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98 Cards in this Set

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basic life support measures
1) assess responsiveness
2) call for help
3) postiion face up on flat surface
4) open the airway
5) assess breathing (if no breathing, perform 2 rescue breaths)
6) check carotid pulse 5-10 seconds (if no pulse, give 30 compressions and two ventilations until help arrives)
asystole and dysrhythmia etiology
"Hi 5, T5": hypoxia, hypo/hyperkalemia, hypothermia, hypoglycemia, hypoveolemia, trauma, toxins, tamponade, tension pneumothorax, thrombosis
advanced cardiac support
if pulseless + shockable --> shock + 5 cycles of CPR + 1mg epi every 3-5min until pulse present
if pulseless + not shockable --> 5 cycles of CPR + 1mg epi + 1mg atropine until electrical activity then check pulse;
shockable rhythms
ventricular fibrillation and ventricular tachycardia
unshockable rhythms
asystole, pulseless electrical activity
signs of hemodynamic instability
hypotension, chest pain, altered mental status, CHF
general measures of tachycardia with pulses
ABC, O2, identify rhythm on ECG, identify reversible causes
hemodynamically unstable patient with pulse and tachycardia
perform immediate cardioversion
IV access and sedation
until stable
hemodynamically stable patient with pulse and tachycardia, narrow QRS, regular rhythm
vagal maneuvers or adenosine
if converts --> probable SVT, treat recurrence with adenosine
if doesn’t convert --> probable atrial flutter, ectopic atrial tachycardia
control rate with diltiazem or betablockers
hemodynamically stable patient with pulse and tachycardia, narrow QRS, irregular rhythm
probable A-fib or MAT; control rate with diltiazem or betablockers
hemodynamically stable patient with pulse and tachycardia, wide QRS, regular rhythm
if VT --> amiodarone 150mg IV over 10min, repeat as needed
if SVT --> adenosine and check for rhythm conversion
hemodynamically stable patient with pulse and tachycardia, wide QRS, irregular rhythm
if WPW --> avoid nodal blocking agents adenosine, digoxin, CCB
consider amiodarone 150mg over 10min
basic algorhythm for tachycardia with pulses
general measures --> check if stable --> check QRS --> check rhtyhm regularity
miosis as sign of toxicity
sugests clonidine, barbiturates, opiates, cholinergics, pontine stroke
mydriasis as sign of toxicity
sugests sympathomimetics, anticholinergics
dry skin as sign of toxicity
sugests anticholinergics
wet skin as sign of toxicity
cholinergics, sympathomimetics
blisters as sign of toxicity
barbiturates, carbon monoxide
common signs of toxicity
miosis, mydriasis, dry skin, wet skin, blisters
measures for toxic ingestion management
induced vomiting
lavage
charcoal
whole bowel irrigation
dialysis
cathartics
forced diuresis
naloxone/dextrose/thiamine
induced vomitting
ipecac can only be used 1-2 hours after toxic ingestion (limited use)
not indicated in children or for caustic substances
lavage
indicated in those with mental status
preceded by intubation
used 1 hour after ingestion (limited use)
contraindicated for caustic substances
charcoal
used if patient arrives more than 1-2 hours after ingestion; decreases absorption and increases removal of absorbed substance
whole bowel irrigation
used when many pills are seen on x-ray; 1-2 liters/hour of GoLytely via gastric tube
dialysis for toxicity management
used for ehtylene glycol, lithium overdose, methanol poisoning, aspirin overdose, theophyline overdose and there is coma, hypotension or apnea
cathartics
useful only when charcoal is used; generally wrong answer
forced diuresis
alkaline diuresis is only useful for salicylates and phenobarbital
naloxone/dextrose/thiamine administration
given to any patient who ingested substance and has altered mental status
acetaminophen toxicity stages
gastritis, nausea, vomitting 12-24 hours after ingestion; 24-48 hours: asymptomatic period with subclinical elevation of transaminases and bilirubin; 48-72 hours: jaundice, abdominal pain, hepatic encephalopathy, renal failure and death
acetaminophen toxicity treatment
N-acetyl-cysteine preferably within first 8 hours
activated charcoal
no gastric emptying
after 24 hours of ingestion no treatment can prevent or reverse toxicity
methanol ingestion sources
paint thinner, sterno, photocopier fluid, solvents, windshield washer solution
ethylene glycol ingestion sources
car antifreeze
methanol and ethylene glycol metabolism
methanol + alcohol dehydrogenase --> formaldehyde + formic acid
ethylene glycol + alcohol dehydrogenase --> oxallic acid/oxalate
general signs of alcohol intoxication
confusion, ataxia, lethargy, drowsiness, slurred speech
isopropyl alcohol intoxication
ketonuria, ketonemia, without acidosis and no increased anion gap
methanol intoxication specific signs
visual disturbances, blindness
ehtylene glycol intoxication specific signs
renal failure and oxalate crystals/stones in urine
alcohol intoxication diagnosis
determine specific alcohol levels in blood
oxalate crystals in urine and ↑BUN/creatinine are characteristic of ethylene glycol
ethylene glycol and methanol produce increased anion gap metabolic aciosis different from isopropyl alcohol which is normal
alcohol intoxication treatment
fomepizole is alcohol dehydrogenase inhibitor which decreases toxic metabolites
carbon monoxide poisoning presentation
dyspnea, tachypnea, shortness of breath, headache, nausea, dizziness, confusion, syncope, chest pain, arrhythmia, hypotension
carbon monoxide poisoning diagnosis
carboxyhemoglobin levels
arterial blood gases (metabolic acidosis with normal PO2)
↑CPK
pulse oximetry not helpful
CO poisoning might present similar to hypoglycemia, if glucose is normal, raise suspicion of CO
carbon monoxide poisoning treatment
removal from source of exposure, 100% O2, hyperbaric O2 if CNS or chest pain
caustic substance intoxication presentation
oral pain, drooling, odynophagia, abdominal pain
esophageal injury and gastric perforation may occur
caustic substance intoxication diagnosis
by history of exposure and upper endoscopy if ingested
caustic substance intoxication management
wash out mouth, eyes or skin with large volumes of cold water
follow eye wash out with fluorescein corneal exam
don't induce emesis or neutralize substance
charcoal and steroids are not effective
digoxin toxicity etiology
from suicide attempt or accidental overdose; hypokalemia predisposes to toxicity
digoxin toxicity presentation
nausea, vomitting, diarrhea, anorexia
blurred vision, color abnormalities
hallucinations
confusion
arrhythmia
digoxin toxicity diagnosis
history + ECG looking for any arrhythmia
check for hyperkalemia
digoxin toxicity management
repeated doses of charcoal, digoxin antibodies, potassium correction
pacemaker might be necessary for refractory bradycardia or 3rd degree heart block
opiate intoxication
respiratory depression
respiratory acidosis
miosis
constipation
bradycardia
hypothermia
hypotension
treat with naloxone
cocaine intoxication
hypertension, hemorrhagic stroke, MI, arrhythmia, seizures
pulmonary edema is specific to crack
treat with benzodiazepines for acute agitation
combined alpha/beta blockers such as labetalol or alpha blockers such as phentolamine
avoid beta blockers
benzodiazepine intoxication
somnolence, dysarthria, ataxia, stupor
death is not from respiratory depression but concomitant ethanol or barbiturates
flumazenil antidote is not always used due to seizures from withdrawal
barbiturate intoxication
hypothermia, loss of deep tendon reflexes
loss of corneal reflexes, coma and death from respiratory depression
no EEG activity can be seen
no specific antidote but increase urinary excretion with bicarbonate
hallucinogens
marijuana, LSD, mescaline, peyote, psilocybin, PCP (angel dust)
hallucinogen toxicity
delirium and bizarre behavior
anticholinergic effects (flushed skin, dry mouth, dilated pupils, urinary retention)
PCP may cause seizures
treat severe intoxication with benzodiazepines
lead sources
ingested paint, soil, dust, drinking water
lead metabolism
absorbed from GI tract, skin or inhalation
5-10% in blood (mostly in RBC)
80-90% in bones, remainder in brain and kidneys
lead poisoning presentation
adults: abdominal pain, anemia, renal disease, neurologic manifestations
children: abdominal pain, anemia, lethargy, seizures, coma, irreversible mental retardation and cognitive damage
lead poisoning diagnosis
best test is blood lead levels (<10ug/dL is normal)
lead lines at metaphyseal plate of long bones in children
anemia
azotemia
lead poisoning treatment
removal of source
chelators (EDTA, dimercaprol, penicillamine or succimer)
acute poisoning: charcoal + urination
mercury poisoning
interstitial pneumonitis from inhalation
irreversible neurologic symptoms (tremors, excitability, memory loss, delirium, insomnia)
GI symptoms from ingestion
treat with succimer or dimercarprol
salicylates intoxication presentation
tinnitus
nausea, vomitting, gastritis
hyperventilation, noncardiogenic pulmonary edema
hyperthermia, CNS toxicity
lactic metabolic acidosis with increased anion gap
salicylates intoxication diagnosis
most specific test is aspirin level
suggestive is elevated anion gap metabolic acidosis but blood may have ↑pH, ↓pH or normal
chest x-ray may be normal or pulmonary edema
salicylates intoxication management
if within 1 hour of ingestion, gastric decontamination + charcoal
mainstay of therapy is alkalinization of urine with aggressive fluid resuscitation
dialysis is sometimes used
tricyclic antidepressant intoxication presentation
anticholinergic (dry mouth, tachycardia, dilated pupils, flushed skin)
cardiac (wide QRS, ventricular tachycardia)
CNS (altered mental status, seizures)
tricyclic antidepressant intoxication diagnosis
serum drug levels is most specific but EKG is more important to do first
tricyclic antidepressant intoxication management
within hours --> charcoal
bicarbonate if cardiac toxicity
don't use flumazenil to reverse concomitant benzodiazepine overdose because it leads to seizures
head trauma presentation
headache, amnesia, loss of consciousness
focal findings are most common with epidural hematomas, then subdural hematomas and contusion
head trauma diagnosis
CT scan always
hemorrahge is visible immediately
subdural hematoma is crescent-shaped
epidural hematoma is lens-shaped
if focal findings consistent with radiculopathy or spinal tenderness --> cervical spine x-ray
concussion diagnosis is loss of consiousness + normal head CT
head trauma treatment
if intracrannial hemorrhage --> hyperventilation to a PCO2 of 30-35
osmotic diuretics and elevation of head of the bed
maintain cerebral perfusion by keeping blood pressure 110-160mmHg
subarachnoid hemorrhage presentation
acute --> sudden headache, loss of consiousness (50%), focal neurologic symptoms (30%)
long-term --> focal deficits, seizures, rebleeding, hydrocephalus, stroke
subarachnoid hemorrhage diagnosis
intial best test is CT scan which has 90-95% sensitivity within first 24 hours
if CT is normal and SAH is still suspect --> lumbar puncture for absence of red cells
angiography to determine site for surgery
inverted or enlarged T-waves on ECG are not alarming
subarachnoid hemorrhage management
maintain blood pressur at 110-160mmHg
nimodipine to prevent spasm and stroke
angiography to determine site of bleeding for surgical correction
shunt if hydrocephalus is present
skin burns classification
first-degree --> skin is intact
second-degree --> blister formation
third-degree --> destruction of skin appendages and pain receptors which result in relative lack of pain
burn presentation
altered mental status, dyspnea, headache and chest pain suggest carbon monoxide poisoning
stridor, hoarseness and dyspnea suggest laryngeal edema
soot in nose and mouth suggests impending airway compromise
rule of nines for burns
arms and head are 9% each
chest, back and legs are 18% each
patchy burns estimated with width of hand which is 1%
watch out for circumferential burns which compromise circulation
diagnosis work-up of burns
aside from actual burn, determine carboxyhemoglobin levels in severe burns
chest x-ray and/or bronchoscopy to determine respiratory injury extent
definition of severe burns
combined second and third-degree burns >20% in adults or >10% in old or young
OR third-degree burns >5% of body surface
burn injury management
if signs of respiratory injury --> intubation is initial step
if carboxyhemoglobin is elevated --> 100% O2
Ringer lactate fluid rescucitation using Parkland formula
H2 blocker prophylaxis, topical silver sulfadiazine to prevent infections
grafts as needed
Parkland formula
4ml of ringer lactate for each % BSA burned per Kg; give 1/2 in first 8 hours, 1/4 in second 8 hours, 1/4 in third
heat stroke
lost ability to romeve heat from body
excessive body temperature elevation
confusion, disorientation, nausea, blurred vision, seizures
hemoconcentration, ↑BUN/creatinine, rhabdomyolysis, anuria, DIC, lactic acidosis
place body in cool temperature, water and fan + IV fluid replacement
malignant hyperthermia
idiopathic reaction to any anesthetic specially halothane and succinylcholine
rhabdomyolysis and hyperthermia
treat with dantrolene
neuroleptic malignant syndrome
reaction to phenothiazines, chlorpromazine, haloperidol
muscular rigidity, hyperthermia, ↑CPK, encephalopathy, rhabdomyolysis
treat by removing agent + bromocriptine or dantrolene
hypothermia
core body temperature <35C
lethargy, confusion, weakness, arrhythmias with J-wave elevation (may mimic ST elevation)
treat with warm bed, bath or blankets
rescucitation efforts from pulselessness can go on beyond 10 minutes until temperature >35C
nonionizing radiation
infrared, ultraviolet and microwave; present primarily as burns
ionizing radiation
bone marrow depression with infections and bleeding
permanent sterility in males around 4-5Gy
nausea and vomitting 100% at 3Gy
supportive therapy with antiemetics, transfusions, colony-stimulating factors, antibiotics as needed
electrocution presentation
local 1st, 2nd and 3rd degree burns
ventricular fibrillation (AC current)
aystole (DC current, lightning)
respiratory arrest (injury to medulla or respiratory muscle paralysis)
neurologic damage
loss of consiousness and amnesia in 75% of lightning cases
renal failure from dehydration and rhabdomyolysis
cataracts in 5-30%
electrocution treatment
cardiopulmonary resuscitation, fluid replacement, local wound care
types of drowinig
dry drowning from laryngospasm, fresh water drowning, sea water drowning
fresh water drowning
hypotonic water alters surfactanct and causes collapse
water is absorbed and results in hypervolemia, hemodilution and hemolysis
lungs have little water
sea water drowning
hypertonic water draws fluid into lungs resulting in pulmonary edema, systemic hypovolemia, hemoconcentration
near drowning presentation
coma
agitation
cyanosis
coughing
sings of pulmonary edema (tachypnea, tachycardia, rales)
near drowning lab exams
arterial blood gases show hypoxia and hypercabia and metabolic acidosis
drowning management
removal from water
ABCs (first step)
endotracheal intubation
O2
positive pressure mechanical ventilation (most effective)
drowning ineffective treatments
abdominal thrusts, antibiotics, steroids
anaphylaxis presentation
hives rash (urticaria), angioedema and swelling, dyspnea, stridor, tachycardia, hypotension, hemodynamic collapse
anaphylaxis management
antihistamine diphenhydramine
if hemodynamic instability --> epinephrine, IV fluids, antihistamines and steroids
cat and dog bites
treat with exploration, debridement, irrigation, proper wound care
prohylactic antibiotic of choice is amoxicillin/clavulanate