Angina - Stable and Unstable

Friday, January 20, 2012 9:03 AM

1. Major detriments of myocardial oxygen supply and demand

a.

2. Ischemia a. Refers to lack of O2 due to inadequate perfusion b. Ischemia occurs if O2 demands are increased (LVH due to AS, AS can cause angina indistinguishable from coronary atherosclerosis) c. Ischemic occurs if O2 carrying capacity of blood is low (severe anemia, carboxyhemoglobin) 3. Effects of Ischemia a. Inadequate perfusion leads to disturbances in mechanical, biochemical, and electrical function b. Mechanical i. HF (LVF or RVF or both) ii. Angina, if ischemia is prolonged or develop coronary occlusion, may lead to myocardial necrosis iii. Segmental akinesis bulging (dyskinesis) c. Biochemical i. FA cant be oxidized ii. Increased lactate production iii. Reduced pH with metabolic acidosis d. Electrical i. Inversion of T wave ii. Transient displacement of ST segment iii. Depression - subendocardial iv. Elevation - subepicardial v. Electrical instability: VT or VF 4. Atherosclerosis a. Most common cause of ischemia b. Decreased CA lumen i. Decreased perfusion and limited increase when demand is needed ii. Supply/demand c. Risk factors that contribute to altered function of vascular endothelium. i. Constriction of vessel (spasm) ii. Clot formation (thrombi, emboli) iii. Abnormal interaction with plts/monocytes
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iii. Abnormal interaction with plts/monocytes 1) Contribute to subintimal collection of fat iv. Leads to reduction in cross sectional area (stenosis) 1) Stenosis of 75-80% is sig d. Plaques are subject to endothelial instability with fissuring, hemorrhage, and thrombosis. i. Reduces CA flow, worsens ischemia, leads to necrosis ii. Location of atherosclerosis will determine the amount of myocardium that is vulnerable. 5. Risk Factors of Atherosclerosis a. Hyperlipidemia i. NCEP Guideline III. Stricter target lipid levels ii. For patients with prior events and a 10 year risk of CHD (20% or greater): 1) LDL - less than 70 mg/dL 2) HDL low is greater than 60 mg/dL 3) TG high is 150 mg/dL 4) Total cholesterol is less than 200 mg/dL a) 1% decrease in TC = 3% decrease risk of CAD b. Smoking c. Hypertension d. DM i. Recognized by AHA as major risk factor (metabolic syndrome) 1) Insulin resistance 2) Hypertension 3) High TG, low HDL 4) Hyperuricemia 5) Hypercoaguable e. Obesity i. Obese - BMI >30 ii. Overweight - BMI 25-30 iii. Desirable - BMI 21-25 1) Desirable waist/hip ratio: a) Men <.9 b) Women <.8 iv. BMI = (lbs*705)/Ht (inches)^2 1) Or Kg/Ht(m)^2 f. Physical Inactivity i. Need 45-60 min of moderate intensity 5-7x/wk g. Age, Gender i. Male - >45 y/o ii. Female - >55y/o h. Family History i. Premature IHD ii. 1st degree men relatives, <45 y/o (55) iii. 1st degree women relatives, <55 y/o (65) 6. Metabolic Syndrome a. Over 25% of US adults have metabolic syndrome b. Need 3 out of 5 to have metabolic syndrome i. Obesity - abdomen over 40'' (men) or 35'' (women) ii. Low HDL - men <40 and women <50 iii. High TG, >150 iv. High BP - Systolic >130 or Diastolic >85 v. High fasting glucose - >110
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v. High fasting glucose - >110 7. Angina a. Due to ischemia, usually caused by an increase in myocardial O2 demand b. Thresholds vary; certain levels of activity may provoke angina attack i. Why? Fixed CA stenosis/fixed O2 supply 1) Produces ischemia b/c of increased O2 demand c. Factors that control MVO2 (myocardial O consumption) i. HR ii. Afterload iii. Contractility iv. Wall Tension 8. Typical history a. Men 50-60 yo, Women 60-70 yo b. Chest discomfort brought on by exertion/emotion, excitement i. Relief on rest usually predictable, stable, not occurring more often, not last longer c. Angina i. Can occur at rest - unstable angina ii. Can occur at night - recumbent or angina decubitus 9. Discomfort a. Description varies; i. Heavy, pressure, squeezing, smothering, choking, dullness, ache, sharp, heart burn, indigestion, gas b. Substernal, clinched fist - levine's Sign c. Crescendo/decrescendo pattern i. Lasts 1-30 min d. May radiate into L shoulder i. Down ulnar surface of forearm/hand; both arms e. May radiate or arise in neck, jaw, teeth, epigastric or back f. May be precipitated by i. Heavy meal, cold exposure g. Duration i. 15-20 mins ii. Longer suggests UA or MI 10. Differential Diagnosis

a.

11. Anginal Equivalent a. Ischemia, but described as dyspnea, fatigue, faintness b. Pathogenesis i. Ischemia causing elevated LV filling pressure that leads to pul edema 1) Diabetics, elderly, women, S/P CABG or transplants are more likely to experience this than classic angina
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likely to experience this than classic angina 12. Angina a. Family History i. Premature IHD b. Risk Factors i. Previously mentioned c. PE i. Typically normal d. Signs of Risk Factors i. Xanthelasma 1) Soft yellowish spots on eyelids ii. Xanthomas iii. Diabetic skin lesions iv. Nicotine stains v. Pale vi. Absent peripheral pulses vii. Abnormal cardiac impulse 1) LV dyskinetic viii. Bruits 1) Carotid, abdominal aorta, femorals ix. Gallop 1) S3, S4, both x. Systolic murmur of MR if papillary muscle is dysfunctional xi. Remember 1) AS, 2) AI 3) Pul hypertension 4) Hypertrophic cardiomyopathy 13. Labs a. Check for DM - HbA1C, fasting glucose, 2hr pp glucose b. Check for renal disease i. BUN, creatinine c. Fasting lipid profile d. CBC e. Check thyroid status - TSH f. Cardiac enzymes i. Troponin 1, CK total, CK-MB 14. ECG a. Normal in 50% of patients b. During anginal attack may have displaced ST segment c. May show old MI 15. Stress Tests (contraindications)

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a.

16. Cardiac Cauterization a. Indication i. Patient being considered for revascularization (CABG or PCI percutaneous coronary intervention) b. PCI - PTCA i. Successful 90% ii. Stent insertion 1) Maintains revascularization of myocardium to prevent restenosis iii. Restenosis occurs in 30-45% of patients in 6 months iv. Mortality 1) .5-1% b; need for emergency coronary

17.

18. Treatment of CAD/Angina a. Identify aggravating conditions b. Treat risk factors c. Diet

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i.

d. Exercise regularly e. Statins for hyperlipidemia f. Unstable Angina i. ACS - acute coronary syndrome ii. New onset angina or pre-existing angina that progresses to point where patient cannot perform less than ordinary activity iii. Tempo has changed; higher number of episodes, lasting longer, more severe intensity symptoms at rest, awaken from sleep, using more medications, a decrease in amount of effort to provide symptoms g. Pathophysiology (UA, ACS) i. Rupture of atherosclerotic plaque from inflammation/mediators released. Activation of platelets, clotting factors, thrombus 19. Pharmacological Treatment of Angina and CAD

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b.

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d.

i.

e.

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f.

g.

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