CCU Management of Arrhythmias in Acute Myocardial Infarction

1. ARRHYTHMIAS IN ACUTE MYOCARDIAL INFARCTION CCU MANAGEMENT K.U.Natarajan, AIMS Kochi

2. # Most of the time # Treating a cardiac arrhythmia # Is based on SIMPLE & LOGICAL THINKING An example ………

3. 32 year old female RHD , severe MR, AF Underwent MVR

4. 8th post OP day On Dopamine 7.5mcg/Kg/min Dobutamine 7.5mcg/Kg/min Adrenaline infusion BP 85/45 Not able to wean off supports – persistent hypotension

8. ACS - > ½ Million deaths /year in the US • Incidence similar if not worse in other developed countries • Incidence is increasing at an alarming rate in the developing countries like India • A majority of the deaths is due to cardiac arrhythmia

9. The CCU • An innovation to improve survival following AMI • Advances in detection & treatment of arrhythmias introduced in 1950s • Set the stage for invention of the CCU concept in early 1960s

10. The CCU • New technologies gave us the power to treat life threatening arrhythmias • “Monitor”,“Defibrillator” & “Pacemaker”

11. A tribute to the masters… • Middle of the 20th century • Several teams of researchers • Electrical Engineers Made discoveries & Cardiologists inventions that lead to Physiologists the introduction of Surgeons defibrillator & pacemaker

12. A tribute to the masters… • 1947 – Claude Beck – Heart surgeon – 1st human resuscitation using defibrillator • Delivered the shock directly to the heart after opening the chest • 1956 – Paul Zoll – cardiologist from Boston • Successful delivery of shock through the chest wall

13. A tribute to the masters… • Early 1930s – Albert Hyman – Cardiologist from New York – invented artificial cardiac pacemaker • Impractical – power supply lasted a few minutes !!! • Late 1950s – William Lillehei – Minneapolis – developed reliable clinically useful pacemaker

14. A tribute to the masters… • The cathode ray oscilloscope made possible continuous ECG monitoring • 1961 – Desmond Julian of Edinburg & Hughes Day of Kansas city • Developed a “team approach” for prompt treatment of cardiac arrest following MI • Creation of the “ CCU Concept”

15. POST MI ARRHYTHMIAS TACHY ARRHYTHMIA BRADY ARRHYTHMIA SUPRAVENTRICULAR VENTRICULAR SINUS BRADY AV BLOCK

16. Supra ventricular arrhythmia • Sinus tachycardia • Atrial ectopics • Atrial Flutter • Atrial Fibrillation • Atrial Tachycardia

17. Ventricular arrhythmias • Ventricular ectopics • AIVR • Ventricular tachycardia • NSVT / Monomorphic / polymorphic • Ventricular Fibrillation

19. Sinus Tachycardia • 1/3rd of patients, commoner in AWMI, augmented sympathetic activity. • Anxiety, pain, ischemia, LVF, fever, pericarditis, hypovolemia, pulmonary embolism • Drugs - Atropine, Isoprenaline, Dopamine, NTG. • Treat cause / BB

20. Atrial Premature Beats No treatment required

21. Atrial Fibrillation • Often occurs in first 24hrs • Usually transient, may recur • Incidence increases with age • Large AWMI, CHF, high grade AV block, atrial infarction, percarditis • In IWMI due to proximal RCA occlusion (involvement of SA nodal artery). • Systemic embolism is a risk

22. Atrial flutter • Least Common arrhythmia 1to 3% • Usually 2:1 AV block, Ventricular rate 150bpm. • Responds to low energy DC shock 25J, over drive atrial pacing

24. Atrial Fibrillation - management • Heparin must be given though AF after AMI is usually transient • No guidelines for class I /class III • Not clear if antiarrhythmic prophylaxis needed after transient AF. • Transient AF no need for long term anticoagulation. If started appropriate to limit to 6weeks if SR restored.

25. Sustained Atrial Fibrillation/ Atrial Flutter • With hemodynamic compromise + ongoing ischemia • Synchronised DC shock – 200J for Fibrillation • 50J for Flutter • Non responder to cardioversion or recurrence • IV Amiodarone • IV Digoxin (LV dysfunction/heart failure) • Brief GA/conscious sedation mandatory

26. Sustained Atrial Fibrillation/ Atrial Flutter No ongoing ischemia & hemodynamically stable Rate control Betablocker Diltiazem/ verapamil

27. Premature ventricular complexes • Most frequent arrhythmia • Incidence 5% to 100% • Highest incidence first 24 - 72hrs • Not an accurate predictor of VF • Frequent complex VPC associated with increased mortality if associated with LV dysfunction.

28. Ventricular Premature Complexes Isolated VPCs, couplets, NSVT + no hemodynamic compromise No need for treatment No role for prophylactic antiarrhythmic therapy (lidocaine)

29. Accelerated idioventricular rhythm • Rate less than 100 • Associated with reperfusion • Can cause loss of AV synchrony • Usually brief, spontaneous termination, hemodynamically non compromising • Treatment generally not required

30. Nonsustained Ventricular tachycardia • Recurrent ischemia /Coronary reperfusion • Not associated with increased risk of VT/VF • Prognosis - occurrence within 24 to 48 hrs not predictive of long term mortality. • In contrast occurrence after acute phase of MI 2 to 3 fold increase in overall mortality and sudden cardiac death. • Only agents that improve survival - beta blockers

31. Acute Polymorphic VT • Rapid rate > 200bpm • Associated with ischemia • Usually nonsustained • May degenerate in to VF • Usually subsides 24 - 48hrs after MI • Late occurrence - recurrent ischemia

32. Monomorphic VT • Occurs less commonly in the acute phase of MI • Patients with primary VT / VF occurring in first 48 hrs • At 21days 20% Vs 2% mortality • Among patients surviving 21days, 1year mortality not different • In contrast sustained VT occurring later than 48hrs • Increased risk of long term mortality • High incidence of arrhythmia recurrence - needs EP study / CAG/ Revascularisation

33. VT - Management • Depends on clinical presentation. • NSVT - brief, asymptomatic, infrequent - no intervention. • In conscious patients - sedation is a must before cardioversion • Only sustained /hemodynamically compromising VT needs treatment

34. Ventricular Tachycardia Sustained (>30s or hemodynamic collapse) polymorphic VT Unsynchronized DC shock 200J, 300J, 360J # # # # # Aggressive anti ischemic treatment – BB, IABP, PCI, CABG, Amiodarone Aggressive normalization of K > 4meq/L, Mg > 2mg/dl If HR < 60 or long QTc – Temporary pacing

35. Ventricular Tachycardia Sustained monomorphic VT + Angina, pulmonary edema, hypotension < 90mm Hg Synchronized DC shock 100J, 200J, 360J Brief anesthesia if hemodynamically stable

36. Ventricular Tachycardia Sustained monomorphic VT No Angina, pulmonary edema, hypotension < 90mm Hg IV Amiodarone 150mg over 10 min repeat 150mg every 10-15 min or 360mg over 6 hrs (1mg /min) 540mg over 18 hrs (0.5mg/min) Synchronised cardio version – 50J (Brief anesthesia must) Procainamide bolus + infusion may be reasonable

37. 50 year old male NIDDM, HTN, ex-smoker CAD , old MI Recurrent palpitations with light headedness. What is the arrhythmia? What does the ECG in sinus rhythm reveal?

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40. Ventricular Fibrillation • Early VF (< 48hrs) ; Late VF (> 48hrs) • Primary VF ( not resulting from shock, hypotension, heart failure) • Peak incidence first hours after MI • Primary VF 2 fold increase in hospital mortality • Patients surviving to hospital discharge have same long term prognosis as patients without primary VF

41. Ventricular Fibrillation VF / Pulse less VT should be treated by Unsynchronized DC shock 200J, 300J, 360J If refractory, reasonable to give Amiodarone 5mg/kg bolus & repeat DC shock may be reasonable to give IV Procainamide bolus (needs longer time to act) After restoration or sinus rhythm, Reasonable to correct electrolytes, acid base disturbance K > 4meq/l, Mg > 2 mg/dl

42. VF – Prophylaxis • Warning arrhythmias lack specificity / sensitivity • Prophylactic Lidocaine -Controversial • BB decreases incidence of early VF • Hypokalemia - arrhythmogenic - risk factor for VF • Tissue depletion of Mg (not low Serum levels), potential risk

43. Role of prophylactic Lidocaine • 21 trials - 12385 patients • Non significant trends towards • Reduced VF (odds ratio 0.71) • Increased mortality ( odds ratio 1.12) • Increased mortality possibly due to increase in brady arrhythmias and asystole. • Routine use of prophylactic Lidocaine in acute MI cannot be recommended.

44. Reperfusion Arrhythmias • Definition • Arrhythmias that develop within seconds after restoration of blood flow to ischemic or infarcted myocardium • Incidence of VT / VF low (6%, range 0 - 17%) • More likely when interval from onset of MI to reperfusion is short.

45. Brady-arrhythmias • AV Block in acute IWMI. • Almost always located in AV node • Pre thrombolytic era - high grade AV block 20% of IWMI, of this 60% CHB

46. AV block in IWMI • Early onset AV block - 67% • Develops in 6hrs, rapid onset, short duration (<12hrs) • Probably hypervagotonia • Responds to Atropine • Rarely requires TPI

47. AV Block in Acute AWMI • Extensive necrosis of septum, His bundle, Bundle branches. • Setting of severe LV dysfunction. • High mortality reflects myocardial damage • Slow unreliable ventricular rhythm at 30-40/min.

48. 55 year old malePresented to Casualty with persistent retrosternal chest discomfort of 4 hrs durationWHAT IS THE ECG FINDING?

50. 62 year old lady Diabetic, Hypertensive. Admitted to CCU with severe persistent chest discomfort of 2 hours duration. WHAT IS THE ECG FINDING?