Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

What type of pain is experienced in myocardial ischaemia?

A

-Tightening

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

What type of pain is associated with pericarditis?

A

-Sharp pain

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

What type of pain is associated with aortic dissection?

A

-Tearing pain

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

What are the common respiratory causes of chest pain?

A
  • Infection (pneumonia)
  • Pulmonary embolism
  • Pneumothorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does respiratory chest pain occur in the thorax?

A

-Lateral chest pain

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

What type of pain is associated with respiratory chest pain?

A

-Pleuritic pain (worsens on inspiration or coughing)

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

What are the common causes of GI chest pain?

A
  • Reflux oesophagitis

- Gastric/gallbladder or pancreatic disease

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

What type of pain is associated with GI chest pain?

A

-Burning pain

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

What are common causes of musculoskeletal chest pain?

A
  • Trauma
  • Muscle pain
  • Bone metastases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of pain is associated with musculoskeletal chest pain?

A

-Often localised pain which may increase on movement

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

Simply, when does myocardial ischaemia occur?

A

-When supply cannot meet demand

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

What determines the O2 demand of the heart?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What determines O2 supply to the heart?

A
  • Coronary bloodflow (perfusion and resistance)

- O2 carrying capacity of the blood

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

-Blood flow occurs from epicardium to endocardium

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

How is flow increased to meet demand?

A

-Vasodilation of coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When do the coronary arteries mainly fill?

A

-During diastole

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

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

Why can aortic stenosis cause IHD?

A

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

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

What are the non-modifiable risk factors for CAD?

A
  • Age
  • Gender (males )
  • Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the modifiable risk factors for CAD?

A
  • Hyperlipidaemia (LDL/HDL ratio)
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Lack of exercise
  • Obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the two main features of an atheromatous plaque?

A
  • Necrotic core

- Fibrous cap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe a stable plaque
-Small necrotic core with a thick fibrous cap, unlikely to fissue/rupture
26
Describe a vulnerable plaque
-Large necrotic core with thin fibrous cap, likely to fissure/rupture
27
Why can thrombus formation occur with vulnerable plaques?
- Fibrous cap undergoes erosion or fissuring - Exposes blood to thrombogenic material in necrotic core - Platelet aggregation followed by fibrin clot formation -> thrombus
28
What is a thrombus?
-Mass of coagulated blood causing partial or complete occlusion of an artery
29
What symptoms are produced from a stable plaque?
-No symptoms or stable angina
30
By how much can the lumen be reduced by in stable angina?
-70%
31
What are the possible consequences of an unstable plaque?
- Plaque fissure with thrombus formation causes sudden reduction in artery lumen-> severe reduction in bloodflow -> ischaemia -> infarction - Acute coronary syndrome
32
What conditions are classified under acute coronary syndrome?
- Stable angina - Unstable angina - STEMI - NSTEMI
33
What type pf plaque is present in stable angina?
-Stable plaque
34
When does pain occur in stable angina and why?
-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
What is characteristic about the pain in stable angina?
-Relieved about 5 mins after rest or nitrates
36
Does necrosis or myocyte injury occur in stable angina?
-No
37
Describe the chest pain caused by ischaemia, including possible radiation sites
-Diffuse central tightening/crushing pain which can radiate to the left shoulder and arm, right shoulder and arm, neck, jaw and upper epigastrium
38
How is stable angina usually diagnosed
-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
Describe the resting ECG in a patient with stable angina
-Normal
40
How is the concluding diagnsosis made if stable angina is suspected?
-Stress ECG
41
When does a stress ECG run till?
``` -Target heart rate reached or -Chest pain occurs or -ECG changes or -Other problems (arrythmias etc) ```
42
Describe a stress ECG in stable angina
-ST depression (horizontal or downsloping) >1mm which disappears when patient at rest
43
What is the aim of treatment for stable angina?
- To reduce myocardial O2 demand through preload/afterload, HR and contractility - Increase bloodflow to arteries
44
Why is aspirin used in CAD?
-To prevent MI as it decreases platelet aggregation and thus thrombus formation if plaque ruptures
45
What is Percutaneous Coronary Intervention and Stenting?
-A method of revascularisation whereby a catheter is introduced into the coronary artery beyond the plaque, a balloon inflated and a stent inserted
46
What is a coronary artery bypass?
-Artery from internal mammary artery, radial artery and saphenous vein used to revascularise the heart
47
What is a STEMI?
-ST elevation MI
48
When does a STEMI occur?
-When there is complete persistent occlusion which affects a large area of myocardium
49
What is an NSTEMI?
-Non ST Elevation MI
50
When does an NSTEMI/unstable angina occur?
-Brief partial occlusion affecting a small area of myocardium as collateral are present
51
Describe the ischaemia and necrosis in STEMI and NSTEMI/unstable angina
- STEMI-> severe ischaemia with lots myocardial necrosis | - NSTEMI/unstable angina -> less severe ischaemia -> necrosis may or may not be present
52
What is the difference between NSTEMI and unstable angina
-Unstable angina there is ischaemia but no necrosis (ie no infarction)
53
In which acute coronary syndromes are biomarkers present?
- STEMI | - NSTEMI
54
In which leads does the ST elevation of a STEMI show in?
-The leads facing the injured area
55
What is the treatment of STEMI?
- emergency PCI if available | - If not available fibrinolysis
56
What is the history of unstable angina?
- Acute worsening of stable angina - More frequent, severe and longer in duration with angina present at rest - Presence of risk factors
57
What are the autonomic features of an MI?
-Sweating, pallor, vomiting
58
What two investigations are used to investigate acute coronary syndrome?
- ECG | - Cardiac biomarkers
59
How is a STEMI differentiated from unstable angina or NSTEMI?
- ECG STEMI will have ST elevation | - ECG UA/NSTEMI will have ST depression or T wave inversion
60
What are the most specific biomarkers of cardiac infarction?
-cTnI and cTnT
61
What is troponin?
-Molecule involved in sliding filament model made of 3 subunits TnI binds to actin TnT binds to tropomyosin TnC binds to Ca
62
What do elevated levels of TnI and TnC in the blood indicate?
-Myocardial infarction
63
When do TnI and TnT levels peak?
-approx 24hours (18-36 hours)
64
How long after an MI does troponin start to rise?
4 hours after onset of pain
65
How long does troponin take to decline?
-10-14 days
66
Which creatine kinase enzyme is the cardiac isoenzyme?
-CK-MB
67
When does CK-MB begin to rise in MI?
-3-8 hours after onset
68
When does CK-MB peak after MI?
-approx, 24 hours
69
How long does CK-MB take to reduce to normal levels?
-48-72 hours
70
What 3 ECG changes occur in a STEMI?
- Q waves - ST elevation - T wave inversion
71
Why do pathological Q waves occur?
-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
Describe pathological Q waves
- Wide -> >1 tiny square - Deep -> 25% of QRS complex - Not always followed by R wave if damage large
73
How is a NSTEMI/UA treated?
- Prevention of extension of thrombus by antithrombotic (aspirin -> antiplatelet) and anticoagulative therapy - Early restoration of perfusion in partially occluded vessels
74
Name some longterm drug treatments after MI
- Aspirin - Beta blocker - ACEI - Statin
75
Name possible complications of an MI
- 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
Simply, why does MI lead to heart failure?
-Loss of myocardium = decreased contractility
77
Why can MI cause cardiogenic shock?
-When >40% myocardium infarcted, there is a severe decrease in CO and systolic BP drops below 90mmHG with inadequate tissue perfusion
78
What are the possible cardiovascular causes of chest pain?
- Myocardial ischaemia - Pericarditis - Aortic dissection

Cardiovascular System (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions