Download Management of Post MI Complications

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 “
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 4th 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
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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
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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
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Aneurysm
 Mechanism:
– Interventricular tension stretches the noncontracting 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,
Sustained ventricular
tachycardia, R on T on phenomenon
and wide QRS tachycardia
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 12-24 hours.
Cardioversion-200-300J
Ventricular Fibrillation
 Electrical cardio version- 260-300J
 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
 1st 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-3rd degree AVB
 There is no relation between
P wave and QRS complex.
 Atrio ventricular
dissociation.
 Bifascicular block with 2nd
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
Trifascicular Block= 1st degree AVB+Bifascicular
block
Use of Pacemaker in Acute MI
 Persistent 2nd degree AVB in the His- purkinje
with bilateral bundle branch block.
 3rd 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 byElevated 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
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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 10-20 mcg/min
 If systolic BP is 70-100 and patient has no signs
and symptoms give dobutamine 2-20mcg/min.
 If systolic BP is 70-100 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.