ALS Lecture 9 - The Cardiac Consequences of Atheroma DONE Flashcards
what is the most serious thing caused by atheroma? (2)
ventricular fibrillation, sudden death
what percentage of patients who have an MI die before they get to hospital?
50%
look at the graphs on cardiovascular disease (A)
done
atheroma
nodular accumulation of degenerative material in the tunica intima of artery wall
what do atheromas consist of? (4)
macrophages, lipids, calcium, fibrous connective tissue
modifiable risk factors for developing heart disease (7)
smoking, diet, obesity, lipids, hypertension, stress, lack of exercise
non-modifiable risk factors for developing heart disease (4)
fh, age, gender, ethnicity
spectrum of coronary disease (1-5)
- asymptomatic
- unstable angina
- acute coronary syndrome
- heart failure
- sudden death
give the 5 steps of atherosclerosis development
- fatty streak forms
- fibrous cap forms over fat deposits
- inside cap becomes necrotic
- fibrous cap ruptures
- thrombus formation leads to arterial occlusion
label the diagram of sequences in progression of atherosclerosis (B)
done
common sites of atheromas (5)
aorta (especially abdominal), coronary, carotid, cerebral, leg arteries
look at the pictures of plaque rupture/fibrous tissue (C)
done
myocardial infarction (MI) occurs when
blood flow stops to part of heart, so lack of oxygen and muscle death
2 types of MI
full thickness (transmural), partial thickness (subendocardial)
full thickness MI involves the
entire thickness of LV wall
example of blocked artery that would cause a full thickness MI
left anterior descending (LAD) artery that supplies left heart
partial thickness MI involves
multi-focal necrosis of inner 1/3 to 1/2 of LV wall
partial thickness MI are caused by blocks of
smaller arteries
other 2 classifications of MI
STEMI, NSTEMI
MI causes (3)
occlusive intracoronary thrombus, vasospasm, emboli
MI pathophysiology steps (5)
- thrombus over atheroma blocks blood flow
- lack of O2 to myocytes
- adrenaline in blood so heart beats faster
- myocytes stop, rest of heart works harder
- myocyte walls break down, leak troponin
label the diagram of a normal 12 lead ECG (C)
done
with acute coronary syndromes, what are we interested in on ECG? (2)
ST elevation, deviation from isometric line
label the diagram of STEMI ECG (D)
done
label the diagram of the coronary arteries (E)
done
right coronary artery arises from
anterior aortic sinus
right coronary artery supplies (2)
RV, inferior wall
left coronary artery arises from
aortic sinus
left coronary artery supplies
LAD ventricle walls, left circumflex LV and LA
if the infarction is in the inferior wall, i.e. right coronary artery the ECG changes will be in leads (3)
II, III, aVF
if the infarction is in the anterior wall, i.e. LAD artery, the ECG changes will be (2)
ST elevation, V1-V6
if the infarction is in the lateral wall, i.e. left circumflex artery the ECG changes will be in leads (3)
V5, V6, aVL
look at the diagrams that show where different wall infarctions will show in the ECF (F)
done
label the leads on the chest diagram (G)
done
look at the diagrams and explanations of the different types of MI (H)
done
drug treatments for MI (4)
anti-platelets, LMWH, statin, anti-ischaemic
anti-platelets used in MI
aspirin + one of clopidogrel, ticagrelor, prasugrel
why do we give anti-platelets in MI?
reduce risk of thrombus growing
why do we give LMWH in MI?
targets thrombus
why do we give statins in MI? (2)
reduce cholesterol, stabilise plaque
anti-ischaemics used in MI
beta-blockers, nitrates
why are beta-blockers (anti-ischaemics) used in MI??
decrease heart rate and stress on plaque
in STEMI we may also treat using (2)
PCI, thrombolysis
marker we use in MI
troponin
how sensitive is troponin?
sensitive to myocardium damage
how specific is troponin?
not specific for MI
why else could troponin be raised? (6)
PE, pulmonary hypertension, septicaemia, subarachnoid haemorrhage, AF, aortic stenosis
to diagnose an MI there must be what in troponin? (2)
20% rise or fall, few hours apart
troponin physiology (6 steps)
- attached to tropomyosin
- when muscle cell stimulated, calcium attaches to troponin
- troponin causes tropomyosin to move from binding site
- exposes myosin binding sites on actin filaments
- myosin binds to actin
- cross-bridge formation and muscle contraction
label the diagrams of actin and myosin (I)
done
myocardial wall rupture
damaged myocardium next to healthy, contracting myocardium can rupture
myocardial wall rupture prognosis
unsurvivable
myocardial rupture of inter-ventricular septum diagram (J)
done
myocardial rupture develops at the margin of the
necrotic and non-necrotic myocardium (hinge point)
myocardial rupture of the interventricular septum causes
left to right shunting
myocardial rupture of interventricular septum prognosis
very bad, ~100% mortality
the papillary muscles hold the
2 cusps of mitral valve
posteromedial papillary muscle is supplied by
posterior descending artery
anterolateral papillary muscle is supplied by
LAD, LCx
which papillary muscles ruptures more frequently?
posteromedial
presentation of ruptured papillary muscle (3)
acute hypotension, pulmonary oedema, holosystolic murmur
left venrticular dysfunction (2)
long term problem with LV, acute/chronic heart failure
left ventricular dysfunction symptoms (4)
SOB, peripheral oedema, orthopnoea, PND
fill in the table of new york heart classification classes (K)
done
left ventricular aneurysm
infarction of inferior cardiac wall, not ruptured but aneurysm formed
cardiac arrest
sudden stop in effective blood flow due to failure of heart to contract
treatment for cardiac arrest (3)
AICD, bradycardia, ventricular tachycardia
stable angina pain character (2)
central, tight
stable angina radiation (3)
arm, jaw, teeth
stable angina aggravating factors (1)
exercise
stable angina relieving factors (2)
rest, nitrates
stress testing (3)
exercise ECG, stress ECHO, myocardial perfusion scan
exercise ECG at rest in stable angina
normal
exercise ECG with exercise in stable angina
depression of ST segment below isoelectric line
stress ECHO (2 steps)
- patient exercises whilst having US of heart
2. if function worsens may be issue with circulation
myocardial perfusion scan (3 steps)
- myocardium takes up radioactive tracer
- at rest lots of uptake
- on exercise there are gaps in orange
aucte coronary syndrome is caused by (3)
STEMI, NSTEMI, unstable angina
STEMI (2)
ST elevation MI, completely occluded vessel
STEMI treatment (2)
clot busting drug, PCI
NSTEMI (2)
no ST elevation, partial occlusion
fill in the flow chart of acute chest pain (L)
done
