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Cardiovascular > Myocardial Infarction > Flashcards

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
Q

changes in what leads shows an anterolateral Myocardial infraction

A

I, aVL, V1-V6

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26
Q

what is bundle branch block

A

when conducting system is effected and ventricles depolarise at different rates- broadening the QRS complex

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27
Q

what enzyme shows and MI, when does it peak and what else does it show

A

creatinine kinase, peaks in 24 hrs, also in skeletal muscle and brain

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28
Q

what protein can be used to diagnose an MI and what different types exist

A

troponin
T and I only found in cardiac muscle
C found in skeletal and cardiac muscle
I highest specificity for MI

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29
Q

how do aspirin and clopidogrel work

A

(antiplatelets) block receptor and prevent to activation and aggregation of platelets

30
Q

what are the two reperfusion therapies used for MI

A

thrombolysis (e.g streptokinase) or PCI

31
Q

what are the risks of thrombolytic therapy

A

failure to re-perfuse, haemorrhage, hypersensitivity

32
Q

what is the early treatment of a STEMI

A

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
Q

what are the complications of a myocardial infarction

A

death, arrhythmic complications, structural complications, functional complications

34
Q

what do structural complications include

A 
cardiac rupture (blood in chambers), ventricular septal defect, 
mitral valve regurgitation,
LV aneurysm,
mural thrombus +/- systemic emboli,
inflammation,
acute pericarditis,
dressler's syndrome
35
Q

what is dresslers syndrome

A

form of pericarditis- an immune system response after damage to heart tissue or to the pericardium, from events such as a heart attack,

36
Q

what are the functional complications of an MI

A

ventricular dysfunction;

  • acute V failure (left, right and both)
  • chronic cardiac failure
  • cardiogenic shock
37
Q

what is cardiac depression a sign of

A

cardiac ischaemia

38
Q

what causes a NSTEMI

A

when artery severely narrowed but not completely occluded

39
Q

blocking of what is effective in inhibiting the coagulation cascade and why

A

factor 10 as in both intrinsic and extrinsic coagulation cascades (e.g. heparin)

40
Q

what do stent patients need

A

dual antiplatelet therapy

41
Q

what is the final common pathway to platelet aggregation

A

group IIb-IIIa protein

42
Q

can an ECG be normal in an NSTEMI

A

YES

43
Q

why is troponin no longer the definitive test for MI

A

as can be raised in a number of other conditions e.g. CCF, renal failur, sepsis, PE, stroke/TIA, pericarditis/ myocarditis,
post arrhythmia

44
Q

what is the pre hospital treatment for an acute MI

A 
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
Q

what tests should be done in hospital for an acute MI

A

ECG, blood test, pulse oxymetry, cardiac monitor, IV line put in, troponins every six hours

46
Q

what is ticagrelor

A

anti platelet

47
Q

which troponins are cardiac

A

I and T

48
Q

what drugs can be prescribed as secondary prevention after an MI

A

statins, beta blockers, aspirin, ACE inhibitors, GTN, clopidegrol/ ticagrelor if stent fitted

49
Q

what are the QRS complexes like in V fib

A

wide

50
Q

what can saline solution be used to treat

A

low BP

51
Q

what is chest expansion like in a pneumothorax

A

low/ unequal

52
Q

how is a pneumothorax treated

A

drain

53
Q

what are the differential diagnosis of acute chest pain

A 
Acute Coronary Syndrome
Aortic Dissection
Pulmonary Embolus
Pneumothorax
Myocarditis
Pericarditis
Oesophagitis
Pancreatitis
Cholecystitis
Biliary Colic
Perforated Viscus
Herpes Zoster
54
Q

what are the ECG changes in an MI

A

ST elevation, T wave inversion, Q waves

MAY BE NORMAL

55
Q

when does the enzyme CK peak in an MI

A

in 24 hours,also in skeletal and brain so not specific

56
Q

when does troponin start to rise

A

within 4-6 hours

57
Q

what is a cardiac specific form of CK

A

isoenzyme CKMB

58
Q

what are the indications for reperfusion therapy

A
  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
Q

what are the contraindications to thrombolytic agents

A 
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
Q

name three types of SVT

A

sinus tachycardia, atrial flutter, atrial fibrillation

61
Q

what are the two types of macrophages involved in myocyte necrosis

A

type 1 eat cells

type 2 repairs, build scar fibrosis

62
Q

when should beta blockers be used in STEMI

A

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
Q

what is fondaparinux

A

anti coagulant

64
Q

what should be given to patient who cant undergo PCI

A

fibrinolytic therapy within 30 mins

65
Q

should you use thrombolysis is NSTEMI

A

no

66
Q

what are the side effects of beta blockers

A

bradycardia, cardiac failure, bronchospasm in asthma & chronic bronchitis, hypotension

67
Q

how is ischaemic VT treated

A

DCCV, cath lab (if needed), electrolyte correction, amiodarone, lidocaine, B-Blockers

68
Q

what is amiodarone

A

potassium channel blocker, class III anti-arrhythmic

69
Q

what is lasix

A

furosemide- diuretic

70
Q

what are IV inotropic agents

A

dobutamine/ dopamine

71
Q

what is a normal ejection fraction

A

more than 50%

72
Q

when should an aldosterone antagonist be used after an MI

A

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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