Tachycardia during Myocardial Infarction Alireza Heidari Bakavoli, M.D Mashhad University of Medical Science

Introduction Ventricular tachyarrhythmia has been one of the most frequent cause of sudden cardiac death in AMI In one report(1985), 60 % of deaths associated with acute MI occurred within the first hour and were related to a ventricular arrhythmia, particularly vf

Introduction Arrhythmic Mortality and Overall in hospital Mortality have been decreased in recent years Ventricular arrhythmias, ranging from isolated ventricular premature beats to VF, are common in the immediate postinfarction period Observations in the prefibrinolytic era : – VPBs 10 to 93 percent – VT 3 to 39 percent – VF 4 to 20 percent

Introduction Early series underestimated the incidence of unstable VT and VF, – they did not include out-of-hospital sudden cardiac death (SCD) The incidence of ventricular arrhythmias appears to be higher with STEMI than NSTEMI VT is less common than VF in the periinfarction period.

Introduction Early (≤4 hours) primary VF (ie, VF in the absence of heart failure or shock) occurred in 3.1 percent. VF recurred during the hospitalization in 11 percent of these patients. Late VF (>4 to 48 hours) occurred in 0.6 percent and was recurrent in 15 percent.

Introduction Most peri-infarct arrhythmias are benign and self- limited However, those that result in hypotension, increase myocardial oxygen requirements, and/or predispose the patient to develop additional malignant ventricular arrhythmias should be aggressively monitored and treated.

Pathophysiology of arrhythmic complications Autonomic dysfunction: – Electrolyte imbalances (eg, hypokalemia and hypomagnesemia) and hypoxia further contribute to the development of cardiac arrhythmia. The damaged myocardium acts as substrate for re- entrant circuits, due to changes in tissue refractoriness.

Classification of peri-infarction arrhythmias Supraventricular tachyarrhythmias – Sinus tach, PACs, PSVT, AFL, Afib Accelerated Junctional Rhythm Bradyarrhythmias Ventricular arrhythmias – PVCs, accelerated idioventricular rhythm, ventricular tachycardia, and ventricular fibrillation – Reperfusion arrhythmias

persistent sinus tachycardia Pain Anxiety Heart failure Hypovolemia Hypoxia Anemia Pericarditis Pulmonary embolism

Sinus tachycardia Treatment strategies: – Pain medication – Diuresis to manage heart failure – Oxygenation – Volume repletion for hypovolemia – Administration of anti-inflammatory agents to treat pericarditis – Beta-blockers and/or NTG to relieve ischemia

Premature atrial contractions Often before the PSVT, AFL, or A fib. The usual cause: – Atrial distention due to LV diastolic pressure or inflammation associated with pericarditis No specific therapy is indicated Attention should be given to identifying the underlying disease process, particularly occult heart failure

Paroxysmal supraventricular tachycardia The incidence: less than 10%. In the absence of definitive data in the patient with AMI, the consensus is that adenosine can be used when hypotension is not present. In patients without clinically significant LV failure, intravenous diltiazem or a beta-blocker can be used instead. In patients who develop severe heart failure or hypotension, synchronized electrical cardioversion is required.

Atrial flutter Occurs in less than 5% of patients with AMI. Is usually transient and results from sympathetic overstimulation of the atria Treatment strategies(same as A fib ) – Rate control with drugs is less easy in AFL than with A fib Synchronized DC shock (50 J, or the biphasic equivalent) may be needed If AFL is refractory to medical therapy – overdrive atrial pacing may be considered.

Atrial fibrillation The rate:10-15% A fib in the first hours of AMI is usually caused by – LV failure – Ischemic injury to the atria – RV infarction – Pericarditis – All conditions leading to elevated LA pressure

Atrial fibrillation The presence of A fib during an AMI is associated with an increased risk of – mortality – stroke, – particularly in patients who have anterior-wall MIs.

Atrial fibrillation Immediate DC cardioversion is indicated for the patient in unstable condition – New or worsening ischemic pain – Hypotension. – Synchronized DC cardioversion to treat A fib begins with 200 J (or the biphasic equivalent). – Conscious sedation (preferred) or general anesthesia is advisable prior to cardioversion.

Atrial fibrillation In stable condition – rate control If the A fib does not respond to cardioversion, IV amiodarone [2] or IV digoxin (in patients with LV dysfx or HF) can be used to achieve rate control.

Atrial fibrillation For patients who do not develop hypotension, a beta- blocker can be used. – metoprolol 5-mg IV boluses every 5-10 min, with a maximum dose of 15 mg. IV diltiazem Is an alternative but it should be used with caution in patients with moderate-to-severe heart failure. In patients with new-onset sustained tachycardia (absent before MI), conversion to sinus rhythm should be considered as an option.

A fib and AFL confer an increased risk of thromboembolism Therefore, anticoagulation with either unfractionated heparin or low molecular weight heparin (LMWH) should be started if contraindications are absent. It is unclear whether anticoagulation is needed in cases of transient atrial fibrillation and how long after the onset of atrial fibrillation should the anticoagulation be started.

Accelerated junctional rhythm and junctional tachycardia A rhythm results from increased automaticity of the junctional tissue that leads to a heart rate of bpm. This type of dysrhythmia is most common in patients who develop inferior myocardial infarctions. Treatment is directed at correcting the underlying ischemia.

Ventricular Arrhythmias

Premature ventricular contractions In the past, frequent PVCs were considered to represent warning arrhythmias and indicators of impending malignant ventricular arrhythmias. However, presumed warning arrhythmias are frequently observed in patients who have an acute AMI and who never develop VF. On the converse, primary VF often occurs without antecedent premature ventricular ectopy

Premature ventricular contractions For these reasons, prophylactic suppression of PVCs with lidocaine, is no longer recommended. Prophylaxis has been associated with an increased risk of fatal bradycardia or asystole because of the suppression of escape pacemakers.

Management A conservative approach Do not routinely administer prophylactic antiarrhythmics. Attention should be directed toward correcting any electrolytic or metabolic abnormalities, plus identifying and treating recurrent ischemia

Accelerated idioventricular rhythm In as many as 20% of patients who have an AMI. A ventricular rhythm characterized by a wide QRS with a regular escape rate faster than the atrial rate, but less than 100 bpm. AV dissociation is frequent. Slow, nonconducted P waves are seen; these are unrelated to the fast, wide QRS rhythm.

AIVR Most episodes are short and terminate spontaneously. Equal frequency in anterior and inferior infarctions. The mechanism – (1) the sinoatrial node or the AV node, which may sustain structural damage and depress nodal automaticity, and/or – (2) an abnormal ectopic focus in the ventricle that takes over as the dominant pacemaker

Management of AIVR The presence of accelerated idioventricular rhythm does not affect the patient's prognosis This rhythm occurs somewhat more frequently in patients who develop early reperfusion than in others; however, it is neither sensitive nor specific as a marker of reperfusion.

Management of AIVR Temporary pacing is not indicated unless the rhythm is sustained and results in hypotension or ischemic symptoms. An accelerated idioventricular rhythm represents an appropriate escape rhythm. Suppression of this escape rhythm with an antiarrhythmic drug can result in clinically significant bradycardia or asystole. Therefore, an accelerated idioventricular rhythm should be left untreated.

Nonsustained VT is defined as 3 or more consecutive ventricular ectopic beats at a rate of greater than 100 bpm and lasting less than 30 seconds. In patients who experience multiple runs of nonsustained ventricular tachycardia, the risk for sudden hemodynamic collapse may be substantial.

Non sustained VT NSVT in the immediate peri-infarction period does not appear to be associated with an increased mortality risk, No evidence suggests that antiarrhythmic treatment offers a morbidity or mortality benefit. However, NSVT occurring more than 48 hours after MI in patients with LV systolic dysfx (LV EF< 0.40) poses an increased risk for sudden cardiac death; If VT is inducible during EPS ICD is indicated (class I, Level of evidence B).

NSVT Multiple episodes of NSVT require intensified monitoring and attention to electrolyte imbalances. Serum potassium levels should be maintained above 4.5 mEq/L, and serum magnesium levels should be kept above 2.0 mEq/L. Ongoing ischemia should aggressively be sought and corrected if found

Sustained VT Defined as 3 or more consecutive ventricular ectopic beats at a rate greater than 100 bpm and lasting longer than 30 seconds or causing hemodynamic compromise that requires intervention. Monomorphic VT is most likely to be caused by a myocardial scar, Polymorphic ventricular tachycardia may be most responsive to measures directed against ischemia. Sustained polymorphic ventricular tachycardia after an AMI is associated with a hospital mortality rate of 20%

Sustained VT Emergency treatment is mandatory because of its hemodynamic effects and because it frequently deteriorates into V fib. Rapid polymorphic VT (rate >150 bpm) associated with hemodynamic instability should be treated with immediate direct-current unsynchronized cardioversion of 200 J (or biphasic energy equivalent). Monomorphic VT should be treated with a synchronized discharge of 100 J (or biphasic energy equivalent).

Sustained VT If VT is well tolerated – Amiodarone (drug of choice) – or procainamide may be attempted before DC cardioversion. Precipitating causes, such as electrolyte abnormalities, acid-base disturbances, hypoxia, or medication, should be sought and corrected. For persistent or recurrent VT, overdrive pacing may be effective in electrically converting the patient's rhythm to a sinus rhythm.

Ventricular fibrillation The incidence of primary ventricular fibrillation is greatest in the first hour after the onset of infarct (4.5%) and declines rapidly thereafter. Approximately 60% of episodes occur within 4 hours, and 80% occur within 12 hours.

Late VF Secondary( late VF) occurring more than 48 hours after an MI is usually associated with pump failure and cardiogenic shock. Risk factors : – Large MI – IVCD – Anteroseptal AMI. Secondary VF in conjunction with cardiogenic shock is associated with an in-hospital mortality rate of 40-60%.

VF treatment Treatment for VF is unsynchronized electrical countershock with at least J (or biphasic energy equivalent) administered as rapidly as possible. Each minute after the onset of uncorrected VF is associated a 10% decrease in the likelihood of survival Electromechanical dissociation, or pulseless electrical activity is generally due to extensive myocardial ischemia and/or necrosis or cardiac rupture.

VF treatment IV amiodarone and lidocaine, facilitate successful electrical defibrillation and help prevent recurrent or refractory episodes. After VF is successfully converted, antiarrhythmic therapy is generally continued as a constant IV infusion for hours. Prophylactic lidocaine is not used because it seems to be associated with an excessive mortality risk owing to bradycardic and asystolic events [4]. Early use of beta-blockers reduces the VF/death