Dr. Hussam Al-Humadi. Cardiac Arrhythmia

Transcription

1 Cardiac Arrhythmia Tachyarrhythmias Cardiac rhythms whose ventricular rate exceeds 100 bpm. 1. Narrow-Complex Tachyarrhythmia (QRS <120 ms) 2. Wide-Complex Tachyarrhythmia (QRS >120 ms) Etiology Disorders of Impulse Conduction (e.g., VT). Disorders of Impulse Formation: Enhanced automaticity (e.g., accelerated junctional and accelerated idioventricular rhythm) and triggered activity (e.g., long QT syndrome and digitalis toxicity) Other less common mechanisms of tachyarrhythmias. Clinical features Dyspnea, angina, lightheadedness or syncope and decreased level of consciousness Palpitations: Sudden onset and termination Symptom abatement with breath holding or Valsalva maneuver (supraventricular tachyarrhythmia AV node is critical in the maintenance of this arrhythmia. History of organic heart disease Endocrinopathy Familial or congenital causes of arrhythmias Medications: (over-the-counter and herbal medications 1. Supraventricular tachyarrhythmia 2. Ventricular tachyarrhythmia (SVT) are often recurrent, occasionally persistent, and a frequent cause of visits to emergency departments and primary care physician offices. Differential Diagnosis (AF) is the most common narrow-complex tachycardia seen : irregular with no p wave pattern If rate is about 150 bpm, suspect atrial flutter (AFl) with 2:1, 4:1 to 3:1, etc sawtooth.(can often accompany AF). 1

2 Like AF, AFl is commonly associated with the postcardiac surgery period, pulmonary disease, thyrotoxicosis, and atrial enlargement. 3. Multifocal atrial tachycardia (MAT) 4. Sinus tachycardia cocaine,amphetamines,methamphetamine and prescription drugs (theophylline, atropine, B-adrenergic agonists 5- Ectopic atrial tachycardia (EAT) EAT with variable block is associated with digoxin toxicity 6. (AVNRT) If rate is >150 bpm, suspect atrioventricular nodal reentrant tachycardia or atrioventricular reentrant tachycardia (AVRT). AVNRT (the most common diagnosis of the paroxysmal SVTs (60%) followed by AVRT (30%) Investigations Serum electrolytes Complete blood count (CBC), Thyroid function tests Serum concentration of digoxin (when applicable) Toxicology screen should be considered for all patients. 2

3 (AFl) Anticoagulation similar to AF Electrical or chemical cardioversion is appropriate. If pacemaker present, cardioversion catheter ablation (MAT) Underlying pathophysiology. K & Mg balance. Antiarrhythmic, BB vs. CCB. DC cardioversion is not effective. (ST) Treatment of underlying pathophysiology (EAT) Acute therapy: Identify and treat precipitating factors like digoxin toxicity if hemodynamically stable, BB & CCB. In rare cases Amiodarone, Flecainide, or Sotalol. Chronic therapy: BB & CCB., If unsuccessful, catheter ablation, Flecainide, Propafenone, Sotalol, or Amiodarone. (AVNRT) Catheter ablation BB, CCB, and digoxin; then consider Propafenone, Flecainide, etc. Valsalva Describe the procedure Vagal stimulation during relaxation phase Exhale forcefully against a closed airway for several seconds followed by relaxation Well tolerated (Toxicity) Patient unable to follow commands (CI) 3

4 No sideffects or antagonists Carotid sinus massage Check for carotid bruits and history of CVA; then place in recumbent position with neck extended Vagal stimulation First, apply enough pressure to simply feel carotid pulse with index and middle fingers. If no effect, then use rotating motion for 3 5 sec Well tolerated. Risk of embolizing carotid plaque. Never massage both carotids (Toxicity) Recent TIA or stroke, or ipsilateral significant carotid artery stenosis or carotid artery bruit (CI) Adenosine Explain the potential side effects to the patient AV nodal blocking agent. Short-acting (serum half-life 4 8 min) Initial: 6 mg IV rapid bolus via antecubital vein, followed by ml saline flush Precipitate prolonged asystole in patients with sick sinus syndrome or 2 nd - or 3rd - degree AV block Significant bronchospasm Potentiators: Dipyridamole & carbamazepine. Effect pronounced in heart transplant Antagonists: Caffeine and theophylline Facial flushing, palpitations, chest pain, hypotension, exacerbation of bronchospasm Atrial Fibrillation Rate control Prevention of thromboembolic events Rhythm control Non pharmacological (Av node ablation) Rate control (limit conduction through the AV node) Nondihydropyridine CCB (diltiazem, verapamil) BB Digoxin 4

5 Lines of treatment of AF 1 ST : Prevention of thromboembolic complications Rate control agents :Digoxine, BB, CCB (non dihy), If no response AV ablation 2nd : Rhythm control (Antiarrhythmic drugs) Prevention of thromboembolic events is a central tenet of AF management Chronic warfarin anticoagulation is currently the most effective therapy for attenuating the risk of stroke associated with AF or(aspirin +clopidogrel) Identify the patients who are at sufficient risk for embolic CVA Patient Features Antithrombotic Therapy <60 yr, + no HD Aspirin ( mg/d) or no <60 yr, HD + no RF Aspirin ( mg/d) yr, + no RF Aspirin ( mg/d) yr + DM or CAD Oral anticoagulation (INR ) 75 yr or >, women Oral anticoagulation (INR ) 75 yr or >, men + no RF Oral anticoagulation (INR ) or aspirin ( mg/d) 65 yr or >, HF LV EF <35% + HT Rheumatic heart disease (MS) Oral anticoagulation (INR ) Prosthetic heart valves; prior thromboembolism Persistant atrial thrombus on TEE Pharmacological agent (control rate) 5

6 I. Without evidence of accessory pathway Esmolol, Metoprolol, Propranolol (BP, HR, HB, HF, bronchospasm) Diltiazem & Verapamil (BP, HB, HF) II. With evidence of accessory pathway Amiodarone (BP, HB, HR, warfarin interaction; dermatologic, thyroid, pulmonary, corneal, and liver side effects III. HF + Without evidence of accessory pathway Digoxin (Digox toxicity, HR, HB) Amiodarone Digoxin: Controlling the resting ventricular rate in AF in the setting of LV dysfunction and CHF Adjunctive with CCB or BB for optimum rate control of chronic AF. It is less useful for rate control during exertion. Digitalis toxicity (nausea, abdominal pain, vision changes, confusion, delirium.) Often seen in renal dysfunction or in patients on agents known to increase digoxin levels (Verapamil, Diltiazem, Eerythromycin, Cyclosporine). 2 nd Rhythm control antiarrhythmic drugs is most effective at preventing recurrence of AF and less effective at chemical cardioversion of AF. Nonpharmacologic methods (catheter or surgical ablation techniques) Rhythm control of AF hospital (life threat. Brady or tachyarrhythmia) Continous ECG monitoring. Ibutilide infus. is the only drug that is approved by FDA The risk for TdP is higher in patients with cardiomyopathy and CHF 6

7 Dofetilide, sotalol, flecainide, and propafenone have some efficacy. Amiodarone has limited efficacy to achieve pharmacologic cardioversion Common drugs used for maintenance of sinus rhythm Flecainide, Propafenone, Sotalol, Dofetilide, Amiodarone Flecainide, Propafenone blockade of active Na channels, High mortality Potent negative inotropes, Exacerbate HF prolong the QRS duration Flecainide should be used with caution (concomitant + AV nodal blocker) lead to paradoxical increase in the ventricular rate (conversion of AF - AFl. Propafenone is less prone to this phenomenon due to intrinsic BB effect. Dofetilide Maintenance of sinus rhythm. Increases the QT interval The main risk of dofetilide is TdP. Contraindicated in a baseline correct QT interval (QT c ) >440 or 500 milliseconds in patients with bundle branch block. If the QT interval exceeds 500 milliseconds, a 50% dosage reduction is indicated. If the QT exceeds 500 milliseconds after the second dose, dofetilide must be discontinued. Several medications block the renal secretion of dofetilide (verapamil, cimetidine, prochlorperazine, trimethoprim, megestrol, ketoconazole) and are contraindicated The advantages of dofetilide are that it is not associated with increased CHF or mortality in patients with LV dysfunction Side effects of some Drugs used to treat arrhythemia: Procainamide GI, CNS, +ANA/SLE-like syndrome, fever, hematologic, anticholinergic. Follow QT serum procainamide Quinidine QT, TdP, BP, thrombocytopenia, cinchonism, GI upset 7

8 Disopyramide Anticholinergic, HF Lidocaine HR, CNS, GI. Adjust dose + /hepatic failure, AMI, HF, or shock Mexilitine GI, CNS Flecainide HF, GI, CNS, blurred vision Propafenone GI, dizziness Sotalol HR, BP, CHF, CNS. Limit QT prolongation to <550 ms Dofetilide QT, VT/TdP, HA, dizziness., <20y: Contraindicated Ibutilide QT, TdP, AV block, GI, HA Amiodarone BP, HB, HR, warfarin interaction; thyroid, pulmonary, corneal, and liver effects Other Nonoperative Therapies surgery DC cardioversion is the safest and most effective method of acutely restoring sinus rhythm Anticoagulation is still critical to minimize thromboembolic events triggered by the cardioversion process If the duration of AF <48 hours, cardioversion may proceed without anticoagulation. If AF >48 hours (or for an unknown duration), patients should be anticoagulated with warfarin, (INR) of 2.0 to 3.0, for at least 3 weeks before cardioversion, and anticoagulation should be continued in the same therapeutic range following successful cardioversion. 8

9 AF -Prevention Statins potent effect on reducing recurrent AF independent of lipid-lowering effect. ACEI and ARBs (prevent atrial remodeling in animals via suppression of the RAAS. Perioperative continuation of BB, Amiodarone, sotalol, magnesium, or omega-3 fatty acids (reduce P.O AF) 2- Ventricular Tachyarrhythmias VT assumption a malignant course until proven otherwise. C.C.C (hemodynamic stability, duration, morphology, and the presence or lack of underlying structural HD determining the patient s risk for SCD and need for device or ablation-based therapy VF (disorganized mechanical contraction, hemodynamic collapse, and sudden death. The ECG reveals irregular and rapid oscillations (250 to 400 bpm) of highly variable amplitude without uniquely identifiable QRS complexes or T waves. VT are the major cause of (SCD). SCD is defined as the death that occurs within 1 hour of the onset of symptoms. 9

10 - Acute therapy of SVT: Chronic IV medications :Adenosine, CCB, or BB CCB & BB can produce hemodynamic instability in patients with VT. Many SVTs are amenable to RFA(Radio frequency ablation), whereas most VTs are malignant and require an antiarrhythmic agent and/or ICD implantation (implanted cardiac defibrillator) Immediate unsynchronized DC cardioversion is the primary therapy for pulseless VT and VF Nonpharmacologic therapy ICD (primary &secondary prevention of SCD Radiofrequency catheter ablation of VT Medications for VT VF that is resistant to external defibrillation requires the addition of IV antiarrhythmic agents. IV Lidocaine is frequently used BUT IV Amiodarone appears to be more effective in increasing survival of VF when used in conjunction with defibrillation After successful cardioversion, continuous IV infusion should be maintained until any reversible causes have been corrected. Chronic antiarrhythmic (recurrent symptomatic VT). hemodynamically unstable VT (ICD, antiarrhythmic drug) 1 st line treatment : 1- Amiodarone Safe and well tolerated for the acute management of VT. Sign. toxicities arising from chronic therapy Prevents the recurrence of sustained VT or VF in up to 60%. A therapeutic latency of > 5 days exists before beneficial antiarrhythmic effects are observed with oral dosing 10

11 Full suppression of arrhythmias may not occur for 4-6 weeks after therapy is initiated. 2- Class II agents (BB) 3- ACEI 1. Only class shown improved survival in post-mi 2. Reduce post-infarction total M 25% -40% and SCD by 32% - 50% 3. After acute therapy of VT/VF +stabilization, BB should be initiated and titrated as BP & HR allow. 4. Idiopathic VT often responds to AV nodal blocking agents Reduce SCD & M in patients with CAD or CHF. 2 ND LINE TREATMENT OF VT 1- Sotalol Class III agent Chronic treatment of VT/VF. Prevents the recurrence of sustained VT & VF in 70% Must be used with caution in CHF 2- Class I agents have not been shown to reduce M in VT/VF. Class Ic agents, Flecainide and Propafenone, are associated with increased M in VT Lidocaine is a class Ib agent available only in IV Toxicities of Lidocaine CNS effects (convulsions, confusion, stupor & rarely, respiratory arrest) all of which resolve with discontinuation of therapy. Negative inotropic effects are seen only at high levels. Mexiletine Similar to lidocaine but in oral form. Used in combination with either Amiodarone or Sotalol for chronic treatment of refractory VT. 11

12 CNS toxicity includes tremor, dizziness, and blurred vision. Higher levels may result in dysarthria, diplopia, nystagmus, and an impaired level of consciousness. Nausea and vomiting are common. Phenytoin NOTES: Primarily in the treatment of digitalis-induced VT IV loading dose is 250 mg/ 10 minutes Frequent monitoring (ECG, BP, and neurologic) Continuous infusion is not recommended Class IV agents have no role in the chronic management of VT IV CCB should never be used in the acute management of VT, as they may cause hemodynamic collapse Oral CCB are not effective in the management of VT. Short-acting Nifedipine is associated with a trend toward increasing mortality when used in the post-mi patient Primary VF that occurs within the first 72 hours of an acute MI is not associated with an elevated risk of recurrence and does not require chronic antiarrhythmic therapy 2- Bradyarrhythmias Ventricular rate of <60 bpm Dysfunction somewhere within the native conduction system Anatomy of the conduction system The sinus node is a collection of specialized pacemaker cells located in the high right atrium. Causes of Bradycardia Intrinsic Congenital disease (may present later in life) Idiopathic degeneration (aging) Infarction or ischemia 12

13 Cardiomyopathy Infiltrative disease: sarcoidosis, amyloidosis, hemochromatosis Collagen vascular diseases: systemic lupus erythematosus, rheumatoid arthritis, scleroderma Surgical trauma: valve surgery, transplantation Infectious disease: endocarditis, Lyme disease, Chagas disease Extrinsic Autonomically mediated Neurocardiogenic syncope Carotid sinus hypersensitivity Increased vagal tone: coughing, vomiting, micturition, defecation, intubation Drugs: -blockers, calcium channel blockers, digoxin, antiarrhythmic agents Hypothyroidism Hypothermia Neurologic disorders: increased intracranial pressure Electrolyte imbalances: hyperkalemia, hypermagnesemia Hypercarbia/obstructive sleep apnea Sepsis Clinical Presentation STABLE SYMPTOMS SHORT-TERM SOURCE SCHEDULE A PACEMAKER A. Asymptomatic B. Nonspecific (lightheadedness, fatigue, weakness, exercise intolerance C. Syncope 13

14 D. signs of poor perfusion (hypotension, confusion, decreased consciousness, cyanosis, etc E. Tolerance (ability to augment cardiac output in response to the decreased HR. Ischemic heart disease (RT) Precipitating circumstances (micturition, coughing, defecation, noxious smells) neurocardiogenic Tachyarrhythmias, particularly in patients with underlying sinus node dysfunction History of structural heart disease hypothyroidism, obstructive sleep apnea, collagen vascular disease, infections (bacteremia, endocarditis, Lyme, Chagas),infiltrative diseases (amyloid, hemochromatosis, and sarcoid) Neuromuscular diseases, and prior cardiac surgery (valve replacement, congenital repair) Medications should be reviewed with particular emphasis on those that affect the sinus and AV nodes (CCB, BB, digoxin). Pharmacologic therapy significant symptoms and hemodynamic instability are considered cardiovascular emergencies Atropine, an anticholinergic agent given in doses of mg intravenously, is the cornerstone pharmacologic agent for emergent bradycardia treatment. Dysfunction localized more proximally in the conduction system (symptomatic sinus bradycardia, 1 ST AV block, Mobitz I 2 ND AV block) tends to be atropine responsive. Distal disease is not responsive and can be worsened by atropine. Reversible causes of bradyarrhythmias should be identified as previously described and any agents (digoxin, CCB, BB) that caused or exacerbated the underlying dysrhythmia should be withheld Nonpharmacologic therapy irreversible etiologies or that are secondary to medically necessary pharmacologic therapy, pacemaker therapy should be considered Temporary pacing is indicated for symptomatic 2 ND or 3 RD HB caused by transient drug intoxication or electrolyte imbalance and complete HB or Mobitz II 2 ND AV block in the setting of an acute MI. 14

15 Sinus bradycardia, AF with a slow ventricular response, or Mobitz I 2 ND AV block should be treated with temporary pacing only if significant symptoms or hemodynamic instability Permanent pacing Complications of placement Pneumothorax Device infection Bleeding, Rarely, cardiac Perforation with Tamponade. Syncope Common clinical problem Primary goal of evaluation is to determine whether the patient is at increased risk of death. Sudden, self-limited loss of consciousness and postural tone caused by transient global cerebral hypoperfusion and followed by spontaneous, complete, and prompt recovery. Neurocardiogenic (most common): vasovagal, carotid sinus hypersensitivity, and situational Orthostatic-hypotension:hypovolemia, medication induced (iatrogenic), and autonomic dysfunction Miscellaneous (not true syncope): seizures, stroke/tia, hypoglycemia, hypoxia, psychogenic, etc Cardiovascular: Arrhythmia: sinus node dysfunction, AV nodal block, pacemaker malfunction, VT, SVT, WPW syndrome, and long QT syndrome. Mechanical: HVM, valvular stenosis, aortic dissection, myxomas, pulmonary embolism, pulmonary hypertension, acute MI, 15