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Semester 2 - CVS > Session 10 - Ischaemic Heart Disease and Chest Pain > Flashcards

Session 10 - Ischaemic Heart Disease and Chest Pain Flashcards

1
Q

Describe the structure of atheromas in stable angina?

A

Atheromatous plaques with a necrotic centre and fibrous cap

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2
Q

What is the effect of atheroma in IHD?

A

Occlude more and more of the lumen as they build up in coronary vessels. This leaves less space for passage of blood and ischaemia in myocardium

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3
Q

At what point does an atheromatous plaque cause angina?

A

When it occludes more than 70% of the lumen

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4
Q

What occurs in stable angina?

A

Brief episode of ischaemia pain brought on by stress.
Predictable pain, relieved by rest or nitrates within five minutes.
Presence of risk factors

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5
Q

What is brief chest pain in ischaemic heart disease typically caused by? How is it described?

A

brought on by exertion, emotion particularly after meals and in cold weather. It is described as mild to moderate pain.

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6
Q

What is the treatment of
acute episodes of angina
preventative episodes of angina

A

Preventative - B blockers, Ca2+ channel blockers, oral nitrates
Prevent cardiac events- Aspirin, statins, ACE inhibitors
Long term - consider revascularisation

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7
Q 
In basic terms, what is the use of 
Nitrates 
Ca2+ blocker
ACE inhibitors 
Beta blockers 
In stable angina
A

Nitrates - decreased preload, venodilation
Ca2+ blocker - decreased after load, peripheral vasodilation
ACE inhibitors - reduced after load
Beta blockers - Reduced HR and contractility

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8
Q

How does unstable angina form?

A

Develops from stable angina, due to increased occlusion of lumen

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9
Q

Define unstable angina

A

Ischaemic Chest Pain that occurs at rest (or with minimal exertion) described as severe pain and occurring with a crescendo pattern (distinctly more severe, prolonged, or frequent than before)

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10
Q

Define MI

A

A MI is a complete occlusion of a coronary vessel, leading to an infarct (death) of the myocardium it supplies.

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11
Q

What can happen to an atheroma to form a thrombosis which will occlude a vessel?

A

The fibrous cap of the Atheromatous plaque can undergo erosion or fissure, exposing blood to the thombogenic material in the necrotic core.The platelet ‘clot’ is followed by a fibrin thrombus, which can either occlude the entire vessel where it forms or break off to form an embolism.

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12
Q

How does MI present?

A

MI presents with typical ischaemic chest pain that is very severe, persistent, at rest and often with no precipitant. It is not relieved by rest or nitrate spray. The patient may also be breathless, faint, feeling of impending doom and autonomic features.

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13
Q

Describe the autonomic features of an MI (adrenaline)

A

Sweating, pallor, nausea and vomiting

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14
Q

What is an NSTEMI

A

Non ST Elevated Myocardial Infarction

Infarct is not full thickness of myocardium

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15
Q

What is a STEMI

A

ST Elevated Myocardial Infarction

Infarct is full thickness of myocardium

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16
Q

What is the clinical diagnosis of angina based on ?

A

History

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17
Q

What are the four risk factors for angina which can be revealed from a cardiovascular exam?

A

Elevated BP
Corneal arcus
LV dysfunction
Signs of peripheral vascular disease

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18
Q

What is the resting ECG of someone with stable angina usually like?

A

Normal, but may show signs of previous MI (pathological Q wave)

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19
Q

How do you confirm stable angina if a resting ECG is normal?

A

Exercise stress test

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20
Q

What is an exercise stress test? How long does it go on for?

A 
Graded exercise on a treatment connected to an ECG until:
Target heart rate reached
OR
Chest Pain
OR
ECG changes
OR
Other problems – arrhythmias, low BP etc…
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21
Q

QUESTION What is a positive ECG after exercise stress test for stable angina?

Why do you get st depression, cell death?

A

Shows ST depressions of >1mm. A strong positive test indicates critical stenosis

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22
Q

What is acute coronary syndrome? What is it a result of?

A

Acute Coronary Syndrome (ACS) relates to a group of symptoms attributed to the obstruction of the coronary arteries. ACS is a result of:
Unstable Angina
NSTEMI
STEMI

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23
Q 
Describe unstable angina 
Occlusion by thrombosis?
Myocardial necrosis?
ECG character?
Biochemical blood markers?
A 
Occlusion by thrombosis?
Partial
Myocardial necrosis?
None
ECG character?
May have ST segment depression, T wave inversion or normal
Biochemical blood markers?
None
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24
Q 
Describe NSTEMI
Occlusion by thrombosis?
Myocardial necrosis?
ECG character?
Biochemical blood markers?
A 
Occlusion by thrombosis?
Partial
Myocardial necrosis?
Some
ECG character?
No ST segment elevation
Biochemical blood markers?
Troponin
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25
Q 
Describe STEMI
Occlusion by thrombosis?
Myocardial necrosis?
ECG character?
Biochemical blood markers?
A 
Occlusion by thrombosis?
Total
Myocardial necrosis?
Large myocardial infarct
ECG character?
ST segment elevation
Biochemical blood markers?
Troponin
26
Q

How can initial ECG be used to to differential STEMI from NSTEMI/Unstable Angina

A

SEE DIAGRAM!

27
Q

What causes ST depression in NSTEMI and unstable angina?

A

K+ leak from injured subendocardial (partial thickness, highest intensity area!) causes depolarisation as ST segment depolarises in ECG lead facing area

28
Q

What do you get minutes to hours after an MI?

A

ST elevation

T wave upright

29
Q

What happens after STEMI diagnosed?

A

Either primary PCI or fibrinolytic therapy

30
Q

What do you get hours to days after MI?

A

ST elevation, decreased T wave
Decreased R wave
Pathological Q wave begins

31
Q

What causes ST elevation in STEMI?

A

K+ leak from injured subepicardial (full thickness!) myocyte, causing depolarisation + ST segment elevation in ECG leads facing injured area

32
Q

What do you get days 1-2 after MI?

A

Deep pathological Q wave
ST elevation, decreased T wave
Decreased R wave

33
Q

What do you get over 2 days after an MI?

A

ST normalises
T wave inverted
Pathological Q wave

34
Q

What do you get weeks after an MI?

A

ST & T normal

Q wave persists

35
Q

How can previous MIs be identified?

A

Persistence of pathological, deepened Q wave

36
Q

How can you determine where someone’s had an MI?

A

The site of an MI can be localised using an ECG, as abnormalities will be seen due to the infarcted, dead myocardium. Look at which lead the abnormality is on and where that lead’s view is allows localisation of the MI.

37
Q

What causes pathological q wave?

A

Q moves from left to right side and vice versa of inter ventricular septum
Area of necrosis in left myocardium provides ‘window’ - only depolarisation going AWAY from lead view shown, so Q depolarisation away massively depolarised down

38
Q

See other deck of flashcards for lead view Mis

39
Q

Name two troponins important in MI detection

A

Cardiac Troponin I (cTnI) and Troponin T (cTnT) are proteins important in actin/myosin interaction, which are released in myocyte death.i

40
Q

Why is it good to test for cardiac troponins?

A

Very sensitive and specific marker, rising 3-4hrs after the first onset of pain and peaking at 18-36 hrs. They will then decline slowly for up to 10-14 days.

41
Q

What is the iso-enzyme found in the blood after MUI?

A

CK-MB, rising 3-8 gours after onset, peaking at 24hrs.

42
Q

What does the prescence of troponin or creatine kinase indicate?

A

Death of the myocardium. It therefore distinguishes between unstable angina and NSTEMI, as there is no tissue death in unstable angina and there is in NSTEMI.

43
Q

How do you treat unstable angina?

A

Prevent UA from progressing to MI and limiting muscle loss in MI
Prevent progression of thrombosis
Restore perfusion of partially occluded vessels

44
Q

How do you prevent progression of thrombosis in unstable angina/MI?

A

Anti Thrombotic therapy
Anti platelet agents: Aspirin
Anticoagulants: Heparin

45
Q

How do you restore perfusion of partially occluded vessels in unstable angina/MI?

A 
High risk
Early Percutaneous Coronary Intervention (Angioplasty) (PCI)
Coronary Artery Bypass Graft (CABG)
Low Risk
Initially medical treatment
46
Q

What are some general treatments for coronary artery syndrome in unstable angina/MI?

A 
O2
Organic Nitrates
B-blockers
Statins
ACE-Inhibitors
47
Q

What are three surgical treatmeants for CAD?

A

Angiography
Percutaneous coronary intervention
Coronary bypass grafting

48
Q

What is angiography used for?

A

to view any vessel occlusions, and from the findings choices can be made about revascularisation surgeries.

49
Q

What does aspirin do?

A

Reduced platelet aggregation, decreased thrombus formation

50
Q

What is percutaneous coronary intervention?

A

Angioplasty and stenting. Inflation of a balloon inside the occluded vessel expands a mesh that holds the vessel open, increasing the lumen size and allowing for more blood to flow.

51
Q

What is involved in a CBPG?

A

involves taking an artery from elsewhere in the body, e.g. internal mammary artery, radial artery, saphenous vein (reversed because of valves) and grafting it to the heart.

52
Q

Describe 5 causes of acute pericarditis?

A 
Infections (viral, TB)
Past MI/cardiac surgery
Autoimmune
Uraemia (kidney failure)
Malignant Deposits
53
Q

Describe the symptoms of acute pericarditis

A

Central/left sided chest pain
Sharp, worse than inspiration
Improved by leaning forward

54
Q

What vessels are used in CABG

A

Reversed great saphenous vein

Radial artery

56
Q

What happens after NSTEMI diagnosed?

A

Anti thrombotic therapy

Early PCI

57
Q

Give some complications of MIl

A

Arrythmia

  • tachycardia (anxiety)
  • bradycardia (SA node ischaemia£
  • heart block (av node ischaemia)
  • Ventricular tachycardia (recently looping)
  • Atrial fibrillation
Heart failure (decreases myocardial contractility) 
Cardiogenic shock
58
Q

What would you see in the ECG of someone with pericarditis?

A

ST elevation with upward concavity in all leads

59
Q

What is a complication of pericarditis?

A

Pericardial effusion

60
Q

What would be the treatment of pericarditis?

A

Pericardiocentesis

61
Q

What is aortic dissection ?

A

Tear in the intima of aorta

62
Q

What are four causes of aortic dissection?

A

Hypertension
Trauma
Marfan’s syndrome
Iatrogenic catheterisation

64
Q

What is acute coronary syndrome?

What is the priority and initial treatments?

A

Chest pain lasting longer than 15 minutes, priority is to separate into STEMI or NSTEMI/unstable angina

ECG, cardiac biomarkers

Semester 2 - CVS (15 decks)

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