Toxic Gases (CO) Flashcards

1
Q

Endogenous source of CO:

A

Catabolism of protoporphyrin ring of Hb
Normally does not exceed 4-6%

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2
Q

Exogenous sources of CO:

A

• Automobile exhaust (mainly)
• Incomplete combustion of Carbon containing material
• All heater types at home
• Fires
• Tobacco cigarettes

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3
Q

Factors affecting CO toxicity:

A
  1. Duration of exposure
  2. Concentration of the gas.
  3. High altitude (low O2).
  4. disease in the CVS or RS
  5. Hematological disease (anemia)
  6. Neonate and infants.
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4
Q

Pathophysiology of CO :

A

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

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5
Q

Other mechanims of CO:

A

• 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.

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6
Q

Clinical manifestations of CO toxicity:
Most common symptoms:

A

N&V, headache, dizziness, lethargy, and feeling of weakness.

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7
Q

When does the recurrent symptoms syndrome occurs:

A

After lucid Interval (1-40 days) in moderate CO toxicity
Incidence: 10-20%

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8
Q

CNS symptoms of CO toxicity:

A

Note : cns is the most sensitive
Headache, dizziness, ataxia, syncope, seizures, and coma.

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9
Q

What is the delayed neuropsychiatric sequence:

A

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.

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10
Q

S&S of DNS:

not domain name system 🙃

A

Depression, emotional liability, hallucinations, personality changes, and verbal aggressiveness.

Children: behavioral changes and learning difficulties

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11
Q

Clinical manifestations of CO in CVS:

A

• 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

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12
Q

Dermal changes in CO toxicity:

A

Cherry red in non survival
Pallor or cyanosis
Blisters due to pressure necrosis and direct effects of CO on the epidermis.

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13
Q

Renal manifestations of CO toxicity:

A

Oliguric and non-oliguric renal failure

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14
Q

CO Eye signs:

A

Retinal vein
- bright red
- congested
- tortuous

vision
- blurred vision
- loss of dark adaptation
- blindness

other
- disk edema
- flame shaped hemorrhage

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15
Q

Respiratory symptoms of CO toxicity:

A

Non-cardiogenic pulmonary edema
Cardiogenic pulmonary edema
Explain why???

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16
Q

Other symptoms of CO toxicity:

A

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.

17
Q

CO investigations:

A

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

18
Q

Management of CO toxicity:

A

• 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

19
Q

What is hyperbaric oxygen?
And what can it do?

A

Oxygen at 2-3 atmospheric pressure.
It decreases CO half-life to 20 min

20
Q

Why should we not treat acidosis above 7.15 in cases of carbon monoxide poisoning?

A

This can increase tissue hypoxia by the left shift of the oxyhemoglobin dissociation curve.

21
Q

Post-mortem appearance of CO toxicity

A

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.