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NUNA 681(pharm) > CV Drugs- ACE Inhibitors, Calcium Channel Blockers, Vasodilators > Flashcards

CV Drugs- ACE Inhibitors, Calcium Channel Blockers, Vasodilators Flashcards

1
Q

concerns with antihypertensives and anesthesia- interference with the sympathetic nervous system’s activity resulting in

A

orthostatic hypotension related to hypovolemia, position change, or decreased venous return (PPV)

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2
Q

concerns with antihypertensives and anesthesia- possible depletion of

A

norepinephrine stores- minimal response to indirect sympathomimetics

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3
Q

concerns with antihypertensives and anesthesia- exaggerated response to

A

direct sympathomimetics- due to no counter- balancing beta 2 activity

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4
Q

beta-blockers may improve

A

the outcome of patients with HTN

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5
Q

other than __, HTN medication should be continued even on the morning of surgery- fewer alteration in BP and HR, fewer arrhythmias

A

diuretics

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6
Q

antihypertensives drug classes

A
  1. beta-adrenergic blockers- negative chronotropic, inotropic
  2. combined alpha1 and beta-adrenergic blocker (labetolol)- negative inotropic, chronotropic, vasodilation; not as potent as beta-blockers or phentolamine
  3. alpha 1-adrenergic blocker (prazosin, phentolamine)- vasodilation
  4. centrally acting alpha 2-adrenergic agonist (clonidine, dex)- decrease sympathetic outflow
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7
Q

ACEi MOA

A
  1. inhibit the ACE in both the plasma and in the vascular endothelium
  2. block the conversion of angiotensin I to angiotensin II
  3. prevent the vasoconstriction from angiotensin II and the stimulation of the SNS
  4. decrease aldosterone-decreased Na and water retention (however, increased K)
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8
Q

ACEi advantage

A

minimal side effects compared to beta-blockers, diuretics

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9
Q

ACEi indications

A
  1. HTN (in diabetes)
  2. CHF
  3. mitral regurgitation (F, F, V)
  4. development of CHF (regression of LVH)
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10
Q

ACEi contraindications

A

patients with renal artery stenosis (their renal perfusion is highly dependent on angiotensin II)

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11
Q

ACEi benefit

A

minimal side effects

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12
Q

most common side effects

A

cough, upper respiratory congestion, rhinorrhea, allergic-like symptoms (potentiation of kinins and inhibition of breakdown of bradykinins)

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13
Q

ACEi angioedema

A

potentially life-threatening (epi 0.30-0.5 ml of 1:1,000 dilution)

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14
Q

ACEi hyperkalemia

A

due to decreased production of aldosterone (especially CHF with renal insufficiency)

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15
Q

ACEi angioedema may occur

A

unexpectedly after prolonged drug use

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16
Q

ACEi hereditary angioedema is due to

A

C1 esterase inhibitor deficiency

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17
Q

ACEi induced angioedema is due to

A

increased availability of bradykinin because bradykinin catabolism is blocked

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18
Q

how is angioedema treated?

A
  1. epi (catecholamines, antihistamines, and antifibrinolytics may be ineffective in acute episodes)
  2. tranexamic acid or aprotinin- inhibits plasmin activation
  3. Icatibant- a synthetic bradykinin receptor antagonist
  4. FFP- 2-4 units- to replace the deficient enzyme
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19
Q

ACEi- captopril (Capoten)- causes

A

decreased SVR- especially in renal

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20
Q

ACEi- captopril (Capoten)- __, __ not effected

A

CO, HR

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21
Q

ACEi- captopril (Capoten)- __ reduced

A

baroreceptor sensitivity (HR does not increase with decreased BP)

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22
Q

ACEi- captopril (Capoten)- may cause

A

hyperkalemia (related to blocking of aldosterone release)

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23
Q

ACEi- captopril (Capoten)- onset

A

15 min

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24
Q

ACEi- captopril (Capoten)- duration

A

6-10 hours

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25
Q

ACEi- enalapril (Vasotec)- dose PO

A

20 mg PO

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26
Q

ACEi- enalapril (Vasotec)- dose IV

A

0.625-1.25 mg

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27
Q

ACEi- enalapril (Vasotec)- onset

A

approx 1 hour

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28
Q

ACEi- enalapril (Vasotec)- duration

A

18-30 hours

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29
Q

ACEi- enalapril (Vasotec)- lacks

A

the rash and pruritus side effects of captopril; rarely angioedema of the face, lips, tongue, and glottis; watch for hypotension

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30
Q

losartan (Cozaar)- MOA

A

blocks the binding of angiotensin II to the receptors (type AT1- found in vascular smooth muscle) to prevent vasoconstriction and aldosterone release

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31
Q

losartan (Cozaar)- side effects

A

similar as ACEi

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32
Q

losartan (Cozaar)- risk of

A

stroke reduction 25% (compared to atenolol)

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33
Q

losartan (Cozaar)- dose

A

50mg

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34
Q

losartan (Cozaar)- may be combined with

A

thiazide diuretic or inhibitor of neprilysin (Entresto)

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35
Q

calcium channel blockers classifications

A
  1. phenylalkylamines
  2. 1,4-dihydropyridines
  3. benzothiazepines
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36
Q

CCB- phenylalkylamines

A

occludes the channel (verapamil)

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37
Q

CCB- 1,4-dihydropryridines

A

arterial vascular smooth cells (nifedipine, nicardipine, nimodipine)

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38
Q

CCB- benzothiazepines

A

AV node, MOA? (diltiazem)

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39
Q

CCB MOA

A
  1. bind to the alpha subunit of the slow L-type calcium ion channels
  2. block calcium entering the cardiac and vascular smooth muscle cells (arterial specific)
  3. reduction of calcium
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40
Q

CCB MOA of reduction of calcium

A
  1. fails to activate myosin- which reduces contraction
  2. slows depolarization of SA and AV nodal tissue
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41
Q

CCB effects- __ inotropic, chronotropic effects

A

negative

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42
Q

CCB effects- __ SA node activity

A

decreased

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43
Q

CCB effects- conduction slowed through the

A

AV node

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44
Q

CCB effects- vaso__, __ BP

A

dilation, decreased

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45
Q

CCB effects- relaxes

A

coronary artery spasm (complements nitrate- different MOA)

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46
Q

CCB uses

A
  1. treatment of coronary artery spasm
  2. unstable angina pectoris
  3. chronic stable angina
  4. essential hypertension
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47
Q

CCB increased risk with dihydrophyrimidine derivates (nifedipine)

A
  1. CV complications (placebo)
  2. perioperative bleeding, GI hemorrhage
  3. development of cancer (beta-blockers, ACE inhibitors)
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48
Q

CCB- verapamil (Calan)- is a derivative of

A

papaverine

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49
Q

CCB- verapamil (Calan)- effects

A
  1. decreases contractility
  2. decreased HR
  3. decreased conduction through AV node
  4. relaxation of vascular smooth muscle, coronary arteries
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50
Q

CCB- verapamil (Calan)- uses

A

treatment of SVT (AV node), HTN

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51
Q

CCB- verapamil (Calan)- dose

A

75-150mcg/kg (2.5-5mg) IV slowly

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52
Q

CCB- verapamil (Calan)- onset

A

1-3 minutes

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53
Q

CCB- verapamil (Calan)- oral nearly complete __ metabolism

A

hepatic

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54
Q

CCB- verapamil (Calan)- IV metabolism

A

70% renal and 15% bile

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55
Q

CCB- verapamil (Calan)- elimination 1.2 life

A

6-12 hours

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56
Q

CCB- verapamil (Calan)- combination with volatile anesthesia

A

has additive myocardial depressant and vasodilation effects, even in normal LV function

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57
Q

CCB- nifedipine (Adalat, Procardia)-

A

dihydropyridine

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58
Q

CCB- nifedipine (Adalat, Procardia)- vasodilation of

A

coronary and peripheral arteries (>verapamil)

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59
Q

CCB- nifedipine (Adalat, Procardia)- __ BP

A

decreases

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60
Q

CCB- nifedipine (Adalat, Procardia)- ___HR

A

indirect baroreceptor-mediated increased

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61
Q

CCB- nifedipine (Adalat, Procardia)- __ contractility, __ chronotropic, and __ effects

A

directly decreased

decreased

dromotropic

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62
Q

CCB- nifedipine (Adalat, Procardia)- admin

A

PO, IV, SL

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63
Q

CCB- nifedipine (Adalat, Procardia)- uses

A
  1. angina
  2. especially coronary artery vasospasm
  3. hypertension emergencies (CAUTION/STOP-cerebrovascular ischemia, MI, severe hypotension)
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64
Q

CCB- nifedipine (Adalat, Procardia)- dose

A

10-20 mg PO or SL

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65
Q

CCB- nifedipine (Adalat, Procardia)- onset

A

20 min

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66
Q

CCB- nifedipine (Adalat, Procardia)- metabolism

A

hepatic

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67
Q

CCB- nifedipine (Adalat, Procardia)- elimination 1/2 life

A

2-5 hours

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68
Q

CCB- nifedipine (Adalat, Procardia)- side effects

A
  1. flushing
  2. HA
  3. vertigo
  4. hypotension
  5. may cause renal dysfunction
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69
Q

CCB- nifedipine (Adalat, Procardia)- abrupt stop has causes

A

coronary artery vasospasm

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70
Q

CCB- nicardipine (Cardene)- __ vasodilation

A

selective arterial (SVR)

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71
Q

CCB- nicardipine (Cardene)- __ vasodilation effects

A

greatest (especially coronary arteries)

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72
Q

CCB- nicardipine (Cardene)- does not effect

A

the SA node of AV node, minimal myocardial depressant effects

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73
Q

CCB- nicardipine (Cardene)- dose

A

25 mg in 240 ml (0.1mg/ml)

titrate- start at 5mg/hr (50ml/hr), increase by 2.5 mg/hr every 5-15 mins to a max of 15 mg/hr

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74
Q

CCB- nicardipine (Cardene)- not compatible with

A

LR

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75
Q

CCB- clevidipine (Cleviprex)-

A

3rd generation dihydropyridine

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76
Q

CCB- clevidipine (Cleviprex)- onset

A

rapid, titratable

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77
Q

CCB- clevidipine (Cleviprex)- __ emulsion

A

lipid (similar to propofol)

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78
Q

CCB- clevidipine (Cleviprex)- metabolism

A

plasma and tissue esterases (organ independent)

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79
Q

CCB- nimodipine (Nimotop)- highly

A

lipid soluble to cross BBB

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80
Q

CCB- nimodipine (Nimotop)- used to treat

A

vasospasm related to subarachnoid hemorrhage

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81
Q

CCB- nimodipine (Nimotop)- dose

A

0.7 mg/kg PO then 0.35 mg/kg q4 hours for 21 days

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82
Q

CCB- nimodipine (Nimotop)- if intracranial compliance is a concern,

A

an increase in ICP could occur

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83
Q

CCB- diltiazem (Cardizem, Dilacor, Tiazac)-

A

benzothiazepine

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84
Q

CCB- diltiazem (Cardizem, Dilacor, Tiazac)- blocks

A

channels in the AV node

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85
Q

CCB- diltiazem (Cardizem, Dilacor, Tiazac)- uses

A

treatment of SVT, angian pectoris

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86
Q

CCB- diltiazem (Cardizem, Dilacor, Tiazac)- dose

A

0.25 mg/kg IV over 2 minutes, may repeat in 15 min if needed

infusion 10mg/hr

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87
Q

CCB- diltiazem (Cardizem, Dilacor, Tiazac)- elimination

A

via bile (60%) and urine (35%)

88
Q

CCB- diltiazem (Cardizem, Dilacor, Tiazac)- elimination 1.2 time

A

3-5 hours

89
Q

CCB drug interactions- volatile anesthetics

A

additive myocardial depression and vasodilation, especially with preexisting LV dysfunction

90
Q

CCB drug interactions- depolarizing and nondepolarizing NMB drugs like mucin antibiotics

A

potentiated (Ca ions are needed to release acetylcholine at the NM junction)

91
Q

CCB drug interactions- LA

A

increased risk of toxicity (inhibition of Na ion movement via Na channels)

92
Q

CCB drug interactions- K replacement

A

hyperkalemia due to inhibition of K moving into cell

93
Q

CCB drug interactions- __ and __ cause hyperkalemia

A

verapamil and dantrolene

94
Q

CCB drug interactions- digoxin

A

increase in digoxin plasma concentration- decreasing its clearance

95
Q

vasodilators- indications

A
  1. treat HTN
  2. induce controlled hypotension
  3. encourage LV SV
96
Q

vasodilators- effects

A
  1. decrease BP
  2. decrease SVR (arterial)
  3. decrease venous return and CO (ventilator)
97
Q

nitric oxide- nitrovasodilators cause

A

both pulmonary and systemic vasodilation be producing NO

98
Q

nitric oxide- increases

A

intracellular cGMP causing smooth muscle relaxation (results ultimately from decreased intracellular calcium similar to the effect of cAMP from beta 2 stimulation)

99
Q

nitric oxide- can be

A

inhaled in the gaseous state to cause pulmonary vasodilation specifically

100
Q

nitric oxide- endogenous- CV effects: release of NO from endothelial cells due to

A

shear stress and pulsatile arterial flow

101
Q

nitric oxide- endogenous- CV effects: regulation

A

SVR and PVR- baseline

102
Q

nitric oxide- endogenous- CV effects: impacts

A

distribution of cardiac output

103
Q

nitric oxide- endogenous- CV effects: autoregulation

A

increased NO production with decreased oxygenation

104
Q

nitric oxide- endogenous- CV effects: __ produce more NO than __

A

arteries

veins

(IMA remains patent longer than saphenous vein grafts)

105
Q

nitric oxide- endogenous- pulmonary effects:

A
  1. bronchodilation
  2. selective dilation of vessels to ventilated alveoli
106
Q

nitric oxide- endogenous- platelet effects:

A

inhibits plt activation, aggregation, and adhesion (antithrombotic)

107
Q

nitric oxide- endogenous- nervous system effects: NT in

A

brain, spinal cord, and peripheral nervous system

108
Q

nitric oxide- endogenous- nervous system effects: may be involved in

A

antinociception and anesthetic effects

109
Q

nitric oxide- endogenous- nervous sytem effects: produce

A

relaxation of smooth muscle of the Gi tract

110
Q

nitric oxide- endogenous- immune response: produced in response to

A

activation of macrophages

111
Q

nitric oxide- endogenous- immune response: can damage

A

bacteria, fungi, and protozoa

112
Q

pathophysiologic effects related to NO- essential hypertension

A

decreased NO release

113
Q

pathophysiologic effects related to NO- sepsis shock

A

excessive NO release

114
Q

pathophysiologic effects related to NO- atherosclerosis

A

decreased NO, plt aggregation, vasoconstriction

115
Q

pathophysiologic effects related to NO- cirrhosis

A

excessive production of NO

116
Q

anesthetic effects on NO- involved in the

A

excitatory neurotransmission

117
Q

anesthetic effects on NO- anesthetics cause suppression of

A

formation of NO to decrease excitatory NT and enhance GABA inhibitory transmission

118
Q

anesthetic effects on NO- administration of NO synthase inhibits have __ in MAC

A

dose dependent reduction in

119
Q

uses of NO

A
  1. inhaled form to treat PH (use in any other than neonates is “off label”)
  2. in neonates, its use has decreased the use of ECMO
120
Q

sodium nitroprusside (SNP, nipride)- is a

A

direct-acting, arterial and venous vascular smooth muscle relaxant

121
Q

sodium nitroprusside (SNP, nipride)- causes vasodilation of

A

arterial and venous

122
Q

sodium nitroprusside (SNP, nipride)- onset

A

60-90 seconds

123
Q

sodium nitroprusside (SNP, nipride)- duration

A

short requiring infusion, titration

124
Q

sodium nitroprusside (SNP, nipride)- monitoring

A

careful, infusion device used

125
Q

sodium nitroprusside (SNP, nipride)- dose

A

0.25-1 mcg/kg/min, up to 5 mcg/kg/min (body can handle only 2 mcg/kg/min continuous)

126
Q

sodium nitroprusside (SNP, nipride)- MOA

A

reacts with hemoglobin to form methemoglobin and releases cyanide and NO; NO causes the vasodilation

127
Q

sodium nitroprusside (SNP, nipride)- is __ cyanide and during metabolism __

A

44%

5 cyanide ions are release making cyanide toxicity possible0 causing tissue anoxia, anaerobic metabolism, and lactic acidosis

128
Q

sodium nitroprusside (SNP, nipride)- susceptible to CN toxicity

A
  1. receiving infusion of > 2 mcg/kg/min
  2. children or young adults- baroreceptor reflexes cause stimulation of SNS, require larger dose
  3. pregnancy- fetal cyanide toxicity
129
Q

sodium nitroprusside (SNP, nipride)- signs and symptoms of CN toxicity

A
  1. unresponsive to previously therapeutic doses of SNP
  2. increased MvO2- inability of tissues to use oxygen
  3. metabolic acidosis
  4. CNS dysfunction, seizures
130
Q

sodium nitroprusside (SNP, nipride)- treatment of CN toxicity

A
  1. stop infusion
  2. 100% O2
  3. sodium bicarb to correct met acidosis
  4. sodium thiosulfate to be a sulfur donor to convert cyanide to thiocyanate
131
Q

sodium nitroprusside (SNP, nipride)- must be protected from

A

the light to prevent breakdown into cyanide; light-protected solution are safe for 24 hours

132
Q

sodium nitroprusside (SNP, nipride)- CV effects:

A

direct partial and venous vasodilation

133
Q

sodium nitroprusside (SNP, nipride)- CV effects: __ BP, SVR

A

decreased

134
Q

sodium nitroprusside (SNP, nipride)- CV effects: __ HR and contractility

A

indirect increase in

135
Q

sodium nitroprusside (SNP, nipride)- CV effects: __ CO

A

may have increased

136
Q

sodium nitroprusside (SNP, nipride)- CV effects: ___ vasodilation which creates __

A

coronary artery

coronary steal from ischemic areas

137
Q

sodium nitroprusside (SNP, nipride)- CV effects: __ diastolic pressure

A

decrease

138
Q

sodium nitroprusside (SNP, nipride)- CNS effects: __ CBF

A

increased

139
Q

sodium nitroprusside (SNP, nipride)- CNS effects: __ CBV

A

increased

140
Q

sodium nitroprusside (SNP, nipride)- CNS effects: if pt has decreased intracranial compline,

A

ICP may become dangerously elevated

141
Q

sodium nitroprusside (SNP, nipride)- CNS effects: ICP increases are maximal if

A

MAP decreases less than 30%; if >30% decrease in MAP, the ICP returns to normal

142
Q

sodium nitroprusside (SNP, nipride)- CNS effects: to prevent the increase in ICP,

A

infuse SNP to slowly lower BP over 5 minutes along with hyperopia and hypocarbia

143
Q

sodium nitroprusside (SNP, nipride)- CNS effects: once the dura is open, ICP

A

problems are not a problem

144
Q

sodium nitroprusside (SNP, nipride)- CNS effects: contraindications

A

patients with increased ICP and inadequate CBF, and patents with carotid artery stenosis

145
Q

sodium nitroprusside (SNP, nipride)- pulmonary effects:

A

decrease in the PaO2

146
Q

sodium nitroprusside (SNP, nipride)- pulmonary effects: alteration of

A

HPV

147
Q

sodium nitroprusside (SNP, nipride)- pulmonary effects: bigger problem in

A

healthy lungs

148
Q

sodium nitroprusside (SNP, nipride)- pulmonary effects: COPD lungs develop

A

vascular changes that prevent the alteration of HPV

149
Q

sodium nitroprusside (SNP, nipride)- pulmonary effects: treatment of alteration in HPV

A

add PEEP

150
Q

sodium nitroprusside (SNP, nipride)- inhibits

A

platelet aggregation (>3 mcg/kg/min); not clinically significant- bleeding not increased

151
Q

sodium nitroprusside (SNP, nipride)- clinical uses:

A
  1. deliberate hypotension
  2. hypertensive emergencies
  3. cardiac disease
  4. aortic surgery
  5. cardiac surgery
152
Q

sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- mostly likely to

A

maintain cerebral perfusion

153
Q

sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- initial rate

A

0.3-0.5 mcg/kg/min

154
Q

sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- should not exceed

A

2 mcg/kg/min

155
Q

sodium nitroprusside (SNP, nipride)- clinical uses: deliberate hypotension- combined with other agents to

A

minimize risk of CN toxicity

156
Q

sodium nitroprusside (SNP, nipride)- clinical uses: HTN emergencies-

A

temporary initial treatment, effective no matter the cause, onset, tritration, quick offset

157
Q

sodium nitroprusside (SNP, nipride)- clinical uses: cardiac disease-

A

decreased afterload (MR, AR, CHF, MI with LV failure but may also need inotrope)

158
Q

sodium nitroprusside (SNP, nipride)- clinical uses: aortic surgery

A

treat HTN related to cross-clamp, spinal cord ischemia- distal hypotension

159
Q

sodium nitroprusside (SNP, nipride)- clinical uses: cardiac surgery

A
  1. rewarming period to cause vasodilation to distribute warmth to periphery
  2. treat PH after valve replacement
160
Q

nitroglycerin-

A

organic nitrate

161
Q

nitroglycerin- dilates

A

venous side except, at elevated doses, it will relax arterial smooth muscle

162
Q

nitroglycerin- MOA

A

produces NO which causes peripheral vasodilation

163
Q

nitroglycerin- sublingual onset

A

4 minutes

164
Q

nitroglycerin- transdermal

A

sustained protection from MI

165
Q

nitroglycerin- infusion requires

A

special tubing and glass bottles to prevent absorption into the plastic

166
Q

nitroglycerin- elimination 1/2 life

A

1.5 minutes; requires infusion

167
Q

nitroglycerin- may cause

A

the production of methgb when the nitrite metabolite oxidizes the ferrous ion in hgb

168
Q

nitroglycerin- methgb treatment

A

methylene blue 1-2 mg/kg IV over 5 minutes to convert back to hgb

169
Q

nitroglycerin- CV effect: __ dilation

A

venous (up to 2mcg/kg/min)

170
Q

nitroglycerin- CV effect: __ venous return, LVEDP, RVEDP

A

decreased

171
Q

nitroglycerin- CV effect: CO __

A

decreased (in normal heart with no CHF; if patient in heart filature, the CO is improved, and pulmonary congestion is relieved)

172
Q

nitroglycerin- CV effect: _ BP

A

decreased (related more to volume than SNP)

173
Q

nitroglycerin- CV effect: __ DBP, coronary blood flow

A

decreased

174
Q

nitroglycerin- CV effect: __ tachycardia, __ inotropic effect

A

baroreceptor-reflex

increased

(increased demand, decrease supply)

175
Q

nitroglycerin- CV effect: dilates

A

larger conductance vessels of the coronary circulation- provides better blood flow to ischemic areas

176
Q

nitroglycerin- CV effect: relaxes

A

pulmonary vessels

177
Q

nitroglycerin- smooth muscle effect: relaxes

A
  1. bronchial smooth muscle
  2. biliary tract smooth muscle (sphincter of ddi)
  3. esophageal muscles
  4. uterine and ureteral smooth muscles
178
Q

nitroglycerin- CNS effect:

A
  1. cerebral vasodilation
  2. inhibition of plt aggregation
179
Q

nitroglycerin- clinical uses:

A
  1. angina pectoris
  2. cardiac failure
  3. acute HTN
  4. deliberate hypotension
180
Q

nitroglycerin- clinical uses: angina pectoris

A

decrease myocardial oxygen demand and vasodilator coronaries to ischemic areas (decrease size of MI-not SNP)

181
Q

nitroglycerin- clinical uses: cardiac failure

A

decrease preload and relieve pulmonary edema

182
Q

nitroglycerin- clinical uses: acute HTN

A

maternal pt during C-section with no effects on fetus

183
Q

nitroglycerin- clinical uses: deliberate hypotension

A

less potent than SNP; decrease in diastolic is less than SNP; intravascular volume has a bigger effect

184
Q

isosorbide dinitrate-

A

oral nitrate- prophylaxis of angina pectoris

185
Q

isosorbide dinitrate- prolonged __ effect, increased __

A

antianginal

exercise tolerance up to 6 hours

186
Q

isosorbide dinitrate- vasodilation of

A

venous circulation and dilation of coronary arteries to redirect blood flow to ischemic areas

187
Q

isosorbide dinitrate- given to

A

CABG patients preop

188
Q

hydralazine (Apresoline)- direct dilation

A

arterial side, some venous

189
Q

hydralazine (Apresoline)- vasodilates

A

coronary, cerebral, renal, and splanchnic, pulmonary vessels

190
Q

hydralazine (Apresoline)- MOA

A

interferences with Ca ion transport

191
Q

hydralazine (Apresoline)- decreases

A

diastolic more than systolic pressure

192
Q

hydralazine (Apresoline)- increases

A

HR (baroreceptor and direct), SV, CO (can cause MI, prevented with beta-blocker)

193
Q

hydralazine (Apresoline)- onset

A

10-20 minutes (prolonged)

194
Q

hydralazine (Apresoline)- duration

A

2-4 hours (unpredictable)

195
Q

hydralazine (Apresoline)- dose

A

10-20 mg

196
Q

hydralazine (Apresoline)- metabolism

A

mostly hepatic

197
Q

hydralazine (Apresoline)- side effects

A
  1. lupus-like syndrome
  2. peripheral neuropahties
  3. vertigo
  4. diaphoresis
  5. nausea
  6. tachycardia
    uncommon in intermittent use
198
Q

trimethaphan- is an

A

ganglionic blocker0 blocks autonomic nervous system reflexes

199
Q

trimethaphan- vasodilation of

A

venous capacitance vessels

200
Q

trimethaphan- __ CO, SVR

A

decreases

201
Q

trimethaphan- blocks

A

receptors for ACh

202
Q

trimethaphan- may have __ that offsets the benefit of __

A

tachycardia

decreased BP

203
Q

trimethaphan- historical use

A

deliberate hypotension

204
Q

adenosine- is an

A

endogenous nucleoside in all cells- maintain the balance of O2 supply and demand of the heart and other organs

205
Q

adenosine- effects

A

dilation of coronary arteries (steal possible); negative chronotropic

206
Q

adenosine- MOA

A

stimulation of K channels in supra ventricular cells to hyper polarize atrial cells and slowing of SA node (can also stimulate release of NO from endothelial cells)

207
Q

adenosine- uses

A
  1. SVT
  2. deliberate hypotension
208
Q

adenosine- uses: SVT for

A

paroxysmal SVT and narrow complex tachycardia (not atrial fib or v tach)

209
Q

adenosine- for SVT dose

A

6 mg IV then 12 mg then 18 mg

210
Q

adenosine- for SVT can repeat dose within

A

60 seconds

211
Q

adenosine- for SVT elimination 1/2 life

A

0.6-1.5 seconds

212
Q

adenosine- uses: deliberate hypotension because of

A

rapid responsiveness, onset and recovery

213
Q

adenosine- for deliberate hypotension: __ SVR, __ HR, __ coronary flow, __ cardiac filling pressures

A

decreased

increased (reflex tachycardia)

increased

unchanged

214
Q

adenosine- for deliberate hypotension: dose

A

220 mcg/kg/min- no tachyphylaxis

215
Q

principle adenosine effects- adenosine 1 receptor effect

A
  1. slowing of the rhythm neg inotropic effects
  2. vasoconstriction
  3. bronchoconstriction
  4. sedation anticonvulsant effect; decrease of NT release
216
Q

principle adenosine effects- adenosine 2 receptor effect

A
  1. vasodilation
  2. bronchodilation
  3. complex stimulant effects
  4. increase of NT release
  5. plt aggregation inhibition

NUNA 681(pharm) (12 decks)

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