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Transcript
Cardiac Arrhythmias II: Tachyarrhythmias Supraventricular Tachycardias (Supraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region) Supraventricular Tachycardia (SVT) Terminology QRS typically narrow (in absence of bundle branch block); thus, also termed narrow QRS tachycardia • Usually paroxysmal, i.e, starting and stopping abruptly; in which case, called PSVT •“Paroxysmal Atrial Tachycardia (PAT)” - the older term for PSVT - is misleading and should be abandoned • AV Junctional Reentrant Tachycardias (typically incorporate AV nodal tissue) Mechanism of Reentry Bidirectional Conduction Unidirectional Block Recovery of Excitability & Reentry AV Nodal Reentrant Tachycardia AV Nodal Reentrant Tachycardia Circuit F = fast AV nodal pathway S = slow AV nodal pathway (His Bundle) During sinus rhythm, impulses conduct preferentially via the fast pathway Initiation of AV Nodal Reentrant Tachycardia PAC PAC PAC = premature atrial complex (beat) Sustainment of AV Nodal Reentrant Tachycardia Rate 150-250 beats per min P waves generated retrogradely (AV node → atria) and fall within or at tail of QRS Sustained AV Nodal Reentrant Tachycardia V1 P P P P Note fixed, short RP interval mimicking r’ deflection of QRS Orthodromic AV Reentrant Tachycardia AP Retrograde conduction via accessory pathway (AP) Anterogade conduction via normal pathway Initiation of Orthodromic AV ReentrantTachycardia PAC Atria AP AVN Ventricles PAC = premature atrial complex (beat) Sustainment of Orthodromic AV Reciprocating Tachycardia Atria AP Rate 150-250 beats per min AVN Ventricles Retrograde P’s fall in the ST segment with fixed, short RP Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-White Syndrome) Sinus beat Hybrid QRS shape “Delta” Wave AP Fusion activation of the ventricles PR < .12 s QRS ≥ .12 s Varying Degrees of Ventricular Preexcitation Intermittent Accessory Pathway Conduction V Preex V Preex Normal Conduction Note “all-or-none” nature of AP conduction Orthodromic AV Reentrant Tachycardia NSR with V Preex SVT: V Preex gone Note retrograde P waves in the ST segment Concealed Accessory Pathway Sinus beat No Delta wave during NSR (but AP capable of retrograde conduction) Summary of AV Junctional Reentrant Tachycardias • Reentrant circuit incorporates AV nodal tissue • P waves generated retrogradely over a fast pathway • Short, fixed RP interval Clinical Significance of AV Junctional Reentrant Tachycardias • Rarely life-threatening • However, may produce serious symptoms (dizziness or syncope [fainting]) • Can be very disruptive to quality of life • Involvement of an accessory pathway can carry extra risks Atrial Tachyarrhythmias Sinus Tachycardia (100 to 180+ beats/min) • P waves oriented normally • PR usually shorter than at rest Causes of Sinus Tachycardia • • • • • • • Hypovolemia ( blood loss, dehydration) Fever Respiratory distress Heart failure Hyperthyroidism Certain drugs (e.g., bronchodilators) Physiologic states (exercise, excitement, etc) Premature Atrial Complex (PAC) V5 Non-Compensatory Pause P P P P’ P Timing of Expected P Premature Atrial Complex (PAC): Alternative Terminology • Premature atrial contraction • Atrial extrasystole • Atrial premature beat • Atrial ectopic beat • Atrial premature depolarization PACs: Bigeminal Pattern P P’ P P’ P P’ • Note deformation of T wave by the PAC • “Regularly Irregular” Rhythm PACs with Conduction Delay/Block P P P Physiologic AV Block P’ Physiologic AV Delay P’ P’ Recovered AV Conduction PAC with “Aberrant Conduction” (Physiologic Delay in the His Purkinje System) V1 P P P’ P RBBB PACs with Aberrant Conduction (Physiologic RBBB and LBBB) V1 RBBB LBBB Normal conduction PACs with Physiologic LBBB and His-Purkinje System Block V1 Non-conducted PAC Non-Conducted PAC V5 V1 P P P’ P Note deformation of T wave by the PAC Bigeminal/Blocked PACs Mimicking Sinus Bradycardia V1 Only the 4th bigeminal PAC conducts Clinical Significance PAC’s • Common in the general population • May be associated with heart disease • Can be a precursor to atrial tachyarrhythmias Atrial Tachycardia V1 Differs from AV nodal or AV reentrant SVT • RP intervals can be variable • RP often > PR • (Example slower than more common rate mof 150-250 beats per min) Clinical Significance of Atrial Tachycardia • Similar to sequela of AV junctional reentrant tachycardias • Must be differentiated from them diagnostically Atrial Flutter (“Typical,” Counterclockwise) Reentrant mechanism Atrial Flutter II 4:1 V1 2:1 Classic inverted “sawtooth” flutter waves at 300 min-1 (best seen in II, III and AVF) Note variable ventricular response Atrial Flutter 2:1 Conduction (common) 2:1 & 3:2 Conduction 1:1 Conduction (rare but dangerous) V. rate 140-160 beats/min Atrial Fibrillation Focal firing or multiple wavelets Chaotic, rapid atrial rate at 400-600 beats per min Atrial Fibrillation V5 V1 • Rapid, undulating baseline (best seen in V1) • Most impulses block in AV node → Erratic conduction Atrial Fibrillation: Characteristic “Irregularly Irregular” Ventricular Response II Atrial Fibrillation with Rapid Ventricular Response II Irregularity may be subtle Atrial Fibrillation: Autonomic Modulation of Ventricular Response Baseline Immediately after exercise Clinical Significance of Atrial Flutter and Fibrillation • Causes – Usually occur in setting of heart disease; sometimes see “lone “ atrial fibrillation – Hyperthyroidism (atrial fibrillation) but • May acutely precipitate myocardial ischemia or heart failure • Chronic uncontolled rates may induce cardiomyopathy and heart failure • Both can predispose to thromboembolic stroke, etc Varying Degrees of Ventricular Preexcitation Atrial Fibrillation with Rapid Conduction Via Accessory Pathway Atrial Fibrillation with Third Degree AV Block V1 V5 Regular ventricular rate reflects dissociated slow junctional escape rhythm Regular Narrow QRS Tachycardias Differential Diagnosis of Regular Narrow QRS (Supraventricular) Tachycardia • Reentrant SVT incorporating AV nodal tissue – AV nodal reentrant tachycardia – Orthodromic AV reentrant tachycardia • SVT mechanism confined to the atria – Sinus tachycardia – Atrial flutter – Other regular atrial tachycardias • Short-RP favors AV node-dependent reentrant SVT Determining AV Nodal Participation in SVT by Transiently Depressing AV Nodal Conduction • Vagotonic Maneuvers – Carotid sinus massage – Valsalva maneuver (bearing down) – Facial ice pack (“diving reflex;” for kids) • Adenosine (6-12 mg I.V.) • If SVT “breaks,” a reentrant mechanism involving the AV node is likely • If atrial rate unchanged, but ventricular rate slows (#P’s > #QRS’s), SVT is atrial in origin SVT Responses to AV Nodal Depressant Maneuvers • SVT termination – AV nodal reentrant tachycardia – Orthodromic AV reentrant tachycardia • No SVT termination (despite maximal attempts) – Sinus tachycardia – Atrial flutter or fibrillation – Most atrial tachycardias (a minority are “adenosinesensitive”) Carotid Sinus Massage Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes Termination of SVT by Vagotonic Maneuver (Carotid Sinus Massage) SVT Carotid Sinus Massage SVT Adenosine 6 mg P P P P Ventricular Tachyarrhythmias Premature Ventricular Complex (PVC): Alternative Terminology • Premature ventricular contraction • Ventricular extrasystole • Ventricular premature beat • Ventricular ectopic beat • Ventricular premature depolarization Premature Ventricular Complex (PVC) Compensatory Pause PVCs: Bigeminal Pattern “Regularly Irregular” Rhythm Accelerated Idioventricular Rhythm (> Ventricular Escape Rate, but < 100 bpm) Fusion beat Ectopic ventricular activation Sinus acceleration Normal ventricular activation AV Dissociation SA Node ATRIA AND VENTRICLES ACT INDEPENDENTLY Ventricular Focus Ventricular Tachycardia (VT) V1 • Rates range from 100-250 beats/min • Non-sustained or sustained • P waves often dissociated (as seen here) Ladder Diagram of AV Dissociation During Ventricular Tachycardia Slower atrial rate Faster ventricular rate Impulses invade the AV node retrogradely and anterogradely, creating physiologic “interference” and block. Under the right conditions, some anterograde impulses may slip through. This phenomenon is not equivalent to third degree AV block Ladder Diagram of AV Dissociation During Third Degree AV Block Faster atrial rate Slower ventricular (escape) rhythm Note that impulses block anterogradely and retrogradely within the AV conduction system Monomorphic VT Polymorphic VT V1 Causes of PVC’s and VT • PVC’s are fairly common in normals but are also seen in the setting of heart disease • Monomorphic VT often implies heart disease, but can sometimes be seen in structurally “normal” hearts • Polymorphic VT can result from myoardial ischemia or conditions that prolong ventricular repolarization • Electrolyte derangements, hypoxemia and drug toxicity can cause PVC’s and VT MI Scar-Related Sustained Monomorphic VT Circuit “Torsade de Pointes” (Polymorphic VT Associated with Prolonged Repolarization) Clinical Significance of PVC’s and VT • Can be a tip-off to underlying cardiac, respiratory or metabolic disorder • VT may (but need not invariably) lead to hemodynamic collapse or more life-threatening ventricular tachyarrhythmias, increasing the risk of cardiac arrest Ventricular Flutter • VT > 250 beats/min, without clear isoelectric line • Note “sine wave”-like appearance Ventricular Fibrillation (VF) • Totally chaotic rapid ventricular rhythm • Often precipitated by VT • Fatal unless promptly terminated (DC shock) Sustained VT: Degeneration to VF Atrial Fibrillation with Rapid Conduction Via Accessory Pathway: Degeneration to VF Diagnosing Regular Wide QRS Tachycardia Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction? V1 Sustained Aberrant Conduction V1 Clinical Clues to Basis for Regular Wide QRS Tachycardia • REMEMBER: VT does not invariably cause hemodynamic collapse; patients may be conscious and stable • History of heart disease, especially prior myocardial infarction, suggests VT • Occurrence in a young patient with no known heart disease suggests SVT • 12-lead EKG (if patient stable) should be obtained Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction? More R-Waves Than P-Waves Implies VT! II Artifact Mimicking “Ventricular Tachycardia” QRS complexes “march through” the pseudo-tachyarrhythmia Artifact precedes “VT”