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Stable Angina template



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Description of Stable AnginaA symptom which results when myocaridal oxygen demand is greater than myocardial oxygen supply. Some pts may not be symptomatic
Risk Factors for Stable AnginaFamily Hx of coronary artery disease Hypertension Hypercholesterolemia Diabetes Mellitus Tobacco/Cocaine Use Obesity Advancing Age
Types of AnginaClassic: Reproducible and predictable, no increase in frequency, severity, or duration Prinzmetal's: Results from coronary artery vasospasm; occurs in typical patterns Unstable: Recent onset, or an increase in severity, frequency or duration from usual, symptoms at rest, or nocturnal symptoms
Assessment Findings in Stable AnginaChange in symptoms warrants further investigation Heaviness, discomfort, pressure, pain, ache radiating to back, chest, arms,jaw, teeth May be precipitated by exercise, stress, cold temperature, ingestion of a heavy meal, and smoking Pain/discomfort relieved after nitro administration SOB with or without activity Asymptomatic Nausea Perspiration Palpitations
Diagnostic Studies in Stable AnginaEKG: may demonstrate ST segment changes Chest X Ray: New or Worsening CHF Lipid Level: May demonstrate hyperlipidemia ECHO Stress Test Coronary Angiography
Nonpharmacologic Management of Stable AnginaCardiac Rehab if appropriate Modify coronary artery disease risk factors Adhere to antianginal medication schedule Stress Management Consumption of low fat diet Smoking Cessation Regular, Aerobic exercise Attain/maintain ideal body weight Pt education
Pharmacologic Management of Stable AnginaNitroglycerin ACE Inhibitor Beta Blockers Calcium Channel Blockers ASA Statins
Nitroglycerin in Stable AnginaProduce arterial and venous dilation by relaxing vascular smooth muscle Tolerance develops; therefore a daily nitrate free period should occur Monitor for hypotension, palpations May produce severe HA
ACE inhibitors in Stable AnginaSuppress renin-angiotensin aldosterone system; Attenuate catecholamine release from adrenergic nerve endings Recommended for secondary prevention of MI Improves morbidity and mortality from MI
Beta Blockers in Stable AnginaBlocks beta receptors in heart which depresses myocardial contractility and decreases sympathetic stimulation Monitor for hypotension, bradycardia, and CHF Abrupt withdrawal can precipitate reflex tachycardia Can worsen symptoms of peripheral artery disease by decreasing cardiac output
Calcium Channel Blockers in Stable AnginaDepress myocardial contractility and increased cardiac blood flow Monitor for arrhythmias, hypotension Can cause ankle edema Significant interaction with Grapefruit Juice
ASA in Stable AnginaPrevent platelet aggregation and exert anti-inflammatory effect in vessels by inhibiting prostaglandin synthesis Monitor for bleeding, tinnitus, GI irritation Cautious use in asthmatics due to hypersensitivity reactions
Statins in Stable AnginaInhibit HMG-CoA, the enzyme which is partly responsible for cholesterol synthesis Monitor for myopathy, rhabdomyolysis Monitor LFTs before starting and at 6 and 12 weeks, after dose increase, and periodically
Follow-up for Stable AnginaDepends on frequency and severity of symptoms Pts with stable angina should be clinically assessed every 4-6 months for the first year, then at least annually
Description of Acute Coronary SyndromeA set of closely related disorders resulting in artheromatous plaque disruption within the coronary arteries and subsequent intravascular clot formation. Myocardial ischemia results that is sufficient to cause damage to the cardiac musculature
Classifications of Acute Coronary Syndrome (ACS)Unstable Angina Non-ST segment MI ST segment MI
Risk Factors for ACSFamily hx of premature CAD (<60yrs) Hyperlipidemia Age (>40 men, postmenopausal women) Cigarette smoking Hypertension Sedentary Lifestyle Diabetes Mellitus Stressful Lifestyle
Assessment Findings in ACSAche, pain, tightness, discomfort, or pressure in chest, arm(s), jaw, teeth, epigastrium or neck usually lasting >20 min; Often unrelieved by nitro Escalating severity of angina Nausea, Vomiting, Diaphoresis Weakness, syncope Feeling on impending doom Hypertension/Hypotension Silent (occurs 20% of time, usually in women, diabetics, or elderly)
Diagnostic Studies for ACSTroponin I: Detectable 3-6 hours after MI EKG: May show elevation/depression of ST segment; presence of Q waves CK-MB isoenzymes; presence in serum indicative of myocardial infarction Coagulation studies Chest X ray: Helps identify cardiomegaly, CHF, and pulmonary diseases which may mimic or exacerbate cardiac disease Anogiography: demonstrates narrowed coronary artery by atherosclerotic lesion ECHO
Nonpharmacologic Management of ACSRe-establish coronary perfusion via angiographic/surgical means ASAP Low Na, low fat diet Patient Education regarding disease, treatment, lifestyle changes, medications
Pharmacologic Management of ACSAcute Phase: IV thrombolytics, Heparin, ASA, anticoagulants, Nitrates, Beta Blockers, Antiarrhythmias, Oxygen, Analgesics Post-MI: BBs, ACEI, Statins and/or fibrates or niacin, nitrates as needed, anticoagulants/antiplatelets
Nitroglycerin in ACSProduce arterial and venous dilation by relaxing vascular smooth muscle Tolerance develops May produce severe HA Monitor for hypotension, palpitations
ACE Inhibitors in ACSSuppress renin-angiotensin aldosterone system; Attenuate catecholamine release from adrenergic nerve endings Recommended for secondary prevention of MI
Beta Blockers in ACSBlock beta receptors in the heart which depress myocardial contractility and decreases sympathetic stimulation Monitor for hypotension, bradycardia, and CHF Abrupt withdrawal can precipitate reflex tachycardia Can worsen symptoms of peripheral artery disease by decreasing cardiac output
Calcium Channel Blockers in ACSDepress myocardial contractility and increase cardiac blood flow Monitor for arrhythmias, hypotension, ankle edema Interacts with grapefruit juice
Statins in ACSInhibit HMG-CoA, the enzyme which is partly responsible for cholesterol synthesis Monitor LFT at start, 6 and 12 wks, and with dose increase Watch for myopathy, rhabdomyolysis
ASA in ACSPrevent platelet aggregation and exerts anti-inflammatory effect in vessels by inhibiting prostaglandin synthesis Monitor for bleeding, tinnitus, GI irritation Caution with use in asthmatics due hypersensitivity reactions
Follow-Up for ACSPer Cardiologist Encourage participation in cardiac rehab program
Consultation for ACSImmediate referral to ED, Give O2, ASA, Nitro, and transport pt)



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