pharmacology GRM week #9 (brief)

Week 9-Chapter 21

1. What do inotropic drugs do
a. change the force of myocardial contraction

2. What do positive chronotropic drugs do?
a. increase the rate at which the heart beats

3. What are the two main classes of positive inotropic drugs?
a. cardiac glycosides and phosphodiesterase inhibitors

4. What is the definition of heart failure?
a. abnormal condition in which cardiac pumping is impaired as a result of myocardial infarction

5. What is ejection fraction and what is the normal value?
a. amount of blood ejected with each contraction, normally 65% of the blood volume in the ventricle

6. When a person is in heart failure, which of their organs are the last to be deprived of blood?
a. those most dependent on blood, the brain and heart

7. What is the relationship of sodium and potassium to heart function?
a. depolarize the heart

8. Define systolic dysfunction and diastolic dysfunction.
a. systolic dysfunction: inadequate ventricular contractions during pumping of the heart
b. diastolic dysfunction: inadequate ventricular filling during ventricular relaxation

9. How does a cardiac glycoside improve myocardial contractility?
a. inhibits the ATPase pump, increasing calcium concentration

10. What are the inotropic, chronotropic, dromotropic and other cardiac effects of digoxin?
a. positive inotropic effect: increase in force and velocity of contractions without increasing oxygen consumption
b. negative chronotropic effect: lowers HR
c. negative dromotropic effect: decreases automaticity at SA node, decreases AV node conduction, reduces conductivity at the bundle of His, and prolongs the atrial and ventricular refractory periods
d. other cardiac effects: increase in stroke volume, reduction in heart size during diastole, decrease in venous BP and engorgement, and increase in coronary circulation

11. What are the primary indications for cardiac glycosides?
a. heart failure and supraventricular dysrhythmias

12. What is the normal therapeutic drug level for digoxin?
a. 0.5-2 ng/ml

13. How do low serum potassium levels affect digoxin therapy?
a. increase potential for toxicity

14. What are the common adverse effects of cardiac glycosides?
a. dysrhythmias, headache, fatigue, malaise, confusion, convulsions, colored vision, halo vision, flickering lights, anorexia, nausea, vomiting, and diarrhea

15. What is the step-by-step management of digoxin toxicity?
a. discontinue administration of the drug
b. begin continuous ECG monitoring for cardiac dysrhythmias, administering appropriate drugs as ordered
c. determine serum digoxin and electrolyte levels
d. administer potassium supplements for hypokalemia if indicated, as ordered
e. institute supportive therapy for GI symptoms like nausea, vomiting, or diarrhea
f. administer digoxin antidote if indicated, as ordered

16. How does digoxin immune Fab (Digibind) work?
a. binds to unbound digoxin to reverse effects and symptoms of toxicity

17. What are the results of inhibition of phosphodiesterase?
a. positive inotrophic response and vasodilation

18. What is an inodilator?
a. a drug producing positive inotrophic response and vasodilation

19. What is the effect of inhibition of phosphodiesterase on the
availability of calcium, systemic and pulmonary vessels and cardiac workload?
a. increases availability of calcium for heart to use for muscle contraction, dilates systemic and pulmonary vessels which decreases cardiac workload

20. How do PDI’s reduce afterload?
a. dilate blood vessels

21. What are the two most common PDI’s?
a. inamrinone and milrinone

22. What serum lab values should the nurse investigate before giving a cardiac glycoside?
a. serum potassium

23. What heart rates in the adult should cause the nurse to withholding a cardiac glycoside?
>?

24. What is the relationship between bran and digoxin?
a. bran in large amounts may decrease the absorption of digoxin

25. What is the safe infusion rate for IV digoxin?
a. usual digitalizing dose: 1-1.5mg/day
b. usual maintenance dose: 0.125-0.5 mg/day

Week 9-Chapter 23

26. How is the heart’s oxygen supply met?
a. delivered by coronary arteries

27. What is angina pectoris?
a. chest pain

28. Define coronary artery disease, myocardial infarction, chronic stable angina, unstable angina, and vasospastic angina.
a. coronary artery disease: supply of oxygen and energy-rich nutrients needed for the heart to meet its demands is decreased due to atherosclerosis
b. myocardial infarction: heart attack; blood flow through the coronary arteries to the myocardium is completely blocked so that part of the heart cannot receive oxygen from blood-borne nutrients
c. chronic stable angina: triggered by exertion or stress causing intense pain for 15 minutes and usually subsides
d. unstable angina: pain episodes increase in severity and frequency
e. vasospastic angina: spasms of the smooth muscle surrounding atherosclerotic coronary arteries often happening during rest

29. Which are two example classes of drugs that aim to correct the imbalance between myocardial oxygen supply and demand and how do they do it?
a. nitrates and nitrites: dilate all blood vessels
b. beta blockers: slow heart rate and reduce blood pressure

30. Explain the process that results in angina.
a. oxygen deprivation of the myocardium under ischemic conditions cause the heart to work anaerobically producing lactic acid and stimulating pain receptors surrounding the heart

31. What is it that actually causes the heart pain called angina?
a. lactic acid causes pain receptors to be stimulated

32. How do nitrates and nitrites vasodilate?
a. relaxes the smooth muscle cells of venous and arterial wall structure

33. What does dilation of coronary arteries by nitrates result in?
a. reverses or prevent exercise induced spasms, encouraging healthy physical activity in patients
34. Explain the way in which nitrates/nitrites reduce preload.
a. cause venous dilation and reduces venous return

35. Why are nitrates/nitrites contraindicated in persons with severe anemia, closed-angle glaucoma, hypotension and severe head injury?
a. conditions can be worsened

36. Why specifically is it risky to give nitrates/nitrites to a person with severe anemia?
a. cause drug-induced hypotensive episode

37. What is reflex tachycardia?
a. cardiovascular overcompensation marked by increased heart rate

38. What is the purpose of the regimen of removing transdermal patches at night for 8 hours and then applying a new patch in the morning?
a. prevent tolerance to nitrates

39. How do beta blockers improve the chances of survival in patients following an MI?
a. block harmful effects of the high levels of circulating catecholamines from irritating the heart

40. How do calcium channel blockers work?
a. promotes muscle relaxation causing coronary artery dilation increasing blood flow and oxygen supply

41. What is the primary beneficial antianginal effect of amlodipine and nifedipine?
a. indicated for angina and hypertension

42. What is the onset time for sublingual nitroglycerine?
a. 2-3 minutes

43. What systolic BP should be reported before giving a nitrate?
a. less than 60 mm Hg

44. Why is it unsafe to take nitrates when taking erectile dysfunction drugs?
a. worsens hypotensive response, paradoxical bradycardia, and increased angina with risk of cardiac or cerebrovascular complications from decreased perfusion

45. When receiving a nitrate, what position should the person be in?
a. seated to avoid falls

46. Where should nitroglycerine ointment be placed?
a. upper arms or body

47. Should nitroglycerine ointment be rubbed in and what is done with it when the dose is changed?
a. it should not be rubbed in and should be cleaned with soap and water and patted dry before applying the changing the dose