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Cardiovascular > Management of CAD > Flashcards

Management of CAD Flashcards

1
Q

what is angina?

A

insufficient oxygen delivery to heart muscle leading to ischaemia

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2
Q

in 2014, CAD was the single most common cause of death, what was the percentage?

A

27%

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3
Q

how many people in the UK have CHD, what is the cost yearly for this?

A

2.3 million costing £9 billion yearly

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4
Q

in the UK, how many admissions are as a result of MI?

A

100,000

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5
Q

what is the pathology of angina?

A
  • Coronary plaque causes decrease in perfusion pressure, decrease in arterial oxygen content
  • Compensates – increase in Hr, preload, afterload, contractibility
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6
Q

describe stable angina?

A
  • Predictable – exertion, exercise, extremes of temp (vasoconstriction)
  • Relieved by rest/ nitrates
  • Long term management prevent attacks coming on and reducing risk of CAD
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7
Q

describe unstable angina?

A
  • Sudden deterioration in angina symptoms – no ECG changes, no troponin rise
  • Result of atheromatous plaque rupture
  • Lasts longer and unresponsive
  • Symptoms control prevention of progression to an MI
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8
Q

what is acute coronary syndromes?

A

spectrum of conditions such as unstable angina/ NSTEMI and STEMI

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9
Q

what is troponin?

A

protein released when cardiac muscle is damaged - not normally present in bloods

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10
Q

what is the pathophysiology in a STEMI MI?

A
  • Plaque ruptures leading to thrombosis
  • Fully occluded lumen
  • MI with irreversible necrosis of the heat can lead to long term complications
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11
Q

what is the pathophysiology in a NSTEMI MI?

A
  • partially blocked lumen eg atherosclerosis
    Myocardial necrosis is evident – risk of progressing to a STEMI
  • Symptomatic relief of ischaemia prevents further MI and death
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12
Q

name a nitrate used to treat angina and acute heart failure?

A

glycerol trinitite - GTN spray

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13
Q

what is the action of GTN spray?

A
  • Action – vasodilating improving coronary blood flow
  • Decrease after/ pre load
  • Decrease myocardial workload
  • Decrease oxygen demand
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14
Q

what are the side effects of GTN spray?

A

headache (means it working as its sublingual), hypotension, syncope (dizziness – take while sat down), facial flushing

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15
Q

what is contra-indicated with GTN spray?

A

acute circulatory failure, shock, head trauma, severe hypotension, aortic stenosis (likely to cause further syncope)

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16
Q

how many hours free of nitrate do you need a day?

A

12hrs

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17
Q

in relation to GTN spray when should an ambulance be called?

A

If no relief after 5 mins of taking spray, repeat if no relief again after 5 mins, call an ambulance

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18
Q

name some anti-platelet drugs?

A

aspirin, ticagrelor, clopidogrel, plasugrel

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19
Q

what is the action of antiplatelets?

A

reduces blood viscosity, disrupts platelet activation including inhibition of platelet agonists, adhesion or aggregation

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20
Q

when are anti-platelets used?

A

revascularisation to restore sufficient blood flow to affected vessel (reperfusion)
- Inhibit clot formation
- Support plaque stabilisation: no thrombus
- Secondary prevention of CV disease, TIA, stroke by aspirin

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21
Q

what are the side effects of antiplatelets?

A

bronchospasm, GI bleeds (blood not sticking together), GI irritation (aspirin), tinnitus

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22
Q

what are contra-indicated with anti-platelets?

A

bleeding risk, low platelet count, allergy

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23
Q

what is the normal dose of aspirin? (anti-platelet)

A

300mg loading, low dose is 75mg

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24
Q

what is the normal dose of ticagrelor? (anti-platelet)

A

180mg loading then 90mg BD

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25
Q

what is the normal dose of prasugrel? (anti-platelet)

A

60mg STAT, then 10/5mg daily while awaiting PCI

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26
Q

name some glycoprotein IIb/IIa antagonists?

A

abicicimab, eptifbratide, tiofibran

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27
Q

what is the action of glycoprotein IIa/ IIb antagonists?

A

inhibit final pathway involved in platelet aggregation
inhibits fibrogen binding

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28
Q

what is the action of glycoprotein IIa/ IIb antagonists?

A

inhibit final pathway involved in platelet aggregation
inhibits fibrogen binding

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29
Q

when is glycoprotein IIb/IIa used?

A

prevention of ischaemic cardiac complications in those undergoing PCI
- Short term prevention of MI in those with unstable angina and waiting for PCI

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30
Q

what are the side effects of glycoprotein IIb/IIa antagonists?

A

bleeding, back pain, fever, headaches, hypotension, nausea

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31
Q

what are contra-indicated with glycoprotein IIb/IIa antagonists?

A

active internal bleeding, hypertensive retinopathy, major surgery in last 2 months

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32
Q

name anticoagulants

A

heparin

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33
Q

what is the action of heparin?

A

prevents blood from clotting by suppressing synthesis or function of various clotting factors
anti-thrombotic
does not thin blood

34
Q

what are types of heparin?

A

low molecular - enoxaparin, daltaparin, tinzaparin (TED)
unfractionated - non seperated
fondaparinux - synthetic heparin

35
Q

what is the dosage of nicrorandil?

A

one tablet 10/20mg BD

36
Q

what is the action of nicrorandil?

A

nitrate like action (vasodilator), K+ channel opener - increase blood flow due to less resistance

37
Q

when is nicrorandil used?

A

prevention and long term management of angina

38
Q

what are the side effects of nicrorandil?

A

headaches, ulceration, dizziness, flushing

39
Q

what is contra-indicated of nicrorandil?

A

severe hypotension, LV failure, hypovolaemia, acute pulmonary oedema

40
Q

what is the action of ranolazine?

A

facilitates myocardial relaxation, reduces flow of Ca2+
does not affect heart rate

41
Q

when is ranolazine used?

A

as an adjunct in stable angina

42
Q

what are the side effects of nicrorandil?

A

dizziness, headache, constipation, nausea, vomiting

43
Q

what is the action of ivabradine?

A

lowers heart rate by acting on sinus node
- Decreased myocardial oxygen demands
- No effect on BP/ contraction

44
Q

when is ivabradine used?

A

treatment of angina in patients with normal sinus rhythm

45
Q

what are the side effects of ivabradine?

A

GI disturbances, nausea, constipation, diarrhoea

46
Q

what is contra-indicated in ivabradine?

A

heart rate <75, acute MI, unstable angina, unstable heart failure

47
Q

what is the action of statins?

A

stabilising plaques by HMG-CoA reductase inhibitors
block enzyme involved in cholesterol synthesis

48
Q

when are statins used?

A

primary (reduce hypercholestrolaemia/ hypertension) or secondary prevention of CV events

49
Q

what are the common side effects of statins?

A

muscle aches and pains
myopathy - rhabdomolysis - muscle tissue releases proteins and electrolytes into blood which can cause permanemt disability/ fatal
nausea, insomnia, vivid dreams

50
Q

what is contra-indicated with statins?

A

liver disease

51
Q

what is the function of reperfusion therapy?

A

to restore blood stores - posterior MI/ left bundle branch block

52
Q

what is PCI?

A

percutaneous coronary intervention - opens up blocked artery

53
Q

how does PCI work?

A

balloon/ stent in artery to open it uo
used with drug eluting stent

54
Q

what are drug eluting stents?

A

slow release medication to prevent clots around stents

55
Q

what better thrombolytics or PCI?

A

PCI -less bleeding, mortality, risk of stroke, re-infarction, infarct angina

56
Q

name some thrombolytic drugs

A

streptokinase, tenecteplase, altepase

57
Q

when do thrombolytic drugs need to be used?

A

within 6-12 hrs of first symptoms

58
Q

how do thrombolytic drugs work?

A

fibrinolytic drug activate plasminogen which turns into plasmin which then degrades the clot, breaking up thrombus

59
Q

when are thrombolytic drugs used?

A

acute MI, PE, ischaemic stroke

60
Q

what are the side effects of thrombolytics?

A

risk of cerebral bleed

61
Q

Name at least 5 absolute contra-indications of thrombolytics

A

haemorrhagic stroke/ stroke at any time. Ischaemic stroke in last 6 months, CNS damage, recent trauma/ surgery, bleed. GI bleeding in last month, known bledding disorders, aortic dissection

62
Q

what are relative contra-indications of thrombolytics?

A

TIA in last 6 mths, dementia, oral anticoagulant drugs, pregnancy within 1 week post-patrum, non compressible punctures, traumatic resuscitation, refractory hypertension, advanced liver disease, ineffective endocarditis, active peptic ulcer

63
Q

what is lifestyle advice of CAD?

A

ineffective endocarditis, active peptic ulcer
Lifestyle:
* Low dose aspirin – decrease death by 25%
* Statins
* Smoking
* Diet and weight modifications
* DVLA needs informing
* Limit alcohol – less than 14 units a week
* Increased exercise
* Control diabetes, hypetension

64
Q

what are the secondary medical management 6As?

A

for CAD
Aspirin – 75mg once a day
Another antiplatelet – eg clopidogrel or tricagrelor (those after PCI, low risk of bleeding)
Atorvastatin – 80mg once a day
ACEi – ramipril titrated as tolerated to 10mg a day
Atenolol- or any beta blocker as high as tolerated
Aldosterone antagonist- for those with heart failure (eplerenone titrated to 50mg once daily)

65
Q

what are the NICE guidelines for stable angina?

A
  • First line – beta blocker/ CCB
  • If symptoms not controlled- consider switching or using combination (DO NOT USE B BLOCKER WITH VERAPAMIL/ DILTIAZEM)
  • Third line – long acting nitrate, ivabradine, ranolazine
  • If patient can not tolerate CCB/ b blocker then monotherapy or nitrate/ ivabradine/ ranolazine
  • Triple therapy while awaiting PCI
66
Q

in those aged 75+ and awaiting PCI which dual anti-platelet combination is best?

A

aspirin with ticagrelor/ clopidogrel

67
Q

what is the management of NSTEMI/ unstable angina?

A

B- beta blockers
A- anti-platelet - aspirin
T- sTaTins
M - morphine
A- another antiplatelet ( ticagrelor/ clopidogrel)
N - nitrates - GTN spray
give oxygen if needed

68
Q

define myocardial infarction

A

necrosis of myocardial tissue following occlusion of coronary artery and subsequent ischaemia
MI is a major manifestation of CAD

69
Q

what type of pain is associated with MI?

A

sudden onset, substernal, crushing, tightness, severe, unrelieved by GTN, may radiate to jaw, shoulder, neck, back

70
Q

what are normal symptoms of MI?

A

dyspnea, syncope, nausea, vomiting, extreme weakness, diaphoresis, denial, increase in Hr

71
Q

what is initial MI treatment?

A
  • Pain relief and antiplatelets: diamorphine, morphine, oxygen, sublingual GTN or IV, aspirin, cyclizine or metoclopramide
  • Thrombolysis – with or without heparin
  • IV beta blockers, IV nitrates
  • Asprin, ACEi, oral B blockers, lipid lowering agents, dual antiplatelets
  • Angiography as needed
  • Revascularization as needed
72
Q

what is initial MI treatment?

A

B- b, blockers
A- antiplatelets (dual)
T- thrombolytics
M- morphine
A- aspirin, ACEi
N- nitrates- GTN spray
Give oxygen as needed

73
Q

what is the role of cardiac rehabilitation?

A

motivates patients with similar conditions but individually meets everyone’s needs - works around medication and exercise capabilities

74
Q

who and when should patients get cardiac rehab?

A

all people regardless of age and should start sessions within 10 days of being discharged

75
Q

can stenting help restonosis?

A

30% less restonosis

76
Q

what drugs help manage stable angina?

A

GTN, ivabradine, ranolazine, nicrovandril, antiplatelets (aspirin + clopidogrel/ tricagrel)
2nd prevention drugs

77
Q

what drugs help manage NSTEMI? unstable angina?

A

antiplatelet (aspirin + clopidogrel/ tricagelor)
PCI route - prasugrel, unfractionated heparin
drug eluting stent
2nd prevention drug

78
Q

what drugs help manage STEMI?

A

antiplatelet (aspirin + tricagrelor/ clopidogrel)
PCI route - unfrectionated heparin + parasugrel
drug eluting stent
fibrinolysis route - altepase/ streptokinase/ tenactapase
2nd prevention drugs

79
Q

when giving another antiplatelet, when is each of them work best (clopidogrel, tricagelor, prasugrel)

A

prasugrel - when undergoing PCI
clopidogrel - if high bleeding risk
tricagelor - any other time

80
Q

other than NSTEMI, what else can increase troponin levels?

A

CKD, sepsis, myocarditis, aortic dissection, PE

Cardiovascular (14 decks)

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