Acute Coronary Syndromes Flashcards

1
Q

What is meant by an acute coronary syndrome?

What are the 3 ‘conditions’ which are examples of ACS’s?

A
  • Signs and symptoms due to myocardial ischaemia- with or without infarction
  • STEMI, NSTEMI, unstable angina
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2
Q

Describe the difference, in terms of pathology, between STEMI, NSTEMI and unstable angina

A
  • STEMI: complete occlusion leading to subendocardial injury/infarction
  • NSTEMI: partial occlusion leading to subepicardial injury/infarction
  • Angina pectoris: partial occlusion leading to ischaemia but with NO infarction
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3
Q

State some risk factors for ACS

A

Non-modifiable

  • Age
  • Sex (male)
  • Ethnicity (asian)
  • Family history
  • Premature menopause

Modifiable

  • Smoking
  • DM
  • Hyperlipidaemia
  • Obesity
  • Diet
  • Physical inactivity
  • Hypertension
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4
Q

How may someone with ACS present?

A
  • Cardiac chest pain >20 mins
  • Pain may radiate to left jaw, shoulder & arm
  • Nausea, vomitting
  • Sweating
  • SOB
  • Palpitations
  • Constant pain
  • Pain at rest

*NOTE: some patients could present ONLY with less typical symptoms e.g. nausea, sweat, SOB etc… don’t always have ‘central crushing chest pain’

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5
Q

What might you find on examination of someone with ACS?

A
  • Tachycardia
  • Tachypnoea
  • Sweating
  • Hypertension (risk factor)
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6
Q

State some differentials for chest pain

A

Respiratory

  • PE
  • Pneumothorax
  • Pleuritis

Cardiology

  • Aortic dissection
  • Pericarditis (usually sharp but may be dull or crushing)

Gastro

  • Oesophagitis
  • Oesophageal spasm
  • Peptic ulcer
  • Pancreatitis
  • Cholecystitis

MSK

  • Rib fracture
  • Costochondritis

Other

  • Sickle cell crisis
  • Panic attack
  • Cocaine use
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7
Q

What bedside tests should you do in patients presenting with ACS?

A
  • ECG
  • Observations (HR, BP, O2 sats, RR, BMs)
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8
Q

What blood tests do you want if a pt is presenting with ACS?

A
  • Troponin: determine if infarction
  • FBC: anaemia, hyperthyroidism, sepsis may precipitte MI
  • U&Es: coronary artery disease may be marker for vascular disease in general and this may result in renal impairment which is important to know as contrast is given in angiogram & may be starting ACE inhibitor
  • LFT’s
  • Coagulation screen: INR needs to be known before taking to cath lab
  • Lipid profile: will need statin therapy
  • HbA1c: poorly controlled diabetes=risk factor
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9
Q

What imaging might you do for someone with ACS?

A
  • CXR: features of heart failure, alternative diagnosis
  • Echocardiogram: assess function of heart

*Don’t delay treatment whilst waiting for these scans in high risk/unstable pt

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10
Q

When determining whether the ACS is a STEMI, NSTEMI or unstable angina, what 3 things do we use/look at?

A
  • Presenting symptom
  • ECG
  • hs-TnI level (high sensity troponnin I release)
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11
Q

Myocardial infarction can be categorised into type 1 and type 2; explain the difference

*NOTE: there are other types of MI (3, 4a, 4b, 5)

A
  • Type 1: ischaemia due to plaque erosion/rupture which causes thrombus formation in the affected coronary artery
  • Type 2: ischaemia due to either increased demand or decreased supply e.g. anaemia, arrhythmia, hyper-/hypotension who has stable coronary artery disease (in summary, ischaemia occured without plaque rupture)
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12
Q

There are different types of MI; we have covered the main types you need to be aware of (type 1 & 2), but what is a:

  • Type 3
  • Type 4a
  • Type 4b
  • Type 5

… MI

A
  • Type 3: diagnosed post mortem
  • Type 4a: related to PCI (e.g. angioplasty blocked side artery)
  • Type 4b: stent thrombosis (if pt stops taking anticoagulants too early or smokes it can occlude the stent)
  • Type 5: related to CABG
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13
Q

How do we distinguish between MI and unstable angina?

A

Rise in hs-TnI

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14
Q

Describe how troponin levels vary over time following myocardial infarction

A
  • Increase within 3-12 hours from onset of chest pain
  • Peak at 24-48hr
  • Return to baseline in 5-14 days
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15
Q

What value will the hs-TnI frequently be above if the patient has had an MI?

A

>100ng/L

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16
Q

Alongside hs-TnI, what other biochemical marker should you also test for in a STEMI?

What value is this marker usually above in a STEMI?

A
  • CK-MB (creatine kinase- myocardial band)
  • Usually >400ng/L
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17
Q

If hs-TnI is above a certain value there is a high likelihood of myocardial necrosis; state this value for men and for women (it is different)

A
  • Males: > 34ng/L
  • Females: >16ng/L
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18
Q

We can use the hs-TnI to predict whether or not the MI was a type 1 myocardial infarction; what levels of hs-TnI have a very high predictive value for a type 1 MI?

A
  • hs-TnI five-fold above the upper limit have very high predictive value for type 1 MI (90%)
  • hs-TnI up to three-fold above the upper limit have a limited predited value for a type 1 MI (50-60%) and can be associated with other conditions
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19
Q

When looking at the troponin, we look at the change in cardiac troponin over time to help us differentiate between acute and chronic cardiomyocyte damage. A rise greater than ______ may indicate ACS

A

Rise greater than 5ng/L may suggest ACS

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20
Q

We look at the change in troponin over time to determine whether cardiomyoctye damage is acute or chronic; however, we must balance this with ensuring we treat the pt quickly. Discuss the time intervals at which hs-TnI should be taken

A
  • Take hs-TnI on admission, then again at 1 hour. *NOTE: if there is uncertainty you can take a further sample 2 hours later (so 3 hours after first sample)
  • HOWEVER, only one hs-TnI is required if the onset of symptoms was 3 or more hours ago
21
Q

State some causes of raised troponin, other than MI

A
  • PE
  • Chronic or acute renal dysfunction
  • Severe sepsis
  • Rhabdomyolysis
  • Aortic dissection
  • Aortic stenosis
  • Hypertrophic cardiomyopathy
  • Takotsubo cardiomyopathy
  • Severe congstive heart failure
  • Acute neurological disease e.g. stroke, SA haemorrhage

*Just remember a few

22
Q

Describe the STEMI criteria

A

At least 20 minutes of clinical symptoms consistent with ACS with persistent (≥20 mins) ECG features, such as:

  • Persistent ST elevation in 2 or more leads from the same zone i.e. 2 contiguous leads (criteria regarding height of elevation varies for sex, age and which lead)
  • Or new LBBB (left bundle branch block)
  • ST depression confied to to leads V1-V4, dominant R waves, tall T waves (may be posterior STEMI)
23
Q

Discuss how the ECG of someone with a STEMI changes over time

A
  1. Hyperacute T wave (minutes)
  2. ST elevation (minutes-hours)
  3. T wave inversion (hours)
  4. Deep Q waves (hours)
  5. Resolution of ST elevation (days)
  6. Resolution of T wave inversion
  7. Persistent Q waves
24
Q

What should the ST elevation be in…

a. ) the limb leads
b. ) the chest leads

… in a STEMI?

A
  • V2-V3
    • Men <40yrs: ≥2.5mm
    • Men >40yrs: ≥ 2mm
    • Women: ≥1.5mm
  • All other leads: 1mm

*Remember, one small square= 1mm. Simplified way mentioned in 3rd year was limb leads >1mm, chest leads >2mm. Check local guidelines as junior doctor.

25
Q

Describe the ECG changes in someone who is having an NSTEMI

A
  • ST depression
  • T wave inversion or flattening
  • T-wave pseudonormalisation
  • Normal
26
Q

Describe the ECG changes in someone with unstable angina

A

ST depression, T wave inversion or may be normal

27
Q

Alongside your usual 12-lead ECG, what should all patients have recorded on or soon after admission?

A
  • Posterior leads (V7-V9)
  • Right ventricular leads
28
Q

Where do you place the ECG electrodes in a 12-lead ECG?

A
29
Q

Where do you place the ECG electrodes when you are doing a 15-lead ECG/posterior leads?

A

Place leads V4-V6 on back:

  • V4 (recorded as V7)- left posterior axillary line
  • V5 (recorded as V8)- tip of left scapula
  • V6 (recorded as V9)- left paraspinal region

*Level of normal V6 placement is good indicator of what level to put leads at

30
Q

ST elevation in what lead, when doing right ventricular leads, is highly sensitive for right ventricular infarction?

A

RV4

31
Q

Describe the immediate management of ACS

*Think MONA

A

*Firstly, gain IV access

  1. Morphine & anti-emetic
  2. Oxygen (if needed- only give is sats <94%)
  3. Nitrates (sublingual or IV)
  4. Aspirin 300mg
32
Q

What dose of aspirin is given in the immediate management of ACS?

What dose of aspirin is given daily for life to patients following ACS?

A
  • 300mg loading dose
  • 75mg daily for life
33
Q

Cardiology booklet says that prasugrel is first line choice of ADP antagonist for STEMI; however, for a pt to have prasugrel they must meet some criteria. State the criteria

A
  • Pt must be undergoing PCI for STEMI
  • <75 years ol
  • Weigh >60kg
  • Not had pior TIA or stroke
  • Can only be used for up to 12 months
34
Q

Clopidogrel can be used as antiplatelet in patients who don’t fulfil the criteria for prasugrel. What loading dose and what daily dose- following initial loading dose- would you give for up to 12 months?

Ticagrelor can also be used if patient cannot have prasugrel OR as first choice for an NSTEMI. What loading dose and what daily dose- followign initial loading dose- would you give for up to 12 months?

A

Clopidogrel

  • Loading: 600mg
  • Daily dose for up to 12 months: 75mg

Ticagrelor

  • Loading dose: 180mg
  • Daily dose for up to 12 months: 90mg
35
Q

What ADP receptor antagonist would be your first choice for:

  • STEMI
  • NSTEMI
A
  • STEMI: prasugrel (clopidogrel if already taking oral anticoagulant)
  • NSTEMI: ticagrelor
36
Q

Following MONA, what is the management for a STEMI?

A

Patients with STEMI need coronary reperfusion therapy, two options:

Percutaneous coronary intervention (PCI) = GOLD STANDARD

  • Offer if presentation within 12hrs symptom onset AND can be delivered within 120 minutes of the time fibrinolysis could have been given. (NOTE: if still have evidence of ongoing ischaemia but present 12hrs after onset symptoms PCI may still be considered)
  • _Prior to PC_I, patients need dual antiplatelet therapy (aspirin + an ADP receptor antagonist):
    • If they are not taking an oral anticoagulant: prasugrel
    • If they are taking an oral anticoagulant: clopidogrel
  • Drug therapy during PCI varies dependent on access:
    • Radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor
    • Femoral access: bivalirudin with bailout glycoprotein IIb/IIIA inhibitor

Fibrinolysis

  • Fibrinolysis (with e.g. alteplase, streptokinase, tenecteplase)
  • Antithrombin drug should also be given at same time as fibrinolysis
  • ECG should be repeated after 60-90 minutes to see if ECG changes resolved, if NOT resolved then PCI should be considered
  • Patient should have ticagrelor as their long term antithrombin drug
37
Q

NICE summary of STEMI mangement

A
38
Q

If the onset of symptoms of STEMI were >12 hours ago, is PCI still beneficial?

A

Still beneficial if there is evidence of ongoing ischaemia

39
Q

Following MONA, what is the management of NSTEMI and unstable angina

A

Following MONA, antithrombin treatment should be given with either:

  • Fondaparinux or LMWH: pts who are not high risk of bleeding and who are not having angiography immediately
  • Unfractionated heparin: if having immediate angiography or creatinine is >265umol/L

You should risk stratify using the GRACE score to determine if should have PCI (may do this prior to deciding what to give in the above):

  • Immediate PCI if pt clinically unstable (e.g. hypotensive)
  • PCI within 72hrs if GRACE score >3% (intermediate or above risk)
  • Consider PCI if ischaemia experienced after admission/continued ischaemia

Further drug therapy prior to PCI:

  • Unfractionated heparin (if not already given?? CHECK). *NOTE: if pts had fondaparinux but then decided to go for PCI still need unfractionated heparin aswell
  • Further antithrombin therapy:
    • Not taking oral anticoagulant: prasugrel or ticagrelor
    • Taking oral anticoagulant: clopidogrel

If patients not having PCI, will need dual antiplatelet therapy (e.g. aspirin + ) lifelong:

  • Not high risk of bleeding: ticagrelor
  • High risk of bleeding: clopidogrel
40
Q

NICE summary of NSTEMI management

A
41
Q

State two scoring systems you can use to assess whether a patient with ACS is low or high risk

A
  • TIMI (thrombolysis in myocardial infarcion)
  • GRACE (global registery of acute coronary events)
42
Q

What is the GRACE score?

State some components of the GRACE scoring system

A

Scoring system used to risk stratify ACS pts by estimating their 6 month mortality risk

  • Age
  • Killip class
  • Heart rate
  • Systolic BP
  • Serum creatinine
  • ST segment deviation
  • Cardiac arrest at admission
  • Elevated cardiac enzymes

*^^All of the above are poor prognostic factors for ACS

43
Q

What is the TIMI scoring system?

State some components of the TIMI scoring system

A

Used to estimate likelihood of ischaemic events and mortality in unstable angina and NSTEMI. Components in scoring system include:

  • Age >/= 65yrs
  • Known CAD
  • Three or more risk factors for CAD
  • Others…
44
Q

What is the Killip classification?

A

Used to risk stratify post-acute MI patients based on heart failure symptoms:

  • Class I: no clinical signs of HF
  • Class II: crackles in lungs, S3, JVP
  • Class III: frank acute pulmonary oedema
  • Class IV: cardiogenic shock/hypotension (BP<90)
45
Q

What medications should someone be sent home with post MI as secondary prevention?

A
  • Beta blocker:
    • Bisoprolol, starting dose 1.25mg OD
  • ACE inhibitor or ARB:
    • ACE-i= amipril, starting dose 2.5mg OD
    • ARB= losartan, starting dose 25mg OD
  • Statin
    • Atorvastatin, 80mg OD
  • Dual antiplatelet therapy​
    • ​​​Aspirin, 75mg OD
    • ADP receptor antagonist if had STEMI or NSTEMI or if high risk unstable angina (e.g. ticagrelor, clopidogrel). **May be discontinued after 12 months but rest of medications lifelong
46
Q

Alongside the medications that everyone should be sent home with post MI, state some other ways to manage a pt post MI

A
  • Consider a PPI
  • Good diabetic control
  • Smoking cessation
  • Exercise
  • Diet
  • Control hypertension
  • Other relevant advice e.g. returning to work etc
47
Q

State some potential complications following an ACS event

*HINT: DREAD

A

DDeath

RRupture of the heart septum or papillary muscles (ventricular rupture)

E – “Edema” (Heart Failure)

AArrhythmia and Aneurysm

DDressler’s Syndrome

*

48
Q

Discuss which pts are best managed on coronary care unit (CCU)

A

In CCU each pt is connected to a cardiac monitor 24/7; staff are able to view this monitor at the working stations and print off the trace whenever they want (e.g. could print off the trace from 2 hours ago). This allows careful monitoring of pts. On CCU there is a specialist multi-disciplinary cardiac team that have access to cardiac investigations & tests at all times. Each nurse will look after fewer pts to ensure adequete and timel care can be given. Pts that are often managed here are those who have any of the following:

  • Myocardial infarction
  • Life threatening arrhythmia
  • Unstable angina
  • Severe heart failure
  • Recovering from cardiac surgery
49
Q

What is Dressler’s sydnrome?

A

Type of pericarditis caused by an immune response following damage to heart tissue