Cardiology: Ischaemic Heart Disease I Flashcards

1
Q

How does angina typically present? [4]

A

Chest pain:
- Left sided
- Tight / squeezing
- Pressure like pain
- Associated SOB
- Radiates down left arm or back

Pain worse with exercise or cold weather

Pain relieved with rest

Pain relieved with GTN

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2
Q

Describe what is meant by cresendo angina [1]

Describe the clinical consequence of this [1]

A

Recent progressive drop in exercise tolerance

Suggests narrowing is getting tighter and vulnerable atherosclerotic plaque may occur

If pain at rest: unstable angina

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3
Q

NICE define anginal pain as what? [3]

A

NICE definition:
1. Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. Precipitated by physical exertion
3. Relieved by rest or GTN in about 5 minutes

Interpretation:
* Patients with all 3 features have typical angina
* Patients with 2 of the above features have atypical angina
* Patients with 1 or none of the above features have non-anginal chest pain

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4
Q

How long does it take for GTN to provide symptomatic relief of angina? [1]

A

~ 2mins

If more: then not GTN

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5
Q

What are the different causes of angina? [3]

A

Coronary Atherosclerosis
- Predominant cause

Also:
Coronary artery vasospasm:
- Constriction of the coronary arteries, leading to transient ischemia.

Microvascular dysfunction:
- Impaired function of the coronary microvasculature, leading to inadequate blood supply to the myocardium.

Extracoronary factors: which increase myocardial oxygen demand or decrease supply.
- Aortic stenosis
- Aortic regurgitation
- hypertrophic cardiomyopathy
- significant anemia

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6
Q

Why does AS and AR cause angina? [1]

A

Coronary arteries emerge just above the aortic valve: so get impeded blood flow

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7
Q

What is the name of this sign when asked for description of chest pain? [1]

A

Levine’s sign

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8
Q

What is decubitus angina? [1]

A

Form of stable angina where get pain when lying down without any apparent cause

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9
Q

What is meant by Prinzmetal’s or variant angina? [1]

A

When you get transient ST elevation due to coronary vasopasm (artery isn’t blocked, but muscle is in spasm)

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10
Q

What is meant by cardiac syndrome X? [1]

A

St depression on excerise ECG but normal angiogram

Sign of microvascular angina

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11
Q

What is meant by St Vincent’s angina? [1]

A

Not actually angina: pharyngitis due to ulcerative ginigivitis

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12
Q

What is the name for this sign of hyperlipdaemia? [1]

A

corneal arcus lipid deposits that appear as rings on the outer region of the cornea

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13
Q

NICE:
What investigations are used to investigate angina? [3]

A

1st line:
- CTCA (+calcium score)

2nd line:
- Non-invasive functional imaging (looking for reversible myocardial ischaemia)

3rd line:
- Invasive coronary angiography

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14
Q

Describe how invasive coronary angiography occurs [3]

A

A catheter is inserted into the patient’s brachial or femoral artery

Directed through the arterial system to the aorta and the coronary arteries under x-ray guidance

Contrast is injected to visualise the coronary arteries and identify any areas of stenosis using x-ray images

This is considered the gold standard for determining coronary artery disease

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15
Q

What function investigations can you conduct for borderline cases of angina / need further investigations? [4]

A
  • Exercise or stress ECHO
  • Nuclear medicine: myocardial perfusion scan
    scans use a small amount of radioactive substance to create images which show blood flow to the heart muscle
  • Cardiac MRI with stress perfusion
  • Exercise ECG
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16
Q

What advice do you give when giving GTN spray? [1]

Why? [1]

A

Can cause dizziness: due to veno-dilatation and BP to drop

17
Q

All patients with angina should be prescirbed which drugs? [2]

A

Aspirin 75mg (prevent risk of MI)

Statin (reduces cholesterol)

18
Q

Describe the treatment algorithm for stable angina patients [5]

A

Sublingual glyceryl trinitrate to abort angina attacks

All patients:
- Aspirin 75 mg
- Statin

1st line:
- Beta blocker: e.g. metoprolol
- CCB: e.g. Amlodopine
- If there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od)
- If a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa

2nd line:
- a long-acting nitrate: Isosorbide mononitrate
- ivabradine
- nicorandil
- ranolazine

3rd line:
- CABG
- PCI

19
Q

Beta blockers shouldn’t be prescribed alongside which angina medication? [1]

Why? [1]

A

Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)

Coadministration of verapamil and β-blockers results in additive negative inotropic, chronotropic and dromotropic (conduction properties) effects on the heart.

20
Q

If a CCB is being used as first line tx for stable angia, what type should be used? [1]

Give two examples [2]

A

If a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used.

21
Q

What do you need to consider about nitrate therapy for stable angina? [1]

How do you modifiy treatment to allow for this? [1]

A

Nitrate tolerance can occur

The BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness

22
Q

Describe the MoA of ivabradine [1]

A

** pacemaker current inhibitor**: slows the HR down (not a Beta blocker)

23
Q

Describe the MoA of ranolizine [1]

A

Late Na current blocker

24
Q

Nicorandil has a rare AE of ? [1]

A

GI ulceration

25
Q

How can you remember the drugs used for secondary prevention of stable angina patients? [4]

A

4 As:

A – Aspirin 75mg once daily
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
A – Already on a beta blocker for symptomatic relief

26
Q

Why do you get nausea, anxiety or sweating when have ACS? [1]

A

Undergoing adrenaline surge:

Due to severe ischaemia; causes necrosis; negative feedback loop causes huge amount of adrenaline released

27
Q

Describe the pathophysiology of ACS ]3

A

Myocardial damage secondary to ischaemia

Generally occurs after following steps:

Step 1 - endothelial dysfunction
* Endothelial injury causes a local inflammatory response.
* If the injury recurs or healing is incomplete, inflammation may continue leading to the accumulation of low-density lipoproteins (LDL).
* These become oxidised by local waste products creating reactive oxygen species (ROS).

Step 2 - plaque formation
* In response to these irritants, endothelial cells attract monocytes (macrophages).
* These engulf (phagocytose) the LDLs swelling to become foam cells and ‘fatty streaks’.

Step 3 - plaque rupture
* Continued inflammation triggers smooth muscle cell migration.
* This forms a fibrous cap, which together with the fatty streaks, develops into an atheroma.
* The top of the atheroma forms a hard plaque.
* This may rupture through its endothelial lining exposing a collagen-rich cap.
* Platelets aggregate on this exposed collagen forming a thrombus that may occlude or severely narrow the vessel.
* Alternatively, the thrombus may break lose, embolising to infarct a distant vessel.

28
Q

How do you assess ACS patient? [4]

A

ABCD

Airway:
- Patent?

Breathing:
- RR?
- Saturations?
- Pulmonary oedema due to LV impairment can cause hypoxia

Circulation:
- HR
- BP

Disability:
- GCS

DONT FORGET GLUCOSE

29
Q

ACS causing bradycardia can indicate MI in which part of heart? [1]

Why? [1]

A

Inferior MI

Right coronary artery perfuses the sinoatrial node, heart block and bradycardia may occur

30
Q

go over heart anatomy & SALI

A
31
Q

What is LDL target for secondary prevention of MI? [1]

A

< 1.4

32
Q

What are target times for coronary angiography for:

STEMI [1]
NSTEMI [1]

A

STEMI: < 6 hours
NSTEMI: < 72 hours

33
Q

In cases of primary PCI, which is the first line P2Y12 inhibitor? [1]

Why? [1]

A

Ticagrelor: most rapidly acting

34
Q

What is the difference between myocardial infarction and myocardial injury? [2]

A

Myocardial injury = trop > 99% percentile ULN

Acute MI = Injury +
- Symptoms
- ECG changes
- Imaging showing loss of viable myocardium
- Evidence of coronary aetiology
Implies ischaemia

35
Q
A