1/1/2013

Chemical Asphyxiants
Pulmonary Respiration

Chemical asphyxiants acting on Cellular Respiration

Carbon Mono oxide (CO):- Colourless, tasteless, odourless, non-irritant gas but is a Silent Killer.
O2 form inhaled air goes to pulmonary blood

Pulmonary Respiration Hb + O2 = HbO2 Artery

HbO2 = Hb + O2

Cellular respiration

Within the cell there are nutrients. If O2 cannot enter into the cell released by HbO2, it is cellular hypoxia. Cytochrome Oxidase play important role in the tissue respiration. It helps to separate oxygen from HbO2. Then Oxygen enters into the cell. Inside the cell oxygen combines 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 severity of the CO toxicity depends upon the % 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 occupiers 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.

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) First line of treatment is 100% Oxygen immediately, till the COHb level returns to normal. On this regimen Half life of COHb is 74 minutes. Lactic Acid 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 is pregnant, because clearance of CO in 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.

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.