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MYOCARDIAL
INFARCTION
 MOHAMMAD RAKIBUL HASAN
 RAISA FATEEMA
 MOHAMMAD ABUL HASNAT
Definition of Myocardial infarction
Myocardial infarction defined as myocardial necrosis which occurs as a result of
critical imbalance between coronary blood flow and myocardial demand due to
occlusion of coronary artery by thrombus.
TYPES OF MI
1) Q wave (Transmural) or ST elevated MI
2) Non Q wave or Non S T elevated or subendocardial MI
ST ELEVATED or Q WAVE MI
Most infarct are transmural involve the full thickness of ventricular wall in the distribution of
single coronary artery.
These infarcts are caused by atherosclerosis, acute plaque change by occlusive thrombi and less
commonly thromboembolI or vasospasm.
NON S T ELEVATED OR SUBENDOCARDIAL
MI
These infarcts involve inner one third to one half of the ventricular wall as sub endocardial zone
is less perfused area of myocardial zone .
The infarcts are caused by hypoperfusion of myocardium and not by coronary occlusion.
These occurs in hypotensive shock and by typical ECG findings these are so called non Q wave
infarction.
SITES OF MI
Inferior MI
Anterior MI
Anteroseptal MI
Lateral MI
Posterior (True) MI
Subendocardial MI
EPIDEMIOLOGY
Industrial countries MI accounts for 10-25% of all deaths
Incidence is higher in elderly people. About 5% occurs at people under age 40
Males have higher risk
Women during reproductive period have low risk
National data on incidence and mortality of coronary heart disease are few in Bangladesh. The
prevalence of coronary heart disease was estimated as 3.3/1000 in 1976 and 17.2/1000 in 1986
indicating 5 folds increase of the disease in 10 years . Socioeconomic improvement and changes
in life style in respect of increase in tobacco consumption and saturated fat intake , decrease in
physical activity, increasing body weight and consequently increasing rate of diabetes mellitus,
hypertension and dyslipidemia in the population contribute to this increase in coronary heart
disease.
RISK FACTOR OF MI
Non modifiable:
Age: common in elderly
Sex: common in male
Family history more common if there is a family history of IHD
Genetic factor: A number of genetic factor linked with coronary artery disease.
Modifiable:
Smoking
Alcohol
Diet
Obesity
Contd.
Hypertension
DM
Hyperlipidemia
Psychosocial factor (Stress, lack of social support, depression and anxiety)
CAUSE OF MI
Coronary blood flow to myocardium may be reduced by obstruction due to the
following-
Atherosclerosis
Thrombosis
Spasm
Embolus
Coronary osteal stenosis
Coronary arteritis (e.g. SLE)
contd.
ANIMATION OF ACUTE MI
CLINICAL FEATURE
SYMPTOMS:
Central chest pain which is severe, stabbing or squeezing or constricting,
radiates to the lower jaw, neck, inner side of the left arm up to the finger, not
relieved by rest and nitroglycerine, persist more than 30 minutes.
Sweating
Fear of impending death
Nausea and vomiting
Breathlessness
Collapse or cardiogenic shock
Contd.
Signs:
o signs of sympathetic activation: pallor, sweating, tachycardia
oSigns of vagal activation: vomiting and bradycardia
oSigns of impaired MI: Hypotension, oliguria, cold peripheries, narrow pulse
pressure, raised JVP, Precordium( quiet 1st heart sound, 3rd and 4th heart sound
and diffuse apical impulse.)
oSigns of tissue damage: fever
oSigns of complication: Mitral regurgitation, pericarditis
INVESTIGATIONS
ECG
Biochemical Cardiac Marker: Troponin I, Troponin T, CK-MB, Myoglobins, AST and LDH
Echocardiography
Chest X ray
Serum creatinine
Fasting lipid profile and Blood sugar
ETT ( Exercise Tolerance Test)
Other stress testing:
•Stress echocardiography
•Myocardial perfusion scan
•Transthoracic echocardiography
ECG FINDINGS
ST ELEVATED MI:
•Elevation of ST segment in 2 or more contiguous leads (1mm or more in limb leads and 2 mm or more
in chest leads)
•New onset left bundle branch block
•Evolution of Q wave along with T wave changes
Associated findings may be as follows –
• reciprocal ST depression- Elevation of ST segment in chest leads may be attended with depression of
ST segment in limb leads and vice versa
•T wave inversion suggestive of myocardial ischemia
•Arrhythmias
•Conduction defect
Contd.
Non ST segment Elevation MI:
•Depression of ST segment of 1mm or more
Associated findings may be as follows-
•T wave changes
•Arrhythmias
•Conduction defect
FINDINGS OF CARDIAC MARKER
CK-MB TROPONIN I,
TROPONIN T
MYOGLOBIN AST LDH
Rise with in 4-6
hours
Rise with in 3
hours
Rise in about 12
hours of attack
Rises relatively late
after 12 hour
Peak appears 12-
24 hours
Reaches to peak in
24-36 hours
Reaches its peak
by 36-48 hours
Normalize after
48-72 hours
Normalize after 2
weeks
Normalize in 3-5
days
Normalizes in 3-5
days
Normalizes by 3
weeks
Complication of MI
Early complication:
Arrhythmia
Cardiogenic shock
Cardiac failure
Acute pericarditis
Thromboembolism
Rupture of papillary muscle or chordae tendineae resulting in MR
Rupture of intra ventricular septum
Rupture or the ventricular wall
Contd.
Late complication:
Ventricular aneurysm
Dressler syndromes
Frozen shoulder
Post infarct angina
PRE HOSPITAL MANAGEMENT OF MI
During this period patient should be treated with-
Absolute bed rest
Sublingual GTN
Aspirin 300mg tablet to be chewed
Clopidogrel 300mg orally ( 4 tablet of 75 mg)
Oxygen inhalation
Main aim should be transferred the patient safely to a center having adequate
facility for the treatment of acute coronary syndrome.
EMERGENCY ROOM CARE
The main aim of the emergency duty doctor is to shorten the door to needle time.
Evaluation of the patient to be made in the emergency on:
 clinical symptoms and sign
ECG
Cardiac biomarker if possible
Emergency steps to be taken:
 drugs particularly aspirin 300mg and clopidogrel 300mg (4 tablet of 75mg )to be given if not
given earlier.
If ECG suggestive of ACS sent the patient to CCU with out delay.
Contd.
If ECG normal keep the patient in observation for 8-12 hours and repeat ECG
and enzyme
If the follow up ECG or enzyme suggestive of ACS admit the patient to CCU and
if normal discharge the patient with advice for further follow up
HOSPITAL MANAGEMENT
GENEREL MANAGEMENT:
 absolute bed rest
Continuous monitoring of heart rate, rhythm and blood pressure
High flow oxygen inhalation
Sublingual GTN
I/V channel for medication
Relieve of pain by morphine or pethidine I/V with prochloroperazine or promethazine
Aspirin 300mg to be chewed and clopidogrel 300 mg orally (if not given earlier)
Contd.
Management of ST MI:/ Non ST MI:
 restoration of coronary blood flow:
Thrombolytic therapy (streptokinase if patient comes with in 12 hours of attack)
Primary PCI if available
Anti ischemic therapy:
Nitrates, beta blocker
Calcium antagonist
ACEI , ARB
Anti platelet therapy:
Aspirin and clopidogrel, GP IIb/IIIa inhibitor
Contd.
Anti thrombin therapy:
Heparin, LMW heparin
 interventions:
PTCA
CABG
CORONARY ARTERY BYPASS GRAFT
MANAGEMENT OF COMPLICTAION
Arrhythmia:
 ventricular ectopics: adequate pain relieve and proper control of heart failure and to keep
electrolytes normal.
 ventricular tachycardia:
Non sustained VT Sustained VT
Asymptomatic patient: Hemodynamically stable patient:
Management of precipitating factor I/V infusion of lignocaine and or
amiodarone.
Anti arrhythmic therapy may be
continued for 24-48 hours
Symptomatic patient: Hemodynamically stable patient:
Anti arrhythmic drug (lignocaine and
amiodarone)
DC cardioversion.
CONTD.
ATRIAL FIBRILLATION:
Ventricular rate <100 bpm, SBP >90 mmHg and there is no associated symptoms – no
treatment
Ventricular rate > 100 bpm associated with SBP >90 mmHG or rate related symptoms – beta
blocker or amiodarone
Rapid ventricular rate, SBP <90 mmHg, heart failure or impaired consciousness – immediate
cardioversion.
Contd.
SINUS BRADYCARDIA SINUS TRACHYCARDIA
If heart rate < 40 bpm or rate related symptoms –
bolus of injection atropine 0.6 mg -1.2 mg I/V
Management of precipitating factor
If sinus bradycardia with symptoms persists despite
repeated bolus of injection atropine (up to 3mg)-
temporary pacing
Beta blocker, diltiazem, verapamil
contd.
1st degree conduction block:
In both anterior and inferior MI no specific treatment other than close observation require.
Mobitz type II and complete heart block:
In inferior MI: asymptomatic and haemodynamically stable patient – no treatment.
If ventricular rate falls < 40 bpm, pause of >3 seconds occur, SBP < 90 mmHg or rate related symptoms
devlop – injection atropine 0.6 mg should be given I/V to be repeated as necessary to maximum of 3
mg.
If symptomatic complete heart block persists despite – injection atropine : temporary pacing indicated
In anterior MI: temporary pacing is indicated.
Contd.
Acute LVF:
Propped up position
High flow oxygen
Nitrates
I/V morphine 3mg and to be repeated on requirement
Loop diuretic: I/V frusemide 40-80 mg and may be repeated on requirement
Vasodilator
ACE inhibitors
Treat identifiable precipitating factor .
Contd.
Cardiogenic shock:
Oxygenation – high flow oxygen via mask (2-4 L/min)
Monitoring: ECG, BP, urine output , pulse oximetry
Improving cardiac output: if SBP< 80 mmHg low dose dopamine 2.5-5
microgram/kg/min infusion, gradually may be increased up to 15
microgram/kg/min
If SBP >80 mmHg dobutamine at the dose of 2.5-15 microgram/kg/min is
preferred present.
Treating reversible myocardial ischemia: IABP support (intra aortic balloon
pump), PTCA or CABG, arrhythmia control and treat other reversible cause.
RISK FACTOR MANAGEMENT
Cessation of smoking
Low fat diets
Eat more vegetables, fruits and fiber containing foods
Control body weight
Regular walking and exercise
Control of DM and HTN
FOLLOW UP MANAGEMENT
Drug:
Individualized on the choice of concerned cardiologists and patient need.
aspirin, beta blocker, trimetazidine, ACEI,ARB, calcium channel blocker, nitrate, clopidogrel and
lipid lowering agents
Assessment of the patient:
Echocardiography
ETT
Radionuclide study
Coronary angiogram
MOBILIZATION AND REHABILITATION
After acute MI in uncomplicated cases :
Sit on chair in day 2
Walk to toilet day 2
Return home on day 5 to day 7
Gradually increasing activity and returning to normal work in 4 to 6 weeks
Counselling and reassurance
In complicated case:
It depends on individual patient conditions and decision of concerned cardiologists.
How to measure Blood Pressure
Myocardial infarction

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Myocardial infarction

  • 1. MYOCARDIAL INFARCTION  MOHAMMAD RAKIBUL HASAN  RAISA FATEEMA  MOHAMMAD ABUL HASNAT
  • 2. Definition of Myocardial infarction Myocardial infarction defined as myocardial necrosis which occurs as a result of critical imbalance between coronary blood flow and myocardial demand due to occlusion of coronary artery by thrombus.
  • 3. TYPES OF MI 1) Q wave (Transmural) or ST elevated MI 2) Non Q wave or Non S T elevated or subendocardial MI
  • 4. ST ELEVATED or Q WAVE MI Most infarct are transmural involve the full thickness of ventricular wall in the distribution of single coronary artery. These infarcts are caused by atherosclerosis, acute plaque change by occlusive thrombi and less commonly thromboembolI or vasospasm.
  • 5. NON S T ELEVATED OR SUBENDOCARDIAL MI These infarcts involve inner one third to one half of the ventricular wall as sub endocardial zone is less perfused area of myocardial zone . The infarcts are caused by hypoperfusion of myocardium and not by coronary occlusion. These occurs in hypotensive shock and by typical ECG findings these are so called non Q wave infarction.
  • 6. SITES OF MI Inferior MI Anterior MI Anteroseptal MI Lateral MI Posterior (True) MI Subendocardial MI
  • 7. EPIDEMIOLOGY Industrial countries MI accounts for 10-25% of all deaths Incidence is higher in elderly people. About 5% occurs at people under age 40 Males have higher risk Women during reproductive period have low risk National data on incidence and mortality of coronary heart disease are few in Bangladesh. The prevalence of coronary heart disease was estimated as 3.3/1000 in 1976 and 17.2/1000 in 1986 indicating 5 folds increase of the disease in 10 years . Socioeconomic improvement and changes in life style in respect of increase in tobacco consumption and saturated fat intake , decrease in physical activity, increasing body weight and consequently increasing rate of diabetes mellitus, hypertension and dyslipidemia in the population contribute to this increase in coronary heart disease.
  • 8. RISK FACTOR OF MI Non modifiable: Age: common in elderly Sex: common in male Family history more common if there is a family history of IHD Genetic factor: A number of genetic factor linked with coronary artery disease. Modifiable: Smoking Alcohol Diet Obesity
  • 10. CAUSE OF MI Coronary blood flow to myocardium may be reduced by obstruction due to the following- Atherosclerosis Thrombosis Spasm Embolus Coronary osteal stenosis Coronary arteritis (e.g. SLE)
  • 11.
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  • 15. CLINICAL FEATURE SYMPTOMS: Central chest pain which is severe, stabbing or squeezing or constricting, radiates to the lower jaw, neck, inner side of the left arm up to the finger, not relieved by rest and nitroglycerine, persist more than 30 minutes. Sweating Fear of impending death Nausea and vomiting Breathlessness Collapse or cardiogenic shock
  • 16. Contd. Signs: o signs of sympathetic activation: pallor, sweating, tachycardia oSigns of vagal activation: vomiting and bradycardia oSigns of impaired MI: Hypotension, oliguria, cold peripheries, narrow pulse pressure, raised JVP, Precordium( quiet 1st heart sound, 3rd and 4th heart sound and diffuse apical impulse.) oSigns of tissue damage: fever oSigns of complication: Mitral regurgitation, pericarditis
  • 17. INVESTIGATIONS ECG Biochemical Cardiac Marker: Troponin I, Troponin T, CK-MB, Myoglobins, AST and LDH Echocardiography Chest X ray Serum creatinine Fasting lipid profile and Blood sugar ETT ( Exercise Tolerance Test) Other stress testing: •Stress echocardiography •Myocardial perfusion scan •Transthoracic echocardiography
  • 18. ECG FINDINGS ST ELEVATED MI: •Elevation of ST segment in 2 or more contiguous leads (1mm or more in limb leads and 2 mm or more in chest leads) •New onset left bundle branch block •Evolution of Q wave along with T wave changes Associated findings may be as follows – • reciprocal ST depression- Elevation of ST segment in chest leads may be attended with depression of ST segment in limb leads and vice versa •T wave inversion suggestive of myocardial ischemia •Arrhythmias •Conduction defect
  • 19. Contd. Non ST segment Elevation MI: •Depression of ST segment of 1mm or more Associated findings may be as follows- •T wave changes •Arrhythmias •Conduction defect
  • 20. FINDINGS OF CARDIAC MARKER CK-MB TROPONIN I, TROPONIN T MYOGLOBIN AST LDH Rise with in 4-6 hours Rise with in 3 hours Rise in about 12 hours of attack Rises relatively late after 12 hour Peak appears 12- 24 hours Reaches to peak in 24-36 hours Reaches its peak by 36-48 hours Normalize after 48-72 hours Normalize after 2 weeks Normalize in 3-5 days Normalizes in 3-5 days Normalizes by 3 weeks
  • 21. Complication of MI Early complication: Arrhythmia Cardiogenic shock Cardiac failure Acute pericarditis Thromboembolism Rupture of papillary muscle or chordae tendineae resulting in MR Rupture of intra ventricular septum Rupture or the ventricular wall
  • 22. Contd. Late complication: Ventricular aneurysm Dressler syndromes Frozen shoulder Post infarct angina
  • 23. PRE HOSPITAL MANAGEMENT OF MI During this period patient should be treated with- Absolute bed rest Sublingual GTN Aspirin 300mg tablet to be chewed Clopidogrel 300mg orally ( 4 tablet of 75 mg) Oxygen inhalation Main aim should be transferred the patient safely to a center having adequate facility for the treatment of acute coronary syndrome.
  • 24. EMERGENCY ROOM CARE The main aim of the emergency duty doctor is to shorten the door to needle time. Evaluation of the patient to be made in the emergency on:  clinical symptoms and sign ECG Cardiac biomarker if possible Emergency steps to be taken:  drugs particularly aspirin 300mg and clopidogrel 300mg (4 tablet of 75mg )to be given if not given earlier. If ECG suggestive of ACS sent the patient to CCU with out delay.
  • 25. Contd. If ECG normal keep the patient in observation for 8-12 hours and repeat ECG and enzyme If the follow up ECG or enzyme suggestive of ACS admit the patient to CCU and if normal discharge the patient with advice for further follow up
  • 26. HOSPITAL MANAGEMENT GENEREL MANAGEMENT:  absolute bed rest Continuous monitoring of heart rate, rhythm and blood pressure High flow oxygen inhalation Sublingual GTN I/V channel for medication Relieve of pain by morphine or pethidine I/V with prochloroperazine or promethazine Aspirin 300mg to be chewed and clopidogrel 300 mg orally (if not given earlier)
  • 27. Contd. Management of ST MI:/ Non ST MI:  restoration of coronary blood flow: Thrombolytic therapy (streptokinase if patient comes with in 12 hours of attack) Primary PCI if available Anti ischemic therapy: Nitrates, beta blocker Calcium antagonist ACEI , ARB Anti platelet therapy: Aspirin and clopidogrel, GP IIb/IIIa inhibitor
  • 28. Contd. Anti thrombin therapy: Heparin, LMW heparin  interventions: PTCA CABG
  • 30. MANAGEMENT OF COMPLICTAION Arrhythmia:  ventricular ectopics: adequate pain relieve and proper control of heart failure and to keep electrolytes normal.  ventricular tachycardia: Non sustained VT Sustained VT Asymptomatic patient: Hemodynamically stable patient: Management of precipitating factor I/V infusion of lignocaine and or amiodarone. Anti arrhythmic therapy may be continued for 24-48 hours Symptomatic patient: Hemodynamically stable patient: Anti arrhythmic drug (lignocaine and amiodarone) DC cardioversion.
  • 31. CONTD. ATRIAL FIBRILLATION: Ventricular rate <100 bpm, SBP >90 mmHg and there is no associated symptoms – no treatment Ventricular rate > 100 bpm associated with SBP >90 mmHG or rate related symptoms – beta blocker or amiodarone Rapid ventricular rate, SBP <90 mmHg, heart failure or impaired consciousness – immediate cardioversion.
  • 32. Contd. SINUS BRADYCARDIA SINUS TRACHYCARDIA If heart rate < 40 bpm or rate related symptoms – bolus of injection atropine 0.6 mg -1.2 mg I/V Management of precipitating factor If sinus bradycardia with symptoms persists despite repeated bolus of injection atropine (up to 3mg)- temporary pacing Beta blocker, diltiazem, verapamil
  • 33. contd. 1st degree conduction block: In both anterior and inferior MI no specific treatment other than close observation require. Mobitz type II and complete heart block: In inferior MI: asymptomatic and haemodynamically stable patient – no treatment. If ventricular rate falls < 40 bpm, pause of >3 seconds occur, SBP < 90 mmHg or rate related symptoms devlop – injection atropine 0.6 mg should be given I/V to be repeated as necessary to maximum of 3 mg. If symptomatic complete heart block persists despite – injection atropine : temporary pacing indicated In anterior MI: temporary pacing is indicated.
  • 34. Contd. Acute LVF: Propped up position High flow oxygen Nitrates I/V morphine 3mg and to be repeated on requirement Loop diuretic: I/V frusemide 40-80 mg and may be repeated on requirement Vasodilator ACE inhibitors Treat identifiable precipitating factor .
  • 35. Contd. Cardiogenic shock: Oxygenation – high flow oxygen via mask (2-4 L/min) Monitoring: ECG, BP, urine output , pulse oximetry Improving cardiac output: if SBP< 80 mmHg low dose dopamine 2.5-5 microgram/kg/min infusion, gradually may be increased up to 15 microgram/kg/min If SBP >80 mmHg dobutamine at the dose of 2.5-15 microgram/kg/min is preferred present. Treating reversible myocardial ischemia: IABP support (intra aortic balloon pump), PTCA or CABG, arrhythmia control and treat other reversible cause.
  • 36. RISK FACTOR MANAGEMENT Cessation of smoking Low fat diets Eat more vegetables, fruits and fiber containing foods Control body weight Regular walking and exercise Control of DM and HTN
  • 37. FOLLOW UP MANAGEMENT Drug: Individualized on the choice of concerned cardiologists and patient need. aspirin, beta blocker, trimetazidine, ACEI,ARB, calcium channel blocker, nitrate, clopidogrel and lipid lowering agents Assessment of the patient: Echocardiography ETT Radionuclide study Coronary angiogram
  • 38. MOBILIZATION AND REHABILITATION After acute MI in uncomplicated cases : Sit on chair in day 2 Walk to toilet day 2 Return home on day 5 to day 7 Gradually increasing activity and returning to normal work in 4 to 6 weeks Counselling and reassurance In complicated case: It depends on individual patient conditions and decision of concerned cardiologists.
  • 39. How to measure Blood Pressure