Environmental-Toxicology Flashcards
What controls thermoregulation?
> Hypothalamus controls thermal regulation by conserving heat and producing heat.
it virtually affects every system, but significantly affects cardiovascular in CNS systems.
Cardiac effects of hypothermia
> bradycardia(epi & atropine will not help)
decreased MAP and CO
Osborne waves( J waves) positive deflection at J point. Seen best in lateral leads.
atrial/ventricular arrhythmias
The height of the J wave equals the degree of hypothermia
CNS effects of hypothermia
> Decreasing metabolism(decreasing oxygen consumption)
Core temp <33°C, electrical activity becomes abnormal
core temp between 19-20°C, EEG may show brain death
Mild hypothermia
> 32 to 35°C (89.6 to 95°F)
Vigorous shivering
May develop altered judgment or dysarthria
respiratory rate may increase
Ataxia/apathy as temperature decreases
tachypnea/tachycardia
Cold diuresis (kidneys are resistant and don’t work well)
Moderate hypothermia
> 28 to 32°C (82.4 to 89.6°F)
O2 consumption decreases
Further CNS depression
stupor/ confusion may occur
loss of shivering
arrhythmia risk increases
bradycardia worsens
cardiac output reduces
dilation of the pupils
Paradoxical undressing
Severe hypothermia
> <28°C (<82.4°F)
susceptible to Vfib
further decrease in myocardial contractility
comatose
pulmonary edema
oliguria
hypotension
decreased/absent activity on EEG
Hypothermia treatment
> Prevent further heat loss
Rewarm Core-temp
Avoid arrhythmias
Avoid inadvertent jerking movements
Monitor for complications
Hypotension is normal, fluid resuscitation is needed.
Watch for hypoglycemia, and treat accordingly.
Thiamine might be helpful
Avoid nasal gastric tube placement
Defibrillate once, but defer all other ALS treatment until Core temp is > 30°C.
Passive external rewarming
> move to warm dry environment
provide insulation
must have intact the regulatory mechanisms
Active external rewarming
> application of heat to the skin
must have intact circulation
Hot water bottles and heating pads
forced air warming systems
you may see Core-temp after drop. You may see increase in acidosis and core temp dropping again.
Active core rewarming
> heated, humidified O2
heated IV fluids
warm lavage of cavities
extra corporeal blood rewarming(echmo)
resuscitative efforts continue until core temp reaches 30 to 32°C (89.6°F)
Hyperthermia
A life-threatening condition characterized by failure of the body to regulate or dissipate heat
Defined as a core of greater than 38.5°C(101 .3°F)
Heat cramps
> mildest form of heat illness; core temp is normal
cause painful muscle cramps/spasms
flushed, moist skin
normally occurs during or after intense exercise/sweating
Heat cramps treatment
> Moved to a cool environment
remove excess clothing
hydration
stretching
Heat exhaustion
> Core temp >38°C( 100.4°F)
muscle cramp
pale, moist skin
N/V/D
HA
fatigue or weakness
feeling faint
Heat exhaustion treatment
> same measures as with heat cramps
humidified O2
cool IV fluid(LR or NS)
check glucose and treat as needed.
Heat stroke
> most severe form of Hyperthermia
Core temp >40°C(104°F)
hot dry skin
rhabdomyolysis
renal failure
worsening CNS symptoms
Heat stroke treatment
> same as heat exhaustion
initiate rapid active cooling
cold water immersion
body temp should be lowered to at least 102°F
remove clothing and cover with sheets, soaked and room temperature water
manage airway is needed
Malignant hyperthermia
> calcium is released into muscle fibers, causing sustained contraction due to rapid depolarization
causes muscle rigidity in excessive heat production
activation of sympathetic nervous system
hyperkalemia
can ultimately lead to DIC and MODS
most often associated with the use of succinylcholine
trismus
increased ET CO2
mixed acidosis
rhabdomyolysis
truncal or extremity rigidity
Malignant hyperthermia treatment
> Dantrolene Na+ 2.5mg/kg. Max 20mg/kg
cool if temp is >39°C
treat dysrhythmias per ACLS guidelines
never combine with calcium channel blockers with Dantrolene(can cause increase in hyperkalemia)
Drowning
> saltwater and freshwater are treated the same initially
contributing factors are hypoxemia and acidosis
cause laryngospasm
leads to inability to breathe
the spasm releases due to drop in PaO2
panic and hyperventilation leads to potentially more water aspiration which worsen hypoxemia.
Pulmonary effects of drowning
> impaired gas exchange
pulmonary vasoconstriction
fluid induced broncospasm
pulmonary hypertension
Drowning treatment
> airway management as necessary
early intubation and peep application or CPAP/BiPAP in cooperative patients
ECMO
volume expansion may be indicated(isotonic fluid)
Inotropic Support
NGT placement
possible bronchoscopy
surfactant therapy
Snakebites in the US
Two types of venomous snakes in the US
>pit vipers- quick onset
>coral snakes-develop of hours
S/S of snakebites
> local tissue destruction: edema, discoloration, or contusions
systemic toxicity: hypotension, coagulopathy(epistaxis/petechia/hemoptysis), diaphoresis, Paresthesia(watch for compartment syndrome) and muscle fasciculations.
Envenomation staging
> Mild: local pain, edema, no sign of systemic toxicity
Moderate: severe local pain; edema, larger than 12 inches surrounding the wound, systemic toxicity, including N/V
Severe: general petechia, ecchymosis, bloody sputum, hypotension, hypoperfusion, renal dysfunction, changes in PT/PTT.
Snakebite treatment
> Support ABC’s
Immobilize area as much as possible
Monitor for systemic reaction
Anti-venom for severe toxicity(neutralizes toxins)
Important to know how much time has elapsed since bite
early notification of need for anti-venom
Scorpion sting
> Generally not aggressive
nocturnal
hide and crevices and burrows during the day
most common sites for a sting or hands and feet
Scorpion sting treatment
> no antivenin
bark scorpion antivenin is most common in the US. Anascorp
administer as early as possible
monitor for serum sickness
administer steroids and antihistamine for anaphylactic type reactions
Brown recluse spider bite
> can see significant tissue necrosis
can have systemic reaction(rare)
cytotoxic and hemolytic venom
minimal initial symptoms
severe pain and pruritus 6-8hrs
edema around bite with a halo
The halo may progress overtime
vesicle develops 24-72 hrs later
tissue necrosis
Brown recluse, spider, bite treatment
> local debridement
elevation
Loose immobilization
cool compress
Analgesics
Antipruritics
Dapsone(cautiously) usually used with leprosy patients
Lethal dose of acetaminophen
7.5 g or 150 mg/kg
Acetaminophen OD, phase 1
> 0-24hr
could be asymptomatic
N/V
anorexia
malaise
pallor
diaphoresis
rise in serum transaminase begins approximately 12 hrs post ingestion
Acetaminophen OD phase 2
> 24-72hr
RUQ pain/tenderness
anorexia
N/V
tachycardia
hypotension
arise in serum transanimase
increased liver enzymes, bilirubin, and PT
oliguria as a result of ATN
Acetaminophen OD phase 3
> 72-96 hrs
N/V, abdominal pain, tender hepatic edge
jaundice, hepatic encephalopathy
coagulopathy(DIC), hypoglycemia
peak of liver function abnormalities
death due to fulminant hepatic necrosis
Acetaminophen OD phase 4
> 4d-3wk
complete resolution of symptoms
complete resolution of organ failure
Caustic ingestion treatment
> airway control
do not administer emetics
gastric lavage contraindicated
NGT suctioning
activated charcoal contraindicated
supportive care: antibiotics, proton pump, inhibitor, pain management.
Alkaline ingestions(caustic)
> cell death occurs from disruption of cell membrane: liquefaction necrosis
in injury occurs immediately; causes tissue edema
Acid ingestions(caustic)
> death occurs from coagulation necrosis
formation of eschatology
stomach is most commonly involved
increase risk of perforation due to granulation tissue
perforation, and upper G.I. hemorrhage most common complications.
Treatment of acetaminophen toxicity
> N-acetylcysteine(NAC), Mucomyst, Acetadote
give within the first 8-12 hrs
G.I. decontamination(activated charcoal)
Aspirin(salicylate) toxicity phase 1
> crosses blood brain barrier
hyperventilation(respiratory alkalosis)- apneustic stimulation
alkaluria(K+ &HCO3- excreted in the urine)
phase may last as long as 12 hours
often mimics early sepsis, and ends up in a metabolic acidosis
Aspirin(salicylate) toxicity phase 2
> continued respiratory alkalosis; paradoxic aciduria due to potassium loss from kidneys
may last 12– 24hrs
Aspirin(Salicylate) toxicity phase 3
> dehydration, hypokalemia, and progressive respiratory acidosis
phase may begin 24 hrs post ingestion
Aspirin(Salicylate) toxicity S/S
> N/V, diaphoresis, and tinnitus are the earliest
vertigo
hyperventilation
tachycardia
hyperactivity/agitation
hallucinations
lethargy/stupor
depressed DTR’s
profound hypocalcemia
hypothermia/low-grade fever
metabolic acidosis(partially compensated)
Aspirin(Salicylate) toxicity treatment
> if hyperventilating and needs to be intubated, match their fast respiratory rate on the vent (Ve 240mL/kg/min)
G.I. decontamination(activated charcoal)
LR or NS (10–20mL/kg/hr until urine output=1mL are/kg/hr
sodium bicarbonate (1-2mEq/kg) this
Beta blocker toxicity treatment
> fluid resuscitation(20mL/kg)
Inotropes and Chronotropes
glucagon (5mg IV)
Milrinone 300mcg/kg
gastric decontamination
cardiac pacing/CPR
insulin(high dose, 1U/kg bolus, 1-10U/kg/hr
Calcium channel blocker toxicity treatment
> gastric decontamination
calcium loading
glucagon
insulin
atropine
vasopressors
cardiac pacing
Digitalis toxicity
> not common anymore
yellow oleander and foxglove plants mimic digitalis toxicity
used for treatment of CHF, a-fib, reentrant SVT.
symptoms: visual disturbance(yellow-green distortion most common), PVCs, bradyarrhythmias, VT, heart blocks
Digitalis toxicity treatment
> Digibind
gastric lavage with activated charcoal
treatment of electrolyte imbalance
don’t give certain antidysrhythmic(quinidine, procainamide,bretyliun)
don’t give calcium it leads to VT/VF
temporary pacing for blocks
cardioversion, only if absolutely necessary
lidocaine, atropine, mag sulfate, good options for dysrhythmics
