Cardiac Arrhythmias II: Tachyarrhythmias Ppt Powerpoint Presentation slides Anonymous Medical Slideshow Cardiac Arrhythmias II : Tachyarrhythmias

Cardiac Arrhythmias II: Tachyarrhythmias

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Notes

Show Notes

Slide 1 :

Cardiac Arrhythmias II: Tachyarrhythmias Michael H. Lehmann, M.D. Clinical Professor of Internal Medicine Director, Electrocardiography Laboratory

Slide 2 :

Supraventricular Tachycardias (Supraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region)

Slide 3 :

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

Slide 4 :

AV Junctional Reentrant Tachycardias (typically incorporate AV nodal tissue)

Slide 5 :

Unidirectional Block Recovery of Excitability & Reentry Bidirectional Conduction Mechanism of Reentry

Slide 6 :

AV Nodal Reentrant Tachycardia

Slide 7 :

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

Slide 8 :

Initiation of AV Nodal Reentrant Tachycardia PAC = premature atrial complex (beat) PAC PAC

Slide 9 :

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

Slide 10 :

P P P P Sustained AV Nodal Reentrant Tachycardia Note fixed, short RP interval mimicking r’ deflection of QRS V1

Slide 11 :

Orthodromic AV Reentrant Tachycardia AP Anterogade conduction via normal pathway Retrograde conduction via accessory pathway (AP)

Slide 12 :

Initiation of Orthodromic AV ReentrantTachycardia AVN Ventricles Atria AP PAC = premature atrial complex (beat) PAC

Slide 13 :

Sustainment of Orthodromic AV Reciprocating Tachycardia Atria AP AVN Ventricles Retrograde P’s fall in the ST segment with fixed, short RP Rate 150-250 beats per min

Slide 14 :

Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-White Syndrome) Fusion activation of the ventricles “Delta” Wave AP PR < .12 s QRS ? .12 s Sinus beat Hybrid QRS shape

Slide 15 :

Varying Degrees of Ventricular Preexcitation

Slide 16 :

Slide 17 :

Intermittent Accessory Pathway Conduction Normal Conduction V Preex V Preex Note “all-or-none” nature of AP conduction

Slide 18 :

Orthodromic AV Reentrant Tachycardia NSR with V Preex SVT: V Preex gone Note retrograde P waves in the ST segment

Slide 19 :

Concealed Accessory Pathway No Delta wave during NSR (but AP capable of retrograde conduction) Sinus beat

Slide 20 :

Summary of AV Junctional Reentrant Tachycardias Reentrant circuit incorporates AV nodal tissue P waves generated retrogradely over a fast pathway Short, fixed RP interval

Slide 21 :

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

Slide 22 :

Atrial Tachyarrhythmias

Slide 23 :

Sinus Tachycardia (100 to 180+ beats/min) P waves oriented normally PR usually shorter than at rest

Slide 24 :

Causes of Sinus Tachycardia Hypovolemia ( blood loss, dehydration) Fever Respiratory distress Heart failure Hyperthyroidism Certain drugs (e.g., bronchodilators) Physiologic states (exercise, excitement, etc)

Slide 25 :

V5 P P P P’ P Timing of Expected P Premature Atrial Complex (PAC) Non-Compensatory Pause

Slide 26 :

Premature Atrial Complex (PAC): Alternative Terminology Premature atrial contraction Atrial extrasystole Atrial premature beat Atrial ectopic beat Atrial premature depolarization

Slide 27 :

PACs: Bigeminal Pattern P P’ P P’ P P’ Note deformation of T wave by the PAC “Regularly Irregular” Rhythm

Slide 28 :

PACs with Conduction Delay/Block Physiologic AV Block Physiologic AV Delay Recovered AV Conduction P P P P’ P’ P’

Slide 29 :

PAC with “Aberrant Conduction” (Physiologic Delay in the His Purkinje System) V1 P P P’ P RBBB

Slide 30 :

V1 PACs with Aberrant Conduction (Physiologic RBBB and LBBB) RBBB LBBB Normal conduction

Slide 31 :

PACs with Physiologic LBBB and His-Purkinje System Block V1 Non-conducted PAC

Slide 32 :

Non-Conducted PAC P P P P’ V5 V1 Note deformation of T wave by the PAC

Slide 33 :

Bigeminal/Blocked PACs Mimicking Sinus Bradycardia V1 Only the 4th bigeminal PAC conducts

Slide 34 :

Clinical Significance PAC’s Common in the general population May be associated with heart disease Can be a precursor to atrial tachyarrhythmias

Slide 35 :

RP intervals can be variable RP often > PR (Example slower than more common rate mof 150-250 beats per min) Atrial Tachycardia V1 Differs from AV nodal or AV reentrant SVT

Slide 36 :

Clinical Significance of Atrial Tachycardia Similar to sequela of AV junctional reentrant tachycardias Must be differentiated from them diagnostically

Slide 37 :

Atrial Flutter (“Typical,” Counterclockwise) Reentrant mechanism

Slide 38 :

II V1 Atrial Flutter 4:1 2:1 Classic inverted “sawtooth” flutter waves at 300 min-1 (best seen in II, III and AVF) Note variable ventricular response

Slide 39 :

Atrial Flutter 2:1 Conduction (common) 2:1 & 3:2 Conduction 1:1 Conduction (rare but dangerous) V. rate 140-160 beats/min

Slide 40 :

Atrial Fibrillation Focal firing or multiple wavelets Chaotic, rapid atrial rate at 400-600 beats per min

Slide 41 :

V5 Atrial Fibrillation Rapid, undulating baseline (best seen in V1) Most impulses block in AV node ? Erratic conduction V1

Slide 42 :

Atrial Fibrillation: Characteristic “Irregularly Irregular” Ventricular Response II

Slide 43 :

Atrial Fibrillation with Rapid Ventricular Response II Irregularity may be subtle

Slide 44 :

Atrial Fibrillation: Autonomic Modulation of Ventricular Response Baseline Immediately after exercise

Slide 45 :

Clinical Significance of Atrial Flutter and Fibrillation Causes Usually occur in setting of heart disease; but sometimes see “lone “ atrial fibrillation Hyperthyroidism (atrial fibrillation) May acutely precipitate myocardial ischemia or heart failure Chronic uncontolled rates may induce cardiomyopathy and heart failure Both can predispose to thromboembolic stroke, etc

Slide 46 :

Varying Degrees of Ventricular Preexcitation

Slide 47 :

Atrial Fibrillation with Rapid Conduction Via Accessory Pathway

Slide 48 :

Atrial Fibrillation with Third Degree AV Block V1 V5 Regular ventricular rate reflects dissociated slow junctional escape rhythm

Slide 49 :

Regular Narrow QRS Tachycardias

Slide 50 :

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

Slide 51 :

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

Slide 52 :

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 “adenosine-sensitive”)

Slide 53 :

Carotid Sinus Massage Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes

Slide 54 :

Termination of SVT by Vagotonic Maneuver (Carotid Sinus Massage)

Slide 55 :

SVT Carotid Sinus Massage

Slide 56 :

SVT Adenosine 6 mg P P P P

Slide 57 :

Ventricular Tachyarrhythmias

Slide 58 :

Premature Ventricular Complex (PVC): Alternative Terminology Premature ventricular contraction Ventricular extrasystole Ventricular premature beat Ventricular ectopic beat Ventricular premature depolarization

Slide 59 :

Premature Ventricular Complex (PVC) Compensatory Pause

Slide 60 :

Slide 61 :

PVCs: Bigeminal Pattern “Regularly Irregular” Rhythm

Slide 62 :

Ectopic ventricular activation Normal ventricular activation Fusion beat Accelerated Idioventricular Rhythm (? Ventricular Escape Rate, but ? 100 bpm) Sinus acceleration

Slide 63 :

SA Node Ventricular Focus ATRIA AND VENTRICLES ACT INDEPENDENTLY AV Dissociation

Slide 64 :

V1 Ventricular Tachycardia (VT) Rates range from 100-250 beats/min Non-sustained or sustained P waves often dissociated (as seen here)

Slide 65 :

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

Slide 66 :

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

Slide 67 :

Monomorphic VT

Slide 68 :

V1 Polymorphic VT

Slide 69 :

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

Slide 70 :

MI Scar-Related Sustained Monomorphic VT Circuit

Slide 71 :

“Torsade de Pointes” (Polymorphic VT Associated with Prolonged Repolarization)

Slide 72 :

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

Slide 73 :

Ventricular Flutter VT ? 250 beats/min, without clear isoelectric line Note “sine wave”-like appearance

Slide 74 :

Ventricular Fibrillation (VF) Totally chaotic rapid ventricular rhythm Often precipitated by VT Fatal unless promptly terminated (DC shock)

Slide 75 :

Sustained VT: Degeneration to VF

Slide 76 :

Atrial Fibrillation with Rapid Conduction Via Accessory Pathway: Degeneration to VF

Slide 77 :

Diagnosing Regular Wide QRS Tachycardia

Slide 78 :

Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction? V1

Slide 79 :

Sustained Aberrant Conduction V1

Slide 80 :

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

Slide 81 :

Regular Wide QRS Tachycardia: VT or SVT with Aberrant Conduction?

Slide 82 :

More R-Waves Than P-Waves Implies VT! II

Slide 83 :

Artifact Mimicking “Ventricular Tachycardia” Artifact precedes “VT” QRS complexes “march through” the pseudo-tachyarrhythmia

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