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Ch 35 Mod IV
Ch 35 cardiac disorders ANGINA and AMI
| Question | Answer |
|---|---|
| CAD occurs when major coronary arteries supplying blood to (epicardium, endo, or myo) are partially or completely ____. | myocardium, blocked |
| Blockage of arteries are caused by what 3 things: | artery spasms, arteriosclerosis, athero |
| Arteriosclerosic and atherosclerosis may result in ____ or ____ of myocardial tissue: what conditions | ischemia, infarction |
| thickening, hardening, loss of elasticity of arterial walls | arterio |
| what causes the innermost layer of the artery to stiffen, thicken, and decrease in diameter for ASHD pts> | collagen and smooth tissues |
| Arteriosclerosis: what 3 things adhere(stick) to the damaged walls | lipids, cholesterol, calcium |
| arteriosclerosis causes 3 conditions, name them: remember acronym HIPA | Hypertension, Impaired tissue Perfusion, aneurysms |
| a form of arteriosclerosis, and is an ___disease that begins with___injury | atherosclerosis inflammatory; endothelial |
| what are seen in advanced stages of atherosclerosis? | Complicated lesions |
| three types of lesions of atherosclerosis | fatty streaks,fibrous plaque, and complicated lesions |
| the earliest lesion in atherosclerosis. | fatty streak |
| fatty streak: what is the color? | Yellow |
| fatty streak: causes an obstruction true or false | false |
| fatty streak: found in what area of the body by age 10? | aorta |
| fatty streak: found in coronary arteries by what age? | 15 |
| fatty streak: are irreversible, true or false | false |
| fatty streak: S/Sx | none |
| Nurse learns that there is fibrous plaque in the pts arteries. She knows this is what stage of atherosclerosis? | progressing stage because fibrous plaque is only seen in the progressing stage. |
| What is the color of fibrous plaque? | whitish, grayish |
| Fibrous plaque contributes to loss of arterial ____ and impairs ____. This impairs the vessels ability to meet increased ___ needs. | elasticity; vasodilate; O2 |
| if plaque formation occur slowly, what type of circulation may develop? | Collateral circulation |
| new branches of blood vessels that grow from existing arteries to provide increased blood flow: | collateral blood vessels |
| non-modifiable risk factors with atherosclerosis-name 4 | gender, age, heridity, race |
| how does gender protect women from developing atherosclerosis? | Hormone secreted-stops protecting women by menopause |
| what are the early signs and symptoms of coronary artery disease? | none: CAD is asymptomatic during early stages |
| Why do pts w/ early stage CAD not show any S/Sx (asymptomatic) | collateral circulation forms to compensate |
| when do S/Sx appear in CAD | when blood supply is reduced by at least 50% |
| CAD: clinical manifestations | angina pectoris, ACS(unstable angina and MI), sudden cardiac death |
| the most common symptom of CAD | angina pectoris |
| Angina pectoris results when? | demand for O2 by Myocaridal cells exceeds supply of O2 delivered |
| name 3 types of angina pectoris | stable, unstable, variant angina |
| stable angina: Characteristics - occurs when? subsides when? constant? not predictable? how long does it last? relieved w/ what med? | occurs w/ activity, subsides w/ rest; intermittent and predictable, lasts only a few minutes, nitro |
| risk factors of stable angina | stress, heavy meals, smoking, exertion |
| viselike, squeeszing, smothering pain on the sternum | stable angina |
| stable angina: pain may radiate to 5 places | arms, shoulder, jaw, neck, epigastrium |
| stable angina S/Sx | diaphoresis, dyspnea, nausea, vomiting |
| two names for unstable angina | pre-infarction angina and crescendo angina |
| unstable angina is treated as what type of condition | acute coronary syndrome: ACS |
| unstable angina characteristics | more severe, occurs at rest or minimal activity, not relieved by NTG, or require frequent NTG, not predictable |
| unstable angina may occur in a patient with a history of? | Stable angina |
| unstable angina pain characteristics | described as more severe, changing pattern |
| what may be the first clinical manifestation of CAD? | unstable angina |
| patients with unstable angina are higher risk for what type of condition? | AMI |
| a type of angina caused by coronary artery spasms | variant angina |
| variant angina characteristics | not associated with CAD, unpredictable, often occurs at rest, pain goes away when spasms stop |
| treatment for variant angina | calcium channel blockers for prevention |
| ABCDE therapy for CAD stands for | aspirin and anginal therapy; beta blockers and blood pressure; cigarette and cholesterol; diet and diabetes; education and exercise |
| low-dose aspirin is administered to interfere with___aggregation; reduce the risk of___. | platelet; MI |
| if patient cannot tolerate aspirin what is given? | another antiplatelet medication (plavix) |
| Antianginal therapy includes three things: | nitrates, beta blockers, calcium channel blockers |
| nitroglycerin are used to treat what two things? | actual episodes of angina, prevent angina |
| two routes of med administration for the onset of angina pain | sublingual, buccal |
| three routes used to admin nitrates for angina attack prevention | oral, transdermal, topical |
| Beta blockers and calcium channel blockers are prescribed for ___management of angina | long-term |
| after initial relief and control of anginal pain, the focus of therapy will turn to__reduction | risk |
| some risk reduction measures are: | blood pressure management, stop smoking, lipid control, diet, exercise, education, glucose control |
| what medication may be prescribed for patients with stable angina to reduce the risk of AMI? | Ace inhibitors |
| medical treatment for unstable angina | same as other angina is; additional anticoagulation therapy with LMWH |
| Cultural: which two americans develop CAD earlier than other americans | Native American and African-Americans |
| coronary artery disease is highest among which Americans? Lower among which Americans? | Caucasian; Latin Americans |
| death of myocardial tissue | AMI |
| myocardial tissue dies as a result of prolonged lack of ____ and ____ supply to the heart | blood, oxygen |
| modifying factors of AMI | smoking, high-fat diet, hypertension, sedentary lifestyle, stress |
| AMI occurs more frequently in men or women | men: considered a risk factor |
| pathophysiology of AMI | begins w/ occlusion of coronary arteries -> ischemia -> injury and infarction |
| how long must ischemia last for damaged tissue to be considered irreversible? | 20 mins |
| how many hours after an MI will the healing process begin | 24hrs |
| what happens on the third day | dead tissue broken down by enzymes and removed by macrophages |
| what develops to supply blood to the injured area? | Collateral circulation |
| between what days after AMI is the myocardium vulnerable to stress? Why | 10 to 14 days; weakness of the healing tissues |
| after an AMI, how long does it take for tissues to heal? | 6 wks |
| two categories of acute coronary syndrome | unstable angina, AMI |
| STEMI and NSTEMI: which is partially occluded, which is completely occluded | partial = NSTEMI; total = STEMI |
| Why is ST segment important to note in an ECG | the segment will look different w/ partial or total lack of oxygen |
| name five complications of AMI | dysrhythmias, heart failure, rupture, cardiogenic shock, thromboembolism |
| a disturbance in heart rhythm is called | dysrhythmias |
| what intervention is ordered for patient w/ dysrhythmias | continuous cardiac monitoring |
| most common complication of AMI | heart failure |
| most frequent cause of death after an AMI | cardiogenic shock |
| after AMI,thrombi may form in what two parts of the body | injured heart chambers, veins of the legs |
| Pulmonary embolism may cause | pallor, cyanosis, heart failure |
| How can ruptures/aneurysms happen after an AMI | weakened, inadequate scars from healing tissue may cause artial walls to buldge and rupture |
| AMI break down | 1) occluded coronary arteries in 4-6 = ischemia = injury = infarction. 2) 20 mins, tissue damage irreversible. 3)after 24 hours, dead tissue breaks down 4) colleteral circulation occurs 5) 10-14 days susceptible to stress 5) complete healing in 6 wks |
| classic symptom of AMI: where is the pain and what is the description | pain located below or behind sternum that is heavy, constrictive |
| AMI pain may radiate where? | arms, back, neck, jaw |
| AMI begins w/ exertion: T or F | false, it is w/ and w/o |
| If AMI progresses what is the S/Sx | same as stable angina: diaphoretic, dsypnea, nausea, vomiting, light head |
| AMI: skin is frequently | cold, clammy |
| AMI: what feelings does pt feel | impending doom, great anxiety |
| Which group shows atypical signs of AMI | older adults, women, diabetics |
| If confusion arises w/ chest pains and other S/Sx of AMI what did Mrs. G say must be done: | immediately put on ECG (not sure of my notes) |
| What confirms AMI? | ECG and lab evidence |
| which lab did Mrs. G say lasts the longest | Troponin: 2 weeks |
| in what extraordinary situation is troponin drawn vs. other enzymes or markers | ER for early diagnosis |
| Mrs G said to remember which is the quickest test for AMI but why is not always useful | Myoglobin, no specific to cardiac injury |
| when does CPK-MB return to normal level after an AMI | 2 to 3 days |
| ECG appearances: ischemia | ST segment is depressed, T wave inverted |
| ECG appearances: when is ST segment elevated | total occlusion |
| ECG appearances: ST segment of partial occlusion | not elevated |
| most frequent dsyrhythmias for AMI | PVC, V-fib, V-tach |
| what is the difference in pain regarding AMI and unstable angina? | Indistinguishable |
| name 3 antiplatelet medications | aspirin, ticlid, Plavix |
| Mrs. G said that calcium channel blockers are more for which type of angina | variant |
| non-modifiable risk factors of AMI | DM, Family Hx, male gender |
| dysrhythmias occur in approximately how many percent of AMI? | 80% |
| CHF can cause what two conditions | cardiogenic shock and death |
| Cardioshock is marked by what syptoms | hypotension, cool, moist skin, decreased alertness, oliguria |
| S/Sx of pulmonary embolism | SUDDEN SEVERE DYSPNEA, pallor, HF, cyanosis |
| T or F: ventricular rupture/aneurysm is not always fatal | false: its always fatal |
| AMI EKG changes | ST elevation in two or more leads, Q is 1/3rd the height of the R wave |
Created by:
Jgar2007
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