Brainscape's Knowledge GenomeTM

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


See full index

OMS III > Emerg Med > Flashcards

Emerg Med Flashcards

1
Q

Initial management of poisoning

GI emptying

A

gastric lavage may be used in the first 2 hours of ingestion. it is dangerous if altered mental status bc pt may aspirate, and causti ingestion causes burning of the esophagus and oropharynx

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

Gastric lavage

A

removes 50% of pills at 1 hour and 15% at 2 hours

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

ipecac in ER

A

always the wrong answer

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

Initial management of poisoning

ipecac

A

althoug ipecac has been used as a home remed in those with accidental overdose or pill injestion prior to coming to the hospital. there is no benefit in using ipecac in the hopstial. ipecac needs 15 to 20 minutes to work and dleays the administartion of antidoes

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

Initial management of poisoning

cathartics

A

sorbitol are always the wrong answer. speeding up gi tranist time does not elminate the ingestion without absorption

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

Initial management of poisoning

forced diuresis

A

giving fluids and diuretics to accelearte urinary excretion is always a wrong answer more pts are harmed iwth pulmonary edema with this method than are helped

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

Initial management of poisoning

whole bowel irrigation

A

placing a gastric tube and flushing out the GI tract with polyethylene glycol-electrolyte solution is almost always wrong. indications are massibe ironr ingestion, lithium, and swallowing drug-filled packets (smuggling)

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

Gastric emptying is always wrong with

A

caustics ( acids and alkali)

altered mental status

acetaminophen oerdose

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

when the answer is not clear and the cause of overdose is asked say

A

acetaminphen or aspirin

they are the most common cause of death by overdose

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

what is useless or dangerous with overdose

A

ipecac, forced diuresis, cathartics

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

best initial management of unknown od with altered mental status

A

opiate antagonist and glucose if this does not work then perfomr intubation to protect the airway possibly followed by a gastric lavage

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

when do you do psych consult with overdose

A

from a suicide attempt, but it is wrong when spcific antidotes and diagnostic tests are needed. you do not need a contultant to tell you to give naloxone and dextrose

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

opiate ovverdose

A

is fatal; give naloxone immediately

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

benzo overdose

A

is not fatal and acute withdrawal causes seizures, do not give flumazenil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

initial management of poisoning

charcoal

A

charcoal is benign and hsould be given to anyone with a pill overdose. charcoal may not be effective for every overdose, but it is not dangerous in anyone. charcoal can also remove toxic substances even after they have been absorbd. blood levels of toxins drop faster in those given repeated odses of charcoal.

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

charcoal is superior to

A

lavage and ipecac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when you dont know what to do intoxicology give

A

charcoal

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

Acetaminophen overdose

A

legal drugs kill more people in the US than illegal drugs bc they are less expensive and more available. toxicity of acetaminphen may occur with ingestions greater than 8 to 10 grams. fatality may occur with ingestion above 12 to 15 grams.

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

Four most common acetaminophen overdose question

A
  1. if a clearly toxic amount of acetaminophen has been ingested (more than 8-10 grams) the answer is n-acetylcysteine
  2. if the overdose was more than 24 hours ago, there is no therapy
  3. if the amount of ingestion is unclear, get a drug level.
  4. charcoal does not make n-acetylcsyteine ineffective. charcoal is not ci with n acetycysteine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Aspirin Overdose

the most common question is what is the most likely diagnosis

A

look for:

tinnitus and hyperventilation

respiratory alkalossi progressing to metabolic acidosis

renal toxicity and altered mental status

increased anion gap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Aspirin causes

A

Aspirin causes diffuse, multisystem toxicity. it caues ARDS. it interferes with prothrombin production and raises the PT. the metabolic acidosis is from lactate. aspirine interfers with ocidative phosphorylation and results in anaerobic glucose metabolism, which produces lactate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Aspirin overdose treatement

A

alkalize the urine which increases the rate of aspirin excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

alcoholism ecreases the amount of

A

acetaminophen needed to cause toxicity

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

keys to diagnosing aspirin overdose

A

tinnitus, respiratory alkalosis, and metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

know what in aspirin overdose

A

blood gas

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

benzos can prevent seizures from

A

tcas

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

what test to run with tcas ovrdose and what dose it show

A

ekg, it shows torsades de pointes bc it prolongs the qt

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

TCA toxicity

A

can cause seizures and arrhytmia leading to death. a wide QRS will tell who is about to have an arrhytmia

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

tcas cause signs of anticholinergic effects like:

A

dry mouth

constipation

urinary retention

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

TCA overdose treatment

A

sodium bicarb. this will protect the heart against arrhytmia. it does not increase urinary excretion of TCAs as it does for aspirin

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

Caustics ingestion

A

caustic ingestion of acids and alkalis (eg drain cleaner) causes mechanical damage to the oropharynx, esophagus, and stomach including perforation.

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

caustic ingestion treatment

A

do not give alkalis or acids to neutralize the other. this would cause heat rom an exothermic rxn and would only make it worse

flush them out. use a lot of water. endoscopy is done to assess the degree of damage

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

Carbon Monoxide Poisoning

overview

A

the most common cause of death in fires. 60% of deaths on the first day after a fire are more from CO poisoning

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

Carbon Monoxide Poisoning

look for a hx of

A

gas heaters or wood burning stoves

automobile exhaust, particularly in an enclosed environment

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

Carbon Monoxide Poisoning

pathology

A

CO binds to hb so tightly that carboxyhemoglobin will not release oxygen to tissues. carboxyhemoglobin acts fucntionally like anemia. there is no functional difference between the absence of blood and carboxyhemoglobing; 60% carboxyhemoglobin acts like th the loss of 60% of blood.

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

Carbon Monoxide Poisoning

presents with

A

dyspnea, lightheadedness, confusion, seizures, and ultimately death from an mi

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

the left ventricle cannot distinguish between

A

anemia, carboxyhemoglobin and a stenosis of coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

co poisoning give a normal

A

po2 bc oxygen does not detah from hemoglobin, this causes lactic acid to build up and you get acidotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Carbon Monoxide Poisoning

test

A

since rouine oximetry will be falsely normal, the most accurate test is a level of carbosyhemoglobin. yuo should expect a low bicar and a low ph

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

Carbon Monoxide Poisoning

therapy

A

best initial therapy is to remove the pt from exposure and give 100% oxygen, which detaches carbon monoxide from hemoglobin and shortens the half-lifeof carboxyhemoglobin. if severe then treat with hyperbaric oxygen, it shortens the half-life of co even more than 100% o2

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

Carbon Monoxide Poisoning severe sx

A

CNS sx

cardiac sx

metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Methemoglobinemia

A

is oxidized hb that is locked into the ferric state. oxidized hb is brown and will not carry oxygen.

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

methemoglobinemia occurs

A

from an idiosyncratic rxn of hb to certain drugs like:

benzocaine and other anesthetics

nitrites and nitroglycerin

dapsone

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

Methemoglobinemia presentation

A

similar to carboxyhemoglobin bc o2 is not delivered to teh tissues. severe sx occur when blood levels rise above 40-50%. there is no functional difference for end organs such as the brain and heart

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

Methemoglobinemia

sx

A

dyspnea and cyanosis

headache, confusion, and seizures

,metabolic acidosis

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

Methemoglobinemia

diagnostic tests

A

can give a normal p02 on blood gas

most accurate test is a mehemoglobin level

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

Methemoglobinemia

therapy

A

best initial therapy is 100% oxygen

most effective therapy is methylene blue which decreases the half-life of mehemoglobing

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

what color is blood with carbon monoxied

A

abnormally red

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

what color is blood with methemoglobinemia

A

abnormally brown

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

cyanosis+normal po2=

A

mehemoglobinemia

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

Organophosphate poisoning and nerve gas

A

Organophosphate poisoning and nerve gas are identical in their effects. nerve gas is faster and more severe. it ccauses a massive increase in the level of acetylcholine by inhibiting its metabolism

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

Organophosphate poisoning and nerve gas

presentation

A

salivation

lacrimation

polyuria

diarrhea

bronchospasm, bronchorrhea, and respiratory arrest if severe

sludge bc these are cholinergic effects

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

acetylcholine causes

A

constriction of bronchi and an increase in bronchial secretions

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

Organophosphate poisoning and nerve gas are absorbed

A

through the skin

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

Organophosphate poisoning and nerve gas

treatment

A

atropine blocks the efffects of acetylcholine

pralidoxime is the antidote and it works by reactivating acetylcholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Digoxin toxicity

etiology

A

hypokalemia predisposes to digoxin toxicity bc potassium and digoxin compete for binding at the same site on the sodium/potassium ATPase. when less potassium is boiund, more digoxin is bound

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

Digoxin toxicity

presentation

A

the most common presentation of Digoxin toxicity is gi problems like nausea vomiting and abdominal pain

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

Digoxin toxicity

other sx

A

heyperkalemia from inhibition of saodium ptassium atapase

confusion

visula distrubance such as yellow halos around objects

rhythm disturbance (bradycardia atrial tachy av block binriculara ectopy and arrhythmias suh as atrial fib with a slow rate)

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

Digoxin toxicity

diagnostic tests

A

the moat accurate test is a digoxin level. the best initial test are k level and an ekg. the ekg will show a downloping of the St segment in all eads. atrial tachy with variable av block is the most common digoxin toxic arrhythmia

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

Digoxin toxicity

treatment

A

control k and give digoxin-specific antibodies. digoxin-binding antiboides will rapidly remove digoxin from circulation

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

hypokalemia>

A

digoxin toxicity

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

digoxin toxicity>

A

hyperkalemia

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

digoxin can produce

A

any arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

The strongest indication for digoxin-binding antibodies are

A

CNS and cardiac involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Lead poisoning

presentation

A

abdominal pain (lead colic)

renal tubule toxicity (ATN)

anemia (sideroblastic)

peripheral neuropathies such as wrist drop

CNS abnormalities such as memory loss and confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Lead poisoning

diagnostic tests

A

most accurate test is a lead level. lead interferes with hb production. this gies anemia. the best initial diagnostic test is an increased level of free erythrocyte protorphyrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

The most accurate test for sideroblastic anemia is a

A

prussian blue stain

this detects increased iron built up in red cell mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Lead poisoning

treatment

A

chelating agnets remove lead fromt he body. succimer is the only oral form of lead chelator. ethylenediaminetetracetic acid (EDTA) and dimercaprol (BAL) are parenteral agents taht bind and remove lead from the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Mercury Poisoning

overview

A

orally ingested mercury causes neurological problems. inhlaed mercury vapor produces lun toxicity that presents as interstitial fibrosis. neurological problems present with pts who are nerous, jittery, twitchy, and somtimes hallucinatory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Mercury poisoning

therapy

A

there is no therapy to reverse the pulmonary toxicity. chelating agents can remove mercury fromt he body. chelating agents such as dimercaprol and succimer are effective in removing mercury form the body and decreasing neurological toxicity. this can prevent progression of pulmonary disease, but cannot reverse fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Toxic Alcohols: methanol and ethylene glycol

A

both produce intoxication and metabolic acidosis with an increased gap. both give an osmolar gap and are treated with fomepizole and dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Methanol toxicity

Source -

toxic metabolite -

presentation -

initial diagnostic abnormality -

A

Source - wood alcohol, cleaning solutions, paint thinner

toxic metabolite - formic acid/formaldehyde

presentation - ocular toxicity

initial diagnostic abnormality - retinal inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Ethylene glycol toxicity

Source -

toxic metabolite -

presentation -

initial diagnostic abnormality -

A

Source - antifreeze

toxic metabolite - oxalic acid/oxalate

presentation - renal toxicity

initial diagnostic abnormality - hypcalcemia, envelope-shpaed oxalate crystals in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Osmolar Gap

A

the osmolar gap is the difference between the measured serum osmolality and the calculated osmolality

serum osmolality = 2 times the sodium + BUN/2.8 + glucose/18

if you calculare the serum osmolality to be 300, but on measurement you find the osmolality to be 350, it is possible that a toxic alcohol such as methanol or ethylene glycol is accounting for the extra osmoles. ordinary alchohol (ethanol) also increase the osmolar gap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Toxic Alcohols: methanol and ethylene glycol

treatment

A

the best initial therapy is fomepizole, which inhibits alcohol dehydrogenase and prevents the production of the toxic metabolite. fomepizole does not remove the substance fromt he body. only dialysis will effectively remove methanol and ethylene glycol from the body

76
Q

Snake Bites

A

the most common injury from snake bites is the local wound 25-35% of bites are not deep enough to deliver venom to the bloodstream, but they do deposit venom into the tissues. proteases and lipases in the venom damage tissue locally.

77
Q

Death from snake bites is from

A

hemolytic toxin: hemolysis and DIC and damage to the endothelial lining of tissues

neeruotoxin: can result in respiratory paralysis, ptosis, dysphagia, and diplopia

78
Q

ineffective snake bite treatment

A

tourniquests blocking arterial flow

ice

incision and suction, especially by mouth

79
Q

beneficial therapy

A

pressure

immobilization decreases movement of venom

antivenin

80
Q

spider bites

A

all spider bites present with a sudden, sharp pain that the pt may describe as “I stepped on a nail” or “a piece of glass was in my shoe”

81
Q

Black widow bite

presentation -

lab test abnormalities -

treatment -

A

presentation - abdominal muscle pain, muscle pain

lab test abnormalities - hypocalcemia

treatment - calcium, antivenin

82
Q

Brown Recluse

presentation -

lab test abnormalities -

treatment -

A

presentation - local skin necrosis, bullae, and blebs

lab test abnormalities - none

treatment - debridement, steroids, dapsone

83
Q

Dog, cat, and human bites

A

they are managed with augmentin and a tetanus vaccination booster if more than 5 years since last injection

dogs and cats: pasteurella multocida

humans: eikenella corrodens

84
Q

Dog, cat, and human bites

which one is the most damaging

A

human

85
Q

Rabies Vaccine only if

A

animal has altered mental status/bizarre behavior

attack was unproved, by a stray dog that cannot be observed or diagnosed

86
Q

Head trauma

overview

A

any head trauma resulting in sufficient injury to cause altered mental status or loc is managed first with a head ct. it does not matter how minor the trauma is if it results in LOC. head ct wo contrast is the best initial test to detect blood. contrast detects mass lesions such as cancer and abscess, not blood

87
Q

LOC=

A

CT

88
Q

Concussion

A

no focal neurological abnormalities. normal ct scan

89
Q

Brain Contusion

A

occasionally (rarely) has focal finding. ecchymoses found on CT (blood mixed in with brain parenchyma)

90
Q

Subdural and epidural hematomas:

A

usually associated with more severe trauma than a concussion. impossible to diagnose without a head CT. even though epidural hematoma ismore frequently associated with skull fracture

91
Q

Lucid interval

A

a lucid interval is a second loc occurring several mintures to several hours after the intial lox. the pt wakes up after the intial lox, but loses cosciousness a second time due to the accumulation of blood. the time between the first and second episodes of loc is the lucid interval

92
Q

concussion treatment

A

no specific therapy. wait at least 24 hours before returning to sports

93
Q

contusion treatment

A

vast majority need no specific treatment. rarely need surgical debridement

94
Q

subdural and epidural hematoma treatment

A

treatment is based on sized ans signs of compression of the brain. small ones are left alone. large hematomes are managed with:

intubation and hyperventialtion

mannitol

drainage

95
Q

Hyperventilation for brain injury

A

works by decreasing pco2. normally, cerebral circulation constricts whent he pco2 is low. a small decraese in volume results in a large decrease in pressure

96
Q

manitol works for brain injury by

A

it is an osmotic diuretic that is used to decrease iv volume. this decreases ic pressure but has only limited benefit

97
Q

hyperventilation briefly slows

A

herniation and is a bridge to surgery

98
Q

both ep and subdural hematomas are

A

associated with a lucid interval

99
Q

those with concustion are sage

A

to go home

hospitalization is not necessary. observe at home for altered mental status

100
Q

Definition of a large intracranial hemorrhage

A

compression of ventricles or sulci

herniation with abnormal breathing and unilateral dilation of the pupil

worsening mental status or focal findings

101
Q

concussion summary

A

no focal finding

no lucid interval

normal CT

no specific treatment; observe at home for lucid interval or new focal fidnings

102
Q

contusion summary

A

rarely focal

no lucid interval

ecchymoses

no specific treatment; observe in hospital

103
Q

subdural summary

A

w/or wo focal finding

w/or wo lucid interval

venous crescent

drain large ones

104
Q

epidural summary

A

w/or wo focal findings

w/or wo lucid interval

arterial, biconvex or lens-shaped hematoma

drain large ones

105
Q

Clear indication for a ppi to prevent stress ulcers

A

head trauma

burns

endotrachela intubation

coagulopathy (pts bleow 50000 or irn over 1.5) with respiratory failure

106
Q

steroids do not benefit

A

ic bleeding but they do decrease edema around mass lesions

107
Q

nimodipine after subarachnoid hemorrhage

A

prevents a stroke

108
Q

Burns

most common cause of death

A

co poisoning

airway burn is second if there is an airway burn

loss of volume is seocnd most common couse if no airway burn

109
Q

burns

therapy

A

best initial therapy is 100% oxygen to treat smoke inhalation and carbon monoxic poising

FLUIDS

110
Q

Burns when to intubate

A

stridor

horseness

wheezing

burns inside the nasopharynx or mouth

111
Q

Burns volume of fluid replacement

overview

A

replace with ringer lactate. if lr is not one of the hcoise then the answer is ns. give one-half in the first 8 hours, a quarter in the second 8 hours and a quarter in the third 8 hours. give 4 ml for each percentage of BSA burned for each kilogram of body weight

112
Q

Burns volume of fluid replacement

BSA

A

head 9%

arms 9% each

legs 18% each

chest and back 18% each

patchy burns use the width of the pts hadn to estimate, each hand width is one percent of BSA

113
Q

short answer for burn fluid replacement

A

give the largest amount of ringer lactate or ns listed, it is probably right

114
Q

Fluid replacement calculation

A

(4ml) x (%BSA burned) x weight in Kg

115
Q

Most common cause of death days to weeks after a burn

A

infection bc of loss of skin you have no barrier which leads to infection with staphy

116
Q

Prophylactic abs for burn

A

topical (silver sulfadiazine) are used not iv antibiotics

117
Q

Heat cramps/exhaustion

risk:

body temp:

CPK and k level:

treatment:

A

risk: exertion; high outside temps

body temp: normal

CPK and k level: normal

treatment: oral fluids and electorlytes

118
Q

Heatstroke

risk:

body temp:

CPK and k level:

treatment:

A

risk: exertion; high outside etmps

body temp: elevated

CPK and k level: elevated

treatment: iv fluids; evaporation

119
Q

Neuroleptic malibnant syndrome

risk:

body temp:

CPK and k level:

treatment:

A

risk: antipsychotic meds

body temp: elevated

CPK and k level: elevated

treatment: dantrolene or dopamine agonists (bromocriptine, cabergoline)

120
Q

Malignant hyperthermia

risk:

body temp:

CPK and k level:

treatment:

A

risk: anesthetics administered systemically

body temp: elevated

CPK and k level: elevated

treatment: dantroline

121
Q

Hypothermia

A

look for an intoxicated person with a low body temp. unintoxicated people do not fall asleep outside in cold temps. the most comon cause of death from hypthermia is cardiac arrhytmia so eck is best initial step

122
Q

Drowning

A

manage with airway and administer positive pressure ventilation

steroid and abs are not beneficial

salt water drowning acts like chf with wet heavylungs

fresh water drowning cuasue hemolysis from absorption of hyptonic fluid into the vasculature

123
Q

wrong answers for drowning

A

steroids

antibiotics

124
Q

Initial management of cardiac arrest

first step

A

make sure the pt is truly unresponsive (breaths and compressions on a breathing pt with a pulse is dangerous)

call for help call 911 active ems

125
Q

Initial management of cardiac arrest

second step

A

open airway: head tilt, chin lift, jaw thrust

give resuc ebreaths if not breathing

check pulse and start chest compression if pulseless

126
Q

what does cpr do

A

it keeps the pt alive until cardioversion can be performed

127
Q

when is a precordial thump the answer

A

very recent onset of arrest (less than 10 minutes) with no defibrillator available

you know it is recent bc you saw it happen

so pretty much never

128
Q

Pulselessness

A

the sudden loss of a pulse can be caused by:

asystole

vfib

vtach

pulseless electrical activity (PEA)

best initial management is CPR

129
Q

Asystole treatment

A

besides CPR, therapy for asystole is with epi. asopressin is an alterntive to epi. they both constrict blood vessels in tissues such as the skin. this shunts blood into critical central areas like the heart and brain

130
Q

V fib initial treatment

A

the best initial therapy for vfib is an immediate, unsynchronized cardioversion is synonymous with defib. generally all electrical cardioversions should be syncrhonized to the cardiac cycle except VF and pulsless VT. in vf there is no organized activity to synchronize with

131
Q

only vf and vt without a pulse get

A

unsynchronized cardioversion

132
Q

Amiodarone is superior to lidocaine for

A

VF

133
Q

Vfib secondary treatment

A

after another attempt at defib the most apprioate next step is epi or vaspression followed by another electrical shock. medications do not restart the heart, they make the next attempt at defib more likely to succeed

134
Q

vfib tertiary treatment

A

amiodarone or lidocaine is given next to try to get subseunt shocks to be more successful. magnesium is given with ventricular arrhythmia without wating for a level. amiodarone isthe first choice.

135
Q

Bretyllium for vfib

A

is always a wrong answer

136
Q

VTAC overview

A

VT is a wide complex tachycardia with a regular rate. Manangment is entirely based on the hemodynamic status

137
Q

VF is managed with

A

shock, drug, shock, drug, shock, drug and CPR at all times in between the shocks

138
Q

Pulseless VT

A

manage in exactly the same way as VF

139
Q

Hemodynamically stable VT

A

treate with meds such as amiodarone, then lidocaine, then procainamide. If all medical therapy fails, then cardiovert the patient

140
Q

Hemodynamically unstable VT

A

perform electircal cardioversion severe times, followed by meds such as amiodarone, lidocaine, or procainamide

141
Q

Hemodynamically instability is defined as

A

chest pain

dyspnea/chf

hypotension

confusion

142
Q

direct intracardiac meds for VT

A

always a wrong answer

143
Q

Pulseless electrical activity

A

pulseless electrical activity formerly called electrical mechanical dissoacion, means that the heart is electrically normal, but there is no motor contraction. in other causes of pea the heart may still be contracting but without blood inside there will be no meaningufl cadiac output

144
Q

VT cardioversion

A

synchronized the electricity to prevent worsening of the arrythmia into ventricular fibirllation or systole

145
Q

to diagnose pea

A

normal ekg and no pulse

146
Q

PEA treatment

A

since the treatment of pea is to correct underlying cuase you need to know what has caused it

147
Q

PEA causes

A

tamponade

tension pneymo

hypvolemia and hypoglycemia

massive PE

hypoxia hypothermia metabolic acidodis

potassium disorders, high or low

148
Q

Atrial arrhytmias

A

not associated with hemodynamic compromise

tpalpitations, dizzinesss, or lightheadedness

exercise intolerance or dyspnea

embolic stroke

149
Q

Afib

A

irregularly irregular

150
Q

aflutter

A

regular rhythm, usually goes back into sinus thythm or deteriorates in fibrillation

151
Q

Afib ant aflutter treatment

A

hemodynamically unstable - treate with synchronized cardioversion. synchronization prevents electricy from being delivered during the regractory perios (ST-T wave). synchronization helps prevent deterioration into VT or VF

152
Q

Chronic afib should be

A

anticoagulated before cardiversion. unstable acute disease does not need anticoagulation

153
Q

chronic Afib

A

defined as lasting for more than 2 days, it takes several days for there to be a risk of clot fomration. routine cardioversion is not indicated. the majority of those who are converted int sinus rhythm will not stay in sinus

154
Q

afib and flutter cause

A

caused by anatomic abnormalitites of the atria from htn or valbular heart disease. shocking hte pt into sinus rhythm does not correct a dilated left atrium. over 90% will rever to fibrillation even with the use of antiarrythmic medications

155
Q

standard of care for afib

A

rate control and anticoagulation

156
Q

Best initial therapy for afib and flutter

A

control the rate with bblockers ccb or digoxin, once the rate is under 100bpm. then give warfarin dabigatran or rivaroxaban

157
Q

do rate control drugs convert to sinus rhythm

A

no

158
Q

does shocking owrk for th elong run

A

no

159
Q

with afib and aflutter is heparing necessary before warfarin

A

no, unless there is a current clot in the atrium

160
Q

what ccbs can you use in afib and flutter

A

diltiazem and verapamil bc they lbock the av node

161
Q

Warfarin, dabigatran, rivaroxaban, and apixabain for afib and flutter

A

without anticoagulation, there will be about 6 embolic strokes per year for every 100 patients with afib. when the inr is between 2 and 3 that cuts in half

162
Q

Acute afib and flutter

A

caused by alcohol, caffeine, cocaine, or transient ischemia will usually convert back to sinus rhythm

163
Q

atrial rhythn problems can cause

A

acute pulmonary edema from loss of atrial contribuation in those with cardimyopathy

164
Q

what does the atrium norammly contribute to cardiac output?

A

10-15% unless the heart is diseased then it is 30-50%

165
Q

Lone afib:

A

chads score

166
Q

Major bleeding from warfarin is defined as

A

intracranial hemorrhage

requiring transfusion

167
Q

CHADS score

A 
C: chf or cardiomyopathy
H: hypertension
A: age>75
D: diabetes
S: stroke or TIA=2 points

when it is 1 or less just use aspirin
when it is 2 or more use warfarin, dabigatran, rivaroxaban, or apixaban

168
Q

Supraventricular Tachycardia

present with

A

palpitations in a pt who is usually hemodynamically stable

169
Q

Supraventricular Tachycardia

best initial step

A

vagal maneuvers (carotid massage, vlasalva, dive reflex, ice immersion)

adenosine if vagal manuevers do not work

beta blockers (metobprolol) ccb (diltiazem) or digoxin if adenosine is not effective

170
Q

adenosine is only therapuetic too

A

svt

171
Q

Supraventricular Tachycardia

on ekg

A

160-108 bpm

narrow complex without p waves, fib waves, or flutter waves

QRS<100msec`

172
Q

Wolf-Parkinson-White syndrome

A

anatomic banormlaity in the cardiac conduction pathway

173
Q

Wolf-Parkinson-White syndrome

mostlikely diagnosis

A

svt alteranting with vtach

svt that gets worse after diltiazem or digoxin

Observing the delta wave on the EKG

174
Q

most accurat test for Wolf-Parkinson-White syndrome

A

cardiac electorpysiology studies

175
Q

Wolf-Parkinson-White syndrome

acute treatment

A

procainamide or amiodarone are useful for obth atrial and ventricular abnormalities. use them only if wpw is currently preseting with an arrhythmia

176
Q

Wolf-Parkinson-White syndrome

chornic therapy

A

radiofrequency catheter ablations is curative for WPW. the tip of the catheter is heated up and siply ablates or eliminates the abnormal conduction tract around the AV node. EP studis will tell you whre the anatomic devect is

177
Q

what is dangerous in Wolf-Parkinson-White syndrome

A

digoxin and calcium channel blockers are dangerous. they block the normal aV node and force conduction in to the abnormal pathway

178
Q

Multifocal Atrial Tachycardia

A

associated with with chronic lung disease such as COPD. treate the undelryind diease. trate it as you would afib but aboid beta blockers bc of the lung disease

has at least 3 different p wave morphologies and is associated with COPD

179
Q

Bradycardia and AV blocke

A

common, can be physiological

can be the initial presentation of third degree or coplete heart block

get an EKG

if asyptomatic sinus bradycardia the you reassure

atropine is the answer for an acutely symptomatic pt with sign of hypoperfusion

pacemaker is used for all pts with third degree AV block

epinephrine is dangerous

180
Q

atropine and pacemaker are used for

A

sinus bradycardia if symptomatic

181
Q

Sinus bradycardia

treatment

A

no treatment is indicated if asymptomatic, no matter how low the heart rate is

is symptomatic, use atropine as the best initial therapy and a pacemeaker as the most effective therapy

182
Q

First-degree AV block

A

use the same management as sinus bradycardia

183
Q

Second-Degree Av Block

mobitz I or Wenckebach block:

A

this is a progressively lengthening PR interval that results in a dropped beat . Mobtiz I is most often a sign or fnormal aging of the oncduction system. if there are not symptoms it is managed in the same way as sinus bradycardia. Do no treat if asymptomatic

184
Q

Second Degree AB Block

mobits II block:

A

mobitz II second-degree AB clock is far more pathologic than Mobitz I. Mobitz II just drops a beat without the progressive lengthening of the PR interval. Mobitz II progresses, or deteriorates into third-degree AV block. Treat it like third-degree AV block. Everyone with Mobitz II block gets a pacemaker even if they are asymptomatic

185
Q

most common cause of death in the 72 hours surroudning an MI

A

ventricular arrhythmia from ischemia, manage by doing andioraphy for angiopblasty or bypass

186
Q

post mi vtac risk of recurrency

A

do an echo most accurate is nuclear ventriculography (MUGA) by you dont do this first

OMS III (21 decks)

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