RED FLAGS
DIFFERENTIALS
RISK FACTORS
DEFINITION
A group of diseases where there is decreased blood flow to part of the heart, usually secondary to plaque rupture & formation of a thrombus. This can result in ischemia & later infarction to that area of the heart.
PATHOPHYSIOLOGY
Damage to endothelial wall of blood vessel –> LDL enters the tissue –> LDL oxidised by macrophages –> macrophages become foam cells –> foam cells accumulate to create fatty streaks –> causing smooth muscle proliferation = fibrinous plaques.
- Stable plaque –> stable angina- chest pain occurs when the heart is put under pressure from stimuli such as exercise or stress –> resolves when the stimulus ceases.
- Unstable plaque –> rupture –> coagulation cascade –> clot formation/thrombus –> clot dislodges & becomes thrombus –> lodges in the coronary arteries –> occlusion of vessel = unstable angina –> AMI.
MANIFESTATIONS
TREATMENT
D. R. A. B: O2. C: IV access, Aspirin, GTN. D. E. Pre-notify hospital.
Pain: Fentanyl/morphine. Other: Ondansetron, thrombolysis clot if >60min from pPCI capable hospital, or administer drugs for pPCI referral if <60 min.
1. pPCI referral: Heparin (anticoagulant). Ticagrelor (antiplatelet) or clopidogrel (antiplatelet).
2. Fibrinolysis: Enoxaparin (low molecular weight heparin – anticoagulant). Clopidogrel (antiplatelet). Tenecteplase (thrombolytic).
Secondary Survey: CVA, pain assessments.
ROLE OF PARAMEDICS
Rule out STEMI mimics, maximise perfusion to heart/decrease O2 consumption, minimise further platelet aggregation, provide pain relief and antiemetic
PHARMACOLOGY
Aspirin
An antiplatelet which blocks prostaglandin synthesis. It inhibits platelet aggregation by irreversibly inhibiting cyclo-oxygenase (COX), reducing synthesis of thromboxane A2 (inducer of platelet aggregation). This action prevents platelets from aggregating to exposed collagen fibres at the site of vascular injury.
- Side effects: epigastric pain, nausea/vomiting, gastritis, GI bleeding, NSAID-induced bronchospasm
Fentanyl
A mu (opioid) receptor agonist which reduce GABAergic neurotransmission & increase parasympathetic activity. GABA release –> hypopolarisation –> CNS depression, activation of dopaminergic pathways in CNS –> change perception/disassociation from pain + euphoria. The inhibition of nociceptive afferent neurons in the PNS impairs transmission of pain messages.
-Side effects: (Boy Does He Need Pain Relief)
GTN
Small doses relax vascular smooth muscles, causing arteriolar/vasodilatation. High doses increase blood flow to the myocardium, reducing cardiac pre-load, myocardial wall stress, coronary artery spasm, vascular resistance, & BP.
- Side effects: dizzy, hypotension, syncope, reflex tachycardia, vascular headaches.
Ondansetron
A serotonin (5-HT3) receptor antagonists which blocks the action of serotonin. Serotonin stimulates vagal & splanchnic nerve receptors that project to the medullary vomiting centre & 5-HT3 receptors in the postrema, initiating the vomiting reflex, causing nausea and vomiting.
- Side effects: headache, constipation.
DEFINITIVE CARE