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Electrical complications of mi

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Electrical complications of MI PPT,Dr Virbhan Balai

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Electrical complications of mi

  1. 1. Electrical Complications of MI Dr. Virbhan Balai Department of cardiology National heart institute, Delhi
  2. 2. Cardiac Arrhythmias and Their Management During Acute Myocardial Infarction
  3. 3. ARRHYTHMIAS • Tachyarrhythmia • Bradyarrythmia • Hemodynamic consequences.
  4. 4. Hemodynamic Consequences • All forms of tachycardia and bradycardia can depress CO. • Myocardial oxygen consumption • Optimal rate - 60 to 80 beats/min.
  5. 5. • Loss of the atrial contribution to ventricular preload. • Loss of atrial transport ↓ LV output by 15%- 20%. • In patients with STEMI, atrial systole boosts – End-diastolic volume by 15% – End-diastolic pressure by 30% – Stroke volume by 35%.
  6. 6. Ventricular Arrhythmias
  7. 7. Ventricular Premature Depolarizations • “warning arrhythmias.” Presage VF. 1. Frequent VPCs = >5/min 2. VPCs with a multiform configuration 3. Early coupling (the “R-on-T” phenomenon) 4. Couplets or salvos
  8. 8. • Primary VF – Occurs without antecedent warning arrhythmias – May even develop despite suppression of warning arrhythmias. • Primary VF and VPCs (esp. R-on-T beats) – Occur during the early phase of STEMI
  9. 9. Management • The incidence of VF in pt`s with STEMI declined. • Prophylactic suppression of VPCs with antiarrhythmic drugs is not indicated . • Suppression may ↑the risk for fatal bradycardic and asystolic events. • Do not routinely prescribe antiarrhythmic drugs, other than beta blockers. • Determine recurrent ischemia or electrolyte or metabolic disturbances .
  10. 10. • When VPCs are accompanied by sinus tachycardia → sympatho adrenal stimulation. • Use beta-adrenergic blockade. • Early administration of an IV beta blocker reduces the incidence of VF in cases of evolving MI.
  11. 11. Accelerated Idioventricular Rhythm • Occurs during the first 2 days • Equal frequency in anterior and inferior infarctions. • Most episodes are of short duration. • Often observed shortly after successful reperfusion established with fibrinolytic therapy.
  12. 12. • Frequent AIVR in pt`s without fibrinolysis & following pri PCI have diff implications . • AIVR does not affect prognosis. • Routine Tt is not required.
  13. 13. Ventricular Tachycardia and Ventricular Fibrillation • Mechanism - re entry • Caused by inhomogeneity of the electrical characteristics of ischemic myocardium. • Cellular mechanisms for reperfusion arrhythmias – – Washout of various various ions such as lactate, k+ and toxic metabolic substances that have accumulated in the ischemic zone.
  14. 14. • Late VT / VF more common in pt`s with transmural infarction and LV dysfunction • More frequently associated with hemodynamic deterioration.
  15. 15. Prophylaxis • Hypokalemia increases the risk for VT • Low K+ levels should be treated promptly. • Pt`s with STEMI have reduced intracellular magnesium levels – not adequately reflected by serum measurements.
  16. 16. • Magnesium should be repleted, achieve a serum level of 2 mEq/liter. • Early beta blocker use reduces VF and can be instituted in pt`s without CI. • Lidocaine prophylaxis to prevent primary VF is no longer advised.
  17. 17. Management • Unstable VT or VF -Electrical cardioversion • I/V Amiodarone- prevention of refractory recurrent episodes • Sod bicarbonate- X, bcz of high osmotic load • Hyperventilation is a more suitable means of clearing the acidosis.
  18. 18. • Correct underlying abnormalities – 1. Hypoxia 2. Hypotension 3. Acid-base disturbances 4. Electrolyte disturbances 5. Digitalis excess.
  19. 19. • Revascularization- Urgent, if caused by ischemia. • Antiarrhythmic drug- extended therapy – Amiodarone – Lidocaine • Defibrillator
  20. 20. • Failure of electrical cardioversion 1. Rapidly recurrent VT or VF 2. Electromechanical dissociation 3. Electrical asystole.
  21. 21. Prognosis • GUSTO-I study, among pt`s who under went fibrinolysis ~10% experienced VT/VF. • APEX-AMI study,-pt`s treated with pri PCI, sustained VT/VF developed in 5.7%. • Worse clinical outcomes in pts with VT/VF than in those without VT/VF.
  22. 22. • Early versus late VT/VF, at 90 days doubles. • VT/VF after(> 48 hrs) without reversible cause, ICD for sec preventions before discharge. • VT/VF before reperfusion therapy-only beta blockers.
  23. 23. Bradyarrhythmias
  24. 24. Sinus Bradycardia • Inf. & post. infarctions • ↑ vagal tone produces sinus bradycardia • May be beneficial • Reduces myocardial O2 demand. • Mortality rate similar
  25. 25. Management • No hypotension or VPCs- observed • IV atropine –In the first 4 to 6 hrs after infarction • If the sinus rate <40/min and associated with hypotension • Doses 0.3 -0.6 mg every 3 to 10 min. • Total dose should not exceed 3 mg.
  26. 26. Atrioventricular and Intraventricular Block • Can produce conduction block at any level • AV or intraventricular conduction system. • Blocks- – AV node – Bundle of His • Produce various grades of AV block • RBBB • LBBB – – LAHB – LPHB
  27. 27. First-Degree Atrioventricular Block • Does not generally require specific Tt. • Beta blockers & CCB- D/c could ↑ischemia • Do not ↓the dosage unless the PR> 0.24 sec • Stopped if a higher-degree block or hemodynamic impairment.
  28. 28. • Atropine- If excessive vagotonia associated with sinus bradycardia and hypotension • Continued ECG monitoring
  29. 29. Second-Degree A-V Block • First-degree and type I second-degree AV blocks do not affect survival • Commonly associated with occlusion of theRCA • Caused by ischemia of the AV node
  30. 30. • Specific therapy is required in pt`s with second-degree type I AV block when- 1. Vent rate >50 beats/min and PVCs 2. Heart failure 3. Bundle branch block are present. • Atropine (0.3 to 0.6 mg) • Temporary pacing systems-not required.
  31. 31. • Type II second-degree AV block • Inferior/posterior STEMI • Usually temporary • Narrow-complex/ junctional escape rhythm. • Managed conservatively.
  32. 32. • Anterior/lateral STEMI- : • Type II second-degree AV block usually originates from below the bundle of His. • May progress to CHB, • Temporary external or trans venous demand pacemaker.
  33. 33. Complete (Third-Degree) Atrioventricular Block • Inferior or anterior infarction • More common in inferior than in anterior MI. • Often progressing from a first-degree or type I second-degree block – – In pt`s with inf infarction
  34. 34. • The escape rhythm is typically stable without asystole and often junctional. • This form of complete AV block is often transient. • May respond to pharmacologic antagonism of adenosine with methylxanthines • Resolves in most patients within a few days
  35. 35. • Pt`s with inferior infarction often have concomitant ischemia or infarction of the AV node secondary to hypoperfusion of the AV node artery, but the His-Purkinje system usually escapes injury in such individuals. • Pt`s with inf STEMI and AV block have larger infarcts and more depressed RV and LV function than do pts with an inf infarct and no AV block. • junctional escape rhythms with narrow QRS complexes occur commonly in this setting.
  36. 36. • Pacing is generally NOT necessary in pt`s with inferior wall infarction • Complete AV block is often transient in nature • Pacing is indicated 1. if symptoms related to a ventricular rate emerge 2. if ventricular arrhythmias 3. hypotension is present 4. if pump failure develops • Atropine only rarely useful
  37. 37. • Only when CHB develops in <6 hrs after the onset of symptoms is atropine likely to abolish the AV block or cause acceleration of the escape rhythm. • In such cases the AV block is more likely to be transient and to be related to increases in vagal tone. • More persistent block seen later in the course of STEMI, which generally requires cardiac pacing.
  38. 38. • In pt`s with ant infarction, third-degree AV block can occur suddenly 12 to 24 hours after the onset of infarction. • It is usually preceded by an intraventricular block and often a type II (not first-degree or type I) AV block. • Such pt`s typically have unstable escape rhythms with wide QRS complexes and rates <40 beats/min • ventricular asystole may occur quite suddenly.
  39. 39. • In pt`s with ant infarction, AV block generally develops as a result of extensive septal necrosis involving the bundle branches. • The high rate of mortality in this group of pts is the consequence of extensive myocardial necrosis resulting in severe left ventricular failure and frequently shock .
  40. 40. • Whether temporary transvenous pacing per se improves survival in pt`s with anterior STEMI remains controversial. • Pacing protects against asystole and may protect against transient hypotension, with its attendant risks of extending the infarction and precipitating malignant ventricular tachyarrhythmias.
  41. 41. Intraventricular Block • The right bundle branch and the left posterior division have a dual blood supply from the LAD and RCA • Left anterior division is supplied by septal perforators originating from the LAD. • Not all conduction blocks in patients with STEMI are complications of infarcts.
  42. 42. • STEMI and bundle branch blocks have higher peak biomarker levels, lower EF, and ↑ed in- hospital and long-term mortality rates. • In the prefibrinolytic era, IVCD of the His- Purkinje system occurred in 5% -10% of pt`s with STEMI. • In the reperfusion era intraventricular blocks occur in ~2% - 5% of pt`s with MI.
  43. 43. Isolated Fascicular Blocks • An isolated left anterior divisional block is unlikely to progress to a complete AV block. • Mortality is increased in these pt`s • The post. fascicle is larger than the ant. fascicle, and in general, a larger infarct is reqd to block it. • Complete AV block is not a frequent complication of either form of isolated divisional block.
  44. 44. Right Bundle Branch Block • Can lead to AV block bcz it is often a new lesion associated with antero septal infarction. • Isolated RBBB is associated with an increased risk for mortality in patients with anterior STEMI – Even if complete AV block does not occur, – But if accompanied by CHF
  45. 45. Bifascicular Block, Including Left Bundle Branch Block • The combination of RBBB with either Lt. ant. or post. divisional block is known as bidivisional or bifascicular block. • If a new block occurs in two of the three divisions of the conduction system, the risk for development of a complete AV block is quite high. • Mortality is also high because of the occurrence of severe pump failure secondary to the extensive myocardial necrosis required to produce such an extensive intraventricular block.
  46. 46. • Preexisting BBB or divisional block is less often associated with the development of complete AV block in pt`s with STEMI. • Bidivisional block in the presence of prolongation of the PR interval may indicate disease of the third subdivision rather than disease of the AV node and is associated with a greater risk for complete heart block than if first-degree AV block is absent
  47. 47. • Complete BBB (either Lt or Rt), the combination of RBBB and left anterior fascicular block, and any of the various forms of trifascicular block are all more often associated with anterior than with inferoposterior infarction. • All these forms are more frequent with large infarcts. • Older patients and have a higher incidence of other accompanying arrhythmias.
  48. 48. Use of Pacemakers in Patients with Acute Myocardial Infarction • Temporary Pacing • Just as is the case for complete AV block, transvenous ventricular pacing has not resulted in a statistically demonstrable improvement in prognosis in patients with STEMI in whom intraventricular conduction defects develop. • Temporary pacing is advisable in some of these patients, however, because of the high risk for development of a complete AV block.
  49. 49. • Temporary pacing • Pt`s with new bifascicular bundle branch block (i.e., RBBB with Lt. ant. or post. divisional block and alternating Rt. and Lt. BBB)
  50. 50. • An isolated new block in only one of the three fascicles, even with PR prolongation and pre existing bifascicular block and a normal PR interval, poses somewhat less risk; • These pt`s should be monitored closely, with insertion of a temporary pacemaker deferred unless a higher-degree AV block occurs.
  51. 51. • Asystole • The presence of apparent ventricular asystole on monitor displays of continuously recorded ECGs may be misleading in that the rhythm may actually be fine VF. • The predominance of VF as the cause of cardiac arrest in this setting suggests electrical counter shock as initial therapy, even if definitive electrocardiographic documentation of this arrhythmia is not available.
  52. 52. • Permanent Pacing • The advisability of permanent pacemaker insertion is complicated because not all sudden deaths in pt`s with STEMI and conduction defects are caused by high-grade AV block. • A high incidence of late VF occurs in CCU survivors with anterior STEMI complicated by either right or left bundle branch block. • VF rather than asystole caused by failure of AV conduction and infranodal pacemakers could be responsible for late sudden death.
  53. 53. • Permanent Pacing 1. when CHB persists throughout the hospital phase in a pt with STEMI, 2. when sinus node function is markedly impaired, or 3. when type II second-degree or third-degree block occurs intermittently. 4. When high-grade AV block is associated with newly acquired BBB or other criteria for conduction system impairment, prophylactic long-term pacing may be justified as well. • Pt. who is candidate for an ICD or has severe heart failure might improve with biventricular pacing.
  54. 54. Supraventricular Tachyarrhythmias • Sinus Tachycardia • Augmented sympathetic activity • Common causes -anxiety, persistent pain, LV failure, fever, pericarditis, hypovolemia, pulmonary embolism • Administration of drugs such as atropine, epinephrine, or dopamine; rarely, it occurs in pt`s with atrial infarction.
  55. 55. • Common in pt`s with anterior infarction, LV dysfunction. • ↑ myocardial O2 consumption &↓time for coronary perfusion→ intensifying the myocardial ischemia & myocardial necrosis. • Persistent sinus tachycardia 1. Persistent heart failure 2. Poor prognosis and excess mortality.
  56. 56. • Tt cause • Analgesics for pain • Diuretics for heart failure • Oxygen, beta blockers, and nitroglycerin for ischemia • Aspirin for fever or pericarditis.
  57. 57. • Beta blockers - sinus tachycardia caused by pain, anxiety, or fever • Beta blockers - CI in pt`s who are tachycardic bcz of pump failure.
  58. 58. Atrial Flutter and Fibrillation • Usually transient in pt`s with STEMI • Augmented sympathetic stimulation of the atria • Reduced cardiac output- – ↑ed vent rate – Loss of the atrial contribution to LV filling
  59. 59. • AF during STEMI is associated with ↑ed mortality and stroke – esp. in pt`s with AWMI
  60. 60. Management • Cardioversion- 1. Hypotension 2. Ongoing ischemia 3. Heart failure • Beta blocker- In stabilized pt`s and in the absence of CI • Digitalis - when AF with ventricular dysfunction. • Amiodarone
  61. 61. • Oral anticoagulants -to reduce the risk for stroke • Even if sinus rhythm is present at the time of discharge.
  62. 62. Thankyou
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Electrical complications of MI PPT,Dr Virbhan Balai


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