Chapter 40: Pts With Acute Coronary Syndromes Flashcards
Chronic stable angina
“Strangling of the chest”
Temporary imbalance between coronary artery’s ability to supply oxygen and cardiac muscle’s demand for oxygen
Ischemia limited in duration and does not cause permanent damage to myocardial tissue
Chronic stable angina. CSA
Unstable angina
Chest discomfort that occurs with moderate to prolonged exertion in a pattern that is familiar to the patient. The frequency, duration, and intensity remain the same. Usually relieved by nitroglycerin or rest.
Coronary artery disease
Includes stable angina, acute coronary syndromes
Ischemia—insufficient oxygen supply to meet requirements of myocardium
Infarction—necrosis or cell death that occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to tissue
Acute coronary syndrome
Patients who present with either unstable angina or acute myocardial infarction
Believed that atherosclerotic plaque in coronary artery ruptures, resulting in platelet aggregation, thrombus formation or vasoconstriction
1. STEMI
2. NSTEMI
3. Unstable angina>30% progress to MI in year
Unstable angina pectoris
Chest pain or discomfort that occurs at rest or with exertion and causes severe activity limitation. There is an increase in the number of attacks and in the intensity of pain. It may last longer than 15 minutes and may or may not be relieved by rest or nitroglycerin
New-onset angina
Variant (Prinzmetal’s) angina from coronary artery spasm usually after rest
Pre-infarction angina in the days or weeks before an MI
Patients present with ST changes on 12-lead ECG, but will not have changes in troponin or CK levels
Myocardial infarction
Most serious acute coronary syndrome
Myocardial tissue abruptly and severely deprived of oxygen. Most are the result of atherosclerosis of a coronary artery, rupture of the plaque, subsequent thrombosis, and occlusion.
Occlusion of blood flow
Necrosis
Hypoxia leads to vasodilation and acidosis.
Subendocardial MI, transmural MI (all 3 layers, anterior wall MI (obstruction of LAD, highest mortality), inferior wall MI(RCA obstruction)
Ventricular remodeling
Divided by ACC/AHA
ØNon-ST MI (NSTEMI)
ØST elevation MI (STEMI)
Modifiable risk factors
Elevated serum cholesterol Cigarette smoking Hypertension Impaired glucose tolerance/DM Obesity Excessive alcohol Limited physical activity Stress Atherosclerosis Metabolic syndrome/syndrome x Elevated homocysteine levels
Labs for MI
Troponin T and troponin I Creatine kinase-MB (CK-MB) Myoglobin Imaging assessment: thallium scan for ischemia, CTCA 12-lead electrocardiograms Cardiac catheterization
Pain management for MI
Nitroglycerin Morphine sulfate: priority with MI Oxygen Position of comfort; semi-Fowler’s position Quiet and calm environment Aspirin 325mg
Interventions for ineffective tissue perfusion cardiopulmonary
Interventions:
ØDrug therapy (aspirin, thrombolytic agents)
ØRestoration of perfusion to injured area limits amount of extension, improves left ventricular function
ØComplete sustained reperfusion of coronary arteries in first few hours after MI has decreased mortality
Thrombolytic therapy
Fibrinolytics dissolve thrombi in coronary arteries, restore myocardial blood flow
ØTissue plasminogen activator
ØReteplase
ØTenecteplase
Medication therapy for MI
Glycoprotein (GP) IIB/IIIa inhibitors Once-a-day beta blockers ACE inhibitors or angiotensin receptor blockers Calcium channel blockers Ranolazine (Ranexa)
Reperfussion therapy
Glycoprotein (GP) IIB/IIIa inhibitors Once-a-day beta blockers ACE inhibitors or angiotensin receptor blockers Calcium channel blockers Ranolazine (Ranexa)
Cardiogenic shock
Necrosis of more than 40% of left ventricle Tachycardia Hypotension Blood pressure <30 mL/hr Cold, clammy skin Poor peripheral pulses Agitation, restlessness, confusion Pulmonary congestion Tachypnea Continuing chest discomfort
Percutaneous Transluminal Coronary Angioplasty
Clopidogrel before procedure
IV heparin after procedure
IV or intracoronary nitroglycerin or diltiazem
Possible IV GP IIb/IIIa inhibitors
Long-term therapy, antiplatelet therapy, beta blocker, ACE inhibitor, or ARB
Indications the clot has been dissolved and the artery reperfused include abrupt cessation of pain or discomfort, sudden onset of ventricular dysrhythmias, resolution of ST segment depression or T wave inversion, a peak at 12 hours of markers of myocardial damage. Large amounts of thrombin are released into the system after lysis which increase the risk of vessel reocclusion. Aspirin and IV heparin is usually prescribed.
· Nonsurgical, invasive procedure to improve severity of discomfort for pts with angina and to bridge pts to CABG. Artery often reoccludes if a stent is not used.
· Pre-procedure: dose of Plavix which is an antiplatelet drug. A heart catheterization is done. Balloon forces plaque open.
· Post-procedure: IV heparin to prevent thrombus, IV nitroglycerin or diltiazem to prevent coronary vasospasm. Re-stenosis can happen in the 1st 24 hours. Monitor for acute closure of vessel (chest pain), bleeding from insertions site, contrast reaction, hypotension, hypokalemia, dysrhythmias. Monitor for hypokalemia. Long term: aspirin with Plavix for antiplatelet therapy. ACE and beta blocker if they had an angioplasty after an MI.
STEMI
STelevation MI which is traditional manifestation