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Cardiology > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

What is included in ACS?

A

ACS basically covers acute presentations of IHD. There are 3 main types included:

  1. ST-elevated MI (STEMI)
  2. Non ST-elevated MI (NSTEMI)
  3. Unstable angina
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2
Q

What is the underlying pathophysiology of IHD?

A
  1. Initial endothelium dysfunction due to smoking, hypertension and hyperglycaemia
  2. Results in a number of changes in the endothelium –> proinflammatory, pro-oxidating, proliferative and reduced nitric oxide bioavailability.
  3. Fatty infiltration of subendothelial space by LDL particles
  4. Monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
  5. Smooth muscle proliferation and migration from the tunica media into the intima results in the formation of a fibrous capsule covering the fatty plaque.
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3
Q

What are the complications of atherosclerosis?

A

Once a plaque has formed a number of complications can develop:

  1. The plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
  2. The plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction
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4
Q

What are the risk factors for ischaemic heart disease? (modifiable and non-modifiable)

A

Unmodifiable risk factors

  1. Increasing age
  2. Male gender
  3. Family history

Modifiable risk factors

  1. Smoking
  2. Diabetes mellitus
  3. Hypertension
  4. Hypercholesterolaemia
  5. Obesity
  6. Sedentary lifestyle
  7. Cocaine use
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5
Q

Ischaemia vs Infarction?

A

Infarction –> Reduced blood supply ; reversible

Ischaemia –> process of cell necrosis/ death has begun. Presence of troponin markers

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6
Q

Symptoms of ACS

A

Acute chest pain lasting > 20 mins often associated with sweatiness, dyspnoea, palpitations.
Silent ACS –> ACS without chest pain. Seen in the elderly and diabetics

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7
Q

Signs of ACS

A

Distress, anxiety, pallor, sweatiness, sweatiness, pulse high or low, BP high or low, 4th heart sounds.
Signs of HF
Pansystolic murmur
Low grade fever
Pericardial friction rub or peripheral oedema may develop later

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8
Q

How is the diagnosis of ACS made?

A
  1. Increase in cardiac biomarkers (e.g. troponin) and EITHER:
    2a. Symptoms of ischaemia
    2b. ECG changes of new ischaemia
    2c. Development of pathological Q waves
    2d. New loss of myocardium
    2e. Regional wall abnormalities on imaging
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9
Q

What investigations would you carry out for ?ACS? List them

A
  1. ECG
  2. CXR
  3. Bloods
  4. Cardiac enzymes
  5. Echo
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10
Q

ECG changes seen in STEMI?

A

Hyperacute (tall) T waves, ST elevation or new LBBB occur within hours.
T wave inversion and pathological Q waves over hours to days

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11
Q

ECG changes seen in NSTEMI/ unstable angina

A

ST depression, T wave inversion, non specific changes or normal

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12
Q

How may a CXR be useful in ACS?

A

May show cardiomegaly, pulmonary oedema or widened mediastinum

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13
Q

What bloods would you carry out for a patient with ?ACS

A 
FBC
U&Es
Glucose
Lipids
Cardiac enzymes
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14
Q

What cardiac enzymes are measured in ACS?

A

Troponin T and I are most sensitive and specific markers of myocardial necrosis.

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15
Q

Give other differentials that could result in a raised troponin level.

A

Myocardial damage : myocarditis, pericarditis, ventricular strain

Non cardiac aetiology: massive PE causing right ventricular strain; subarachnoid haemorrhage, burns or sepsis; renal failure (common!!)

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16
Q

What are the differential diagnoses to chest pain?

A

Stable angina; ACS; pericarditis; myocarditis; aortic dissection; PE; oesophageal reflux/ spasm ; pneumothorax; MSK pain; pancreatitis

17
Q

How would you manage a STEMI?

A
  1. Percutaneous coronary intervention (PCI) is first line - to revascularise myocardium => CATH LAB

Offer primary PCI to patients who present within 12 hours of onset of symptoms, if it can be delivered within 120 minutes of the time when fibrinolysis could have been given.

  1. Sublingual glyceryl trinitrate and intravenous morphine + metoclopramide should be given to help relieve the symptoms.
  2. Oxygen should only be given if the oxygen saturations are < 94%
  3. Aspirin 300mg should be given to all patients (unless contraindicated).
  4. A second antiplatelet is normally given, usually ticagrelor, clopidogrel or prasurgel (all are antagonists of the P2Y12 adenosine diphosphate receptor).
  5. Other treatments that may be given include bivalirudin (a direct thrombin inhibitor, usually given alongside aspirin + clopidogrel) and a form of heparin (either low-molecular weight or unfractionated).
18
Q

What are the broad principles in the management of ACS?

A
  1. Symptom control
  2. Modify risk factors
  3. Optimise cardioprotective medications
  4. Revascularisation
  5. Manage complications
  6. Discharge plan
  7. General advice reg work and driving
19
Q

How would you manage an NSTEMI?

A

All patients should receive:

  1. aspirin 300mg
  2. nitrates or morphine to relieve chest pain if required
  3. Antithrombin treatment. Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patients creatinine is > 265 µmol/l unfractionated heparin should be given.
  4. Clopidogrel 300mg should be given to all patients and continued for 12 months.
  5. Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.
  6. Coronary angiography should be considered within 96 hours of first admission to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically unstable.
20
Q

MoA of aspirin

A

Antiplatelet - inhibits the production of thromboxane A2

21
Q

MoA of clopidogrel

A

Antiplatelet - inhibits ADP binding to its platelet receptor

22
Q

MoA of enoxaparin

A

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

23
Q

MoA of fondaparinux

A

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

24
Q

MoA of bivalirudin

A

Reversible direct thrombin inhibitor

25
Q

MoA of Abciximab, eptifibatide, tirofiban

A

Glycoprotein IIb/IIIa receptor antagonists

26
Q

What are poor prognostic factors for ACS?

A

Based on GRACE scoring

  1. Age
  2. Development (or history) of heart failure
  3. Peripheral vascular disease
  4. Reduced systolic blood pressure
  5. Killip class*
  6. Initial serum creatinine concentration
  7. Elevated initial cardiac markers
  8. cardiac arrest on admission
  9. ST segment deviation
27
Q

What is the Killip Class?

A

Killip class - system used to stratify risk post myocardial infarction

Killip class    Features    30 day mortality
I	No clinical signs heart failure	6%
II	Lung crackles, S3	17%
III	Frank pulmonary oedema	38%
IV	Cardiogenic shock	81%
28
Q

How would you advise on modifying risk factors post ACS?

A
  1. Smoking cessation help + advice
  2. Identify and treat DM, HTN and hyperlipidaemia
  3. Diet high in oily fish, fruit, vegetables and fibre and low in saturated fats
  4. Encourage daily exercise. Refer to cardiac rehab program
  5. Mental health - flag if depression or anxiety present
29
Q

What cardioprotective medications are the patients prescribed?

A
  1. Antiplatelets (X2) - aspirin 75mg OD + 2nd Antiplatelet (e.g. clopidogrel) for atleast 12 months. Consider adding a PPI
  2. Anticoagulate e.g fondaparinux until discharge
  3. B-blocker - reduces myocardial oxygen demand. Start low and increase slowly monitoring pulse and BP
  4. ACE-i - in patients with LV dysfunction, HTN or diabetes, Titrate up slowly monitoring renal function
  5. High dose statin eg atorvastatin 80mg
  6. Echo to assess LV function. Eplerenone improves outcome in MI patients with HF (EF <40%)
30
Q

How do you categorise urgency of an angiography for different ACS presentations?

A
  1. STEMI and very high risk NSTEMI patientd (haemodynamically unstable) = immediate angiography +/- PCI
  2. NSTEMI patients with GRACE score >140 = angiography within 24hrs
  3. Intermediate risk eg GRACE score of 109 - 140 within 3 days
  4. Low risk = non invasive testing
31
Q

When would you consider a CABG instead of PCI?

A

Patients with multivessel disease

32
Q

What driving advice are patients given?

A
  1. Group 1 license holders:
    a. Successful angioplasty - driving after 1 week
    b. ACS without successful angioplasty, if EF > 40% - driving after 4 weeks
  2. Group 2 license holders:
    a. Inform DVLA of ACS and stop driving
    b. Can restart driving after 6 weeks depending on results of functional tests
  3. CABG - 4 weeks off driving
33
Q

What is the initial management of a patient presenting with ?ACS? (GP)

A
  1. GTN
  2. Aspirin 300mg - dont give other antiplatelets outside of hospital
  3. Do not routinely give Oxygen, only if sats <94%
  4. Perform ECG asap but do not delay transfer to hospital
    A normal ECG DOESNT exclude ACS
34
Q

What are the guidelines for referral to hospital in patients with ?ACS

A
  1. Current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission
  2. Chest pain 12-72 hours ago: refer to hospital the same-day for assessment
  3. Chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action
35
Q

What are NICE guidelines regarding administration of oxygen therapy?

A

Monitor oxygen sats using pulse oximeter

Only offer supplemental oxygen to:
1. People with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%

  1. People with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

Cardiology (4 decks)

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