffeine, nicotine, or alcohol, cocaine sympathomimetic drugs, ischemic heart disease Clinical Significance Tachycardia Rapid rates can cause a marked reduction in cardiac output because of inadequate ventricular filling time Treatment Manage with tachycardia algorithm Click here to view the Tachycardia Management diagram. Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Care,” Circulation 2005, Volume 112, IV-70. © 2005 American Heart Association. Rules of Interpretation Atrial Flutter Rate Rhythm Pacemaker Site P Waves Atrial rate 250–350 Ventricular rate varies Usually regular Atrial (outside SA node) F waves are present PRI Usually normal QRS Usually normal Atrial Etiology Results when the AV node cannot conduct all the impulses Flutter Impulses may be conducted in fixed or variable ratios Usually associated with organic disease such as congestive heart failure (rarely seen with MI) Clinical Significance Generally well tolerated Rapid ventricular rates may compromise cardiac output and result in symptoms May occur in conjunction with atrial fibrillation Atrial Flutter Treatment Electrical Therapy Consider if ventricular rate >150 and symptomatic Synchronized cardioversion starting at 100 J Pharmacological Therapy Diltiazem or beta blockers Do not use a calcium channel and beta blockers concomitantly Rules of Interpretation Atrial Fibrillation Rate Atrial rate 350–750 Ventricular rate varies Rhythm Irregularly irregular Pacemaker Site P Waves PRI QRS Atrial (outside SA Node) None discernible None Normal Atrial Etiology Fibrillation Results from multiple ectopic foci; AV conduction is random and highly variable Often associated with underlying heart disease Clinical Significance Atria fail to contract effectively, reducing cardiac output Well tolerated with normal ventricular rates High or low ventricular rates can result in cardiac compromise Atrial Fibrillation Treatment Electrical Therapy Consider if ventricular rate >150 and symptomatic Synchronized cardioversion starting at 100 J Pharmacological Therapy Diltiazem or beta blockers AV junction serves two important physiological purposes: Slows the impulse between the atria and the ventricles Backup pacemaker if the SA node or cells higher in the conductive system fail to fire AV Locations Blocks At the AV node At the Bundle of His Below the Bundle of His Classifications First-Degree AV block Type I Second-Degree AV block Type II Second-Degree AV block Third-Degree AV block Rules of Interpretation First-Degree AV Block Rate Rhythm Pacemaker Site P Waves PRI QRS Depends on underlying rhythm Usually regular SA node or atrial Normal >0.20 Seconds Usually <0.12 seconds First-Degree Etiology Delay in the conjunction of an impulse through the AV node May occur in healthy hearts, but often indicative of ischemia at the AV junction Clinical Significance AV Block Usually not significant, but new onset may precede a more advanced block Treatment Generally, none required other than observation Avoid drugs that may further slow AV conduction Rules of Interpretation Type I Second-Degree AV Block Rate Rhythm Pacemaker Site P Waves Atrial, normal; ventricular, normal to slow Atrial, regular; ventricular, irregular SA node or atrial Normal, some P waves not followed by QRS PRI Increases until QRS is dropped, then repeats QRS Usually <0.12 seconds Type Etiology Also called Mobitz I, or Wenckebach Delay increases until an impulse is blocked Indicative of ischemia at the AV junction Clinical Significance I Second-Degree AV Block Frequently dropped beats can result in cardiac compromise Treatment Generally, none required other than observation Avoid drugs that may further slow AV conduction Treat symptomatic bradycardia Rules of Interpretation Type II Second-Degree AV Block Rate Rhythm Pacemaker Site Atrial, normal; ventricular, slow May be regular or irregular SA node or atrial P Waves Normal, some P waves not followed by QRS PRI Constant for conducted beats, may be >0.21 seconds QRS Normal or >0.12 seconds Type Etiology Also called Mobitz II or infranodal Intermittent block of impulses Usually associated with MI or septal necrosis Clinical Significance II Second-Degree AV Block May compromise cardiac output and is indicative of MI Often develops into full AV blocks Treatment Avoid drugs that may further slow AV conduction Treat symptomatic bradycardia Consider transcutaneous pacing Atropine Rules of Interpretation 2:1 AV Block Rate Rhythm Atrial, normal; ventricular, slow Regular Pacemaker Site SA node or atrial P Waves 2 P waves for each QRS PRI QRS Constant for conducted beats, may be >0.21 seconds Normal or >0.12 seconds 2:1 Etiology Second degree AV block where there are two P waves for each QRS Associated with acute myocardial infarction and septal necrosis Clinical significance AV Block Can compromise cardiac output Can develop into full AV block Treatment Prepare for transcutaneous pacing Atropine Rules of Interpretation Third-Degree AV Block Rate Atrial, normal; ventricular, 40–60 Rhythm Both atrial and ventricular are regular Pacemaker Site SA node and AV junction or ventricle P Waves Normal, with no correlation to QRS PRI No relationship to QRS QRS 0.12 seconds or greater Third-Degree Block) Etiology Absence of conduction between the atria and the ventricles Results from AMI, digitalis toxicity, or degeneration of the conductive system Clinical Significance AV Block (Complete Heart Severely compromised cardiac output Treatment Transcutaneous pacing for acutely symptomatic patients Treat symptomatic bradycardia Avoid drugs that may further slow AV conduction Dysrhythmias Premature junctional contractions Junctional escape complexes and rhythm Junctional bradycardia Accelerated junctional rhythm Characteristics of all junctional rhythms Inverted P Waves in Lead II PRI of <0.12 Seconds Normal QRS Complex Duration Rules of Interpretation Premature Junctional Contractions Rate Depends on underlying rhythm Rhythm Depends on underlying rhythm Pacemaker Site Ectopic focus in the AV junction P Waves Inverted, may occur after QRS PRI QRS Normal if P occurs before QRS Usually normal Premature Etiology Single electrical impulse originating in the AV node May occur with use of caffeine, tobacco, alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic Clinical Significance Junctional Contractions Limited, frequent PJCs may be precursor to other junctional dysrhythmias Treatment None usually required Rules of Interpretation Junctional Escape Complexes and Rhythms Rate Rhythm Pacemaker Site P Waves PRI QRS 40–60 Irregular in single occurrence, regular in escape rhythm AV junction Inverted, may occur after QRS Normal if P occurs before QRS Usually normal Junctional Etiology Results when the AV node becomes the pacemaker Results from increased vagal tone, pathologically slow SA discharges, or heart block Clinical Significance Escape Complexes and Rhythms Slow rate may decrease cardiac output, precipitating angina and other problems Treatment None if the patient remains asymptomatic Treat symptomatic episodes with atropine or pacing Rules of Interpretation Junctional Bradycardia Rate Rhythm Pacemaker Site P Waves PRI QRS Less than 40 Irregular in single occurrence, regular in escape rhythm AV junction Inverted, may occur after QRS Normal if P occurs before QRS Usually normal, may be greater than 0.12 Junctional Etiology Junctional dysrhythmia with a heart rate less than the intrinsic rate of the AV node Increased vagal tone, pathological slow SA node discharge, heart block, intrinsic disease Clinical Significance Bradycardia Decreased cardiac output Treatment Prepare for transcutaneous pacing Consider Atropine Rules of Interpretation Accelerated Junctional Rhythm Rate 60–100 Rhythm Regular Pacemaker Site P Waves PRI QRS AV junction Inverted, may occur after QRS Normal if P occurs before QRS Normal Accelerated Etiology Results from increased automaticity in the AV junction Often occurs due to ischemia of the AV junction Clinical Significance Junctional Rhythm Usually well tolerated, but monitor for other dysrhythmias Treatment None generally required in the prehospital setting Rules of Interpretation Accelerated Junctional Rhythm Rate Rhythm Pacemaker Site P Waves PRI QRS 60-100 Regular AV junction Inverted, may occur after QRS Normal if P occurs before QRS Normal Accelerated Etiology Results from increased automaticity in the AV junction Ischemia of the AV junction Clinical Significance Junctional Rhythm Patient should be monitored for other dysrhythmias Treatment Prehospital treatment generally is unnecessary Ventricular escape complexes and rhythms Accelerated idioventricular rhythm Premature ventricular contraction Ventricular tachycardia Torsades de pointes Ventricular fibrillation Asystole Artificial pacemaker rhythm Rules of Interpretation Ventricular Escape Complexes and Rhythms Rate Rhythm Pacemaker Site 15–40 Escape complex, irregular; escape rhythm, Regular Ventricle P Waves None PRI None QRS >0.12 seconds, bizarre Ventricular Rhythms Etiology Safety mechanism to prevent cardiac standstill Results from failure of other foci or high-degree AV block Clinical Significance Escape Complexes and Decreased cardiac output, possibly to life-threatening levels Treatment For perfusing rhythms, administer atropine and/or TCP For nonperfusing rhythms, follow pulseless electrical activity (PEA) protocols Rules of Interpretation Accelerated Idioventricular Rhythm Rate Rhythm Pacemaker Site 60-100 Escape complex, irregular; escape rhythm, Regular Ventricle P Waves None PRI None QRS >0.12 seconds, bizarre Accelerated Etiology A subtype of ventricular escape rhythm that frequently occurs with MI Ventricular escape rhythm with a rate of 60–110 Clinical Significance Idioventricular Rhythm May cause decreased cardiac output if the rate slows Treatment Does not usually require treatment unless the patient becomes hemodynamically unstable Primary goal is to treat the underlying MI Rules of Interpretation Premature Ventricular Contractions Rate Underlying rhythm Rhythm Interrupts regular underlying rhythm Pacemaker Site Ventricle P Waves None PRI None QRS >0.12 seconds, bizarre Premature Ventricular Contractions Etiology Single ectopic impulse resulting from an irritable focus in either ventricle Myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid-base disturbances, electrolyte imbalances, or as a normal variation of the ECG May occur in patterns Bigeminy, trigeminy, or quadrigeminy Couplets and triplets Premature Ventricular Contractions Clinical Significance Malignant PVCs More than 6/minute, R on T phenomenon, couplets or runs of ventricular tachycardia, multifocal PVCs, or PVCs associated with chest pain Ventricles do not adequately fill, causing decreased cardiac output Premature Ventricular Contractions Treatment Nonmalignant PVCs do not usually require treatment in patients without a cardiac history Cardiac patient with nonmalignant PVCs Administer oxygen and establish IV access Malignant PVCs: Lidocaine 1.0 –1.5 mg/kg IV bolus Repeat doses of 0.5-0.75 mg/kg to max dose of 3.0 mg/kg If PVCs are suppressed, administer lidocaine drip 2–4 mg/min Reduce the dose in patients with decreased output or decreased hepatic function and patients >70 years old Rules of Interpretation Ventricular Tachycardia Rate Rhythm Pacemaker Site P Waves PRI QRS 100–250 Usually regular Ventricle If present, not associated with QRS None >0.12 seconds, bizarre Ventricular Etiology 3 or more ventricular complexes in succession at a rate of >100 Causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acidbase disturbances, or electrolyte imbalances VT may appear monomorphic or polymorphic Tachycardia Torsade’s De Pointes Clinical Significance Decreased cardiac output, possibly to life-threatening levels May deteriorate into ventricular fibrillation Click here to view an animation on dysrhythmia. Click here to view the Tachycardia Management diagram. Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Care,” Circulation 2005, Volume 112, IV-70. © 2005 American Heart Association. Torsades de pointes Polymorphic VT Use of certain antidysrhythmic drugs Exacerbated by coadministration of antihistamines, azole antifungal agents and macrolide Torsades Typically occurs in nonsustained bursts de pointes Prolonged QT interval during “breaks” QRS rates from 166–300 RR interval highly variable Treatment Do not treat as standard VT Administer magnesium sulfate 1–2 g diluted in 100 ml D5W over 1–2 minutes Overdrive pacing Rules of Interpretation Ventricular Fibrillation Rate Rhythm No organized rhythm No organized rhythm Pacemaker Site Numerous ventricular foci P Waves Usually absent PRI None QRS None Ventricular Etiology Fibrillation Wide variety of causes, often resulting from advanced coronary artery disease Clinical Significance Lethal dysrhythmia with no cardiac output and no organized electrical pattern Ventricular Fibrillation Treatment Initiate CPR Defibrillate with 360 J (or biphasic equivalent) Control the airway and establish IV access Administer epinephrine 1:10,000 every 3–5 minutes Consider 40 IU Vasopressin IV (one time only) Consider second-line drugs Amiodarone Lidocaine Provide continuous compressions Rules of Interpretation Asystole Rate Rhythm Pacemaker Site No Electrical Activity No Electrical Activity No Electrical Activity P Waves Absent PRI Absent QRS Absent Asystole Etiology Primary event in cardiac arrest, resulting from massive myocardial infarction, ischemia, and necrosis Final outcome of ventricular fibrillation Clinical Significance Asystole results in cardiac arrest Poor prognosis for resuscitation Asystole Treatment Administer CPR and manage the airway Treat for ventricular fibrillation if there is any doubt about the underlying rhythm Administer medications: Epinephrine and Atropine Click here to view the Pulseless Arrest diagram. Reproduced with permission from “2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Care,” Circulation 2005, Volume 112, IV-59. © 2005 American Heart Association. Rules of Interpretation Artificial Pacemaker Rate Rhythm Pacemaker Site P Waves PRI QRS Varies with pacemaker May be regular or irregular Depends upon electrode placement None produced by ventricular pacemakers; pacemaker spike If present, varies >0.12 seconds, bizarre Artificial Etiology Pacemaker Rhythm Single vs. dual chamber pacemakers Fixed-rate vs. demand pacemakers Clinical Significance Used in patients with a chronic high-grade heart block, sick sinus syndrome, or severe symptomatic bradycardia Artificial Problems with Pacemakers Battery failure “Runaway” pacers Displaced leads Management Considerations Pacemaker Rhythm Identify patients with pacemakers Treat the patient Use of a Magnet Characteristics Electrical impulses are present, but with no accompanying mechanical contractions of the heart Treat the patient, not the monitor Causes Hypovolemia, cardiac tamponade, tension pneumothorax, hypoxemia, acidosis, massive pulmonary embolism, ventricular wall rupture Treatment Prompt recognition and early treatment Epinephrine 1 mg every 3–5 minutes Treat underlying cause of PEA Categories of Conductive Disorders Atrioventricular Blocks Disturbances of Ventricular Conduction Pre-excitation Syndromes Disturbances Aberrant Conduction All supraventricular beats are conducted through the ventricles in a delayed manner Causes A single supraventricular beat conducted through the ventricles in a delayed manner Bundle Branch Block of Ventricular Conduction Ischemia or necrosis of a bundle branch PAC or PJC that reaches one of the bundle branches in a refractory period Differentiation of SVT and Wide-Complex Tachycardias Pre-excitation Syndromes Excitation by an impulse that bypasses the AV node Creates Delta wave slur Wolff-Parkinson-White (WPW) syndrome Conduction from the atria to the ventricles is abnormal Associated with tachydysrhythmias Wolfe- ParkinsonWhite Syndrome Hypokalemia Normal potassium levels are 3.5–-5.0 mEg/L Flattened T waves Prominent U waves Hyperkalemia Tall Ts Suspect in patients with a history of renal failure Hypocalcemia Can be caused by the use of diuretics and certain endocrine conditions Prolongs ST segment Hypercalcemia Can be caused by adrenal insufficiency, hyperparathyroidism, kidney failure, or malignancies Shortens ST segment Digitalis use Sagging or scooping of the ST segment Prolonged PR interval Hypothermia Osborn wave (“J” wave) T wave inversion, sinus bradycardia, atrial fibrillation or flutter, AV blocks, PVCs, VF, asystole Cardiovascular Anatomy Cardiovascular Physiology Electrocardiographic Monitoring Dysrhythmias
