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Cardiovascular 2 > Unstable angina > Flashcards

Unstable angina Flashcards

1
Q

What is ACS

A

encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).

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2
Q

What does ACS typically manifest as

A

sudden, new-onset angina, or an increase in the severity of an existing stable angina.

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3
Q

What are the clinical classifications for unstable angina?

A
  • Cardiac chest pain at rest
  • Cardiac chest pain with crescendo pattern
  • New onset angina – angina out of the blue – somethings happened to the coronary artery
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4
Q

Epidemiology

A
  • STEMI = 5/1000 per annum in UK
  • M>F
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5
Q

Non modifiable RFs for ACS

A
  • Age (>65 years of age)
  • Male
  • Family history of premature coronary heart disease
  • Premature menopause
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6
Q

Modifiable RFs

A
  • Smoking
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Obesity
  • Sedentary lifestyle
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7
Q

Pathophysiology: Atherosclerotic plaque formation

A
  • Accumulation of LDLP cholesterol in inner layer of BV
  • Leukocytes adhere to endothelium - gain entry to intima where they combine with lipids to become foam cells
  • artery remodelling + calcification + foam cells causes atherosclerotic plaque to form
  • plaque rupture causes platelet activation, thrombus formation and coronary artery occlusion
  • results in ischaemia and infarction
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8
Q

What is a dianosis of angina based on?

A

history
ECG
troponin (no significant rise in unstable angina)

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9
Q

Occlusions

A
  • Unstable angina + NSTEMI: Partial occlusion
  • STEMI - occlusion is complete
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10
Q

Signs

A
  • Hypotension or hypertension
  • Reduced 4th heart sound
  • Signs of heart failure: e.g. increased JVP, oedema; **red flag symptom
  • Systolic murmur: if mitral regurgitation or a ventricular septal defect develops
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11
Q

Symptoms

A
  • Chest pain
    • Central, ‘heavy’, crushing pain
    • Radiation to the left arm or neck
    • Symptoms should continue at rest for more than 20 minutes
  • Shortness of breath
  • Sweating and clamminess
  • Nausea and vomiting
  • Palpitations
  • Anxiety
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12
Q

Investigations

A
  • ECG:perform within 10 minutes. Aim to perform serial ECGs every 10 minutes to detect dynamic changes.
  • Troponin:for a STEMI and NSTEMI, troponin levels will begin to elevate 4-6 hours after injury and will remain elevated for roughly 10 days. In unstable angina, there isnoelevation in troponin.
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13
Q

ECG findings

A
  • Unstable angina: non-specific changes
  • NSTEMI: ST-segment depression; T-wave inversion; pathological Q waves; a normal ECG may be seen
  • STEMI: ST-segment elevation; T-wave inversion; new left-bundle branch block
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14
Q

Other investigations

A
  • Coronary angiogram:aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice
  • FBC
  • UEs
  • CXR
  • Echocardiogram
  • HbA1C
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15
Q

Unstable angina + NSTEMI Immediate management

A
  • Oxygen:only if SpO2is <94%, and aim for 94-98%
  • Analgesia:morphine and sublingual glyceryl trinitrate
  • Dual antiplatelets: Aspirin +
  • Prasugrel, ticagrelor or clopidogrel - if undergoing PCI - just T+ C if not
  • Anticoagulation:
  • Fondaparinux or unfractionated heparin
  • BBs
  • Remember ‘MONA’: Morphine,Oxygen,Nitrates,Aspirin
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16
Q

Immediate STEMI Management

A
  • Oxygen:only if SpO2is <94%, and aim for 94-98%
  • Analgesia:morphine and sublingual glyceryl trinitrate
  • Dual antiplatelets: Aspirin +
  • Prasugrel, ticagrelor or clopidogrel - if undergoing PCI - just T+ C if fibrinolysis
  • Anticoagulation - U Heparin + glycoprotein IIB/IIA inhib
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17
Q

If ineligible for PCI management for STEMI

A
  • Thrombolysis e.g. alteplase or tenecteplase
    • IV administration of a fibrinolytic agent
    • Offered if symptom onset is greater than 12h OR PCI not available within 120 mins
  • Anticoagulation
    • An antithrombin agent such as unfractionated heparin is usually given alongside thrombolysis
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18
Q

ECG for STEMI MI

A

If the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI

19
Q

2ndary prevention of CVD

A
  • Lifestyle changes: exercise, diet change, smoking cessation, reducing alcohol intake
  • Manage cardiovascular risk factors: lipid, diabetes, hypertension management
  • Antiplatelet therapy:
    • Aspirin 75mg OD continued indefinitely
    • The second antiplatelet depends on the one chosen in the acute setting i.e. prasugrel, ticagrelor, or clopidogrel, and is usually continued for 12 months.
  • Statin
  • ACEi
20
Q

Early complications of Angina

A
  • Post-MI pericarditis:inflammation of the pericardium usually occurs afew dayspost-MI due to irritation of the pericardium; usually benign
  • Cardiac arrest/tachyarrhythmias:most commonly**due to ventricular fibrillation
  • Bradyarrhythmias:heart block is more common after an inferior myocardial infarction
  • Cardiogenic shock:extensive ventricular damage may lead to impaired ejection fraction and the development of cardiogenic shock
  • Ventricular septal defect:seen within the first week and may present with acute heart failureand a pansystolic murmur
  • Mitral regurgitation
21
Q

Later complications

A
  • Dressler’s syndrome:presents similarly to post-MI pericarditis but occurs2-6 weekspost-MI, and reflects anautoimmuneprocess against neo-antigens formed by the heart
    Diagnosis:ECG(global ST elevationandT wave inversion),echocardiogram (pericardial effusion) and raisedinflammatory markers(CRPandESR).
    Management:NSAIDs(aspirin/ibuprofen) and in more severe cases steroids (prednisolone). May needpericardiocentesisto remove fluid around the heart.
  • Heart failure:ventricular dysfunction following extensive damage can lead to chronic heart failure
  • Left ventricular aneurysm: bulge or ballooning of a weakened area of the heart
22
Q

Type of MI

A
  • Type 1: a classic MI and occurs due to atheromatous plaque rupture
  • Type 2: secondary to ischaemia due toeitherincreased oxygen demandordecreased supply, such as vasospasm, anaemia and sepsis. Management involves treating the underlying cause.
  • Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
  • Type 4: MI associated with PCI / coronary stenting / CABG
23
Q

What are ST elevation MI and MI assosciated with LBBB related to?

A

larger infarcts
unless effectively treated more likely to lead to pathological Q wave formation, heart failure or death

24
Q

R wave MI

A

R wave generated by electrically viable myocardium under ECG lead – if we replace this with scar tissue lose R wave and you get pathological R wave

25
Q

What is the initial management for acute coronary syndrome?

A

Get in to hospital quickly – 999 call
Need defibrillator

Paramedics – if ST elevation, contact primary PCI centre for transfer

Take aspirin 300mg immediately

Pain relief

26
Q

Hospital management for MI

A

Make diagnosis
Bed rest
Oxygen therapy if hypoxic
Pain relief – opiates/ nitrates
Aspirin +/- platelet P2Y12 inhibitor
Consider beta-blocker
Consider other antianginal therapy
Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy

27
Q

What is troponin?

A

Troponin C Troponin I and Troponin T
Protein complex regulates actin:myosin contraction
Highly sensitive marker for cardiac muscle injury
Not specific for acute coronary syndrome
May not represent permanent muscle damage

28
Q

Positive troponine is found in?

A

gram negative sepsis
pulmonary embolism
myocarditis
heart failure
arrhythmias
cytotoxic drugs

29
Q

Agonists for platelet activation

A

Thrombin > Coagulation
Thromboxane A2
Collagen
5HT
ADP
ATP
Fibrinogen > Fibrin

30
Q

Aspirin effect

A

Irreversible inactivation of cyclo-oxygenase 1
Stops conversion of collagen to Thromboxane A2

31
Q

What does thrombin do?

A

activates platelets – final factor in coagulation cascade as it cleaves fibrin from fibrinogen

32
Q

What is the fibrinolytic system?

A

Endothelium releases tissue plasminogen activator (TPA)
TPA > Plasminogen > plasmin > Fibrin to fibrin degradation products

33
Q

What is P2Y12 and what is its antagonists / inhibitors

A
  • important amplification process in platelet activation -Makes response of platelets much more aggressive
  • Clopidogrel, ticagrelor, prasugrel
34
Q

What do P2Y12 inhibs do?

A

Used in combination with aspirin in management of ACS = ‘dual antiplatelet therapy’
Increase risk of bleeding so need to exclude serious bleeding prior to administration

35
Q

What are adverse effecrs of P2Y12 inhibs

A

Bleeding e.g. epistaxis, GI bleeds, haematuria
Rash
GI disturbance
Dyspnoea

36
Q

What are some GPIIb/IIIa antagonists?

A

Abciximab
Tirofiban
Eptifibatide

37
Q

What do GPIIb/IIIa antagonists do?

A

Only intravenous drugs available

Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS

Increase risk of major bleeding so used selectively

38
Q

What do anticoagulants do?

A
  • Used in addition to antiplatelet drugs
  • Target formation and activity of thrombin
  • Inhibit both fibrin formation and platelet activation
39
Q

When is fondaparinux used?

A

used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used

40
Q

When do you use full dose anticoagulation

A
  • used during PCI: options are:
  • heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin)
  • direct thrombin inhibitor: bivalirudin
41
Q

When is high dose heparin used

A

cardiopulmonary bypass for CABG surgery

42
Q

When is a coronary angiography usually performed?

A

for patients with troponin elevation or unstable angina after medical therapy

43
Q

What is the most used revascularisation procedure?

A

PCI

Cardiovascular 2 (10 decks)

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