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Myocardial Infarction Flashcards

1
Q

what is demand led ischaemia and in what type of angina is it found

A

when fixed stenosis causing ischaemia during exertion. in chronic stable angina

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2
Q

how is cardiac chest pain characterised

A

heavy, pressure, tightness, gripping, squeezing, crushing

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3
Q

what is an acute coronary syndrome

A

any acute presentation of coronary artery disease

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4
Q

what conditions can cause acute coronary syndrome

A

unstable angina, NSTEMI, STEMI, cardiac death

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5
Q

what is the pathogenesis of acute coronary syndromes

A

normal- endothelial injury- fatty streak- atherosclerotic plaque- fibrous plaque- plaque rupture/fissure and thrombosis

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6
Q

what affects the chances of a spontaneous plaque rupture/ fissure

A

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

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7
Q

what causes unstable angina and what type of ischaemia does it exhibit

A

dynamic stenosis

supply led ischaemia (due to subtotal or complete occlusion)

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8
Q

what initiates the platelet cascade

A

vascular damage exposes tissue elements (subendothelial collagen, von willebrand factor) to circulating blood

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9
Q

what does the exposition of tissue factors to the circulating blood cause

A

platelet recruitment anf adhesion at the site of injury forming a monolayer

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10
Q

what does the adhesion of platelets lead to

A

activation of platelets which leads to the release of activators (ADP and thromboxane A2) via degranulation

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11
Q

how is thromboxane A2 generated

A

via the enzyme system cycloxygenase

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12
Q

what do the activators released by activated platelets bind to

A

surface receptors of circulating platelets activating them, amplifying platelet activation and resulting in platelet aggregation

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13
Q

what does the amplification of platelet activation lead to and how

A

triggers the inflammatory cascade- activated platelets express adhesion receptors for leukocytes = platelet-leukocyte conjugates

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14
Q

how does a previous MI lead to heart failure

A

as scarred tissue doesn’t pump properly

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15
Q

what does ST elevation show

A

infarction- muscle artery is blocked and muscle is dying

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16
Q

what is the one condition that has a worse prognosis than an acute MI

A

lung cancer

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17
Q

what are the associated symptoms of an MI

A

sweating, nausea and often vomiting

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18
Q

what mimics cardiac chest pain

A

pneumothorax, bronchopneumonia, muscular skeletal, heart burn

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19
Q

what ECG changes are often seen in an acute STEMI

A

ST elevation, T wave inversion, Q waves

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20
Q

when in an MI does Q wave formation and T wave inversion happen

A

within the first day

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21
Q

what is the sign of an ‘old’ MI

A

Q waves +/- inverted T waves

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22
Q

changes in what leads shows an inferior Myocardial infraction

A

II, III, AVF

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23
Q

changes in what leads shows an anterior Myocardial infraction

A

V1-V6

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24
Q

changes in what leads shows an anteroseptal Myocardial infraction

A

V1-V4

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25
changes in what leads shows an anterolateral Myocardial infraction
I, aVL, V1-V6
26
what is bundle branch block
when conducting system is effected and ventricles depolarise at different rates- broadening the QRS complex
27
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
28
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
29
how do aspirin and clopidogrel work
(antiplatelets) block receptor and prevent to activation and aggregation of platelets
30
what are the two reperfusion therapies used for MI
thrombolysis (e.g streptokinase) or PCI
31
what are the risks of thrombolytic therapy
failure to re-perfuse, haemorrhage, hypersensitivity
32
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
33
what are the complications of a myocardial infarction
death, arrhythmic complications, structural complications, functional complications
34
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 ```
35
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,
36
what are the functional complications of an MI
ventricular dysfunction; - acute V failure (left, right and both) - chronic cardiac failure - cardiogenic shock
37
what is cardiac depression a sign of
cardiac ischaemia
38
what causes a NSTEMI
when artery severely narrowed but not completely occluded
39
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)
40
what do stent patients need
dual antiplatelet therapy
41
what is the final common pathway to platelet aggregation
group IIb-IIIa protein
42
can an ECG be normal in an NSTEMI
YES
43
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
44
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
45
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
46
what is ticagrelor
anti platelet
47
which troponins are cardiac
I and T
48
what drugs can be prescribed as secondary prevention after an MI
statins, beta blockers, aspirin, ACE inhibitors, GTN, clopidegrol/ ticagrelor if stent fitted
49
what are the QRS complexes like in V fib
wide
50
what can saline solution be used to treat
low BP
51
what is chest expansion like in a pneumothorax
low/ unequal
52
how is a pneumothorax treated
drain
53
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 ```
54
what are the ECG changes in an MI
ST elevation, T wave inversion, Q waves MAY BE NORMAL
55
when does the enzyme CK peak in an MI
in 24 hours,also in skeletal and brain so not specific
56
when does troponin start to rise
within 4-6 hours
57
what is a cardiac specific form of CK
isoenzyme CKMB
58
what are the indications for reperfusion therapy
1. Chest pain suggestive of acute myocardial infarction - more than 20 minutes, less than 12 hours 2. ECG - acute ST elevation or new Left Bundle Branch Block 3. No contraindications
59
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 ```
60
name three types of SVT
sinus tachycardia, atrial flutter, atrial fibrillation
61
what are the two types of macrophages involved in myocyte necrosis
type 1 eat cells | type 2 repairs, build scar fibrosis
62
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
63
what is fondaparinux
anti coagulant
64
what should be given to patient who cant undergo PCI
fibrinolytic therapy within 30 mins
65
should you use thrombolysis is NSTEMI
no
66
what are the side effects of beta blockers
bradycardia, cardiac failure, bronchospasm in asthma & chronic bronchitis, hypotension
67
how is ischaemic VT treated
DCCV, cath lab (if needed), electrolyte correction, amiodarone, lidocaine, B-Blockers
68
what is amiodarone
potassium channel blocker, class III anti-arrhythmic
69
what is lasix
furosemide- diuretic
70
what are IV inotropic agents
dobutamine/ dopamine
71
what is a normal ejection fraction
more than 50%
72
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.

Cardiovascular (34 decks)

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