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ESA2 LKM > CVS - chest pain and ischaemic heart disease > Flashcards

CVS - chest pain and ischaemic heart disease Flashcards

1
Q

What are potential causes of chest pain?

A
  1. Musculoskeletal pain (ribs and muscles)
  2. Pneumonia
  3. MI or angina
  4. Cholecystitis (gallbladder inflammation)
  5. GORD
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2
Q

Describe the differences in pain between MI, pericarditis and aortic dissection:

A

All central pain.

  1. Ischaemia - tightening pain
  2. Pericarditis - sharp pain
  3. Dissection - tearing pain
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3
Q

What is the imbalance that leads to ischaemic heart disease?

A

An imbalance of myocardial oxygen supply and myocardial oxygen demand.

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4
Q

What is the direction of coronary blood flow?

A

Epicardium -> endocardium

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5
Q

Which muscle of the heart is most vulnerable to ischaemia?

A

Sub endocardial muscle

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6
Q

What is the most common cause of IHD?

A

Fixed narrowing of coronary arteries due to atherosclerosis.

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7
Q

Where are collateral arteries found in the heart?

A

There are none between major arteries (they are functional end arteries) but some are found between smaller arteries and arterioles.

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8
Q

What two main factors determine myocardial oxygen supply?

A
  1. Coronary blood flow

2. Oxygen carrying capacity of blood

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9
Q

What two factors determine coronary blood flow?

A
  1. Perfusion pressure (diastolic BP)

2. Coronary artery resistance

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10
Q

What are the three factors that myocardial oxygen demand depend on?

A
  1. Heart rate
  2. Wall tension
  3. Contractility
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11
Q

What determines the wall tension of the heart?

A

Preload and afterload

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12
Q

List some non-modifiable risk factors for coronary artery disease:

A
  1. Increasing age
  2. Male gender (females catch-up after menopause)
  3. Family history
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13
Q

List some modifiable risk factors for coronary artery disease:

A
  1. Hyperlipidaemia
  2. Smoking
  3. Hypertension (high diastolic or systolic)
  4. Diabetes (doubles IHD risk)
  5. Lack of exercise
  6. Obesity
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14
Q

Describe a stable atheromatous plaque:

A

It has a small necrotic core, thick fibrous cap and so is less likely to rupture.

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15
Q

Describe an vulnerable/unstable atheromatous plaque:

A

It has a large necrotic core, thin fibrous cap and therefore the cap is less likely to rupture.

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16
Q

Name three acute coronary syndromes:

A

Unstable angina, NSTEMI and STEMI.

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17
Q

What are typical features of chest pain?

A
  1. Central (sometimes on left or right side)
  2. Tightening/ constricting
  3. Characteristic pattern of radiation.
18
Q

What coronary pathology can stable plaques cause?

A

Stable angina

19
Q

What coronary pathology can ruptured plaques cause?

A

Acute coronary syndromes: unstable angina, NSTEMI and STEMI.

20
Q

What is the difference between stable angina and acute coronary syndromes?

A

Stable angina has no pain at rest but is precipitated by stress or exertion - which is relived within 5 minutes by nitrates or rest. ACSs have pain at rest or minimal exertion which is not relieved by nitrates and is of longer duration.

21
Q

How does a plaque form a thrombus?

A
  1. Fibrous cap undergoes rupture or fissuring
  2. Exposes blood to the thrombogenic material in the necrotic core
  3. Platelet ‘clot’ followed by fibrin thrombus.
22
Q

How does sub-endocardial ischaemia present itself on the ECG?

A

ST segment depression of >1mm.

23
Q

Why is aspirin given for IHD?

A

It reduces platelet aggregation and therefore reduces thrombus formation.

24
Q

Why are statins given for IHD?

A

Decrease LDL cholesterl and therefore slow the progression of atherosclerosis and increase the plaque stability.

25
Q

Why are long-lasting (transdermal or oral) nitrates given for IHD?

A

They cause venodilation and therefore reduce preload (decrease wall tension) and therefore myocardial oxygen demand.

26
Q

Why are calcium channel blockers given for IHD?

A

They cause peripheral vasodilatation and therefore reduce afterload and therefore myocardial oxygen demand.

27
Q

Why are beta-blockers given for IHD?

A

They reduce heart rate and contractility and therefore myocardial oxygen demand.

28
Q

List two revascularisation techniques:

A
  1. PCI: percutaneous coronary intervention (angioplasty and stenting)
  2. CABG: coronary artery bypass grafting.
29
Q

How is it determined which revascularisation technique is best for a patient?

A

They undergo coronary angiography which identifies the sites of occlusion. The choice of procedure is influenced by these findings.

30
Q

Which blood vessels are used for graft for CABG?

A
  1. Internal mammary artery (internal thoracic artery)
  2. Radial artery
  3. Saphenous vein (using reversed segment of vein)
31
Q

What is the difference in blood flow between NSTEMI and STEMI?

A

NSTEMI blood flow obstruction is typically incomplete whereas STEMI is complete obstruction.

32
Q

How does a STEMI cause ST elevation?

A

Total occlusion of an artery causes transmural (full-thickness) injury which extends to the sub-epicardial area. ECG leads that face that area

33
Q

How do you localise ST depression?

A

You can’t! Unlike ST elevation it cannot be localised.

34
Q

What are the diagnostic criteria for ST elevation?

A

Elevation greater than 1 small square in limb leads or 2 small squares in chest leads above the baseline. Seen in two contiguous leads.

35
Q

Why is it important to recognise a STEMI?

A

90% are due to total occlusion and there if proved benefit from EMERGENCY RE-OPENING of the artery.

36
Q

How can NSTEMIs and unstable angina be differentiated?

A

No biomarkers (e.g. troponin I) of myocyte necrosis seen in blood test of unstable angina as no myocyte necrosis has occurred.

37
Q

What ECG changes may be seen in unstable angina or NSTEMI?

A

ST depression in leads facing injured area and/or T wave inversion. ECG may be normal.

38
Q

What clues in the history of a patient with unstable angina MAY enable you to diagnose unstable angina over acute MI?

A
  1. Acute worsening of stable angina
  2. Angina at rest
  3. Recent onset of new, effort limiting angina.
  4. Or the story may be the same as in acute MI.
39
Q

List some examination finding in an acute myocardial infarction:

A
  1. Patient anxious, distressed
  2. Sweating, pallor
  3. Cold, clammy skin
  4. Tachycardia/ arrhythmias (+/-)
  5. Low BP (+/-)
  6. Signs of heart failure: S3/S4, crackles in lung bases (left ventricular failure).
40
Q

When do troponin levels peak? How long does it take their levels to decline?

A

Peak: 18-36 hours
Decline: slowly, up to 10-14 days

41
Q

When do CK-MB (creatine kinase cardiac isoform) levels peak? How long does it take them to decline? When is it useful to measure?

A

Peak: 24 hours
Decline: back to normal 48-72 hours
Uses: when new episode of chest pain occurs within 10 days (troponin levels will be high from previous episode still but CK-MB will have come back down).

ESA2 LKM (45 decks)

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