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Med-Surg II - wk 3

Problems of Oxygenatio: Perfusion: Nursing Management of Acute Coronary Syndrome

Systematic Approach to Assessing Cardiac Rhythm: 1. Look at a P wave. Is there 1 P for every QRS? Yes, NSR. represent atrial depolarization and repolarization.
Systematic Approach to Assessing Cardiac Rhythm: 2. evaluate atrial rhythm. Is atrial rate the same or different than ventricular rate?
Systematic Approach to Assessing Cardiac Rhythm: 3. Evaluate atrial rate. Do I have an atrial rate that is different from the ventricular rate?
Systematic Approach to Assessing Cardiac Rhythm: 4. measure PR interval (0.12-0.20). the amount of time it takes the message to get from atria to Vs. Long PR interval: conduction problem - impulse isn't getting there when it should. could be a problem in the bundle of His.
Systematic Approach to Assessing Cardiac Rhythm: 5. evaluate ventricular rate.
Systematic Approach to Assessing Cardiac Rhythm: 6. calculate ventricular rate.
Systematic Approach to Assessing Cardiac Rhythm: 7. measure QRS complex. WIDE: PVCs. do the QRSs look like the normal pattern?
Acute Coronary Syndreme the heart is not getting the perfusion that it needs (perfusion problem). pt's may have underlying diseases that cause this to happen (CHF, HTN, diabetes, hx rheumatic fever). "happens really fast" - sudden cardiac death.
Heart Disease "silent killer" . leading cause of death in men and women, worldwide.
What do people do that make coronary arteries sick? fatty foods, smoking, lack of exercise, obesity, etc. some people are pre-disposed.
Complications of CAD one of 2 ways: develop chronic stable angina, or have an episode of acute coronary syndrome. CAD can lead to angina or MI.
Angina (basic) pain due to ischemia.
MI (basic) nothing is getting to that part of the heart muscle = tissue death.
CAD type of lesions Stenotic lesion; non-stenotic lesion
Stenotic Lesion lesions with a "cap" over it (body recognizes the plaque as not normal, immune response, eventually "protective" layer over it. blood is still getting though the open part. anytime the myocardial O2 demand increases they will have angina.
lesion build up of plaque
plauqe build up of cells, fatty cells, making a fibrous plaque (fabric-like). decreases the diameter of the artery. develops
Stenotic Lesion Treatments localized therapy: PTCA, stent,or CABG. (go in and try to fix the clogged area.
Non-Stenotic Lesion more complicated. inflammatory mediators move in, clot develops, less space for blood, protective cap begins to dissolve, blood cells collect. high risk of thrombus and MI.
Non-Stenotic Lesion: Treatment very dangerous to mess with an artery as fragile as this. Lifestyle modification. Drug therapy.
Developing a Lesion plaque begins to develop, narrowing the lesion. Body begins to develop collateral circulation to get blood around the plaque.
Developing a Lesion: Complicated Lesion totally blocked lumen, but collateral circulation is providing tissue with nutrients and O2. takes a long time for this to develop.
Developing a Lesion: someone who develops CAD and doesn't have collateral circulation and younger people they have no back-up when the artery is blocked. "silent killer"
Assessment of Ischemia (PQRST). Precipitating (what brought the pain on?). Quality (how does it feel?). Radiating (where is the pain?). Severity (0-10 scale). Timing (how long have you had the pain? how long did it last?)
Chronic Stable Angina person living with this: have some pattern of angina (associated with CAD), they know they have CAD (they've had testing).
Chronic Stable Angina: Treatment: Drug Therapy Anti-platelet. Nitroglycerin. Beta-blockers, calcium-channel blockers, ACE inhibitors Lipid lowering drugs.
Anti-Platelets prevent platelet aggregation. Baby aspirin Q day. Plavix.
Nitroglycerin potent vasodilator. sublinginal, patch. 3 nitro then stop, 1 Q 5 min, up to 3 doses.
Beta-blockers, Calcium-channel blockers, ACE inhibitors trying to decrease the work of the heart. given for HTN. rate control. give medication that decrease how hard the heart has to work so they don't get into angina episodes.
Lipid-lowering Drugs statins. side effects: rhabdomyolysis - making HR worse, diabetes worse,
Chronic Stable Angina: Management of Risk Factors lifestyle changes, loose weight, start exercising (ease into it)
PCTA/I Percutaneous Translumin Coronary Angioplast/Intervention (w/ or w/o stent).
PCTA (balloon angioplast) cath lab, cath up femoral artery to the artery that needs cleaned out. then they blow up a balloon that pushes the plaque aside, hopefully opening up the lumen making more room for blood flow.
PCTA/I (stent) mesh material covers the outside of the balloon. When the balloon is blown up, the stent is pushed onto the artery walls, pull the balloon out and the stent stays. works well if compliant (lifestyle mods). palliative measure!
Coronary Artery Bypass Graft CABG. Cabbage Patch. either use the sephrenous vein from pt, or pig graft/artificial graft. Go in, take out the damaged artery, replace it w/ healthy artery.
CABG: cntd MAJOR surgery (open-heart). major complications can occur (TCDB). don't want to open chest unless completely necessary. can do valves and a few bypasses with scope.
Acute Coronary Syndrome: unstable angina chest pain that occurs at rest, new in onset, has a change in pattern, or severity for the pt w/ stable angina. more serious than stable. provoked by minimal or no activity. EMERGENCY - need attention right away.
Myocardial Infarction a thrombus formation occlude perfusion distal to the clot. in 4-6 hrs, the heart muscle can become necrotic - EMERGENCY.
MI: Clinical Manifestations Pain (acute pain r/t tissue ischemia). Sympathetic NS stimulation (anxious, increased HR and BP, diaphoretic). Cardiovascular: will start to see affect in LV function - pulmonary (crackles, fluid backs-up).
MI: Diagnostics ECG: shows changes that tell us the patient is experiencing ischemia.
ECG: what shows that there is myocardial ischemia? ST segment depression, T wave inversion. haven't had an MI yet, but they could.
ECG: What shows that there has been myocardial injury? ST segment elevation - there is some injury to the myocardium.
ECG: what shows that an MI has occurred? T wave inversion after an ST elevation.
serum cardiac markers markers int eh blood from damage to muscle. Myoglobin and CK-MB are NOT specific to cardiac tissue. Troponin IS specific to cardiac tissue.
Myoglobin marks injury to muscle. detected early. can't say for sure that this means they have damage to their heart muscle, but we can say they have damage to muscle.
Troponin and CK-MB elevate later than myoglobin. confirms muscle damage (troponin is the one specific to myocardial tissue).
serum cardiac markers: how often are the drawn? Q 6hrs. so we can see these patterns for a patient.
Hospital: C/O of chest pain suspicion of MI, will order serum cardiac markers. and coronary antgography. cath lab for dx or tx.
STEMI vs NSTEMI NSTEMI - there is still time, MI hasn't happened quite yet. STEMI - MI has happened (there is tissue injury and possibly death).
STEMI protocol send straight to cath lab. time = muscle: if we can intervene before there is ischemia and death to the cardiac tissue, that will be better for the patient.
Unstable Angina/NSTEMI nitroglycerin. low-molecular weight heparin (increase clotting time, hopefully they haven't thrown clot yet). plavix (decrease platelet aggregation). Coronary angiography.
Patient with chest pain 1. O2 - 2-3L nasal canula. 2. pulse ox, titrate O2 (>95%) >6L = non-rebreather mask. call another nurse. look into the orders (nitro? ECG - 12 lead? implement these orders, BUT NOT ALONE).
MEWS Modified Early Warning System. EMR calculates this.
derease in myocardial tissu perfusion? 1. O2. 2. ECG 3. Nitro (if ordered). (want ECG before nitro so you can see what is happening).
STEMI immediate reperfusion therapy. get them to cath lab (may go to surgery from there). fibrinolytic therapy (dissolves clots).
Therapy for ACS and MI o2. emergent PTCA. fibrinolytic/thrombolytic therapy. possible CABG.
Therapy for ACS and MI: drugs IV nitroglycerin. IV morphine (viasodilates the airways). beta-blockers ACE inhibitors. anti-dysrhythmics. antiplatelets and anti-coagulants. cholesterol meds.
Sudden Cardiac Death abrupt disruption in cardiac functions resulting in unexpected death (not the people with long-standing CAD). commonly 2ยบ to VFib or VTach. may be result of MI relaated structural damage.
Created by: malysab14