Toxic Inhalations Flashcards
Simple Asphyxiants
Reduce oxygen from the air below the typical 21%/
Chapter 7, page 121
Systemic Asphyxiants
Interfere with oxygen transport by hemoglobin, with oxygen use by cytochrome-c oxidase, or with both.
Methemoglobin-forming compounds interfere with oxygen transport when they convert hemoglobin to methemoglobin that cannot carry oxygen.
Cyanides, azides, and sulfides interfere with cytochrome-c oxidase’s ability to react with molecular oxygen.
Chapter 7, page 119
Methemoglobin-Forming Compounds
Oxidize ferrous iron in hemoglobin to ferric iron, producing methemoglobin that is incapable of transporting oxygen.
Examples include inorganic nitrirte or nitrate salts.
Chatper 7, page 121
Hydrogen Cyanide
Highly water-soluble irritant gas that can irritate mucous membranes including the upper airway.
Chapter 7, page 123
Chocolate-brown blood
Caused b y Methemoglobin-forming compounds.
Skin also appears blusish resulting in central and peripheral (acral) cyanosis.
Chapter 7, page 123
Level of Methemoglobin to causes cyanosis
1.5 g/dL of methemoglobin in the blood or approximately 10% methemoglobinemia.
Chapter 7 page 123
Exposure to high concentrations of Hydrogen Sulfide can cause….
Sudden loss of consciousness, known as “knock down”.
Chapter 7, page 123
Simple asphyxiants can produce hypoxemia that cause cyanotic skin.
Cause ?
Lack of circulating oxygen with high concentrations of deoxyhemoglobin.
This cyanosis is usually visible when there is 5g/dL of deoxyhemoglobin in the bood or approximately 33% deoxyhemoglobin.
Chapter 7, page 123
At what level can Methemoglobin-forming compounds produce central and peripheral cyanosis ?
When the methemoglobin concentration reaches 10%.
Chapter 7, page 123
Hydrogen Sulfide
A systemic asphyxiatn and intermedicately water-solubel irritant gas can irritate skin and mucous membranes.
Can cause chemical conjunctivitis, keratitis, lacrimation.
Commonly referred to as gas eye in the oil and gas industry.
Chapter 7 page, 123
Nitrites, Nitrates and Azides
Shock
Are all potent vasodilators. They can cause distributive shock by decreasing pre-load and after-load.
Large quantities of intravenous isotonic crystalloid may be required because the intravascular space is expanded by potent vasodilation.
Chapter 7, page 130
Hyperbaric Oxygen
Indications
Carbon monoxide poisoning
Carboxyhemoglobin level > 25%
Carboxyhemoglobin level > 20% in a pregnant patient
Significant cyanide or cyanogenic compound poisoning
Chapter 9, pager 168
Hyperbaric Oxygen
Dosage
100% oxygen at 2.5 to 3 atmospheres absolute (ATA) for 90 minutes with 5 minute air breaks every half hour.
Chapter 9, page 169
Methylene Blue
Indications
Methemoglobinemia with signs or symptoms of cardiac or cerebral hypoxia such as dyspnea, chest pain, ischemic ECG.
Lactic acidosis
Methemoglobinemia > 30%
Chapter 10, page 174
Methylene Blue
Dosage
1 to 2 mg/kg IV, slowly over 5 minutes
Repeat every 30 to 60 minutes
Chapter 10, page 175
Methylene Blue
Relative Contraindications
A patient usually doens not require treatment with methylene blue if he is cyanotic, but is not in cardiorespiratory distress, has no lactic acidosis, and has a methemoglobin level < 30%
Chapter 10, page 174
Methylene Blue
Complications
Nausea
Vomiting
Abdominal pain
Blue-green urine (expected side effect)
Hemolysis if given to a patient with G6PD deficiency.
Chapter 10, page 174
Methylene Blue
Mechanism of Action
Cofactor for NADPH-dependent methemoglobin reductase, allowing more rapid reduction of ferric iron of methemoglobin back to the ferrous iron of normal hemoglobin.
Chapter 10, page 175
Amyl Nitrite
Indications
Life-threatening Cyanide or Cyanogenic compound poisoning, followed by sodium nitrite and/or sodium thiosulfate.
Amyl nitrite is not indtended for use alone.
Chapter 11, page 180
Sodium Nitrite
Indications
Cyanide or cyanogenic compound poisoning followed by sodium thiosulfate.
Chapter 12, page 186
Sodium Nitrite
Complications
Nausea
Headache
Hypotension
Reflex tachycardia
Excessive methemoglobinemia
Chapter 12, page 186
Sodium Nitrite
Dosage
1 vial (300 mg) over 5 minutes
Dosage is not titrated to any specific methemoglobin level.
Administer IV or IO over 5 minutes. Dose can be diluted into 50 to 100 mL of D5W or NS
Chapter 12, page 187
Sodium Nitrite
Mechanism of Action
Induces methemoglobinemia
Increases nitric oxide production to produce vasodilation and improve perfusion to cyanide-poisoned tissues.
Chapter 12, page 187
Sodium Thiosulfate
Indications
Cyanide or cyanogenic compound poisoning
Chapter 13, page 192
Sodium Thiosulfate
Complications
Nausea
Vomiting
Hypotension
Headache
Prolonged bleeding time
Chapter 13, page 192
Sodium Thiosulfate
Dosage
1 vial (50 mL, 12.5 g), over 10 minutes
Chapter 13, page 192
Sodium Thiosulfate
Mechanism of Action
Provides sulfane sulfur that is needed by the hepatic enzyme thiosulfate sulfurtransferase to change cyanide into thiocyanate that is then excreted in the urine.
Chaper 13, page 193
Hydroxocobalamin
Indications
Suspected or confirmed cyanide or cyanogenic compound poisoning.
Confined-space fire victims with smoke inhalation and suspected cyanide poisoning, based on soot in the nose, mouth, or throat, carbonaceous expectorations, altered mental status or hypotension.
Chapter 14, page 198
Hydroxocobalamin
Complications
Chromaturia (reddish-brown urine) in 100% of patients. Harmless and transient, due to the color of the antidote.
Reddish-brown discoloration of skin, sclera, and mucous membranes in at least 94% of patients.
Transient blood pressure elevation in 18% of patients.
Chapter 14, page 198
Hydroxocobalamin
Lab Abnormalities
Artifically increased
Creatinine
Bilirubin
Glucose
Hemoglobin
Chapter 14, page 198
Hydroxocobalamin
Dosage
5 grams IV or IO over 15 minutes
Chapter 14, page 199
Hydroxocobalamin
Mechanism of Action
Direct binding of the cyanide anion to the cobalt moiety of hydroxocobalamin, displacing hydroxide anion and forming essentially non-toxic cyanocobalamin (vitamin B12) that is readily excreted in the urine.
Hydroxocobalamin is a nitric oxide scavenger which results in increased blood pressure.
Chapter 14, page 199
