• Acute Myocardial Infarction is precipitated by exer­tion, exercise, emotional stress, medical and surgical disease and interventions.
  • Circadian variation – AMI is more common in early morning hours due to increase in sympathetic tone and increased thrombolytic tendency from 4 to 12 AM.
  • Acute myocardial infarction (AMI) is the rapid development of myocardial necrosis resulting from a sustained and complete absence of blood flow to a portion of the myocardium



Acute Myocardial Infarction is precipitated


  • Pain is the most common and typical symptom of AMI.
  • There is very severe pain.
  • It is located in cen­tral portion of chest and sometimes epigastrium.
  • It radiates to Arms; Abdomen; Jaw; Back and Neck.
  • Pain may be present up to occiput or to umbilicus in front but not lower than umbilicus.
  • It is a deep pain.
  • It may be a severe discomfort, heavi­ness, squeezing, crushing pain.

Risk Factors

  • Diabetes mellitus
  • Dyslipidemia
  • Advanced age
  • Poorly controlled hypertension
  • Tobacco use
  • Family history of premature onset of coronary artery disease (CAD)
  • Sedentary lifestyle

Chest pain is accompanied by :

  • Weakness
  • Sweating
  • Pain may occur during rest.
  • Painless MI – occurs in:
  • Diabetes mellitus –
  • old age
  • Nausea
  • Vomiting Anxiety
  • Sense of doom.
  • Pain occurs during exertion – is not relieved with rest.
  • In Old age – Acute MI may present with acute aysponea (pulmonary edema).

Less Common presentations


  • Loss of consciousness Confusion
  • Extreme weakness Arrhythmia
  • Pulmonary embolism Falling Blood pressure.

Associated Conditions

  • Extracranial cerebrovascular disease
  • Abdominal aortic aneurysm
  • Atherosclerotic peripheral vascular disease


  • Acute pericarditis Pulmonary embolism Acute aortic disease Costochond ritis Gastrointestinal disorders.


  • Severe pain – Resulting in restless movements.
  • Pallor
  • Cold extremities Profuse sweating
  • Severe substernal pain for >30 minutes
  • In anterior infarction :
    • Tachycardia
    • Hypertension
  • In Inferior infarction:
    • Bradycardia
    • Hypotension


  • Apical impulse difficult to palpate.
  • In Anterior wall M~ – dyskinetic bulge seen due to
  • ‘nfarcted myocardium-in periapical area.
  • S4 may be present S3 may be present
  • Decreased intensity of heart sound Paradoxical splitting of 2nd heart sound
  • Mid or late systolic murmur at apex due to MR due to dysfunction of Mitral valve apparatus. Pericardial friction rub.
  • Decreased cardiac pulsations-decreased stroke volume.
  • Temperature increased for a week.
  • Feeble apex beat and increased JVP is Seen in right ventricular infarction.
  • Systolic BP decreases by 10- 15 mmHg. –


  • Acutephase
  • Total occlusion results in ST elevation, with Q waves developing in hours or days.
  • Q.waves ultimately de­velop.
  • Q Wave MI is usually Transfmural infarction.
  • In Sub total occlusion no ST elevation called Unstable angina. Non QMI is usually Non ST elevation MI.
  • Non Q MI has positive serum cardiac marker with clini­cal Picture of MI.
  • If no ST elevation is seen in a patient with clinical picture of MI with negative serum cardiac marker it is Unstable Angina.-


  • 1.Acute few hrs to 7 days
  • 2.Healing 7 to 28 days
  • 3. Healed —- 29 days
  • · ECG
  • · Serum cardiac markers
  • · Cardiac imaging
  • · Non specific.


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