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NPS Modules > Acute Coronary Syndrome (2022) > Flashcards

Acute Coronary Syndrome (2022) Flashcards

1
Q

Markers for Very High Risk ACS?

A

Mechanical cardiac failure (haemodynamic instability, heart failure, cardiogenic shock or mechanical complications of myocardial infarction)

life-threatening arrhythmias or cardiac arrest

recurrent or ongoing ischaemia
OR
recurrent dynamic ST segment and/or T wave changes,
( particularly with intermittent ST segment elevation, de Winter T wave changes or Wellens syndrome, or widespread ST segment elevation in two coronary territories)

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2
Q

Markers for High Risk ACS?

A
  • trop rise
  • dynamic ST/ T-wave changes
  • GRACE Score > 140
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3
Q

Markers for Intermediate Risk ACS?

A
  • DM
  • Renal Filaure
  • HFrEF
  • prior angio intervention
  • GRACE score 110 - 140
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4
Q

Components of GRACE score for ACS?

A

age,

Killip class,

cardiac arrest at admission,

heart rate,

systolic blood pressure,

ST segment deviation,

creatinine,

elevated cardiac markers,

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5
Q

Mechanism of action for heparins?

A

Neutralise clotting factors thrombin and Xa by binding to antithrombin III.

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6
Q

Mechanism of action for warfarin?

A

Inhibits synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and the antithrombotic factors protein C and protein S.

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7
Q

In which ACS patients are beta-blockers indicated?

A

Beta-blockers are indicated in all patients unless there is a contraindication

Contraindications:

  • significant bradycardia,
  • heart block,
  • hypotension,
  • clinically apparent heart failure,
  • uncontrolled asthma.

The benefit of beta-blocker therapy persists long term, and beta-blockers should be continued indefinitely in high-risk patients. The available beta-blockers vary in their affinity for beta receptors and mode of clearance from the body.

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8
Q

Which receptor(s) does Atenolol act upon?

A

beta1 selective

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9
Q

Which receptor(s) does Carvidolol act upon?

A

non-selective beta blocker, which also has α1-blockade

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10
Q

Which receptor(s) does Metoprolol act upon?

A

non-selective beta blocker, which also has α1-blockade

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11
Q

Which receptor(s) does propranolol act upon?

A

non-selective beta blocker, which also has α1-blockade

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12
Q

What are the consequences of whether a beta-blocker is lipophilic or hydrophilic?

A

Atenolol is hydrophilic and therefore cleared by the kidney, requiring dose adjustment in the setting of renal impairment.

The hydrophilic nature of atenolol makes it less likely to cross the blood brain barrier and cause central nervous system adverse effects such as sleep disturbance and nightmares.

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13
Q

When should propranolol be used in MI?

A

The use of propranolol in the setting of myocardial infarct should be based on the recommendation of a cardiologist. Most commonly, propranolol is used in situations where the non-selectivity is desirable such as essential tremor.

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14
Q

How should you titrate beta-blocker dose after MI?

A

Aim to titrate doses to the maximum tolerated dose in the recommended range, provided that systolic blood pressure does not fall below 95 mm Hg and heart rate does not fall below 55 beats per minute.

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15
Q

Which beta-blockers are recommended post MI?

A

Atenolol or metoprolol (short acting)

If HFrEF use: carvedilol, bisoprolol, nebivolol or metoprolol succinate

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16
Q

In which MI patients should calcium channel blockers be considered?

A

The use of calcium channel blockers should be reserved for patients with post–myocardial infarction angina.

A dihydropyridine such as amlodipine could be considered for anginal symptoms.

Verapamil can also be considered for rate control if a beta-blocker is contra-indicated, but shouldn’t be used with a beta-blocker.

17
Q

Antiplatelets if STEMI** for **PCI?

A

Aspirin 300mg AND a P2Y12 Inhibitor

clopidogrel 600 mg STAT, then 75 mg daily

OR

ticagrelor 180 mg STAT, then 90 mg twice daily

OR (if patient is not at increased bleeding risk)

prasugrel 60 mg STAT, then 10 mg daily.

(ETG 2021)

18
Q

Which patients should you not use prasugrel in?

(In STEMIs)

A

patients who weigh less than 60 kg,

are aged 75 years or older, or

had a previous stroke or TIA

19
Q

Which patients should you not use tigagrelor in?

(In STEMIs)

A

2nd- or 3rd degree AV block patients

20
Q

Antiplatelets if STEMI** for **Fibrinolysis?

A

Aspirin 300mg AND

clopidogrel 300 mg STAT, then 75 mg daily

21
Q

Indications for repercussion therapy in STEMI?

(ETG 2022)

A

continuing ischaemia (persistent pain)

viable myocardium (preservation of R waves in infarct-related ECG leads)

major complications (eg cardiogenic shock).

(Advanced age, frailty and comorbidities influence a patient’s overall survival, and should be considered when deciding to intervene with reperfusion therapy.)

22
Q

Reperfusion options for STEMI?

A

percutaneous coronary intervention (PCI)—transluminal coronary balloon angioplasty and stenting

fibrinolytic therapy.

23
Q

When should you use PCI over fibrinolysis for STEMI?

A

PCI is more beneficial than fibrinolytic therapy in reducing mortality, recurrent myocardial infarction and stroke. The benefit of PCI over fibrinolytic therapy increases as the time between symptom onset and patient presentation increases.

If PCI is available within 90 minutes of first medical contact, PCI is preferred over fibrinolytic therapy.

If PCI cannot be delivered promptly, fibrinolytic therapy should be given within 30 minutes of the patient arriving at the hospital.

24
Q

Indications for transfer to PCI centre in STEMI?

(Assuming outside of 90min window)

A

If fibrinolytic therapy:

  • is contraindicated; see Box 3.5
  • is unlikely to be effective (eg cardiogenic shock) and the patient is deemed to be at very high acute risk of mortality and recurrent cardiovascular events (see Box 3.4)
  • has been unsuccessful (failed reperfusion), with 50% or less ST recovery after 60 to 90 minutes and/or haemodynamic instability.
25
Q

Medications to give prior to PCI for STEMI?

A

Aspirin 300mg

\+
 P2Y12 Inhibitor (Clopidogrel/ ticagrelor/ prasugel)

+

Heparin

+/-

Glycoprotein IIb/IIIA inhibitor

26
Q

Should you give heparin with fibrinolysis?

A

Yes

27
Q

Antiplatelets if STEMI** for **PCI?

A

Aspirin 300mg AND a P2Y12 Inhibitor:

clopidogrel 600 mg STAT, then 75 mg daily

OR

ticagrelor 180 mg STAT, then 90 mg twice daily

OR

prasugrel 60 mg STAT, then 10 mg daily.

(ETG 2021)

28
Q

When should Glycoprotein IIb/ IIIa inhibitors be considered in NSTEACS?

A

When immediate access to a cardiac catheterisation laboratory is not available, glycoprotein IIb/IIIa inhibitors may be used for patients with:

  • abnormal ECGs
    OR
  • positive troponin,

especially if there is recurrent ischaemia

29
Q

Examples of Glycoprotein IIb/ IIIa Inhibitors?

A
  • abciximab,
  • eptifibatide,
  • tirofiban
30
Q

Medications for ongoing anginal pain?

A

GTN

ISMN

For patients already taking a beta blocker, verapamil or diltiazem for angina, the dose of that drug should be maximised

31
Q

How long should DAPT be continued after a MI?

A

Dual antiplatelet therapy is usually recommended for 12 months after an acute coronary syndrome.

Dual antiplatelet therapy for less than 12 months may be appropriate for patients at high risk of bleeding, and longer than 12 months may be appropriate for selected patients at high risk of recurrent ischaemic events.

(ETG 2022)

32
Q

What medications should be given long term after an MI?

A
  • DAPT then to aspirin (else the P2Y12 anti-platelet)
  • Statin
  • Beta-blocker (metoprolol/ atenolol unless HF)
  • ACEi/ ARB
  • Aldosterone Antagonist
33
Q

Choice of P2Y12 anti-platelet in ACS?

A

Generally, prasugrel and ticagrelor are preferred over clopidogrel as they are more effective but have higher risk of bleeding events than clopidogrel.

34
Q

How does tirofiban work?

A

glycoprotein IIb/IIIa receptor antagonist, occupies the receptor site on platelets, thus preventing binding of fibrinogen.

35
Q

Do glycoprotein IIb/ IIIa inhibitors being reversibly or not?

A

Clopidogrel and prasugel irreversibly bind to the P2Y12 receptor, ticagrelor reversibly binds to the P2Y12 receptor.

36
Q

Mechanism of action of nitrates in ACS?

A

Exogenous source of nitric oxide, producing vasodilation, reducing venous return and pre-load to the heart, subsequently reducing oxygen requirement.

NPS Modules (15 decks)

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