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
What are some side effects of epinephrine?
Platelet aggregation and infarction - don't give to patients having an MI!
26
Describe how PDE inhibitors work
increase contractility through an increase in intracellular Ca act independently of beta receptors potent vasodilators
27
What are the hemodynamic effects of PDE inhibitors?
improve systolic and diastolic functioning (increased CO) decreased SVR improve exercise intolerance inhibit platelet aggregation minimal change in HR!
28
What are some cautions of working with PDE inhibitors?
can cause significant hypotension
29
Amrinone
PDE inhibitor can cause thrombocytopenia
30
Milrinone
stronger PDE inhibitor no thrombocytopenia more selective eliminated by the kidney
31
atropine (What is it?)
atropine, competitive antagonist for muscarinic receptors
32
What are the effects of atropine?
increase HR, decrease refractoriness, decrease parasympathetic SVR decrease
33
What are the clinical uses of atropine?
prevent vagal reaction restore AV conduction in disorders of AV refractoriness
34
prazosin
alpha 1 antagonist results in decreased PVR and blood pressure
35
doazosin/terazosin
alpha antagonist
36
Describe the uses of beta blockers
decrease HR decrease impulse conduction decrease contractility and metabolic rate
37
Describe the adverse effects of beta blockers
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
Procainamide
Class IA -- targets sodium and potassium currents
39
Propanolol
non selective beta blocker lipid soluble eliminated by liver
40
Metoprolol
Beta1 selective Moderate solubility hepatic elimination
41
Atenolol
beta1 selective low lipid solubility renal excretion
42
Carvedilol
non selective with alpha1 blockade moderate lipid solubility hepatic elimination
43
Lidocaine
Targets Sodium currents
44
Flecainide
Targets sodium channel
45
Dofetilide
Potassium channel target
46
Adenosine
agonist for adenosine receptor lowers calcium currents acts VERY quickly
47
What are the mechanisms available by which to block reentry?
class 1 drugs, decrease excitability class 1A and class III drugs increase ERP
48
What are the associated risks in treating reentry tachy?
Prolonging ERP - long APD decrease excitability - slow conduction facilitates reentry
49
Statins
target HMGcoA reductase step, upregulate LDL receptor
50
Ezetimibe
cholesterol absorption drug - targets NPC1 receptor and then upregulates LDL receptor
51
Bile acid sequestrants
get rid of bile acids, more cholesterol used to make them; upregulates the receptor
52
What is PCSK9? WHy is it a target?
targets receptors for degradation - removing it upregulates receptors
53
fibrates
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
Omega 3 fatty acids
decrease TG levels
55
niacin
reduces FFA release and flux to liver increases HDL, decreases LDL
56
Enlalapril
ACEi (all end in april)
57
58
ARB
losartan (all end in -artan)
59
What are the arterial vasodilators
hydralazine Sodium nitroprusside
60
Sotalol
Class III
61
venodilators
organic nitrates
62
Edrophonium