Ischaemic Heart Disease (11) Flashcards
What is pre load and after load?
- Preload: end diastolic pressure
- Afterload: pressure of the wall of left ventricle during ejection
What is the definition of heart failure?
- The chronic inability of the heart to perfuse tissues of the body despite adequate filling pressure
What is coronary blood flow affected by?
- Perfusion pressure
- Coronary artery resistance
What is meant by supply?
- O2 carrying capacity of the blood
What myocardial causes are there for IHD?
- Increase in myocardial demand: tachycardia, thyrotoxicosis, aortic stenosis increasing afterload
- Decrease in myocardial O2 supply: decreased coronary blood flow, severe hypotension, leads to severe anaemia, strictures
What are the risks of having unstable plaques?
- Fibrous cap undergoes erosion/fissuring -> exposing blood to thrombotic material in necrotic core -> platelet clot can then lead to fibrin thrombus
Outline how plaque fissuring may lead to myocyte injury.
- Sudden decrease in artery lumen
- Acute severe decrease in blood flow
- Ischaemia
- Cause myocyte injury/necrosis
What is meant by stable angina pectoris?
- Brief episodes from exertion or stress
- Presence of risk factors
- Relieved after 5 mins
What is a stable plaque?
- Moderate decrease in blood flow
- Flow is sufficient at rest
- Exercise -> transient ischaemia
- No necrosis or myocyte injury
Where are collaterals found?
- Smaller arteries
- Absent in major arteries
What are the treatments available for IHD?
- B blockers: decrease hr and contractility strength
- Statins: increases stability of plaques, decreases progress of atherosclerosis
- Aspirin: anti-platelet aggregation, decreases thrombus formation
- Ca channel blockers: decreases afterload by peripheral vasodilation
- Organic nitrates: venodilators -> decreases preload
- Revascularisation
What is revascularisation?
- Percutaneous coronary intervention and stenting
- Internal mammary artery grafts
- Saphenous and radial grafts
- Coronary artery bypass grafting (CABG)
What is a STEMI?
- ST elevation MI: due to randomly depolarising myocytes
- 90% occlusion
- Lots of necrosis
- Biomarkers present (Tropanin & Creatin kinase)
- PCI needed
- Thrombolysis
What is a NSTEMI?
- No ST elevation MI
- Positive to Biomarkers
- Necrosis
- Adequate collateral circulation to keep alive
- Not full thickness myocyte death
What is unstable angina?
- No ST elevation
- No necrosis
- Partial/brief occlusion
- Adequate collateral circulation
What is the treatment for STEMI?
- Re-establish perfusion: PCI/stenting, Thrombolysis
- Anti platelet agents: aspirin
- Anti ischaemic therapy
What is the treatment for long term MI?
- Risk factor management
- ACE inhibitors
- Statins
- B blockers
- Aspirin
What is the treatment for unstable angina/NSTEMI?
- Prevent MI/muscle loss
- Risk assessment
- Prevent progression of thrombus: anti platelet, anticoagulant
What are the signs and symptoms of acute MI?
- Tachycardia
- Arrhythmias
- Low bp
- S3/S4 crackles
- Sweating
What is the history for an Acute MI?
- Central, crushing chest pain and radiation
- Distressed
- Persistent, severe pain
- Pallor
- Sweating
- Nausea
- Vomiting
- Not relieved by rest
What are the possible complications of acute MI?
- Arrhythmias
- Heart block
- Atrial fibrillation
- Heart failure: loss of myocardium, decrease myocardial contractility
- Cardiogenic shock
- Ventricular fibrillation, tachycardia
What are the two main biomarkers for IHD?
- Tropanin: cardiac tropanin 1/tropanin T
- Creatin kinase
Where is creatin kinase released from and when does it first show, peak and disappear?
- Skeletal muscle
- Brain
- HEART
- 3-8hrs first shows
- Peak: 24hrs
- Normal 48-72hrs
What is tropanin and when does it first show, peak and disappear?
- Cardiac tropanin 1: cTn1
- Tropanin T: cTnT
- 3-4hrs after onset of pain
- Peak: 18-36hrs
- Slow decline 10-14 days
