S K Haldar CLI Mumbai Notes

1. 1/1/2013 Chemical Asphyxiants
PulmonaryRespiration
Chemical asphyxiantsactingon
CellularRespiration
Carbon Mono oxide (CO):-Colourless,tasteless,odourless,non-irritantgasbutisa SilentKiller.
O2 form inhaledairgoestopulmonaryblood
PulmonaryRespirationHb+ O2 = HbO2 HbO2 = Hb + O2
Artery
Cellularrespiration
Withinthe cell there are nutrients.If O2cannot enterintothe cell releasedbyHbO2, it is cellular hypoxia.
Cytochrome Oxidase playimportantrole inthe tissue respiration. Ithelpsto separate oxygen from HbO2.
ThenOxygenentersintothe cell. Insidethe cell oxygencombines with the nutrients and produce energy
& CO2
N + O2 = E + CO2
Nutrients Energy
Hb has 200 to 300 times more affinity to CO than O2.
1) CO combines with Hb to form Carboxy haemoglobin (HbCO)
2) CO also depresses Cytochrome Oxidase (aa3)
3) CO has direct toxic effect on the cell. It increases acid secretion inside the cell, which kills the cell.
Endothelial cells & platelets release nitric acid.
The severityof the COtoxicitydependsuponthe % of HbCO in the blood. Above 40 gms/100gms of Hb in
the blood can kill the person.
CoHb is measured by Dedicated Carboxy Meter by which CO contents are measured of heparinised
arterial or venous blood, in a live person. In dead person it measured by Gas Chromatography of the
blood.
It is an occupier’s responsibility that the worker working in the area where there is a possibility of CO
Poisoning, the worker should be observed from outside. If worker becomes unconscious he may die.
Methylene choloride (Paint strippers) fume inhalation sometimes causes CO Poisoning.
Pathophysiology:-
Sign & Symptoms of CO Poisoning:- Symptoms usually start when conc. Rises above 10%. Mainly
Cardiovascular & Neurological signs
General:-Headache, Nausea, vomiting, dizziness, lethargy, weakness.

2. Neurological signs:- Basal ganglia have high consumption of O2. Thus they are affected most.
confusion,disorientations, visual disturbances,syncope &seizures. Cogwheel type rigidity, opisthotonus
& flaccidity or spasticity
Cardiac:- Patients with coronary heart disease may experience angina, arrhythmias & myocardial
infarction. Hypotension.
Retinal :- Retinal haemorrhages,
Skin:- Cherry red colour of skin “when you are red you are dead”
Muscle necrosis:- Creatine Phosphokinase
Treatment:- 1) Firstline of treatmentis100% Oxygenimmediately, till the COHb level returns to normal.
On thisregimenHalf life of COHbis74 minutes. LacticAcid produced due to anaerobic respiration of the
tissue facilitates tissue Oxygen diffusion.
2) Hyperbaric Oxygen:- Indications:- 1) If COHb is more than 40 gm/100gm of Hb
2) If he is unconscious
3) If Cyanosed
4) If female ispregnant,becauseclearance of COin Foetal
Carboxy Hb is slower than adult Hb
5) If suffering from some other illness
Advantages of Hyperbaric Oxygen:- 1) Half life of COHb at 3ATA (Absolute Atmosphere) of
Oxygen is only 23 minutes.
2) Improves Mitochondrial Function
3) Impairment of platelet adhesion in the capillaries
4) Inhibition of lipid peroxidation
In UK most of the centres use hyperbaric oxygen if COHb is above 25 to 30 %. Myocardial Ischemia &
Neurological signs especially Coma are treated with Hyperbaric O2 irrespective of the concentration of
HbCO in the blood.
Hyperbaric baric oxygen is given at 252 Kilo Pascal pressure.
Side effect:- Alveolar Rupture. Main complication is Ear Barotraumas.
Delayed Symptoms of CO Poisoning:- Weeks after the recovery form CO Poisoning the patient show
neuropsychiatric symptoms. Mush more pronounced in elderly patients. Parkinsonism can be clearly
detected, but the personality, cognitive changes are not easily detected. Children may present with
behavioural or educational problems. Some of the signs may remain permanent.
HCN
HCN has no affinity for Oxygen. Thus at in the lungs HbO2 is formed as usual. Both HbO2 and HCN
reaches at tissue level. HCN has strong affinity for Cytochrome Oxidase. So at tissue level it forms
cytochrome Oxidase Cyanide complex. Cellular transport of oxygen is blocked causing tissue hypoxia,
causing cell death.
Treatment:- First Aid:- Immediate Amyl Nitrate inhalation:- Amyl nitrate capsule is broken &
spread over the handkerchief and patient is given the inhalation for 15 -30 seconds. This process
must be repeated after every 2-3 minutes, until the capsule is exhausted.
Amyl nitrite converts Hb to Meth hemoglobin. Meth Hb has more affinity to CN than Cytochrome
Oxidase. So Cyn- meth-Hemoglobin complex is formed and cytochrome oxidase is released, and
cellular oxygenation will start again.
However Cyn-Meth-Haemoglobin is toxic. So the further treatment is done in hospital.
2) Hospital Treatment:-i) So when patient arrives at the hospital Sodium Thiosulphate is given
IV. Sodium Thiosulphate is a Sulpher Donor, combines with
Cyn-Meth-Haemoglobin to form Thiocyanate, which is nontoxic and is
excreted through urine.

3. 12.5 Gm. Of Sodium Thiosulphate in 25 Ml. of glucose or normal saline
solution produces 50% solution of Sodium Thiosulphate, which is to be
given slow IV for 5-6 minutes.
ii) Chelating Agents:- Cobalt EDTAte will combine with Cyn Meth Hb to
form Cobalti Cynide, which is non toxic. It is given if the patient is in
comatose condition. Dose 300Mg in 20Ml. of Glucose Soution IV slowly for
3-4 minutes. It is a chelating agent combines with Cyanide to form an inert
complex Cobalti Cyanide.
iii) Conversion of cynide into cyn-cobalamine by Vit B12 (cobalamine).
Under research.