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145 Cards in this Set
- Front
- Back
CHD stands for? This is a ______ term |
CORONARY HEART DISEASE; Umbrella term
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CHD includes things such as? (4) Don't really need to know |
Angina, MI, SILENT myocardial ischemia, CHD deaths r/tCAD |
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CAD =Coronary Artery disease, a PATHOLOGICAL process that affects the? Name a main example |
Coronary Arteries. Example: Atherosclerosis (Plaque build up in artery wall) |
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CVD=Affects ENTIRE _____ Circulation. Name 5 examples |
Cardiovascular Disease (arteries THROUGHOUT body are all affected). Affects entire ARTERIAL circulation Stroke, TIA (interruption in blood supply/neuro dysfunction, prior to stroke) Angina, MI claudication, limb ischemia |
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While over 17 million Americans have CHD, the incidence in the US is _____ d/t? |
DECREASING; medication interventions (Ex: Statins/Lower cholesterol) |
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There has been a reduction in risk factors, improvement in _____ prevention, and heart failure treatment |
Secondary :) |
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However, ______ and ______ INCREASES WITH AGE for men and women |
Incidence + Prevalence (Although postmenopasual women catch up to their male counterparts) |
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We are treating a lot more of the risk factors: Such as? |
1) Stopping Smoking 2) Lowering cholesterol 3) Anti-platelet Therapy (Ex: Aspirin) Prevent blood cells called platelets from forming clots 4) AGGRESSIVELY treating HTN 5) AGGRESSIVELY treating DIABETES All of these DECREASES THE INCIDENCE in this country |
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Whats the difference between anticoagulants and anti platelets? |
Antiplatlets (Ex: Aspirin) Prevent blood cells called platelets from forming clots Anticoagulants (Ex: Heparin/Warafrin aka Coumadin): Work on chemical reactions in your body to LENGTHEN the amount of time it takes your body to form a clot |
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Problem- GLOBABLY, the incidence of cardiovascular disease rapidly increasing outside of the US- WHY? |
(Our diet/lifestyle) is influencing other countries. People don't have to walk as far (2nd/3rd developing countries) |
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Estrogen is protective against heart disease. This is why ____ women catch up to their male coutnerparts Add a new card (or press TAB) |
Postmenopausal (RISK FOR MEN + WOMEN=SAME) |
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What is the MAJOR cause of CVD? (MESSES UP THE WHOLE CIRCULATION) A very ____ process |
ATHEROSCLEROSIS (PLAQUE BUILD UP IN ARTERIES, EVERYWHERE) Complex |
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While many people have plaque in their arteries, it isn't until about ___ of artery blocked that they are SYMPTOMATIC |
75% (Now they will show symptoms) Need a fair amount of narrowing, before you become symptomatic |
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With atherosclerosis there is damage to the outer lining of the artery, known as the? |
Endothelium (inner wall) |
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Substances traveling in the blood such as?(3) can accumulate that are responsible for the narrowing |
Cholesterol, Fats, +Cellular Waste products can gather in arterial wall/damaged area. Chemical reactions then happen d/t build up--> cause cholesterol molecules to OXIDIZE |
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Oxidized cholesterol/inflammatory response leads to the release of? |
Monocytes that turn into macrophages |
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While the MACS eat the cholesterol, they change in shape and accumulate to form? |
PLAQUE |
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As the plaque increase in size, the arterial wall HARDENS and? |
THICKENS |
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Smooth muscle cells within arterial wall begin to? |
MULTIPLY |
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They cover the plaque (YAMS), but this ends up reducing overall? |
Blood supply/oxygen to tissues |
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Overtime the plaque can erode and break off, being released into the? This can form a ___ AND STOP BLOOD FLOW |
Bloodstream; CLOT |
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Limited blood supply to organs and this can lead to _____ death |
Tissue |
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Blood flow can be reduced or completely ____ |
BLOCKED |
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There are NON MODIFIABLE and MODIFIABLE risk factors for CAD. What are the NON-MODIFIABLE risk factors (3) |
1) Gender 2) Age 3) Heredity |
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Name modifiable risk factors |
Smoking, high cholesterol, HTN, physical inactivity obesity/overweight, DM (we can help), stress, alcohol |
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What are 5 things we must OBTAIN when ASSESSING for the presence of CAD? ("ND GAP") |
1) Number of risk factors present 2) Description of symptoms 3) Gender 4) Age 5) PRIOR history |
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Description of symptoms= N-T |
N: Normal O: Onset P: Precipitating and Palliative Factors (What was going on when you noticed the symptoms. What makes it go away?) Q: Quality R: Region/Radiation S: Severity (0-10/how long) T: Time |
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What are some associated symptoms that we may see? |
Dyspnea, Diaphoresis/ N/V |
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Prior history is important. For example, upon assessing for CAD if you have someone come in that notes they had a prior stent in place and notes similar symptoms, we would want to act FAST and call? |
911 |
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What are the main categories/branches of CAD? |
1) CHRONIC STABLE ANGINA 2) ACUTE coronary syndrome |
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Acute Coronary Syndrome is divided into 2 more categories, including? |
1) Unstable Angina+ NON-st segment elevation MI 2) ST-segment elevation MI |
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CAD. Chronic Stable Angina. = Paroxysmal meaning? _____ pain. The pain is usually _____ |
It comes and goes. SUBSTERNAL pain; predictable (pattern, onset, duration of symptoms) |
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Usually occurs with? |
Physical exertion OR EMOTIONAL stress (Ex: Grandma knows when she goes downstairs, she is going to have some chest pain.) |
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Caused by? |
TRANSIENT (short time), REVERSIBLE myocradial ischemia |
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WITH CHRONIC STABLE ANGINA, pain lasts for? |
LESS THAN 15 minutes Transient/Short lasting, predictable, + REVERSIBLE |
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Reversible in that Chronic Stable angina can be relieved by what 2 main things? |
1) Rest 2) Medications: (Nitro-Vasodilator) |
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Grandma may have narrowed arteries, but not___ blockage |
75% (so she can be diag with CHRONIC stable angina) |
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What is the GOAL of Chronic stable angina? To either? |
1) Increase oxygen supply 2) Decrease oxygen demand |
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Pharmacological Intervention for CAD- What is the main medication and how does it work? |
Nitroglycern (Vasodilates and reduces that myocardial demand by DECREASING PRELOAD |
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NITRO DECREASES______ |
PRELOAD/MYOCARDIAL DEMAND |
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What are the 2 ways we can give Nitro? |
1)IV 2) PO |
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Name 5 main medications affiliated with tx of CAD? |
1) ACE Inhibitors (EF <40%) 2) Antiplatelet Therapy: Asprin, PLAVIX, Effient 3) Beta Blockers: reduce mycardial consumption because they reduce contractility, conduction, rate+ velocity(slow) (reduces o2 demand) 4) CCB's- decrease AFTERload, contractility, HR 5) Nitroglycerin: MAINSTAY of therapy |
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Relieved by? |
REST OR NITRO |
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Most of the interventions go towards ___ oxygen demand |
Decreasing |
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How do we educate for Nitroglycerin? |
3 doses, after call 911 (might get 3 more), then if not working, IV |
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PO: 2 types |
1) QUICK sublingual (under the tongue) 2) Long acting (take routinely) Ex: Indir prn |
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Antiplatelets keep further clots/___ from happening |
Narrowing |
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People can stay with Chronic Stable Angina, or they can progress to? |
Acute Coronary Syndrome. |
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CAD. Acute Coronary Syndrome |
:) |
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With Acute Coronary Syndrome, Ischemia=_____ NOT IMMEDIATELY REVERSIBLE |
PROLONGED |
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With Acute Coronary Syndrome, what are the 2 distinct problems |
1) Unstable angina -----ACUTE MYCOARDIAL INFARCTION (AMI) 2) NSTEMI: Non St Elevation MI: NO set elevations on ECG. But ischemia still severe enough to cause Myocardial damage+ release cardiac biomarkers 3) STEMI: St Elevation MI: ST elevations seen on ECG + POSITIVE cardiac biomarkers |
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As things collect, they can form a? |
THROMBOUS (d/t platelet aggregation) |
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As severity increases, there is a decrease in lumen and INCREASE in |
THROMBOUS |
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Order of 3 categories based on amount of lumen? |
1)Unstable Angina 2) NSTEMI 3) STEMI |
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With unstable angina, while you have a fair amount of lumen left you are still having? |
CHEST PAIN |
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However, once you enter the "EMI's" you are causing |
MYOCARDIAL INJURY (don't have enough room to push blood through to perfuse heart) |
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STEMI |
LUMEN COMPLETELY OCCLUDED WITH THROMBUS/PLATLETS. IT ALSO HAS RUPTURED |
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Thrombus happens when? |
The plaque RUPTURES. It's that thrombus that occludes/restricts blood flow |
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Eventually STEMI will lead to? |
Myocardial necrosis/cell death. COMPLETELY OCCULUDES |
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Thrombous= |
CLOT |
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Unlike Chronic Stable Angina, UA doesn't just occur during predictable periods of activity. It is ____ NEW, OCCURS EVEN AT REST + can worsen |
UNPREDICTABLE (EMERGENCY) |
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With UA there are ischemic symptoms that last LONGER THAN? |
20 minutes (not less than 15) |
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With unstable angina there is NO elevation in? |
Trops EVEN THOUGH SYMPTOMS, NO ELEVATION OF TROPONIN !!! |
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Unstable angina may reflect ECG changes or not. Typically indicate? |
ISCHEMIA (reduced blood flow) -May or may not see ischemic changes in EKG |
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Who can develop Unstable Angina?
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Those with previous Chronic Stable Angina, or FIRST STEP OF CAD |
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Unstable Angina has SAME symptoms as NSTEMI (chest pain, radiating, symptoms, may or may not see EKG changes, BUT- WHAT IS THE DIFFERENCE?) |
YOU WILL SEE ELEVATION IN TROPONIN (Refecting that myocardial damage more so now) |
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Usually elevation happens around after ___ hours of symptoms |
6-8 |
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BUT no ST elevations, rather |
depressions |
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May see ____ of a ___ wave |
INVERSION OF T WAVE |
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Just as in UA, a _____ partially is occluding the coronary artery |
Thrombus |
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Someone may be experiencing ischemia, but not any of the "emis" which reflect? |
Muscle Damage |
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Ischemia= Reversible with? |
Rest, Nitrates |
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What kind of ECG changes with Ischemia? |
T wave inversion or ST depression IMBALANCE between myocardial oxygen demand/mycocardial oxygen (SAME AS NSTEMI) |
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It is with INJURY to that myocardium that we will see. Is stemi reversible? |
ST ELEVATION in leads facing injured area, cellular damage BEYOND ischemia Yes, but only if RAPID Intervention (within hour) cells SCREAMING FOR O2 (STEMI) (Grandma who doesn't get better with rest or meds) |
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Infarction - development of what kind of ways? INFARCT= |
Q waves (downward DEFLEX of QRS complex) Q waves represent disruptions in electricity/movement d/t nectroic muscle NECROSIS, DEAD TISSUE (CANT REVERSE) |
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Can reverse Ischemia, Can reverse injury if WITHIN AN HOUR, but CANT reverse?
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INFARCTION. ITS DEAD TISSUE ABSENCE OF DEPOLARIZATION |
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Acute Coronary Syndrome: STEMI (ST ELEVATIONS). STEMI= S for _____ Ischemia |
SUSTAINED/SUCKS. Not reversible. Only NSTEMIS/ISCHEMIA are. THIS IS IRRIVERSIBLE myocardial cell death (necrosis) |
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TIME IS MUSCLE. We need to HURRY up & get people to ___ labs |
CATH |
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Takes about ____ before cell death starts to occur. How long for ENTIRE thickness of muscle to die/necrose |
20 minutes; 4-6 hours |
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STEMIS usually described by location of? |
DAMAGE |
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With STEMI that rhonbus forms- Blood flow ___ to blockage stops |
DISTAL , causing that tissue necrosis/death |
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LAD supplies o2 to? |
ANTERIOR WALL OF LV. ANY MI's here can cause SIGNIFICANT damage |
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With vessel occlusion, what is one way the body compensates? |
By forming collateral circulation (blood can bypass thrombous on own, so NO intervention necessary) |
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ACS. Clinical Manifestations of STEMI (IRREVERSIBLE DAMAGE) |
1) PAIN: 2) SKIN: Not getting that good blood supply: Cool, clamy, ashen 3) HR/BP: Both may initially elevate for compensation and then BP drops with decrease CO/HR eventually+other signs of decreased CO 4) N/V: From pain/vagus nerve stimulation 5) FEVER: Slightly elevated d/t systemic INFLAMMATORY process, caused by the tissue death |
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Won't always be just the "elephant on the chest" could be? (RARE) |
The guy who burped - previous heart attack, that was his only symptom |
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Signs of decreased CO |
1) Hypotension 2) Crackles of lungs 3) TACHY (trying to compensate) |
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How do we assess for ACS (Not just plan old CAD) |
1) History and Physical 2) ECG: Compare to previous if available. Is it reflecting Dysrythmia, MIschemia, Myocardial injury, or Myocardial Infarction? 3) LAB WORK: CARDIAC MARKERS (TROPONIN) 4) CXR 5) Stress Testing 6) Electrocardiogram 7) Angiogram |
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Other lab values other than looking at Trop levels include? |
CBC, Chemistries, Coags + Lipids (Trops, Lipids, CCC) |
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While a Chest X Ray won't show you if they are having an acute MI. But it can show you if they have a? |
Large Cardiomyopathy, dropped lung that is causing chest pain, pnuemonia? (could be chest pain) |
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Diangostic Lab Tests of Serum Cardiac Markers include? |
1) TROPONIN (T and I) 2) Creatine Kinase |
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Troponin = ____ released with? |
PROTEINS; heart muscle damage |
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In MI, trop will elevate when? |
3-6 hours |
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Peaks at? |
12-18 hours and remains elevated for 5-9 days |
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TROP has GREATER sensitivity and specificity for Myocardial injury than does? |
Creatine Kinase |
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This is why we hang onto a lot of chest pain people for? |
24 hours (WE WANT TO DRAW SERIAL TROPONIONS) Want to make sure no elevations. |
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Creatine Kinase is an ______ found mainly in? |
Enzyme; HEART and SKELETAL muscles |
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Heart muscle damage releases? |
CK into the blood (TROP still preferred) |
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CK-MB damage comes from the HEART though, not ____ muscle |
Skeletal |
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When does this one elevate? |
6-8 hours |
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If Troponin positive, but NO changes on EKG- What does the person have? |
NSTEMI (ELEVATED TROP) |
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If you have chest pain and there are ST elevations, what do I have? |
STEMI |
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History of chest pain, Chronic stable angina chest pain. Can turn into? Not relieved by medications/rest |
UNSTABLE ANGINA (Acute Coronary Syndrome) |
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ACS MANAGEMENT (STEMI) MANAGE ___ |
FAST |
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For someone with a STEMI, we are going to see? |
INFARCTION/ST ELEVATION (MI on 12 lead ECG showing these elevations) |
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Management: What are the steps that we are going to do? What medications are we going to give? |
1) IV access 2) Labs drawn 3) CONTINUOUS TELEMETRY 4) GIVE MEDICATIONS -Aspirin (325 mg PO, chew & swallow, Oxygen (Controversial), SL Nitro, Morphine (if other stuff not working) 5) Make decision about a REPERFUSION strategy |
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For US, reperfusion strategy typically involves? |
PCI: Percutaneous Intervention (SAME AS CARDIAC CATH, ANGIOGRAPHY) OR Fibrinolytic Strategy (8 hours away by car, live in mountains, go to ED with STEMI) |
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If you live forever away, you will get? |
The Fibrolytic Strategy |
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Explain this: |
CLOT BUSTIN. Will break up clot, but NONSELECTIVE (very dangerous) every place you clot, you can disrupt the clot and can have significant bleeding (WHEN PCI not available) |
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How do we ensure progress? |
SERIAL ECG's (With Fibrolytic Therapy) waiting to see if ST elevations get better (breaking up the clot) |
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CLOT Lysis= |
LYSE coronary thrombi by CONVERTING pasminogen to plasmin, causes DEGRADATION OF FIBRIN AND FIBROGEN. |
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This will stop the ____ process |
Infarction:) (DISSOLVES THAT THROMBIS) |
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Only done when ___ not available |
PCI/Angiogram/Cardiac Cath Lab |
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Has to be done within? |
12 hours |
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If pt. can't get to PCI center within ___ hours |
3 of arrival to ED |
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Ideally infused within ___ upon arrival to hospital |
30 (Patient selection criteria important) |
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What is the TREATMENT OF CHOICE for confirmed MI? |
ANGIOGRAM |
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What medications will we typically see with angiogram? |
1) ASPIRIN (ANTI-platelet) ALWAYS 2) P2Y12 receptor blockers (Ex: Ticarelor. Prasugrel, loading dose preferred over clopidogrel (plavix) .Sometimes IV GP (Anciximab) |
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With Balloon angioplasty, the plaque is ____ up against |
arterial wall. STENT will then be put in place. |
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Risk: |
Can reocclude (body sees it as foreign) MOST COMMON SITE: RADIAL ARTERY |
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Reperfusion Intervention Complications |
1) CHEST PAIN- Could indicate reocclusion 2) Hemodynamic Instability 3) Evidence of bleeding (Thrombolytic Therapy: CLOT LYSIS non selective, so patient can bleed anywhere) PCI therapy/assess insertion site |
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Complications of MI/Hemodynamic Complications (5) |
1) Cardiogenic SHOCK- may require IABP 2) WALL RUPTURE 3) PERICARDITIS 4) Thromboembolic events 5) DYS |
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Patient Teaching after MI: |
1) Pathphysiology of MI 2) Treat risk factors 3) Env. of hospital-tests, procedures 4) lifestyle modifications 5) Emotional adapation 6) Cardiac Rehabilitation (help with adverse physiological/psychological events. |
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Things that can help with MI |
Exercise, stop smoking, lipid management, weight control, bp control, psychological support, return to work, activity (dont ignore sexual activity) |
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Medications for UA/NSTEMI |
1) Antiplatelets 2) BB /CCB 3) LIPID/DM meds 4) Nitrates (short/long acting) |
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If stent doesn't work, failed medical management, not a candidiate for PCI, failed PCI with chest pain, when long term-benefits of this are superior to those with PCI, presence of LEFT MAIN CORONARY ARTERY or 3 vessel disease= |
CABG |
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When people are taking Statins, we want to see that their lipid levels/cholesterol are going down. We monitor through? |
LIVER FUNCTION TESTS . If not, we need to increase the dose. |
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All chest pain, ___ until proven otherwise |
Cardiac |
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To diagnosis a heart attack, the MOST IMPORTANT THING TO GATHER FROM A PATIENT= |
THEIR OWN INDIVIDUAL STORY |
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Other things to diagnosis a heart attack include |
1) LAB (TROP) 2) ECG changes (Q wave, T inversions, ST elevation) 3) Draw blood |
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When patient is not getting a good blood supply, we will see this with? |
Dysrhythmias |
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We will usually treat the Dysrhythmias with? |
MEDICATIONS |
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So people with heart problems, will need to have a ____ lock in place |
SALINE (we want to be able to intervene quickly) |
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People with heart problems will also have an abnormal? |
Na/K/Mg pump. Electrolyte Imbalances, LOW 02 (meaning they are becoming acidodic) ALL CAUSES OF DYS. |
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Drugs to treat HEART ATTACK: |
OXY, NITRO, ASP, MORPHINE (MONA) Not always in that order. |
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The chest pain is due to? |
Ischemia/ACID building up |
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Nitrate guide = Q ___ min, ___ doses 5; |
5, 3 |
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If not any relief, call? |
911 (TIME IS MUSCLE) |
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Nitrates help to decrease workload of heart, so the heart wont have to? (VASODILATE)
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Pump as hard. Hopefully will vasodilate coronary arteries |
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Side effects of nitrates? |
HA, HYPOTENSION Helps the heart to get the o2 that it needs. |
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You don't want to give the pt. acet/ibu because these dont help with the? |
Vasodilation |
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Nitroglycern: AMBER bottle, active for? |
6 months Check for sizzle |
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Usually patients would be home, then to ER, get their nitro, if nitro doesn't work, get? |
MORPHINE |
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If patient still not better after morphine, nurse will give? |
IV NITRO (Monitor pain, BP (Hypotension) |
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If they are STILL in pain they are going to increase the dose until? |
NO pain or BP is dropping too much |
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Coronary= ___ sided for artery. Hemodynamic pressure paramers= |
L; R |