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Y3 CBLs > CBL_1 ACS > Flashcards

CBL_1 ACS Flashcards

1
Q

What Acute Coronary Syndrome (ACS) refers to (in terms of presentation)?

A

Acute Coronary Syndrome ACS refers to acute chest pain of cardiac origin

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2
Q

What underlying conditions may ACS refer to? (6)

A
  • ST elevation Myocardial infarction (STEMI)
  • Non ST elevation Myocardial Infarction (NSTEMI)
  • Unstable angina (UA)

There are also

  • chronic angina
  • undiagnosed CHD
  • atheroma
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3
Q

How to differentiate STEMI from Non-STEMI?

A

ST elevation Myocardial infarction (STEMI): cardiac enzyme release and ST elevation on the ECG

Non ST elevation Myocardial Infarction (NSTEMI): cardiac enzyme release

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4
Q

What are characteristics on Ix of unstable angina?

A

Unstable angina (UA): no cardiac muscle necrosis -> ECG changes reverse; no cardiac enzyme release

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5
Q

BP targets for secondary prevention

A

Secondary prevention - treated hypertension targets

  • below 140/90 mmHg if aged under 80 years
  • below 150/90 mmHg if aged 80 years and over
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6
Q

Normal lipids/ cholesterol results

A

Total cholesterol < 5 mmol/l

Triglycerides < 2 mmol/l

HDL cholesterol > 1 mmol/l

LDL cholesterol < 3 mmol/l

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7
Q

What’s the normal glucose range?

A
  • Fasting; normal: <5.5 (> 7.0 = diabetic)
  • oral glucose tolerance; normal: <7.8 (>11.1 = diabetic)
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8
Q

Patient with not known angina and central chest pain

What to do?

A

Call 999

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9
Q

Patient with known angina and central chest pain

What to do?

A
  • Use GTN spray -> repeat after 5 mins if pain hasn’t gone
  • If after further 5 mins, pain hasn’t gone -> call 999
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10
Q

Causes of secondary MI

A

Secondary MI = not due to atheroma

  • anemia
  • hypoxia
  • shock
  • tachyarrhythmia
  • bradyarrhythmia
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11
Q

Possible causes of cardiac chest pain

A
  • reduction of oxygen supply into the myocardium
  • aortic dissection
  • coronary artery spasm
  • oesophageal rupture
  • pericarditis
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12
Q

What are the features of cardiac chest pain?

A

Ischaemic symptoms e.g. chest pain with radiation to arm/ jaw

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13
Q

Possible associated features with chest pain (in ACS) (2)

A
  • vomiting
  • sweating
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14
Q

Why is there vomiting and sweating in MI?

A

visceral pain -> pain from nociceptors -> commonly refer in a diffuse way over a number of dermatomes with autonomic features

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15
Q

Who may have no pain in MI?

A
  • elderly
  • diabetics

This is due to autonomic nervous system degeneration

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16
Q

Aspirin MoA

A

Aspirin is “anti-platelet aggregation”-> inhibits cyclo-oxygenase (COX) enzyme and so preventing production of certain prostaglandins and thromboxane production, all of which encourage platelet aggregation -> sp less platelet aggregation (less clot is formed)

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17
Q

What to do if a patient has MI in GP surgery?

A
  1. Give aspirin 300mg
  2. Call 999 and do ECG while waiting for the ambulance
  3. Record keeping: note with med and dose/time administrated + PMH (with referral to the hospital)
  4. Help: defibrillator equipment should be kept ready + extra staff should attend the patient
  5. Give oxygen if sats <95%
  6. GTN spray (if suspicion of angina and if not too hypotensive BP systolic >90 mmHg)
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18
Q

Investigations in ACS

A
  • IV access
  • Serial ECGs showing ST elevation and this can relate to sites of damage , changes in rhythm, new Q waves or LBBB
  • Serial Troponins: Troponin is a protein released from damaged cardiac myocyctes
  • CXR for LVF and cardiomegaly and differentials
  • oxygen (sats)
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19
Q

What are enzymes and markers used in Ix of possible MI?

A
  • Troponin I or T rises in 3-12 hours of chest pain, peaks at 24-48 and is the baseline at 5-14 days so do at presentation and 10-12 hours after chest pain started. Amount released relates to size of MI

Other enzyme biomarkers are not as sensitive or specific:

  • Myoglobin rises first, creatinine kinase in about 3 hours, also WCC can rise, ESR and CRP can rise and BNP may rise
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20
Q

What happens in PCI?

A

Percutaneous coronary intervention (PCI)

21
Q

2 first steps of PCI

A
  1. Aspirin 300mg given in primary care
  2. One of three oral ADP receptor antagonist antiplatelet medications given in secondary care. Clopidogrel initially as a loading dose or

prasugrel or ticagrelor

*the last two medications work more quickly at 30 minutes rather than clopidogrel at 3–4 hours.

22
Q

Why do we give so many anti-platelet and anticoagulation meds to the patient with PCI?

A

Patient receives a number of anticoagulants to improve perfusion and prevent further thrombus; undergoes angioplasty with stent insertion; then antiplatelet medication to take home

23
Q

What further meds a patient undergoing PCI is given in a catheter lab?

A

3. In the catheter lab other agents such as unfractionated heparin given (factor 10 inhibitor and antithrombin) or bivalirudin (f2 thrombin inhibitor) to prevent clotting during the procedure

4. A minority of patients get another antiplatelet group, the GP2B/3A platelet receptor antagonists, GPIs, which are abciximab or eptifibatide or tirofiban

24
Q

Step 5 and 6 in PCI (after meds are given)

A
  1. A catheter is fed via radial or femoral artery to the coronary artery for angiogram

6. The thrombus in the coronary artery may be aspirated and then balloon angioplastied with a stent being expanded in the previously occluded area

25
Q

What is the compilation of stent insertion in PCI?

A

Stent restenosis: the recurrence of abnormal narrowing of an artery or valve after corrective surgery

Bare metal stents have a 20% restenosis rate by re-endothelialisation at six months and so drug eluting stents were produced to reduce this

26
Q

What is offered to a patient if PCI did not work or to the patient with the extensive disease?

A

Coronary artery bypass grafting (CABG)

27
Q

What meds do patients with unstable angina/NON-STEMI MI do receive in the hospital?

A

Initially:

  • high dose aspirin and clopidogrel
  • they may get O2
  • morphine and metclopramide

on the CCU they receive

  • statin
  • B-blocker
  • LMWH
  • ACEI
28
Q

What score is used to determine if a patient with unstable angina/ non-STEMI MI needs an angiogram?

A
  • GRACE score to determine if they can go home on therapy or require an angiogram
  • It stratifies patients into low risk (<1.5%) up to highest risk (>9%) of death at six months post ACS and uses this to suggest therapy
29
Q

What GRACE score is used for?

A

Grace Score is used to predict patient mortality at 6 months and helps decide therapy and management

30
Q

What would you expect to be in the Grace score to predict a poor outcome after a MI?

A
  • advancing age
  • severity of heart failure
  • pulse rate
  • systolic blood pressure
  • renal function
  • ST changes on ECG
  • raised troponins
  • cardiac arrest at admission
31
Q

What meds do most patients receive after hospital admission for MI?

A

Most patients receive aspirin and clopidogrel (dual antiplatelet therapy/ DAPT)

  • In addition for angina - patients may have nitrates
  • For prognosis improvement: B blocker (bisoprolol), ACEI (ramipril) and DAPT 12 months and then assess as probably only need one antiplatelet at that stage
32
Q

What meds do most patients receive after hospital admission for MI?

A
  • aspirin (lifelong) + copidogrel/ticaglerol (12 monrs)
  • Statin
  • B-blocker (Bisoprolol)-> to reduce myocardial demand (continued for 12 months or lifelong if LV dysfunction)
  • ACE inhibitor (Ramipril) -> prevents adverse cardiac remodeling
  • GTN spray (when required)
  • Aldosterone antagonist (eplerenone) if LV is =<40%

Advise: *BP control, lifestyle modification, cardiac rehabilitation and smoking cessation

33
Q

Initial steps in management of ACS (2 x mnemonics)

A

A B C D E approach if critically ill

M - morphine IV (+ metoclopramide IV)

O - oxygen (if sats below target 94%-98%)

N - nitrate

A - aspirin - loading dose 300mg; then 75mg

C - clopidogrel

34
Q

Regions on ECG and possible MI location

A
35
Q

The classic triad of Dressler’s syndrome

A
  • Pericarditis
  • Fever
  • Pericardial effusion

*seen 2-10 weeks after MI

36
Q

Features of Dressler’s syndrome

What’s physical examination like?

A

Features include:

  • central stabbing chest pain (worse on inspiration and lying flat)
  • fever and lethargy
  • pericardial and pleural effusions

Examination is often irrelevant, although a pericardial rub might sometimes be heard

37
Q

What Dressler’s syndrome is a result of?

A

It is thought to be autoimmune condition secondary to the generation of the new myocardial antigens after an MI. they have a raised ESR secondary to the inflammation process.

38
Q

Management of Dressler’s syndrome

A
  • usually settles with NSAIDS and analgesia
  • sometimes steroids are needed
39
Q

What anti-coagulation start in NSTEMI for a short-term?

A

Fondaparinux or LMWH or Heparin for 5 days

40
Q

Are glycoprotein IIb/IIIa inhibitors often used?

A

Not, used in very selective patients only

Examples of IIb/IIIa: Abciximab, eptifibatide, tirofiban

41
Q

What’s gold standard reperfusion therapy for AC?

A

PCI (Percutaneous Coronary Intervention)

42
Q

When is thrombolysis (as Rx for ACS) used? (indications)

A

It’s rarely used (many contraindications related to bleeding risk)

  • if PCI unavailable within 2 hours
  • STEMI in two contiguous ECG leads
  • new LBB
43
Q

Contraindications for thrombolysis

A

Related to bleeding risk

  • active internal bleeding
  • bleeding disorder
  • aortic dissection
  • stroke
  • surgery/trauma <2 weeks
  • Hx of CNS bleed/aneurysm/neoplasm
  • GI bleed <1 month
44
Q

Indications for PCI

A

Any ACS:

  • SEMI (any ST elevation or new LBBB)
  • NSTEMI
  • Unstable angina

Contraindications: significant comorbidities

*PCI is a gold standard Rx for ACS

45
Q

MoA of unfractionated heparin

A

Factor X inhibitor and anti-thrombin

46
Q

Clopidogrel MoA

A

Antiplatelet -inhibits ADP binding to its platelet receptor

47
Q

Bivalirudin MoA

A

Reversible direct thrombin (factor II) inhibitor

Class: thrombin inhibitor

48
Q

Class and MoA of Fondaparinux

A

Fondaparinux

class: anti-thrombotic agent

MoA: activation of antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

49
Q

Enoxaparin

class

MoA

A

Enoxaparin

Class: LMWH

MoA: Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

Y3 CBLs (13 decks)

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