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7. CVS > 17. Chest Pain and Ischaemic Heart Disease > Flashcards

17. Chest Pain and Ischaemic Heart Disease Flashcards

1
Q

Why does an anatomical sieve have to be used to generate a list of causes of chest pain?

A

Because it is so common and can be life threatening if underlying cause is not dealt with.

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2
Q

Where does cardiac caused chest pain occur?

A

Central pain.

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3
Q

Where does respiratory caused chest pain occur?

A

Lateral chest pain.

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4
Q

Where does GI caused chest pain occur?

A

Chest and epigastric pain.

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5
Q

Where does musculoskeletal caused chest pain occur?

A

Localised to the area of damage.

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6
Q

What would tightening pain in the central chest region suggest?

A

Myocardial ischaemia.

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7
Q

What would sharp pain in the central chest region suggest?

A

Pericarditis.

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8
Q

What would tearing pain in the central chest region suggest?

A

Aortic dissection.

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9
Q

What respiratory problems can cause chest pain?

A

Infections, like pneumonia, pulmonary embolism, pneumothorax.

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10
Q

What type of pain is there with respiratory caused chest pain?

A

Pleuritic pain - gets worse on inspiration and coughing.

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11
Q

What GI problems can cause chest pain?

A

Reflux oesophagus, gastric/ gall bladder/ pancreatic problems.

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12
Q

What type of pain is there with GI caused chest pain?

A

Reflux - a burning pain that moves upwards.

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13
Q

What musculoskeletal problems can cause chest pain?

A

Trauma, muscle pain from excessive use, bone metastases.

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14
Q

What is the normal response to increased myocardial O2 supply and how is that changed in ischaemic heart disease?

A

Normally there is an increased coronary blood flow, in myocardial ischaemia, the coronary blood flow cannot meet the O2 supply.

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15
Q

What is the direction of coronary blood flow?

A

From epicardium to endocardium.

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16
Q

What type of tissue is most vulnerable to ischaemia in ischaemic coronary blood flow?

A

Sub endocardial, as it’s usually the last to be reached.

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17
Q

When does coronary heart flow occur?

A

In diastole.

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18
Q

How does tachycardia worsen ischaemia?

A

The rapid heart rate means diastole shorten, so the time available for coronary blood flow shortens and ischaemia is worsened.

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19
Q

What is the most common cause of ischaemic heart disease?

A

Fixed narrowing of a coronary artery/arteries due to coronary atheorsclerosis.

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20
Q

What does myocardial oxygen supply depend on?

A

Coronary blood flow (in turn depends on perfusion pressure and coronary artery resistance), and O2 carrying capacity of blood.

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21
Q

What does myocardial oxygen demand depend on?

A

Heart rate, wall tension (in turn depends on pre load and afterload), and contractility.

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22
Q

How does anaemia cause ischaemia?

A

It reduces the O2 carrying capacity of the blood.

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23
Q

How can aortic stenosis cause ischaemia?

A

Perfusion pressure and afterload are affected, the blood has to push against more pressure so effectively has a higher afterload.

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24
Q

What are some non modifiable risk factors for coronary artery disease?

A

Increasing age, male gender (although females catch up after menopause), and family history.

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25
What are some modifiable risk factors for coronary artery disease?
Hyperlipidaemia, cigarette smoking, hypertension, diabetes mellitus, lack of exercise, obesity, diet low in fruit and vegetables, psychosocial factors.
26
What is the structure of atheromatous plaques?
Necrotic centre and fibrous cap.
27
What is the structure of stable atheromatous plaques?
Small necrotic core, thick fibrous cap, cap less likely to fissure/rupture.
28
What is the structure of vulnerable atheromatous plaques?
Large necrotic core, thin fibrous cap, cap more likely to fissure/ rupture.
29
Why are unstable plaques so worrying?
The fibrous cap can undergo erosion or fissuring, this exposes the blood to the thrombogenic material in the nectrotic core so a platelet clot forms followed by a fibrin thrombus.
30
What are the features of ischaemic chest pain?
Central, tightening/ constricting, characteristic pattern of radiation: left shoulder, left arm, right arm, jaw, and throat.
31
What are the symptoms of stable angina?
No pain at rest, typical pain (moderate), precipitated by stress of exertion, relived by rest or nitrates within 5 minutes.
32
What are the symptoms of unstable angina/ acute coronary syndrome?
Pain at rest/ minimal exertion, more severe pain than stable angina, no relief with nitrates, long duration of pain.
33
How can a diagnosis of stable angina be confirmed?
Stress ECG testing.
34
How are exercise stress ECG tests performed?
Patient is connected to ECG machine, graded exercise on the treadmill. Stopped when: the target heart rate is reached, or ECG changes occur, or chest pains occur, or any other problems occur.
35
What are the results of exercise ECGs with stable angina?
Transient sub-endocardial ischaemia with exercise - ST depression. But this disappears with rest and ST segment returns to baseline. ST depression >1mm shows stable angina.
36
How are acute episodes of stable angina treated?
Sublingual nitrates (tablets under tongue or spray) for immediate relief of ischaemia and pain.
37
How is stable angina dealt with in the long run?
Lifestyle changes: patient education, modify risk factors. Medication: long acting nitrates, B-blockes, Ca2+ channel blockers, statins, and aspirin. Revascularisation to restore circulation.
38
How do nitrates work to treat stable angina?
Venodilators, so lessen preload.
39
How do calcium channel blockers work to treat stable angina?
Decrease after load by peripheral vasodilatation.
40
How do beta blockers work to treat stable angina?
Decrease heart rate and contractility.
41
How does aspirin work to treat stable angina?
Decreases platelet aggregation so reduces thrombus formation if the plaque is disrupted.
42
How do statins work to treat stable angina?
Decrease LDL cholesterol, hence reducing progression of atherosclerosis, increases plaque stability. It's a secondary prevention.
43
How does revascularisation work to treat stable angina?
Mechanically restores blood flow.
44
How is revascularisation performed?
A coronary angiography is performed to identify sites of occlusion and study coronary anatomy. The next step is based on these findings: percutaneous coronary intervention angioplasty and stenting, or coronary arteyr bypass grafting.
45
What are the three types of graft available for coronary artery bypass grafting?
Internal mammary artery grafts, radial artery grafts, or saphenous vein grafts (reversed segment of vein so blood flows the correct way).
46
What is acute coronary syndrome?
Includes unstable angina, and acute myocardial infarction.
47
What are the two types of myocardial infarction according to ECG changes?
NSTEMI - non-ST elevation myocardial infarction. | STEMI - ST elevation myocardial infarction.
48
What are acute coronary syndromes triggered by?
Fissuring or rupture of an atheromatous plaque, which stimulates a thrombotic response, causing variable obstruction to flow in the coronary arterial lumen with downstream ischaemic myocardial injury.
49
How do NSTEMI and STEMI differ in obstruction to flow?
NSTEMI is often incomplete occlusion, STEMI is complete obstruction to flow.
50
Why does total occlusion cause ST elevation?
It causes transmural injury - across the whole thickness of the vessel. This subtends to the sub-epicardial area and manifests as ST elevation in leads facing the injured area.
51
What is the difference between unstable angina and NSTEMI?
Unstable angina is an unprovoked or prolonged episode of chest pain raising suspicion of acute myocardial infarction. There is ST depression but no biomarkers of myocyte necrosis. NSTEMI - is non ST segment elevation MI. Theres is ST depression and release of troponins, signalling myocyte necrosis.
52
What are the biochemical markers of myocyte damage?
Cardiac troponin I (cTnI) and cardiac troponin T (cTnT). These are proteins present in myocytes which are important in actin/ myosin interaction and are released on myocyte death.
53
When are cardiac troponin I and T levels raised?
In NSTEMI and STEMI, not in unstable angina.
54
What is the typical history of unstable angina?
Acute worsening of stable angina, angina at rest, recent onset of new, effort limiting angina.
55
What is the typical history of myocardial infarction?
Pain at rest: severe, persisten, central, crushing chest pain, with typical radiation, and not relieved by rest/ nitrate spray. The patient is distressed and sweating, pallor (sympathetic nervous system), also nauseous and vomiting (parasympathetic stimulation). Feeling of breathlessness and faint.
56
What are the examination findings in acute MI?
Anxious, distressed patient. Sweating and pallor,cold, clammy skin. Tachycardic with arrythmias, low blood pressure, and sign of heart failure - S3/S4 sounds, and crackles in lung bases.
57
What are the ECG features of a fully evolved STEMI?
Q waves from area of necrosis, ST segment elevation from injury zone, T wave inversion.
58
What are the measurements of a pathological Q wave?
Wide - >1 small square, deep - >25% of the QRS complex.
59
Which artery causes inferior area of infarction and which leads does this show on?
Right coronary, and II, III, aVF leads.
60
Which artery causes anteroseptal area of infarction and which leads does this show on?
Left anterior descending, leads V1 and V2.
61
Which artery causes anteroapical area of infarction and which leads does this show on?
Ledt anterior descending, distal part, leads V3 and V4.
62
Which artery causes anterolateral area of infarction and which leads does this show on?
Circumflex, leads I, aVL, V5, and V6.
63
Which artery causes extensive anterior area of infarction and which leads does this show on?
Proximal left coronary artery, leads I, aVL, V2, and V6.
64
Which artery causes true posterior area of infarction and which leads does this show on?
Right coronary artery, leads V1 - tall R wave.
65
When do cardiac troponin levels rise?
4 hours after onset of pain in MI. They peak at 18-36 hours and decline slowly over 10-14 days.
66
Which creatine kinase iso enzyme is used for identifying an MI?
CK-MB the cardiac iso enzyme.
67
How do CK-MB levels change over the course of a MI?
Rise after 3-8 hours of onset of pain, peak at 24 hours and return to normal within 48-72 hours.
68
When is STEMI diagnosed over NSTEMI?
ST elevation in >2 leads facing the same area - 1mm in limb leads or 2mm in chest leads. Or new left bundle branch block.
69
When is NSTEMI or unstable angina diagnosed over STEMI?
ST segment depression, and T wave inversion. Or no ECG changes.
70
What are the aims of acute coronary syndrome treatment?
Restore perfusion, prevent muscle loss.
71
How are STEMI immediately dealt with?
If an emergency percutaneous coronary intervention is available in 90-120 minutes, then that is performed, if not fibrinolytic therapy is given.
72
How are partial occlusions in acute coronary syndrome immediately dealt with?
Anti thrombotic therapy to prevent extension of thrombus, risk assessment performed - if high risk, then early restoration of perfusion in partially occluded vessels using angiography or percutaneous coronary intervention or bypass.
73
What is the goal of treating STEMI?
Save the myocardium.
74
How are STEMI treated?
Pain control, dual anti platelet therapy - aspirin and ticagrelor, perfusion reestablished as soon as possible, anti ischaemic therapy - IV nitrates and B-blockers, ACE inhibitors and statins.
75
What is the goal of treating NSTEMI and unstable angina?
Prevent MI and muscle loss.
76
How are NSTEMI and unstable angina treated?
Pain control, dual antiplatelet therapy - aspiring and ticagrelor, prevent progression of thrombosis with antiplatelets and anticoagulatns, risk assessment, anti ischaemic therapy - IV nitrates and B blockers, ACE inhibitors and statins.
77
What groups of drugs are used in acute coronary syndrome?
Fibrinolytic agents to dissolve the thrombus if STEMI, anti platelet drugs to prevent thrombosis, anti coagulants to act on coagulation cascade to prevent thrombosis.
78
What are the long term treatments following MI?
Aspirin, B blockers, ACE inhibitors, statins, managing risk factors.
79
What are the complications of MI?
Sudden cardiac death, arrhythmias: sinus tachycardia, sinus bradycardia, heart block, ventricular tachycardia, ventricular fibrillation, or atrial fibrillation, also heart failure from loss of myocardium, and cardiogenic shock if >40% of myocardium is infarcted.

7. CVS (21 decks)

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