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
2
Q
Gastric lavage
A
removes 50% of pills at 1 hour and 15% at 2 hours
3
Q
ipecac in ER
A
always the wrong answer
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
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
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
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)
8
Q
Gastric emptying is always wrong with
A
caustics ( acids and alkali)
altered mental status
acetaminophen oerdose
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
10
Q
what is useless or dangerous with overdose
A
ipecac, forced diuresis, cathartics
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
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
13
Q
opiate ovverdose
A
is fatal; give naloxone immediately
14
Q
benzo overdose
A
is not fatal and acute withdrawal causes seizures, do not give flumazenil
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.
16
Q
charcoal is superior to
A
lavage and ipecac
17
Q
when you dont know what to do intoxicology give
A
charcoal
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.
19
Q
Four most common acetaminophen overdose question
A
- if a clearly toxic amount of acetaminophen has been ingested (more than 8-10 grams) the answer is n-acetylcysteine
- if the overdose was more than 24 hours ago, there is no therapy
- if the amount of ingestion is unclear, get a drug level.
- charcoal does not make n-acetylcsyteine ineffective. charcoal is not ci with n acetycysteine
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
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
22
Q
Aspirin overdose treatement
A
alkalize the urine which increases the rate of aspirin excretion
23
Q
alcoholism ecreases the amount of
A
acetaminophen needed to cause toxicity
24
Q
keys to diagnosing aspirin overdose
A
tinnitus, respiratory alkalosis, and metabolic acidosis
25
know what in aspirin overdose
blood gas
26
benzos can prevent seizures from
tcas
27
what test to run with tcas ovrdose and what dose it show
ekg, it shows torsades de pointes bc it prolongs the qt
28
TCA toxicity
can cause seizures and arrhytmia leading to death. a wide QRS will tell who is about to have an arrhytmia
29
tcas cause signs of anticholinergic effects like:
dry mouth
constipation
urinary retention
30
TCA overdose treatment
sodium bicarb. this will protect the heart against arrhytmia. it does not increase urinary excretion of TCAs as it does for aspirin
31
Caustics ingestion
caustic ingestion of acids and alkalis (eg drain cleaner) causes mechanical damage to the oropharynx, esophagus, and stomach including perforation.
32
caustic ingestion treatment
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
33
Carbon Monoxide Poisoning
overview
the most common cause of death in fires. 60% of deaths on the first day after a fire are more from CO poisoning
34
Carbon Monoxide Poisoning
look for a hx of
gas heaters or wood burning stoves
automobile exhaust, particularly in an enclosed environment
35
Carbon Monoxide Poisoning
pathology
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.
36
Carbon Monoxide Poisoning
presents with
dyspnea, lightheadedness, confusion, seizures, and ultimately death from an mi
37
the left ventricle cannot distinguish between
anemia, carboxyhemoglobin and a stenosis of coronary arteries
38
co poisoning give a normal
po2 bc oxygen does not detah from hemoglobin, this causes lactic acid to build up and you get acidotic
39
Carbon Monoxide Poisoning
test
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
40
Carbon Monoxide Poisoning
therapy
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
41
Carbon Monoxide Poisoning severe sx
CNS sx
cardiac sx
metabolic acidosis
42
Methemoglobinemia
is oxidized hb that is locked into the ferric state. oxidized hb is brown and will not carry oxygen.
43
methemoglobinemia occurs
from an idiosyncratic rxn of hb to certain drugs like:
benzocaine and other anesthetics
nitrites and nitroglycerin
dapsone
44
Methemoglobinemia presentation
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
45
Methemoglobinemia
sx
dyspnea and cyanosis
headache, confusion, and seizures
,metabolic acidosis
46
Methemoglobinemia
diagnostic tests
can give a normal p02 on blood gas
most accurate test is a mehemoglobin level
47
Methemoglobinemia
therapy
best initial therapy is 100% oxygen
most effective therapy is methylene blue which decreases the half-life of mehemoglobing
48
what color is blood with carbon monoxied
abnormally red
49
what color is blood with methemoglobinemia
abnormally brown
50
cyanosis+normal po2=
mehemoglobinemia
51
Organophosphate poisoning and nerve gas
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
52
Organophosphate poisoning and nerve gas
presentation
salivation
lacrimation
polyuria
diarrhea
bronchospasm, bronchorrhea, and respiratory arrest if severe
sludge bc these are cholinergic effects
53
acetylcholine causes
constriction of bronchi and an increase in bronchial secretions
54
Organophosphate poisoning and nerve gas are absorbed
through the skin
55
Organophosphate poisoning and nerve gas
treatment
atropine blocks the efffects of acetylcholine
pralidoxime is the antidote and it works by reactivating acetylcholinesterase
56
Digoxin toxicity
etiology
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
57
Digoxin toxicity
presentation
the most common presentation of Digoxin toxicity is gi problems like nausea vomiting and abdominal pain
58
Digoxin toxicity
other sx
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)
59
Digoxin toxicity
diagnostic tests
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
60
Digoxin toxicity
treatment
control k and give digoxin-specific antibodies. digoxin-binding antiboides will rapidly remove digoxin from circulation
61
hypokalemia>
digoxin toxicity
62
digoxin toxicity>
hyperkalemia
63
digoxin can produce
any arrhythmia
64
The strongest indication for digoxin-binding antibodies are
CNS and cardiac involvement
65
Lead poisoning
presentation
abdominal pain (lead colic)
renal tubule toxicity (ATN)
anemia (sideroblastic)
peripheral neuropathies such as wrist drop
CNS abnormalities such as memory loss and confusion
66
Lead poisoning
diagnostic tests
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
67
The most accurate test for sideroblastic anemia is a
prussian blue stain
this detects increased iron built up in red cell mitochondria
68
Lead poisoning
treatment
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
69
Mercury Poisoning
overview
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.
70
Mercury poisoning
therapy
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
71
Toxic Alcohols: methanol and ethylene glycol
both produce intoxication and metabolic acidosis with an increased gap. both give an osmolar gap and are treated with fomepizole and dialysis
72
Methanol toxicity
Source -
toxic metabolite -
presentation -
initial diagnostic abnormality -
Source - wood alcohol, cleaning solutions, paint thinner
toxic metabolite - formic acid/formaldehyde
presentation - ocular toxicity
initial diagnostic abnormality - retinal inflammation
73
Ethylene glycol toxicity
Source -
toxic metabolite -
presentation -
initial diagnostic abnormality -
Source - antifreeze
toxic metabolite - oxalic acid/oxalate
presentation - renal toxicity
initial diagnostic abnormality - hypcalcemia, envelope-shpaed oxalate crystals in urine
74
Osmolar Gap
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
75
Toxic Alcohols: methanol and ethylene glycol
treatment
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
Snake Bites
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
Death from snake bites is from
hemolytic toxin: hemolysis and DIC and damage to the endothelial lining of tissues
neeruotoxin: can result in respiratory paralysis, ptosis, dysphagia, and diplopia
78
ineffective snake bite treatment
tourniquests blocking arterial flow
ice
incision and suction, especially by mouth
79
beneficial therapy
pressure
immobilization decreases movement of venom
antivenin
80
spider bites
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
Black widow bite
presentation -
lab test abnormalities -
treatment -
presentation - abdominal muscle pain, muscle pain
lab test abnormalities - hypocalcemia
treatment - calcium, antivenin
82
Brown Recluse
presentation -
lab test abnormalities -
treatment -
presentation - local skin necrosis, bullae, and blebs
lab test abnormalities - none
treatment - debridement, steroids, dapsone
83
Dog, cat, and human bites
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
Dog, cat, and human bites
which one is the most damaging
human
85
Rabies Vaccine only if
animal has altered mental status/bizarre behavior
attack was unproved, by a stray dog that cannot be observed or diagnosed
86
Head trauma
overview
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
LOC=
CT
88
Concussion
no focal neurological abnormalities. normal ct scan
89
Brain Contusion
occasionally (rarely) has focal finding. ecchymoses found on CT (blood mixed in with brain parenchyma)
90
Subdural and epidural hematomas:
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
Lucid interval
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
concussion treatment
no specific therapy. wait at least 24 hours before returning to sports
93
contusion treatment
vast majority need no specific treatment. rarely need surgical debridement
94
subdural and epidural hematoma treatment
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
Hyperventilation for brain injury
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
manitol works for brain injury by
it is an osmotic diuretic that is used to decrease iv volume. this decreases ic pressure but has only limited benefit
97
hyperventilation briefly slows
herniation and is a bridge to surgery
98
both ep and subdural hematomas are
associated with a lucid interval
99
those with concustion are sage
to go home
hospitalization is not necessary. observe at home for altered mental status
100
Definition of a large intracranial hemorrhage
compression of ventricles or sulci
herniation with abnormal breathing and unilateral dilation of the pupil
worsening mental status or focal findings
101
concussion summary
no focal finding
no lucid interval
normal CT
no specific treatment; observe at home for lucid interval or new focal fidnings
102
contusion summary
rarely focal
no lucid interval
ecchymoses
no specific treatment; observe in hospital
103
subdural summary
w/or wo focal finding
w/or wo lucid interval
venous crescent
drain large ones
104
epidural summary
w/or wo focal findings
w/or wo lucid interval
arterial, biconvex or lens-shaped hematoma
drain large ones
105
Clear indication for a ppi to prevent stress ulcers
head trauma
burns
endotrachela intubation
coagulopathy (pts bleow 50000 or irn over 1.5) with respiratory failure
106
steroids do not benefit
ic bleeding but they do decrease edema around mass lesions
107
nimodipine after subarachnoid hemorrhage
prevents a stroke
108
Burns
most common cause of death
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
burns
therapy
best initial therapy is 100% oxygen to treat smoke inhalation and carbon monoxic poising
FLUIDS
110
Burns when to intubate
stridor
horseness
wheezing
burns inside the nasopharynx or mouth
111
Burns volume of fluid replacement
overview
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
Burns volume of fluid replacement
BSA
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
short answer for burn fluid replacement
give the largest amount of ringer lactate or ns listed, it is probably right
114
Fluid replacement calculation
(4ml) x (%BSA burned) x weight in Kg
115
Most common cause of death days to weeks after a burn
infection bc of loss of skin you have no barrier which leads to infection with staphy
116
Prophylactic abs for burn
topical (silver sulfadiazine) are used not iv antibiotics
117
Heat cramps/exhaustion
risk:
body temp:
CPK and k level:
treatment:
risk: exertion; high outside temps
body temp: normal
CPK and k level: normal
treatment: oral fluids and electorlytes
118
Heatstroke
risk:
body temp:
CPK and k level:
treatment:
risk: exertion; high outside etmps
body temp: elevated
CPK and k level: elevated
treatment: iv fluids; evaporation
119
Neuroleptic malibnant syndrome
risk:
body temp:
CPK and k level:
treatment:
risk: antipsychotic meds
body temp: elevated
CPK and k level: elevated
treatment: dantrolene or dopamine agonists (bromocriptine, cabergoline)
120
Malignant hyperthermia
risk:
body temp:
CPK and k level:
treatment:
risk: anesthetics administered systemically
body temp: elevated
CPK and k level: elevated
treatment: dantroline
121
Hypothermia
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
Drowning
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
wrong answers for drowning
steroids
antibiotics
124
Initial management of cardiac arrest
first step
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
Initial management of cardiac arrest
second step
open airway: head tilt, chin lift, jaw thrust
give resuc ebreaths if not breathing
check pulse and start chest compression if pulseless
126
what does cpr do
it keeps the pt alive until cardioversion can be performed
127
when is a precordial thump the answer
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
Pulselessness
the sudden loss of a pulse can be caused by:
asystole
vfib
vtach
pulseless electrical activity (PEA)
best initial management is CPR
129
Asystole treatment
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
V fib initial treatment
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
only vf and vt without a pulse get
unsynchronized cardioversion
132
Amiodarone is superior to lidocaine for
VF
133
Vfib secondary treatment
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
vfib tertiary treatment
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
Bretyllium for vfib
is always a wrong answer
136
VTAC overview
VT is a wide complex tachycardia with a regular rate. Manangment is entirely based on the hemodynamic status
137
VF is managed with
shock, drug, shock, drug, shock, drug and CPR at all times in between the shocks
138
Pulseless VT
manage in exactly the same way as VF
139
Hemodynamically stable VT
treate with meds such as amiodarone, then lidocaine, then procainamide. If all medical therapy fails, then cardiovert the patient
140
Hemodynamically unstable VT
perform electircal cardioversion severe times, followed by meds such as amiodarone, lidocaine, or procainamide
141
Hemodynamically instability is defined as
chest pain
dyspnea/chf
hypotension
confusion
142
direct intracardiac meds for VT
always a wrong answer
143
Pulseless electrical activity
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
VT cardioversion
synchronized the electricity to prevent worsening of the arrythmia into ventricular fibirllation or systole
145
to diagnose pea
normal ekg and no pulse
146
PEA treatment
since the treatment of pea is to correct underlying cuase you need to know what has caused it
147
PEA causes
tamponade
tension pneymo
hypvolemia and hypoglycemia
massive PE
hypoxia hypothermia metabolic acidodis
potassium disorders, high or low
148
Atrial arrhytmias
not associated with hemodynamic compromise
tpalpitations, dizzinesss, or lightheadedness
exercise intolerance or dyspnea
embolic stroke
149
Afib
irregularly irregular
150
aflutter
regular rhythm, usually goes back into sinus thythm or deteriorates in fibrillation
151
Afib ant aflutter treatment
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
Chronic afib should be
anticoagulated before cardiversion. unstable acute disease does not need anticoagulation
153
chronic Afib
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
afib and flutter cause
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
standard of care for afib
rate control and anticoagulation
156
Best initial therapy for afib and flutter
control the rate with bblockers ccb or digoxin, once the rate is under 100bpm. then give warfarin dabigatran or rivaroxaban
157
do rate control drugs convert to sinus rhythm
no
158
does shocking owrk for th elong run
no
159
with afib and aflutter is heparing necessary before warfarin
no, unless there is a current clot in the atrium
160
what ccbs can you use in afib and flutter
diltiazem and verapamil bc they lbock the av node
161
Warfarin, dabigatran, rivaroxaban, and apixabain for afib and flutter
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
Acute afib and flutter
caused by alcohol, caffeine, cocaine, or transient ischemia will usually convert back to sinus rhythm
163
atrial rhythn problems can cause
acute pulmonary edema from loss of atrial contribuation in those with cardimyopathy
164
what does the atrium norammly contribute to cardiac output?
10-15% unless the heart is diseased then it is 30-50%
165
Lone afib:
chads score
166
Major bleeding from warfarin is defined as
intracranial hemorrhage
requiring transfusion
167
CHADS score
```
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
Supraventricular Tachycardia
present with
palpitations in a pt who is usually hemodynamically stable
169
Supraventricular Tachycardia
best initial step
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
adenosine is only therapuetic too
svt
171
Supraventricular Tachycardia
on ekg
160-108 bpm
narrow complex without p waves, fib waves, or flutter waves
QRS<100msec`
172
Wolf-Parkinson-White syndrome
anatomic banormlaity in the cardiac conduction pathway
173
Wolf-Parkinson-White syndrome
mostlikely diagnosis
svt alteranting with vtach
svt that gets worse after diltiazem or digoxin
Observing the delta wave on the EKG
174
most accurat test for Wolf-Parkinson-White syndrome
cardiac electorpysiology studies
175
Wolf-Parkinson-White syndrome
acute treatment
procainamide or amiodarone are useful for obth atrial and ventricular abnormalities. use them only if wpw is currently preseting with an arrhythmia
176
Wolf-Parkinson-White syndrome
chornic therapy
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
what is dangerous in Wolf-Parkinson-White syndrome
digoxin and calcium channel blockers are dangerous. they block the normal aV node and force conduction in to the abnormal pathway
178
Multifocal Atrial Tachycardia
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
Bradycardia and AV blocke
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
atropine and pacemaker are used for
sinus bradycardia if symptomatic
181
Sinus bradycardia
treatment
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
First-degree AV block
use the same management as sinus bradycardia
183
Second-Degree Av Block
mobitz I or Wenckebach block:
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
Second Degree AB Block
mobits II block:
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
most common cause of death in the 72 hours surroudning an MI
ventricular arrhythmia from ischemia, manage by doing andioraphy for angiopblasty or bypass
186
post mi vtac risk of recurrency
do an echo most accurate is nuclear ventriculography (MUGA) by you dont do this first
