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Medicine - 3rd year > ACS > Flashcards

ACS Flashcards

1
Q

ACS - definition

A

Refers to a spectrum of acute myocardial ischaemia and/or infarction. Decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. 3 conditions:

  • unstable angina
  • NSTEMI
  • STEMI
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2
Q

Stable vs Unstable Angina

A
  • Stable angina = at least 70% stenosis; chest pain only on exertion (supplies tissue at rest but heart needs to work harder on exertion)
  • Unstable angina = usually rupture of plaque with thrombosis -> subendocardial ischaemia. Pain at REST
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3
Q

ACS - cardiac tissue involvement

A
  • UA = subendocardial ischaemia
  • NSTEMI = subendocardial infarction (20-40 min after onset)
  • STEMI = transmural infaction (3-6 h after onset)
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4
Q

Cardiac biomarkers and ECG changes

A

UA - no changes in cardiac markers
- ECG may be normal or have changes (ST depression, T wave inversion

NSTEMI - elevated cardiac markers
- ECG changes: ST depression, T wave inversion

STEMI - elevated cardiac biomarkers
- ECG changes: ST elevation of at least 1 mm in 2 or more contiguous leads, may have new LBBB or pathological Q waves

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5
Q

Cardiac biomarkers in ACS

A
  • Troponins (I and T): increase 3-12h from onset, peak at about 24-48 h and overall last 10-14 days
  • CK-MB: rises after 3 h, peaks at about 24 h and lasts up to 72 h (more useful to determine re-infarction)
  • myoglobin: first one to rise so useful for rapid Dx
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6
Q

ACS - risk factors

A
  • Increasing age
  • Gender (male for STEMI, female for UA)
  • Diabetes
  • Smoking
  • Hypertension
  • Hx of coronary artery disease
  • Hyperlipidaemia
  • PVD
  • CKD
  • Obesity
  • Inflammatory conditions e.g. RA
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7
Q

What is type 2 MI and some causes?

A

MI not due to atheroma

  • Supply and demand mismatch – cardiac muscle not receiving enough oxygen, often due to subendothelial tissue hypoxia – better prognosis than type 1 MI. Causes:
  • Anaemia
  • Hypoxia
  • Shock
  • Tachyarrhythmia
  • Bradyarrhythmia
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8
Q

What is type 3 MI?

A

Type 3 MI: sudden cardiac death due to thromboembolism (no time to measure cardiac enzyme therefore classified as type 3 MI as unknown if they had previous atheroma)

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9
Q

UA - presentation

A
  • increasing frequency of chest pain (several times a day, instead of occasionally)
  • increasing severity of chest pain (decreasing levels of activity needed to trigger pain and may occur at rest)
  • retrosternal pressure or heaviness radiating to jaw, arm, or neck that is improved by nitrates
  • dyspnoea
  • 4th heart sound (Indicates reduced myocardial relaxation due to ischaemia)
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10
Q

Acute MI - presentation

A
  • central crushing chest pain (sensation of tightness, heaviness, aching, burning, pressure, or squeezing)
  • diaphoresis, pallor
  • dyspnoea
  • N and/or V
  • dizziness or light-headedness
  • weakness and anxious
  • tachycardia
  • may have S3 or S4 heart sounds
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11
Q

Rarer causes of MI

A
  • Aortic dissection – tearing pain that radiates to the back, different bp in the different arms, widening of mediastinum, risk of pericardial effusion and tamponade; worst at onset, then lingering pain with time
  • Coronary artery spasm
  • Oesophageal rupture - excessive retching, vomiting
  • Pericarditis – saddle shaped ST elevation, relieved by learning forward; can have viral prodrome
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12
Q

ACS - investigations

A
  • ECG
  • cardiac biomarkers (tropinin, CK-MB +/- myoglobin)
  • FBC (normal or low Hb)
  • U+Es / electrolytes (usually normal)
  • blood glucose
  • lipid profile (normal or high total cholesterol and LDL)
  • coagulation profile (should be normal)
  • CXR (excludes HF, PE, aortic dissection, etc)
  • consider echo (regional wall motion abnormalities)
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13
Q

ACS - criteria for hospital admission

A

Suspected acute coronary syndrome (ACS), who:

  • Have current chest pain
  • Have signs of complications (such as PE)
  • Are pain-free, but have had chest pain in the last 12 hours and have an abnormal ECG
  • A recent history of ACS, and they develop further chest pain.
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14
Q

Stable angina - treatment

not ACS

A

(The first-line investigation recommended by NICE is contrast-enhanced CT coronary angiogram)

  • GTN spray (for use before performing activities known to cause symptoms of angina)
  • BB or CCB
    OR either one of:
    a long-acting nitrate (isosorbide mononitrate)
    Nicorandil
    Ivabradine
    Ranolazine
  • antiplatelet treatment (low dose aspirin - 75 mg daily)
  • statins
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15
Q

What to give to people with angina and:

  1. stroke
  2. diabetes
A

STROKE
clopidogrel instead of aspirin
(long term ischaemic stroke Rx also includes warfarin)

DIABETES
consider adding ACEi

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16
Q

ACS - immediate management

A

IMMEDIATE

  • IF SATS < 94%: Supplemental Oxygen - use a simple face mask. Adjust the flow rate to 5–10 L/min to achieve a target SpO2 of 94–98%.
  • Treat pain with sublingual glyceryl trinitrate (GTN spray) and/or opioid (for example IV diamorphine 2.5 mg to 5.0 mg); also consider metoclopramide
  • Give aspirin 300 mg*. Send a written record with the person that aspirin has been given.
  • Take a resting 12-lead ECG. Send the results to the hospital

*chew for 30 seconds, then swallow

17
Q

UA - further management (after MONA)

A
  • antiplatelet therapy (clopidogrel or prasugrel or ticagrelor)
  • BB or CCB
  • anticoagulant (heparin -unfractionated- or a low molecular weight heparin, or fondaparinux sodium)
  • glycoprotein IIb/IIIa inhibitors (eptifibatide) for high risk pts
  • consider ACEi if HTN persists after BB
  • chest pain not resolved: consider IV nitrates
18
Q

NSTEMI - further management (after MONA)

A
  • antiplatelet therapy (clopidogrel or prasugrel or ticagrelor)
  • BB or CCB
    Assess need for invasive or conservative approach - risk stratification tool (such as GRACE) is used to decide upon further management. If a patient is considered high-risk or is clinically unstable then coronary angiography will be performed during the admission.
  1. Invasive:
    PCI + anticoagulant (heparin -unfractionated- or a low molecular weight heparin, or fondaparinux sodium)
    +/- glycoprotein IIb/IIIa inhibitors (eptifibatide)
  2. conservative = anticoagulation only
19
Q

STEMI - definitive management (haemodynamically stable)

A

PCI - gold standard

  • performed within 90 min of diagnosis
  • should also receive anticoagulant -> either heparin (unfractionated) or a LMWH (e.g. enoxaparin sodium) or bivalirudin to prevent clotting during the procedure
  • no-reflow or a thrombotic complication -> glycoprotein IIb/IIIa inhibitors (eptifibatide)

> 90 min –> thrombolytic therapy

  • alteplase or reteplase
  • PCI after thrombolysis recommended in high-risk pts
    • anticoagulation

For both cases (additional Rx):
aspirin, antiplatelet therapy (clopidogrel or prasugrel or ticagrelor), BB, statin, ezetimibe (if require additional lowering of LDL after statin)

20
Q

STEMI - definitive management (haemodynamically unstable)

A

1st line- PCI
2nd line - coronary artery bypass graft (CABG)

+ anticoagulation
+ aspirin
+ antiplatelet
- no-reflow or a thrombotic complication -> glycoprotein IIb/IIIa inhibitors (eptifibatide)

21
Q

What is PCI?

A

Percutaneous coronary intervention (PCI or angioplasty with stent)

  1. A catheter is fed via radial or femoral artery to the coronary artery for angiogram to locate the thrombus
  2. A deflated balloon attached to a catheter (a balloon catheter) is passed over a guide-wire into the narrowed vessel and then inflated to a fixed size.
  3. The balloon forces expansion of the blood vessel and the surrounding muscular wall, allowing an improved blood flow.
  4. A stent may be inserted at the time of ballooning to ensure the vessel remains open, and the balloon is then deflated and withdrawn.
22
Q

ACS - lifestyle measures (2ary prevention)

A

Cardiac Rehabilitation Programme - exercise,
education, relaxation and emotional support

In addition to adequate control of HTN, DM, and hyperlipidaemia, risk-factor intervention includes:

  • smoking cessation
  • regular physical activity with 30 minutes of moderate-intensity aerobic activity at least 5 times/week
  • a healthy diet (low salt intake, decreased intake of saturated fats, regular intake of fruit and vegetables)
  • weight reduction
23
Q

ACS - long term management (2ary prevention)

A
  • low dose aspirin continued indefinitely (75 mg daily)
  • clopidogrel (or alternative) for 12 months
  • BB
  • statin
  • ACEi

Consider angiotensin II antagonist eg valsartan if intolerant to ACEi; consider aldosterone antagonist and anticoagulants (for high risk or recurrence only)

(remember CRABS = clopidogrel, ramipril, aspirin, BB, statin)

24
Q

Other causes of acute chest pain (NICE)

A
  • pulmonary embolism
  • tension pneumothorax
  • sudden-onset cardiac arrhythmia
  • cardiac tamponade
  • aortic dissection
  • ruptured oesophagus
25
Q

MI - complications

A
  • complication of Rx: bleeding (eg intracranial hrg,
  • complication of Rx: thrombocytopenia
  • congestive HF
  • ventricular arrhythmias eg VT and VF*
  • BBB, heart block
  • acute mitral regurgitation (from rupture of papillary muscle)
  • VSD (from septal rupture)
  • acute pericardial tamponade (from ventricular free wall rupture)
  • post-infarction pericarditis (Dressler’s syndrome)
  • recurrent ischaemia and infarction
  • cardiac arrest

*VF is the most common cause of death following MI

26
Q

Anterior MI’s show most in which leads? Which artery is affected?

A

V1-V4

Left anterior decending

27
Q

Inferior MI’s show most in which leads? Which artery is affected?

A

II, III, aVF

Right coronary

28
Q

How do posterior MI’s present on an ECG?

A

Tall R waves in V1-V2

Possible ST depression (not elevation) in V1-V4 (reciprocal change)

29
Q

Lateral MI’s show most in which leads? Which artery is affected?

A

I, aVL, V5, V6

Left circumflex artery

30
Q

Within 48 hours of an MI a patient presents with signs of LVF, dropping BP and a new murmur, what is most likely diagnosis?

A

Papillary muscle rupture / MR

or ventricular septal rupture

31
Q

What are the criteria for PCI in suspected ACS? (3 things on ECG and time criteria)

A
  • ST elevation (2mm in anterior leads, 1mm in I,II,III,avF)
  • Any new LBBB
  • Posterior changes (ST depression + big R waves in V1-V3)
  • Must be within 12 hours of symptom onset
32
Q

What is the grace score?

A 
Estimates admission-6 month mortality for patients with ACS. Based on:
age
heart rate
systolic blood pressure
renal function
congestive heart failure
ST-segment deviation
cardiac arrest
elevated biomarkers

6 Month Estimated Mortality eg
1 to 69 Points = less than 1%

  • Low risk <1.5%
  • High risk >9%
33
Q

Primary prevention of CVD

A

Lifestyle factors:

  • smoking
  • alcohol
  • diet
  • physical activity
  • weight management

Lipid modification therapy (offered when CV risk > 10%)

  • 1st line: atorvastatin 20 mg
  • 2nd line: Ezetimibe
34
Q

Angina

  • drug for prevention
  • drug for relief
A
  • prevention: BB eg bisoprolol*
  • relief: short acting nitrate eg GNT
  • 2nd line - CCB (verapamil or diltiazem)
    3rd line - long acting nitrates (Nicorandil or Ivabradine/Ranolazine)

Medicine - 3rd year (8 decks)

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