COMPLICATIONS OF ACUTE CORONARY SYNDROME.pptx

Complications of Myocardial infarction

1. COMPLICATIONS OF ACUTE CORONARY SYNDROME

2. HAEMODYNAMIC Acute LVF Cardiogenic SHOCK RV Failure Free wall Rupture Ventricular septal rupture Acute MR PERICARDIAL PERICARDITIS PERICARDIAL EFFUSION ARRYTHMIC VENTRICULAR ARRYTHMIA SUPRAVENTRICULAR ARRYTHMIA BRADYARRYTHMIAS OTHERS THROMBOEMBOLISM TRUE ANEURYSM RECURRENT ISCHEMIA

3. HAEMODYNAMIC COMPLICATIONS 25% ACUTE PULMONARYEDEMA 40% CARDIOGENIC SHOCK 20% LVS3 8% LVS4

4. Causes of acute LV failure: Pump failure - LMCA/LAD/MVD Acute diastolic dysfunction Mechanical complications- Acute MR, VSR Excessive IVF Cardiac arrythmias (AF with Rapid ventricular rate).

5. MANAGEMENT Maintain Oxygen saturation O2 or NIV. Reopen the infarct Related Artery / IRA: Fibrinolysis or Primary angioplasty or bypass surgery (rarely). NTG most important drug. Diuretics. lonotropes (if BP is low). Ionodilators .

6. CARDIOGENIC SHOCK BP < 90 mm Hg or MAP reduction of 30 mm Hg. CI<1.8 L/min/ma without support or <2.2 l/min/ma with support. Elevated EDP >18 mm Hg: LV & >10-15 mm Hg: RV End organ hypoperfusion . The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Cardiogenic shock has 80% mortality with medical Rx & a 50% mortality with intervention. Do not diagnose it lightly.

7. Open up the artery by: PCA/ lysis /CABG (NCL PCA not to be done) medical management Afterload reduction. lonotropes . Mechanical circulatory support mechanical circulatory support devices : ECMO / extracorporeal membrane oxygenation. Impela LVAD/ LV assist device.

8. Right Ventricular Myocardial Infarction Infarction is a misnomer RV is seldom infracted / necrosed . Reason Thin walled-4 mm (Complication of perforation uhle placing temporary pace maker is command. Hence gets nourishment rom blood within Rv cavity RCA Is supplied both in systole and diastole. Rv ejects against a lower after load : Less workload Prognosis : High risk IWMI Low risk IWMI+ PWMI = Intermediate risk. INF+LATERAL/RIGHT= High risk.

9. FREE WALL RUPTURE Primary PCI > Thrombolysis A Noradrenaline B. Noradrenaline Dopamine C IV Fluids D Immediate lysis. Not immediate lysis, as patient is in hypotension. Normotension { normal circulation is essential for thrombolytic agents to act. what drug to avoid : Nitrates. Given I litre of V Normal saline -> Bp-1 00 / 70 mm Hg Hypotension in RVMI : Rv becomes dysfunctional, blood is not pumped into pulmonary circuit and does not reach the LV. LW stroke volume falls, resulting in hypotension In RVMI , Right Atrium plays a central role in maintaining cardiac output. RA gets stretched -increases contraction by IV Fluids

10. Fbrinolytic therapy increases risk. Elderly hypertensive females. MC site-anterior wall - transmural infarct, junction of infarcted and non infarcted myocardium MC artery involved- occlusion of poorly collateralised LAD/First MI/ SVD Risk - Non reperfused >Fibrinolysis therapy> primary PCI Preceded by infarct expansion. Clinical Features Sudden death Hypotension/shock. Nausea/ Vomiting • Pericardial pain . EMD/PDA-monitor.

11. Types: Bimodal presentation either within 24 hrs or 3-5 Days Acute -Blow out type-Results in immediate death. Subacute -oozing type . Thrombus partially occludes the rupture, with slow oozing of blood, chance of survival if immediately repaired. Chronic - LW pseudoaneurysm 1 rupture occurs in-between the area of 2 congenital pericardial adhesions.

12. True Ventricular aneurysm: Bounded by all layers.. Seen in AWMI, when the area becomes infracted it becomes dyskinetic Psuedoaneurysm:Only pericardium forms a barricade, if ruptured results in death Complications - Rupture-3-5 days Thromboembolism Large psuedoaneurysm - 50% risk of rupture-must do Sx

13. Chronic complication LAD tX MC-4x times IW Dyskinetic segment+thinned out myocardium Contains all 3 layers. Chronic total occlusion of a poory collateralised LAD. Rarely occurs in multi-vessel disease

14. Course L V aneurysm increases mortality in comparison with patients with similar eF May remain stable or years Heart failure Arrhythmia -SCD Thromboembolism

15. Psuedoaneurysm Only pericardium Narrow neck Psuedoaneurysm Risk ot rupture high Surgery -TOC True Aneurysm All 3 layers wide neck Rupture risk low Usually conservative

16. VENTRICULAR FREE WALL RUPTURE Incidence :1-3 % • Bimodal peak (<24hrs or > 3 to 5 days) Elderly female with CKD-MC. Less common in Dm /SHT /Smokers / prev angina/ MI Occurs at junction between infarcted and non infarcted tissue Biventricular Failure AKI MODS Death- 40-75% mortality

17. ACUTE MR Incidence Bimodal course. MR post MI causes. • Partial rupture Posteromedial papillary muscle 6-12 times more common IWMI - MC Posteromedial papillary muscle has single blood supply by PDA Left dominant- LPDA branch of LCx right dominant-RPDA- branch of RCA Anterolateral muscle has dual blood supply

18. Acute MR and acute HF Sudden transmission of LV pressure into LA due to free mR . LA pressure increases. Pulmonary capillary wedge pressure increases Results in acute pulmonary oedema. Treatment • Aterload reduction : NTG, nitroprusside , dobutamine / IABP • Surgery-mv repair/replacement

19. Arrhythmic COMPLICATIONS Usually occurs in first 6 hours , early in course of MI IWMI+RVMI >IWMI>AWMI

20. Present in as many patients who do not develop VF as those who do. No role for prophylactic PVC Suppression with antiarrhythmics . Determine/treat recurrent ischemia and electrolyte/ metabolic disturbance. When augmented Sympatho -adrenal stimulation accompanies PvCs > beta-adrenergic blockade. VPCS post mi increases mortality , Suppression of VPCs by antiarrhythmics also increases mortality, established by CAmiAT trial, emiAT trial, CASS trial

21. Accelerated Idio ventricular rhythm Poor marker for RA patency 20 % of MIs -independent of size /type of MI Equal frequency in AW or IWMI Does not affect prognosis Mechanism: Enhanced automaticity, Increased Vagal dominance (especially in reperfusion, which suppresses atrial pacemakers, and ventricles takes Over, Treated by vagolytics like atropine

22. Ventricular Fibrillation • Primary VF- Occurs within 24 hrs due to electrical instability Inhomogenous repolarisation. Does not affect mortality. Treated by Betablockers Secondary VF occurs after 48 hrs Bad prognosis - large Infarct, LVF, RBBB, AF Treatment Reperfusion Beta blocker Correct electrolyte abnormalities, hypoxia, Amiodarone. DC shock

23. COMPLETE HEART BLOCK IWMI Predictable occurrence Suprahissian stable Rhythm Recovery is the rule AWMI Highly unpredictable Comes suddenly Infrahissian unstable rhythms Frequently require PPI

24. PERICARDIAL COMPLICATIONS PERICARDITIS Occurs within 24 hours, can occur up to 8 weeks Dressler's Syndrome, is an autoimmune disease, treated with Aspirin 250mg four times per week Glucocorticoids & NSAIDs are avoided as it can delay post MI healing PERICARDIAL EFFUSION # Heparin is being given, can continue but keep a watch for Increase in pericardial effusion & tamponade .