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Flashcards in CARDIAC Deck (94):
1

What effect do BB's and nitrates have on ejection time?

nitrates decrease ejection time and BB's increase injection time

2

Name 5 drugs commonly used to Tx malignant HTN

nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam

2

Which aspect of the heart is most sensitive to the effects of Class II antiarrhythmics?

AV node

3

Which lipid-lowering agents act by upregulating LPL?

Fibrates

3

2 clinical indications of cardiac glycosides

CHF to increase contractility; Atrial Fibrillation to depress SA node and decrease AV conduction

4

What are 4 AE of bile acid resins

CHOLESTEROL GALLSTONES, decreased fat soluble vitamin absorption (ADEK), GI discomfort, tastes bad

5

Why does renal failure predispose to digoxin toxicity?

decreased clearance

5

Althought most beta blockers fit into class ____ antiarryhthmics, sotalol is actually a class _________

II; III

6

How does the effect of class IC antiarrhythmics on AP duration differ from Ia and Ib

IC does NOT affect AP duration, Ia increases, Ib decreases

7

What are 5 determinants of myocardial oxygen demand?

End Diastolic Volume (preload), Blood Pressure (afterload), heart rate, contractility, and ejection time

7

What are 2 partial beta agonists that are contraindicated in angina?

pindolol and acebutolol

8

What autoantibodies might you expect in the blood of a patient who is on hydralazine having an AE?

anti-histone, these are the autoantibodies present in drug induced lupus, which hydralazine can cause

9

Which lipid lowering agents do patients not like because they taste bad?

bile acid resins

9

What are 6 EKG findings with digoxin toxicity?

increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block

9

What class is quinidine when used to tx the heart? What is its major AE?

Class Ia; cinchonism = headache and tinnitus

10

Name 2 class IC antiarrhythmics

propafenone, flecainide

11

Which class Ia anti-arrhythmic is associated with lupus-like syndrome? What antibodies?

procainamide, anti-histone

13

Which 3 organ systems should you regularly monitor when a person is on amiodarone?

LFT's (hepatoxicity), PFT's (pulmonary fibrosis), and TFT's (hypo/hyperthryoidism)

14

Which CCB's are most effective on the heart (as opposed to vessels)?

Verapamil and diltiazem

14

What are 4 side effects of hydralazine?

Compensatory Tachycardia, Fluid Retention, Nausea, Headache, and LUPUS-LIKE SYNDROME

14

What are the 3 AE of fibrates?

Myositis, hepatoxicity, cholesterol gallstones

14

What are the 3 AE of Class Ib antiarrhythmics?

CNS stimulation or depression and CV depression, also can be a local anesthetic

15

What are 3 class I anti-arrhythmics

quinidine, disopyramide, procainamide

17

Compare and contrast the effect of BB's and nitrates on the End Diastolic Volume

BB's increase EDV because they decrease HR and increase filling time; Nitrates decrease EDV by decreasing preload

17

What is blocked by Class I, II, III, and IV antiarrhythmics?

Class I = Na channels, Class II = beta blockers, Class III = K channels, Class IV = Ca channels

18

What 3 factors predispose to digitalis toxicity?

Hypokalemia, renal failure, co-administration of quinidine

19

What toxicities do ALL class Ia anti-arryhthmics cause?

thrombocytopenia and torsades due to QT prolongation

20

Name 3 bile acid resins

Cholestyramine, Colestipol, Colesevelam

20

What drug is DOC for diagnosing and abolishing SVT?

adenosine

22

Which drugs are first line for increasing HDL?

niacin

22

3 AE of niacin

Flushing, Acanthosis nigricans (hyperglycemia), Hyperuricemia (precipitating gout)

23

Which drug ONLY decreases LDL and does not affect HDL or TG's?

ezetimibe = decrease in LDL uptake by intestines

25

What is the treatment for beta blocker OD?

glucagon

26

Why does quinidine predispose to digoxin toxicity?

it displaces digoxin from tissue binding sites and decreases its clearance

27

Why is it that class II antiarrhythmics act so heavily on SA and AV nodes?

Because, being beta blockers they decrease Ca currents which are necessary for upstroke in nodal tissue

29

What is the MOA of hydralazine? What drugs are often co-prescribed and why?

It increases cGMP in the ARTERIOLES thereby reducing afterload. It is co-administered with beta-blockers to prevent reflex tachycardia

30

The effect of adenosine is blocked by what 2 drugs?

theophylline and caffeine

31

What class is procainamide in? Major AE?

Class Ia antiarrhythmic; SLE like syndrome with anti-histone abs

31

Name 4 Class III antiarrhythmics. What is the mnemonic?

Amiodarone, Ibutilide, Dofetilide, and Sotalol (AIDS)

32

Why do DM pts get ACE inhibitors?

They are protective against diabetic nephropathy

33

Which drug prevents cholesterol reabsorption at the small intestine brush border?

Ezetimibe

34

Why would a CCB cause constipation?

Because Ca is needed for smooth muscle contraction in the gut

35

In whom (2) is hydralazine contraindicated? Why?

Coronary Artery Disease and Angina patients because it causes a reflex tachycardia due to its effect on reducing afterload

36

Which CCB's are most effective on vascular smooth muscle?

Amlodipine and nifedipine

38

How do cardiac glycosides increase contractility AND decrease HR?

CONTRACTILITY = inhibition of Na/K pump inhbits the Na/Ca antiport leading to greater Ca in cytoplasm = more contractility? HR is mediated by increasing vagal tone to heart

39

Name 3 class Ib antiarrhythmics

Lidocaine, tocainide, mexilitine

40

Which calcium channel is blocked by diltiazem? What about ethosuximide?

L type; T type

41

What is the major AE of ibutilide?

torsades

42

2 indications for nitrates

angina and pulmonary edema

42

What is the MOA of adenosine?

it increases K efflux out of the cell and hyperpolarizes it. It is thus the DOC in diagnosing and abolishing supraventricular tachycardia

43

What aspect of cardiac depolarization do ALL class I drugs acts on?

all decrease the slope of phase 0 depolarization

44

What cholinergic side effects occur with cardiac glycosides?

N/V, diarrhea, BLURRY YELLOW VISION

45

What is "Monday Disease" in industrial exposure?

People working with nitrates can develop tolerance to the vasodilating effects and then loss of tolerance during the weekend causes a reflex tach and hypotension with facial flushing on Monday

46

What are the 2 MOA's of niacin?

it inhibits lipolysis in adipose tissue and reduces VLDL secretion from the liver

47

Which drug used in malignant HTN is a D1 agonist?

fenoldopam

48

What class is disopyramide in? Major AE?

Class Ia antiarrhythmic ; heart failure!

49

What is the antidote to digoxin toxicity?

Slowly normalize K, LIDOCAINE, cardiac pacer, anti-digoxin Fab fragments, Mg

50

What is the shortest acting class II antiarrhythmic?

ESMOLOL

52

Magnesium is useful for what 2 cardiac conditions?

torsades de pointes and digoxin toxicity

54

What is the MOA of nitroprusside?

Short acting increase in cGMP to decrease afterload by primarily acting on arterioles

56

Co-administration of what drug predisposes to digoxin toxicity?

quinidine

57

Which CCB's are similar to BB's in their effect? Which are more similar to nitrates?

Similar to BB's = verapamil and diltiazem; similar to nitrates = nifedipine and amlodipine

58

Which drug are first line for decreasing triglycerides?

fibrates

60

How is the effect of nitroglycerin and isosorbide dinitrate different from that of hydralazine?

All increase cGMP to dilate vessels; however, hydralazine predominately affects arterioles and the nitrates affect veins so they decrease preload

62

Which Class I class is best for MI and which is contraindicated?

Class I B = B est; Class I C = C ontraindicated

63

The formation of which molecule is prevented by statins?

mevalonate (produced from HMG-CoA reductase)

64

Class IV antiarrhythmics are used to prevent _________ and have this MOA _______

nodal arrhythmias (SVT) and they are CCB's

65

Which subset of class I drugs is particularly useful in treating digitalis toxicity?

Class Ib (LIDOCAINE, mexilitine, and tocainide)

66

In which setting of heart failure must you be cautious with the use of beta blockers?

Acute decompensated heart failure--they need all the contractility they can get

67

What are the AE of class IC antiarrhythmics?

proarrhythmic ESPECIALLY post-MI, and significant prolongation of AV node refractory period

69

Which cardiac drug can cause cyanide toxicity?

nitroprusside

69

Which anticonvulsant drug can function as a class Ib antiarrythmic?

phenytoin

70

How do class II antiarrhythmics depress abnormal pacemakers?

decreasing slope of phase IV depol

71

Which lipid lowering agents can cause cholesterol gallstones and why?

Bile acid resins because the liver needs to use cholesterol to create new bile acids; also, fibrates

73

Which drugs are first line for decreasing LDL?

statins

75

What effect to BB's and nitrates have on A) contractility and B) heart rate

BB's decrease contractility and HR but nitrates cause a reflex increase in HR and contractility

76

Name 6 AE of CCB's

Cardiac Depression, AV block, Peripheral edema, flushing (vasodilation), dizziness, and constipation

77

What is first line Tx of HTN in pregnancy?

Hydralazine and methyldopa

78

Which drug decreases VLDL secretion from the liver and inhibits lipolysis in fat tissue?

Niacin

79

What are 2 AE of ezetimibe?

diarrhea (probably osmotic), and rarely, increase in LFTs

80

What is the major AE of sotalol?

torsades and excessive beta blockade

81

Compare and contrast the effect of Class Ia antiarrhythmics and Class Ib on the action potential duration

Class Ia increases AP duration so is useful for reentrant tachycardias; Class Ib decreases AP duration so is useful for ischemic tissue and POST-MI

82

What electrolyte imbalance may be present with digoxin toxicity?

hyperkalemia--a poor prognostic indicator

84

Why does hypokalemia predispose to digoxin toxicity?

it is permissive for digoxin to bind to the Na/K pump and have a more potent effect

85

2 AE of statins

increased LFT's (hepatotoxicity) and rhabdomyolysis

86

What is the physiological goal of anti-anginal therapy?

Decrease myocardial oxygen demand

87

What is the MOA of fenoldopam?

D1 agonist that acts on coronary, peripheral, renal, and splanchnic vessels causing vasodilation to decrease BP and facilitate natriuresis

88

Why does amiodarone have class I, II, III, and IV effects?

it alters the lipid membrane, thereby affecting all of the channels

89

Name 2 class IV antiarrhythmics

Verapamil and diltiazem

90

What cardiac drug can cause yellow vision?

digoxin

91

Why wouldn't you give propanolol to a person using cocaine?

it can exacerbate prinzmetal's variant angina

92

Why is it that amiodarone can cause hypothyroidism?

It is heavily comprised of iodine, this can result in the Wolff-Chaikoff effect in the thyroid whereby there is autoregulation and decreased synthesis of T3/4

93

What does the statement "Class I anti-arryhthmics are state-dependent" mean

they selectively act on DEPOLARIZED tissue (i.e. their activity depends on the "state" of the tissue)

94

What is a unique AE of metoprolol? Of propanolol?

Metoprolol = dyslipidemia; propanolol = exacerbates prinzmetal angina vasospasm