CVS S10 - Ischaemic Heart Disease Flashcards Preview

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Flashcards in CVS S10 - Ischaemic Heart Disease Deck (33):
1

What are the 4 major areas of the body that may contribute to chest pain?

Lungs and pleura

GI system

Chest wall

CVS (Heart and great vessels)

2

What might be the cause of chest pain with origin in the lungs and pleura?

Pneumonia

Pulmonary embolism

Pneumothorax

3

What might be the cause of chest pain with origin in the GI system?

Acid Reflux

Peptic ulcer disease

Gall bladder (Biliary colic, cholecystitis)

4

What might be the cause of chest pain with origin in the chest wall?

Rib (Fractures, bone metastases)

Muscles

Skin

5

What might be the cause of chest pain with origin in the CVS?

Myocardium (Angina, MI)

Pericardium (Pericarditis)

Aorta (Aortic dissection)

6

What are the risk factors for coronary atheroma?

Non-modifiable:

- Increasing age

- Male (Females post menopause)

- Family history

Major Modifiable:

- Hyperlipidaemia

- Smoking

- Hypertension

- Diabetes mellitus

Minor Modifiable:

- Exercise

- Obesity

- Stress

7

Describe Ischaemic chest pain

Location?

Quality?

Variation?

Central, retrosternal or left sided

Pain may radiate (more commonly left sided than left in these locations):

- Neck

- Jaw

- Epigastrum

- Back

Pain in these locations may appear without chest pain

Pain described as:

- Crushing

- Heavy

- Constricting

- Sometimes burning epigastric pain (inferior MI)

Can vary in:

- Intensity and duration

- Onset

- Precipitating or relieving factors

- Associated symptoms

However everything tends to get progressively worse from Stable angina to unstable angina to MI

8

Describe the pathophysiology of stable angina

Atheromatous plaque with a necrotic core and fibrous cap build up in the coronary vessels, occluding more and more of the lumen

This leads to transient ischaemia of the myocardium when heart is stressed, relieved when O2 demand falls

Angina occurs after >70% occlusion

9

Describe in specific the chest pain associated with stable angina

Chest pain is in brief episodes and is mild to moderate Precipitating factors:

- Cold weahter

- Exertion

- After meals

- Emotion

10

What are the treatments for stable angina?

Hint: 4 categories of treatment

To treat acute episodes:

- Sublingual nitrate sprays/tablets

To prevent episodes:

- B-blockers

- Ca2+ channel blockers

- Oral nitrates

Prevent acute cardiac events:

- Aspirin

- Statins

- ACE inhibitors

Long term:

- Consider revascularisation

11

Describe how unstable angina differs from stable angina in terms of pathophysiology and pain

Angina worsens due to progression of the formation of the atheromatous plaque and increased vessel occlusion

Ischaemic chest pain occurs at rest or with minimal exertion

Described as severe pain that is more prolonged and occurring in crescendo pattern

12

Describe the pathophysiology of an MI

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

The fibrous cap of the atheromatous plaque undergoes erosion or fissuring exposing blood to thrombogenic material in the necrotic core

The platelet clot is followed by a fibrin thrombus which completely occludes the vessel (or embolises)

13

Describe the pain associated with an MI

What are some of the associated symptoms?

Typical ischaemic chest pain that is very severe, persistent, at rest and often no precipitant It is not relieved by nitrates or rest

The patient may also be:

- Breathless (due to LV dysfunction)

- Have a feeling of impending death

- Sweating, Pallor, Nausea/vomiting

- Tachycardia/arrhythmia

- Low BP

14

Why is a patient having an MI likely to be sweating, pale and vomiting?

Sympathetic nervous system overdrive to try and compensate for LV dysfunction by raising heart rate

15

Describe the investigation of a patient with suspected angina

Initial investigation based on history, looking for risk factors

Risk factors include:

- Elevated BP

- Corneal Arcus

- LV dysfunction

- Evidence of atheroma (E.g. Peripheral vascular disease)

Resting ECG is usually normal, but may show signs of previous MI (pathological Q wave)

Exercise stress test is undertaken to confirm

16

Describe the process of performing an exercise stress test What is a positive result for angina?

Graded exercise on a treadmill attached to an ECG until either:

- Target heart rate reached

- Chest pain

-ECG changes

- Other problems (E.g. Arrhythmia/low BP etc)

Test positive for angina when ECG shows ST depressions of >1mm (stronger = critical stenosis) when exercising

17

What is acute coronary syndrome?

A group of symptoms attributed to the obstruction of the coronary arteries ACS is a result of:

- Unstable angina

- NSTEMI

- STEMI

18

DIfferentiate Unstable angina, STEMI and NSTEMI based on these 4 criteria (listed in this order under condition headings):

- Occlusion by thrombus

- Myocardial necrosis

- ECG

- Biochemical markers in blood

UA:

- Partial (or full w/ collaterals)

- None

- May be ST depression/T wave inversion/normal

- None

NSTEMI:

- Partial (or full w/ collaterals)

- Some (confined to endocardium)

- No ST elevation

- Troponin

STEMI:

- Complete (not adequate collaterals)

- Large myocardial infarct extending to sub-epicardium

- ST elevation

- Troponin

19

What are these ECG traces showing?

What features of the trace do you look at to come to a conclusion?

Q image thumb

Right shows the typical trace of someone with Unstable angina or having an NSTEMI as evidenced by:

- ST depression >1mm

- T wave inversion

- May be normal however

Left shows typical trace seen in a STEMI as evidenced by:

- ST elevation of >1mm (make sure it's in >2 leads)

 

20

What does this diagram show?

For each picture fill in the white boxes describing how the trace has changed

Q image thumb

Diagram shows progression of ECG trace following a STEMI

1. Normal

2. ST elevation and upright T wave

3. ST elevation, inverted T wave, Q wave deepens

4. Q wave deepens further

5. ST normalises, T wave inverted, Q wave persists

6. ST and T normal, pathological Q wave persists

21

How can the site of an MI be determined?

By looking at ECG leads, abnormalities due to dead myocardium will be seen in different leads

Looking at which leads are abnormal and their view allows for localisation of the MI

22

There are 6 broad areas of the heart that an MI can be localised to, give each and state which leads will be abnormal and which coronary artery is affected when an MI occurs in that area

 

Table overleaf, cover it with your hand and reveal it a row or column at a time?

 

Just a suggestion, I'm a flashcard, not your supervisor.

A image thumb
23

Describe the involvement of Troponins in acute coronary syndrome

Cardiac troponin 1 (cTnI) and Troponin T (cTnT)  are proteins involved in the actin myosin interactions in cardiac myocytes

Released on cardiomyocyte death

Very sensitive and specific marker

Rising 3-4 hrs after onset of pain and peaking at 18 - 36 hrs

Then decline for up to 10 - 14 days

24

Describe the involvement of Creatine Kinases in acute coronary syndrome

CK-MB is the cardiac isoenzyme of CK

Released into blood after cardiomyocyte death

Rises 3-8 hrs after onset of pain, peaking at 24hrs

Levels return to normal in 2 - 3 days

25

How does the presence of CK-MB and cardiac troponins in the blood help our differential diagnoses for acute chest pain?

Distinguishes between unstable angina and an NSTEMI

No tissue death in UA, therefore no biomarkers in blood as there is in a NSTEMI

26

What is the goal of treatment for unstable angina/MI?

Prevent UA from progression to MI and limiting muscle loss in MI

27

What are the treatments for unstable angina/MI?

Categorise by treatment targets

Prevent progression of thrombosis:

- Antithrombotic therapy

- Aspirin, Heparin

- Thrombolytics (If PCI not available)

Restore perfusion to highly occluded vessels:

High risk

- Percutaneous coronary intervention (angioplasty)

- Coronary artery bypass graft (CABG)

Low risk

- Initial medical treatment

- Followed by elective angioplasty

Long term:

- Pain control

- O2

- Organic nitrates

- B-blockers

- Statins

- ACE inhibitors

- Manage risk factors (E.g. Stop smoking)

28

Why is an angiogram useful to treatment of coronary artery disease?

Can be used to view vessel occlusions

Use the findings to make a choice about revascularisation surgery

29

Describe percutaneous coronary intervention

Why is it useful in treatment of coronary artery disease?

Angioplasty and stenting

Inflation of a ballon inside the occluded vessel expands a mesh that holds the vessel open

This increases lumen size allowing more blood flow and relieving ischaemia

30

Describe coronary bypass grafting (CABG)

Why is it useful in the treatment of coronary artery disease?

Involves taking an artery or reversed vein (E.g. Radial artery, Saphenous vein) and grafting it to the heart

This allows the occlusion to be bypassed by blood flow, so blood flow increases

This relieves ischaemia

31

What are the causes of pericarditis?

Infection (viral, TB)

Post MI/cardiac surgery

Autoimmune

Uraemia (kidney failure)

Malignant deposits

32

What are the symptoms of pericarditis?

Central/left sided chest pain

Sharp, worse on inspiration

Improved by leaning forward

33

GIve some complications of MI

Sudden cardiac death (VFib/asystole)

Arrhythmia:

- Sinus tachycardia

- Sinus bradycardia (SAN ischaemia)

Heart block (All degrees)

2nd and 3rd degree may require temporary pacemaker

V Tachycardia / VFib:

Ventricular ischaemia causing re-entry loops

Heart Failure

 - Loss of myocardium, reduced contractility

Cardiogenic shock

- >40% of myocardium infarcted

- Severe output reduction

- Systemic BP >90mmHg, inadequate for proper perfusion