Complication of MI.pptx

Complications of MI
DR.NOORUL QAMAR MALIK
DM CARDIOLOGY IInd YR

 Electrical Complications
 Mechanical Complications
 Heart failure
 Pericarditis
 Post infarction angina or Reinfarction

A- Electrical Complications
1-Arrhythmias / Heart block:
Almost any cardiac arrhythmia may occur in acute
MI.
LAD supplies most of the conduction
system below the A-V node (His-Purkinje system).
RCA supplies most of the conduction system at and
above the A-V node (including the S-A node and the A-
V nodes ).
Any type of infarct can lead to abnormal conduction.
Normal tissue is adjacent to injured tissue, which may
lead to re-entry rhythms including ventricular
tachycardia and atrial flutter.

2-Hypotension:
Hypotension - acute MI
1) Hypovolemia
2) Decreased left ventricular filling, secondary to right
ventricular infarction.
3) Marked reduction in cardiac output due to
extensive infarction or to a mechanical complication of
MI.

B-Major mechanical complications
-Rupture -left ventricular free wall,
- Acute severe MR
- papillary muscle displacement
- papillary muscle rupture
- Ventricular septal rupture.
- Pseudo aneurysm formation
- RV infarction
- Dynamic LV outflow obstruction
- LV thrombus

Free wall rupture
Most common least recognized complication:
 < 1% to 6.2% patients with acute MI
 14 to 26% of Infarct related mortality
 7% in hospital deaths
Time Course :
 First 5 days post MI in 50%
 90% occur within 2 weeks

Mid ventricle and lateral wall are most common sites
May affect any wall
 Can involve RV
 Atria may be affected rarely
Adjacent to junction of normal with infarcted tissue

Clinical signs :
 Pericarditis , emesis and agitation
 Recurrent chest pain
 Transient hypotension and
bradycardia

Echocardiographic features include;
Pericardial effusion in end –diastole > 5mm
High density intrapericardial echoes (thrombus)
RV/RA compression (Tamponade)
Direct 2D identification of tear is unusual
- Contrast may be helpful

Suspected LVFWR
Echo confirmation
Hypotension
No EMD
IV fluids, Inotropes, IABP,
Pericardiocentesis(?)
Emergency Surgery

LV pseudo aneurysm
 Incomplete rupture
 Sealed by pericardium and hematoma
 Echo- lucent space external to LV
 Narrow neck
 Ratio of the diameter of the entry point to the
maximal diameter is <40 -50%
 May contain thrombus
 Characteristic Doppler Profile
 Bidirectional ( “to- and –fro”) flow pattern

 Narrow base
 Walls composed of
pericardium and
thrombus
 High risk of rupture
 Wide base
 Walls composed of
myocardium
 Low risk of rupture
Aneurysms
Pseudo-aneurysms

Aneurysms Pseudo-aneurysms
Location 3% posterior Posterior or inferior
Echocardiography
Anatomy Thinned myocardium Ruptures
Contractility Non contractile Dyskinesia
Consequences/Complica
tions
Congestive heart failure
Embolic events Ventricular
arrhythmias
Congestive heart failure
Embolic events
Ventricular arrhythmias
Therapy Medical or Surgical
therapy
Surgery
Surgical risk Dubious Lower than medical
therapy

Ventricular septal rupture
Occurs in 0.2 to 1% patients with MI
- Bimodal distribution – 24 hrs.and days 3-5
 Any portions of septum may be involved margin
between necrotic and non necrotic myocardium
 Anterior VSR s tend to located distally with defects
septum at the same level- “simple”
Inferior VSRs located more toward the base and
follows a serpingenious course“ complex”

Presentation
 Holosystolic murmur (often loud)
 Thrill
 Heart failure

Treatment
 Medical Therapy
 Diuretics
 Inotropes
 Vasodilators
 IABP
 Surgery
 Percutaneous Closure

Papillary Muscle Rupture
 Least common mechanical complication
 Pathology
 Complete
 Partial – muscle heads/tips
 Posteromedial papillary muscle more often involved
( single blood supply)

 Presentation
 1 to 7 days after MI
 Heart failure
 Shock
 MR murmur
- may be soft/indistinct
- often no thrill present

Echocardiographic features
 Flail mitral leaflet with systolic cusp prolapse to LA
 Mobile echogenic mass attached to the chordae tendinae and to
the mitral valve
 No prolapse of papillary head to LA is observed in 35%
 Abnormal cutoff of one papillary muscle
 Severe MR
- Color –flow disturbance area can be small
- Cut-off sign in CW spectral profile
 Hyper dynamic LV function

Acute Mitral Regurgitation
Treatment
 Medical therapy
 Inotrophic support
 Diuretics
 Afterload reduction
 IABP
 Surgery

Right ventricular MI
 Common association with inferior MI
 RV apical segments may be involved in LAD occlu
 ST segment elevation in V1and or V4R- V6R
 Mortality high vs inferior MI
 Clinical presentation
 Hypotension
 Clear lung fields
 Increased JVP
 Lack of pulmonary congestion
 Hypoxemia
 Right to left shunting via PFO

Echocardiographic features
 Focal RV wall motion abnormalities – McConnell's sign
 Paradoxical septal motion due to acute volume overload
 Dilation of RV (RA)
 Small LV
 Bowing of interatrial septum from right to left
 RV thrombus
 Tricuspid regurgitation
 TAPSE and RVS’ reduced
 IVC plethora
 Right to left shunting via PFO

Dynamic LV outflow obstruction
 In setting of apical infarction sparing the base
 Basal hyper kinesis
 Systolic anterior motion of mitral leaflet
 Dynamic LVOT obstruction
 Hypotension
 Systolic murmur
 Exacerbation by inotropic agents and IABP

Left ventricular thrombus
Anterior wall infarcts
20-40% (60% in large anterior-wall AMIs, not treated
with anticoagulant therapy)
High risk of systemic embolization (Anticoagulant
therapy ↓
rate of embolic events by 33%
anticoagulation)
Most common presentation is Stroke (within the first
10 days after AMI)

 Transthoracic echocardiography is modality
of choice (92% sensitivity, 88% specificity)
 Management - heparin treatment
followed by oral warfarin therapy for 3-6
months, lifelong anticoagulation if a clot
persists.
Left ventricular thrombus

Etiologies , Incidence and Mortality

Summary for LAD Infarct
Left anterior descending artery
40% of LV myocardium His-Purkinje System
Cardiogenic shock due to loss
of large amount of myocardium
Intraventricular septum
(upper two – thirds)
Antero-apical wall
Acute VSD
Apical LV aneurysm
Ventricular
arrhythmias
Apical thrombus
formation
Arterial embolism originating in
the LV
Advanced Heart Block
(LBBB, 3rd degree A-V
block
And Mobitz II 2nd degree)

Summary for RCA (or Circumflex) Infarct
Right coronary artery
RV Infarct
Hypotension due to
Decreased LV filling
SA –nodal infarct
A-V nodal infarct
Brady arrhythmias
1st degree A-V block
Mobitz 2nd degree
block
A-V dissociation
Posteromedial
Papillary muscle
infarct
(
Acute MR
with or without papillary
muscle rupture )

Complication of MI.pptx

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