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Environmental Flashcards

1
Q

What are consequences of CO toxicity that are unrelated to Hb

A
  • Binding to myoglobin -> myocardial and muscular hypoxia -> arrhythmia, rhabdomyolysis
  • Binding to guanylyl cyclase -> increased cGMP -> vasodilation (including cerebral) ->altered mentation
  • Binding to cytochromes oxidase system -> disrupted oxidative metabolism -> generation for free radicals -> neuronal necrosis
  • Increased platelet adherence -> increased risk of thromboembolic event
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2
Q

What are the 2 consequences of CO toxicity on Hb

A
  • CO binds 2 of the 4 available hemes ->reduces O2 carrying capacity by 50%
  • CO shifts the Hb dissociation curve to the left -> decreased O2 release to tissues
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3
Q

What is the affinity of CO for Hb compared to O2

A

200-240 times the affinity

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4
Q

What is the normal COHb

A

Up to 1%

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5
Q

What contributes to VQ mismatch following smoke inhalation

A
  • Inhalation of irritants -> inflammatory response with secretion of neurokinins, calcitonin-gene related peptides (CGRP), other pro-inflammatory peptides -> bronchoconstriction, vasoconstriction, airway fluid accumulation
  • Increased production of NO -> inhibition of hypoxic vasoconstriction
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6
Q

What is the mechanism of cyanide toxicity

A
  • Inhibition of electron transport chain in the mitochondria -> impaired cellular ATP production
  • Neurotoxicity
  • Stimulation of chemoreceptors -> tachypnea
  • Arrhythmias
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7
Q

What is the common delay for development of lung injury / neurological signs following smoke inhalation

A

Lung injury: 24-48h
Neuro signs: 10h to 6 days

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8
Q

In smoke inhalation, hydrogen cyanide toxicosis should be suspected in case of combustion of what materials

A

Wool, silk, cotton, paper, plastic

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9
Q

What is the half-life of CO in patients breathing room air vs breathing 100% O2

A

Room air -> 320 min
100% O2 -> 70 min

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10
Q

What inhaled therapies could be beneficial in smoke inhalation patients

A
  • Beta2-agonists: cause bronchodilation, decrease inflammation, help airway clearance
  • Epinephrine: causes bronchodilation and vasoconstriction, help airway clearance
  • N-acetylcysteine: mucolytic, could help airway clearance but causes bronchoconstriction
  • Heparin: reduces fibrin casts formation
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11
Q

What antidotes can be used for hydrogen cyanide toxicity

A
  • Hydroxocobalamin (vitamin B12a) -> binds cyanide to form cyanocobalamin which is excreted via the kidney
    (/!\ most commercially available vitamin B12 is already in the form of cyanocobalamin which has no benefit)
  • Amyl nitrate and sodium thiosulfate -> transform Hb into MetHb which binds cyanide, but also decreases O2 distribution to tissues
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12
Q

What are the different degrees of severity of primary hypothermia and their common clinical signs

A
  • Mild (32-37°C): ataxia, thermoregulatory mechanisms intact (-> shivering, vasoconstriction)
  • Moderate (28-32°C): decreased level of consciousness, hypotension, atrial dysrhythmias, loss of shivering
  • Severe (20-28°C): coma, ventricular dysrhythmias (prone to Vfib), no shivering
  • Critical (<20°C): imminent death

/!\ stages are different for secondary hypothermia

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13
Q

Where are temperature-sensing receptors located

A
  • Anterior hypothalamus
  • Spinal cord, abdominal viscera, great abdominal and thoracic veins (-> input to posterior hypothalamus)
  • Skin (-> input to posterior hypothalamus)
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14
Q

What are the 4 mechanisms of heat loss

A
  • Convection: transfer of heat from body surfaces to surrounding air
  • Conduction: transfer of heat from body surfaces to objects in contact
  • Radiation: transfer of heat to objects not in contact (eg. walls) regardless of the temperature of air
  • Evaporation: loss of heat from moisture on body surfaces or through respiratory tract

(70% lost via radiation and convection)

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15
Q

What are the effects of hypothermia on cardiac rhythm

A
  • Mild hypothermia leads to sympathetic activation -> vasoconstriction, tachycardia
  • With progressive hypothermia -> decreased rate of SA node depolarization -> bradycardia (non-responsive to atropine)
  • Prolonged duration of action potential and decreased conduction -> widening of QRS, prolonged PR interval, positive deflection of ST segment (“J-wave”)
  • Progression to atrial fibrillation then ventricular arrhythmias and eventually Vfib
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16
Q

What are the effects of hypothermia on coagulation

A
  1. Primary hemostasis
    - Sequestration of platelets in liver and spleen -> thrombocytopenia
    - Decreased production of thromboxane B2, decreased platelet granule secretion, decreased P selectin expression, decreased vWF receptor expression -> decreased platelet aggregation
  2. Secondary hemostasis
    - Decreased enzymatic activity of coagulation factors
    - Hypercoagulability and DIC due to release of catecholamines, steroids, thromboplastin

Coagulation testing commonly performed at 37°C ->will not reflect function in vivo

17
Q

What is the effect of hypothermia on urine production

A
  • Early peripheral vasoconstriction -> sensed increased effective circulating volume -> increased diuresis
  • With progressive hypothermia, the distal tubule becomes less responsive to vasopressin
  • Ultimately, decreased CO leads to decreased GFR
18
Q

What electrolyte imbalances can be seen with hypothermia

A

Hyponatremia and hyperkalemia due to decreased Na-K ATPase function

19
Q

What are the risks with Active external rewarming

A
  • Cardiovascular shock due to peripheral vasodilation
  • Rewarming acidosis (blood carrying lactate and metabolites returning to the core)
  • Afterdrop (colder blood from extremities returning to the core)
  • Thermal skin injury
20
Q

What are methods of active core rewarming

A
  • Heated intravenous fluids infusion (only works with high rates)
  • Delivery of warmed humidified air (face mask, ET tube, HFNC)
  • Warm peritoneal or thoracic lavage
    (- Extracorporeal life support)
21
Q

List different warming methods and their warming rates

A
  1. Passive external rewarming (only efficient if patient able to produce heat) -> 0.5-5°C/h
  2. Active external rewarming -> 0.5-4°C/h
  3. Active core rewarming:
    - Warm air inhalation -> 1.0-2.5°C/h
    - Peritoneal / thoracic lavage -> 1.5-2.5°C/h
    - Extra-corporeal life support -> 4-10°C/h
22
Q

What are the 3 mechanisms of protection from heat (which fail in heat stroke)

A
  • Thermoregulation
  • Acute-phase response: balanced production of pro-inflammatory and anti-inflammatory mediators
  • Heat shock proteins
23
Q

Explain the pathophysiology of heat stroke

A
  • Failure of thermoregulation due to increased heat load (environment / exercise) and/or failure of heat loss mechanisms (airway obstruction, obesity) -> increased core temperature
  • Direct injury of muscles due to heat -> rhabdomyolysis, release of IL-6 and IL-1
  • Direct injury of GI -> translocation of endotoxin
    -> trigger of inflammatory response
  • Inflammation + direct endothelial injury by heat -> activation of coagulation (release of thromboplastin = factor III which activates factor VII + release of kallikrein which activates intrinsic pathway), inhibition of fibrinolysis -> microthrombi + factor and platelet consumption
  • Direct heat injury + hypoperfusion + cytokines + myoglobinuria + endotoxemia (tubular and glomerular damage) -> AKI
  • Direct heat injury + cytokines -> endothelial injury in lungs and myocardium -> ARDS, myocardial injury, arrhythmias
  • Cerebral hypoperfusion, hypoxia, hypoglycemia, microthrombi ->cerebral damage (very little direct heat injury in brain)

=> SIRS, MODS, DIC

24
Q

What CBC parameter has a prognostic value in heat stroke

A

Nucleated red blood cells

nRBC > 18 / 100 WBC on presentation has Se 91% and Sp 88% to predict death

25
Q

What are mechanisms of VQ mismatch in drowning

A
  • Bronchospasm
  • Wash out of surfactant by water leading to atelectasis
  • Alveoli filled with water
  • Infectious or chemical pneumonitis
  • NCPE, ARDS

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