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patho 2 cad
| Question | Answer |
|---|---|
| What % of all death in western society is related to CAD | 33% |
| resting coronary blood flow is | 225ml/min->8 ml of O2/100g of tissue/min |
| what % of CO is going to the heart's circulation | 4-5% |
| T or F Exercise can increase coronary BF up to 4X | True |
| What is the O2 requirement to maintain the life of a cell? | 1.3ml of O2/100g of tissue/min |
| T or F coronary BF is controlled by the nervous system | False, it's controlled by local metabolism |
| The most important factor in local BF regulation | O2 demand |
| Effects of the sympathetic NS | ^HR+strength of contraction+^vasoconstrict |
| Effects of the parasymp NS | decrease HR decrease strength of contraction..no effect on vessels |
| Cardiac muscle uses ______ 70% of the time, but in emergencies ________ is used | fatty acids, glycolysis |
| The most frequent cause of decreased coronary BF | Atherosclerosis |
| Death due to CAD is caused by 2 things | Acute coronary occlusion or cardiac fibrillation |
| 3 biological processes in the creation of atherosclerosis | -proliferation of intimal smooth musc. cells(macroph.+Tlymph)-form. lg amts of connective tissue(collagen & elastin)-accum. of lipids(mostly chol)- |
| 3 independant risk factors for the dev. of atherosclerosis | plasma cholesterolsmokinghigh BP |
| Response to injury theory | injury in the endothelium triggers eventsby changing the funct. act of the endoth. comb. w/ ^ chole.,smooth musc prolif., and platelet activity lead to plaque |
| monoclonal theory | Each of the lesions is a benign neoplasm, resulting from a cell affected by a virus, chem, or mutation |
| Coronary insufficiency | When the blood supply is lower than what is requiredfor normal cardiac metab. |
| Hypoxia | decreased O2 supply to tissue despite adequate perfusion |
| Anoxia | no O2 supply despit adequate perfusion |
| ischemia | decreased O2 supply +insuff. removal of wastes as a result of decreased perf. |
| Angina Pectoris | pain due to ischemia, begins when the load on the heart is too great in relation to coronary BF |
| Where is Angina felt and how does it feel | beneath the upper sternum ext to L arm and shoulder, neck, side of face, opp arm, and shoulder. hot pressing, constricting |
| T or F there is myocardial necrosis in angina | that's a BIG FAT NO!!! |
| Chronic or stable angina | begins gradually reaching top intensity over a couple of minutes before dissipating,after sesation of the activity that caused it |
| Events that cause an episode of chronic or stable angina | events causing an inc. in O2 demand-phys. activity, emotions, eating, tachy, fever, chills, etc.. |
| Chronic/stable angina has ____O2 demand and ___O2 supply | increased, fixed |
| Findings w/ chronic/stable angina | HTN, non specific ST and T changes; LBBB |
| T wave inversion is usually indicative of | ischemia |
| ST segment elevation is usually indicative of | injury |
| Diagnosis of stable/chronic angina | Exercise EKG, thallium stress test, myocardial perf imaging,exer. radionucleotide angiography, CXR, enzymes norm, ^chol., echo, cath |
| Definative diagnosis for chronic/stable angina | coronary arteriography+LV Arteriography |
| How does myocardial perfusion imaging work? | radionucleotide is injected at peak exercise and image obtained min.later with pt. at rest->pattern of perfusionduring exercise. defect areas are areas of stress induced ischemia or infarct.still shows defect in 2-3h=MI |
| Management of chronic/stable angina | lifestyle changes, drugs, revascularization |
| methods of revascularization | PTCA, CABG,laser angioplasty, athrectomy |
| Acute/unstable angina happens @___ | rest |
| Acute angina has ____O2 demand and ____O2 supply | fixed, decreased |
| T or F bed rest an nitro can eliminate the pain of acute angina completely or permanently | False |
| Findings of acute angina on EKG | transient deviations of ST segment and/or inv. T wave |
| Findings in acute angina in the cath lab | show collat circ. less dev. than chronic and higher % of more than one vessel disease. inc incidence coronary thrombi. |
| Pt's w/ acute angina have a faster prog. of atheros due to | inc. platelet aggreg., and thrombosis+coronary spasms |
| Diagnosis of acute angina | exer. ekg, echo, thallium 201 test, cath and angiography |
| management of acute angina | hospitilization,(tx fever, anemia, infections, arrythm, thyrotoxicosis), drugs(nitrates b-block anti coag, anti plate), thrombolytics, IABP, CABG, PTCA |
| If the whole thickness of the myocardial wall is infarcted what type of MI? | Transmural |
| If the MI only involves the subendocardium, the intramural myocardium or both w/o extending to the epicardium what type of MI | sub-endocardial |
| Acute coronary thrombosis is most common w/ what type of MI | Transmural |
| When is a CABG contraindicated? | pt's with uncomplicated transmural infarcts more than 6 hours after onset. |
| When is a CABG indicated? | when PTCA was not successful, multi vessel CAD even in absence of an AMI. Should be w/in 4-6h, best in first 2h |
| Prinzmetal's angina | occurs at rest, elev. of ST seg.,result of coronary artery spasm, |
| Diagnosis of Prinzmetal's angina | dev. ST elevation w/pain, Ergonovine test(will cause chest pain & ST^ |
| Treatment of Prinzmetal's angina | nitrates and Ca antagonists |
Created by:
jenbirne69
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