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Sp: Pharm 1 > Pharm Unit 2 Cardiac > Flashcards

Pharm Unit 2 Cardiac Flashcards

1
Q

positive inotropes

A

increase strength of heart muscle contraction

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2
Q

vasopressors

A

increase BP by contracting blood vessels

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3
Q

adrenergic neurons

A

norepinephrine
epinephrine

postganglionic neurons

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4
Q

B1 receptor location

A

heart
kidney

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5
Q

beta 2 receptor

A

kidney
peripheral

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6
Q

beta 1 receptor causes

A

increase HR and contractilioty

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7
Q

beta 2 receptor on kidney causes

A

renin release
- RAAS (incr Na+/H2O retention)
increases blood volume
increases blood pressure

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8
Q

beta 2 receptor peripheral causes

A

peripheral vasodialtion
- bronchodilation
- decrease GI motility
- glucagon release
- increase glucose

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9
Q

alpha 1 receptors

A

walls of blood vessels
eyes
bladder

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10
Q

alpha 1 receptor causes

A

vasoconstriction
pupil dilation
urinary retention

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11
Q

alpha 2 receptor

A

synaptic cleft
NE binds and decreases NE in synaptic cleft

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12
Q

cellular actions are driven by

A

Ca2+

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13
Q

higher Ca2+ means

A

faster
more foreceful contraction
faster relaxation

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14
Q

contractility

A

strength of contraction

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15
Q

preload

A

amount of blood returning to heart

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16
Q

afterload

A

peripheral resistance
(arterial)
force resisting myocardial fiber contraction at the start of systole

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17
Q

stroke volume determinants

A

contractility (EF)
afterload

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18
Q

ejection fraction

A

percentage of EDV ejected each contraction

normal: 55-60%

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19
Q

contractility

A

reasonably estimatd by Ejetion fraction

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20
Q

what lowers afterload

A

afterial vasodilation

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21
Q

increases in afterload causes

A

decreases in SV

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22
Q

severe LV dysfunction is impacted by what

A

afterload
increased afterload significantly decreases SV

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23
Q

frank-starling mechanism

A

describes relationship between preload and cardiac output

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24
Q

increased preload causes

A

increased SV

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25
Q

stroke volume calculation

A

SV = EDV-ESV

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26
Q

CO calulation

A

CO = (EDV-ESV) x HR

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27
Q

HFpEF

A

diastolic dysfunction (dec EDV)

cannot fully relax so will not fully fill

pump is still functioning: No change to EF

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28
Q

HFrEF

A

systolic dysfunciton (incr ESV)
loss of contractile strength
decreased EF due to inability to contract

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29
Q

inotrope receptors

A

beta agonists
increases contracility

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30
Q

vasopressor receptors

A

alpha 1 agonists
increases SVR

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31
Q

positive inotrope drugs

A

dobutamine
dopamine
milrinone

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32
Q

dobutamine

A

beta 1 agonist (highly selective)
– incr Ca2+ (incr contractility/HR)
beta 2 agonist (some selectivity)
– vasodilation (incr CO)

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33
Q

dobutamine indications

A

systolic heart failure (B1)
-schemic heart disease
acute heart failure (b2)
cardiogenic shock (b2)

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34
Q

dobutamine CI

A

chronic heart failure
(due to tolerance)

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35
Q

dobutamine SE

A

tachycardia
palpitations
arrhythmias
tolerance

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36
Q

PDE

A

breaks down cAMP

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37
Q

PDE inhibitors

A

prevent breakdown of cAMP
incr Ca2+
incr contraction
vasodilation

“inodilator”

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38
Q

common PDE inhibitor

A

milrinone

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39
Q

milrinone indication

A

acute heart failure

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40
Q

milrinone CI

A

chronic heart failure
(incr morbidity/mortality)

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41
Q

dopamine: low dose

A

<3 mcg/kg/min
vasodilation
incr naturesis (Na+/H2O elim)d

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42
Q

dopamine: mod dose

A

4-10 mcg/kg/min
beta 1 agonist (incr Ca2+)
incr CO

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43
Q

dopamine: high dose

A

> 10 mcg/kg/min
alpha 1
vasopressor (incr Ca2+)
vasoconstriction
incr BP

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44
Q

dopamine indications

A

severe hypotension
acute heart failure
shock (vasodlatory/cardiogenic)
severe bradycardia

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45
Q

dopamine SE

A

tachycardia
atrial/ventricular dysrhythmias
nausea/vomiting
ischemia of digits/organ systems

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46
Q

norepinephrine

A

potent a1 receptor agonist
- vasoconstriction
- incr BP
moderate beta 1 stimultor
- incr CO
- minimal HR change

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47
Q

norepinephrine indidcations

A

hypotension
shock-like state w/periph vasodilation

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48
Q

norepinephrine adverse effects

A

atrial/ventricular dysrhythmias
ischemia of digits/organs

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49
Q

which is safer: NE or dopamine?

A

NE

causes less arrythmias

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50
Q

epinephrine

A

balanced (nonselective) b1, b2, a1 agnonist (Cardiac stimulator)
incr contractility
incr HR
incr SVR

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51
Q

which drug is a cardiac stimulator

A

epinephrine

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52
Q

epinephrine indications

A

cardiac arrest
shock
bronchospasm/anaphylaxis
symptomatic bradycardia

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53
Q

epinephrine SE

A

atrial/ventricular dysrhythmias
ischemia of digits/organs
cardiac toxicity (high/prolonged doses)
severe hypertension (cerebral hemorrhage)

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54
Q

phenylephrine

A

potent alpha 1 agnoist
incr SVR
incr BP
minimal HR/contractility change

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55
Q

phenylephrine indications

A

vasodilatory hypotension
vagal / drug induced hypotension

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56
Q

phenylephrine SE

A

reflex bradycardia
ischemia of digits/organs
tissue necrosis (extravasation)
severe hypertension

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57
Q

digoxin

A

blocks Na+/K+ atpase
which inhibits NCX
- Ca2+ stays IN cell
incr Ca2+
incr contraction force

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58
Q

digoxin indications

A

atrial flutter/afib
HFrEF

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59
Q

digoxin therapeutic window

A

narrow
0.5-2.0 ng/ml
<1.0 in HF

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60
Q

digoxin low dose

A

increases parasympathetic tone

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61
Q

digoxin SE (toxicity)

A

GI upset
altered color perception (halo vis)
malaise
bradycardia
AV block
VTAC
fibrillation

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62
Q

cardiovascular mortality risk _____ for every _____ incr in BP

A

cardiovascular mortality risk doubles with each 20/10 mmHg BP increase

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63
Q

hypertension

A

Systolic >130
and/or
Diastolic > 80

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64
Q

2 ways to decrease blood pressure

A

decrease CO
decrease SVR

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65
Q

3 ways to decrease CO

A

decrease BV
decrease HR
decrease SV

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66
Q

5 anatomic sites of BP control

A

arteries (SVR)
veins
heart (CO/HR/SV)
kidney (BV)
CNS

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67
Q

RAAS antagonists

A

ACE inhibitoprs
ARBS
neprilysin inhibitor + ARB
aldosterone antagonist (K+ sparing diuretic)

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68
Q

aldosterone

A

promotes Na+/H2O retention
increases BV
incr BP

can cause myocardial/renal/vascular fibrosis

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69
Q

angiontensin II

A

vasoconstriction
incr aldosterone
Na+/H2O retention
incr NE release

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70
Q

ACE breaks down

A

bradykinin

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71
Q

bradykinin function

A

vasodilation

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72
Q

ACE inhibitors mechanism

A

incr bradykinin = vasodilation
decr antiontensin II = vasodilation

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73
Q

ACE inhibitor indications

A

HF
CAD
hypertension
chronic renal disease w/proteinuria

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74
Q

ACE inhibitor SE

A

incr K+
acute renal failure
dry cough
angioedema
hypotension (volume/Na+ depleted pts)

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75
Q

ACE inhibitor CI

A

pregnancy
renal insufficiency pts
renal artery stenosis

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76
Q

ACE inhibitors drugs

A

end in -pril

Benazepril
capropril
quinapril
etc

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77
Q

ARBS mechanism

A

block angiotensin II receptors
= vasodilation
decr aldosterone
decr Na+/H2O retention
decr BV
decr BP

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78
Q

ARBS indications

A

HF
CAD
hypertension
chronic renal diseas w/proteinuria

alt to ACE inhibitors for pts w/dry cough

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79
Q

ARBS CI

A

renal failure pts
pregnancy

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80
Q

ARBS SE

A

incr K+
acute renal failture
hypotension (volume/Na+ depleted pts)

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81
Q

ARBS drugs

A

end in -Sartan

candesartan
losartan
etcf

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82
Q

Neprilysin Inhibitor Plus ARB

A

neprilysisn breaks down bradykinin
vasodilation
decr BP

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83
Q

neprilysin inhibitor plus ARB drug

A

sacubitril/valsartan (enstrest)

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84
Q

neprilysin inhibitor plus ARB indication

A

heart failure

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85
Q

neprilysin/ARB SE

A

hyperkalemia
cough
angioedema
renal function deterioration
hypotension

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86
Q

neprilysin/ARB CI

A

pregnancy
bilateral renal artery stenosis

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87
Q

neprilysin/ARBs should not be used within ____ hrs of ACE inhibitors

A

36 hrs

increased risk of angioedema

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88
Q

aldosterone antagonists indications

A

hyperaldosteronism
hypertension (resistant HTN)
HF
MI w/LV dysfunction

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89
Q

aldosterone antagonist SE

A

renal dysfunction
hyperkalemia
endocrine abnormalities
- dynecomastia
- breast pain
- menstrual irregularities
- impotence

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90
Q

aldosterone antagonist CI

A

Cr >2.5 (males)
Cr >2.0 (women)
K+ >5meq/mL

91
Q

aldosterone antagonist drugs

A

spironolactone
eplerenone

92
Q

diuretics mechanism

A

incr Na+/H2O excretion
decr BV (decr SV)

93
Q

types of diuretics

A

loop
thiazide
potassium sparing

94
Q

loop diuretics site of action

A

kidney -
ascending loop of henle

blocks Na+ reabsorption

95
Q

loop diuretics indications

A

treatment/prevention of:
edematous condition
hyperkalemia
HTN (2d line)

96
Q

loop diuretics SE

A

hypotension
renal insufficiency
hypokalemia (arrythmias)
hypocalcemia (tetany)
hypomagnesemia (arrythmias)
metabolic alkalosis
hyperuricemia (gout)
ototoxicity (tinnitus, deafness, vertigo)

97
Q

loop diuretics drugs (4)

A

furosemide (lasik)
bumetanide
ethacrynic acid
torsemide

98
Q

which loop diuretic is good for pts w/sulfa allergy?

A

ethacrynic acid

99
Q

loop diuretics excretion

A

renal
- furosemide
- torsemide
renal/hepatic
- bumetanide
- ethacrynic acid

100
Q

which loop diuretic has the lowest oral bioavailability?

A

furosemide

101
Q

which loop diuretic has the shortest duration of action?

A

furosemide and dumetanide
(4-6hrs)

102
Q

thiazides diuretic site of action

A

distal convoluted tubule

103
Q

4 most common thiazides

A

hydrochlorothiazide
chlorthalidone
indapamide
metolazone

104
Q

thiazade potency

A

less potent than loops

105
Q

thiazide indications

A

hypertension (1st line treatment)

106
Q

thiazide SE

A

hypovolemia
hypokalemia
hyponatremia
hypochloremia
hypomagnesemia
hypercalcemia
hyperuricemia (gout)
metabolic alkalosis

107
Q

what drug can be combined with loop diuretic to increase diuretic effects?

A

thiazide diuretics potentiate loop effects

108
Q

potassium sparing diuretics site of action

A

collecting tubule
Na+ channel

109
Q

potassium sparing diuretics (2 types)

A

Na+ channel blockers
aldosterone receptor antagonists

110
Q

Na+ channel blocker drugs (2)

A

triamterene
amiloride

111
Q

Na+ channel blocker mechanism

A

block Na+ reabsorption
increases K+ retention
minimal diuresis

112
Q

potassium sparing diuretics

A

weak unless used for specific states
combine w/loop or thiazides to minimize K+ loss

113
Q

potassium sparing diuretics SE

A

hyperkalemia

114
Q

central anti-adrenergics mechanism

A

target adrenergic neurons in CNS
prevent NE release

115
Q

alpha 2 receptor agonists drugs

A

clonidine
guanabenz
guanfacine

116
Q

alpha 2 receptor agonist mechanism

A

decr NE release
decr sympa firing
incr parasympa

117
Q

methyldopa

A

false neurotransmitter
causes methylnorepinephrine release
methyl-NE can activate alpha 2
- inhibits NE release
methyl-NE cannot activate adrenergic receptors

118
Q

central anti-adrenergic SE

A

bradycardia
hypotension
rebound HTN w/withdrawal (250/120)
dry mouth
drowsiness/sedation
lethargy
GI upset

119
Q

methydopa SE

A

all central anti-adrenergic effects
+
hepatoxicity
hemolysis

120
Q

central anti-adrenergic indications

A

hypertension (not first line)
resistant hypertension
ADHD (guanfacine)
pregnancy hypertension (methyldopa)
withdrawal (narcotics/alcohol)

121
Q

which drug is used for ADHD

A

guanfacine

122
Q

which drug is safe for treating hypertension in pregnancy?

A

methyldopa

123
Q

non-selective alpha antagonists drugs

A

phenoxybenzamine
phentolamine

124
Q

selective alpha-1 antagonists drugs

A

prazosin
terazosin
doxazosin

125
Q

non-selective alpha antagonists mechanism

A

alpha 1 antagonist = vasodilation
alpha 2 antagonist = reflex tachycardia
- incr NE = incr HR

126
Q

phenoxybenzamine

A

irreversible
non-competitive alpha antagonist

127
Q

phentolamine

A

reversible
competitive alpha antagonist

128
Q

what drugs are used to treat phochromocytoma?

A

phenoxybenzamine
phentolamine

129
Q

what drug reverses soft tissue anesthesia/IV extravisation toxicity

A

phentolamine

130
Q

nonselctive alpha antagonists SE

A

reflex tachycardia
postural hypotension
cardiac arrythmias
iscehmic cardiac events

131
Q

phenotlamine-sepcific SE

A

stimulates GI
increases GERD

132
Q

phenoxybenzamine-specific SE

A

metagenic (causes cancer)

133
Q

which alpha antagonists should you use emergently?

A

non-selective

134
Q

which alpha antagonists should you use chronically?

A

selective alpha 1

135
Q

selective alpha 1 antagonists mechanism

A

inhibit NE binding to alpha 1
relax arterial/venous smooth muscle
= vasodilation
decr PVR / preload

136
Q

selective alpha 1 antagonist indications

A

hypertension (not first line)
- benign prostatic hypertrophy

137
Q

benign prostatic hypertrophy selective alpha 1 mechanism

A

inhibits alpha 1 in lower urinary tract
decr resistance to urinary flow
(tamsulosin)

138
Q

which drug is selective for urinary tract?

A

tamsulosin

139
Q

selective alpha 1 antagonist SE

A

postural hypotension
syncope
fluid retention
nasal congestion
drowsiness

140
Q

first dose phenomenon (selective alpha 1 antagonists)

A

faintness/syncope that occurs 30 min to 6 hrs after initial dose

start w/low dose at bedtime

141
Q

why do selective alpha 1 antagonists cause syncope?

A

block the natural vasoconstriction mechanism
decr BF to brain when shifting from sitting to standing

142
Q

b1 receptor location

A

heart
SA/AV node
kidney

143
Q

b2 receptor location

A

lung
vascular smooth muscle
liver/pancreas

144
Q

Beta Blockers

A

bind to beta-adrenergic receptors preventing binding of epi/NE
inhibits normal sympathetic stimulation of the heart

145
Q

which beta blockade is better for decreasing BP

A

beta 1 blockade

146
Q

non-selective beta blocker drugs

A

nadolol
propranolol
timolol

147
Q

cardioselective beta blocker

A

Beta-1 inhibition only:
decr HR
decr cardiac output,
decr renin release
decr BP

148
Q

cardioselective beta blocker drugs

A

atenolol
betaxolol
bisprolol
metoprolol

149
Q

vasodilating beta blocker drugs

A

carvedilol
labetalol
nebivolol

150
Q

vasodilating beta blocker

A

inhibit beta receptors
also inhibit alpha-1 receptors, causing vasodilation

151
Q

beta blocker cardia effects

A

negative chronoitropic (decr HR)
negative dromotropic (decr HR)
anti arrythmic
negative inotropic (decr contractility)
anti-ischemic
decr CO

152
Q

what drugs can cause nodal depression in the heart?

A

verapamil
diltiazem
digoxin
amiodarone

153
Q

non-vasodilating beta blockers effects

A

acute decr in CO (20%)
(compensatory reflex rise in SVR)
SVR return to baseline
chronic BP lowering

154
Q

non-vasodilating beta blockers are _____line antihypertensive

A

not a first line
- low CV protection
lowers brachial BP
does not lower central BP

155
Q

wich drug has higher mortality than other antihypertensives

A

atenolol

156
Q

beta blocker CI

A

bradycardia
- 2d degree/complete heart block
- sick sinus
severe asthma (COPD)
severe depression
cardiogenic shock
hypotension

157
Q

beta blocker smooth muscle SE

A

bronchospams
cold extremities

greater w/non-selective

158
Q

beta blocker cardiac SE

A

bradycardia
heart block
hypotension
excess negative inotropic effect

159
Q

beta blocker CNS SE

A

insomnia
derpression

greatest w/lipid soluble

160
Q

beta blocker QoL SE

A

weight gain
fatigue
erectile dysfunction

161
Q

beta blocker metabolic SE

A

loss of glycemic control
incr triglycerides
decr HDL
hides hypoglycemia

less common w/cadioselective and vasodilating BB

162
Q

beta blocker withdrawal phenomenon

A

surge of sympathetics if you stop the drug abruptly

tachycardia
incr BP

163
Q

beta blocker indications

A

ischemic heart disease
HFrEF
tachyarrythmias
2nd line antihypertensive
hyperthyroidism
migraine prevention
acute pain symptoms
glaucoma
variceal bleeding (portal hypertension/cirrhosis)

164
Q

which beta blocker is best for HFrEF

A

metoprolol, carvedilol, bisoprolol

165
Q

which beta blocker is best for migraine prevention

A

propranolol
metoprolol

166
Q

T-type Ca2+ channels

A

SA Node

opens at more negative potentials

167
Q

L-type Ca2+ channels

A

AV Node
located in vasc smooth muscle, cardiac myocytes, cardiac nodal tissue

CICR from SR
phase 0 of nodal AP
phase 2 of cardiac myocyte AP
increased by cataecholamines

168
Q

non-dihydropyridine Ca2+ channel blockers mechanism

A

bind L-type channels on vascular smooth muscle/cardiac myocytes/cardiac nodals (AV/SA)

decr Ca2+ entry into cell

169
Q

non-dihydropyridine effects

A

decr Ca2+ into cell:
- vasodilation
- decr contractility (neg inotropic)
- decr HR (neg chronotropic - AV)

170
Q

non-dihydropyridine indications

A

hypertension
tachyarrhythmia
- afib
- aflutter
angina
coronary spasm

171
Q

non-dihydropyridine drugs

A

diltiazem
verapamil

172
Q

non-dihydropyridine SE

A

flushing
headache
peripheral edema
hypotension
bradycardia
impare electrical conduction (AV block)
decr contractility

173
Q

non-dihydropyridine CI

A

bradycardia
heart conduction defects
HFrEF (EF<40%)
severe hypotension
cardiogenic shock

174
Q

non-dihydropyridine has minimal______effects

A

cardiovascular
it is very hemodynamically stable

175
Q

verapamil

A

more cardioselective
more potent HR lowering
stronger contractility suppression

176
Q

diltiazem

A

more effective vasodilator
better antihypetensive
moderate contractility suppression

177
Q

varapamil main SE

A

constipation

178
Q

dihydropyridine calcium channel blockers mechanism

A

prevent flow of Ca2+ through L-type channels in vascular smooth muscle

179
Q

dihydropyridine calcium channel blocker drugs

A

amnlodipine
felodipine
nicardipine
nifedipine

…end in -[dipine]

180
Q

dihydropyridine ca2+ blocker effects

A

vasodilation
decr SVR
decr BP

181
Q

dihydropyridine Ca2+ blocker indications

A

hypertension
chronic stable angina
coronary spasm
raynauds
hypertensive emergency
subarachnoid hemmorrhage
migraine prevention

182
Q

best DHP blocker for hypertensive emergency?

A

nicardipine
celveidipine

183
Q

best DHP for subarachnoid hemorrhage?

A

nicardipine prolonged release implants

184
Q

DHP blocker SE

A

ankle edema
flushing
headache
hypotension
reflex tachycardia

185
Q

DHP is a _______ line treatment for hypetension

A

1st line
regardless of race

186
Q

nifedipine

A

least vascular selective DHP
short acting
rapid vasodilator
worse outcomes for MI pts

187
Q

nifedipine SE

A

muscle cramps/myalgia
hypokalemia
gingival swelling
worse MI outcomes

188
Q

are longer or shorter acting DHPs preferred?

A

long acting DHPs are preferred

189
Q

direct vasodilators drugs

A

hydralazine (IV/oral)
minoxidil (oral)

190
Q

direct vasodilators mechanism

A

directly relaxing arteriolar smooth muscle
little effect on veins
decr SVR

exact mechanism unknown

191
Q

direct vasodilators indications

A

hypertension
HFrEF
- black pts
- pts who cannot tolerate ACE/ARBs
- hyperkalemia
- renal insufficiency

192
Q

which antihypertensive is commonly used to treat preeclampsia?

A

hydralazine

193
Q

which antihypertensive is used to treat poor response to other HTN drugs?

A

minoxidil

must have maxed out diuretic and 2 other anti-HTN meds

194
Q

which is more potent: hydralazine or minoxidil?

A

minoxidil is more potent

195
Q

direct vasodilator SE

A

headaches
flushing
barorecptor tachycardia
Na+/H2O retention
edema
lupus (hydralazine)
hair growth (minoxidil)
pericardial effusion (minoxidil)

196
Q

direct vasodilators CI

A

CAD (can cause angina)

197
Q

parenteral vasodilator drug

A

fenoldopam
sodium nitroprusside

198
Q

fenoldopam mechanism

A

stimulates D1-like dopamine receptors
vasodilation

199
Q

fenoldopam effects

A

rapid arteriolar vasodilation
natriuresis/diuresis
incr renal BF

200
Q

fenoldapam indications

A

hypertensive emergencies
post-op HTN
acute renal failure prevention during cardiac surgery

201
Q

fenoldapam SE

A

reflex tachycardia
headache
flushing
hypokalemia
incr ocular pressure

202
Q

fenoldapam CI

A

glaucoma (incr ocular pressure)
beta-blockers
- inhibit sympa reflex response

203
Q

nitrates mechanism

A

incr NO
- dilation of veins/arteries

204
Q

nitrates effect

A

vasodilation veins
–decr preload
vasodilation arteries (high dose)
–decr afterload (decr SVR)

decr O2 consumption by heart
incr O2 delivery to heart

205
Q

nitrate drugs

A

glyceryl trinitrate/NTG (nitroglycerin)
isosorbide dinitrate (ISDN)
isosorbide mononitrate (ISMN)

206
Q

which nitrate is a prodrug?

A

ISDN

207
Q

NTG types

A

sublingual (rapid onset)
IV
transdermal patch

208
Q

ISDN

A

prodrug
high first past metabolism (low avail)
oral (2-3x daily)

209
Q

ISMN

A

no first pass metabolism (high avail)
more predictable
1x dailty

210
Q

Nitrates indications

A

hypertension
chronic HF
angina
MI

211
Q

nitrate CI

A

right ventricular infarction
–sensitive to preload changes

212
Q

nitrate SE

A

headache
hypotension
reflex tachycardia
dizziness/syncope
tachyphylaxis (tolerance)

213
Q

sodium nitroprusside risk

A

thiocyanate toxicity due to CN- release

214
Q

nitrates drug interactions

A

PDE inhibitors

drugs potentiate effects
incr hypotension
decr coronary perfusion

(cGMP overload — massive vasodilation)

215
Q

sodium nitroprusside

A

iron
CN-
nitroso moiety

216
Q

sodium nitroprusside mechanism

A

uptake into RBCs
- release NO and CN-
NO incrs cGMP
incr cGMP == vasodilation

217
Q

sodium nitroprusside effects

A

decr preload
decr SVR/afterload

works equally in veins/arteries

218
Q

the hemodynamic effect of sodium nitroprusside is determined by

A

LV function

severely impaired LV:
- decr afterload = incr SV/CO

219
Q

nitroprusside SE

A

CN- toxicity
lactic acidosis
hedache/anxiety/vertigo/seizures
arrythmias
hypotension
coronary steal
incr ICP

220
Q

nitroprusside indications

A

hypertensive ermgencies
- aortic dissection
- pulmonary edema
acute decompensated HF
regurgitant mitral valve disease
periop hypetension (cardiac sx)

221
Q

nitroprusside requires what type of monitoring

A

continuous BP
- central line or art-line

222
Q

nitroprusside toxicity risk factors

A

prolonged treatment (>24-48 hrs)
renal issuesd
doses >2mcg/kg/min

223
Q

nitroprusside toxicity treatment

A

hydrocobalamin
sodium thiosulfate

224
Q
A

Sp: Pharm 1 (9 decks)

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