Angina, ACS and MI Flashcards
what is the main difference between stable and unstable angina?
stable predictable, comes on during exercise and relieved by rest
unstable can come on at any point (including rest) and can’t always be relieved by rest
what are the conditions that make up acute coronary syndromes?
unstable angina
NSTEMI
STEMI
what are some of the causes of acute coronary syndromes?
atherosclerosis vasospasm cocaine emboli coronary dissection coronary vasculitis
what investigations should be done to diagnose an ACD?
HR, BP
ECG
blood test for markers (troponin, CK)
chest xray
if troponin levels are elevated if a patient presents with chest pain, what can that be a sign of?
STEMI
NSTEMI
if troponin levels are not elevated if a patient presents with chest pain, what can that be a sign of?
unstable angina
stable angina
non-cardiac reasons
what other conditions could show elevated troponin levels?
pulmonary embolism
sepsis
kidney failure
subarachnoid hemorrage
where on an ECG would a lateral MI show abnormalities?
SLL1
aVF
might involve the Cx
where on an ECG would an inferior MI show abnormalities, and which vessel would it normally involve?
aVF
SLL2
SLL3
might involve the RCA
where on an ECG would an anterior MI show abnormalities, and which vessel would normally be involved?
V1-V4
might involve the LAD
what is the pharmacological treatment management for ACS?
morphine (pain relief) oxygen if sats low nitrates IV aspirin \+ clopidogrel/ticagrelor/prasugrel fondaparinux/heparin beta blockers (when pt stable) statins ACEIs
what are more invasive treatment options for ACS/MI?
PCI
CABG
what is the main protocol for treating a STEMI?
PCI within two hours of event
if no PCI facility available (fast enough), thrombolysis
what are the thrombolysis options for MI and their characteristics?
tenecteplase, alteplase: fibrin-specific
streptokinase: older drug, not fibrin-specific
what is the mechanism of action of aspirin?
it stops production of Thromboxane A2 at the beginning of the platelet activation process
what is the mechanism of action of clopidogrel, and what are its pharmacological properties?
prodrug - activated in liver
it stops the ADP receptor, which in turn acts on the GP IIb/IIIa receptor
what is the difference between clopidogrel and ticagrelor?
clopidogrel is a pro-drug, some patients don’t metabolise it
ticagrelor is not a prodrug
what are some signs/symptoms of ACS/MI?
variable, especially with NSTEMI crushing chest pain/discomfort pain may radiate to neck/arms cold/clammy/sweaty SoB nausea/vomiting collapse
which layers of the heart muscle are affected in NSTEMI and STEMI?
NSTEMI - endocardial layer = mural/endocardial MI
STEMI - all three layers = transmural MI
what are the possible changes on an ECG during and after a STEMI?
ST elevation
hyperacute T waves
Q waves after a few days (dead tissue)
what are the possible changes on an ECG during and after a NSTEMI?
ST depression
inverted T wave
normally no Q waves
how can a posterior MI be diagnosed?
by putting V leads on the patient’s back in opposite places as V1/V2
what is used to support the diagnosis of an MI?
biomarker presence (CK, troponin) + ECG changes, symptoms, autopsy changes, other imaging evidence of cardiac damage
what is the pathological difference between an NSTEMI and a STEMI?
STEMI - complete occlusion of a vessel
NSTEMI - severe narrowing but not complete obstruction of vessel
what are some of the risks associated with PCI?
coronary artery damage/perforation
MI/stroke
bleeding
kidney damage from contrast
what is used for imaging during PCI?
radiography (XR) with contrast
what are possible complications following an MI?
arrythmias mechanical damage (tears in myocardium, papillary muscle snapping, pericardial tamponade)
why should patients be left on dual antiplatelet therapy for a while after a PCI?
because stopping them before the stent is covered in endothelium may cause clotting/risk of further MI/stroke
what are disadvantages of giving dual antiplatelet therapy?
high risk of bleeding
what are some contraindications to thrombolysis?
recent bleeding/menstrual bleeding
recent brain damage (structural, ischemic stroke, haemorrage,)
suspected aortic dissection
what are the benefits and disadvantages of prasugrel compared to clopidogrel?
prasugrel works faster on ADP receptor
prasugrel doesn’t need to be metabolised for activation
prasugrel has higher incidence of bleeding
what is the difference in administration between low molecular weight heparin and unfractionated heparin?
LMWH is administered subcutaneously
UFH is administered intravenously
what are some types of low molecular weight heparin?
tinzaparin
deltaparin
fondaparinux
what is the main symptom of stable angina?
chest pain on exertion
what can be some symptoms of stable angina in absence of chest pain, and who might have them?
SoB/fatigue/syncope or presyncope on exertion
diabetics - they may not feel pain as much (diabetic neuropathy)
what is the most common physiological cause of stable angina?
mismatch in O2 supply/demand because of narrowed coronary artery
what are less common physiological causes of stable angina?
pathological increase in O2 demand
reduced O2 distribution (anemia)
what are the main investigations done to diagnose stable angina?
Blood test (FBC, U&E, glucose, biochemistry)
ECG
CXR
ETT (stress test)
Myocardial perfusion imaging
if the above inconclusive: CT coronary angiogram
what are possible signs of stable angina?
tar staining (smoking)
xanthalasma and corneal arcus (high cholesterol)
obesity
retinopathy (diabetic or hypertensive)
crackles, raised JVP, possible murmur (heart failure)
pallor (anemic)
what are the non-pharmacological treatment options for stable angina?
manage underlying cause
smoking cessation, weight management
what is the main aim of pharmacological treatment for stable angina?
aimed at controlling risk factors
reduction of symptoms
improve survival
what are the pharmaceutical treatment options for stable angina?
morphine, oxygen, nitrates, aspirin/clopidogrel beta blockers ivabradine (funny ion channel inhibitors) nicorandil (K+ channel activators) ranolazine (late Na+ channel blocker) statins CCBs ACEIs
what invasive treatment options are available for stable angina, when are they carried out and what is their purpose?
PCI and CABG
if investigations show severe stenosis
PCI - symptom relief
CABG - better prognostic but higher risks in procedure
what should be the first line pharmaceutical therapy in stable angina?
GTN
beta blockers/CCB
what should be the second line pharmaceutical therapy in stable angina?
ivabradine ranolazine nicorandil long acting nitrates trimetazidine
what should be the first line medical and non-medical prevention therapy in stable angina?
- lifestyle advice, smoking cessation, weight loss
- aspirin/clopidogrel
statins
ACEIs/ARB
why should nifedipine never be given immediate release?
because it may precipitate MI/heart failure
what are the mechanisms of action of nicorandil?
K channel opening
some nitrate effect (vasodilation)
what is the mechanism of action of ranozaline?
closes late Na+ channels
what are some contraindications for beta blockers?
asthma
peripheral vascular disease
sometimes heart failure
bradychardia/heart block
what are some side effects of beta blockers?
fatigue
depression
lethargy
bradychardia
what are possible side effects of nitrates and vasodilating CCBs?
headache flushing dizzyness hypotension syncope (GTN syncope)
what are the two main side effects of GTN and isosorbide mono/dinitrate?
headache!
hypotension (GTN syncope)
which angina medication has side effects which can mimic Crohn’s disease?
nicorandil
what is the lowest heart rate someone can have to be “safely” put on beta blockers?
60bpm
which angina medications can interact with macrolide antibiotics?
ivabradine
ranolazine
with what types of medication is drug-drug interaction of ivabradine important?
macrolides (eg clarythromycin)
antifungals
antivirals (HIV)
