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Arrhythmias. Steven M. Costa, M.D. Assistant Professor Department of Medicine Division of Cardiology. Scott & White Memorial Hospital and Clinic Texas A&M University Health Science Center. Objectives. Common Arrhythmias: Sinus Tachycardia Atrial Fibrillation Atrial Flutter MAT VT.
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Arrhythmias Steven M. Costa, M.D. Assistant Professor Department of Medicine Division of Cardiology Scott & White Memorial Hospital and Clinic Texas A&M University Health Science Center
Objectives • Common Arrhythmias: • Sinus Tachycardia • Atrial Fibrillation • Atrial Flutter • MAT • VT
CLUES Width? NCT vs WCT Regular? Irregular? Rate? P waves? No P waves Relation to QRS? Morphology (s) RP Interval
Sinus Tachycardia General HR > 100 bpm Upper Limits: 220 – age Behavior: Warm up, Cool Down Etiology Hyperadrenergic States Hypovolemia Fever Pain Hyperthyroidism Treatment Correct underlying cause
ECG #2 • You’ve Just admitted at patient • 68 y/o with CAP-Pneumonia • h/o COPD • You tuck him away • Nurse calls you – they’re Tachycardic
Multifocal Atrial Tachycardia General Seen in Elderly, Critically Ill pts Etiologies Pulmonary Disease COPD, Hypoxia Theophylline Electrolytes – i K+, Mg+ Infxns Metabolic Disturbances Acidosis ECG Recognition 3 different P wave morphologies Rate: 100 – 180 bpm Treatment Treat the underlying cause!!!!
Case #3 • 76 y/o WM • HPI: 3 hours history of “fluttering in chest” with SOB; never had this before; came on at rest • No chest pain or symptoms consistent with heart failure • PMHx: significant for HTN (not on meds), Obesity, and Anxiety • FHx positive for mother and two brothers with irregular heart rhythms • Exam unremarkable except for irregularly irregular rhythm and BMI of 31
A.Multiple-wavelet reentry Wavelets (indicated by arrows) randomly reenter tissue previously activated by them or by another wavelet. B. Focal activation. The initiating focus often lies within the region of the pulmonary veins.
What are the important issues in managing this gentleman? • Etiology/Risk Factors • Initial Rate control • Do we anti-coagulate? • Convert? • Should we do other test? • What medicines do we send him out on?
Background • Atrial fibrillation is the most common sustained arrhythmia • Affects 2 million Americans • 6% over the age of 65 experience it • Responsible for 15% strokes • Benjamin E: Epidemiology of Atrial Fibrillation. In Falk RH, Podrida PJ, eds:Atrial Fibrillation: Mechanisms and Management. 2nd Ed, Lippincott-Raven Press, New York 1997, pp.1-22.
Atrial Fibrillation Demographics by Age U.S. populationx 1000 Population with AFx 1000 Population withatrial fibrillation 30,000 20,000 10,000 0 500 400 300 200 100 0 U.S. population <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 Age, yr Adapted from Feinberg WM. Arch Intern Med. 1995;155:469-473.
Symptoms • Inappropriate heart rate response • Tachycardia induced cardiomyopathy • Irregular rate • Loss of atrial systolic function • CHF- reduced EF Lots of patient have no symptoms present with Thromboembolic event
Atrial Fibrillation: Causes • Cardiac • Non-cardiac • “Lone” atrial fibrillation
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
Atrial Fibrillation: Non-Cardiac Causes • Pulmonary • COPD • Pneumonia • Pulmonary embolism • Metabolic • Thyroid disease: hyperthyroidism • Electrolyte disorder • Toxic: alcohol (‘holiday heart’ syndrome)
“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 • These patients have a favorable prognosis with respect to thromboembolism and mortality. 1 Brand FN. JAMA. 1985;254(24):3449-3453.2 Van Gelder IC. Am J Cardiol. 1991;68:41-46.
RATE CONTROL • Digoxin is NOT the first line of therapy • Beta-blockers and nondihydropyridine CCBS are the first line of therapy • Rare patient can’t be controlled with meds - AV node ablation and pacing • Tachycardia mediated cardiomyopathy • Chicken or Egg
New Onset AFib Work Up Work Up ECG - Telemetry TSH Electrolytes, Magnesium Echo – TTE vs TEE Ingestion History – EtOH, Cocaine PE Work up (if indicated)
Other tests • Echo • Left atrial enlargement • LV function • Valvular Heart disease • Shunt – ie ASD is young • “Smoke” (TEE) • Poorly contractile LA appendage (TEE)
Immediate Treatment • Significant symptoms • Restore NSR +/- Antiarrhthymics • Minimal symptoms • Strongly Consider rate control • AFFIRM Trial
Afib Management Unstable Shock! • Stable • < 48 Hrs > 48 Hrs Rate Control Rate Anticoag Anticoag 1. TEE-DCCV CCV/DCCV 2. Coumadin +/- DCCV
Therapeutic Approaches to Atrial Fibrillation • Anticoagulation • Antiarrhythmic Suppression • Control of Ventricular Response • Pharmacologic • Catheter modification or ablation of the AV node. • Curative Procedures • Surgery • Cox-Maze III • Pulmonary Vein Isolation - “Mini-Maze” • Catheter based ablation
Benefit of Warfarin Absolute Risk of Stroke • Age < 65 years and no risk factors, “lone AF”: 1%/yr. • All others: lowered to ~1.5%/yr by warfarin The Atrial Fibrillation Investigators Arch Intern Med 1994;154:1449
CHADS2 SCORECHF=1, HTN=1, Age>75=1, Diabetes=1, Stroke/TIA=2 ScoreStroke RateCHADS risk 0 1.9 Low 1 2.8 Low 2 4.0 Moderate 3 5.9 Moderate 4 8.5 High 5 12.5 High 6 18.2 High
AF: Anticoagulation - General Points • Anticoagulation (INR 2.0 - 3.0) can reduce risk of stroke by 2/3 1,2 • Aspirin has little effect on risk of stroke due to AF – lone AF consider ASA • 1 Hylek EM and Singer DE. Arch Intern Med 1994;120:897 • 2 Hylek EM et al. New Engl J Med 1966;335:540 • 3 The Atrial Fibrillation Investigators. Arch Intern Med 1997;157:1237
Stroke/Bleeding Risk ACC/AHA Guidelines
Anti-coagulation for AFib • Afib accounts for 15% of strokes nationwide • Chronic and Paroxysmal have the same risk • 70% of strokes in Afib are cardioembolic • Only 50-60% of qualified patients are on coumadin
Stroke/Bleeding Risk ACC/AHA Guidelines
Cardioversion • Acutely Yes, if : • Hemodynamically unstable • CHF • Angina • Electively if pt remains symptomatic despite rate control • Electrical vs Chemical
AFib Summary • Think about precipitating causes • Rate control with beta blockers and calcium channel blockers • Use safe, effective anti-dysrhythmic drugs • Don’t be afraid to anticoagulate • EP guided ablation of Afib is slowly becoming a reality; • Aflutter can usually be easily ablated- remember Afib-Aflutter closely related • Afib and Aflutter have similar stroke risks
Case #4 Wide QRS complex tachycardia with cycle length 250ms. Mechanism of tachycardia cannot be determined from this trace alone.
IV adenosine causes transient atrioventricular block and reveals the underlying atrial flutter.
Wide complex tachycardia • One of three things: • SVT w/ BBB or aberration • SVT w/ conduction over accessory pathway • VT – *important to differentiate • CAD/LV dysfxn think VT > 90%
Atrial Flutter • (Macro) Reentrant Circuit located in the RA • Typical Flutter = Cavotricuspid Isthmus Dependent • Atrial Rate: 250-350 bpm • Ventricular Rate: Depends on degree of conduction
Atrial Flutter (A-Flutter) • Rapid and regular form of atrial tachycardia • Usually paroxysmal • Sustained by a macro-reentrant circuit • Circuit is confined to the right atrium • Episodes can last from seconds to years • Chronic atrial flutter may progress to atrial fibrillation Morady F. N Engl J of Med. 1999;340:534-544.
Ventricular Tachycardia Potentially lethal arrhythmias arising in ventricle Rate 100 – 280 bpm Usually 130 – 200 bpm Shape Monomorphic Polymorphic