Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

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

At what point does an atheromatous plaque cause angina?

A

When it occludes more than 70% of the lumen

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

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

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

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

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

How does unstable angina form?

A

Develops from stable angina, due to increased occlusion of lumen

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

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

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

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

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

Describe the autonomic features of an MI (adrenaline)

A

Sweating, pallor, nausea and vomiting

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

What is an NSTEMI

A

Non ST Elevated Myocardial Infarction

Infarct is not full thickness of myocardium

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

What is a STEMI

A

ST Elevated Myocardial Infarction

Infarct is full thickness of myocardium

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

What is the clinical diagnosis of angina based on ?

A

History

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

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

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

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

A

Exercise stress test

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
``` Describe STEMI Occlusion by thrombosis? Myocardial necrosis? ECG character? Biochemical blood markers? ```
``` Occlusion by thrombosis? Total Myocardial necrosis? Large myocardial infarct ECG character? ST segment elevation Biochemical blood markers? Troponin ```
26
How can initial ECG be used to to differential STEMI from NSTEMI/Unstable Angina
SEE DIAGRAM!
27
What causes ST depression in NSTEMI and unstable angina?
K+ leak from injured subendocardial (partial thickness, highest intensity area!) causes depolarisation as ST segment depolarises in ECG lead facing area
28
What do you get minutes to hours after an MI?
ST elevation | T wave upright
29
What happens after STEMI diagnosed?
Either primary PCI or fibrinolytic therapy
30
What do you get hours to days after MI?
ST elevation, decreased T wave Decreased R wave Pathological Q wave begins
31
What causes ST elevation in STEMI?
K+ leak from injured subepicardial (full thickness!) myocyte, causing depolarisation + ST segment elevation in ECG leads facing injured area
32
What do you get days 1-2 after MI?
Deep pathological Q wave ST elevation, decreased T wave Decreased R wave
33
What do you get over 2 days after an MI?
ST normalises T wave inverted Pathological Q wave
34
What do you get weeks after an MI?
ST & T normal | Q wave persists
35
How can previous MIs be identified?
Persistence of pathological, deepened Q wave
36
How can you determine where someone's had an MI?
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
What causes pathological q wave?
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
See other deck of flashcards for lead view Mis
yay..
39
Name two troponins important in MI detection
Cardiac Troponin I (cTnI) and Troponin T (cTnT) are proteins important in actin/myosin interaction, which are released in myocyte death.i
40
Why is it good to test for cardiac troponins?
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
What is the iso-enzyme found in the blood after MUI?
CK-MB, rising 3-8 gours after onset, peaking at 24hrs.
42
What does the prescence of troponin or creatine kinase indicate?
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
How do you treat unstable angina?
Prevent UA from progressing to MI and limiting muscle loss in MI Prevent progression of thrombosis Restore perfusion of partially occluded vessels
44
How do you prevent progression of thrombosis in unstable angina/MI?
Anti Thrombotic therapy Anti platelet agents: Aspirin Anticoagulants: Heparin
45
How do you restore perfusion of partially occluded vessels in unstable angina/MI?
``` High risk Early Percutaneous Coronary Intervention (Angioplasty) (PCI) Coronary Artery Bypass Graft (CABG) Low Risk Initially medical treatment ```
46
What are some general treatments for coronary artery syndrome in unstable angina/MI?
``` O2 Organic Nitrates B-blockers Statins ACE-Inhibitors ```
47
What are three surgical treatmeants for CAD?
Angiography Percutaneous coronary intervention Coronary bypass grafting
48
What is angiography used for?
to view any vessel occlusions, and from the findings choices can be made about revascularisation surgeries.
49
What does aspirin do?
Reduced platelet aggregation, decreased thrombus formation
50
What is percutaneous coronary intervention?
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
What is involved in a CBPG?
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
Describe 5 causes of acute pericarditis?
``` Infections (viral, TB) Past MI/cardiac surgery Autoimmune Uraemia (kidney failure) Malignant Deposits ```
53
Describe the symptoms of acute pericarditis
Central/left sided chest pain Sharp, worse than inspiration Improved by leaning forward
54
What vessels are used in CABG
Reversed great saphenous vein | Radial artery
56
What happens after NSTEMI diagnosed?
Anti thrombotic therapy | Early PCI
57
Give some complications of MIl
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
What would you see in the ECG of someone with pericarditis?
ST elevation with upward concavity in all leads
59
What is a complication of pericarditis?
Pericardial effusion
60
What would be the treatment of pericarditis?
Pericardiocentesis
61
What is aortic dissection ?
Tear in the intima of aorta
62
What are four causes of aortic dissection?
Hypertension Trauma Marfan's syndrome Iatrogenic catheterisation
64
What is acute coronary syndrome? | What is the priority and initial treatments?
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)

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