What are the 4 major areas of the body that may contribute to chest pain?
Lungs and pleura
CVS (Heart and great vessels)
What might be the cause of chest pain with origin in the lungs and pleura?
What might be the cause of chest pain with origin in the GI system?
Peptic ulcer disease
Gall bladder (Biliary colic, cholecystitis)
What might be the cause of chest pain with origin in the chest wall?
Rib (Fractures, bone metastases)
What might be the cause of chest pain with origin in the CVS?
Myocardium (Angina, MI)
Aorta (Aortic dissection)
What are the risk factors for coronary atheroma?
- Increasing age
- Male (Females post menopause)
- Family history
- Diabetes mellitus
Describe Ischaemic chest pain
Central, retrosternal or left sided
Pain may radiate (more commonly left sided than left in these locations):
Pain in these locations may appear without chest pain
Pain described as:
- Sometimes burning epigastric pain (inferior MI)
Can vary in:
- Intensity and duration
- Precipitating or relieving factors
- Associated symptoms
However everything tends to get progressively worse from Stable angina to unstable angina to MI
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
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
- After meals
What are the treatments for stable angina?
Hint: 4 categories of treatment
To treat acute episodes:
- Sublingual nitrate sprays/tablets
To prevent episodes:
- Ca2+ channel blockers
- Oral nitrates
Prevent acute cardiac events:
- ACE inhibitors
- Consider revascularisation
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
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)
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
- Low BP
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
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
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
- Other problems (E.g. Arrhythmia/low BP etc)
Test positive for angina when ECG shows ST depressions of >1mm (stronger = critical stenosis) when exercising
What is acute coronary syndrome?
A group of symptoms attributed to the obstruction of the coronary arteries ACS is a result of:
- Unstable angina
DIfferentiate Unstable angina, STEMI and NSTEMI based on these 4 criteria (listed in this order under condition headings):
- Occlusion by thrombus
- Myocardial necrosis
- Biochemical markers in blood
- Partial (or full w/ collaterals)
- May be ST depression/T wave inversion/normal
- Partial (or full w/ collaterals)
- Some (confined to endocardium)
- No ST elevation
- Complete (not adequate collaterals)
- Large myocardial infarct extending to sub-epicardium
- ST elevation
What are these ECG traces showing?
What features of the trace do you look at to come to a conclusion?
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)
What does this diagram show?
For each picture fill in the white boxes describing how the trace has changed
Diagram shows progression of ECG trace following a STEMI
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
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
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.
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
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
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
What is the goal of treatment for unstable angina/MI?
Prevent UA from progression to MI and limiting muscle loss in MI
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:
- Percutaneous coronary intervention (angioplasty)
- Coronary artery bypass graft (CABG)
- Initial medical treatment
- Followed by elective angioplasty
- Pain control
- Organic nitrates
- ACE inhibitors
- Manage risk factors (E.g. Stop smoking)
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
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
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