Case Presented by Final Year MBBS sudents of Frontier Medical College at the 1st Clinico-Pathological Conference for the year 2015.The Presentation is divided into two parts. First part is about a case of an Acute ST Segment elevated Myocardial Infarction with. Its management at the Hospital and the findings. Second part is about the pathophysiology, Cinical signs and symptoms and an effective gold standard treatment of MI.

1. Clinico-pathologicalconference
1st
Myocardial
infarctionPresentation by
1605- Abubakkar
Raheel
1622- Haider Ali
1606- Ahmed Arsalan
Final Year MBBS
27th February, 2015

2. Long Case
• Muhammad Shareef, a 65 year old male patient from
Abbottabad, known case of Diabetes since last 12
years and Coronary Artery Disease for the last 2
years presented in King Abdullah Teaching Hospital
with the complaints of Chest pain and breathlessness
for the last 6 hours. Patient had an episode of
vomiting. He was conscious and well oriented.
Overall health state was weak and meagre.
Dept of Medicine
Frontier Medical and Dental College

3. Dept of Medicine
Frontier Medical and Dental College

4. Dept of Medicine
Frontier Medical and Dental College

5. History of Patient
• Name: Muhammad Shareef
• Sex: Male
• Age: 65 years
• Marital Status: Married
• Occupation: Retired Govt. servant
• Address: Abbottabad
• D.O.A: 20th February, 2015
• T.O.A: 9:30 am
• M.O.A: OPD
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6. Chief Complaints
• Chest pain – 6 hrs
• Shortness of Breath – 6 hrs
• Vomiting - 5 hrs
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7. History of Present illness
• Known case of Diabetes - 12 yrs &
Ischemic Heart Disease – 2 yrs
• Chest pain started 6 hrs back
• Sudden in onset
• Retrosternal
• Crushing in nature
• Radiating to left arm, back and neck
• Aggravated on exertion
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8. History of Present illness
• Shortness of breath – 6hrs
• Sudden onset
• present at rest
• Vomiting – 5hrs
• 2 episodes of vomiting
• Vomitus was yellowish
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9. History of Present illness
Associated symptoms:
• Moderate fever
• Sweating
• Dizziness
• Patient was completely conscious
• Palpitations
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10. History of Present illness
• Systemic Inquiry
1. General
a. Reduced apetite
b. Sleep disturbed
c. Weakness
2. Respiration
Cough, wheezing and hemoptysis not
present
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11. History of Present illness
• Alimentary system: Nausea & Vomiting
present
• Urinary system: No significant history
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12. History of Past illness
• Past Medical History
– Diabetes : 12 yrs
– IHD : 2 yrs
– HTN : Positive
– TB : Negative
– Asthma : Negative
• Past Surgical History
No significant past surgical history
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13. Family History
• Positive for IHD, HTN and DM
• 2 brothers died of MI
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14. Drug & treatment History
• Patient was taking anti diabetics and anti
hypertensive drugs
• Drug compliance was poor
• No other significant drug history
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15. Personal History
• Chronic Smoker
• No history of drinking
• Sedentary lifestyle
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16. Socio-economic History
• Satisfactory
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17. History based Differential Diagnosis
• Acute Myocardial Infarction
• Unstable Angina
• Pleurisy
• Pericarditis
• Pneumothorax
• Pulmonary embolism
• Reflex Esophagitis
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18. General Physical Examination
Patients general appearance
• Pale and anxious
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19. General Physical Examination
• Vitals
– B.P: 160/90mmHg in lying position
– Pulse: 115 b/m, regular, tachycardia
– Temp: 101 F
– Resp: 30/m
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20. General Physical Examination
• No Clubbing, pallor, splinter
hemorrhages koilonychias or leconichia
• Mild tobacco staining observed
• Xanthomas present on extensor
surface of hands
• Carotid pulse: thin
• JVP: Not raised
• Eyes: Anemia not present
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21. General Physical Examination
• Jaundice not present
• Dental hygiene good
• Carotid briut not audible
• No abnormality on fundoscopy
• No abnormality seen on thyroid
examination
• Lymph nodes not palpable
• Pedal and Sacral edema absent
• No other significant findings
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22. Systemic Examination
1. CVS Systemic Examination
a. Inspection:
• No Chest deformity
• No sternotomy or any other surgical
scar
b. Palpation:
• Apex beat: Lateralized from mid
clavicular line at 6th intercoastal spacece
due to LVH
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23. General Physical Examination
• Heave: well sustained (at apex)
• No left parasternal lift
c. Auscultation:
Mitral, Tricuspid, Aortic, Pulmonary
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24. General Physical Examination
• S1- Normal (Apex)
• S2- Audible (Left sternal edge)
• No added sounds
• No murmurs
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25. General Physical Examination
c. GIT:
• Liver not palpable
• Spleen not palpable
• Ascites not present
d. Respiration:
• Chest clear
• No tracheal shift
• No remarkable findings
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26. General Physical Examination
e. CNS:
No remarkable findings
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27. Examination based Differential Diagnosis
• Myocardial Infarction
• Unstable Angina
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28. Investigations - ECG
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29. Investigations
ECG:
Done within 25 mins of patient arrival
Findings:
• Rate: 78.9
• Rhythm: Sinus Rhythm
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30. Investigations
Leads showing ECG Changes:
• V1 to V6, AvL
• Changes include:
• ST Segment Elevation
• Q wave development
• Loss of R Wave
• T wave inversion
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31. Investigations
• Left Axis deviation seen by thumb rule on
Lead 1 and AvF
(For inferior wall MI, changes are seen in:
Leads 2, 3 and AvF)
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32. Investigations
 Cardiac biomarkers
• Trop T raised
• CK-MB raised
Chest Xray
• Cardiothoracic ratio increased showing LV
Dilatation
• Pulmonary edema not evident
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33. Investigations – Xray
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34. Investigations
Other Blood Tests
• ESR and CRP raised
Echocardiography could not be done due
to the non availablity of facility.
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35. Investigations based Diagnosis
Anterolateral ST Segment Elevation
Myocardial Infarction with Left Axis
Deviation
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36. Management
• Patient was immediately admitted in ICU. Within 10
mins, ECG was performed and based upon
diagnosis, following treatment was given.
• Oxygen + Cardiac rhythm monitoring
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37. Management
• Aspirin 300mg PO
• (Therapy should be continued indefinitely if there
are no side affects)
• Clopidogrel 600mg PO followed by 150mg daily for
1 week and 75mg daily thereafter.
• Streptokinase 1.5ml I.V in 100ml sol at 6ml/hr
• Inj Morphine
• Inj Metoclopromide I.V Stat
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38. Late Management
• Patient advised on the following:
• Lifestyle Modification:
• Lipid Lowering diet
• Cessation of Smoking
• Regular exercise
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39. Late Management
• Secondary Drug therapy:
• Aspirin
• B blocker
• Ace Inhibitor/ARB
• Statin
• Additional therapy for DM and HTN
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40. The patient was given Streptokinase (Thrombolysis)
within 8 hours of his arrival. He is still in the ICU
undergoing 24/7 observation and treatment. He
was advised angiography due to the unavailability of
the facility at the Hospital. We wish him a speedy
recovery. 
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41. What is MI ?
• Detection of rise and/or fall of cardiac biomarker
values (preferably cardiac troponin) with atleast one
of the following:
• Symptoms of Ischemia
• Significant ST segment-T wave changes or new LBBB
• Development of pathological Q waves
• Imaging evidence of new loss of viable myocardium
• Angiographic identification of Intra coronary
thrombus
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42. Types of MI
On the basis of ECG, there are two main types of MI
• STEMI (major coronary artery complete obstruction)
• Non-STEMI (Complete occlusion of a minor vessel or
partial occlusion of a major coronary vessel
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43. Arterial Supply of the Heart
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44. Arterial Supply of the Heart
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45. Arterial Supply of the Heart
There are two major arteries which supply the heart
• Left coronary artery
• Right coronary artery
1. Left Coronary Artery:
It is further divided into two main branches:
 LAD (I/V septum, Ant. Wall of LV and Apex)
 LCx (Lateral, Posterior and Inferior Walls)
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46. Arterial Supply of the Heart
2. Right Coronary Artery
It supplies RA, RV and inferio-posterior part of LV
Branches include:
 PDA (supplies I/V septum inferior part) In 90%
individuals PDA is a branch of RCA. (Right Dominant
people)
In 10% individuals PDA is a branch of LCA (Left
Dominant)
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47. Arterial Supply of SA & AV Node
• SA Node: RCA in 60% individuals
• AV Node: RCA in 90% individuals
Clinical Significance:
• Proximal RCA occlusion may result in Sinus
Bradycardia and may also cause AV Nodal block
• Abrupt occlusion of RCA may lead to infarction of
inferior part of LV
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48. Conducting system of Heart
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49. Nerve Supply of Heart
• Adrenergic Nerves from the Cervical Sympathetic
chain supply atria and ventricles
• Parasympathetic: Vagus nerve
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50. Pathophysiology of MI
Atheromatous plaque formation
Interplaque haemorrhages
Exposure of Subendothelial
collagen fibers
Formation of micro thrombi
Full blown thrombus
vasospasm
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51. Pathophysiology of MI
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52. Pathophysiology of MI
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53. Pathophysiology of MI
• LCA Occlusion:
 LAD occlusion (40-50) leads to
Anterior wall infarction of LV
Anterior portion of ventricular septum
Apex
 LCx Occlusion 15-20%
Lateral wall of LV
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54. Pathophysiology of MI
 RCA Occlusion (30-40%)
RCA occlusion leads to infarction of
• Posterior wall of RV
• Inferior wall of LV
• Posterior 1/3rd of I/V septum
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55. Clinical features
 Symptoms:
• Pain: Crushing, retrosternal chest pain radiating to
back, left arm, neck or jaw
• Anxiety and fear of impending death
• Nausea and Vomiting
• Breathlessness
• Diaphoresis
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56. Clinical features – Pain Areas
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57. Clinical features
• Signs
 Sympathetic activation:
- pallor
- sweating
- tachycardia
 Vagal activation:
-bradycardia
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58. Clinical features
 vomiting
• Signs of impaired myocardial function:
 Hypotention
 Narrow pulse pressure
 JVP may be raised
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59. Clinical features
 3rd heart sound
 Quiet 1st heart sound
 Diffuse apical impulse
 Lung crepitations
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60. Clinical features
• Signs of tissue damage
 fever
• Signs of complications e.g Mitral regurgitation,
pericarditis etc
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61. Clinical features
• Silent MI
 diabetic patients
 Older individuals
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62. Investigations
• ECG
• Cardiac biomarkers
• Chest X-Ray
• Echocardiography
• ESR & CRP
• Angiography
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63. Investigations
• ECG
It is central to confirming the diagnosis but may be
difficult to interpret if there is bundle branch block
or previous MI. so repeated ECGs are very
important.
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64. Investigations – Normal ECG
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65. Investigations – Normal ECG
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66. Investigations - ECG
Earliest changes are seen in ST-segment
1. STEMI
• ST-segment elevation
• progressive loss of R wave .
• Development of Q wave .
• Resolution of ST-segment
• T-wave inversion
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67. Investigations - ECG
2. NSTEMI
• St-segment depression
• T-wave changes
• Loss of R-wave
• Absence of Q-wave
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68. Investigations – ECG - STEMI
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69. Investigations - ECG
 Significance of chest leads
 Antero-septal infarct
v1 ,v2,v3,v4
 Antero-lateral
v4,v5,v6 and AVL and 1
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70. Investigations - ECG
 Inferior infarction
leads II , III and AvF
 Posterior wall infarction doesn’t cause ST elevation
or Q-waves in the standad leads but can be
diagnosed by the reciprocal changes that is st
depression and a tall R-wave and leads V1-V4.
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71. Cardiac Biomarkers
1. Troponins
2. Creatinine kinases
3. LDH
4. AST
5. Myoglobins
6. Most specific are troponins and CK-MB
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72. Cardiac Biomarkers
1. CK-MB
Rises in 4-6 hours and peaks a 12 hours and falls to
normal within 48-72 hours . It is very important.
For diagnosis of recurrent MI’s.
2. Troponins: Trop-T and trop-I are gold standards for
diagnosis of MI, Troponins rise in 4 to 6 hours and
remains elevated for 2 weeks
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73. Investigations- Chest Xray
• Chest Xray to determine cardiomegaly and
pulmonary edema
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74. Investigations - Echocardiography
• Useful for assessing ventricular function and
determining complications
Eg. Mural thrombus, cardiac rupture , VSD and
pericardial effusion etc
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75. Investigations - Other blood tests
1. ESR raised
2. Leucocytosis
3. CRP raised
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76. Management
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77. Management
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78. Drugs used in treatment of MI
1. Analgesics
- Opiates: Morphine Sulphate dimorphine
2. Anti-emetics: metoclopromide
3. Anti-thrombotic drugs
a. Anti platelets: Aspirin
- Clopidogrel
- Ticagrelor
- Gycoprotien 2b and 3a
receptor antagonists: Abciximab
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79. Drugs used in treatment of MI
b. Anticoagulants :
– LMW Heparin, HMW Heparin,
pentasaccharide - fondaparinux
– Warfarin
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80. Drugs used in treatment of MI
4. Anti anginal drugs
- Nitrates: GTN, isosorbide dinitrate
- B blockers: metoprolol and atenolol
5. Dihydropyridine CCBs:
- Nifedipine, amlodipine
6. Thrombolytics:
- Alteplase, streptokinase, retiplase, tenecteplase
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81. Invasive modalities used in the treatment of MI
• PCI (Percutaneous Intervention)
• CABG (Coronary Artery Bypass graft) Surgery
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82. Late Management of MI
Lifestyle modifications
Diet
Cessation of smoking
Weight control
Reguar exercise
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83. Late Management of MI- Sec prevention
• Anti platelet therapy
• B blockers
• Ace inhibitors
• Statins
• Additional therapy for diabetes and HTN control
• Mineralocorticoid receptor antagonist
• Devices: Implantable Cardiac Defibrillators
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84. Complications
• Arrythmias
• Bradycardia
• Acute Circulatory failure
• Pericarditis
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85. Complications - Mechanical
• Rupture of papillary muscle
• Rupture of I/V septum
• Rupture of ventricle which can lead to fatal cardiac
temponade
• Embolism
• Impaired ventricular function, remodeling and
ventricular aneurysm
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86. Prognosis
• If medical care is not provided, death occurs in
almost 1/4th of the cases. Half of the death occurs
within 24nhours of the onset of symptoms and
about 40% of all affected patients die within the
first month.
• Patients who reach the hospital and survive
have much better prognosis with a 28 day survival
of more than 85%. The prognosis of anterior
infarcts is worse as compared to inferior infarcts.
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87. Prognosis
OF THOSE WHO SURVIVE AN ACUTE ATTACK, MORE THAN
80% LIVE FOR A FURTHER YEAR. ABOUT 75% FOR 5 YEARS.
50% FOR 10 YEARS & 25% FOR 20 YEARS.
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88. Thankyou everyone 
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