Asphyxiants: Carbon Monoxide (CO)

D i.e. None

A i.e. Cherry red cyanosis

Ans. is ‘d’ i.e., All of the above

Pollutant  Sources

Carbon monoxide Combustion equipment,stove, Gas heater.

Nitrogen dioxide Gas cookers, Cigarattes

Sulphur dioxide  Coal combustion

Carbone dioxide Combustion, respiration

Ozone Electric arcing, UV light sources

Ans. C: Anaemic hypoxia

When carbon monoxide is inhaled, it takes the place of oxygen in hemoglobin

Levels of carbon monoxide bound in the blood can be determined by measuring carboxyhemoglobin, which is a stable complex of carbon monoxide and hemoglobin.

The affinity between carbon monoxide and hemoglobin is 240 times stronger than the affinity between hemoglobin and oxygen.

CO binds to hemoglobin, producing carboxyhemoglobin (COHb), which decreases the oxygen-carrying capacity of the blood. This inhibits the transport, delivery, and utilization of oxygen.

This causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue.

Levels of oxygen available for tissue use are decreased. This situation is described as CO shifting the oxygen dissociation curve to the left.

Blood oxygen content is actually increased in the case of carbon monoxide poisoning; because all the oxygen is in the blood, none is being given to the tissues, and this causes anemic hypoxic.

Carbon monoxide binds to hemoglobin (reducing oxygen transportation), myoglobin (decreasing its oxygen storage capacity), and mitochondrial cytochrome oxidase (inhibiting cellular respiration).

Hallmark pathological change following CO poisoning is bilateral necrosis of the pallidum.

Hemoglobin acquires a bright red color when converted to carboxyhemoglobin, so a casualty of CO poisoning is described as looking pink-cheeked and healthy.

The main medical treatment for carbon monoxide poisoning is breathing 100% oxygen.

Ans. Anemic hypoxia

Ans. is ‘b’ i.e., Blue skin discoloration

Postmortem findings of CO-poisoning

• Fine froth at mouth and nose.
• Bright cherry red discolouration of skin, mucous membranes, nail-beds, blood, tissues and internal organs. Cyanide poisoning and exposure to cold causes similar redness.
• Blood is fluidish thin, hyperemia (congestion) is general, and serous effusion are common.
• Skin blisters or red patches due to hypoxia in areas that contact the ground or appositional skin e.g. axilla, inner thigh, buttock, calves, knee.
• Lungs show congestion with pink fluid blood, followed by pulmonary edema and bronchopulmonary consolidation.
  Pleural and pericardial anoxic haemorrhage, tiny focal necroses in myocardium are late changes (5 days).
• Bilateral symmetrical necrosis and cavitation of basal ganglia (esp globus pallidus and putamen) is most characteristic feature in delayed deaths (prolonged hypoxia) may be confused with PM finding of parkinsons patient. Although cerebral cortex, cerebellum, hippocampus and substantia nigra of brain stem may also be affected. Ring shaped punctiform haemorrhage in white matter, wide spread brain oedema, punctate haemorrhage in meninges, cortex and cellular necrobiosis of ganglionic cells in cortex are other features.
• Spectroscopic examination, Hoppe – Seyler’s test (10% NaOH), kunkel’s (tannic acid) test and adding water (15 ml) in 2 drops of blood can detect CO.

Ans. is `b’ i.e., > 10%