Acute & Chronic Coronary Syndromes Flashcards
(39 cards)
What is ischaemia?
the restriction of blood flow to the coronary arteries
what percentage of the lumen has to be occluded to be symptomatic?
50% of the diameter; 75% of the cross-sectional area
components of a plaque
soft lipid core and fibrous cap
components of the lipid core
LDL and cholesterol
what are foam cells?
macrophages that have eaten up too much cholesterol and lipid to toxic amounts
how is a thrombus formed?
- platelet aggregation which starts through singular fibrin links and the formation of a white thrombus
- this breaks off due to the bursting of the foam cells and release of proteases from the cells, the thrombus then occludes small arterioles
characteristics of an NSTEMI
- rise in troponin
- ST depression
- chest pain
treatment for angina
- antiplatelets eg aspirin/clopidogrel
- anticoagulants eg LMWH
white vs red thrombi
- red thrombi have a tighter, more organised fibrin matrix which traps red cells in it; can occlude the whole lumen
- white thrombi are not capable of blocking the whole lumen; can trap platelets in it
characteristics of a STEMI
- ST elevation
- relatively higher troponin rises
treatment for STEMIs
- fibrinolytic eg alteplase
- angioplasty
stable vs unstable angina
- stable: simple mismatch of supply and demand; consistent symptoms in intensity
- unstable: the unpredictable intensity of symptoms
symptoms of angina
chest pain, shortness of breath, sweating, fatigue, belching, nausea and vomiting
describe the chest pain
retrosternal, diffuse, discomfort-type, radiates to the jaw, neck, shoulder and arm
haemodynamic symptoms of angina
hypotension, low cardiac output, shock, pulmonary congestion, pulmonary oedema, heart failure
cause of death in angina
arrhythmias secondary to the ischaemia
questions to ask when administering antithrombolytics
- are you on thrombolytics already?
- do you have: bleeding PR, bleeding tumour, haematuria
- recent surgeries?
- recent strokes?
- have you used anticoagulants?
contraindications of beta-blockers
- obstructive pulmonary diseases eg asthma, COPD
- heart failure
short-term complications of a myocardial infarction
- arrhythmia
- ventricular rupture
- mitral regurgitation due to papillary muscle rupture
- pulmonary oedema
- low cardiac output
- heart failure
- pain (managed by opiates or heroin)
- acquired septal defect (septal rupture)
- ventricular aneurysm
long-term complications of a myocardial infarction
- arrhythmia due to the fibrosis (treat as a potential VT0
- Dressler’s (autoimmune pericarditis)
treatment of MI
- antiplatelets
- anticoagulants
- ACE inhibitors
- beta blockers
- statins
- manage pre-existing comorbidities
- lifestyle changes
follow-up of MI
- reinforce lifestyle changes
- monitor heart rhythm, BP, glucose, lipids to keep the other comorbidities in check
ST changes in which leads?
- inferior MI (RCA territory) - II, III, avF
- anterior MI (LAD territory) - V1-V6
- lateral MI (Cx territory) - avL, I, V5, V6
differentials of a myocardial infarction
- cardiac (aortic dissection; angina; myocarditis; Prinzmetal’s)
- respiratory (pulmonary embolism; pneumothorax; pleuritic chest pain)
- gastrointestinal (oesophageal reflux; oesophageal spasm, oesophagitis; oesophageal tumour)
