Toxic Gases (CO) Flashcards
Endogenous source of CO:
Catabolism of protoporphyrin ring of Hb
Normally does not exceed 4-6%
Exogenous sources of CO:
• Automobile exhaust (mainly)
• Incomplete combustion of Carbon containing material
• All heater types at home
• Fires
• Tobacco cigarettes
Factors affecting CO toxicity:
- Duration of exposure
- Concentration of the gas.
- High altitude (low O2).
- disease in the CVS or RS
- Hematological disease (anemia)
- Neonate and infants.
Pathophysiology of CO :
• Hypoxia high affinity to Hb (210 times than O2)
• ⬇⬇O2 release: shifting of dissociation curve of remaining oxyhemoglobin to the left less O2 available to tissues
Other mechanims of CO:
• Myoglobin impairment: Affinity is 40 times more than O2 ( myocardial depression & arrhythmia )
• Mitochondrial impairment: bind to mCytochrome aa3 and block of cellular O2 uptake.
• brain reperfusion injury: **lipid peroxidatin & luekocyte mediated inflammatory change … demylination of brain.
Clinical manifestations of CO toxicity:
Most common symptoms:
N&V, headache, dizziness, lethargy, and feeling of weakness.
When does the recurrent symptoms syndrome occurs:
After lucid Interval (1-40 days) in moderate CO toxicity
Incidence: 10-20%
CNS symptoms of CO toxicity:
Note : cns is the most sensitive
Headache, dizziness, ataxia, syncope, seizures, and coma.
What is the delayed neuropsychiatric sequence:
delayed neuropsychiatric sequence (DNS) can occure in 50% of patients who have survived from acute CO poisoning.
It’s characterised by slowness, Parkinsonism and cognitive impairment.
S&S of DNS:
not domain name system 🙃
Depression, emotional liability, hallucinations, personality changes, and verbal aggressiveness.
Children: behavioral changes and learning difficulties
Clinical manifestations of CO in CVS:
• Tachycardia is common. Bradycardia occurs in severe cases. Why?🙃
• Palpitation and chest pain.
• Patchy myocardial infarction with ECG changes of ischemia (ST-segment deviations, T wave inversion, and Q-waves).
• A&V arrhythmia
• Hypotension
Dermal changes in CO toxicity:
Cherry red in non survival
Pallor or cyanosis
Blisters due to pressure necrosis and direct effects of CO on the epidermis.
Renal manifestations of CO toxicity:
Oliguric and non-oliguric renal failure
CO Eye signs:
Retinal vein
- bright red
- congested
- tortuous
vision
- blurred vision
- loss of dark adaptation
- blindness
other
- disk edema
- flame shaped hemorrhage
Respiratory symptoms of CO toxicity:
Non-cardiogenic pulmonary edema
Cardiogenic pulmonary edema
Explain why???
Other symptoms of CO toxicity:
GIT: N&V, abdominal pain, may be diarrhea, so may be misdiagnosed as gastroenteritis or food poisoning, especially in children.
Bood: DIC and TTP
Muscles: rhabdomyolysis
Metabolic: lactic acidosis, hyperglycemia, and hypercalcemia.
CO investigations:
Carboxy Hemoglobin level:
Measured by oximeter :10% in smoker and 0-5% in normal
ABG:
O2 may be normal
Oximeter shows false ⬆ O2 saturation and can not be relied
Metabolic acidosis if preset usually from lactic acidosis which is bad prognosis sign
Management of CO toxicity:
• Rapid removal from continued exposure
• 100% O2 should be provided
• Cardiac monitoring and IV access
• Hyperbaric oxygen (HBO)
• Do not aggressively treat acidosis with pH above 7.15
What is hyperbaric oxygen?
And what can it do?
Oxygen at 2-3 atmospheric pressure.
It decreases CO half-life to 20 min
Why should we not treat acidosis above 7.15 in cases of carbon monoxide poisoning?
This can increase tissue hypoxia by the left shift of the oxyhemoglobin dissociation curve.
Post-mortem appearance of CO toxicity
• Cherry red appearance especially in the area of postmodern lividity
• Skin Blisters are seen sometimes in claves, buttocks, wirst, and knee.
• Cherry pink color of blood and tissues.
• Pulmonary edema
• in delayed death: necrosis and cavitation of basal ganglia, especially globus pallidus.
