The document provides an extensive overview of coronary arteries and their role in myocardial infarction (MI), including risk factors, symptoms, diagnosis, and management strategies. Key components highlighted include the importance of various cardiac markers for diagnosis, ECG changes, and management protocols such as reperfusion therapy and lifestyle modifications. The prognosis for MI patients is discussed, with statistics on survival rates and factors affecting outcomes.

3. CORONARY ARTERIES

4. Distribution of coronary blood
supply
Right Coronary Artery Left Coronary Artery
Right atrium
Right ventricle
SA node (85%)
AV node
Inter-atrial septum
Portion of left atrium
Postero-inferior 1/3 of Inter-
ventricular septum
Portion of posterior part of left
ventricle
Left atrium
Left ventricle
Most of the Interventricular
septum
Atrio-ventricular bundle and its
branches

5. ACUTE MYOCARDIAL INFARCTION
• Cardiac muscle
necrosis secondary
to protracted lack
of coronary
perfusion
• Usual etiology:
Thrombus at site of
vascular injury

6. OTHER ETIOLOGIES OF ACUTE
MYOCARDIAL INFARCTION
• Coronary embolus
• Coronary spasm
• Coronary anomoly
• Primary in situ thrombosis
• Vasculitis
• Hypotension

7. DETERMINANTS OF EXTENT OF DAMAGE
• Territory supplied
• Duration of occlusion
• Existence of collaterals
• Oxygen demand at time of occlusion
• Vasospasm

8. RISK FACTORS
Risk factors for atherosclerosis are generally risk factors for
myocardial infarction
Diabetes (with or without insulin resistance) – the single
most important risk factor for ischaemic heart disease (IHD)
Tobacco smoking
Hypercholesterolemia
Low HDL

9. High blood pressure
Family history of ischaemic heart disease (IHD)
Obesity
Age: Men at age 45 & Women at age 55
Hyperhomocysteinemia (high homocysteine, a toxic
blood amino acid that is elevated when intakes of
vitamins B2, B6, B12 and folic acid are insufficient)
Stress
Alcohol
Males are more at risk than females

10. Presenting Symptoms of Acute MI
• Pain-
*typical-crushing substernal chest pain
*atypical - jaw, neck, shoulder, back pain, indigestion
*painless - “silent”
• Dyspnea-
systolic and/or diastolic dysfunction
• Dizziness-hypotension, arrhythmia
• Nausea, vomiting
• Elderly patients: Failure to thrive
• Anxiety, restlessness

11. CHEST PAIN

12. Presenting Signs in Acute MI
• Appearance: Pallor, diaphoretic, anxious
• Vital Signs: Normal or abnormal BP and P
– Hypertension and tachycardia: SNS
– Hypotension and tachycardia:
• Cardiogenic shock
• Myocardial rupture
• Tachyarrhythmia
– Hypotension and bradycardia
• vagal stimulation
• Bradyarhythmia

13. Presenting Signs in Acute MI (Cont.)
• Lungs: Rales - CHF
• Heart: Displaced LV impulse
–S3
–S4
–Murmur of mitral regurgitation
–Murmur of ventricular septal
rupture
–Pericardial rub

14. DIAGNOSIS
The diagnosis of myocardial infarction can be
made after assessing
Patient's complaints and physical status
ECG changes
Coronary angiogram
Levels of cardiac markers

16. ORDER OF ECG CHANGES IN AMI
 Earliest: Increased R and T wave amplitudes; giant R wave and
Hyperacute T waves
 Progressive ST elevation
 Q waves appear
 Loss of R waves
 “T wave” inversion (because of change in ventricular repolarisation)
and it persists

18. HYPERACUTE “T WAVES”

19. Electrocardiographic Differential Diagnosis
of the Hyperacute T Wave
A: AMI
B: AMI
C: Hyperkalemia
D: Benign Early Repolarization
E: Acute Pericarditis
F: LBBB
G: LVH

20. T Wave Inversion in ACS

21. INFARCTION DISTRIBUTION
TERRITORY ECG LEADS ARTERY
Anterior V2-V6 LAD
Inferior II,III, aVF RCA
Lateral I, aVL, V5-V6 Circumflex
Posterior Tall R in V1-V2 Variable

22. ANTERIOR AMI
STE in V1-V4

24. ANTEROLATERAL AMI
STE in V2-V4 Anterior
STE in I, aVL, V5-V6 Lateral

26. LATERAL AMI
STE in I, aVL
*Note the ST depression in II, III, aVF consistent
with reciprocal changes, as well as in V2-V3 which
may represent a posterior MI

28. INFERIOR AMI
STE in II, III, aVF
*Note the ST depression in I, aVL consistent with
reciprocal change, as well as in V1-V4 representing a
posterior MI

30. POSTERIOR WALL AMI
ST Segment Depression in V1-V3 and posterior thoracic
leads with STE

32. PLASMA MARKERS
CK-MB
Increases at 4-6 hours
Peaks at 12 hours
Normalizes in 48-72 hours
TROPONIN T & I
Increases at 4-6 hours
Remains elevated for 2
weeks

33. Creatine Phosphokinase (CK)
• Rises within 4-8 hours, rapidly cleared by 24-24 hours
• Other Sources:
– Skeletal
– Hypothyroidism
– Renal failure
– Stroke
• Isoenzymes
– MM skeletal muscle
– BB brain
– MB cardiac
• CKMB≥ 4% suggests acute myocardial infarction+++

34. Cardiac Specific Troponins (cTnT, cTnI)
• Rise within 4-8 hours, remain elevated 7-14
days (T>I)
• 30% of patients with UAP show ↑ levels cTnT
or I, indicating increased risk of adverse
outcome

36. OTHER TESTS
BLOOD leukocytosis, ESR and CRP is elevated
Chest X-ray Pulmonary edema
Echocardiography
Mural thrombi
Cardiac rupture
VSD
MR
Pericardial effusion

37. DIAGNOSIS OF MYOCARDIAL
INFARCTION (American college of cardiology
and the Europeon society of cardiology)
Elevated Troponins or CK-MB above 99th
centile with
one of the following
Ischemic symptoms
Development of Q-waves on ECG
Ischemic ECG changes (ST elevation/depression)
Coronary artery intervention

38. A. IMMEDIATE
MANAGEMENT
B. MAINTAINING
VESSEL PATENCY
C. PREVENTION
OF FURTHER
COMPLICATIONS
D. LATE
MANAGEMENT
Defibrillation
services
Resuscitation
Reperfusion
Detection and
Management of
acute
complications
Drugs
Adjunctive
therapy
Arrythmias
Ischemia
Acute circulatory
failure
Pericarditis
Mechanical
complications
Embolism
Impaired
ventricular function
Ventricular
aneurysm
Risk stratification
and management
Life style
modification
Drug therapy in
Secondary
Prevention
Mobilization and
Rehabilitation

39. A. IMMEDIATE MANAGEMENT
DEFIBRILLATOR
IMMEDIATE MEASURES
1.High flow oxygen
2.IV access
3.ECG monitoring
4.IV analgesics (Morphine Sulphate 5-10 mg)
5.Anti-emetics (Metoclopramide 100mg)
6.Anti-platelets (Aspirin 300mg)

40. REPERFUSION
 Primary PCI is the treatment of choice
 Thrombolysis (Greatest benefits if in 2 hours)
Streptokinase 1.5 Million Units in 100ml of N/S over 1 hour
Alteplase 15mg bolus then 0.75mg/kg in 30 mins (50mg)
followed by 0.5mg/kg in 60 min (35mg)
Major hazard is Cerebral Haemorrhage
DETECTION AND MANAGEMENT OF ACUTE
COMPLICATIONS
 Arrythmias
 Ischemia
 Heart failure

41. Major Contraindications To the Use of
Thrombolytic Therapy
• Any previous history of hemorrhagic stroke
• History of stroke, dementia, or central nervous system
damage within 1 year
• Head trauma or brain surgery within 6 months
• Known intracranial neoplasm
• Suspected aortic dissection
• Internal bleeding within 6 weeks
• Active bleeding or known bleeding disorder
• Major surgery, trauma, or bleeding within 6 weeks
• Traumatic cardiopulmonary resuscitation within 3 weeks

42. Relative Contraindications To the Use of
Thrombolytic Therapy
• Oral anticoagulant therapy
• Acute pancreatitis
• Pregnancy or within 1 week postpartum
• Active peptic ulceration
• Transient ischemic attack within 6 months
• Dementia
• Infective endocarditis
• Active cavitating pulmonary tuberculosis
• Advanced liver disease
• Intracardiac thrombi
• Uncontrolled hypertension (systolic blood Pressure >180 mm Hg, diastolic blood pressure >
110 mm Hg
• Puncture of noncompressible blood vessel within 2 weeks
• Previous streptokinase therapy

43. Risks of Coronary Angiography: (all
are rare)
• Stroke
• Myocardial infarction
• Arrhythmia
• Renal failure
• Allergic reaction to contrast agent

44. B. MAINTAINING VESSEL PATENCY
• Anti-platelets
Aspirin 75-300mg daily and/or Clopidogrel 75mg daily
• Anti-coagulants
S/C Heparin 12,500 units twice daily
IV Heparin (within 48-72 hrs of thrombolysis)
Warfarin in Persistant A.Fibrillation & Extensive anterior
infarction
• Adjunctive therapy
B-Blockers Atenolol 5-10mg to dec. pain and arrythmias but
should be avoided in HF, AV Block and severe bradycardia
Nitrates S/L GTN 300-500 mcg in threatened MI and IV nitrates
(Nitroglycerin 0.6-1.2mg/hour or Isosorbide dinitrate are
useful in treating LVF and Ischemic pain relief.

45. C. FURTHER COMPLICATIONS AND THEIR
PREVENTION
1. ARRYTHMIAS (VF, VT, AF, AT, Heart blocks and
Ventricular ectopics)
Can be avoided by Pain relief, Rest and Correction of
hypokalemia
• Vent. Fib….5-10% cases…..prompt defibrillation
• Atrial Fib….transient and rarely requires treatment
….DC cardioversion, Digoxin or B-Blocker are
TOCs…..Patient can go into LVF so give
Anticoagulants
• AV block….Atropine 0.6mg IV + Temporary
pacemaker

46. 2. ISCHEMIA 50% cases known as post-infarct Angina
Managed as Unstable Angina
• IV nitrates (0.6-1.2mg/hour)
• IV heparin (1000 units/hour)…dose adjusted to PT
• LMWH
• GP IIb/IIIa receptor antagonists…..selected cases
3. ACUTE CIRCULATORY FAILURE in extensive myocardial
damage
4. PERICARDITIS (on 2nd
and 3rd
day)
Opiod based analgesics
Also called Post-Infarction syndrome/Dressler’s
syndrome…..fever, pericarditis and pleurisy (due to
auto-immunity)….may require High dose Aspirin,
other NSAIDS and Cortico-steriods.

47. 5. MECHANICAL COMPLICATIONS
Papillary muscle damage…..acute onset pulmonary
edema due to severe MR (PSM + S3)…..diagnosed by
doppler’s echocardiography and treated by
emergency mitral valve replacement
Ruptured IV septum…..Left to right shunt (PSM
radiating to right sternal border difficult to
distinguish from MR) …..diagnosed on doppler’s
echocardiography …..fatal condition
Ventricular rupture…..cardiac tamponade…..fatal
6. EMBOLISM risk is decreased by prophylactic ani-
coagulants and early mobilization

48. 7.IMPAIRED VENTRICULAR FUNCTION
Due to infarct expansion…..lead to progressive
dilataion of the infarcted area and hypertrophy of
the rest of the portion
8. VENTRICULAR ANEURYSM 10% cases
Leads to HF, Ventricular arrythmias, Mural thrombus
and systemic embolism
Echocardiography is diagnostic
Surgical removal improves the chances of survival

49. D. LATE MANAGEMENT
1. RISK STRATIFICATION
LV FUNCTION ISCHEMIA ARRYTHMIAS
•Physical findings …
tachycardia, S3,
Crackles at lung
bases and elevated
venous pressure
•ECG changes
•Size of heart and
Pulmonary edema
on CXR
•Post-infarct angina …
treat like unstable angina
•CABG
•Implantable cardiac
defibrillators

50. 2. LIFE STYLE MODIFICATION
 Quit smoking (5 year mortality twice if you don’t
quit)
 Regular exercise (20min/day for 3 days/week)
 Diet control to decrease weight and lipid lowering

51. 3. DRUG THERAPY (Secondary prevention)
Statins…best results when level of LDL is greater than 3.2
mmol/L….Atovstatin 80mg OD
Anti-platelets…Aspirin/Clopidogrel
B-Blockers….but contra-indicated in Bradycardia, AV block,
hypotension and Asthma
ACE inhibitors….Enalapril 10mg BD, Ramipril 2.5-5mg BD
Angiotensin receptor antagonists….valsartan 40-160mg OD,
Candesartan 4-16mg OD
Control of HTN and DM
4. MOBILIZATION AND REHABILITATION start working in 4-6
weeks

52. CARDIAC REHABILITATION
•Healthcare professionals,
should actively promote
cardiac rehabilitation.
•Cardiac rehabilitation
should be equally accessible
and relevant to all patients
after an acute MI.

53. COMPONENTS OF CARDIAC
REHABILITATION
• The guideline recommends that cardiac
rehabilitation should include:
• education
• exercise
• stress management

54. CARDIOLOGICAL ASSESSMENT
All patients should be
offered a cardiological
assessment to consider
whether coronary
revascularisation is
appropriate.

55. ABCs of Treatment and Secondary
Prevention of AMI
• Aspirin-prophylactic Rx for recurrent ischemic events;
give for at least 3 mo. after AMI, probably indefinitely
• Beta blockers-prophylactic, for reduction of cardiac
mortality; Rx for 2 yr-indefinitely
• Converting enzyme inhibitors-all pts with LV
dysfunction to reduce risk of progressive heart failure
and death.
• Diet and lipid lowering Rx-statins have been shown to
reduce risk of subsequent MI, need for
revascularization and mortality (4S, Care)
• Exercise and rehabilitation-essential in restoration of
confidence and improvement in quality of life

56. PROGNOSIS
• 1/4th
of the patients suffering acute MI die in few
min due to any arrythmia
• Half of the MI deaths occur in 1st
24 hours
• 40% of the rest die in 1st
Month
• Anterior infarcts are worse than Inferior infarcts
• BBB and increased enzymes reflects that the
damage is extensive
• Increased mortality is associated with old
age,depression and social isolation

57. SURVIVAL CHANCES
After surviving an acute attack….
• 80 % Survive the 1st
year
• 75 % Survive upto 5 years
• 50% Survive upto 10 years
• 25% survive upto 20 years