Management of Post MI Complications Dr. A.M. Thirugnanam MD.,FRSH.,MSICP.. Interventional Cardiologist Sreem Remedy Hospitals, Hyderabad.

What is Myocardial Infarction? “ Sudden rupture of thin fibrous cap of Plaque which leads to immediate occlusion of a coronary artery “ “ Sudden rupture of thin fibrous cap of Plaque which leads to immediate occlusion of a coronary artery “

Complications in Acute Myocardial Infarction  Mechanical complications  Electrical Instability  Pump Failure  Other complications

Mechanical complications of STEMI  Ventricular Septal Rupture  Papillary Muscle Rupture  Free Wall Rupture  Aneurysm

Ventricular Septal Rupture  Clinical Feature: Occurrence 1-3% Equally occurs among Inferior and Anterior wall Myocardial Infarction. Typically occurs in first episode of MI with little or no collaterals formation. Peak occurrence 3-5 days, sometimes less than 24 hours.

Signs and Symptoms of VSR Hypotension, Cardiogenic shock, Dyspnea, Pan systolic murmur with clear lungs.

Diagnosis of VSR  Pan systolic murmur in the 4 th intercostal space.  2D echocardiogram ( left to right shunt )  Large ‘v’ on PCWP  Left Venrticulography  Right heart Catheterization.

Prognosis and Management of VSR Prognosis depends on RV function, location of MI, hemodynamic status, and associated MR. Infero-posterior MI is more worse than anterior wall MI. Management: IABP, Presser drugs and surgical.

Papillary Muscle Rupture  Occurs in 1% of acute myocardial infarction  20% of PMR occurs with in 24 hours of acute MI.  50% of the PMR occurs in smaller infarcts.  Average period 3-7 days after post MI.  Most common with infero-posterior MI than anterior MI.

Signs and Symptoms of PMR  Cardiogenic shock  Pulmonary Edema  Apical Holosystolic murmur and absence of S1  Thrill may be absent

Diagnosis of PMR  2D Echocardiogram : Flail mitral leaflet with severe MR  LV angiogram

Treatment for PMR  Poor prognosis with medical management.  Stabilisement of Hemodynamics with Presser drugs, Inotropes and after load reductions  Intubations  Intra aortic counter pulsation  Corrective surgery

Free Wall Rupture  Occurrence-1-2% of Acute MI  30% of FWR occurs in 24 hours  Mostly occurs by 7 days

Risk Factors causing FWR  Advanced age  Female sex  Hypertension  First episode of MI  Late thrombolysis  Use of corticosteroids

Consequences of FWR  Pulse less electrical activity  Cardiac Tamponade  No premonitory symptoms  Occurrence manifest by chest pain and vagal episode  Usually fatal

Aneurysm  Mechanism: –Interventricular tension stretches the non- contracting infarcted cardiac muscle, thus producing infarct expansion. Thin layer of necrotic muscle and fibrous tissue that bulges with each cardiac contraction. –Aneurysm is rarely seen with multi vessel disease.

True aneurysm and Pseudo aneurysm  Pseudo aneurysm contains wall of pericardium with thrombus.  Represent free wall rupture.  Narrow neck  May be associated with CHF and arrhythmias  May be silent and found incidentally on LV angiogram and 2D echo

True aneurysm  True aneurysm contains broad neck with myocardial wall.  Very rarely ruptures  Not Fatal  Symptomatic true aneurysm needs surgical correction.

Electrical instability / Arrhythmias Fatal arrhythmias : Ventricular Fibrillation, Fatal arrhythmias : Ventricular Fibrillation, Sustained ventricular tachycardia, R on T on phenomenon and wide QRS tachycardia Sustained ventricular tachycardia, R on T on phenomenon and wide QRS tachycardia Non fatal arrhythmias: Non fatal arrhythmias: AF, atrial flutter, junctional tachycardia, atrioventricular junctional tachycardia, VPC, sinus tachycardia, sinus bradycardia and accelerated idiovenrticular rhythm.

What type of arrhythmias should be treated in the setting of acute MI?  Reperfusion arrhythmias: Sinus bradycardia occurs with inferior wall MI, premature ventricular contraction, accelerated idioventricular rhythm and early after depolarization. Washout of various ions like lactate,pottasium and toxic metabolic substances from ischemic myocardium

Treatment for Arrhythmias  Ventricular Tachycardia  AADs- Amiodarone: 150mg iv bolus for 10min, 450mg /6 900mg for 18hr. Lidocaine: 100mg bolus, followed by 2-4mg /min for hours. Lidocaine: 100mg bolus, followed by 2-4mg /min for hours. Cardioversion J Cardioversion J

Ventricular Fibrillation  Electrical cardio version J  Lidocaine: 1-2mg/kg rate of 20-50mg/min, second dose ½ of the first dose, infusion0.5mg/kg  Amiodarone: 15mg/min for 10min, 1mg/min for 6hr, 0.5mg/min for 18hr.  NaHCO3, adrenalin, atropine

Venrticular Premature complex  Treatment : Correction of electrolytes, sympathetic tone- potassium, magnesium, beta blockers. Prophylaxis amiodarone against VT.

Treatment for Accelerated Idioventricular Rhythm  Observation unless hemodynamic function is compromised.  For hemodynamically unstable patients: atropine, AADS and atrial pacing.

Atrioventricular and Bundle Branch Block  1 st degree AV block: Prolongation of PR interval.  Clinically not significant unless associated with fascicular block.

2nd Degree AVB  Mobitz type I; Progressive prolongation of PR interval.  Clinically not significant, when symptomatic temporary pacing

Type-II AVB  Fixed PR interval with non conducted P wave.  This will lead to complete heart block.  Temporary pace maker, atropine

Complete Heart Block-3 rd degree AVB  There is no relation between P wave and QRS complex.  Atrio ventricular dissociation.  Bifascicular block with 2 nd degree AVB can leads to CHB.  Tri fascicular block with wide QRS complex always leads to CHB

Fascicular Block Bifascicular block= RBBB+LAFB(RBBB+LAD) RBBB+LPFB(RBBB+RAD RBBB+LPFB(RBBB+RAD Trifascicular Block= 1 st degree AVB+Bifascicular block

Use of Pacemaker in Acute MI  Persistent 2 nd degree AVB in the His- purkinje with bilateral bundle branch block.  3 rd degree AVB within or below the His-purkinje system after MI.  Transient advanced infra nodal AVB and associated bundle branch block.  Persistent and symptomatic second or third degree AVB.

Cardiogenic Shock  Low cardiac output state is characterized by- Elevated LV filling pressures, low cardiac output, systemic hypotension and evidence of vital organ hypo perfusion. Cardiogenic shock is the main cause of death in about 60% of death after MI.

Hemodynamic Abnormalities  Normal perfusion with out pulmonary congestion = normal CO and normal PCWP  Normal perfusion with pulmonary congestion = normal CO and elevated PCWP  Decreased perfusion with out pulmonary congestion= decreased CO and normal PCWP  Decreased perfusion with pulmonary congestion = decreased CO and increased PCWP

Cardiogenic shock Incidence in AMI  LV failure-74.5%  Acute MR-8.3%  VSR-4.6%  RV shock-3.4%  Tamponade-1.2%  Others-7.5%

Diagnosis of Cardiogenic shock  Persistent hypotension for more than 30min.  Systolic BP less than 80mmHg.  Marked cardiac output reductions. <1.8l/min.m2  Increased Pulmonary capillary wedge pressure.

Management of cardiogenic shock  Immediate 2D echocardiogram to rule out mechanical defects.  Swan catheter to determine filling pressure, cardiac output and systemic vascular resistance.

Indication for IABP in AMI  Hemodynamically unstable  Cardiogenic shock with unresponsive to medical treatment  Persistent ischemic pain unresponsive to treatment

Management of cardiogenic shock in MI  If systolic BP is >100 and patient is asymptomatic give NTG mcg/min  If systolic BP is and patient has no signs and symptoms give dobutamine 2-20mcg/min.  If systolic BP is and patient is symptomatic give Dopamine 5-15 mcg/min.  If Systolic BP is <70 and patient symptomatic give adrenalin 30mcg/min.

Other complications in AMI  Pericarditis: Pericarditis chest pain occurs day one and lasts as late as 6 wks. This may be confused with post MI angina. Discomfort usually more during deep inspiration but can be relieved when the patient sits up or leaning forward.

Treatment for Pericarditis  650 mg of Aspirin 4 times a day for 4 weeks.  Steroids should be avoided in AMI condition because they may interfere with myocardial formation.

Other complications in AMI  Dressler’s syndrome: Usually occurs in 1-8wks after infarction. 3-4% of the acute MI complications Present with malaise, fever, pericardial discomfort, leucocytosis, increased ESR, and pericardial effusion. RX- ASA 650 mg 4 times a day for 1 month.

Other complications of AMI  Venous thrombosis and Pulmonary embolism Bed rest and congestive heart failure predispose to venous thrombosis and subsequent pulmonary embolism in 20% of acute MI patients.