ahmad hersi consultant electrophysiologist assistant professor
DESCRIPTION
Dysrhythmias. Ahmad Hersi Consultant Electrophysiologist Assistant Professor. Sinus Tachycardia Atrial Tachycardia Atrial Flutter Atrial Fibrillation AVRT AVNRT Junctional Tachycardia. Ventricular Tachycardia (VT) Ventricular Fibrillation (VF) Torsade de point Polymorphic VT. - PowerPoint PPT PresentationTRANSCRIPT
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Ahmad HersiConsultant Electrophysiologist
Assistant Professor
Dysrhythmias
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• Ventricular Tachycardia (VT)• Ventricular Fibrillation (VF)• Torsade de point• Polymorphic VT
•Sinus Tachycardia• Atrial Tachycardia• Atrial Flutter• Atrial Fibrillation• AVRT• AVNRT•Junctional Tachycardia
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Atrial fibrillation accounts for 1/3 of all
patient discharges with arrhythmia as principal diagnosis.
2% VF
Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.
34% Atrial
Fibrillation
18% Unspecified
6% PSVT
6% PVCs
4% Atrial Flutter
9% SSS
8% Conduction
Disease3% SCD
10% VT
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Outline Atrial FibrillationDescription
Chaotic and disorganized atrial activity Irregular heartbeat Can be paroxysmal, persistent or
permanent (chronic) Most common sustained arrhythmia Can be symptomatic or asymptomatic Incidence increases with age
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Atrial Fibrillation Demographics by Age
Adapted from Feinberg WM. Arch Intern Med. 1995;155:469-473.
U.S. population
Population withatrial fibrillation
Age, yr
<5 5-9
10-14
15-19
20-24
25-29
30-34
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
80-84
85-89
90-94
>95
U.S. populationx 1000
Population with AFx 1000
30,000
20,000
10,000
0
500
400
300
200
100
0
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Atrial Fibrillation
Common and age-dependent2 - 4% over age 60
Significant risk of stroke4% per year (Framingham Study)
High risk of embolism with cardioversion
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Incidence of AF
The Framingham Study 1982,The Framingham Study 1982, New England New England Journal of MedicineJournal of Medicine
Annual Incidence 0.1% Per YearAnnual Incidence 0.1% Per Year
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Atrial Fibrillation: Causes
Cardiac Non-cardiac “Lone” atrial fibrillation
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Atrial Fibrillation: Cardiac Causes Hypertensive heart disease Ischemic heart disease Valvular heart disease
– Rheumatic: mitral stenosis– Non-rheumatic: aortic stenosis, mitral regurgitation
Pericarditis Cardiac tumors: atrial myxoma Sick sinus syndrome Cardiomyopathy
– Hypertrophic– Idiopathic dilated (? cause vs. effect)
Post-coronary bypass surgery
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Atrial Fibrillation: Non-Cardiac Causes
Pulmonary– COPD– Pneumonia– Pulmonary embolism
Metabolic– Thyroid disease: hyperthyroidism– Electrolyte disorder
Toxic: alcohol (‘holiday heart’ syndrome)
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“Lone” Atrial Fibrillation
Absence of identifiable cardiovascular, pulmonary, or associated systemicdisease
Approximately 0.8 - 2.0% of patients with atrial fibrillation (Framingham Study)1
In one series of patients undergoing electrical cardioversion, 10% had lone AF.2
1 Brand FN. JAMA. 1985;254(24):3449-3453.
2 Van Gelder IC. Am J Cardiol. 1991;68:41-46.
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Forms of AF
– Paroxysmal Paroxysmal lasting less than 48 hours, transient
– Persistent An episode of AF lasting greater than 48 hours, which can still be
cardioverted to sinus rhythm
– Permanent – Inability of pharmacologic or non-pharmacologic methods to restore
sinus rhythm
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Symptoms
Palpitations Presyncope Fatigue Chest pain Dyspnea Syncope
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Work-up
EKG ECHO TFT 24 h Holter Others…..
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ECG Recognition
Atrial Rate: > 300 bpm Rhythm: Irregular
– Ventricular Rate: Variable • Dependent upon: • AV node conduction properties • Sympathetic and parasympathetic ton
Recognition: Absence of P waves
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Atrial Fibrillation: Clinical Problems Embolism and stroke (presumably due to LA clot) Acute hospitalization with onset of symptom Congestive heart failure
– Loss of AV synchrony
– Loss of atrial “kick”
– Rate-related cardiomyopathy due to rapid ventricular response
Rate-related atrial myopathy and dilatation Chronic symptoms and reduced sense of well-being
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Management Strategies
Prevention of Thromboembolis
Rate control
Restoration of sinus rhythm
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Therapeutic Approaches to Atrial Fibrillation
Anticoagulation
Antiarrhythmic suppression
Control of ventricular response– Pharmacologic
– Catheter modification/ablation of AV node
Curative procedures– Surgery (maze)
– Catheter ablation
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Prevention of Thromboembolis
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Atrial Fibrillation and Stroke
Risk: 5 - 8% per year in high-risk patients
Anticoagulant therapy is clearly indicated and beneficial in rheumatic atrial fibrillation.
In non-rheumatic atrial fibrillation, major randomized trials have provided useful guidelines for identifying and treating patients at risk.
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Predictors of Thromboembolic Risk in Atrial Fibrillation
Congestive Heart Failure
Hypertension
Age ≥75 years
Diabetes
Stroke or TIA
CHADS2
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CHADS2 Score and Risk of Stroke
JAMA 2001;285:2864
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Restoration of sinus rhythm
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Antiarrhythmic Drugs to SuppressAtrial Fibrillation
Class I agents– IA: quinidine, procainamide, disopyramide
– IC: flecainide, propafenone
Class III agents– amiodarone, sotalol
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Chronic1 month coumadin cardioversion (CV)
Uncertain durationStable 1 month coumadin CVUnstable TEE CV
Acute
Timing of Cardioversion for Atrial Fibrillation
coumadin repeat TEE CV
no clot
clot
Heparin TEECV coumadin
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Rate control
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Control of Ventricular Rate in Atrial Fibrillation
Digoxin
Calcium channel blockers
Verapamil, diltiazem
Beta blockers
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Sinus Tachycardia (ST)
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Clinical Conditions Associated with Persistent Clinical Conditions Associated with Persistent Sinus TachycardiaSinus Tachycardia
Fever
Volume depletion
Anemia
Sepsis (due to profound vasodilatation reflex tachycardia)
Pain / anxiety
Hypoxemia (PE / COPD)
Cardiac conditions decreased cardiac output (CHF / MI)
Medications (B2 agonists)
Drugs (crack / ephedrine)
Hyperthyroidism
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Rx – Sinus TachycardiaRx – Sinus Tachycardia
Sinus tachycardia is almost always a physiologic response to a given stimulus or disease state
In most situations, do not treat sinus tachycardia, treat the underlying process
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Focal Atrial Tachycardia
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Causes – Atrial TachycardiaCauses – Atrial Tachycardia
Onset is often precipitated by increased sympathetic stimulation
Specific examples:• Digoxin toxicity (especially if AV block noted)• Theophylline (beta-agonist)• EtOH• Myocardial ischemia• Hypoxia
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Rx – Atrial TachycardiaRx – Atrial Tachycardia
Rhythm often spontaneously resolves with normalization of sympathetic tone
If rhythm recurs repeatedly, consider Rx:• Step #1 – beta-blockers (BB)• Step #2 – amiodarone (not if dig toxic)• Step #3 – radio-frequency ablation is curative
Kowey PR. Arch Int Med. 1998; 158: 325
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Atrial Flutter with 2:1 AV block
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Background - Atrial FlutterBackground - Atrial Flutter
Underlying mechanism – large “macro re-entrant circuit” in the atrium, typically moves counter-clockwise
Atrial rate range: 250-350 bpm Ventricular response depends on the degree of AV block:
• 2:1 block ventricular rate = 150 bpm• 3:1 block 100 bpm• 4:1 block 75 bpm
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Causes – Atrial FlutterCauses – Atrial Flutter
Most commonly occurs in male patients with dilated or distended atria with elevated left atrial pressure
Clinical scenarios:– Systolic CHF with low EF– Mitral regurgitation (MR)
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Rx – Atrial FlutterRx – Atrial Flutter
Unstable pt (i.e. low BP / CP / AMS):• Synchronized cardioversion as per ACLS • 50J 100J 200J 300J 360J
Stable pt:• Rate control - just like atrial fibrillation (AFib)• Elective cardioversion - just like AFib• Anti-coagulation – just like AFib
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Atrioventricular Nodal Re-entrant Tachycardia
(AVNRT) or AVRT
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AVNRT or AVRT
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Rx – AVNRT / AVRTRx – AVNRT / AVRT Unstable:
– Synchronized cardioversion start @ 50J (avoid if EF < 40%)
Stable:– Step #1 – attempt to terminate rhythm with vagal
maneuvers (carotid massage / Valsalva)– Step #2 – adenosine 6mg IVP 12mg 2min later
18mg 2min later– Step #3 – AV nodal blocking agents (BB / CCB > digoxin)– Step #4 – amiodarone 150mg IV over 10min 1mg/min
x 6hrs 0.5mg/min x 18hrs (max dose 2.2g/24hrs)
– Step #5 – in pts with bypass tracts not tolerating the medications, consider radio-frequency ablation
ACLS 2000 / Wang YS, et al. JACC. 1991; 18:1711
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Wolf-Parkinson-White (WPW) Syndrome
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Take Home Messages - WPWTake Home Messages - WPW Syndrome features:
• Short PR• Broad irregular QRS complexes due to Delta waves• Ventricular rates up to 300 bpm
Conduction along the accessory pathway:• Orthodromic – conduction to ventricles over normal AV
node-His-Purkinje path• Antidromic – conduction to ventricles via accessory path
Medical Rx:• 1st choice – procainamide 20mg/min IV (max 17mg/kg)• Drugs to avoid – AV nodal blocking agents!!!• Radio-frequency ablation curative > 95% cases
ACLS 2000 / Krahn AD. Ann Intern Med. 1992; 116: 456
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So What Is Actually Meant By So What Is Actually Meant By Supraventricular Tachycardia?Supraventricular Tachycardia?
Arrhythmias of supraventricular origin using a re-entrant mechanism with abrupt onset & termination
AVNRT (60%)
AVRT (30%)
Atrial tachycardia (10%)
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Ventricular Tachycardia (VT)
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Brugada EKG Criteria for VTBrugada EKG Criteria for VT
AV dissociation
R-S interval > 100 ms
No RS morphology in pre-cordial leads
Dr. Brugada (Cardiology) @ Noon Conference – The Methodist Hospital 9/00
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Classification - VTClassification - VT Duration:
– Sustained VT (> 30 seconds or hemodynamic compromise)
– non-Sustained VT (< 30 seconds)• Risk factor for sudden death among pts with heart dz
QRS morphology:– Monomorphic (common in pts with CAD)– Polymorphic (usually associated with a prolonged QT)
ACP - MKSAP 12. Cardiovascular Medicine: 24
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Rx – VTRx – VT
Hemodynamically Unstable:– Unsynchronized cardioversion as per ACLS protocol for VF /
pulseless VT
Unstable (CP / AMS):– Synchronized cardioversion as per ACLS protocol
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Rx – VTRx – VT Stable:
– Rx ischemia– Correct electrolytes (K / Mg / Ca)– Consider cardioversion (yes even in stable pts!!)– EF > 40%:
• Procainamide / sotalol (class IIa)• amiodarone (class IIb)
– EF < 40%:• amiodarone (class IIa)
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Torsades de Pointes
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Causes – Torsades de PointesCauses – Torsades de Pointes
Underlying Mechanism – prolongation of the QT interval coupled with R-on-T phenomenon
Medications (Class Ia anti-arrhythmics / TCAs)
Electrolyte abnormalities (Mg / K)
Bradycardia (usually s/p inferior MI)
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Rx – Torsades de PointesRx – Torsades de Pointes
Unstable:• Cardioversion as per ACLS protocol for VT based on
hemodynamics (refer to prior slides)
Stable:• Correct electrolytes (K / Mg)• Hold any culprit medications • magnesium sulfate 2g IVP + repeat prn• Transcutaneous overdrive pacing
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Summary - WideSummary - Wide
Ventricular tachycardia (VT)
Torsades de Pointes (sub-type of VT)
Any supraventricular tachycardia with aberrancy (e.g. sinus tach with pre-existing bundle branch block)