Cardiac II

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Cardiac II
2013-03-23 16:00:09

Cardiac II, HF, CAD CHOL
Show Answers:

  1. What is unstable angina caused by and how do you treat it?
    • Caused by vasospasm, platelet aggregation, transient thrombi, or emboli. 
    • Treatment= MONA (morphine, oxygen, nitroglycerin and aspirin)
    • Any pt w/hx of MI should be on BB
  2. What is variant angina caused by and how do you treat it?
    • Caused by coronary artery spasms (restricted myocardial blood flow)
    • Can occur anytime (even rest or sleep)
    • Not r/t plaque, just vasospasm
    • Treat by severity: oxygen, vasodilators, Calcium channel blockers, or nitrates
    • DO NOT GIVE BB!!!
  3. What is the goal of angina treatment?
    • Prevent Death or MI
    • STOP angina pain=pain level of ZERO
    • Decrease frequency & intensity 
    • Decrease myocardial O2 demand
    • Decrease HR, contractility, afterload & preload
    • (NITRO)
  4. What is NITROglycerin's mechanism of action on stable angina?
    • Decreases pain by decreasing cardiac O2 demand
    • Dilates veins, decreases venous return, decreases preload
  5. What is NITROglycerin's mechanism of action for variant angina?
    • Acts by relaxing or preventing coronary artery spasms
    • NTG increases oxygen supply
  6. Tell me about the absorption and metabolism of Nitroglycerin
    • HIGHLY lipid soluble so you can give it multiple ways (SL, Transdermal,  PO, IV)
    • Does have big 1st pass effect (most of PO dose is destroyed)
    • Rapidly metabolized by liver-short 1/2 life of 5-7 minutes
  7. TRUE or FALSE
    NITROglycerin patches should be on intermittently (taken off at night for 8hrs)
    TRUE but can use nitro if attack occurs
  8. Can you use Nitroglycerin as an ointment?
    • Yes, onset is 20-60min and lasts 12hrs so it provides sustained protection.
    • NOT for use during attack (doesn't work quickly enough!)
  9. TRUE or FALSE
    You must taper Nitroglycerin slowly when discontinuing to prevent risk of vasospasm
  10. TRUE or FALSE
    It's okay to chew and swallow the sub lingual Nitroglycerin.
    • FALSE. SL dose is meant to have no 1st bypass effect so it contains a much lower dose than the PO form.
    • DO NOT CHEW or SWALLOW SL dose!
  11. Name 3 side effects of NITROglycerin
    • HA, Orthostatic HYPOtension, Tachycardia
    • but generally well tolerated
  12. TRUE or FALSE
    Nitroglycerin (SL) bottle is good for 12months
    FALSE! It's good for 24months. Teach patient to discard after it's expired...otherwise dose may be ineffective in an emergency (and that would suck!)
  13. Bob is on a Phosphodiesterase Type 5 inhibitor (Viagra, Cialis, or Levitra) and and wants to take Nitroglycerin. Can he?
    • NO! Vasodilation is greatly increased when taking these medications together
    • PS. this was the only medication questions I had on my NCLEX :)
  14. What happens if Bob takes a betablocker (or Ca Channel blocker like Verapamil or Diltazem) with his Nitroglycerin?
    It could suppress the NTG induced tachycardia.
  15. What is the goal HR of Betablockers?
  16. Name some uses of Betablockers (There are a ton!)
    • STABLE ANGINA (not vasospasms!)
    • Makes heart more efficient
    • Dec. cardiac O2 demand
    • Dec. afterload
    • Dec. HR (allows longer filling time)
    • Dec. contracility (caution w/CHF patients!)
    • Dec. intensity and frequency of angina
    • INCREASEs exercise tolerance (eventually)
  17. TRUE or FALSE
    You should never stop a Beta blocker abruptly
    TRUE! IT could cause a very intense angina attack and lead to an MI
  18. Name some side effects of a betablocker
    • Bradycardia
    • Decreased AV node conduction
    • Decreased contractility (caution in HF)
    • Can block Beta 2 as well (caution w/asthma and COPD)
    • Insomnia, bizarre dreams
    • Sexual dysfunction (educate pt!)
  19. If your patient has asthma and needs to be on a betablocker, which one is best?
    Metoprolol (more Beta 1 selective) but still be cautious!
  20. Calcium channel blockers are used to treat what two types of angina?
    Stable and Variant
  21. Name the three drug categories used in prevention of an MI for the patient w/chronic stable angina.
    • Anti-platelet (ASA or plavix)
    • Cholesterol lowering drug (for all pt w/stable angina)
    • ACE (for most pt's w/CAD and strongly recommended for those w/DM bc it's renal protective)
  22. Explain the strategy for angina treatment (start with one drug class, if not effective then....etc.)
    • SL Nitroglycerin, if not effective...
    • Add a beta blocker, (gold standard for previous MI) if not effective....
    • Add a Ca channel blocker, if not effective....
    • Add a long-acting nitrate.....if not effective
    • Get a referral!
  23. What is the first line of treatment for management of HF and what does it do?
    • Diuretics are the 1st line of therapy.
    • Decreases preload/afterload and pulmonary/peripheral edema (decreases fluid to it doesn't have so much to pump out!)
  24. Vasodilators are used to treat CHF. Name three types and how they work.
    • ACE, ARB, and Nitrates
    • Reduces workload of the heart, increases O2 demand, and decreases afterload
  25. Inotropic agents can be used to treat HF (sometimes). How do they work?
    Increases the strength of the contraction (increased contractility of a weak ventricle)
  26. TRUE or FALSE 
    Betablockers can be used for treatment of HF and are indicated if history of MI
  27. Thiazide diuretics (like Hydrocholorthiazide) are used for early stage HF (1st line therapy). Can you use it in a patient w/low GFR?
    NO it will be ineffective, use a loop diuretic (Lasix, Bumex, or Demadex)
  28. What is an adverse effect of both Thiazide and Loop diuretics?
    Hypokalemia (caution w/ Digoxin because it can cause toxicity!)
  29. TRUE or FALSE
    High ceiling loop diuretics are drug of choice for MODERATE to SEVERE CHF
    TRUE! They are good because they can mobilize a lot of water and are NOT DEPENDENT on GFR and cardiac output.
  30. Why diuretic can cause otoxicity?
    LASIX (FUROSEMIDE)=High ceiling loop diuretic
  31. Why bother giving Aldactone to a patient w/CHF if it only promotes a scant diuresis?
    It is used to counteract K+ loss by thiazides and loop diuretics.
  32. When prescribing Aldactone, what three drugs do you need to use caution with?
    • ARBs, ACE inhibitors, and Digoxin
    • d/t risk for hyperkalemia!!
  33. TRUE or FALSE
    Aldactone is the only K+ sparing diuretic proven to prolong survival in HF patients
  34. How does Aldactone work?
    It blocks aldosterone receptors
  35. TRUE or FALSE
    ACE inhibitors (think -pril) are the drug of choice for HF patients and should be prescribed to ALL HF patients unless contraindicated
    TRUE! They increase functional status and prolong life. They also decrease morbidity and mortality.
  36. How do ACE inhibitors (-pril) work?
    • They block Angiotensin II production which in turn decreases the release of aldosterone from adrenal cortex. This also suppresses the degradation of kinins. 
    • They dilate arterioles and veins (decreased afterload and workload, increased CO and SV, increased renal bld flow)
  37. ACE inhibitors decrease edema, pre load and ventricular dilation. HOW?
    • By decreasing aldosterone, kidneys will secrete fluid and retain K+ (watch for hyperkalemia)
    • Also increase renal blood flow so the kidneys can excrete more water and Na+
  38. What are two major side effects of ACE inhibitors that can be attributed to the accumulation of bradykinin?
    • Intractable cough, may improve after 3M
    • Angioedema
  39. TRUE or FALSE
    ACE inhibitors are safe to use when  pregnant
    FALSE! Fetal lung injury in 2nd and 3rd trimester!
  40. What is a major contraindication to using an ACE inhibitor (-pril)?
    • Bilateral renal artery stenosis!
    • Kidney's release Renin to increase angiontensin II to preserve GFR. If this is inhibited, then decreased GFR and decreased UO
  41. ARBs are similar to ACE inhibitors, so why switch from an ACE inhibitor to an ARB?
    ARBs don't increase the level of kinins like ACE you won't get the cough!
  42. What is the only ARB (-sartan)currently used for tx of HF?
    • Valsartan.
    • Although you can use the others (Candesartan or Losartan)..just use caution and monitor symptoms
  43. TRUE or FALSE
    After 2 weeks, the full benefits of a betablocker should be reached
    FALSE. Full benefits are not seen for 1-3 months. START LOW and GO SLOW. A gradual increase will minimize effects of decreased contractility.
  44. How do Betablockers (-lol) work to protect the heart?
    • They protect the heart from excessive sympathetic stimulation and protect against dysrhythmias. 
    • Help exercise tolerance, improve LV function, slow progression of HF, and reduce hospitalization and mortality.
  45. Why do you need to use caution in placing a patient w/CHF on a beta blocker?
    • A side effect of Betablockers is fluid retention and worsened HF from the decreased contractility. 
    • Also can have SOB, night cough, weight gain, and extremity swelling (from same problem)
  46. TRUE or FALSE
    Digoxin (inotropic agent) is a second line agent in treatment of HF and does not prolong life, it's actually less effective in women.
    TRUE! And it has a narrow therapeutic window so it's a very risky drug!
  47. How does digoxin work?
    • It increases contractile force
    • Decreases sympathetic tone
    • Increases urine production
    • Decreases renin release
  48. It takes ___ days for Digoxin levels to plateau.
    SIX. Check levels at routine intervals until at goal and then recheck is S/S of digoxin toxicity.
  49. What kind of labwork do you need to monitor w/Digoxin?
    • Renal function (BUN/Cr)
    • BMP (K+, Na, Mg, Ca)
    • ABG for hypoxemia or acidosis.
  50. How do antacids and kaopectate interact with digoxin?
    They decrease absorption and you will have subtherapeutic Dig levels
  51. How do chloestyramine and metoclopropamide effect Digoxin levels?
    They impair absorption (so space the dosing!)
  52. TRUE or FALSE
    Ca Channel blockers can increase digoxin levels.
    TRUE=toxicity risk!
  53. How is digoxin metabolized?
    In the liver and gut by bacteria. So if you give abx, then you may increase digoxin levels d/t interference w/bacterial flora!

    *20-30% of Digoxin is protein bound....
  54. Todd is a bit earthy crunchy and is taking siberian ginseng and licorice that his herbal store recommended. Can you prescribe Digoxin to him?
    NO! It will enhance Digoxin toxicity. NEED to ask patients about any OTC and herbal supplements!
  55. TRUE or FALSE
    Decreased renal function can increase half life of Digoxin from 30-40hours to FOUR days.
  56. Why should you always get an EKG prior to beginning Digoxin.
    • Toxicity can cause non-specific ST depression or T wave flattening
    • PS. I hate getting EKGs
  57. Visual disturbances of Digoxin toxicity are....
    yellow and green halos!
  58. HYPOkalemia or HYPERkalemia can cause Digoxin toxicity?
    • HYPOkalemia!
    • (Increased K can cause Subtherapeutic levels)
    • Digoxin is like Goldilocks-K needs to be JUST RIGHT!
  59. What three agents do you need to avoid in HF?
    • Antidysrthymic agents (Amio and Defetilide) will make HF worse
    • Ca Channel blockers (make HF worse)
    • NSAIDS: increase fluid retention and peripheral vasoconstriction
  60. First line of therapy for HF includes three them!
    • Diuretics
    • ACE or ARB
    • Beta blocker 
    • *only add Digoxin if symptoms can't be managed w/these three*
  61. Which category of Dislipidemic agents are most effective at lowering LDL-C?
  62. Statins have very few SE but what is the common one?
    • Leg cramps..
    • Myopathy/rhabdomyolysis (renal caution!)
    • Also can cause hepatoxicity
  63. STATINS (HMG-COA Reductase Inhibitors) should be given AT  NIGHT, why?
    • Endogenous cholesterol increases during the night (increased synthesis)
    • most effective before bed (don't need to worry about taking w/ or w/out meals)
  64. What's so great about STATINS (HMG-COA Reductase inhibitors)
    • Decrease LDL-C  (25-63%)
    • Increase HDL-C (5-17%)
  65. Name some non-lipid benefits of Statins...there are quite a few!
    • Promote plaque stability
    • Reduces inflammation
    • Slows progression of CAD
    • Improves endothelial dysfunction
    • Enhances vasodilation
    • Reduces risk of A-fib
    • Reduces risk of thrombosis
  66. What is the MOA for STATINS (HMG-COA Reductase inhibitors)?
    • Competitive inhibitor of HMG-COA Reductase that is responsible for conversion of HMG-CoA to mevalonate which is a precursor of cholesterol.
    • Stimulates synthesis of LDL receptors leading to an increase in uptake of LDL particles
  67. How often should you monitor LFTs when when your patient is on STATINS?
    Check LFTs Q3M, then Q6M, then QYR
  68. TRUE or FALSE
    Pregnant patients can take STATINs
  69. Name 5 drugs that interact with STATINs
    • Cimetidine
    • Aldactone (increases risk of endocrine dysfunction)
    • Digoxin (can elevate levels)
    • Erythromycin/Genfibrozil (increased risk of rhabdomyolysis)
    • Warfarin (increased anticoagulant effect)
  70. How do NICOTINIC acids work?
    • They inhibit lipolysis in adipose tissue which decreases hepatic esterification of triglycerides
    • Increase lipoprotein lipase activity
    • Reduces serum cholesterol & TG levels
  71. Nicotonic Acids (Niacin) is good for triclycerides. It's also good for ___.
    Good for HDL but not as good for LDL
  72. What are some indications to give Niacin?
    • Adjunct tx of hyperlipidemia & hypercholesteremia
    • Pellagara (vitamin B deficiency)
    • Peripheral Vascular disease
  73. Patients often complain of _____ so they should take Niacin at night and not have hot food or drink with it.
    • Flushing (d/t excessive peripheral vasodilation)
    • Regular schedule and starting low and going slow will decrease SE.
  74. Niacin can also cause ___ and ____ so use caution in patients with DM or gout.
    Hyperglycemia and Hyperuricemia
  75. Niacin is contraindicated with these four things...
    • Hepatic dysfunction
    • Active Peptic Ulcer Disease
    • Severe hypotension
    • Arterial hemorrhage
    • (seriously, is someone is hemorrhaging  don't give Niacin, should probably fix the hemorrhage first....)
  76. Niacin is used with caution in the following situations (tricky Nancy might ask...hateful!)
    • Liver disease (contraindicated w/dysfunction)
    • PUD (contraindicated if ACTIVE)
    • Gout
    • DM
    • Gallbladder disease
  77. What happens if you give ASA with Niacin (nicotinic acid)?
    Decreased metabolic clearance of nicotinic acid
  78. what happens if you give a sympathetic blocker with Niacin?
    Causes vasodilation and hypotension
  79. How does Gemfibrozil (fibrate) work?
    • It decreases TG levels and VLDL while increasing HDL
    • Inhibits lipolysis of adipose tissue
    • Reduces hepatic TG synthesis
    • *Good for high TG and Low HDL*
  80. TRUE or FALSE
    Giving a Fibrate (Gemfibrozil) and a statin together will increase occurance of myopathy.
  81. Why should you advise the patient to call you if they experience diarrhea, nausea, epigastric pain, chills, fever, or sore throat when they are taking a fibrate (Gemfibrozil)?
    Could indicate leukopenia!
  82. Your patient is on a fibrate (Gemfibrozil) and when you check their serum lipoprotein concentration, there was NOT a significant change What do you do now?
    DC the drug.
  83. What labwork should you obtain for your patient on a fibrate (Gemfibrozil)?
    • Serum lipoprotein concentration
    • LFTs/BUN/Cr (ensure appropriate metabolism and excretion)
    • CBC & Electrolytes
    • If on anticoagulant then PT/INR (Fibrates can increase effects of oral anticoagulants)
  84. When should the patient take Gemfibrozil?
    30min prior to meals in the morning and evening.