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Cardiac drugs > Cardiac drugs > Flashcards

Cardiac drugs Flashcards

1
Q

thiazides (PK, response, toxicities)

A

distal diuretics

PK
renal excreted
long duration of action

Variable response
african Americans, elderly most responsive
response depends on vigor of adaptation

Toxicities
sulfa allergy
hypokalemia

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2
Q

Non-dihydropine

A

bind in an open state, therefore if stimulation of cell is increased, blockade is increased

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3
Q

verapamil

A

NHP,

effective in SVT, angina, hypertension
(increases coronary blood flow)
side effect: constipation

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4
Q

◦
diltiazem

A

NHP

blocks Ca in both cardiac and vascular tissue

(good for SVT, not good for hypertension)

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5
Q

Dyhydropyridine (What are they used for? What are the hemodynamic effects?)

A

binds in resting state, good for vasodilation on SMC

treatment of SV dysrhythmia in setting of hypertension/angina

profound vasodilation

can produce reflex tachycardia, increase in myocardial contractility – > increase in workload, may be detrimental to pts. at risk for MI

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6
Q

nifedipine

(actions, side effects)

A

DHP

(mostly vasodilatory - good for hypertension

contraindicated in MI, HFside effects: facial flushing, headaches, dizziness

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7
Q

Epinephrine

(SVR, HR, CO)

A

mixed alpha, beta1, beta2 agonist activity
mixed actions on SVR
increased HR
increased CO

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8
Q

Norepinphrine

(SVR, CO, HR)

A

mixed alpha, beta1 agonist
increases SVR
decreases HR by baroreceptor reflex
CO unchanged

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9
Q

dopamine

A

mixed alpha, beta1 activity

has different effects at different doses

low doses - renal vasodilation

intermediate dose - beta1 action, increases CO with no effect on SVR

high dose - alpha action

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10
Q

Phenylephrine

A

alpha agonist
increase SVR
decrease HR by baroreceptor reflex
drops CO - uncompensated increase in LV afterload
no beta activity to increase contractility

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11
Q

Isoproterenol

A

beta1 and beta2 agonist
increase cardiac inotropy and chronotropy
decreases SVR
increase in CO (increase in inotropy and drop in SVR)

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12
Q

Dobutamine

A

beta1 agonist with little effect on HR, little effect on BP, mostly just an inotrope

increases CO

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13
Q

digoxin (actions, hemodynamic effects, advantage)

A

binds Na K ase
note: high levels of K+ may compete with digoxin, may be protective for toxicity
causes upwards and leftwards shift of the starling curve

increases CO
increases LVEF and decreases LVEDP
increases exercise intolerance, decreases neurohormonal activation

no sensitization

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14
Q

What are the hemodynamic effects of digoxin?

A

increases CO
increases LVEF and decreases LVEDP
increases exercise intolerance, decreases neurohormonal activation

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15
Q

What are the neurohormonal effects of digoxin?

A

decreases norepinephrine
decreases peripheral nervous system activity
increases vagal tone
normalizes arterial baroreceptors

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16
Q

What are the electrophysiologic impacts of digoxin in the atria and AV node?

A

makes RMP less negative - buildup of extracellular K+- inactivates Na current – > slow conduction

causes increase in vagal tone and decrease in sympathetic activity
can get abnormal automaticity and increase refractory period of the AV node
can result in bradycardia or heart block

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17
Q

What are the effects of digoxin in the ventricle?

A

at therapeutic doses, increases inotropy; at toxic doses, can get delayed afterdepolarizations from buildup of too much intracellular Ca+

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18
Q

What conditions could predispose someone for digoxin toxicity?

A

hypokalemia
hypomagnesemia
hypothyroidism
hypoxia and acidosis

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19
Q

What are the contraindications for digoxin use?

A

digoxin toxicity
hypokalemia
ventricular arrhythmias
bradycardia
atrial fibrillation

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20
Q

What are potential extracardiac toxicities of digoxin?

A

gastrointestinal – nausea, vomiting, diarrhea
nervous - depression, disorientation, paresthesias
visual - blurred vision, scotomas, yellow green vision
hyperestrogenism - gynecomastia, galactorrhea

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21
Q

How do you treat digoxin toxicity?

A

give antibody against digoxin
avoid hypokalemia

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22
Q

Side effects of dopamine

A

infiltration of IV site causing necrosis, gangrene,

tachycardia,

nausea, vomiting,

hypertension

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23
Q

What are some disadvantages of dobutamine?

A

chronic infusions can lead to desensitization

inhibited by beta blockers

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24
Q

What are some side effects of dobutamine?

A

Ischemia, arrhythmia, hypotension, tachycardia, atrial fibrillation, nausea

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25
Q

What are some side effects of epinephrine?

A

Platelet aggregation and infarction - don’t give to patients having an MI!

26
Q

Describe how PDE inhibitors work

A

increase contractility through an increase in intracellular Ca
act independently of beta receptors
potent vasodilators

27
Q

What are the hemodynamic effects of PDE inhibitors?

A

improve systolic and diastolic functioning (increased CO)

decreased SVR
improve exercise intolerance
inhibit platelet aggregation

minimal change in HR!

28
Q

What are some cautions of working with PDE inhibitors?

A

can cause significant hypotension

29
Q

Amrinone

A

PDE inhibitor

can cause thrombocytopenia

30
Q

Milrinone

A

stronger PDE inhibitor

no thrombocytopenia
more selective
eliminated by the kidney

31
Q

atropine (What is it?)

A

atropine, competitive antagonist for muscarinic receptors

32
Q

What are the effects of atropine?

A

increase HR, decrease refractoriness, decrease parasympathetic SVR decrease

33
Q

What are the clinical uses of atropine?

A

prevent vagal reaction
restore AV conduction in disorders of AV refractoriness

34
Q

prazosin

A

alpha 1 antagonist

results in decreased PVR and blood pressure

35
Q

doazosin/terazosin

A

alpha antagonist

36
Q

Describe the uses of beta blockers

A

decrease HR
decrease impulse conduction
decrease contractility and metabolic rate

37
Q

Describe the adverse effects of beta blockers

A

AV block
Fatigue
Withdrawal phenomenon (sudden increase in HR after stop taking)
heart failure
MI
arrhythmia
hypertension
can worsen limb ischemia
effect on lipids (can increase lipids)

38
Q

Procainamide

A

Class IA – targets sodium and potassium currents

39
Q

Propanolol

A

non selective beta blocker

lipid soluble

eliminated by liver

40
Q

Metoprolol

A

Beta1 selective

Moderate solubility

hepatic elimination

41
Q

Atenolol

A

beta1 selective

low lipid solubility

renal excretion

42
Q

Carvedilol

A

non selective with alpha1 blockade

moderate lipid solubility

hepatic elimination

43
Q

Lidocaine

A

Targets Sodium currents

44
Q

Flecainide

A

Targets sodium channel

45
Q

Dofetilide

A

Potassium channel target

46
Q

Adenosine

A

agonist for adenosine receptor

lowers calcium currents

acts VERY quickly

47
Q

What are the mechanisms available by which to block reentry?

A

class 1 drugs, decrease excitability

class 1A and class III drugs increase ERP

48
Q

What are the associated risks in treating reentry tachy?

A

Prolonging ERP - long APD

decrease excitability - slow conduction facilitates reentry

49
Q

Statins

A

target HMGcoA reductase step, upregulate LDL receptor

50
Q

Ezetimibe

A

cholesterol absorption drug - targets NPC1 receptor and then upregulates LDL receptor

51
Q

Bile acid sequestrants

A

get rid of bile acids, more cholesterol used to make them; upregulates the receptor

52
Q

What is PCSK9? WHy is it a target?

A

targets receptors for degradation - removing it upregulates receptors

53
Q

fibrates

A

activate PPAR receptor in liver
increase HDL production
decrease VLDL production
increase VLDL clearence

have been shown to reduce TG, good for pts. with really high levels

54
Q

Omega 3 fatty acids

A

decrease TG levels

55
Q

niacin

A

reduces FFA release and flux to liver

increases HDL, decreases LDL

56
Q

Enlalapril

A

ACEi (all end in april)

57
Q
A
58
Q

ARB

A

losartan (all end in -artan)

59
Q

What are the arterial vasodilators

A

hydralazine

Sodium nitroprusside

60
Q

Sotalol

A

Class III

61
Q

venodilators

A

organic nitrates

62
Q

Edrophonium

A

Cardiac drugs (1 decks)

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