ARRHYTHMIAS. REENTERY occurs when propagating impulse fails to die out after normal activation of heart and persist to re excite the heart.
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1 ARRHYTHMIAS Arrhythmia is defined as loss of cardiac rhythm, especially irregularity of heartbeat. PATHOPHYSIOLOGY Ectopic complexes (ectopic beats) 1. By definition, arise from a site other than the sinus node - may be atrial, AV nodal (or junctional), ventricular. 2. May be premature (arise prior to the next expected sinus activation). Premature atrial ectopic complexes, or beats (may be abbreviated PAC's, APC's, and APB s). Premature ventricular ectopic complexes, or beats (PVC's, VPC's, VPB's). Ectopic tachycardias REENTERY: Rate > 100/min. arise from a site other than the sinus node. may be "paroxysmal" (start and stop abruptly, usually by initiating or terminating factor) or "nonparoxysmal" (present constantly, tend to appear or disappear by gradual changes in rate). may also be "nonsustained" (terminating spontaneously) or "sustained" (continuing for prolonged periods or until stopped by an intervention). Most common are ventricular tachycardia (VT), paroxysmal atrial tachycardia (PAT). REENTERY occurs when propagating impulse fails to die out after normal activation of heart and persist to re excite the heart. Continuous repetitive propagation of excitatory waves traveling in circular path, returning to its site of origin to reactive that site. OR Reentrant arrhythmias can arise anywhere in the heart provided there are two pathways connected proximally (here at X) and distally (Y). Such anatomic structures are present in many areas of the heart, but the conditions permitting reentry to occur are very specific. This kind of arrangement is particularly common in the AV node, in which there can be 2 distinct alternative conduction pathways. It can also occur in any area of the heart with fibers interconnected at more than 1 point.
2 An impulse must first arrive from above at a time when one pathway (here designated B) is still refractory, but the other (A) has recovered excitability. Since the refractory period is usually over well before the next expected sinus beat, a premature beat is much more likely than a sinus beat to encounter refractoriness in one of the pathways. (Proper timing is crucial, however - if the premature beat arrives too early, both A and B will be refractory.) The impulse travels down pathway A and arrives at the terminal portion of pathway B (which has not been activated from above). If the distal end of pathway B has recovered excitability, the impulse can travel retrogradely over pathway B. It will now arrive at the proximal end of pathway A. If the proximal end of pathway A has recovered excitability by the time the impulse re-enters it, the impulse will now propagate antegradely down pathway A. Thus, under certain very specific conditions, a premature beat can block in B, travel antegradely down A, come back retrogradely through B, activate A again, and then the cycle can keep repeating itself. One premature impulse can thereby initiate a self-sustaining tachycardia.
3 The conditions necessary for reentry include: Premature beats. Differences in refractoriness between alternate pathways. Conduction which is slow enough so that the reentrant impulse never encounters refractory tissue (otherwise it would be blocked and reentry would terminate). Consider for a moment only the reentry circuit (comprising the two pathways and their connections): The time (T) to complete one circuit of the pathway is given by: T = L/V The circuit time has to be longer than the longest refractory period- otherwise the impulse would leave the area of greatest refractoriness and return to it before excitability is restored. So for reentry to be sustained, T must be greater than RP, i.e. T > RP and L/V > RP Thus reentrant arrhythmias can be terminated or prevented by increasing the refractory period so that it exceeds conduction time Fast conduction (V large) makes reentry less likely, while slow conduction facilitates reentry There are two other important consequences of the above relationship: 1. Consider the path lengths necessary for reentry to occur in tissue with normal conduction. An average refractory period (RP) is about 0.25 seconds, and conduction velocity (v) in fast channel tissue (atria, ventricles, His-Purkinje system) is > 1 m/sec. In slow channel tissue (SA and AV nodes) the average refractory period is similar but mean conduction velocity is in the order of 0.04 m/sec. Calculate the minimal path length in each type of tissue that could support reentry, assuming L/V > RP (i.e., minimum length= V x RP).
4 These calculations will demonstrate why reentry within the AV node (which sometimes behaves as though it consists of two separate pathways connected above and below) frequently occurs in otherwise normal individuals, while reentry in the atria or ventricles is usually associated with diseases that cause slowed conduction and/or chamber dilation. 2. The heart rate during the reentrant tachycardia will depend on the circuit time. If one circuit takes T seconds, the number of circuits per minute will be 60/T. Since the impulse leaves the circuit in an antegrade direction (at Y) once during each circuit, the heart rate (HR) will equal 60/T. But T = L/V, so: If conduction is accelerated (i.e. V becomes greater), there will be a larger number of circuits completed per unit time and the heart rate during reentrant tachycardia will be increased. Therefore, while theoretically an increase in conduction velocity might prevent reentry; in practice increasing conduction velocity might dangerously accelerate a reentrant tachycardia if it failed to immediately terminate it. Thus, reentrant arrhythmias are usually treated by interventions that increase refractoriness or cause block, rather than interventions that accelerate conduction. Factors predisposing to reentry Prevention or termination of reentry premature beats variability in refractoriness slow conduction, short refractory periods (L/V > RP) drugs that decrease the number of premature beats drug therapy to equalize refractory period in the two pathways (easier if pathways contain different types of tissue) drugs which increase refractory period
5 Reentry may involve one consistent circuit. This will result in a regular reentrant arrhythmia such as AV node reentrant tachycardia (PAT), atrial flutter, or ventricular tachycardia. Reentry can also occur in a discontinuous, irregular pattern of a large number of re-entrant wave fronts. This produces a rapid, chaotic arrhythmia (e.g. atrial fibrillation or ventricular fibrillation). When the atria are firing rapidly (e.g. atrial flutter, 300/min: or atrial fibrillation, /min) the ventricular response rate (rate of the ventricles) is determined by the filtering effect of the AV node. Tachycardias produce problems by limiting the diastolic period available for ventricular filling and subendocardial blood flow. For rapid atrial arrhythmias, the ventricular response rate usually determines the consequences of the arrhythmia. Alternate (non-drug) approaches to stopping or preventing reentry 1. Electric shock - Stops reentry by depolarizing strongly cardiac tissue, thereby restoring electrical synchrony to cardiac activity. Treatment of choice for termination of most life-threatening reentrent arrhythmias (e.g. ventricular fibrillation). Implantable devices (e.g. implantable ventricular defibrillator) are now available, that can detect and automatically terminate ventricular tachycardia and fibrillation These are probably TREATMENT OF CHOICE for chronic therapy of life-threatening ventricular tachyarrhythmias. 2. Destruction of arrhythmic tissue - Can prevent a variety of reentrant arrhythmias. Originally required surgery, can now be performed in many cases by delivering radiofrequency energy via electrode catheter (introduced via an artery or vein, and positioned under fluoroscopic guidance) Treatment of choice for recurrent AV reentry tachycardias (e.g. AV node reentry). Becoming very effective and more widely used for certain kinds of ventricular arrhythmias and atrial fibrillation
6 Potentially Beneficial Effects of Drugs 1. Arrhythmia termination - by interrupting reentry, or by suppressing enhanced or abnormal forms of automaticity. 2. Arrhythmia prevention - by eliminating or altering the factors that either initiate or sustain an arrhythmia. 3. Arrhythmia control - if the ventricular response rate is controlled, patients with atrial flutter or fibrillation may be clinically well despite continued atrial fibrillation or flutter. Drugs to stop reentry (arrhythmia termination) - can act by stopping conduction in the reentry circuit (especially in slow-channel reentry). AV node reentry is a common form, and can be treated by drugs that suppress conduction in slow-channel (Ca2+current dependent) tissue. Examples: Mechanism by which drugs depress slow response (slow-channel) action potentials and can stop reentry in slow-channel tissue 1. Sympathetic antagonism - reduces camp dependent calcium entry through receptor operated channel (beta blockers, sympatholytic drugs). 2. Vagal enhancement - reduces Ca2+ entry by both direct and indirect (antisympathetic) mechanism (digitalis, acetylcholinesterase inhibitors), hyperpolarizes AV node cells by activating K+ current, and brings cells further from threshold (harder to fire). 3. Calcium channel blockers - reduce Ca2+ entry through voltage - dependent calcium channel (verapamil, diltiazem, nifedipine). 4. Purinergic agonists - adenosine or ATP - produce "vagal - like" effects via purinergic receptor activation.
7 AUTOMATICITY 1. Enhanced Automaticity Automaticity can be enhanced by: Less negative diastolic potential (closer to threshold). Steeper slope of phase 4. More negative threshold (closer to maximum diastolic potential). Catecholamines enhance automaticity by increasing slope of phase 4. can result in arrhythmias e.g. with exercise, pheochromocytoma. Catecholamine-induced arrhythmias can be eliminated by interventions that prevent beta-adrenergic cardiac stimulation (e.g. beta blockers like propranolol). Myocardial infarction (MI) may enhance automaticity by enhancing catecholamine release (from nerve endings in the infarct and from the adrenal medulla) and by depolarizing tissue towards threshold. Some ventricular arrhythmias after acute MI can be reduced or eliminated by drugs that suppress automaticity. Enhanced automaticity can be suppressed by: reducing phase 4 depolarizing current (Ca2+ current in SA and AV node, Na+ current in His-Purkinje system) making threshold potential more positive (e.g. by suppressing current needed to fire cell during phase 0, Ca2+ current in SA/AV nodes, Na+ current in HP system) antagonizing components that enhance automaticity, e.g. beta blockers in situations where beta-adrenergic stimulation contributes to enhanced automaticity
8 Abnormal Forms of Automaticity: EARLY AFTERDEPOLARIZATIONS (EAD'S) occur when the action potential has been markedly prolonged, causing Ca2+ current to depolarize cell. arise on the plateau phase of the action potential (before full repolarization). occur in His Purkinje cells. can depolarize surrounding tissue to threshold, resulting in premature activation of the heart. long series of early afterdepolarizations can cause a ventricular tachycardia (VT), often with characteristic ECG appearance ("Torsades de Pointes" - rapid VT, with alternation of the points of the QRS) EAD - induced arrhythmias tend to be caused by factors that increase APD, such as: 1. certain antiarrhythmic drugs (e.g. quinidine, disopyramide, procainamide, sotalol) that block K+ channels involved in repolarization 2. slow heart rate 3. hypokalemia (low extracellular K+ concentration, which directly inactivates certain K+ channels) 4. since the QT interval on the surface ECG is largely determined by ventricular APD, arrhythmias caused by early afterdepolarizations are usually associated with marked QT prolongation ("long QT syndromes"). Treatment of arrhythmias due to EAD's eliminate reversible factors (e.g. drug therapy) that may be causative or contributory. treat hypokalemia if present. increase heart rate (electrical pacemaker or isoproterenol).
9 DELAYED AFTERDEPOLARIZATIONS (DAD'S) result from cellular calcium overload in fast channel tissues free cytosolic (Ca2+) in resting cardiac cell is in the range of l0-7 M (extracelluar conc. > 10-3 M). During systole, release from SR stores increases free calcium concentration 10-fold, resulting in contraction. During diastole, calcium is rapidly pumped back into subcellular stores, allowing the cell to relax. Increases in total cellular calcium are handled by increased uptake into SR, so that free resting cytosolic calcium is not increased (systolic calcium release may, however, be augmented). With more severe calcium overload, there is a diastolic "spillover" of calcium from SR. This "spillover" modulates properties of the cell membrane, resulting in inward current and an afterdepolarization. If the afterdepolarization reaches threshold, it can cause premature activation (premature beat); a series of afterdepolarizations which reach threshold can cause a tachycardia. Factors enhancing DAD's (All increase intracellular calcium): increased heart rate, premature complexes. hypercalcemia. catecholamines (via camp). methylxanthines (e.g. theophylline). Digitalis (via enhanced Na+, Ca2+ exchange) arrhythymias caused by DAD's probably occur only with fairly severe Ca2+ overload, so drug toxicity or a number of interacting factors are usually necessary to cause them. Treatment of arrhythmias caused by DAD's eliminate reversible contributory or causative factors. Various drugs can reduce delayed afterdepolarizations: o Calcium antagonists (e.g. verapamil) - reduce calcium entry during each action potential. o Sodium channel blockers (e.g. lidocaine, quinidine) - make threshold potential more positive, harder for DAD's to reach threshold. o Eliminate factors tending to increase heart rate. PROARRHYTHMIA : Antiarrhythmic drugs can sometimes paradoxically worsen or cause arrhythmias (so-called "proarrhythmic effects") - if they alter the underlying substrate to favour arrhythogenesis - e.g. drugs that prolong APD can produce EADmediated tachycardias; drugs that slow conduction can favour the occurrence of reentry; drugs that increase cellular Ca2+ load like digitalis, when in excess (toxicity) can result in DAD-induced tachycardias.
10 TYPES OF THE DRUG AND ITS EFFECTS:
11 TYPES OF ARRHYTHMIA AND ITS RESPECTIVE DIAGNOSTIC ECG PATTERN: TYPE CAUSE DIGNOSIS TREATMENT Normal sinus rhythm Is the standard against which all other rhythms are compared 1. Rhythm: regular 2. Heart rate: QRS: less than P wave: only one precedes each QRS, all have same size, shape and deflection 5. PR interval: Interpretation: Sinus Rhythm Sinus Tachycardia Characterized by heart rate greater than 100 Causes: fever, any type of hypovolemia such as dehydration or blood loss 1. Rhythm: regular 2. Heart rate: QRS: less than P wave: only one precedes each QRS, all have same size, shape and deflection 5. PR interval: Interpretation: Sinus Tachycardia Sinus Bradycardia Characterized by heart rate less than Rhythm: regular 2. Heart rate: Treated only if accompanied by symptoms of hypoperfusion, such as dizziness, chest pain, changes in LOC 3. QRS: less than P wave: only one precedes each QRS, all have same size, shape and 2. Medical treatment may include atropine or pacemaker
12 deflection 5. PR interval: Sinus Arrhythmia 1. Usually caused by respiratory cycle 2. Inspiration causes slight increase in rate and exhalation causes a slight decrease in rate due to vagal tone during the different phases of respiration 3. Seen most often in children and young adults 1. Rhythm: irregular 2. Heart rate: normal, or slow, QRS: less than P wave: only one precedes each QRS, all have same size, shape and deflection 5. PR interval: Atrial Tachycardia 1. Digoxin toxicity, most common cause 2. Also, Rheumatic heart disease, hyperthyroidism, Cor pulmonale 1. Rhythm: usually regular 2. Heart rate: QRS: usually normal, less than Vagal maneuvers Valsalva, carotid massage 2. Adenosine to chemically cardiovert 3. Cardioversion 4. P wave: may not always be discernible due to fast rate, frequently obscured in the preceding T wave 4. Also, Cardizem, Verapamil, Digoxin, Rapid atrial pacing Caution, Cardioversion + Digoxin + Ca channel blocker can cause sustained systole 5. PR interval: not measurable Paroxysmal Atrial Tachycardia Characterized by an abrupt start and end of Atrial tachycardia. Is often initiated by a PAC C. 3 or more consecutive PACs are considered to be atrial tachycardia 1. Rhythm: usually regular 2. Heart rate: QRS: usually normal, less than P wave: may not always be discernible due to fast rate, frequently obscured in
13 the preceding T wave 5. PR interval: not measurable Supraventric ular Tachycardia A. Characterized by narrow complex tachycardia with P waves hidden in the previous T wave, it is not possible to tell where the rhythm originates B. Is a general term that refers to the origin as being above the ventricles 1. Rhythm: regular 2. Heart rate: >150 beats/min 3. QRS: normal, less than P wave: difficult or unable to visualize Treatment: if associated with rapid ventricular response needs immediate attention. Treatment of choice is synchronized cardioversion, also may give Digoxin, Quinidine, Corvert C. Includes rapid response atrial flutter, atrial tachycardia, junctional tachycardia 5. PR interval: not measurable Atrial Flutter A. Occurs when an ectopic pacemaker site in the atria discharges impulses at a very rapid rate B. The atrial muscles respond to the rapid stimulation producing wave deflections called flutter waves 1. Rhythm: atrial regular, ventricular regular if conduction is regular 2. Heart rate: atrial , ventricular varies depending on conduction but will be less than atrial rate C. Characterized by flutter waves D. Cause: 1. Mitral valve disease, hyperthyroidism, pericardial disease, MI, COPD 3. QRS: less than P waves: sawtooth looking, more P waves than QRS 5. PR interval: not measurable 2. Rarely seen in healthy people, usually have some underlying heart disease
14 Atrial Fibrillation A. Multiple ectopic pacemakers in the atria discharge at a very rapid rate B. The impulses are so rapid it causes the atria to quiver instead of contracting regularly C. If left untreated may cause thrombus formation due to blood pooling in the atria from inadequate contractions D. Characterized by irregular rhythm, absence of P waves, and presence of fibrillation waves E. Cause: 1. Valvular heart disease, hyperthyroidism, infection, CAD, MI, hypoxia, pericarditis, Aminophylline, Digoxin 1. Rhythm: atrial and ventricular irregular 2. Heart rate: atrial (400 average), ventricular or depending on conduction 3. QRS: less than P waves: absent, irregular fibrillation waves seen instead 5. PR interval: not measurable Treatment: 1. Try to keep ventricular rate under Drugs: Cardizem, Verapamil, Digoxin, Corvert, Quinidine, Pronestyl, beta blockers 3. Chemical or electrical cardioversion a) Electrical cardioversion most successful if used within the 1 st 3 days b) If unsure how long patient has had the rhythm, check for thrombus formation before cardioversion, because conversion to NSR may dislodge clots if not anticoagulated c) Patient is at risk for CVA while in A-fib due to release of micro-emboli 2. Commonly associated with CHF Ventricular Tachycardia A. Originates in an ectopic focus in the ventricles B. Usually associated with increased automaticity or reentry C. May develop without warning, but is often associate with frequent PVCs D. Characterized by rapid heart rate made up of 1. Rhythm: usually regular, may be somewhat irregular 2. Heart rate: QRS: wide and bizarre, greater than 0.12 seconds 4. P wave: none associated, the SA node does continue to fire independently, so P waves may be seen at random, but I. Treatment: Check the patient 1. If there is no pulse, begin CPR and other code measures 2. If there is a pulse and the patient is unstable - cardiovert and begin drug therapy 3. With chronic or recurrent VT a) Give antiarrhythmics
15 ventricular beats E. May occur as a 1. Sustained rhythm lasting longer than 30 seconds are usually hidden in the QRS complexes 5. PR interval: not measurable b) Long term may need ICD placed c) Ablation may be used for reentry 2. Nonsustained rhythm lasting less than 30 seconds 3. Burst of VT a series of 3 or more consecutive PVCs F. Cause: 1. Usually occurs with underlying heart disease 2. Commonly occurs with myocardial ischemia or infarction 3. Certain medications may prolong the QT interval predisposing the patient to ventricular tachycardia 4. Other causes include electrolyte imbalance and mechanical stimulation of the endocardium Torsade de Pointes A. A unique variant form of ventricular tachycardia B. Characterized by QRS complexes that seem to twist around the baseline, changing back and forth from negative to positive C. Is commonly an immediate forerunner to ventricular fibrillation 1. Rhythm: somewhat irregular 2. Heart rate: QRS: wide and bizarre, greater than 0.12 seconds, polarity changes from positive to negative around the isoelectric line 4. P wave: none associated Treatment protocol includes: 1. Begin CPR and other code measures 2. Eliminate predisposing factors - rhythm has tendency to recur unless precipitating factors are eliminated 3. Administrate magnesium sulfate bolus 4. Overdrive pace, especially if
16 D. Cause: 1. Is associated with prolonged QT interval 5. PR interval: not measurable precipitated by bradycardia 5. Defibrillation 2. Is often caused by drugs conventionally recommended in treating VT 3. Phenothiazine or tricyclic antidepressant overdose 4. Electrolyte disturbances, especially hypokalemia and hypomagnesemia Ventricular Fibrillation A. A disorganized, chaotic electrical focus in the ventricles which takes control of the heart B. The ventricles do not beat in any coordinated fashion, instead quiver asynchronously and ineffectively C. Characterized by an erratic series of waves 1. Rhythm: chaotic 2. Heart rate: none 3. QRS: no complexes are present 4. P waves: none 5. PR interval: none Treatment: Begin CPR and other code measures D. Is the most common cause of sudden cardiac death E. May occur spontaneously, but is most often preceded by VT or dangerous forms of PVCs (pairs, runs, multifocal, or R-on-T type) F. There is no cardiac output, peripheral pulses, or blood pressure and the patient become unconscious immediately
17 G. Death is imminent H. Two types of V-fib 1. Coarse - waves are large, usually indicates a more recent onset and is more likely to be reversed by defibrillation 2. Fine - waves are small, must be differentiated from asystole
18 TREATMANT AND MANAGEMENT OF ARRHYTHEMIAS: ATRIAL FIBRILLATION OR ATRIAL FLUTTER:
19 NOTE: Anticoagulation should be initiated prior to cardioversion because return of atrial contraction increases risk of thromboembolism. Current recommendations are to initiate warfarin (international normalized ratio [INR] 2 to 3) for at least 3 weeks prior to cardioversion and continuing for at least 1 month after effective cardioversion. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA Paroxysmal supraventricular tachycardia (PSVT) arising by reentrant mechanisms includes arrhythmias caused by AV nodal reentry, AV reentry incorporating an anomalous AV pathway, sinoatrial (SA) nodal reentry, and intraatrial reentry. ALGORITHUM: AUTOMATIC ATRIAL TACHYCARDIAS Underlying precipitating factors should be corrected by ensuring proper oxygenation and ventilation and by correcting acid-base or electrolyte disturbances. If tachycardia persists, the need for additional treatment is determined by symptoms. Patients with asymptomatic atrial tachycardia and relatively slow ventricular response usually require no drug therapy. In symptomatic patients, medical therapy can be tailored either to control ventricular response or to restore sinus rhythm. Calcium antagonists (e.g., verapamil) are considered first-line drug therapy for decreasing
20 ventricular response. Type I agents (e.g., procainamide, quinidine) are only occasionally effective in restoring sinus rhythm. DCC is ineffective, and β blockers are usually contraindicated because of coexisting severe pulmonary disease or uncompensated heart failure. VENTRICULAR TACHYCARDIA Acute Ventricular Tachycardia If severe symptoms are present, DCC should be instituted to restore sinus rhythm immediately. Precipitating factors should be corrected if possible. If VT is an isolated electrical event associated with a transient initiating factor (e.g., acute myocardial ischemia, digitalis toxicity), there is no need for long-term antiarrhythmic therapy after precipitating factors are corrected. Patients with mild or no symptoms can be treated initially with antiarrhythmic drugs. IV amiodarone is usually the first step in this situation. Procainamide or lidocaine given IV is suitable alternatives. If lidocaine fails to terminate tachycardia, IV procainamide (loading dose and infusion) can be tried. DCC should be instituted or a transvenous pacing wire should be inserted if the patient's status deteriorates, VT degenerates to VF, or drug therapy fails. Sustained Ventricular Tachycardia Patients with chronic recurrent sustained VT are at extremely high risk for death; trial-and-error attempts to find effective therapies are unwarranted. Neither electrophysiologic studies nor serial Holter monitoring with drug testing is ideal. These findings and the side-effect profiles of antiarrhythmic agents have led to nondrug approaches. The automatic implantable cardioverter defibrillator (ICD) may be the most effective method for preventing sudden death due to recurrent VT or VF. It resulted in better overall survival at 3 years than chronic antiarrhythmic therapy with amiodarone, the most effective drug known. Patients with complex ventricular ectopy should not receive type I or III antiarrhythmic drugs. Nonsustained Ventricular Tachycardia The approach to NSVT is controversial. Patients with long symptomatic episodes require drug therapy, but most patients are asymptomatic. Patients with NSVT and coronary disease are at risk for sudden death, particularly if they have inducible sustained VT after programmed stimulation. Consequently, these patients should undergo electrophysiologic studies and be given chronic preventive therapy with an ICD or empiric amiodarone if sustained VT/VF is inducible. Proarrhythmia Proarrhythmia is resistant to resuscitation with cardioversion or overdrive pacing. Some clinicians have had success with IV lidocaine (competes for the sodium channel receptor) or sodium bicarbonate (reverses the excessive sodium channel blockade).
21 Torsades de Pointes For an acute episode, most patients require and respond to DCC. However, TdP tends to be paroxysmal and often recurs rapidly after countershock. IV magnesium sulfate is considered the drug of choice for preventing recurrences of TdP. If ineffective, strategies to increase heart rate and shorten ventricular repolarization should be instituted (i.e., temporary transvenous pacing at 105 to 120 beats/min or pharmacologic pacing with isoproterenol or epinephrine infusion). Agents that prolong the QT interval should be discontinued, and exacerbating factors (e.g., hypokalemia) corrected. Drugs that further prolong repolarization (e.g., IV procainamide) are contraindicated. Lidocaine is usually ineffective. Ventricular Fibrillation VF (with or without associated myocardial ischemia) should be managed according to the American Heart Association's recommendations for advanced cardiac life support. After successful resuscitation, antiarrhythmics should be continued until the patient's rhythm and overall status are stable. Long-term antiarrhythmics or ICD implantation may or may not be required. EVALUATION OF THERAPEUTIC OUTCOMES The most important monitoring parameters include (1) mortality (total and due to arrhythmic death), (2) arrhythmia recurrence (duration, frequency, symptoms), (3) hemodynamic consequences (rate, blood pressure, symptoms), and (4) treatment complications (need for alternative or additional drugs, devices, or surgery). BY: DEEP [36] Reference and further reading: pharmacotherapy- a pathophysiologic approach by josepth t. dipiro, sixth edition.
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