CVS S10 - Chest pain and IHD Flashcards
List the 4 general types of chest pain
Cardiovascular, Respiratory, GI, Musculoskeletal
List the different causes of cardiovascular chest pain and how the pain would feel
MI - Tightening
Pericarditis - Sharp
Aortic dissection - Tearing
Give an example for each of the other types of pain (GI/ Musculoskeletal/ Respiratory)
Respiratory - Infection, pneumothorax
GI - reflux oesophagitis, pancreatic disease
MSK - trauma, bone metastases, muscle pain
List the modifiable and non-modifiable risk factors for CAD
M- hyperlipidaemia, diabetes, smoking, hypertension
NM- increasing age, male gender, family history
What is the cause of stable angina?
Stable plaque- small necrotic core, thick fibrous cap, cap less likely to fissure
Moderate reduction in blood flow results in transient ischaemic attacks during periods of high oxygen demand
How would the chest pain present in a patient with stable angina?
- Central tightening pain
- Brief episodes with radiation to left/right/both arms or shoulders and neck, jaw or back
- Brought on by exertion and relieved by rest or nitrates
How would a diagnosis of stable angina be made?
- Based on history
- No specific signs on examination but may have signs related to risk factors e.g. increased BP, corneal arcus, signs of atheroma elsewhere due to absent pulses
- Resting ECG usually normal
What can be done if the diagnoses of stable angina is uncertain?
- Exercise stress ECG Test
- Patient connected to ECG and undertakes graded exercise on a treadmill until target heart rate reached or chest pain occurs/
- ECG changes/ other problems such as fall in BP
What would be the results of an exercise stress test in a patient with stable angina?
- Transient sub-endocardial ischaemia with exercise- ST depression of more than 1mm
- With rest ST segment goes back to baseline
What does a strongly positive exercise test indicate?
Critical stenosis
What are the aims of treatment for stable angina?
- Reduce myocardial oxygen demand
- Increase blood flow by revascularisation
- Prevent progression of atheroma, stabilise plaque, prevent thrombosis
What factors does myocardial oxygen supply depend on?
O2 carrying capacity of blood and coronary blood flow (depends on perfusion pressure (DBP) and coronary artery resistance)
What factors must be altered to reduce myocardial oxygen demand?
Wall tension, heart rate, contractility
What drugs can be given to reduce myocardial oxygen demand?
Nitrates, calcium channel blockers, beta blockers
What are the two potential methods of revascularisation?
Percutaneous Coronary Intervention and stenting (PCI)
Coronary Artery Bypass Grafting (CABG)
What are the two different types of Acute Coronary syndrome?
STEMI- occlusion complete, persistent, no collaterals, severe ischaemia and necrosis
NSTEMI/Unstable Angina- non occlusive thrombus, brief, collaterals present, less severe ischaemia
How does unstable angina differ from NSTEMI?
NSTEMI is a non ST segment elevation MI with necrosis and biomarkers present
Unstable angina is ischaemia but no infarction so no necrosis and no biomarkers present
How would a patient with unstable angina present?
- Acute worsening of stable angina- more frequent, more severe and longer duration
- Angina at rest
- Recent onset of new, effort limiting angina
- Presence of risk factors
How would patient with MI present?
- Severe central crushing chest pain with typical radiation
- Persistent and continues at rest
- Not relieved by rest/ nitrate spray
- Autonomic features present e.g. sweating/pallor
- Nausea/ vomiting/ breathlessness/ faint
What would you find on examination of a patient with an MI?
- Sweating, pallor
- Cold, clammy skin
- Tachycardia/ Arrythmias
- Low BP
- Signs of heart failure- S3/S4, crackles in lung bases
What are the main biochemical markers of myocyte damage?
Cardiac Troponin I and Cardiac Troponin T
Rise 4 hours after onset of pain, peak 18-36 hours, decline slowly up to 10-14 days
What other biochemical marker can be used to detect myocyte damage?
Creatine Kinase (CK-MB)
Rise 3-8 hours after onset, peak at 24 hours, back to normal 48-72 hours
How would a STEMI be treated?
Emergency Percutaneous coronary intervention (PCI) within 90-120 minutes
If not available then fibrinolytic therapy
How would an NSTEMI be treated?
Prevent extension of thrombus with anti-thrombotic therapy
Possible PCI/CABG but not emergency
What are the long term treatments given after an MI and why?
Aspirin- decrease mortality and re infarction
Beta Blocker- decrease mortality and re infarction
ACE Inhibitors- improved survival
Statins- decrease mortality and re infarction
Manage risk factors via lifestyle modifications
List some potential complications of MI
- Sudden cardiac death
- Arrhythmias- tachycardia/ bradycardia
- Heart block- primary/ secondary/ tertiary
- Ventricular tachycardia/ fibrillation
- Atrial fibrillation
- Heart failure
- Cardiogenic shock
How can MI lead to bradycardia?
SA node ischemia
How can MI lead to ventricular tachycardia?
Ventricular ishaemia causes re-entry circuits or increased automatic firing
How can MI lead to heart failure?
Loss of myocardium causes decreased myocardial contractility
How can MI lead to cardiogenic shock?
- > 40% myocardium infarcted
- Severely decreased CO
- Systolic BP
