→ cranial syndrome usually characterized by episodes of paroxysm of the pain or pressure in the anterior chest.

→ cause is insufficient coronary blood flow that results in low oxygen supply.


→ most common cause of angina pectoris is atherosclerotic disease. → associated with significant obstruction of a major coronary artery. physical exertion exposure to cold eating heavy meal stress or emotion provoking situation


Precipitating Factors

Chest pain → poorly localized → may radiate to neck, jaw, shoulders & inner aspects of the upper arms → retrosterna
stable angina → predictable & consistent pain that occurs on exertion & relieved by rest. unstable angina/ preinfarction angina/ crescendo angina → symptoms occurs frequently, last longer pin. The threshold for pain is lower & pain occur at rest. intractable/ refractory angina → severe incapacitating chest pain. variant angina → pain at rest. ST segmentation elevation – caused of vasospasm. silent ischemia/ obstructive ischemia → no symptoms

Clinical Manifestations


objective: • decrease oxygen demand & increase oxygen supply

Medical Management

nitroglycerin → remain the mainstay for treatment of angina to decrease myocardial oxygen consumption w/c decrease ischemia & pain. → vasodilators (especially in high dose) → administered to decrease cardial oxygen consumption w/c decrease ischemia & pain. → Decrease pre & afterload sublingual/ spray → alleviates the pain after 3mins. Nitroglycerin effect → hypotension If the symptoms is free, nitroglycerin is switched to topical preparation Mouth should be moist Saliva is not swallowed until the nitroglycerin is dissolved


If severe, patient crush the tablet between the teeth to hasten the absorption

IV → given if there is recurring symptoms of ischemia → for unstable angina
Propanolol, Metaprolol, Atenolol → blocks the beta-adrenergic sympathetic stimulation to the heart. → this help to control chest pain & delays the onset of ischemia during work exercise. → produce the cardiac mortality, recurrent angina, infarction.


Beta-adrenergic blocking agents

hypotension bradycardia advance atrioventricular block decompensated failure hyperlipidemia decreased libido

Side effects:


Caution: not to stop abruptly decrease gradual over several days

→ if given intravenously for an acute cardiac event ∙ ECG, BP ,HR monitored Mode of Action

→ ↓ conduction → ↓HR & ↓ heart contraction → ↓ workload → relax blood vessels → ↓ BP → ↑ coronary perfusion → dilating the coronary arteries → most commonly drug use are Amlodipine, verapamil, Diltiazem use of Nifidepine was found poorly tolerated % to increase the risk of MI in patient w/ hypertension & the risk of death in patient with ACS first generation calcium channel blockers should take w/ caution especially patient w/ HF → Amlodopine & Felodipine


Antiplatelet & Anticoagulant Medications

→ prevents platelet activation & reduces the incidence of MI & death in patients w/ CAD. 160-325mg Dose of aspirin should be given to the patient w/ angina & then 81-325mg/day → causes intestinal upset & bleeding, treatment for helicobacter pylori & use of H2-blockers (Cimetidine, Famotidine, Ranitidine, Misoprostol) should be considered to allow continued aspirin.

→ given if the patient is allergic to aspirin → take few days to achieve their antiplatelet effect → given with aspirin in patient w/ high risk for MI & GI upset, N&V, diarrhea & ↓ neutrophil level.
→ prevents the blood clots → use alone in treating patients w/ unstable angina, reduces the occurrence of angina → if cardiac event → patient is hospitalized & IV bolus of heparin & continuous infusion / IV bolus every 4-6hrs → Heparin is given in base on result of activated partial thromboplastin time (aPTT) → Heparin is therapeutic when the aPTT is 1.5-2 times the normal aPTT

Clopidogrel & Ticlodipine


→ SC- injection of LMWH Enoxoparin or Dalteparin to treat unstable angina

→ more stable & effective anticoagulation → because Heparin & LMWH ↑ the risk of bleeding (IRE) so monitor the patient BP, ↑HR, ↓ serum hemoglobin & hematocrit levels → Heparin-induced thrombocytopenia → an antibody-mediated reaction to heparin that may result to thrombosis → IV agents ABCIXIMAB, TIROFIBAN, EFTIFIBATIDE → prevent platelet aggregation by blocking GIIb/IIIa receptor on the platelet → initiated at the onset o chest pain in attempt to increase the amount of oxygen delivered to the myocardium & to ↓ pain. → necrosis → myocardial cells in the heart are permanently destroyed → like angina, MI is usually caused by reduced blood flow in coronary artery due to atherosclerosis & occlusion of embolus/thrombus → acute coronay syndrome (ACS) term for the diagnose

Elevation MI

GPIIb/IIIa Agents

Oxygen Administration



Vasospasm ↓ Oxygen Supply

→The area of infarction takes time to develop as the cells deprived of oxygen


Chest pain occurs and continues despite rest and medication is presenting symptoms. Shortness of breath ↓ 55 age.
Patient’s History 2 parts → Presenting Symptoms → Previous illness and family history

Clinical Manifestations

↓ Ischemia Develops ↓ Cellular Injury ↓ Lack of Oxygen ↓ Infarction

Assessment and Diagnostic Findings

→ The classic ECG changes are T- wave inversion, ST segment elevation and development of Q- wave. →The first ECG signs of an acute M.I are from myocardial injury & ischemia.


Injury ↓

→ Causes T-wave to become enlarge and

→ Causes also to ST-segment changes. → Injured Myocardial cells depolarize normal but repolarization is more rapidly than normal cells, causing the ST-segment rises to 1 mm above the isoelectric line. → If the Myocardial Injury is n the Endocardial tissue the ST-segment is usually horizontal or downward slope.

Symmetric. altered and delayed, causing

Myocardial repolarization is altered & delayed causing T-wave to invert

Ischemia ↓

M.I is classified as Q-wave or Non Q-wave Infarction
Develops 1-3 days → Because there is no Deporalization Current conducted from necrotic tissue. → Abnormal Q-wave is 0.04c op longer 25% of R-wave. Non Q-wave Infarction ↓ Do not develop a Q-wave on the ECG after ST-Segment and T-wave changes. Q-wave ↓

→ During Recovery to M.I, ST- segment is the first to return normal (1-6 weeks) T-wave become large symmetric for 24 hours, and it then inverts within 1-3 days for 1-2 weeks. → Q-wave alteration → Can detect hypokinetic and akinetic wall motion and can determine the ejection fraction.
Creatinine kinase and its isoenzymes 3 CKI CK-MM (Skeletal Muscle) CK-BB (Brain Tissue) CK-MB (Heart Muscle) Specific Cardial specimen Isoenzymes Found mainly in Cardiac cells and therefore rises only when there is damage cells. → The level starts to ↑ 4-8 hours, peaks 24-36 hours that will last for 1-3 days.

Echocardiogram Laboratory Test

→ It is a Heme protein that helps transport Oxygen.


→ Found in Cardiac and Skeletal Muscle starts to ↑ 13 and peaks within 12 hours.
→ ↑ in myoglobin; not specific acute Cardiac event. → ↓ (-) ruling out M.I Troponin, a found in the myocardium, regulates the myocardial contractile process. → 3 Isomers ( C, I and T) → Use more frequently → 3-4 peaks 4-24 last from 1-3 weeks

After Onset of Surgery

Goal: Minimize myocardial damage Preserve myocardial function Prevent complications

Medical Management

Thrombolytics → IV given → To dissolve and lyse the thrombus in a coronary artery allowing reperfusion. → Administration 20 minutes unrelieved by Nitroglycerin → Administer after the onset of symptom → Not given to unstable Angina → Door-to-needle time → administer within 30 minutes from the time the patients arrive in the emergency department.

Pharmacological Therapy

→ Increase the amount of plasminogen Activator, which then increase the amount of circulating and clot- bound plasmin. → Vasculitis occurred up to 9 days after administration. → Tissue Plasminogen avtivator, ( t- PA)



→ Activates the plasminogen on the clot more. → Heparin with ( t- PA)

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