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
NSTEMI
non ST elevation MI common in women
Angina pain
Sub sternal chest discomfort radiating to the left arm, precipitated by exertion or stress, relieved by nitroglycerin or rest, lasts less than 15 minutes, few if any associated symptoms
Myocardial infarction pain
Sub sternal chest pain radiating to the left arm, pain in the jaw back shoulder or abdomen, occurring without cause usually in the morning, relieved only by opioids, last 30 minutes or more. Associated symptoms include nausea and vomiting, diaphoresis, dyspnea, anxiety, dysrhythmias, fatigue, palpitations, epigastric distress, dizziness, disorientation, feeling short of breath
Assessment MI
Pain: onset, location, radiation, intensity, duration, precipitating and relieving factors. Assess associated symptoms. Blood pressure, heart rate, and dysrhythmias. Sinus tachycardia with PVCs frequently occur a few hours before an MI. Assess distal pulses, skin temperature, auscultate for S3 Gallup indicating heart failure, respiratory rate, crackles or wheezes with left-sided failure, S4 heart sound with previous MI or hypertension, jugular venous distention, peripheral Edema, temperature
ECG changes
ST elevation caused by coronary vasospasm and variant angina
ST depression and Twave inversion. During anginal episode
The above return to normal after.
Qwave wider than .04 or more than 1/3 height of QRS from necrosis. This may be permanent
Nursing diagnosis for coronary artery disease
Acute pain, ineffective tissue perfusion, activity intolerance, ineffective coping.
If experiencing an MI the most important collaborative problems are potential for dysrhythmias, potential for heart failure, potential for recurrent symptoms and extension of injury.
Additional nursing diagnoses include ineffective sexuality pattern, impaired physical mobility, potential for acute renal failure
Nitroglycerin
.3-.4 SL q5 min x 3 in 15.
Do not give to patients being treated with sexual dysfunction. Fatal interactions may occur. Lie down with the head of bed at a level of comfort because hypotension can be immediate. Monitor blood pressure. If less than 100 systolic or 25 lower than previous, call doc. Pay Attention to orthostatic changes. Allow the tablet to dissolve do not swallow the tablet. Check the expiration date. Tablet should be replaced every 3 to 5 months. Reevaluate pain every five minutes. Monitor for headache. Vasodilation is generalized.
If on long-term they should have an 8 to 12 hour free. To prevent tolerance. Give acetaminophen before to ease headache pain.
Aspirin
81-325 mg po q day
Take daily dose with food to decrease gastric irritation. Tinnitus may occur with toxicity. Should be continued unless the doctor tells them to stop.
It inhibits platelet aggregation and vasoconstriction, decreasing the likelihood of thrombosis. Patient should chew and swallow the drug. Observed for bleeding tendencies.
Contraindications for thrombolytic therapy
Any prior intracranial hemorrhage. Known structural cerebral vascular lesion. Known malignant intracranial neoplasm. Ischemic stroke within three months. Suspected aortic dissection. Active bleeding or bleeding diastasis. Significant closed head or facial trauma within three months
Relative: history of chronic severe poorly controlled hypertension. Severe uncontrolled hypertension on presentation greater than 180/110. History of prior ischemic stroke within three months, dementia, or known intracranial pathology not covered in contraindications. Dramatic or prolonged CPR over 10 minutes or major surgery in 3 weeks. Recent internal bleeding within 2 to 4 weeks. Noncompressive all vascular punctures. For streptokinase prior exposure over five days ago or prior allergic reaction. Pregnancy. Active peptic ulcer. Current use of anticoagulants, the higher the INR the higher the risk of bleeding