Cardiac Medication

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  1. Systemic Vascular resistance
    Cardiac output
    • Resistance against which the left ventricle must pump blood thru out  the systemic system
    • - diameter/tone of the blood vessels
    • - viscosity
    • - resistance from the inner lining
    • increase SVR- the more the heart will pump therefore more energy used

    • Cardiac Output
    • The amount of blood the heart pumps in one minute
    • HR SV
  2. Preload
    • Preload- when u blow up a balloon
    • end diastolic ventricular volume (when blood is sitting in the ventricle)
    • strenching of the muscle fibers in the ventricles
    • Starlings Law

    • Afterload
    • resistance ie like tieing a knot then balloon has to work harder to get the air out
    • - systemic vascular resistance
    • - pressure that the ventricle must generate to overcome the pressure in the aorta

    when u strench the fiber too much the blood will sit in the ventricle causing heart failure

    • Cardiac Workload- influence by the heart rate and venous return- how much work does the heart have to do to get the blood out. the greater the cardiac workload the more work the heart has to do. 
    • great workload= more O2 demand
  3. Heart failure
    • Inability of the heart to meet the body's demand
    • - ventricular hypertrophy
    • - decrease contractile force
    • - too tired to pump
    • - s/s right and left sided heart failure
    • - tx decrease SVR decrease venous return
  4. Beta Blocker 1
    Ex- Propanolol (inderal) and Metoprolol (lopressor)

    MOA- blocks Beta 1 receptors (decrease, HR, contractlity, blocking renin)

    CI- primary line of therapy HTN, prevent angina (increase O2 supply bc it vasodilates, decrease O2 demand because of de hr), blocks aldosterone
  5. SE beta blockers 1
    Bradycardia, hypotension, CNS (dizzy, headache), bronchospasm, reduce HDL and increase cholesterol and triglycerides

    NI- see previous handouts.
  6. Alpha 1 Blocker

    MOA- blocks Alpha 2 receptor (vasodilates)

    CI: HTN

    SE: significant hypotension, first dose effect (dizziness, headache, drowiness)

    NI: see neuro
  7. Centrally acting agents (alpha 2 stimulants)
    ex. Clonidine (catapress), Methyidopa (aldomet)

    • MOA: acts on the brainstem to suppress sympathetic outflow. decrease sns (stimulation)- vasodilate 
    • stimulant alpha 2 receptor- inhibits NE release
    • used for alcohol abuse
    • Not first line choice

    CI: HTN Severe to moderate, decrease s/s from withdrawl from opiates and alcohol
  8. Centrally acting agents (alpha 2 stimulants)
    • SE: orthostatic hypotension, CNS, rebound HTN following abrupt withdrawl
    • methylopa- hemolytic anemia (red blood gets broken down and see as foriegn)

    • NI: 
    • Assess BP and associated s/s
    • patient teaching safety
    • assess CBC
    • slow withdraw of medication
  9. Ace inhibitor
    • MOA: blocks the conversion of Angiotensin I to Angiotensin II- it vasodilate
    • then it block aldosterone

    Angiotensin converting enzyme inhibitors

    ex- Captopril (Capoten), Enalapril (Vasotec)
  10. Ace Inhibitor End results
    • decreases peripheral vascular resistance 
    • lowers blood pressure
    • increases renal blood flow- can use for renal patient
  11. Ace Inhibitor CI SE NI
    CI: Htn, CHF, DM nephropathy (renal damage caused by DM less blood flow to the kidneys)

    SE: hypotension, CNS, chronic cough A1 converts to A2 in the lungs, Angioedema (swellen in the lips face, neutrapenia (risk for infection)

    • NI: 
    • Assess BP
    • patient teaching 
    • best on empty stomach
    • careful with other drugs- hypotension
    • assess edema, WBC
    • enhance of effect of thiazide diurectics
  12. Angiotensin II receptor antagonist ARB
    Ex. Irbesrtian (Avapro)

    Blocks Angiostensin II

    used for pts who cannot tolerate the ace inhibitor- less side effects 

    CI: adjunct HTN (used for dm pt with HF who cannot tolerate Ace inhibitor, treat kidney damage in pt with DM)
  13. A II NI
    • Assess BP
    • response seen in 2-3 weeks
    • assess renal function
    • drug interaction
    • NSAIDs will decrease diurectics effects
    • additive effect with other drugs
    • addess K (can cause hyperkalemia)
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Cardiac Medication
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