1、Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.EKG Characteristics: Regular narrow-complex rhythmRate 60-100 bpmEach QRS complex is proceeded by a P waveP wave is upright in lead II & downgoing in lead aVR
2、Sinus BSinus tachycardiaJunctional tachycardiaEctopic atrial normal (sinus) beatssinus node doesnt fire leading to a period of asystole (sick sinus syndrome)p-wave has different shape indicating it did not originate in the sinus node, but somewhere in the atria. QRS is slightly different but still n
3、arrow, indicating that conduction through the ventricle is relatively normalAtrial Escape Beats A single ectopic focus fires near the AV node, which then conducts normally to the ventricles (usually initiated by a PAC)The rhythm is always REGULARProlonged runs of PSVT may result in atrial fibrillati
4、on or atrial flutter May be terminated by carotid massage Treatment: carotid massage, adenosine, Ca+ channel blockers, ablationAdenosine preferred in hypotension, previous IV B-blockerNote REGULAR rhythm in the tachycardiaRhythm usually begins with PAC Multiple ectopic foci fire in the atria, all of
5、 which are conducted normally to the ventriclesThe rhythm is always IRREGULAR P-waves of different morphologies (shapes) may be seen Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF Treatment: Ca+ channel blockers, beta blockers, but antiarrhythmic drugs are often ineffe
6、ctive potassium, magnesium (McCord et al, Chest 1998), Note IRREGULAR rhythm in the tachycardiathere is no p wave, indicating that it did not originate anywhere in the atria, but since the QRS complex is still thin and normal looking, we can conclude that the beat originated somewhere near the AV ju
7、nction. Junctional Escape BeatsQRS is slightly different but still narrow, indicating that conduction through the ventricle is relatively normala retrograde” p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back
8、up through the atria from the ventriclesQRS is wide and much different looking than the normal beats. This indicates that the beat originated somewhere in the ventricles. Ventricular Escape Beats“PVCs”no p wave, indicating that the beat did not originate anywhere in the atriaThey are frequent ( 30%
9、of complexes) or are increasing in frequency The come close to or on top of a preceding T-wave (R on T) Three or more PVCs in a row (run of V-tach) Any PVC in the setting of an acute MI PVCs come from different foci (multifocal or multiformed)These may result in ventricular tachycardia or fibrillati
10、on.sinus beatsUnconverted V-tach to V-fib V-tach“R on T phenomenon”time hypoxic myocardium - chronic pulmonary disease, pulmonary embolus ischemic myocardium - acute MI, expanding MI, angina sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism drugs & electrolyte imbalances - antiar
11、rhythmic drugs, hypokalemia, imbalances of calcium and magnesium bradycardia - a slow HR predisposes one to arrhythmias enlargement of the atria or ventricles producing stretch in pacemaker cellsFast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryThe Reentry Mechanism of Ectopic Beats
12、& RhythmsElectrical ImpulseCardiac Conduction TissueTissues with these type of circuits may exist: in the SA node, AV node, or any type of heart tissue in a “macroscopic” structure such as an accessory pathway in WPWFast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryPremature Beat Imp
13、ulseCardiac Conduction Tissue1. An arrhythmia is triggered by a premature beat 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only Repolarizing Tissue (long refractory period)The Reentry Mech
14、anism of Ectopic Beats & Rhythms3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrograde (backwards) up the fast pathway Fast Conduction PathSlow RecoverySlow Conduction PathFast RecoveryCardi
15、ac Conduction TissueThe Reentry Mechanism of Ectopic Beats & Rhythms4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation re-enters the pathway and continues in a circular movement. This creates the re-entry circuitFast Conduction
16、PathSlow RecoverySlow Conduction PathFast RecoveryCardiac Conduction TissueThe Reentry Mechanism of Ectopic Beats & RhythmsAtrial Re-entry atrial tachycardia atrial fibrillation atrial flutterAtrio-Ventricular Re-entry Wolf Parkinson White supraventricular tachycardiaVentricular Re-entry ventricular
17、 tachycardiaventricular fibrillationAtrio-Ventricular Nodal Re-entry supraventricular tachycardiaReentry Circuits as Ectopic Foci and Arrhythmia GeneratorsRate 100-270Normal QRSAberrancy possibleAcute Rx: Vagal maneuversAdenosine 6-12 mg IV push beware of pro-arrhythmiaCa+ channel blockersAtrial flu
18、tter is caused by a reentrant circuit in the wall of the atriumEKG Characteristics:Typical: “sawtooth” flutter waves at a rate of 300 bpmFlutter waves have constant amplitude, duration, and morphology through the cardiac cycleThere is usually either a 2:1 or 4:1 block at the AV node, resulting in ve
19、ntricular rates of either 150 or 75 Unmasking of flutter waves with adenosine.Acute Rx: ventricular rate control can be difficultAV nodal blockers prevent 1:1 conductionIbutilide 1-2mg rapid IV infusion have paddles readyRapid pacing or low voltage DC cardioversion is effectiveAnticoagulation as per
20、 atrial fibrillationBeware: Accelerated idioventricular rhythm. Rate below 150, stable hemodynamics, benign prognosis.SVT with aberrancy. Look at the 12 lead not just a rhythm stripMonomorphic vs. Polymorphic (long QT, bradycardia, ischemia)Rx:Unstable DC cardioversionStable monomorphic Procainamide
21、, AmiodaroneStable polymorphic - treat underlying etiologyRate 100-20Wide QRSMonomorphic vsPolymorphicAtrial fibrillation is caused by numerous waves of depolarization spreading throughout the atria, leading to an absence of coordinated atrial contraction.Classified as:Recurrent: when AF occurs on 2
22、 or more occasionsParoxysmal: episodes that generally last /= 7 days (most last /=7 daysPermanent: paroxysmal or persistent AF with failure to cardiovert or not Absent P wavesIrregularly irregular ventricular responseAcute Rx: rate control not rhythm control AFFIRM trial (NEJM 2002): B-blockers, Ca+
23、 channel blockers, digoxin, amiodaroneIbutilide 1-2mg rapid IV infusion have paddles readyOral propafenone or flecainide beware pro-arrhythmiaLow voltage DC cardioversion Anticoagulation as per atrial fibrillationOn the horizon: vernakalant, an atrial-selective Na and K channel blocker for conversio
24、n of short-duration atrial Ventricular fibrillation is caused by numerous waves of depolarization spreading throughout the ventricles simultaneously, leading to disorganized ventricular contraction and immediate loss of cardiac function.EKG Characteristics:Absent P wavesDisorganized electrical activ
25、ityDeflections continuously change in shape, magnitude and directionEKG Characteristics:Prolongation of the PR interval, which is constantAll P waves are conductedUsually benignThe Alan E. Lindsay ECG Learning Center ; http:/medstat.med.utah.edu/kw/ecg/Mobitz 1(Wenckebach)EKG Characteristics:Progres
26、sive prolongation of the PR interval until a P wave is not conducted.As the PR interval prolongs, the RR interval actually shortensUsually benign unless associated with underlying pathology, i.e. MIEKG Characteristics: Constant PR interval with intermittent failure to conduct Rhythm is dangerous as
27、the block is lower in the conduction system May cause syncope or may deteriorate into complete heart blockCauses: anterioseptal MI, fibrotic disease of the conduction system Treatment: may require pacemaker in the case of fibrotic conduction systemMobitz 2EKG Characteristics:No relationship between
28、P waves and QRS complexesConstant PP intervals and RR intervals May be caused by inferior MI and its presence worsens the prognosis May cause syncopal symptoms, angina, or CFHTreatment: usually requires pacemaker1.Depolarization spreads from the left ventricle to the right ventricle.2.This creates a
29、 second R-wave (R) in V1, and a slurred S-wave in V5 - V6.3.The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.1.Depolarization
30、 enters the right side of the right ventricle first and simultaneously depolarizes the septum from right to left.2. This creates a QS or rS complex in lead V1 and a monophasic or notched R wave in lead V6. 3.The T wave should be deflected opposite the terminal deflection of the QRS complex. This is
31、known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.Antiarrhythmia AgentsClass 1A agents: Procainamide, quinidine UsesWide spectrum, but side effects limit usageQuinidine : maintain sinus rhythms in atrial fibrillation a
32、nd flutter and to prevent recurrent tachycardia and fibrillation Procainamide: acute treatment of supraventricular and ventricular arrhythmias (no longer in production) Side effectsHypotension, reduced cardiac outputProarrhythmia (generation of a new arrhythmia) eg. Torsades de Points (QT interval)
33、Dizziness, confusion, insomnia, seizure (high dose) Gastrointestinal effects (common) Lupus-like syndrome (esp. procainamide)Class 1B agents: Lidocaine, phenytoinUsesacute : Ventricular tachycardia and fibrillation (esp. during ischemia)Not used in atrial arrhythmias or AV junctional arrhythmias Sid
34、e effects Less proarrhythmic than Class 1A (less QT effect) CNS effects: dizziness, drowsinessClass 1C agents: Flecainide, propafenoneUsesWide spectrumUsed for supraventricular arrhythmias (fibrillation and flutter) Premature ventricular contractions (caused problems) Wolff-Parkenson-White syndromeS
35、ide effectsProarrhythmia and sudden death especially with chronic use (CAST study) Increase ventricular response to supraventricular arrhythmiasCNS and gastrointestinal effects like other local anestheticsClass II agents: Propranolol, esmololUsestreating sinus and catecholamine dependent tachy arrhy
36、thmiasconverting reentrant arrhythmias in AVprotecting the ventricles from high atrial rates (slow AV conduction)Side effects bronchospasm hypotension beware in partial AV block or ventricular failureClass III agents: Amiodarone, sotalol, ibutilideAmiodaroneUsesVery wide spectrum: effective for most
37、 arrhythmiasSide effects: many serious that increase with timePulmonary fibrosisHepatic injuryIncrease LDL cholesterolThyroid diseasePhotosensitivityMay need to reduce the dose of digoxin and class 1 antiarrhythmicsClass III agents: Amiodarone, sotalol, ibutilideSotalolUses Wide spectrum: supraventr
38、icular and ventricular tachycardia Side effects Proarrhythmia, fatigue, insomniaClass III agents: Amiodarone, sotalol, ibutilideIbutilideUsesconversion of atrial fibrillation and flutter with rapid IV infusion Side effectsTorsades de pointesClass IV agents: Verapamil and diltiazemUsescontrol ventric
39、ular rate during supraventricular tachycardiaconvert supraventricular tachycardia (re-entry around AV)Side effectsCaution when partial AV block is present. Can get asystole if blocker is on boardCaution when hypotension, decreased CO or sick sinus Some gastrointestinal problemsAdditional agentsAdeno
40、sineAdministration rapid i.v. bolus, very short T1/2 (seconds)Cardiac effectsSlows AV conductionUsesconvert re-entrant supraventricular arrhythmiashypotension during surgery, diagnosis of CADMagnesiumtreatment for tachycardia resulting from long QTAdditional agentsDigoxin (cardiac glycosides)Mechani
41、smenhances vagal activity, inhibits Na/K ATPase refractory period, slows AV conductionUsestreatment of atrial fibrillation and flutterAtropineMechanismselective muscarinic antagonist Cardiac effectsblocks vagal activity to speed AV conduction and increase HRUsestreat vagal bradycardiaSelected References:ACC/AHA/ESC Practice Guidelines:Supraventricular Arrhythmias JACC 2003;42:1993-531.Atrial Fibrillation JACC 2006;48:854-906Ventricular Arrhythmias JACC 2006;48:1064-1108Thanks, and questions?
