Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anesthesia Drug Test Quick Facts > Nicole's Study Guide Anes Pharm 2015 > Flashcards

Nicole's Study Guide Anes Pharm 2015 Flashcards

1
Q

SVT management drugs of choice

A

Adenosine
verapamil
diltiazem

“in SVT give A,V,D”

A>D>V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

dose of adenosine in SVT

A

6 mg rapid IV push

12 mg rapid IV push second dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

dose of verapamil in SVT

A

75-150 mcg/kg IV

= 2.5-10 mg IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

dose of diltiazem in SVT

A

SVT 5-10 mg /2 min repeat after 5 min

75-150 mcg/kg bolus of 0.2 mg/kg /2 min repeat 0.35 mg/kg bolus after 15 min

infusion 5-15 mg/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

alternatives for SVT

A

Esmolol, metoprolol, amiodarone, digoxin

DAME- the first lines didn’t work!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

dose of esmolol with SVT

A

0.5 mg/kg over 1 minute

35 mg for 70 kg pt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

dose of metoprolol for SVT

A

1-2.5 mg

repeat 2.5 min double dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

dose of amiodarone with SVT

A

150 mg IV slowly over 10 minutes

may repeat once

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

dose of digoxin in SVT

A

0.5-1 mg IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Liver failure + asthma

drugs to avoid

A

Opiods- histamine release: morphine, codeine, meperidine
NDMB- atracurium and mivacurium- histamine
non-selective BB- timolol, propranolol, labetalol
esterLA’s- PABA allergic reactiosn
Succ- histamine (OK WITH RSI) give benadryl or famotidine- H1/H2 respectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

asthma pateint questions

A

asthma severity
hospitilizations
intubations in last 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pre-treat asthmatic pt with…

A

beta-agonist (albuterol)

steriods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

drugs to use with asthma + liver failure

A

Ketamine- bronchodilator
propofol- bronchodilator
fentanyls- no histamine
NMB- pancuronium, Vec, Roc, Cisatracurium - no histamine

*if also liver NO Panc or Vec

maintenance of Cis @ 0.03 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does liver failure affect drug PD/PK

A 
increases Vd
decreased plasma protein binding of drugs
decreased clearance 
BLEEDING- caution renals
heptopulmonary or hepatorenal pathology
encephalopathy
decreased plasma pseudocholineserases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

liver failure and benzos

A

metabolism impaired

prolonged elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

liver failure prolongs the elimination of what drugs?

A 
benzos
lidocaine
meperidine
morphine
phenobarbitol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

liver failure delays the metabolism of which induction agents

A

vecuronium (50-60%) biliary)
rocuronium (70-90% biliary)
Succ- d/t decreased psudocholinesterases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which drugs are highly protein bound that liver failure effects

A

opiods
benzo
increased free drug with hypoalbuinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

drugs preferred for induction with liver failure and asthma

A

etomidate
propofol
iso
cisatracurium (metabolism independent of liver may need larger dose because Vd is increased - use PNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

plan for liver failure induction with asthma

A 
Versed 1-2 mg
lidocain 1 mg/kg
fentanyl 1mcg/kg
propofol 1-1.5 mg/kg
succs 1-1/5 mg/kg
cisatracurium for maintenance NMB 0.03mg/kg
sevo 2% 
reverse
*fentanyl * albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what can cross the BBB

A 
water- unpolarized
CO2- small
O2-small
lipid-soluble free forms of steroids
glucose- via GLUT1 transporters
Thyroid hormones
organic acids
choline
nucleic acid precursors
neutral, basic, and acidic amino acids in BBB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

CAN NOT cross BBB

A 
protiens
polypeptides
ionized/charged
water soluble drugs- lipophilic
large molecules
highly protein bound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

are NMB lipophilic or hydrophilic

A

hydrophilic- degree of ionization determined by dissociation constatnt pKa of agent and its pKa gradient HIGHLY ionized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what affects/can alter the BBB

A 
being a neonate- immature
uremia
head trauma
infections
tumors
strokes
seizures- sustained
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

do local anesthetics pass the BBB?

A

they can- unbound lipophilic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what 5 factors contribute to crossing the BBB

A

serum concentration (passive diffusion)
active transport (“in” or “out”)
lipophilicity (predisposition to dissolve in fat vs water)
the electrical charge (polarity)
molecular size and configuration (bulk not purely molecular weight but also the way the molecule aligns)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

which anticholinergics cross the BBB?

A

ONLY tertiary amines- atropine, scopolamine (have CNS effects)
glycopyrolate does NOT quaternary amine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

which Ach-ase-Inhibitors cross the BBB?

A

ONLY physostigmine to reverse anticholinergic effects too

AChase- Inhibitors: neostigmine and edrophonium have quarternary ammonium structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

where does parkinson’s affect the CNS

A

dopamine containing neurons of the substantial nigra

neurodegenerative disease`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

EPS symptoms of Parkinson’s

A

extrapyramidal motor dysfunction
tremor (pill rolling)
rigidity
hypokinesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the goal of treatment with parkinson’s

A

increase dopamine in the basal ganglia (not periphery)

decrease s/e of Ach on neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what drugs are patients with Parkinson’s likely taking?

A

levodopa
MAO-B Inhibitors (selegiliine, rasagiline)
SSRI- concern with 5Ht3 blockers risk seratonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what medications should be avoided with a pt with parkinson’s

A

Ephedrine b/c MAO-B -I use
antidopaminergics (butyrophenones = haloperidol and droperidol) butyrophenones, phenothiazines, phenergan metoclopramide - all reverse dopamine effects at the basal gaglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which anti-emetics can be used in Parkinsons?

A

5HT3 antagonists = -onsetron
i.e. ondansetron 4 mg 30 minutes before emergence

H1 antagonist diphenhydramine- (10-50 mg IV) Benadryl 25 mg

NK1 receptor blocker - 5-HT blocker of substance P- 3 hours before ages- 8-12 hours active chemo drug = Aprepitant

steriod = Dexamethasone 2.5-10 mg IV 4 mg!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

anti emetics to AVOID with Parkinsons

A

Promethazine
Droperidol- no antidopaminergic drugs
Metoclopramide - Reglan- antagonizes central and peripheral dopamin receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

considerations with N/V

A

make sure adequate volume recitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the systemic clinical effects of repeated dosing of narcan?

A 
discomfort
withdrawl
reversal of RD
catecholamine release
pulmonary edema
sudden death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the systemic side effects of repeated dosing of narcan?

A 
HTN
CV instability
increased HR
pulmonary edema
nausea
vomiting
sweating
tachycardia
seizures
pulmonary edema
arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

how does RD compare to analgesia with opiods- how does this effects narcan dosing?

A

RD from opiods occurs at higher receptor occupancy rates than analgesia
Analgesia is NOT compromised with CAREFUL titration of naloxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the opoid overdose dose of narcan/naloxone

A

0.4-2 mg/dose
titrate SLOWLY 0.1-0.2 mg to start
q 2-3 incremental increases * usually no more than 0.2 needed

dilute 0.4mg in 9mL NS = 0.04mg/mL and give 0.5-1mcg/kg q 3-5 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are the s/e of rapid withdrawal or unmasking of pain by narcan

A 
catecholamine replease!
pain
htn
sweating
agitation
irritabilty
vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

MOA of naloxone

A

derivative of oxymorphone
small structural change converts to pure ovoid antagonist
NO agonist properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

onset of naloxone

A

1-3 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

duration of naloxone

A

60 minutes
CAUTION- may have to redoes d/t renarcotization
caution with liver failure

RAPIDLY metabolized by the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Demerol:morphine potency

A

0.1x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

morphine:morphine potency

A

1x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

hydromorphone:morphine potency

A

8x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

alfentanil:morphine potency

A

10x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

fentanyl:morphine potency

A

100x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

remifentanil:morphine potency

A

100 (some sources say 200)x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

sufentanil:morphine potency

A

1000x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

where is epidural location?

A

Outside the dura mater

contains blood vessels nerve roots fat connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

where is the spinal space located

A

Spinal-intrathecal- subarachnoid
= between arachnid and piamater
baths the spinal cord- CSF is here

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

which opiods are hydrophilic?

A

Morphine
Hydromorphone
meperidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

which opiods are LIPOphilic

A 
Fentanyls love FAT
Fentanyl
sufentanil
alfentanil
remifentanil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

rank the fentanils in order of lipophiliciry

A

sufentenil (1600 x’s MS04)
fentanyl (800x MSO4)
Alfentanil
Remifentanil least- rapidly off b/c of ester hydrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what property of the drug does lipophilic/hydrophilic affect the most?

A

PEAK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how is the peak affected by lipophilicity?

A

Morphine is hydrophilic- SLOWER peak

fentanyl is the least lipophilic of the fentanils and still peaks in only 20 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is the peak of sufentanil

A

6-8 minuts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is the peak of morphine and why is it this time?

A

1-4 hours

because it is hydrophilic and peaks slower- slower to cross the dura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is the greatest risk of opiods intrathecally?

A

Respiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

how is the RD different for the hydrophilic vs. the lipophilic drugs

A

Neuroaxial opioid RD occurs in 2 way
1- early phase- systemic absorption with parenteral dosing- similar with all fentanyls- lipophilic

2- insidious depressoin- 8-12 hours
rostral flow of CSF delivery of morphine to the brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

describe the properties of lipophilic opiods epidural/intrathecal doses

A 
Fentanyls
rapid absorbed into the spinal tissues 
FASTER onset
Smaller area of distribution
more limited area of analgesia
faster clearance of the drug out of the epidural and intrathecal space
shorter duration of action
higher blood concentrations of the opioid 
GOOD for selective anesthesia
64
Q

asthmatic treatment with Des v. Iso v. Halothane

A

Des- pungent-airway irriatant- bronchodilator
Iso- less pungent than des-
halothane-bronchodilator but hepatotoxic

65
Q

Vapor pressure and MAC of Des, Iso, Halothane

A

Halothan- 243/0.75
Iso- 240/1.2
Des- 669/6
Sevo- 160/2

66
Q

local anesthetics are weak-

A

bases

67
Q

infected tissue is…

A

acidic

68
Q

weak base in acid =

A

Ionization increases
water soluble
-locals loose their effect when they are more ionized
it is the LIPID soluble- NON-ionized portion of the local that takes effect

69
Q

-locals loose their effect when..

A

they are more ionized
it is the LIPID soluble- NON-ionized portion of the local that takes effect
can not cross fatty nerve sheeth- NOT effective

70
Q

what determines the degree of ionization for an individual drug?

A

pKa of the agent
AND
its pKa gradient across the membrane

71
Q

acids are…

A

proton donors

72
Q

bases are…

A

proton acceptors

73
Q

where do local anesthetics act

A

uncharged form crosses the neuronal cell membrane

acts on the Na channel INSIDE

74
Q

what does the ability to counteract a non depolarizing blocking agent depend on?

A

the amount of spontaneous recovery before the administration of a reversal drug

75
Q

how much time is required for several of anticholinesterse take?

A

15-30 minutes

76
Q

when should you reverse with anti cholinesterase drugs?

A

alway

4 hours or less and even 4/4 twiches still may have unto 75% blocked

77
Q

what else could be affecting prolonged blockade after NMDA

A 
overdose
inadequate reversal dose
adjunctive agents contributing to the pt weakness
metabolism of relaxant decreased
excretion of the relaxant slowed
acid-base status
temp
age
drug interactions
78
Q

what is the MAX DOSE of neostigmine?

A

0.07 mg/kg

5 mg total

79
Q

what diseases affect neuromuscular blockade reversal with a ACHE-Inhibitor

A

Myasthenia Gravis

over treatment with ACH can precipitate cholinergic crisis

80
Q

when should reversal agent not be given for a NMBA

A

when 0-2 twitches are present
TOF stimulation 2 or less may have prolonged recovery
do not attempt until T1 > 25%

0 twitches- 95% ACh receptor blocked
90% = 1 twitch
80% = 2 twitch
75= 3 twitch
4 twitch  STILL can have just under 75% blocked!!
81
Q

when TOF > 0.9 how long is the block typically

A

15 minutes

82
Q

all acetecholinesterase- Inhibitors all experience

A

a ceiling effect
lower doses may be just as effective

overdose in fact may lead to ACh on muscarinic and nicotinic receptors in PNS- leading to bradycardia, prolonged QT, systole

MUST maintain airway- Sp02, CV monitor, BP, CRNA to stay with pt

Reintubate if needed

83
Q

intermediate active NMBA

A

vecuronium
rocuronium
cisatricurium
atracurium

84
Q

what drug interactions prolong NMBA

A

halogenated agents
when continued after neostigmine administration
prolong time to full reversal
EVEN when d/c at time of reversal that is OK- b/c of wash out
aminoglycosides
Mg

85
Q

what happens if you exceed the max dosage of reversal agent of a NMBA?

A

choACh accumulates in sufficient amounts at the NMJ
ACh is sustained
block develops just as it would with Sch.

86
Q

what are the s/s of excessive Anti-cholinesterase activity?

A 
cholinergic overactivity
bradcardia
increased secretions
Abdominal cramp
n/v
resp distress
miosis
skeletal muscle paralysis
weakness
87
Q

what do you give to treat overdose of anti-cholinesterase drugs?

A

Atropine

88
Q

electrolyte imbalance that may prolong paralysis

A

Hypomagnesium
hypokalsemia
hypophosphatemia
hypocalcemia

89
Q

what electrolyte is affected by Succinylcholine?

A

Potassium
0.5-1 mEq/L increase
within 3 minutes
for 10-15 minutes

90
Q

why does K increase with Succ administration?

A

When the muscle depolarizes-
Na influx and K efflux occurs
this efflux = potassium release during normal muscle
do influx back of K slow to enter back into cell
signaling and the response to Succ

91
Q

What pathologic states result in an up-regulatoin (increase) of AChRs spreading throughout the muscle membrane

A 
Upper or lower motor denervation
infection
direct muscle trauma
muscle tumor
muscle inflammation
burn injury
immobilization- disuse atrophy
prolonged chemical denervation by muscle relaxants, drugs or toxins (NDMR, Mg, clostridial toxin)
muscular dystrophies
92
Q

where are AChR in the normally innervated mature muscle

A

only in the junctional area

93
Q

what depolarizes the nicotinic actylcholine receptors in the muscle that leads to hyperkalemia?

A

ACh
Succ
AND choline

94
Q

when are ACh receptors up-greulated after a burn and Succ is unsafe to give?

A

24-48 hours

95
Q

when is it ok to use Succ in a post-burn victim?

A

NEVER

96
Q

how do you treat hyperkalemia from Succ- emergently?

A

promote the cellular uptake of K
insulin with glucose
catecholamines
sodium bicarbonate

97
Q

what are the most common causes of delayed awakening during emergence?

A

prolonged action of anesthetic drugs
metabolic causes
neurologic injury

98
Q

what is the most common cause of delayed awakening?

A

prolonged action of anesthetic drugs

99
Q

why does prolonged action of anesthetic drugs occur?

A

secondary to alterations in drug PK/PD
pt status
hypoventilation
combo anesthsia- opiods, IV anesthetics, inhalational agetns

100
Q

PK alterations leading do delayed awakening

A

changes in drug distribution secondary to
mobilization of drugs from body tissue stores
redistribution
decreased protien binding
changes in metabolism
excretion secondary to renal or hepatic dysfunction

101
Q

PD alterations leading to delayed awakening

A

increased pt sensitivity to drug effects b/c of extremes of age
hypothermia
concomitant alcohol or drug use

102
Q

who is at risk for delayed awakening?

A

pre-existing cognitive or psych disorders
chronically take sedatives
intoxicated etoh/drugs at the time of induction
physically exhausted prior to surgery

103
Q

how does hypoventilation affect inhalational drugs

A

hypoventilation limits exhalation
prolongs elimination of inhalational agents \
CO2 narcosis

104
Q

how do benzodiazepines affects delayed awakening?

A

long-acting benzos (lorazepam and diazepam) may contribute to delayed awaking
esp. in elderly

105
Q

what herbal supplements affect emergence?

A

delayed: kava kava, St. John’s wart, valerian

106
Q

metabolic causes of delayed awakening

A

Hypoglycemia *monitor diabetics peri and post ob BG!
hyperglycemia
electrolyte imbalance - Na, Ca, Mg

107
Q

what electrolyte imbalance occurs post TURP that leads to delayed emergence?

A

dilutional hyponatremia
transurethral prostate resection
sedation, coma, hemiparesis

108
Q

conditions that lead to HHNK

A 
BG > 600 mg/dL
can lead to sedation post-op/delayed emergence
type 2 DM
severe dehydration (esp old)
uremia
pancreatitis
sepsis
pneumonia
CVA
large surface burns
109
Q

hypocalcemia post parathyroidectomy can lead to

A

delayed awakening

110
Q

hyperMg from prolonged MgSO4 during labor with pre-eclamptic pt may result in

A

sedation, muscle weakness after general/regional

111
Q

what are potential causes of neurologic injury responsible for delayed awakening?

A 
RARE
CVA
Intracranial hemorrhage
IICP
HTN uncontrolled
air/fat emboli
HypoTN uncontrolled esp if previously a HTN pt with carotid disease
112
Q

how to manage a pt on a BB post op bradycardia

given succs, propofol, and vec

A

1) perfusion, pulses, blood pressure, O2
2) baseline HR- consider 12 lead EKG for underlying rhythm/electrolyte disturbances
3) hold next dose of atenolol
4) if stable monitor, cardiology, fluids
5) if hypotensive, SOB, CP, diaphoresis, decreased pulses
- O2/ventilate if needed, - glyco 0.2 mg or atropine 0.5 mg if severe, Ephedrine 5-10 mg, Epi 10-20 mcg’s or infusion of epi 2-10 mcg/min or transcutaneous pace until cards can place temporary pacing wires

113
Q

during a lap chili- pneumoperitoneum is created- bradycardia and dropping actions include:

A 
Ask surgeon to release pressure
admin 100% O2
increase IV fluids to increase preload
assess for 4 possible complications
consider medications 
transcutaneous pacing? @ 80 bpm
ABG, hemoglobin, lytes
EKG troponins
114
Q

Intra-abdominal pressure

A

increased venous return
increased CO
hypertension

115
Q

Intra-abdominal pressure > 15 s/e

A

decreased venous return
decreased CO
hypotension

116
Q

bradycardia during intrabdominal surrey causes:

A

IIAP
vagal stimulation- trochar CO2 emboli, mesentary stretch
reduced lung volumes, PAP increased, V/Q mismatch, pneumothorax
IICP
decreased blood flow

117
Q

4 possible complications of pneumoperitoneum

A

pneumomediastinum
pneumopericardium
pneumothorax
CO2 gas embolism

118
Q

what medications to give in bradycardia post pneumomediastinum lap chile?

A

BP and pulse check
Ephedrine 5-10 mg
glycopyrolate 0.2 mg or atropine 0.5 mg
ACLS doses if PEA/Asystole

119
Q

max dose of atropine

A

3 mg

120
Q

infusions to consider during unstable bradycardia

A

dopamine 2-20 mcg/kg/min

epinephrine 2-10mcg/min

121
Q

PEA arrest steps

A

1) call for help
2) CPR 100/min >2 in deep ETCO2 >10
3) turn off agent 100% FiO2
4) 10 breaths/min NO over vent
5) IV good, IO?, Art?
6) Epinephrine 1 mg 3-5 min
7) vasopressin 40 units x1
8) rhythm check Vt/Vf shockable
9) causes- Hemorrhage, anesthetic overdose, septic shock, shock, auto PEEP, anaphylaxis, med error, high spinal, pneumo, local anes tox, vagal stimulation, PE
H &T

122
Q

causes of PEA arrest

A 
Hemorrhage
anesthetic overdose
septic shock, shock
auto PEEP
anaphylaxis
med error
 high spinal
pneumo
local anes tox
vagal stimulation
PE
123
Q

Pt has a spinal and now BP is 80/40 hypotensive- how would you treat this?

A

sympathetic blockade in1) Fluids

2) Ephedrine is bradycardia 5-10 mg
3) Phenylephrine is normal/tachy - 10-20 mcg (may decrease CO because increased SVR)
4) dopamine? low dose consider
5) vassopression 2-4 units consider if RAAS depressed

124
Q

why does hypotension occur with neuroaxial blockade?

A

sympathetic blockade -> arterial vasodilation
decreased SVR
venous pooling
reduction in venous return

125
Q

a high block can cause what CV complication?

A

T1-T4 blockade = sympathetic innervation of the heart is blocked
cardiac accelerators anesthetized
vagal fibers and heart rate slows leading to HYPOTENSION

126
Q

what factors are involved in the cardiovascular response to neuroaxial anesthesia?

A

baroreceptor reflex
volume receptor reflexes
decreased central sympathetic outflow
-loss of ability to handle normal CV stresses and normal CV homeostatic reflexes

127
Q

what is allowable decrease in BP?

A

20%

*previously HTN or elderly with CA disease

128
Q

pre-treating with fluids for hypotension induced by spinal

A

15mL/kg of glucose free crystalloid or colloid solutions
15 minutes pre-op
including post-op deficits by NPO status

129
Q

which vasoactives are more effective for spinal induced bradycardia?

A

alpha and beta adrenergic active- IE ephedrine

phenylephrine is only an alpha agonist- will not increase HR

130
Q 
lap chole 
DM
hx- PONV
hx- spontaneous pneumothorax
what gas would you not give and why not?
A

Nitrous:

PONV - activation of chemoreceptor trigger zone and the vomiting center in the medulla

potential for pneumo
N2O can expand a pneumothorax to double or triple its site in 10 to 30 minutes respectively

expansion of air filled structures/bubbles

131
Q

what is the property of N2O that allows it to worsen pneumothorax?

A

greater solubility in blood compared to nitrogen

diffuses into air-containing cavities more rapidly than nitrogen is absorbed by the blood spream

N20 delivered to a patient diffuses from the blood into these closed gas spaces easily- until the partial pressure equals that of the blood and alveoli
complaint spaces will expand until sufficient pressure is generated to oppose N20

132
Q

how much more soluble is N20 than nitrogen in the blood?

A

35 X

*N20 is insoluble compared to other inhalation agents

133
Q

how would you induce a pt with open globe emergently- intoxicated, smokes, MJ

A

succ- rapid sequence full stomach is more of the concern!
IOP will increase, but aspiration is more likely
-research does not support extrusion of ocular contents
-coughing must be avoided also

*modified RSI with >1 mg/kg (0.6-1.2)of Roc approaches the onset of Succ
K replacement
decrease mac d/t etoh decrase opioids and benzos

134
Q

how much dose such increase IOP and for how long

A

5-10 mmHg

for 5-10 minutes

135
Q

what induction/anesthetic agents increase IOP or should be avoided?

A

Succ
and ketamine- unclear by how much
etomidate- risk of myoclonus

136
Q

what drugs and dose for induction with open globe?

A

lidocaine 1.5 mg/kg to blunt the response to laryngoscopy
opioid other option-
remifentanil 0.5-1 mcg/kg
alfentanil 20 mcg/kg
propofol- rapid onset but does not blunt sympathetic response to DL
fentanyl 1-3 mcg/kg
esmolol 0.5-1 mg/kg

137
Q

how should you manage open globe with full stomach

A 
NO NG- may make them cough/gag IIOP
metoclopramide 10mg
Ranitidine 50 mg
cimetidine 300 mg
famotidine 20 mg
all options
must give anti-emetic before extubation need to avoid vomiting IIOP
138
Q

If you give Succ what should you give also with an open globe injury on induction

A

defaciculating dose of Rocuronium

atropine or glyco- decrease oculocardiac reflex

139
Q

How to treat a bronchospasm

A

1) 100% 02
2) I:E to allow for adequate exhalation 1:3
3) deepen agent- use sego
4) rule out maintop, kink, secretions
5) Beta 2 agonist- albuterol, ipratropium
6) Consider epinephrine @ 10 mcg IV increase PRN
7) Ketamine 0.2-1 mg/kg IV
8) hydrocortisone 100 mg IV
9) nebulized racemid epinephrine
10) R/u anaphylaxis
11) ABGs

140
Q

s/sx of bronchospasm

A

1) increased peak airway pressure
2) wheezing on lung exam
3) increased expiratory time
4) increased ETCO2- UPSLOPING
5) decreased tidal volumes if pressure control

141
Q

How do you sedate a pt with multiple allergies

A

1) ASK QUESTIONS- egg allergy- do you eat them, do you eat products with eggs cooked in it- what happens- do you get a flu shot- if YES then proposal OK
2) pre-med for allergic rxn.

142
Q

how do you treat a beta blocker overdose?

A 
ABC #1 stabilize airway breathing circulation 
bolus of IV fluids 
atropine 1 mg IV unto 3 doses #1 for brady/hypotension
IV glucagon- 
IV calcium slats
vasopressor
IV high dose insulin (with glucose)
IV lipid
143
Q

s/sx of BB overdose?

A

hypotension and bradycardia
Electrocardiogram - show PR prolongation or any bradydysrhythmia
hyperkalemia
hypoglycemia

144
Q

IV glucacon dose in BB overdose

A

5 mg IV bolus

145
Q

dose of calcium chloride in BB overdose

A

10-20 mL of 10% solution or

146
Q

calcium gluconate IV dose in BB overdose

A

30-60 mL of 10% solution

147
Q

high-dose insulin and glucose dose in BB overdose

A

1 unit/kg bolus IV regular insulin short acting THEN
continuous infusion 0.5 units/kg per hour
titrate until hypotension is corrected
MAX 2 units/ kg

148
Q

which vasopressor to use for BB overdose

A

ephedrine 5-10 mg

149
Q

lipid emulsion dose in BB overdose

A
  1. 5 mg/kg over 2 minutes

1. 5 mL/kg infusion over 60 minutes

150
Q

Carotid endarterectomy hypotension and bradycardia considerations:

A 
Carotid sinus baroreceptors 
cerebral perfusion
no less than 20% change
Ephedrine with brady
phenylephine with tacky
Fluids- crystalloi/colloid depending on comorbidities
151
Q

AA male HTN peri-op how to treat this

A

no > 20% increase
ok to start case if chronic

Increase sedation- gas
give proposal
pain medication
give esmolol 10-20 mg or gtts
nipride gtts
152
Q

Characteristics of depolarizing NMB

A

ACh agonist
binds to nicotinic ACh receptors
generate AP
Phase 1 block : depolarize NMB NOT degraded by Achase
NO FADE- Na inactivated- confirmational change- BOTH subunits bound

Phase 2 block: resembles NDNMB - FADES

153
Q

characteristics of Non-depolarizing block

A

ACh antagonists binds to nicotinic ACh receptors
no conformational change- JUST block
only 1 alpha subunit bound for blockade

FADE in PNS

prejunctionally also block ACh receptors
decreasing mobilization of ACh and this is seen with contraction fade

154
Q

which induction drugs should you avoid with renal failure?

A

pancuronium

vecuronium

155
Q

B1 selective Beta blockers

A

Atenolol
Metoprolol
Esmolol

156
Q

Asthma avoid…. MAST drugs

A

Mivacurium
Atricurium
Succs
Temolol (B non selective drugs)

157
Q

contraindications with Succ

A

persons with personal or familial history of malignant hyperthermia
skeletal muscle myopathies
known hypersensitivity to the drug.

patients after the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury,

because succinylcholine administered to such individuals may result in severe hyperkalemia which may result in cardiac arrest

Anesthesia Drug Test Quick Facts (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions