CLINICAL PRESENTATION

• 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

Pain:

• 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

DIFFERENTIAL DIAGNOSIS

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

PHYSICAL FINDINGS

• 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

Precordium –

• 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 2^nd 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. –

ECG

• 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.-

LAB FINDINGS

• 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.