Week 126 - Chronic Stable Angina Flashcards
What are some of the differential diagnoses for angina?
- MI
- PE
- Reflux Oesophagitis
- Pneumothorax
- Aortic Dissection
What investigations should be performed for a suspected case of angina?
ECG, Blood profile, Exercise Stress Test, Angiography
What are some of the lifestyle management options for chronic stable angina?
- Smoking Cessation
- Diet
- Exercise
What are the medical treatment options for chronic stable angina?
• Drugs-
- Antiplatelets
- Beta-blockers
- Statins
- Nitrates
- Calcium channel blockers
- *• Treat related conditons-**
- Anaemia
- Diabetes
What are the revascularisation options for chronic stable angina?
- Percutaneous coronary intervention - Plain old balloon angioplasty, bare metal stents, drug eluting stents.
- Coronary Artery Bypass Surgery
Coronary Artery Bypass Surgery for Chronic Stable Angina: What are the indications, risks and benefits?
Indications -
- 3VD, 2VD with LV impairment or LMS.
Risks -
- Risk stratification, unit results, individual results.
Benefits -
- Symptoms and prognosis.
What is a the definition of Hypoxia?
A lack of oxygen resulting in a decrease in oxidative respiration leading to tissue damage.
What is the definition of ischaemia?
- A lack of blood supply from a stenotic/occluded artery or reduced venous drainage causes ischaemia.
- This causes a lack in oxygen **and **metabolites, causes cell injury more rapidly than hypoxia.
What is the definition of infarction?
Irreversible cell death due to hypoxia or ischaemia.
What are the four main pathophysiological outcomes of cell injury?
- Decreased ATP
- Membrane damage
- Increased intracellular calcium
- Increased oxygen derived from free radicals
What is the impact of decreased ATP during cell injury?
• Decreased activity of Na/K pump leads to;
- Influx of Ca, H2O, Na
- Eflux of K leading to cell swelling, loss of microvilli.
• Increased anaerobic glycolysis leading to;
- Decreased pH and Glycogen
• Detachment of ribosomes;
- Decreased protein synthesis.
What occurs to the membrane during cell damage?
- Decreased ATP leads to decreased production of phospholipids.
- Influx of Ca activates phospholipases and proteases leading to destruction of cytoskeleton.
During cell damage their is an influc of Ca, what effect does this have on the cell?
- ATPase causing decrease in ATP.
- Increase in phospholipases, causes a decrease in phospholipids.
- Increase in proteases, causes destruction of membrane and cytoskeleton.
- Increase in endonucleases, leading to chromatin breakdown.
What is iscahemia-reperfusion injury? What are the hypothesis for its mechanism?
- Some cells which are reversibly damaged for ischaemia may then die when blood flow returns.
- Oxygen free radicals, Mitochondrial permeability transition, inflammation associated injury, Complement.
What is atheroscleorsis?
- Atheroma is the accumulation of lipid and fibrous tissue within the antima of the artery.
- These localised collections are called ‘plaques’.
What is the difference between a stable and unstable plaque?
• **Stable **-
- Concentric, rish in firbous stroma, rich in smooth muscle.
- *• Unstable - **
- Eccentric, rich in lipid, Macrophages, Inflammation, endothelial cell injury.
What are the risk factors for atherosclerosis?
- Age, Gender, Family history
- Smoking, Hypertension, Hyperlipidaemia, Diabetes Melitus.
What are the four life-threatening causes of chest pain that you should **never **miss?
- MI
- PE
- Tension pneumothorax
- Dissecting aortic aneurism
What is the definition of stable angina?
• Reversible ischaemia to myocardiam brought about due to increased stress and relieved by rest.
What are the four classifications of stable angina?
- Class I - Strenuous or protracted exercise.
- Class II - Slight limitation with vigorous exercise.
- Class III - Marked limitation with activities of everyday living.
- Class IV - Inability to perform daily activites.
What initial investogations should be performed for stable angina?
- ECG
- Bloods
- CXR - For determining causes of chest pain.
What is the drug-therapy for chronic stable angina?
- Nitrates
- Beta-Blockers
- Calcium Channel Blockers
- Longer-acting nitrates
- Potassium channel activators
- Ivabradine
- Ranolazine
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Nitrates?
- 1st line choice for rapid relievement of symptoms, can also be used as prophylaxis.
- Release of NO to activate cAMP which causes smooth muscle relaxation and subsequent vasodilation.
- Sideffects - Hypotension, Headache, Flushing.
- Contraindications - Hypotension, Aortic and mitral stenosis, Hypertrophic cardiomyopathy.
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Beta-blockers?
- 1st line treatment.
- Causes reduction in sympathetic stimulation to cause a reduction in heart rateand myocardial contractability.
- Side-effects - Bronchospasm, bradycardia, cold extremities, numbness, sleep disturbance, fatigue, sexual dysfunction.
- Contra-indications - Asthma, bradycardia, uncontrolled heart failure, 2˚ and 3˚ heart block, severe peripheral artery disease.
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Calcium Channel Blockers (dihydropyridines)?
- Amlodipine, Nifedipine, Felodipine.
- 2nd-line addition to Beta-blockers.
- Smooth muscle relaxation by inhibiting influx of calcium ions.
- Side-effects: Flushing, headaches, dizziness, ankle oedema, hypotension.
- Contraindications: Uncontrolled heart failure, MI in past month, significant aortic stenosis.
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Calcium channel blockers (Non-dihydropyridines)?
- Verapamil, Diltiazem.
- Option for patiens where beta-blockers are contraindicated.
- Conduction of AV node, has rate limiting mechanism.
- Side-effects - SA/AV block, constipation.
- Contraindications - 2˚/3˚ heart block, uncontrolled heart failure.
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of **Longer-acting nitrates? **
- Added into beta-blocker for symptom control.
- Release of NO to activate cAMP to cause smooth muscle relaxation and subsequent vasodilation.
- Side-effects: Hypotension, headache, flushing.
- Contra-indications: Hypotension, aortic and mitral stenosis, hypertrophic cardiomyopathy.
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Potassium-channel activator?
- Nicorandil
- 3rd-line added in drug.
- NO donor to activate cAMP, smooth muscle relaxation, vasodilation.
- Opens K+ channels resulting in decreased Ca influx.
- Side-effects: Headache, Hypotension, GI irritation.
- Contra-indications: Left ventricular failure, hypotension.
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Ivabradine?
- 3rd line treatment.
- Blocks a pacemaker or ‘funny’ current channel in SA node.
- Side-effects: Visual disturbances, Bradycardia, 1˚ heart block, Headache and dizziness.
- Contraindications: Bradycardia, 2˚/3˚ heart block, Acute MI.
Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Ranolazine?
- Add-on for symptomatic control if no relief from previous medical therapy.
- Inhibits ‘late’ sodium channels - resulting in decreased influx of Ca resulting in relaxation of smooth muscle.
- Side-effects: Constipation, Nausea and Vomitting, Dizziness and headache.
- Contradindications - Moderate to severe hepatic impairment.
