Definition, causes, pathophysiology, clinical presentation and collaborative care

1. Myocardial Infarction /MI
Prepared by
Mrs. Safoora
Qureshi
CON, PIMS

2. Myocardial Infarction/ MI
• MI or Heart Attack is the
irreversible damage of
myocardial tissue cased by
prolonged ischemia &
hypoxia
• MI, occurs as result of sustained
ischemia, irreversible myocardial
cells death (necrosis)
• MI is a disease condition
caused by reduced blood
flow to the heart muscles
due to atherosclerosis &
occlusion of a coronary
artery by an embolism or
thrombosis

3. Causes
95% of heart attacks occurs due blockage of one of the
major vessels supplying blood to heart
• Atherosclerosis and rupture plaque, is the most common cause
Other 5% contributing factors are:
• Spasm of the artery
• Trauma
• Rare medical conditions
• Electrolyte imbalances such as
• hyperkalemia or hypokalemia
• Obstruction, from elsewhere in the body
• Eating disorders

4. Pathophysiology
• 80 to 90% of all acute MIs are secondary to thrombus formation
• Perfusion to the myocardium distal to the occlusion is halted, result in
necrosis
• Contractile function of the heart stops in necrotic area(s)
• The degree of altered function depend on the area
of the heart involved and the size of infarction
• The location of MI correlates with the
involve coronary artery such as:
• Inferior wall MI result from occlusion of right coronary artery
• Anterior wall MI, result from occlusions in the left anterior descending artery
• Lateral or posterior MIs, result from occlusion of circumflex artery

5. Atherosclerosis Spasm
Atherosclerosis + Plaque
split + thrombosis
Gradual
obstruction
Sudden reversible
obstruction
Sudden Occlusion,
usually irreversible
Hypoxia
Ischemia
Coronary thrombosis
Necrosis
Angina
Unstable angina
MI
Myocardial infarction Pathophysiology

6. Types of MI
1. ST segment Elevation MI
(STEMI)
2. Non-ST segment Elevation MI
(NSTEMI)
3. Coronary Spasm or
unstable Angina

7. Clinical Manifestation
Pain
• Severe, immobilizing chest pain
not relieve by position change, or
nitrate admin, is the hallmark of
an MI
• Persistent and unlike other pain
• Describe; as a heaviness, pressure,
tightness, burning, constriction or
crushing
• Location; Substernal, retrosternal, or
epigastric area
• Radiate to: the neck, jaw, arms, or
to the back
• Occurs; while the patient is active,
at rest, or asleep or awake
• Time; commonly occurs in
morning
• No pain / Silent MI:
in some pts of DM & cardiac
neuropathy
Other Symptoms
• shortness of breath
• sweating
• nausea, vomiting,
• abnormal heart beating,
• anxiety, fatigue,
• weakness,
• stress, depression

8. Complications:
Dysrhythmias:
• The most common complication, in 80 % of MI pts, is the most common cause of
death in prehospital patients
Heart Failure
• Occurs when pumping power of the heart has diminished.
Papillary Muscles dysfunction:
• Occurs when infarcted are includes or is adjacent to the papillary muscles that
attached to the mitral valve
Ventricular aneurysm: infarcted myocardium become thickened and bulged out
during contraction
Pericarditis: reduce ventricular filling and emptying and cause HF
Dressler Syndrome: pericarditis with pericardial effusion and fever as a result of
antibody-antigen reaction to necrotic myocardium
Cardiogenic Shock:
• Occurs when inadequate oxygen and nutrients are supplied to the tissues in sever
left ventricular failure

9. Diagnosis
Unstable Angina and MI
• History and physical assessment
• ECG: is the primary tool to rule out or confirm, UA or MI
• Changes in QRS complex , ST segment and T wave caused by ischemia and
infarction can develop quickly in both UA and MI
• UA or NSTEMI: tend to have transient thrombosis or partial occlusion
• STEMI: tend to have a more extensive MI, associated with prolonged and
complete coronary occlusion and development of pathological Q wave on
ECG
• Serum Cardiac Markers: are released into the blood in large quantities
from necrotic heart muscles
• Cardio Angiography (PCI): to evaluate the extent of the disease and to
determine the most appropriate therapeutic modality

10. ST segment & Q Wave Changes In MI

12. ENZYMES INITIAL RISE PEAK BACK TO
NORMAL
Myoglobulin < 2 hrs. 6 – 9 hrs. 1 day
CK - MB 3 --- 6 hrs. 12 --- 24 hrs. 2 – 3 days
Troponin I < 4 hrs. 14 – 24 hrs. 3 – 5 days
CARDIAC MARKERS

13. Collaborative Care
Emergency Treatment
• Strict bed rest
• 12- leads, continue ECG monitoring
• Maintain IV line
• Oxygen therapy via Nasal cath at rate
2 to 4 L/min
• Drugs:
• Nitroglycerin IV
• Morphine sulfate IV
• Aspirin
• Heparin
• Beta-Blockers
• AC inhibitors
• Monitor oxygen saturation, and vital
signs

14. stable Angina
Non- ST- segment-Elevation MI
• Acute intensive drug therapy
• Nitroglycerin S/L
• Low-molecular-weight Heparin
• Clopidogrel / anti-platelets medicine
• Glycoprotein IIb/IIIa inhibitors
• Coronary Angiography
• Percutaneous coronary Intervention PCI

15. Unstable Angina
 Immediate reperfusion therapy
• PCI is the first line treatment
within 90 /mins of MI
• Fibrinolytic therapy to dissolve clots
• Streptokinase
• urokinase
• Recombinant Human tissue- type plasminogen
• Anisoylated plasminogen-streptokinase
activator complex
• Emergency CABG