Myocardial Infarction Flashcards
what is demand led ischaemia and in what type of angina is it found
when fixed stenosis causing ischaemia during exertion. in chronic stable angina
how is cardiac chest pain characterised
heavy, pressure, tightness, gripping, squeezing, crushing
what is an acute coronary syndrome
any acute presentation of coronary artery disease
what conditions can cause acute coronary syndrome
unstable angina, NSTEMI, STEMI, cardiac death
what is the pathogenesis of acute coronary syndromes
normal- endothelial injury- fatty streak- atherosclerotic plaque- fibrous plaque- plaque rupture/fissure and thrombosis
what affects the chances of a spontaneous plaque rupture/ fissure
lipid content of plaque,
thickness of fibrous plaque,
sudden changes in intraluminal pressure/tone,
bending or twisting if an artery during each heart contraction,
plaque shape,
mechanical injury
what causes unstable angina and what type of ischaemia does it exhibit
dynamic stenosis
supply led ischaemia (due to subtotal or complete occlusion)
what initiates the platelet cascade
vascular damage exposes tissue elements (subendothelial collagen, von willebrand factor) to circulating blood
what does the exposition of tissue factors to the circulating blood cause
platelet recruitment anf adhesion at the site of injury forming a monolayer
what does the adhesion of platelets lead to
activation of platelets which leads to the release of activators (ADP and thromboxane A2) via degranulation
how is thromboxane A2 generated
via the enzyme system cycloxygenase
what do the activators released by activated platelets bind to
surface receptors of circulating platelets activating them, amplifying platelet activation and resulting in platelet aggregation
what does the amplification of platelet activation lead to and how
triggers the inflammatory cascade- activated platelets express adhesion receptors for leukocytes = platelet-leukocyte conjugates
how does a previous MI lead to heart failure
as scarred tissue doesn’t pump properly
what does ST elevation show
infarction- muscle artery is blocked and muscle is dying
what is the one condition that has a worse prognosis than an acute MI
lung cancer
what are the associated symptoms of an MI
sweating, nausea and often vomiting
what mimics cardiac chest pain
pneumothorax, bronchopneumonia, muscular skeletal, heart burn
what ECG changes are often seen in an acute STEMI
ST elevation, T wave inversion, Q waves
when in an MI does Q wave formation and T wave inversion happen
within the first day
what is the sign of an ‘old’ MI
Q waves +/- inverted T waves
changes in what leads shows an inferior Myocardial infraction
II, III, AVF
changes in what leads shows an anterior Myocardial infraction
V1-V6
changes in what leads shows an anteroseptal Myocardial infraction
V1-V4
changes in what leads shows an anterolateral Myocardial infraction
I, aVL, V1-V6
what is bundle branch block
when conducting system is effected and ventricles depolarise at different rates- broadening the QRS complex
what enzyme shows and MI, when does it peak and what else does it show
creatinine kinase, peaks in 24 hrs, also in skeletal muscle and brain
what protein can be used to diagnose an MI and what different types exist
troponin
T and I only found in cardiac muscle
C found in skeletal and cardiac muscle
I highest specificity for MI
how do aspirin and clopidogrel work
(antiplatelets) block receptor and prevent to activation and aggregation of platelets
what are the two reperfusion therapies used for MI
thrombolysis (e.g streptokinase) or PCI
what are the risks of thrombolytic therapy
failure to re-perfuse, haemorrhage, hypersensitivity
what is the early treatment of a STEMI
Analgesia- diamorphine + antiemetic (stops vomiting) IV
Oxygen if hypoxic
aspirin 300mg chewed
GTN if BP more than 90 mmHg
ticagrelor 180mg
thrombolysis if delay more than 120 mins
what are the complications of a myocardial infarction
death, arrhythmic complications, structural complications, functional complications
what do structural complications include
cardiac rupture (blood in chambers), ventricular septal defect, mitral valve regurgitation, LV aneurysm, mural thrombus +/- systemic emboli, inflammation, acute pericarditis, dressler's syndrome
what is dresslers syndrome
form of pericarditis- an immune system response after damage to heart tissue or to the pericardium, from events such as a heart attack,
what are the functional complications of an MI
ventricular dysfunction;
- acute V failure (left, right and both)
- chronic cardiac failure
- cardiogenic shock
what is cardiac depression a sign of
cardiac ischaemia
what causes a NSTEMI
when artery severely narrowed but not completely occluded
blocking of what is effective in inhibiting the coagulation cascade and why
factor 10 as in both intrinsic and extrinsic coagulation cascades (e.g. heparin)
what do stent patients need
dual antiplatelet therapy
what is the final common pathway to platelet aggregation
group IIb-IIIa protein
can an ECG be normal in an NSTEMI
YES
why is troponin no longer the definitive test for MI
as can be raised in a number of other conditions e.g. CCF, renal failur, sepsis, PE, stroke/TIA, pericarditis/ myocarditis,
post arrhythmia
what is the pre hospital treatment for an acute MI
M-diamorphine + anti emetic IV O-oxygen if hypoxic N-GTN if BP > 90 mmHg A-aspirin 300mg chewed T-ticagrelor 180 mg
thrombolysis if delay more than 120 mins
what tests should be done in hospital for an acute MI
ECG, blood test, pulse oxymetry, cardiac monitor, IV line put in, troponins every six hours
what is ticagrelor
anti platelet
which troponins are cardiac
I and T
what drugs can be prescribed as secondary prevention after an MI
statins, beta blockers, aspirin, ACE inhibitors, GTN, clopidegrol/ ticagrelor if stent fitted
what are the QRS complexes like in V fib
wide
what can saline solution be used to treat
low BP
what is chest expansion like in a pneumothorax
low/ unequal
how is a pneumothorax treated
drain
what are the differential diagnosis of acute chest pain
Acute Coronary Syndrome Aortic Dissection Pulmonary Embolus Pneumothorax Myocarditis Pericarditis Oesophagitis Pancreatitis Cholecystitis Biliary Colic Perforated Viscus Herpes Zoster
what are the ECG changes in an MI
ST elevation, T wave inversion, Q waves
MAY BE NORMAL
when does the enzyme CK peak in an MI
in 24 hours,also in skeletal and brain so not specific
when does troponin start to rise
within 4-6 hours
what is a cardiac specific form of CK
isoenzyme CKMB
what are the indications for reperfusion therapy
- Chest pain suggestive of acute myocardial infarction - more than 20 minutes, less than 12 hours
- ECG - acute ST elevation
or new Left Bundle Branch Block - No contraindications
what are the contraindications to thrombolytic agents
Trauma/Haemorrhage Recent surgery (within 2 weeks) Recent stroke (within 6 months) Severe hypertension (>200/120 mmHg) Known active peptic ulceration Traumatic cardiopulmanory resuscitation Streptokinase more than five days or less than 2 years previously Proliferative retinopathy Oral anticoagulant therapy Cardiogenic shock
name three types of SVT
sinus tachycardia, atrial flutter, atrial fibrillation
what are the two types of macrophages involved in myocyte necrosis
type 1 eat cells
type 2 repairs, build scar fibrosis
when should beta blockers be used in STEMI
to relax heart and prevent cardiac rupture when patients have no;
signs of heart failure,
evidence of a low output state
increased risk for cardiogenic shock, or
relative contraindications to beta blockade
what is fondaparinux
anti coagulant
what should be given to patient who cant undergo PCI
fibrinolytic therapy within 30 mins
should you use thrombolysis is NSTEMI
no
what are the side effects of beta blockers
bradycardia, cardiac failure, bronchospasm in asthma & chronic bronchitis, hypotension
how is ischaemic VT treated
DCCV, cath lab (if needed), electrolyte correction, amiodarone, lidocaine, B-Blockers
what is amiodarone
potassium channel blocker, class III anti-arrhythmic
what is lasix
furosemide- diuretic
what are IV inotropic agents
dobutamine/ dopamine
what is a normal ejection fraction
more than 50%
when should an aldosterone antagonist be used after an MI
in patients with symptoms or signs of heart failure and LVSD should be offered a licensed aldosterone antagonist within 3–14 days of the acute MI.
