Management of Acute Myocardial Infarction Flashcards Preview

Cardiology (Phase 3) > Management of Acute Myocardial Infarction > Flashcards

Flashcards in Management of Acute Myocardial Infarction Deck (11):

What is the pathophysiology of CAD?

- Endothelial dysfunction (damage, usually as a result of smoking and high LDL, activates endothelial cells, upregulating inflammatory adhesion molecules and promoting monocyte and platelet adhesion, also increases permeabiloty to lipids allowing their accumulation in the intima)

- Formation of a fatty streak (monocytes adhere to endothelium, migrate into intima and differentiate into macrophages, local oxidation of LDL attracts macrophages and once in the intima they become foam cells, platelets also adhere and cause endothelial cells and macrophages to release PDGF causing smooth muscle cell migration from the media to the intima)

- Development of a lipid plaque (smooth muscle proliferation and increased ECM occur in the intima, cytokines and GFs promote more infiltration)

- Advanced plaques (consists of a lipid rich core and a fibrois cap, cors is free lipid/macrophages/smooth muscle/cellular debris, cap is collagen)


What is the pathophysiology of ACS?

- Most common cause is rupture of atherosclerotic plaques leading to exposure of subendothelial matrix elements (i.e. collagen) stimulating platelet activation and thrombus formation

- Release of tissue factor directly activates the coagulation cascade and promotes formation of fibrin

- Arterial inflammation may stimulate plaque rupture

- NSTEMI can also be caused by vascspasm, narrowing from stenosis, inflammatory mechanisms and extrinsic factors leading to poor coronary perfusion


What are the signs and symptoms of CAD?

- Chest pain

- Back pain

- Jaw pain

- Indigestion

- Sweatiness/clamminess


- Death

- Tachycardia

- Distress

- HF

- Shock

- Arrhythmia


What are the different types of MI?

- 1) Spontaneous MI due to ACS

- 2) Increased O2 demand of decreased O2 supply (HF, sepsis, anaemia, arrhythmias, HTN, hypotension)

- 3) Sudden cardiac death

- 4a) Associated with PCO

- 4b) MI stent thrombosis

- 5) Associated with CABG


How is MI diagnosed?

A image thumb

What are the non-coronary causes of elevated troponin?

- Congestive HF

- Tachyarrhythmias

- Pulmonary embolism

- Sepsis

- Apical ballooning syndrome

- Renal failure


Which vessels cause which types of MI?

- RCA or LCx causes inferior

- Cx or RCA causes posterior

- LCx causes lateral

- LAD causes anteroseptal


How is STEMI treated?

- If shock thenPPCI

- If no shock and <90mins then PPCI

- If no shock and >90mins then thrombolysis (rescue PCI is no reperfusion)


What are the complications of MI?

- Arrhythmias

- Heart failure

- Cardiogenic shock

- Myocardial rupture

- Psychological


What is the immediate management following MI? (ACUMA)


- Aspirin

- Clopidogrel (600mg for PPCI, 300mg for thrombolysis)

- Unfractionated heparin

- Morphine

- Anti-emetics


What is used for secondar prevention of MI? (COBRA-A)

- Clopidogrel (antiplatelet)

- Omacar (Omega 3)

- Bisoprolol (BB)

- Ramipril (ACE-I)

- Aspirin (antiplatelet)

- Atorvastatin (statin)