Chest Pain, ACS and Myocardial Ischaemia Flashcards

1
Q

Chest pain is a common presenting complaint and the spectrum of pathology ranges from non-urgent to life threatening. What leads to diagnosis?

A

History, clinical examinations and investigations.

SQUITARS for history taking, but time may be of the essence.

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2
Q

What are the different types of causes of chest pain?

A

Cardiac (Ischaemic or pericarditis), respiratory (pneumonia, PE), upper gastrointestinal (oesophageal reflux) or musculoskeletal (rib fracture or costal chondritis).

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3
Q

What is the difference between pleural/pericardial pain and lung/heart tissue pain and how do they present?

A

Pleural/pericardial pain is somatic and so is often sharp and well localised, worsening on inspiration/coughing/positional movement.
In contrast lung/heart tissue pain is visceral, so dull and poorly localised, worsened by exertion.

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4
Q

What may be the cause of non-cardiac chest pain that’s sharp, radiates to the back and is life-threatening?

A

Aortic dissection.

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5
Q

Who might present with pericarditis and what are the changes seen on an ECG?

A

Pericarditis is more common in adults and men and may be secondary to a viral infection.
On an ECG there will be widespread/saddle shaped ST elevation.

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6
Q

How does one present with pericarditis (inflammation of the pericardium)?

A

Present with chest pain that’s: retrosternal, sharp and localised to the front of the chest, aggravated with inspiration/ a cough / lying flat and eased with sitting up and leaning forward. A pericardial rub (coarse, harsh noise), may be heard on auscultation.

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7
Q

What is cardiac/ischaemic chest pain about?

A

Pain secondary to pathology involving the heart (coronary heart disease aka IHD). The initial primary concern is to rule out urgent, life threatening causes.

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8
Q

What is a pathway of pathophysiology of coronary heart disease?

A

Atherosclerosis - builds up over time, lipid-laden core with fibrous external cap.

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9
Q

Risk factors for atherosclerosis are the same as those for IHD, name some that are modifiable and not modifiable.

A

Modifiable: smoking, hypertension/cholesteraemia, diabetes, obesity, sedentary lifestyle.
Non-modifiable: advanced age, family history, male.

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10
Q

Explain stable angina.

A

The atherosclerotic plaque is ‘stable’ - ischaemia only when the demands of the cardiac muscle are greater than what can be delivered by the coronary arteries.

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11
Q

What is the typical patient history for someone with stable angina?

A

Dull retrosternal pain, triggered by exertion and relieved completely by rest (as well as GNT spray). It may radiate to the neck/shoulders, but the patient will not feel particularly unwell.

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12
Q

What does Acute Coronary Syndrome include?

A

Unstable angina, MI - NSTEMI & and STEMI. Each may progress to the next.

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13
Q

How is Acute myocardial ischaemia caused?

A

Atherosclerotic coronary artery disease: an atheromatous plaque ruptures with thrombus formation causing an acute increased occlusion (of an already partially occluded lumen), leading to ischaemia. The rupture leads to platelet aggregation and thrombus formation, which goes from partially to completely occlusive.
There is a spectrum of increased occlusion form a common pathophysiologic mechanism.

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14
Q

When will cardiac enzymes leak?

A

In the case of heart tissue infarction, but not if only ischaemia, as the enzymes come from necrosed muscle cells.

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15
Q

What is the typical patient history for someone with Unstable angina?

A

Similar to that of stable angina (dull, retrosternal, may radiate to shoulders/neck), but the pain occurs at rest. It may be more intense and last longer - there’s a risk of deteriorating further to a NSTEMI/STEMI.

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16
Q

What is the typical patient history for someone with Myocardial infarction?

A

Dull retrosternal (central) chest pain, heavy/crushing (more severe than angina), can radiate to neck/shoulders, present at rest, they look unwell, increased autonomic output - sweaty/pallor/nauseous. Pain persists for over 15 minutes with no relieving factors.

17
Q

How can examinations differentiate stable angina and Acute Coronary Syndrome?

A

Stable angina often yields normal examinations and ACS may do the same, but patients often may appear sweaty, anxious and pale, with or without clinical signs secondary to complications of cardiac tissue death (MI) e.g. Acute Heart Failure or a heart murmur.

18
Q

What are the diagnostic tests for suspected ACS?

A

ECG- chances suggestive of current ischaemia/infarct, look at ST segments, T waves +/- pathological Q waves.
Blood tests - troponin presence indicates cardiac myocyte death.
Other investigations to exclude any other potential diagnoses and identify potential complications.

19
Q

What are the ECG changes seen with a STEMI?

A

ST segment elevation, hyperacute T waves, localisation of changes help determine the site.
Repeat the ECG as it may evolve over time. It is different if there is a new left bundle branch block.

20
Q

What are the ECG changes seen with unstable angina/NSTEMI?

A

Patterns of ischaemia - ST segment depression and/or T wave flattening/inversion.

21
Q
If ECG leads are showing abnormalities in the following groups, which coronary artery does it suggest may be occluded:
II, III and aVF,
II, aVL and V5, V6
V1, V2
V3, V4
aVR?
A

II, III and aVF are inferior so right coronary artery.
I, aVL, V5 and V6 are lateral so the circumflex artery.
V1, V2 do anteroseptal and V3, V4 do anteroapical, so both suggest the left anterior descending artery (the latter more distal).
aVR looks at the right atrium.

22
Q

What is the significance of the Vagus nerve supplying the heart from the top of the thorax (T1-4)?

A

Any irritation stimulates it here an dermatomes go out to the neck/jaw/arm, hence the spread out pain in cases of myocardial ischaemia.

23
Q

Explain stable angina investigations.

A

Bloods (Hb-anaemia? Cholesterol), ECG (Q wave is past MI), chest X-ray (cardiomegaly?), test for ischaemia if appropriate e.g. Elderly man won’t exert himself much anyway, so may not do treadmill test/stress echo, test coronary anatomy.

24
Q

How may unstable angina be treated?

A

Aspirin (anti-platelet), beta-blocker, statin, ACE inhibitors, oral nitrate, nicorandil, calcium channel blocker, PCI or CABG.

25
Q

What are PCI and CABG?

A

Percutaneous coronary intervention, for revascularisation - balloon or stent angioplasty.
CABG - coronary artery bypass surgery (grafting) - rerouted blood flow around blockage (may use mammary artery).

26
Q

Other than atherosclerosis, what may cause a myocardial infarction?

A

Coronary spasm, coronary embolism, coronary dissection, aortic root dissection, mechanical obstruction during cardiac intervention.

27
Q

What may cause the release of cardiac troponin?

A

Acute coronary occlusion/ severe stenosis, myocarditis, acute heart failure (+/- valvular heart disease), prolonged tachycardia, cardiac amyloidosis, cardiac trauma, Takotsubo syndrome, defibrillation - CRR, aortic dissection.

28
Q

What may cause the release of non-cardiac troponin?

A

Acute pulmonary embolism, hypertension, haemodynamic challenge, systemic illness, severe anaemia, Rhabdomyolysis, Polymyositis, seizures, carecholamine release, SAH - intercranial haemorrhage and kidney failure.

29
Q

When is intervention on coronary arteries with stents appropriate?

A

Intervention of coronary arteries with stents is only necessary if ACS is related to plaque rupture.

30
Q

How is unstable angina treated?

A

Optimise general condition, pharmacological and reperfusion (PCI/CABG).

31
Q

What is the treatment for MI?

A

Oxygen, pain relief, GTN sublingually (glycotrinitrite spray - dilates blood vessels), second anti-platelets and reperfusion.