Disturbances_of_heart_rate_and_rythm.ppt

Disturbances of heart rate and rhythm Mechanisms of arrhythmias 1. 2. 3. 4. Disorders of impulse formation in the sinus node Disorders of impulse conduction- at sinus or atrioventricular node, in the IV conduction system, within atria and ventricles Reentry- paroxysmal supraventricular arrhythmi...

Disturbances of heart rate and rhythm Mechanisms of arrhythmias 1. 2. 3. 4. Disorders of impulse formation in the sinus node Disorders of impulse conduction- at sinus or atrioventricular node, in the IV conduction system, within atria and ventricles Reentry- paroxysmal supraventricular arrhythmias, atrial flutter Triggered activity. Techniques for evaluating rhythm disturbances 1. 2. 3. Electrocardiographic monitoring- the ideal way of establishing a causal relationship between a symptom and rhythm disturbance Electrophysiologic testing- employs intracardiac electrocardiographic recordings and programmed atrial or ventricular stimulations Autonomic Testing- evaluation of individuals with an imbalance between sympathetic and parasympathetic autonomic activity. Antiarrhythmic drugs  Class I agents block membrane sodium channels. Three subclasses are further defined by the effect of agents on the Purkinje fiber action potential. -class Ia slow the rate of rise of the action potential (Vmax) and prolong its duration, thus slowing conduction and increasing refractoriness (quinidine, procainamide). -class Ib agents shorten action potential duration; they do not affect conduction or refractoriness (lidocaine, mexiletine) -class Ic agents prolong Vmax and slow depolarization, thus slowing conduction and prolonging refractoriness, but more so than class Ia drugs (flecainide, propafenone) . Antiarrhythmic drugs  Class II agents: beta-blockers, which decrease automaticity, prolong atrioventricular conduction and prolong refractoriness.  Class III agents block potassium channels and prolong repolarization, widening the QRS and prolonging the QRS interval. They decrease automaticity and conduction and prolong refractoriness.(ex: amiodarone, sotalol)  Class IV agents are the slow calcium channel blockers, which decrease automaticity and atrioventricular conduction. (ex: diltiazem, verapamil) All antiarrhythmic drugs can exacerbate arrhythmias (proarrhythmic effect), and most depress LV function. Normal Impulse Conduction Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers Impulse Conduction & the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers The “PQRST”  P wave - Atrial depolarization • QRS - Ventricular depolarization • T wave - Ventricular repolarization The PR Interval Atrial depolarization + delay in AV junction (AV node/Bundle of His) (delay allows time for the atria to contract before the ventricles contract) Pacemakers of the Heart  SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.  AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.  Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm. Arrhythmia Formation Arrhythmias can arise from problems in the: • Sinus node • Atrial cells • AV junction • Ventricular cells SA Node Problems The SA Node can:  fire too slow  fire too fast Sinus Bradycardia Sinus Tachycardia Sinus Tachycardia may be an appropriate response to stress. Respiratory sinus arrhythmia Sinus arrhythmia is a cyclic increase in normal heart rate with inspiration and decrease with expiration. It results from reflex changes in vagal influence on the normal pacemaker and disappears with breath holding or increase in heart rate due to any cause. It has no clinical significance; common in the young and elderly. Sinus bradycardia is a heart rate that is slower than 50/min due to: - vagal influence on the normal pacemaker or - organic disease of the sinus node. The rate usually increases during exercise or adm. of atropine. Severe sinus bradycardia may be an indication of sinus node pathology, especially in elderly patients and pacing may be required. Sinus tachycardia      Is defined as a heart rate faster than 100 beats/min that is caused by rapid impulse formation from the normal pacemaker; it occurs with fever, exercise, emotion, pain, anemia, heart failure, shock, thyrotoxicosis, or in response to many drugs. Alcohol and alcohol withdrawal are common causes of sinus tachycardia and other supraventricular arrhythmias. The onset and termination are usually gradual, in contrast to paroxysmal supraventricular tachycardia that is due to reentry. The rhythm is basically regular. Sinus tachycardia Atrial Cell Problems Atrial cells can:  fire occasionally Premature Atrial from a focus  Contractions (PACs) fire continuously due to a looping re-entrant circuit PSVT Atrial Flutter Atrial Premature Beats (Atrial Extrasystoles)    They occur when an ectopic focus in the atria fires before the next sinus node impulse The contour of the P wave usually differs from the patient’s normal complex. They occur frequently in normal hearts; Atrial Premature Beats Re-entrant tachycardias  A re-entrant pathway occurs when an impulse loops and results in selfperpetuating impulse formation. Paroxysmal supraventricular tachycardia Paroxysmal tachycardia often occurs in patients without structural heart disease. Attacks begin and end abruptly and may last a few seconds to several hours or longer. The heart rate may be 140-240/min (usually 160220/min) and is perfectly regular.   The most common mechanism is reentry, which may be initiated or terminated by an atrial or ventricular premature beat. The reentry circuit may involve the sinus node, the AV node, or an accessory pathway. Paroxysmal supraventricular tachycardia Treatment of the Acute Attack  A. Mechanical Measures: - Valsalva’s maneuver, stretching the arms and body, lowering the head between the knees, coughing, breath holding, carotid sinus pressure; these measures stimulate the vagus, delay AV conduction and block reentry mechanisms, terminating the arrhythmias. Vagal Stimulation with Carotid Sinus Pressure     This procedure should not be performed if the patients has carotid bruits or a history of transient cerebral ischemic attacks. With the patient relaxed in a semi recumbent position, firm but gentle pressure and massage are applied first over the right carotid sinus for 10-20 sec. and then over the other. Pressure should not be exerted on both carotid sinuses at the same time Continuous ECG or auscultatory monitoring of the heart rate is required so that the carotid sinus pressure can be relieved as soon as the attack ceases; carotid sinus pressure will interrupt up to half of the attacks, especially if the patient has been sedated. Drug Therapy If mechanical measures fail, 2 rapidly acting i.v. agents will terminate more than 90% of episodes. - i.v. adenosine has a brief duration of action and minimal negative inotropic activity; a 6 mg bolus is adm.; if no response is observed after 1-2 min., a second and third 12 mg bolus should be given. Nearly 20% of patients will experience transient flushing and some sever chest discomfort. Drug Therapy Ca channel blockers also rapidly induce AV block and break most reentry SV tachycardia. i.v. Verapamil may be given as a 2.5 mg bolus, followed by additional doses of 2.5 mg to 5 mg every 1-3 min up to a total of 20 mg if BP and rhythm are stable. In patient with WPW syndrome, in which an accessory pathway is involved, these agents may be contraindicated. Cardioversion   If the patient is hemodynamically unstable or if adenosine and verapamil are contraindicated or ineffective, synchronized electrical cardioversion (beginning at 50100 J) is almost universally successful. If digitalis toxicity is present or strongly suspected, as in the case of paroxysmal tachycardia with AV block, electrical cardioversion should be avoided. Prevention of attacks  A. Drugs: Verapamil and beta-blockers are the drugs of choice.  B. Radiofrequency ablation: preferred approach to patients with recurrent SVT. Atrial Cell Problems Atrial cells can also: • fire continuously from multiple foci or fire continuously due to multiple micro re-entrant “wavelets” Atrial Fibrillation Atrial Flutter Atrial fibrillation    Atrial fibrillation is the commonest chronic arrhythmia; it occurs in rheumatic heart disease, dilated cardiomyopathy, atrial septal defect, hypertension, mitral valve prolapse, hypertrophic cardiomyopathy, as well as in patients with no apparent cardiac disease. Atrial fibrillation often appears paroxysmally before becoming the established rhythm Pericarditis, chest trauma or surgery, pulmonary disease (as well as medications as theophylline and beta-adrenergic agonists) may cause attacks in patients with normal hearts. Atrial fibrillation    Alcohol intoxication and alcohol withdrawal may precipitate atrial fibrillation (“holiday heart”) The ventricular rate is rapid and the rhythm very irregular; the atrial rate is 400-600/min, but most impulses are blocked at the atrioventricular node. The ventricular response is completely irregular, ranging from 80 to 180/min Difference between apical rate and pulse rate = “pulse deficit” Atrial fibrillation CLASSIFICATION AFIB Acute Management      Short-term complications are primarily hemodynamic Rapid ventricular rate may cause progressive deterioration of LV function Acute management includes determination of whether there is underlying heart disease, achieving rate control and restoring sinus rhythm Except with holiday heart or a transient precipitating cause, most patients with new onset of atrial fibrillation do not revert to sinus rhythm spontaneously. Unless the patient is unstable (either from ischemia or hypotension), the initial approach is usually rate control. Acute management    Acute rate control can be obtained with i.v. betablockers (metoprolol 5 mg), i.v. verapamil or diltiazem, or i.v. digoxin (0.5-0.75mg over 30-60 min, followed by 0.125-0.25 mg very 2-4 h until rate is controlled). Electrical cardioversion may be necessary if rate control cannot be achieved and the patient is hemodynamically unstable. However, if atrial fibrillation has been present for more than 48 h, the risk of embolizing during conversion to sinus rhythm increases. Atrial fibrillation      If the arrhythmia has been present for >48h= anticoagulation should be initiated and maintained for 3-4 weeks prior to cardioversion an alternative strategy involves transoesophageal echocardiography and early cardioversion in individuals without evidence of left atrial thrombi Pharmacologic cardioversion: if no LA thrombi or effective anticoagulation for 3-4 weeks: amiodarone, or a short acting class III agent: ibutilide Electrical cardioversion: initial 200 J shock adm. in synchrony with R wave+ an additional attempt with 400 J Anticoagulation maintained 4-6 weeks after cardioversion Treatment of Chronic Atrial Fibrillation      Disadvantages: symptoms related to arrhythmia and increased risk of thrombembolic phenomena Rate control obtained with: digoxin, a beta-blocker or a Ca channel blocker, or amiodarone. Atrial fibrillation is a major risk for stroke- as high as 20% per year (especially with MS, increasing age, reduced LV function and heart failure, hypertension and diabetes). Antithrombothic therapy with warfarin or acenocumarol (maintained for an INR=2-3) has been shown to reduce the risk of stroke in virtually all subgroups of pts. with chronic AF. NOACs: apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa)- effective in non-valvular AF Atrial Flutter    Less common than AF, usually occurs in pts. with COPD, rheumatic or CHD, congestive heart failure or ASD. Ectopic impulse formation occurs at atrial rates of 250- 350/min, with transmission of every second, third, or fourth impulse through the AV node to the ventricles. Ventricular rate control accomplished using the same agents utilized in AF Atrial Flutter     1-2 mg Ibutilide i.v.- 50-70% conversion to sinus rhythm within 60-90 min. Electrical cardioversion with 25-50 J = 90% efficacy Systemic embolization lower than in AF Chronic atrial flutter: - rate control with amiodarone - radiofrequency ablation Ventricular Cell Problems Ventricular cells can:  fire occasionally from 1 or more foci  fire continuously from multiple foci  fire continuously due to a looping re-entrant circuit Premature Ventricular Contractions (PVCs) Ventricular Fibrillation Ventricular Tachycardia Ventricular Arrhythmias Ventricular premature beats -wide QRS complexes that differ in morphology from the patient’s normal beats, usually not preceded by P waves, followed by a fully compensatory pause Ambulatory ECG monitoring or during exercise test may reveal more frequent and complex ventricular premature beat`s When VPB are frequent- exclude electrolytic abnormalities, hyperthyroidism and organic heart disease Ventricular Arrhythmias Pharmacologic treatment:  indicated only for symptomatic patients;  beta-blockers are the agents of first choice Ventricular Tachycardia      Three or more consecutive ventricular premature beats; usual rate= 160-240/min and is moderately regular but less so than atrial tachycardia. Carotid sinus pressure has no effect Usual mechanism: reentry, but abnormally triggered rhythms may occur. VT- either nonsustained (lasting less than 30 sec) -either sustained Ventricular Tachycardia    may be asymptomatic or associated with syncope or symptoms of impaired cerebral perfusion VT is a frequent complication of AMI and dilated cardiomyoparthy, hypertrophic cardiomyopathy, mitral valve prolapse, myocarditis Torsade de pointes may occur spontaneously or after quinidine or any drug that prolongs the QT interval Ventricular tachycardia Treatment of VT Acute Ventricular Tachycardia- treatment determined by the degree of hemodynamic compromise and the duration of the arrhythmia  If hypotension, heart failure or angina is presentsynchronized DC cardioversion with 100- 369 J should be performed immediately.  If the patient is tolerating the rhythm, lidocaine 1 mg/kg as an i.v. bolus injection , i.v procainamide 100 mg every 5 min (up to 1000mg), bretylium 5 mg/kg repeated after 20 min  Treatment of VT Amiodarone with a loading dose of 150 mg over 10 min, followed by slow infusion of 1mg/min for 6 hours and a maintenance dose of 0.5 mg/min for an additional 18-42 h. Chronic Recurrent Ventricular Tachycardia      Nonsustained ventricular tachycardia: poor prognosis if associated with organic heart disease, marker for increased mortality Major factor post AMI: degree of LV dysfunction Best treatment: implantable cardiac defibrillator Beta-blocking agents: occasionally effective More recent data favor the class III agents: sotalol or amiodarone, because proarrhythmia may be less frequent Chronic Recurrent Ventricular Tachycardia   Sustained ventricular tachycardia: sotalol or amiodarone, implantable cardiac defibrillator (ICD) Ablation of ventricular tachycardias that originate in the right ventricular outflow tract (appearing as a left bundle branch block with inferior axis morphology) Nonsustained VT Severe Ventricular Arrhythmias Ventricular fibrillation: the patient is in cardiac arrest emergency CPR and electrical cardioversion Ventricular fibrillation Torsade de pointes A-V Conduction Disturbances    Sick sinus syndrome- an imprecise diagnosis applied to patients with sinus arrest, sinoatrial exit block, persistent sinus bradycardia. These rhythms are often caused or exacerbated by drug therapy (digitalis, Ca channel blockers, beta- blockers, sympatholythic agents, antiarrhythmics) Another presentation is of recurrent SVT, atrial flutter and fibrillation, associated with Brady arrhythmias (“tachy-brady syndrome”). A-V Conduction Disturbances     ECG features are mostly noted in elderly patients- reason: patchy fibrosis of the sinus node or cardiac conduction system ( various cardiomyopathies) Patients asymptomatic or experiencing syncope, dizziness, confusion, palpitations Pharmacologic therapy: difficult; Most symptomatic patients will require permanent pacing Sick sinus syndrome Atrioventricular Block  First –degree AV block: PR interval>0.21 s, with all atrial impulses conducted Atrioventricular Block Second-degree AV block: -Mobitz type I (Wenckebach): PR interval progressively lengthens, with the RR interval shortening, before the blocked beat; -Mobitz type II block is abrupt, not preceded by lengthening AV conduction time; the width of the QRS complexes assists in determining whether the block is nodal or infranodal 2nd Degree AV Block, Type I – PR interval progressively lengthens, then the impulse is completely blocked (P wave not followed by QRS). 2nd Degree AV Block, Type I  Etiology: Each successive atrial impulse encounters a longer and longer delay in the AV node until one impulse (usually the 3rd or 4th) fails to make it through the AV node. 2nd Degree AV Block, Type II Occasional P waves are completely blocked (P wave not followed by QRS). Etiology: Conduction is all or nothing (no prolongation of PR interval); typically block occurs in the Bundle of His. 2nd Degree AV Block, Type II 3rd Degree AV Block – The P waves are completely blocked in the AV junction; QRS complexes originate independently from below the junction. Atrioventricular Block  Complete (third- degree) heart block is a more advanced form of block due to a lesion distal to the His bundle  the ventricular pacemaker maintains a slow, regular ventricular rate, usually less than 45/min. Treatment of complete AV block  Insertion of a pacemaker