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Cardiovascular System > Session 10 - Chest pain and IHD > Flashcards

Session 10 - Chest pain and IHD Flashcards

1
Q

Where does cardiovascular chest pain occur in the thorax?

A

-Central

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2
Q

What type of pain is experienced in myocardial ischaemia?

A

-Tightening

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3
Q

What type of pain is associated with pericarditis?

A

-Sharp pain

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4
Q

What type of pain is associated with aortic dissection?

A

-Tearing pain

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5
Q

What are the common respiratory causes of chest pain?

A
  • Infection (pneumonia)
  • Pulmonary embolism
  • Pneumothorax
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6
Q

Where does respiratory chest pain occur in the thorax?

A

-Lateral chest pain

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7
Q

What type of pain is associated with respiratory chest pain?

A

-Pleuritic pain (worsens on inspiration or coughing)

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8
Q

What are the common causes of GI chest pain?

A
  • Reflux oesophagitis

- Gastric/gallbladder or pancreatic disease

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9
Q

What type of pain is associated with GI chest pain?

A

-Burning pain

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10
Q

What are common causes of musculoskeletal chest pain?

A
  • Trauma
  • Muscle pain
  • Bone metastases
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11
Q

What type of pain is associated with musculoskeletal chest pain?

A

-Often localised pain which may increase on movement

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12
Q

Simply, when does myocardial ischaemia occur?

A

-When supply cannot meet demand

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13
Q

What determines the O2 demand of the heart?

A

-HR, Wall tension (pre-load and after load), contractility

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14
Q

What determines O2 supply to the heart?

A
  • Coronary bloodflow (perfusion and resistance)

- O2 carrying capacity of the blood

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15
Q

What is the most common cause of ischaemic heart disease?

A

-A fixed narrowing of the arteries due to atheromatous coronary artery disease

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16
Q

Why is the sub-endocardial muscle most vulnerable to ischaemia?

A

-Blood flow occurs from epicardium to endocardium

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17
Q

How is flow increased to meet demand?

A

-Vasodilation of coronary arteries

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18
Q

When do the coronary arteries mainly fill?

A

-During diastole

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19
Q

Why are collaterals relevant in IHD?

A

-There is little collateral circulation in the heart, meaning narrowing and occlusion severely deplete the supple to the heart

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20
Q

What are the rare causes of IHD?

A
  • Severe anaemia
  • Severe hypotension
  • Non-atheromatous causes of coronary artery narrowing
  • Thyrotoxicosis (increased BMR)
  • Tachycardia
  • Aortic stenosis
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21
Q

Why can aortic stenosis cause IHD?

A

-Pressure in root of aorta decreased and thus less blood driven through coronary arteries

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22
Q

What are the non-modifiable risk factors for CAD?

A
  • Age
  • Gender (males )
  • Family history
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23
Q

What are the modifiable risk factors for CAD?

A
  • Hyperlipidaemia (LDL/HDL ratio)
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Lack of exercise
  • Obesity
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24
Q

What are the two main features of an atheromatous plaque?

A
  • Necrotic core

- Fibrous cap

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25
Q

Describe a stable plaque

A

-Small necrotic core with a thick fibrous cap, unlikely to fissue/rupture

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26
Q

Describe a vulnerable plaque

A

-Large necrotic core with thin fibrous cap, likely to fissure/rupture

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27
Q

Why can thrombus formation occur with vulnerable plaques?

A
  • Fibrous cap undergoes erosion or fissuring
  • Exposes blood to thrombogenic material in necrotic core
  • Platelet aggregation followed by fibrin clot formation -> thrombus
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28
Q

What is a thrombus?

A

-Mass of coagulated blood causing partial or complete occlusion of an artery

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29
Q

What symptoms are produced from a stable plaque?

A

-No symptoms or stable angina

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30
Q

By how much can the lumen be reduced by in stable angina?

A

-70%

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31
Q

What are the possible consequences of an unstable plaque?

A
  • Plaque fissure with thrombus formation causes sudden reduction in artery lumen-> severe reduction in bloodflow -> ischaemia -> infarction
  • Acute coronary syndrome
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32
Q

What conditions are classified under acute coronary syndrome?

A
  • Stable angina
  • Unstable angina
  • STEMI
  • NSTEMI
33
Q

What type pf plaque is present in stable angina?

A

-Stable plaque

34
Q

When does pain occur in stable angina and why?

A

-Only during periods of increased O2 demend, as flow is adequate at rest (ie exertion/emotional stress) as the narrowing of the coronary arteries means vasodilation cannot occur and also upon exertion diastole is shortened which means coronary arteries have less time to fill

35
Q

What is characteristic about the pain in stable angina?

A

-Relieved about 5 mins after rest or nitrates

36
Q

Does necrosis or myocyte injury occur in stable angina?

A

-No

37
Q

Describe the chest pain caused by ischaemia, including possible radiation sites

A

-Diffuse central tightening/crushing pain which can radiate to the left shoulder and arm, right shoulder and arm, neck, jaw and upper epigastrium

38
Q

How is stable angina usually diagnosed

A

-Based on history -> patient has no specific signs but may have signs of risk factors eg high bp, corneal arcus, signs of atheroma elsewhere (PVD)

39
Q

Describe the resting ECG in a patient with stable angina

A

-Normal

40
Q

How is the concluding diagnsosis made if stable angina is suspected?

A

-Stress ECG

41
Q

When does a stress ECG run till?

A 
-Target heart rate reached
or
-Chest pain occurs 
or
-ECG changes 
or
-Other problems (arrythmias etc)
42
Q

Describe a stress ECG in stable angina

A

-ST depression (horizontal or downsloping) >1mm which disappears when patient at rest

43
Q

What is the aim of treatment for stable angina?

A
  • To reduce myocardial O2 demand through preload/afterload, HR and contractility
  • Increase bloodflow to arteries
44
Q

Why is aspirin used in CAD?

A

-To prevent MI as it decreases platelet aggregation and thus thrombus formation if plaque ruptures

45
Q

What is Percutaneous Coronary Intervention and Stenting?

A

-A method of revascularisation whereby a catheter is introduced into the coronary artery beyond the plaque, a balloon inflated and a stent inserted

46
Q

What is a coronary artery bypass?

A

-Artery from internal mammary artery, radial artery and saphenous vein used to revascularise the heart

47
Q

What is a STEMI?

A

-ST elevation MI

48
Q

When does a STEMI occur?

A

-When there is complete persistent occlusion which affects a large area of myocardium

49
Q

What is an NSTEMI?

A

-Non ST Elevation MI

50
Q

When does an NSTEMI/unstable angina occur?

A

-Brief partial occlusion affecting a small area of myocardium as collateral are present

51
Q

Describe the ischaemia and necrosis in STEMI and NSTEMI/unstable angina

A
  • STEMI-> severe ischaemia with lots myocardial necrosis

- NSTEMI/unstable angina -> less severe ischaemia -> necrosis may or may not be present

52
Q

What is the difference between NSTEMI and unstable angina

A

-Unstable angina there is ischaemia but no necrosis (ie no infarction)

53
Q

In which acute coronary syndromes are biomarkers present?

A
  • STEMI

- NSTEMI

54
Q

In which leads does the ST elevation of a STEMI show in?

A

-The leads facing the injured area

55
Q

What is the treatment of STEMI?

A
  • emergency PCI if available

- If not available fibrinolysis

56
Q

What is the history of unstable angina?

A
  • Acute worsening of stable angina
  • More frequent, severe and longer in duration with angina present at rest
  • Presence of risk factors
57
Q

What are the autonomic features of an MI?

A

-Sweating, pallor, vomiting

58
Q

What two investigations are used to investigate acute coronary syndrome?

A
  • ECG

- Cardiac biomarkers

59
Q

How is a STEMI differentiated from unstable angina or NSTEMI?

A
  • ECG STEMI will have ST elevation

- ECG UA/NSTEMI will have ST depression or T wave inversion

60
Q

What are the most specific biomarkers of cardiac infarction?

A

-cTnI and cTnT

61
Q

What is troponin?

A

-Molecule involved in sliding filament model made of 3 subunits
TnI binds to actin
TnT binds to tropomyosin
TnC binds to Ca

62
Q

What do elevated levels of TnI and TnC in the blood indicate?

A

-Myocardial infarction

63
Q

When do TnI and TnT levels peak?

A

-approx 24hours (18-36 hours)

64
Q

How long after an MI does troponin start to rise?

A

4 hours after onset of pain

65
Q

How long does troponin take to decline?

A

-10-14 days

66
Q

Which creatine kinase enzyme is the cardiac isoenzyme?

A

-CK-MB

67
Q

When does CK-MB begin to rise in MI?

A

-3-8 hours after onset

68
Q

When does CK-MB peak after MI?

A

-approx, 24 hours

69
Q

How long does CK-MB take to reduce to normal levels?

A

-48-72 hours

70
Q

What 3 ECG changes occur in a STEMI?

A
  • Q waves
  • ST elevation
  • T wave inversion
71
Q

Why do pathological Q waves occur?

A

-Dead myocardium is used as a window for electrical activity, so electrical activity is not recorded from damaged myocardium, producing a downwards Q wave as depolarisation is away from the lead

72
Q

Describe pathological Q waves

A
  • Wide -> >1 tiny square
  • Deep -> 25% of QRS complex
  • Not always followed by R wave if damage large
73
Q

How is a NSTEMI/UA treated?

A
  • Prevention of extension of thrombus by antithrombotic (aspirin -> antiplatelet) and anticoagulative therapy
  • Early restoration of perfusion in partially occluded vessels
74
Q

Name some longterm drug treatments after MI

A
  • Aspirin
  • Beta blocker
  • ACEI
  • Statin
75
Q

Name possible complications of an MI

A
  • Sudden cardiac death (Ventricular fibrillation)
  • Arrythmias (sinus tachycardia due to pain, anxiety, heart failure/sinus bradycardia due to SA node ischaemia)
  • Heart block (1st, 2nd and 3rd degree due to AV node ischaemia)
  • Ventricular tachycardia -> re-entry circuits due to ischaemic tissue or increase in spontaneous depolarisation of damaged tissue)
76
Q

Simply, why does MI lead to heart failure?

A

-Loss of myocardium = decreased contractility

77
Q

Why can MI cause cardiogenic shock?

A

-When >40% myocardium infarcted, there is a severe decrease in CO and systolic BP drops below 90mmHG with inadequate tissue perfusion

78
Q

What are the possible cardiovascular causes of chest pain?

A
  • Myocardial ischaemia
  • Pericarditis
  • Aortic dissection

Cardiovascular System (19 decks)

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