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Angina pectoris
Angina pectoris is characterized by chest pain due to cardiac ischemia, often manifesting as squeezing or pressure-like sensations typically felt substernally and radiating to areas such as the neck and arms. It can result from atherosclerosis, vasospastic events, or unstable angina, with several risk factors including smoking, obesity, and physical inactivity. Diagnosis involves identifying typical symptoms and may utilize tests like ECGs and angiograms, while treatment includes medications like vasodilators and beta blockers, as well as procedures like balloon angioplasty.
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Angina pectoris
- 1. ANGINA PECTORIS PRESENTED BY BATCHC1 (199-220)
- 2. Angina Pectoris ■ Asudden characteristics Cushing, strangling, squeezing, burning, chocking or pressure like sensation due to cardiac ischemia. Sites Typical location substernally radiating to: ■ Neck ■ Shoulders ■ Arms ■ Neck ■ Jaws
- 3. Types 1. Atherosclerosis Angina: ■Classic or angina of effort.. ■ Atherosclerotic plaques occlude coronary arteries.. ■ Cardiac workload increase.. ■ Obstruction to flow. ■ Decrease O2 delivery.. ■ Accumulation of lactic acid .. ■ Ischemia, myocardial pain. ■ 90% of angina cases. ■ Relieved by rest, within 15 min of period.
- 4. 2. Vasospastic angina: ■Reversible spasm of coronary arteries usually at the site of atherosclerotic plaque. ■ Spasm can occur even during sleep. ■ It can lead to unstable angina. ■ 10% of angina cases.
- 5. 3. Unstable Angina ■Increased frequency and severity of attack resulting from condensation of atherosclerotic plaque.. ■ Platelet aggregation at that site and vasospasm which leads to MI
- 6. Causes of AnginaPectoris Major Risk Factors: ■ Females less than or equals 45 years, Males less than or equals 35 years. ■ Smoking ■ Dyslipidemia ■ Family history of CVS diseases ■ HIN ■ Kidney disease ■ Obesity ■ Physical inactivity ■ Prolonged psychosocial stress
- 7. Other conditions: ■ Provokingangina medications ■ Vasodilation ■ Vasoconstriction ■ Excessive thyroid replacement ■ Polycythemia ■ Hypovolemia ■ Hypothermia ■ Anemia ■ Hypothyroidism ■ Hypoxemia
- 8. Symptoms ■ It canbe painful or there is only chest discomfort and radiating pain in sites discussed before.. Associated symptoms: ■ Breathlessness ■ Sweating ■ Nausea ■ Vomiting, ■ Pallor ■ Vitals : increased bp , increased pulse rate
- 9. Pathophysiology ■ Imbalance betweenheart and oxygen’s demand & supply. ■ The imbalance usually occurs during strenuous work like exercise. Diagnosis It is suspected when patient comes with the complaints of heavy chest discomfort retrosternal on left sided radiates to left arm, neck, jaw or back. Associated with exertion or emotional stress and relieved in within several minutes by taking rest. It is precipitated by cold weather or meal. Pain is not relieved by antacid and simple analgesics however relieved by glyceryl trinitrate.
- 10. ■ St segmentmay be depressed or elevated, constant monitoring of Bp and pulse is also done. ■ Thallium scintigram is done in patients of asthma or arthritis, in others, treadmill teats are done. ■ Coronary angiogram for identifying the nature of lesion. Aggravator factors ■ Stress ■ Strenuous work (exercise) Relieving factors ■ Medication ■ Rest
- 11. Drugs used inAngina Pectoris Vasodilators Cardiac Depressants Other Drugs Calcium Blockers (veraparnil) Nitrates Beta Blockers (Propranolol) Metabolism Modifiers, Rate Inhibitors Short Duration(sub lingual nitroglycerin ) Intermediate (oral nitroglycerin) Long Duration (transdermal nitroglycerin)
- 12. Drugs Used InAngina Pectoris1. Vasodilators 2. Nitrates: ■ Short actins (within minutes) Sublingual ■ Intermediate (within 4-6 hours) Oral ■ Long actins (8-10 hours)Transdermal Mode of Action Increases CGMP, Relaxation of SM muscles PK Short actins, rapid onset (limit) duration is up to Intermediate actins, slow onset , duration up to 2-4 hours Long actins, slow onset , duration up to 8-10 hours Ultra short actins, onset seconds, duration 1-5 minutes S/E Tachycardia orthostatic hypotension due to headache Example Nitroglycerin, Amyl nitrate
- 13. Calcium channel blockers ModeOf Action ■ Block calcium channel in SM muscles & heart, depress I.C calcium (intracellular calcium) PK ■ Oral parenteral and slow release for arteries available. S/E ■ Constipation ■ Pretibial edema ■ Flushins, dizziness ■ Increased dose results in cardiac depression and hypotension Example Verapamil, Nifedipine.
- 14. Beta Blockers Mode OfAction ■ Block sympathetic effect on heart & blood pressure, reduce renin release. PK ■ Oral parenteral S/E ■ Bradycardia ■ AV blockage ■ Heart failure, Fatigue ■ Sleep problems ■ Sexual dysfunction Example Propranolol, atenolol, metoprolol etc..
- 15. Na- channel blockers(ranolazine) ModeOf Action ■ Blocks late sodium channel in myocardium, reduces cardiac rate. PK ■ Oral given duration 10-12 hours. S/E ■ QT Prolongation on ECG ■ InhibitCYP 3A & 2D6 Example Verapamil, Nifedipine.
- 16. Ivabradine Mode Of Action ■Block pacemaker sodium Current ion, SA node reduces heart rate. PK ■ Given Oral twice a day. NOT KNOWN SIDE EFFECTS!
- 17. Treatment Strategy 1. DecreasedOxygen demand (vasodilators) 2. Decreased cardiac work loads (Beta blocks, Calcium blocks) Balloon Angioplasty ■ Balloon inserted at the end of catheter inflated to widen arterial lumen. Stents ■ Stents also used to mountain arterial widening. coronary bypass Coronary bypass ■ Exercise ■ Healthy life plan ■ Diet