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UTA NURS 4581 Exam 1

UTA NURS 4581 Adults with Complex Needs Exam 1

Resilience being resourceful, being flexible, and having good problem-solving strategies.
Sense of coherence parts of the individual’s functions with synchronization (working together with multiple factors) will give them optimal power
Hardiness physically or mentally strong
General Adaptation Syndrome (GAS) stages alarm reaction, stage of resistance, and stage of exhaustion
Alarm reaction GAS stage fight-or-flight response
Stage of resistance GAS stage physiologic reserves are mobilized to increase the resistance to stress
Stage of exhaustion GAS stage all energy is expended; it is common to become ill and even die if assistance from an outside source is not available
Effects of aging on drug-receptor interaction brain receptors become more sensitive, making psychoactive drugs very potent.
Effects of aging on drug metabolism liver mass shrinks, hepatic blood flow and enzyme activity decline, metabolism drops, and enzymes lose ability to process some drugs, prolonging drug half-life.
Effects of aging on drug absorption gastric emptying and motility slow, absorption capacity of cells and active transport decline.
Effects of aging on drug circulation vascular nerve control less stable, may cause increased effect (anti-HTN drops BP too low, Digoxin slows HR too much)
Effects of aging on drug excretion kidney function declines, blood flow and waste removal slow, lengthening half-life for renally excreted drugs (oral antidiabetic stay in body longer)
Effects of aging on drug distribution lean body mass decreases and adipose stores increase, total body water declines, raising concentration of water-soluble drugs (increased digoxin can cause heart dysfunction), plasma protein diminishes, raising blood levels of free protein-bound drugs.
Creatine kinase (CK)-MB serum cardiac markers found in the blood after myocardial infarction; begin to rise 6 hrs, peak 18 hrs, and return to baseline within 24-36 hrs after myocardial infarction (MI)
Myoglobin serum cardiac markers found in the blood after myocardial infarction; begin to rise 2 hrs, peak 3-15 hrs, and return to baseline within 24 hrs after myocardial infarction (MI)
Troponin serum cardiac markers found in the blood after myocardial infarction; begin to rise 4-6 hrs, peak 10-24 hrs, and return to baseline within 10-14 days after myocardial infarction (MI)
Cardiac Chest X-Ray depicts cardiac contours, heart size and configuration, and anatomic changes in individual chambers; records any displacement or enlargement of the heart, presence of extra fluid around the heart (pericardial effusion), and pulmonary congestion.
Electrocardiogram The basic P, QRS, and T waveforms are used to assess cardiac function.
ECG changes seen during myocardial injury ST segment elevation, pathologic Q wave (≥25% of the height of the R wave), and T wave inversion.
Echocardiogram ultrasound waves record movement & provides info abt abnormalities of valvular structures & motion, cardiac chamber size & contents, ventricular muscle & septal motion & thickness, pericardial sac, ascending aorta & ejection fraction.
Exercise (or Stress) Testing a method used to evaluate the cardiovascular response to physical stress.
Cardiac MRI can detect and localize areas of MI in a 3-D view; sensitive enough to find even small MIs; can assist in the final diagnosis of MI and the assessment of EF; helps predict recovery from MI and to diagnose congenital heart and aortic disorders.
Cardiac Computed Tomography heart-imaging test that uses CT technology with or without intravenous contrast (dye) to visualize the heart anatomy, coronary circulation, and great blood vessels (e.g., aorta, pulmonary veins, arteries); detects calcification.
Cardiac Catheterization insertion of catheter into heart through a vein (R side) and/or an artery (L side) to obtain information about O2 levels and pressure readings within heart chambers.
Electrophysiology study Invasive study used to record intracardiac electrical activity using catheters (with multiple electrodes) inserted via the femoral and jugular veins into the right side of the heart.
Peripheral Vessel Blood Flow Useful in the diagnosis of occlusive disease and venous thromboembolism. Assessed by using duplex imaging and injecting contrast media into the appropriate arteries or veins (arteriography and venography).
Hemodynamic monitoring used to assess cardiovascular status and monitor patient response to interventions. intraarterial and pulmonary artery catheters can be used to monitor arterial BP, intracardiac pressures, and CO.
Coronary Artery Stent expandable mesh-like structure designed to maintain vessel patency by compressing the arterial walls and resisting vasoconstriction. used to treat abrupt or threatened abrupt closure and restenosis following balloon angioplasty.
coronary artery disease (CAD) an abnormal condition that may affect the heart's arteries and produce various pathologic effects, especially the reduced flow of oxygen and nutrients to the myocardium.
Atherosclerosis athere: “fatty mush” and sklero: “hard”; formation of focal deposits of cholesterol and lipids known as atheromas or plaque, primarily within the intimal wall of arteries, that obstruct circulation
myocardial infarction (MI) irreversible cardiac cellular death caused by sustained myocardial ischemia
MI resulting from left anterior descending artery inferior wall MI
MI resulting from left circumflex artery lateral and/or posterior wall MI
Causes of atherosclerosis HTN, tobacco use, hyperlipidemia, hyperhomocysteinemia, hemodynamic factors, diabetes, infections, immune reactions
Developmental stages of CAD (1) fatty streak, (2) fibrous plaque resulting from smooth muscle cell proliferation, and (3) complicated lesion.
CAD fatty streaks stage the earliest lesions of atherosclerosis; characterized by lipid-filled smooth muscle cells which cause a yellow tinge to appear starting around age 15 and increasing in surface area as patient ages.
CAD fatty streaks stage management Treatment that lowers LDL cholesterol may reverse this process
CAD fibrous plaque stage second stage in the development of an atherosclerotic lesion which can appear by age 30 and increase with age; narrowing of the vessel lumen and a reduction in blood flow to the distal tissues caused by formation of fibrous plaque.
CAD complicated lesion stage final stage in the development of an atherosclerotic lesion and the most dangerous; continued inflammation results in plaque instability, ulceration, and rupture, causing platelet accumulation and thrombus.
collateral circulation development of arterial branching that occurs within the coronary circulation when occlusion of the coronary arteries occurs slowly over a long period
Nonmodifiable Risk Factors for CAD Increasing age, Gender (men > women until 65 yr of age), Ethnicity (whites > African Americans), Genetic predisposition and family history of heart disease
Modifiable Risk Factors for CAD elevated cholesterol, triglycerides, or LDL, low HDL, elevated BP, DM, Tobacco use, physical inactivity, obesity, elevated blood glucose, pscychosocial risk factors (e.g., depression, hostility and anger, stress), elevated homocysteine levels
Cholesterol normal level <200 mg/dL
HDL normal level Male: >40 mg/dL; Female: >50 mg/dL
LDL recommended level <100 mg/dL (Near optimal: 100-129 mg/dL)
LDL level with Moderate to High risk for CAD Moderate risk: 130-159 mg/dL; High risk: >160 mg/dL
Triglyceride level with risk for CAD ≥150 mg/dL
Hypertension >140/90 (or >130/80 in patients with diabetes or CKD)
BP with risk for CAD elevated systolic BP >160 mm Hg
Obesity BMI > 30 and Waist circumference ≥40” in men and ≥35” in women
Homocysteine an amino acid formed from methionine that is believed to contribute to atherosclerosis by (1) damaging the inner lining of blood vessels, (2) promoting plaque buildup, and (3) altering the clotting mechanism to make clots more likely to occur
Diet for decreasing risk of CAD reduce total fat, animal (saturated) fat, and salt intake. Increase amount of complex carbohydrates and vegetable proteins in diet.
angina chest pain that is a clinical manifestation of reversible myocardial ischemia
chronic stable angina chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms
CAD manifestations angina
Silent ischemia asymptomatic ischemia that may damage the heart
Nocturnal angina occurs only at night but not necessarily when the person is in the recumbent position or during sleep
Angina decubitus chest pain that occurs only while the person is lying down and is usually relieved by standing or sitting
Prinzmetal’s (variant) angina variant angina; occurs at rest, usually in response to reversible, severe spasm of a major coronary artery
Microvascular angina chest pain is related to myocardial ischemia associated with abnormalities of the coronary microcirculation (vs. coronary atherosclerosis or coronary spasm)
Drug therapy for chronic stable angina drugs that decrease O2 demand and/or increase O2 supply, including Nitrates, β-Adrenergic blocker, Calcium channel blockers, and ACE inhibitors
acute coronary syndrome (ACS) develops when the oxygen supply to the myocardium is diminished and not immediately reversible. includes unstable angina (UA), non–ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI)
unstable angina (UA) angina that is new in onset, occurs at rest, or has a worsening pattern
myocardial infarction (MI) irreversible cardiac cellular death caused by sustained myocardial ischemia (>20 min)
MI manifestations Pain, stimulation of sympathetic nervous system, cardiovascular: elevated BP & HR, then decreased cardiac output and BP; crackles (left ventricle); Jugular venous distention, hepatic engorgement, and peripheral edema (right ventricle), n/v, fever
MI Healing process Within 24 hrs, leukocytes infiltrate area and the inflammatory process begins. At 10 to 14 days, new scar tissue is still weak and vulnerable to increased stress. By 6 weeks, scar tissue has replaced necrotic tissue and injured area is considered healed.
MI Complications Dysrhythmias, HF, Cardiogenic Shock, Papillary Muscle Dysfunction, Ventricular Aneurysm, Pericarditis, Dressler Syndrome
dysrhythmias r/t MI intrinsic rhythm of the heartbeat is disrupted, causing a fast HR (tachycardia), a slow HR (bradycardia), or an irregular beat, all of which adversely affect the ischemic myocardium.
heart failure an abnormal clinical condition involving impaired cardiac pumping that results in pathophysiologic changes in vasoconstriction and fluid retention
heart failure manifestations subtle signs such as mild dyspnea, restlessness, agitation, or slight tachycardia; pulmonary congestion on chest x-ray, S3 or S4 heart sounds on auscultation, crackles on auscultation of breath sounds, and jugular vein distention.
cardiogenic shock shock occurring when either systolic or diastolic dysfunction of the myocardium results in compromised cardiac output
cardiogenic shock management control of dysrhythmias, intraaortic balloon pump (IABP) therapy, and support of contractility with the use of vasoactive drugs to maximize oxygen delivery, reduce oxygen demand, and prevent complications such as acute renal failure.
Papillary Muscle Dysfunction complication of MI; occurs if infarcted area includes or is adjacent to papillary muscle attached to the mitral valve; causes mitral valve regurgitation, which increases the volume of blood in the left atrium and reducing CO even further.
Papillary Muscle Rupture rare and life-threatening complication of MI causing massive mitral valve regurgitation, which results in dyspnea, pulmonary edema, and decreased CO. There is rapid clinical deterioration of the patient.
Papillary Muscle Rupture management rapid afterload reduction with nitroprusside (Nipride) and/or IABP therapy and immediate cardiac surgery with mitral valve replacement.
Ventricular Aneurysm complication of MI; infarcted myocardial wall is thin and bulges out during contraction. May experience HF, dysrhythmias, and angina. Besides ventricular rupture, which is fatal, ventricular aneurysms harbor thrombi that can lead to an embolic stroke.
Pericarditis complication of MI; an inflammation of the visceral and/or parietal pericardium occurring 2-3 days after MI; may result in cardiac compression, decreased ventricular filling and emptying, and HF.
Pericarditis manifestations Chest pain, which may vary from mild to severe, and is aggravated by inspiration, coughing, and movement of the upper body; friction rub; fever.
Pericarditis management aspirin or corticosteroids
Dressler Syndrome complication of MI; pericarditis with effusion and fever that develops 4 to 6 weeks after MI or cardiac surgery.
Dressler Syndrome manifestations pericardial pain, fever, a friction rub, pericardial effusion, arthralgia.
Dressler Syndrome management Short-term corticosteroids
Acute Coronary Syndrome emergency management establish IV, draw blood, initiate O2, ECG monitoring, sublingual NTG & aspirin (then morphine if pain unrelieved), monitor vitals, emergent PCI, fibrinolytic therapy, surgical revascularization (CABG, transmyocardial laser revascularization)
Goal for emergent PCI (percutaneous coronary intervention) to open the affected artery within 90 minutes of arrival to a facility with an interventional cardiac catheterization lab.
Medication management for ACS MONA: morphine, oxygen, NTG, and aspirin
Fibrinolytic therapy fibrinolytic given IV to stop the infarction process by dissolving the thrombus in the coronary artery and reperfusing the myocardium.
Coronary Artery Bypass Graft (CABG) surgery the placement of new vessels to transport blood between the aorta, or other major arteries, and the myocardium distal to the obstructed coronary artery (or arteries).
Transmyocardial laser revascularization (TMR) an indirect revascularization which involves the use of a high-energy laser that is triggered electrocardiographically to create channels between the left ventricular cavity and the coronary microcirculation (ventriculocoronary anastomoses).
sudden cardiac death (SCD) unexpected death from cardiac causes
srongest predictors of sudden cardiac death (SCD) left ventricular dysfunction (EF <30%) and ventricular dysrhythmias following MI
Created by: camellia