Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where does cardiac caused chest pain occur?

A

Central pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where does respiratory caused chest pain occur?

A

Lateral chest pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does GI caused chest pain occur?

A

Chest and epigastric pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does musculoskeletal caused chest pain occur?

A

Localised to the area of damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What would tightening pain in the central chest region suggest?

A

Myocardial ischaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What would sharp pain in the central chest region suggest?

A

Pericarditis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What would tearing pain in the central chest region suggest?

A

Aortic dissection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What respiratory problems can cause chest pain?

A

Infections, like pneumonia, pulmonary embolism, pneumothorax.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Pleuritic pain - gets worse on inspiration and coughing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What GI problems can cause chest pain?

A

Reflux oesophagus, gastric/ gall bladder/ pancreatic problems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

Reflux - a burning pain that moves upwards.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What musculoskeletal problems can cause chest pain?

A

Trauma, muscle pain from excessive use, bone metastases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the direction of coronary blood flow?

A

From epicardium to endocardium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When does coronary heart flow occur?

A

In diastole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most common cause of ischaemic heart disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does myocardial oxygen demand depend on?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does anaemia cause ischaemia?

A

It reduces the O2 carrying capacity of the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are some modifiable risk factors for coronary artery disease?

A

Hyperlipidaemia, cigarette smoking, hypertension, diabetes mellitus, lack of exercise, obesity, diet low in fruit and vegetables, psychosocial factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the structure of atheromatous plaques?

A

Necrotic centre and fibrous cap.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the structure of stable atheromatous plaques?

A

Small necrotic core, thick fibrous cap, cap less likely to fissure/rupture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the structure of vulnerable atheromatous plaques?

A

Large necrotic core, thin fibrous cap, cap more likely to fissure/ rupture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why are unstable plaques so worrying?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the features of ischaemic chest pain?

A

Central, tightening/ constricting, characteristic pattern of radiation: left shoulder, left arm, right arm, jaw, and throat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the symptoms of stable angina?

A

No pain at rest, typical pain (moderate), precipitated by stress of exertion, relived by rest or nitrates within 5 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the symptoms of unstable angina/ acute coronary syndrome?

A

Pain at rest/ minimal exertion, more severe pain than stable angina, no relief with nitrates, long duration of pain.

33
Q

How can a diagnosis of stable angina be confirmed?

A

Stress ECG testing.

34
Q

How are exercise stress ECG tests performed?

A

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
Q

What are the results of exercise ECGs with stable angina?

A

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
Q

How are acute episodes of stable angina treated?

A

Sublingual nitrates (tablets under tongue or spray) for immediate relief of ischaemia and pain.

37
Q

How is stable angina dealt with in the long run?

A

Lifestyle changes: patient education, modify risk factors.
Medication: long acting nitrates, B-blockes, Ca2+ channel blockers, statins, and aspirin.
Revascularisation to restore circulation.

38
Q

How do nitrates work to treat stable angina?

A

Venodilators, so lessen preload.

39
Q

How do calcium channel blockers work to treat stable angina?

A

Decrease after load by peripheral vasodilatation.

40
Q

How do beta blockers work to treat stable angina?

A

Decrease heart rate and contractility.

41
Q

How does aspirin work to treat stable angina?

A

Decreases platelet aggregation so reduces thrombus formation if the plaque is disrupted.

42
Q

How do statins work to treat stable angina?

A

Decrease LDL cholesterol, hence reducing progression of atherosclerosis, increases plaque stability. It’s a secondary prevention.

43
Q

How does revascularisation work to treat stable angina?

A

Mechanically restores blood flow.

44
Q

How is revascularisation performed?

A

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
Q

What are the three types of graft available for coronary artery bypass grafting?

A

Internal mammary artery grafts, radial artery grafts, or saphenous vein grafts (reversed segment of vein so blood flows the correct way).

46
Q

What is acute coronary syndrome?

A

Includes unstable angina, and acute myocardial infarction.

47
Q

What are the two types of myocardial infarction according to ECG changes?

A

NSTEMI - non-ST elevation myocardial infarction.

STEMI - ST elevation myocardial infarction.

48
Q

What are acute coronary syndromes triggered by?

A

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
Q

How do NSTEMI and STEMI differ in obstruction to flow?

A

NSTEMI is often incomplete occlusion, STEMI is complete obstruction to flow.

50
Q

Why does total occlusion cause ST elevation?

A

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
Q

What is the difference between unstable angina and NSTEMI?

A

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
Q

What are the biochemical markers of myocyte damage?

A

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
Q

When are cardiac troponin I and T levels raised?

A

In NSTEMI and STEMI, not in unstable angina.

54
Q

What is the typical history of unstable angina?

A

Acute worsening of stable angina, angina at rest, recent onset of new, effort limiting angina.

55
Q

What is the typical history of myocardial infarction?

A

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
Q

What are the examination findings in acute MI?

A

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
Q

What are the ECG features of a fully evolved STEMI?

A

Q waves from area of necrosis, ST segment elevation from injury zone, T wave inversion.

58
Q

What are the measurements of a pathological Q wave?

A

Wide - >1 small square, deep - >25% of the QRS complex.

59
Q

Which artery causes inferior area of infarction and which leads does this show on?

A

Right coronary, and II, III, aVF leads.

60
Q

Which artery causes anteroseptal area of infarction and which leads does this show on?

A

Left anterior descending, leads V1 and V2.

61
Q

Which artery causes anteroapical area of infarction and which leads does this show on?

A

Ledt anterior descending, distal part, leads V3 and V4.

62
Q

Which artery causes anterolateral area of infarction and which leads does this show on?

A

Circumflex, leads I, aVL, V5, and V6.

63
Q

Which artery causes extensive anterior area of infarction and which leads does this show on?

A

Proximal left coronary artery, leads I, aVL, V2, and V6.

64
Q

Which artery causes true posterior area of infarction and which leads does this show on?

A

Right coronary artery, leads V1 - tall R wave.

65
Q

When do cardiac troponin levels rise?

A

4 hours after onset of pain in MI. They peak at 18-36 hours and decline slowly over 10-14 days.

66
Q

Which creatine kinase iso enzyme is used for identifying an MI?

A

CK-MB the cardiac iso enzyme.

67
Q

How do CK-MB levels change over the course of a MI?

A

Rise after 3-8 hours of onset of pain, peak at 24 hours and return to normal within 48-72 hours.

68
Q

When is STEMI diagnosed over NSTEMI?

A

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
Q

When is NSTEMI or unstable angina diagnosed over STEMI?

A

ST segment depression, and T wave inversion. Or no ECG changes.

70
Q

What are the aims of acute coronary syndrome treatment?

A

Restore perfusion, prevent muscle loss.

71
Q

How are STEMI immediately dealt with?

A

If an emergency percutaneous coronary intervention is available in 90-120 minutes, then that is performed, if not fibrinolytic therapy is given.

72
Q

How are partial occlusions in acute coronary syndrome immediately dealt with?

A

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
Q

What is the goal of treating STEMI?

A

Save the myocardium.

74
Q

How are STEMI treated?

A

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
Q

What is the goal of treating NSTEMI and unstable angina?

A

Prevent MI and muscle loss.

76
Q

How are NSTEMI and unstable angina treated?

A

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
Q

What groups of drugs are used in acute coronary syndrome?

A

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
Q

What are the long term treatments following MI?

A

Aspirin, B blockers, ACE inhibitors, statins, managing risk factors.

79
Q

What are the complications of MI?

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions