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What is an MI
35-45 min of ischemia leads to
What natural compensatory mech can help?
- occulsion of th coronary artery
- cellular damage, necrosis across they myocardium
- artherosclerosis or an embolus (air, gas, tissue, or thrombus).
- collateral circulation
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?
- 24 h
- cardiac enzymes
- phagocytes (neutrophils)
- 6 weeks post MI, necrotic tiss turns to scar tissue
How is an MI diagnosed?
CKMB, MYoglobin, Troponin I (cardiac spec), EKG changes, risk factors. Elevated WBC w large MI
Similar to Angina, but may last longer. Pain.
s s/x MI?
heavy pressure, pain, anx, dyspnea, weakness, faintness, NV, pallor, erratic beh, hypotension, shock, cardiac rhythm, fever
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
- *O2, morphine can dilate coronary arteries, anticoags (APLT, heparin), BBs, stool softeners to prevent straining
MI nursing interventions
min act 1-2 days. Lifestyle ^ Ysocial issues, pt teaching. Possible ICU 1-2 days
MI clinical pathway:
standard door to balloon time?
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.
coronary artery bypass graph
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
How do resting on channels work w anti Ds?
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?
- 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
Na channel blockers
Sub class IB Lidocaine (Xylocaine)
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
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
- beta blockers- HTN, MI, dysrhythmias
- Most common cardiac med
- slows HR and conduction velocity through AV
Beta adrenergics Blockers- treat what? end in what?
Metoprolol (Lopressor, toprolol)
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?
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
weekly dose till angina free
- yes, better absorption
BBs Propanolol (Inderal)
Treats dysrhythmics and also____ and _____
On own or combined w other dysrhythmics, usually?
- angina migraines
K+ channel blockers
How do they work?
Can they cause serious SEs?
tx of _______ ________
half life long or short?
- 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)
- severe pulm tox, pneumonia-like synd
- CV-brady, HF, Heart block, sinus arrest HTN
K+ channel blockers
Amiodarone (cordarone) con't
- Inc Dig
- enhances anticoags
- cautn w herbal supps
- monitor pulm, CV, liver piror and reg, IV- cont EKG monitoring
- mon for pulm tox (fatal)
how does it work?
Only a few approved to treat ____
only effective against _______
blocks Ca_ channels, slows cond velocity, slows impulse thru AV node, prolongs resting stage
- vasospastic angina *helps CAs relax)
- HTN, AFib
AV block, brady, arrhyth, HF, hypotension, headache, insomnia, photosensitivity, ab discomfort
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
- 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+)
SEs arrhythnmias, HF, hypotenstion, anorex, hyperKalemia
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 ___
how does it help? Dilates______
- 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.
- B Blockers, Ca_ blockers, thrombolytics, antiplatelets
- resp dep, resp arrest, thrombocytopenia, brady, hypo, cardiac arrest, sedation, euphoria, seizures, urinary ret, itching, N/V, constipation
Nitrates Nitroglycerin (Nitrostat, Nitrobid)
- Fast acting for acute angina/MI
- subling, IV drip, topical. Watch out for Viagra. severe hypotension. S