Cardiac Meds 2 final

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Cardiac Meds 2 final
2014-06-24 23:20:45

Fun last week
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  1. Vasodilating agents
    directly acting vasodilators- acts directly on the smooth muscle not first line agents

    calcium channel blockers

    Big open road- vasodilates so the BP can decrease
  2. Direct Acting Vasodilators
    • Ex- hydralazine (apresoline)
    • - netroprusside (DOC for HTN crisis)

    MOA- works directly on the vascular smooth muscles to vasodilate. 

    CI- HTN (not first choice), reduce afterload with CHF by openning up because it vasodilate
  3. Direct Acting Vasodilators 
    Netroprusside SE NI
    • SE: Hypotension
    • reflex tachycardia palpitations- 
    • CNS
    •  (hypotension stimulates baroreceptors send msg to SNS- stimulates beta 1)
    • fast HR increase O2 demand

    • NI: give beta 1/alpha 2 stimulant to bring down HR
    • peaks in 10-20 mins
    • assess BP HR urinary output, edema, safety
  4. Calcium Channel Blockers
    ex- Diltiazem (cardizem)

    • MOA: prevents the entry of calcium into the cardiac cell and vascular smooth muscle
    • - vasodilation (VSM)
    • - decrease rate and conduction
    • - decrease contractibility
  5. Ca channel blockers
    VSM Cardiac
    Agents work on VSM and cardiac

    direct effect- decreases hr, conduction (ca needed for nerve conduction), contractions, bp

    indirect effect- reflex tachycardia

    • end effects- direct and indirect effects negate each other 
    • little or no effect on rate and conduction
    • but it will cause this to vasodilate
  6. Ca channel blocker VSM
    • direct- decrease BP
    • indirect- reflex tachycardia
    • end effects- unopposed tachycardia
    • - give beta blocker
  7. Ca Channel blockers CI
    angina HTN, cardiac arrhythmias (change rate u change rhythm), migraine headache
  8. Ca Channel blocker SE
    • constipation (most common)
    • hypotension
    • reflex tachycardia (VSM dilation)
    • arrhythmias
    • CNS effects (headache, dizziness, flushing, fatigue)
    • muscle fatigue
  9. Ca Channel Blockers NI
    • Assess BP and HR
    • parameters BP S< 100, HR< 60
    • assess type of Ca channel blockers
    • drug interaction
    • patient teaching
  10. Medications to treat Angina
    • Angina- chest pain that results from ischemia
    • - when the O2 demand exceeds the O2 supply
    • - underlying- atherosclerosis

    O2 supply- determined by the myocardial blood flow

    O2 demand- determined by the heart rate, contractility, preload and afterload
  11. Treatment Strategies
    goal: to decrease the frequency and intensity of agina

    reduce O2 demand and increase O2 supply

    • nitrates
    • calcium channel blockers
    • beta blocker
  12. treatment strategies (beta blockers, calcium channel blocker)
    • Beta Blockers
    • - decrease HR, contraction, conduction
    • - decrease preload (how much blood in ventricle if u reduce this the heart wont have to work hard), afterload (SVR)
    • - decrease cardiac workload (O2 demand)
    • - improves O2 supply (vasodilation)

    • Ca Channel blockers (works the same way)
    • - decrease HR, contraction, conduction
    • - decrease preload, afterload
    • - decrease cardiac workload (O2 demand)
    • - improves O2 supply (vasodilation)
  13. Nitrate
    ex. Nitroglycerin

    MOA: acts directly on Vascular smooth muscle (VSM) causing vasodilation

    • **sulfahydride- converts drug from inactive form to active form (prodrug) decrease uptake of Ca into the smooth muscle (no muscle contraction, vasodilate)
    • - decrease venous return (vasodilate)
    • - decrease preload, afterload (vasodilate)
    • - decrease cardiac workload (vasodilate)
  14. Nitrate CI SE
    CI: Angina, prevention for angina, HTN, CHF, to reduce pre/afterload, MI, adjunct PVD

    put under the tongue works within seconds- for agina

    • SE: headache (common) vasospasm over time h/a will reduce treat with tylenol
    • - orthostatic hypotension
    • - reflex tachycardia (beta blocker)
    • - CNS effects dizziness
    • - local skin irritation 
    • - stinging in mouth
    • - nitrate flush- vasodilate- feels hot
  15. Nitrate routes of administeration
    • Rapid onset- to terminate an immediate attack
    • long term- used for prevention

    • sublingual- under the tongue (burning in mouth)
    • translingual- spray under tongue
    • Buccal in the gum line
    • above all work in seconds. used for treating an attack/preventive if ur doing work, no longer (u can take up to three doses 5 mins apart max 15 mins 2nd not reduces agina call 911)
    • Sustained release oral tablets- slower onset 30-1hr 8 hr lasting
    • topical ointment- paste/disk
    • transdermal- last up to 24hr
    • IV infusion- ICU htn/mi/angina is resistant therapy. works within minutes gone within minutes. needs to be on a drip
    • check BP s>100

    problem with sulhydride- u need this for patches/cream to convert into active form. keep on for 12 and keep off for 12 to restore sulhydride (once in the system last 24 hr)
  16. Nitrate NI
    • assess bp
    • assess risk of tolerance (sulhydride)
    • approriate use- chest pain (immediate), preventative
    • cautious of other hypotension agent
    • pt teaching regarding sublingual use
    • slowly withdrawl to avoid vasospasm
  17. Isosorbide dinitrate
    • Nitrate
    • prevents agina, acute attacks (subling)
    • MOA- vasodilation
    • SE: hypotension, tachycardia, h/a, dizziness
    • NI: similar to Nitrate
  18. Cardiac Glycoside Agent
    Ex. digoxin

    • MOA: inhibits Na-Ktpase pump. if u block this energy level in the cell Na will increase in cell and then it will increase the release of Ca, so we increase contractility 
    • drops the HR b/c it stimulates the vagus nerve
    • increase contractlity- bc of the na-k pump (enzyme energy pump)
    • increase CO

    CI: HF (increase contractlity)
  19. Terms to describe digoxin *
    Positive inotropic effect (increase contractility)

    negative Chronotropic effect -  decrease rate

    negative dromotropic- decrease velocity
  20. Digoxin Cardiac Glycoside agent CI SE
    CI- HF, a. fib, and flutter, tachyarrhythimias 

    • SE: (non cardiac usually precede cardiac effects)
    • GI: N/v lack of appetite (early s/s of problem with digoxin- look at dig level)
    • CNS- fatigue, visual disturbance (halos yellow to green), blurred vision
    • Cardiac- arrythimas, bradycardia
  21. Relationship of K to digoxin
    K competes with dig with binding to the enzyme.

    whoever has more wins and binds to the pump (na-k pump)
  22. digoxin risk facter
    Hypokalemia, hypomagnesia, anything that decrease O2 level, elderly

    dig toxicity- non cardiac s/s precede cardiac

    • Digoxin level- .5-2 mcg/mg
    • K 3.5-5 meq 

    Antidote- digibind - binds to dig so it can be excreted
  23. Digoxin NI
    • Assess BP, HR
    • assess apical HR for full min
    • if suspect toxicity then do ekg (arrhythimia)
    • monitor K and dig level
    • loading and mainentance dose
    • drug interaction  
    • assess for risk factors for dig toxicity 
    • monitor renal function