GOOD

1. DR HIRALAL

2.  The term myocardial infarction should be used when
there is evidence of myocardial necrosis in a clinical
setting consistent with myocardial ischaemia. Under these
conditions any one of the following criteria meets the
diagnosis for myocardial infarction:
• Detection of rise and/or fall of cardiac biomarkers
(preferably troponin) with at least one value above the 99th
percentile of the upper reference limit (URL) together with
evidence of myocardial ischaemia with at least one of
the following:
• Symptoms of ischaemia.
• ECG changes indicative of new ischaemia (new ST-T
changes or new left bundle branch block [LBBB]).
• Development of pathological Q waves in the ECG.
• Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality. (Kristian Thygesen, et al
2007)

3. Complications
Electrical Complications
Mechanical complications
Heart Failure
Pericarditis
Post Infarction Angina or ReInfarction .
Take Home Message

4. Cardiogenic shock and heart failure are the most
common causes of death in patients hospitalized
with acute myocardial infarction.
At least 75% of patients with acute myocardial
infarction (MI) have an arrhythmia during the
periinfarct period.

5. Electrical Complications :
In acute M.I , Arrythmias are mainly due to reentry
caused by inhomogenicity of ischaemic myocardium .
While Reperfusion Arrythmias are due to washout of the
accumlated ions and metabolites .
Ventricular Arrythmias
1. Ventricular premature beats ( PVCs )
No correlation to the development of primary vent.
Fibrillation .
Treated by correction of the electrolyte or metabolic
disturbances . If associated with sinus tachycardia , Beta
Blockers are used to suppress the sympathetic overdrive.

6. 2. Accelerated idioventricular rhythm :
occurs in 20% of patients with STEMI , most often
after successful reperfusion .
3. Ventricular Tachycardia :
Non-Sustained V.Tach. isn’t associated with
increase mortality during hospitalization or one year
after .
Sustained V.tach with haemodynamic stability
should be treated immediately by amiodarone or
procainamide , while if it's not aborted or
associated with chest pain or haemodynamic
deterioration ,
DC shock should be used for cardioversion .

7. 4. Ventricular fibrillation :
 Primary V.F
 Secondary V.F
 Late V.F
- Treatment Consists of:
 Unsynchronized DC shock with at least 200 – 300 joules
monophsic
 Amiodarone I.V , helps interruption of the attack and
prevent recurrence .
 Treatment of hypokalaemia and magnesium deficits . ( aim K
≥ 4.5
 Prophylactic Lidocaine is no longer recommended .

8. Supraventricular Arrythmias
1. Sinus Tachycardia :
very common in patients with acute M.I esp. Ant. M.I , it
may be caused by other post-infarction causes as anxiety ,
persistant pain , LV dysfunction , fever , hypotension ,
hypovolaemia , pericarditis , pulmonary embolism , etc …..
2. Premature Atrial beats :
may be due to atrial ischaemia or pericarditis .
No specific therapy is indicated .
3. Paroxysmal SVT :
usually transient and needs rate control using carotid
massage , adenosine , verapamil , diltiazem or Beta
blockers .

9. 4. Atrial Flutter and Fibrillation :
both are usually transient and may occur with patients with
LV dysfunction , extension of ischaemia or pulmonary
embolism .
Bradyarrythmias
1. Sinus Bradycardia :
it’s common especially in Inferior and posterior Infarctions . If
heart rate is below 40-50 , Atropine is administered .
2. First Degree A-V block :
it may be caused by the use of Beta blockers or Calcium
channel blockers

10. 3. Second degree AV block :
Type I: Does not require treatment except if ventricular
rate is below 50 bpm , then atropine is indicated.
Type II: has a potential to progress to complete heart
block so temporary pacing is indicated and set at about
60 bpm.
4. Complete AV block :
 If associated with Inferior infarctions , it’s usually transient and
resolves within 72 hrs . Pacing is indicated if Ventricular rate is
less than 40- 50 bpm
 If associated with with anterior infarction , it usually occurs
suddenly , after 12-24 hrs , they have unstable escape rhythm
and a wide complexes at a rate ≤ 40 bpm . They are associated
with an extensive septal necrosis and may need permenant
pacing .

11. 5. Intraventricular block :
RBBB with ant. MI is associated with increased
mortality .

12. Indications of Temporary Pacing in Acute M.I :
1. Asystole
2. Symptomatic bradycardia not responsive to atropine
3. Complete Heart Block
4. Second degree H.B ( Mobitz type II )
5. New Bifasicular block
6. Bilateral Bundle branch block
7. Sinus pauses > 3 sec. , not resposive to atropine
8. Incessant Vent. Tachycardia ( overdrive pacing )

13. Mechanical complications
1. Acute Mitral Regurge :
Papillary muscle dysfunction:
Caused by posteromedial papillary ms dysfunction , It’s usually
transient during ischaemia .
It usually presents with an apical systolic murmur , confirmed by
echocardiography .
It requires no specific therapy , in intermediate cases it may require
antifailure treatment , while in severe cases it requires treatment like
that of papiilary ms rupture .
Papillary ms Rupture :
It occurs with Inferior Infarction 6-12 times more than Anterior
infarctions .
It may present with acute pulmonary oedema or even sudden cardiac
death , it can occur upto 2-7 days post infarction .
Intra-Aortic Balloon , vasodilators or inotropic therapy may be
required for temporary stabilization before surgery ( CABG + Mitral
Valve Repair or Replacement )

14. Papillary muscle rupture complicating acute inferior myocardial infarction;
magnified four-chamber view. The ruptured head of the posteromedial
papillary muscle (arrow) prolapses freely into the left atrium; the posterior mitral
valve leaflet (arrowhead) is flail.

15. 2. Ventricular Septal Rupture
 It occurs within the first week post-Infarction .
 It occurs equally with Inferior and Anterior infarctions.
 Rupture with Anterior Infarctions tend to be apical while
it’s basal and has a worse prognosis with inferior
infarctions .
 It usually presents with a new onset murmur ( new harsh
holosystolic murmur along the left sternal border ) . The
patient is usually stable and develops sudden clinical
deterioration .
 Patients with acute VSR usually lie flat , while patients
with acute MR develop pulmonary oedema & cann’t Lie
flat .
 Medical therapy is ineffective , Emergency Surgical
Intervention is the treatment of choice .

16. Transthoracic sub-costal 4-chamber echocardiographic findings
showing a large ventricular septal rupture (VSR)

17. 3. Free wall Rupture :
 Occurs within 2 weeks , and most common cause of death after
cardiogenic shock and arrythmias .
 Early use of thrombolytic therapy appears to reduce the
incidence of cardiac rupture , while late use appears to increase
the incidence .
 It usually presents by sudden Death.
 Few cases can be salvaged by immediate pericardiocentesis ,
emergency Thoracotomy and surgical repair .

18. Cardiac free wall rupture post
myocardial
infarction.
Pericardial tamponade from left
ventricular free
wall rupture and hemopericardium.

19. 4. Ventricular Aneurysm :
Diff. between True and Pseudo-aneurysm .
True Aneurysm Pseudo-Aneurysm

20. Clinically : abnormal precordial impulse in the 3rd
left intercostal space
ECG : ST Seg. Elevation persists more than 2 weeks . ( it may indicate
a large infarction with RWMA not necessarily Aneurysm ) .
Other Mechanical Complications
5.Pulmonary Embolism :
• Post-infarction patients have greater tendancies for Pulmonary
embolism ( P.E ) due to decreased cardiac output and
immoblization ,
• Early mobilization and treatment aiming to increase Cardiac
output are the most effective prophylactic methods .

21. 7. Systemic embolism :
 LV thrombi occurs in 20-40 % of ant. Infarction Patients .
 If LV thrombus is clearly demonstrated in Echocardiography ,
Systemic anticoagulation should be given for 3-6 months .

22. Heart Failure and Cardiogenic shock:
Heart Failure occurs when LV function decrease by 30% of
normal function .
Killip Class: Clinical Examination
I No S3 or rales
II Rales in less than half of lung field
III Rales in more than half of lung field
IV Cardiogenic shock
May present acutely after MI ( killip class II or III ) or as a
delayed presentation ( NYHA II-IV) .

23. Cardiogenic shock is persistent hypotension with a
systolic pressure <80 mm Hg for more than 30
minutes in the absence of hypovolemia. It occurs
when ≥ 40 % of myocardium is affected .
The most common causes of cardiogenic shock
include
1) large left ventricular infarct (usually >40% of
left ventricle) seen in about 80% of shock patients
2)right ventricular infarct in 10% of shock patients
3) mechanical complications of myocardial infarction
(ventricular septal defect, acute mitral regurgitation,
tamponade) in 10% of shock patients.

24. Pericarditis :
1. Early post-infarction Pericarditis
 Occurs 2-4 days following acute infarction .
 Patients who develop this condition usually have larger infarcts ,
lower EF and higher incidence of CHF .
 Presented by Fever , Chest pain and friction rub .
 Pain is aggrevated by movement and inspiration , Radiated to
the trapezius .
 Treated by Aspirin 160 – 325 mg daily ( although higher doses
may be required 650 mg / 4-6 hrs ) , Anticoagulants are
relatively contraindicated .

25. 2. Post MI syndrome ( Dressler’s Syndrome )
Fever , chest pain , friction Rub .
Occurs after 1 week up to several weeks of MI .
Treatment as that of early post-MI pericarditis except
that an oral corticosteroid course maybe required .
Anti-Coagulants should be stopped .
May cause pericardial effusion but rarely tamponading .

26. Take Home Message
Cardiac Rehabilitation and extended follow up of the
post-Infarction patient clinically and by imaging
modalities are as important as the early follow up.
Anticipate complications in every patient , so you won’t
miss it when it occurs .