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Silverollbars
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2011-05-21 20:21:56
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  1. What is an MI
    leads to
    35-45 min of ischemia leads to

    caused by?
    What natural compensatory mech can help?
    • occulsion of th coronary artery
    • ischemia
    • cellular damage, necrosis across they myocardium

    • artherosclerosis or an embolus (air, gas, tissue, or thrombus).
    • collateral circulation
  2. How does the body respond to an MI?
    within how long?
    What is releasedf rom dead cardiac cells?
    How is the area cleared?
    How long until scar tissue formed?
    • inflammation.
    • 24 h
    • cardiac enzymes
    • phagocytes (neutrophils)
    • 6 weeks post MI, necrotic tiss turns to scar tissue
  3. How is an MI diagnosed?

    Clinical manifestations
    CKMB, MYoglobin, Troponin I (cardiac spec), EKG changes, risk factors. Elevated WBC w large MI

    Similar to Angina, but may last longer. Pain.
  4. s s/x MI?
    heavy pressure, pain, anx, dyspnea, weakness, faintness, NV, pallor, erratic beh, hypotension, shock, cardiac rhythm, fever
  5. Med mgmt of MI- 1st priority?

    How long do myo cells take for entire thickness of muscle to necrose?

    When is reperfusion most effective?
    • Open blockage!
    • Dec heart workload w O2, Meds*, anxiety, treat PVCs or irreg HB, thrombolytic
    • PCTA!
    • *O2, morphine can dilate coronary arteries, anticoags (APLT, heparin), BBs, stool softeners to prevent straining
    • 4-6h

    30-60m
  6. MI nursing interventions
    min act 1-2 days. Lifestyle ^ Ysocial issues, pt teaching. Possible ICU 1-2 days
  7. MI clinical pathway:
    standard door to balloon time?
    Meds given?
    Prognosis?
    Mod vs non mod risk facts
    • 90 min
    • antigcoags and anti platelets, tissue plasminogen, nitrates, BBs, CaBs, salicylates, antidysrhythmias, stool softener, diuretics, Elyte replcmt

    many not tx before getting to hospital die.
  8. What's CABG?
    coronary artery bypass graph
  9. Dysrhythmia, what is it?
    Harmless or deadly?
    How to you know for sure?
    Atrial dysrhythmias- how many have strokes?
    • abnormailites of e conduction in heart
    • either
    • EKG
    • 15%
  10. How do resting on channels work w anti Ds?
    Resting?
    ions out?
    ions in?
    mycard mem neg or pos charge? polarized or non? channel gates open or closed?

    Depolarization (action potential)
    what channels open?
    What goes in or out and what causes myo contr?

    Refractory
    when?
    what wave?

    Repolarization
    what's happening?
    • Resting:
    • out- more Na and Ca
    • in- K_Myocardial memb slight neg charge- polarized, channel gates closed.

    • Depolarization (action potential)
    • Na and Ca channels open
    • Na and Ca rush in
    • Ca ion resp for mycardial contraction

    • immediately after depolarization
    • T wave

    everything is resetting, returns to rest
  11. Na channel blockers
    Sub class IB Lidocaine (Xylocaine)
    For what?
    SEs?
    Must be on what? Monitor what? Stop if what?
    • slows impulse cond across my.
    • res. for rapid control of V dysryth.
    • hypotension, worsened arrhyth, brady, heart block, resp arrest (rare, status asthmaticus)
    • Must be on card monitor,
    • mon vitals and Elytes, tox *seiz, confusion, stop if widening of QRS
  12. Antidysrhymics
    Beta-adrenergic blockers
    End in what?
    What does it treat besides dysrhythmias?
    Beta 1-receptors in heart
    Beta 2-receptors in lungs
    How common a med?
    How does it work and where?
    Result is it _________myo contractility
    • olol
    • beta blockers- HTN, MI, dysrhythmias

    • Most common cardiac med
    • slows HR and conduction velocity through AV
    • decreases
  13. Beta adrenergics Blockers- treat what? end in what?
    Metoprolol (Lopressor, toprolol)
    affects Beta___
    How is it good in an acute MI, monitor what? How given at first and how given later? Don't give below __bpm

    How good in angina? How long given weekly for angina?

    Where metabolized?
    When given w multiple CV meds: multiple antihypertensives can cause severe____in BP
    Combined with dig may cause_____
    give w food or not?
    can pt stop suddenly?
    • HTN, MI, antidysrhythmics, angina (weekly till it goes away)
    • Beta 1
    • Metoprolol (lopressor, toprolol)
    • Early intervention, IV push q 2-5 min, monitor vitals every 2-5min, then start PO
    • 60

    weekly dose till angina free

    • liver
    • drop
    • brady
    • yes, better absorption
    • no.
  14. BBs Propanolol (Inderal)
    Treats dysrhythmics and also____ and _____
    Affects Beta____
    On own or combined w other dysrhythmics, usually?
    monitor
    • angina migraines
    • 1&2
    • combined
    • vitals
  15. Antidysrhythmics
    K+ channel blockers
    How do they work?
    Can they cause serious SEs?
    Amiodarone (cordarone)
    tx of _______ ________
    half life long or short?
    _________
    SEs?
    • block K+ ions channels in myo cells and lengthens resting stage of myo cell
    • w caution, yes, bradycaria, hypotension, hepatic dysfunction, photosensitivity

    • V tach
    • A tach (fib)
    • long
    • severe pulm tox, pneumonia-like synd
    • CV-brady, HF, Heart block, sinus arrest HTN
  16. Antidysrhythmics
    K+ channel blockers
    Amiodarone (cordarone) con't
    DDIs?
    Monitor
    • Inc Dig
    • enhances anticoags
    • cautn w herbal supps

    • monitor pulm, CV, liver piror and reg, IV- cont EKG monitoring
    • mon for pulm tox (fatal)
  17. Ca+blockers
    how does it work?
    Only a few approved to treat ____
    only effective against _______

    Diltiazem (Cardiaem
    also treats?
    SEs?

    Varapamil (Calan)
    blocks Ca_ channels, slows cond velocity, slows impulse thru AV node, prolongs resting stage

    SVT

    • vasospastic angina *helps CAs relax)
    • HTN, AFib

    AV block, brady, arrhyth, HF, hypotension, headache, insomnia, photosensitivity, ab discomfort
  18. Digoxin
    Primarily for ____
    How does it work?
    ________ _______of SA node
    ____ ____ through AV node
    ______ ____ in myo cells
    Excessive levs cause _____ ______

    Must take _________ one full min prior to giving
    SEs?
    • HF, also for arrhythmias
    • decreases automaticity of SA node
    • slows conduction through AV node
    • Inc contractility in myocardial cells
    • excessive levels cause serious dysrhythmias
    • (interacts w lots of meds, monitor drug levels, more so w hypoK+)

    apical pusle

    SEs arrhythnmias, HF, hypotenstion, anorex, hyperKalemia
  19. Meds for angina, MI?
    Give ___ first
    nitrates- Venous dilation decreases______
    arterial dilation decreases _______
    Dilates and relaxes spasms in ______
    short acting long acting or both?
    Morphine- schedule ___
    antidote?
    how does it help? Dilates______
    resp____
    SEs?
    • O2,Nitrates, B Blockers, Ca_ blockers, thrombolytics (anticoags), morphine, antiplatelets,
    • O2- give first!!
    • nitrates- vasodilation.
    • Relaxes both arterial and venous smooth muscle.
    • Venous dilation decreases preload.
    • Arterial dilation decreases afterload. Decreases BP
    • Coronary arteries.
    • Both.
    • B Blockers, Ca_ blockers, thrombolytics, antiplatelets
    • Morphine
    • II
    • narcan
    • CAs
    • resp dep, resp arrest, thrombocytopenia, brady, hypo, cardiac arrest, sedation, euphoria, seizures, urinary ret, itching, N/V, constipation
    • BBlockers
  20. Nitrates Nitroglycerin (Nitrostat, Nitrobid)
    • Fast acting for acute angina/MI
    • subling, IV drip, topical. Watch out for Viagra. severe hypotension. S

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