This document discusses various types of asphyxiants including irritants, chemical asphyxiants, simple asphyxiants, and volatile and systemic asphyxiants. It provides detailed information about specific asphyxiants such as carbon monoxide, hydrogen cyanide, hydrogen sulfide, carbon dioxide, and methyl isocyanate. For each one, it describes properties, sources, mechanisms of action, signs and symptoms, treatment, and post-mortem findings. Common features of asphyxiation and approaches to management are also outlined.

1. ASPHYXIANTS
Dr. Ayushi Gera

2. • Asphyxiants are gases that deprive body tissues of oxygen.

3. HANDERSON AND HAGGARD
CLASSIFICATION
1. Irritants
Irritate air passages and produce inflammatory changes
 Smoke
 tear gases
 ammonia
 formaldehyde
 chlorine
 phosgene
 nitrogen dioxide
 sulphur dioxide

4. 2. Chemical asphyxiants
Inrerrupt with either delivery or utilization of oxygen
 Carbon monoxide
 Cyanide
 hydrogen sulphide etc.

5. 3 . Simple asphyxiant
Inert gases
When breathed in hight concentration displaces oxygen in alveoli .
Clinical effect due to hypoxia
 carbon dioxide,
 methane,
 helium,
 nitrogen,
 nitrous oxide

6. 4. Volatile -
act after getting absorbed in blood either as anaesthetic or agent toxic to liver , kidney
or other organ.
 Aliphatic hydrocarbon
 halogenated hydrocarbon
 aromatic htdrocarbon .
5. Systemic –
These are insecticide,arsine, stibine .

7. CARBON MONOXIDE
PROPERTIES –
• Colorless
• Tasteless
• Non-irritating gas
• Lighter than air
• burns with blue flame
• Produced due to incomplete combustion of carbon
• Mostly accidental poisoning

8. SOURCES
INHALATION OF SMOKE IS MAIN CULPRIT

9. MECHANISM OF ACTION
 Hemoglobin – it has 240 times more affinity for haemoglobin as compared to oxygen
 It binds with haemoglobin to form CARBOXYHAEMOGLOBIN .
 Reduce total oxygen carrying capacity of blood .
 Myoglobin – it has 40 times more affinity than oxygen (decreasing its oxygen
storage capacity)
 Mitochondrial –inhibit cytochrome a3 oxidase & cytochrome p 450 thereby
inhibiting cellular respiration.

10. OXYGEN
HAEMOGLOBIN
DISSOCIATION
CURVE
Shift to left
Increase affinity of oxygen to hb so
decrease unloading of oxygen

11. SIGNS & SYMPTOMS
USUALLY START WHEN CONC. RISES ABOVE 10%.

13. LATE COMPLICATIONS
• Personality disorder
• Short term memory loss
• Parkinsonism
• depression

14. TREATMENT
1. First aid is to immediately remove the victim from the exposure
2. CPR if needed.
3. Firstline of treatmentis100% Oxygen immediately, till the COHb level returns to normal.
4. Hyperbaric Oxygen
• Half life with
1. 21% oxygen=4 – 5 hours
2. 100% oxygen=80 – 90 min
3. Hyperbaric oxygen=30 min
Indications for hyperbaric oxygen
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

15. OTHER IMPORTANT POINTS
• Saturation required to cause the death varies with age and the health. Death usually
occurs when 80% of Hb is saturated with CO.
• Senility / co-existing respiratory or circulatory diseases / anaemia / in association with
CNS depressant drugs like barbiturates, alcohol result in significant decrease in the
lethal saturation of the COHb & death can occur from as little as 30% saturation.
• CO can cross the maternal blood to foetal blood & may cause IUD of the foetus.
• Physical activity increases the rate of saturation.
• Children saturate their blood more rapidly than adults because of their rapid rate of
respiratory exchange.

16. POST MORTEM CHANGES
External
1. Cherry red color of skin, mucous membrane , comjunctiva , nail beds, hypostasis .
2. Cutaneous bullae
Internal
1.Cherry red color of blood n tissues
2. Pulmonary n cerebral edema
3. Necrosis n cavitation of basal ganglia, globus pallidus

18. HYDROCYANIC ACID ( PRUSSIC ACID )

19. Cynide
Solid form
KCN FD
200-300 mg
NaCN FD
200-300 mg
gas
HCN FD
50-60 mg

20. PROPERTIES
• vegetable acid (distributed in many fruits n leaves) in the form of harmless glucoside
amygdalin
• colorless gas or pale blue, highly volatile liquid
• has a faint, bitter almond-like odor
• Other names - Hydrocyanic acid ,Prussic acid, Formonitrile,Formic anammonide
Carbon hydride nitride, Cyanane,Cyclon

21. ROUTE OF POISONING
• Inhalation – cyanide gas
• Ingestion – KCN, NaCN – in acidic ph of stomach get concerted to HOCL & and
become poisonous
• Skin absorption

22. SOURCE

23. -- CHERRIES, APRICOTS, APPLES, BITTER ALMONDS
--100 G OF CRUSHED APPLE SEEDS CAN YIELD 219 MG OF AMYGDALIN WHICH CAN
GENERATE ~10 MG OF HCN

25. MECHANISM OF ACTION
• 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.
HISTOTOXIC ANOXIA

27. TREATMENT : CYANIDE ANTIDOTE KIT

28. • 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.

29. • Cyn-Meth-Haemoglobin is toxic.
• 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.
• VIT B12 iv infusion – hydroxycobalamine contain cobalt which binds with cyanide
with more affinity than cytochrome oxidase to form cynocobalamine which is less
toxic and get excreted in urine .
• EDTA chelating agent

30. POST MORTEM CHANGES
External
• Odor of bitter almonds
• Brick red color of skin and mucous membranes
• Cyanosis of extremities
• Froth at mouth and nostrils
Internal
• stomach mucosa red &congested
• Pulmonary and cerebral edema
• Disseminated petechiae in brain, meninges, pleura, lungs, and pericardium

31. HYDROGEN SULPHIDE
Properties –
• Colourless
• heavy
• flammable gas
• Rotten egg odour

32. SOURCE
• Hydrogen sulfide is produced naturally
by decaying organic matter and is
released from sewage sludge, liquid
manure, sulfur hot springs, and natural
gas.
• It is a by-product of many industrial
processes including petroleum refining,
tanning, mining, wood- pulp processing,
rayon manufacturing, sugar-beet
processing

33. MECHANISM OF ACTION
• Exposure of hydrogen sulphide is mainly by inhalation .
• Inhibit cytochrome oxidase thereby inhibiting oxidative phosphorylation

34. SIGNS & SYMPTOMS

35. TREATMENT
• Remove patient from site of exposure and take him to fresh air
• Artificial respiration & 100 % oxygen given
• Amyl nitrate and sodium nitrate given to form less toxic sulphahaemoglobin .
Which is less toxic & can easily be excreted through kidney .

36. POST MORTEM CHANGES
• Rotten egg smell
• Signs of asphyxia
• Viscera – greenish purple

37. CARBON DIOXIDE
• Heavy colorless gas with a faintly sweet odour
• Act as simple asphyxiant by preventing the tissue from obtaining oxygen
• SOURCES- produced by complete combustion of carbon containing compounds
decomposition of organic matter
manholes, wells
mine explosions

38. CLINICAL FEATURES
• vary with % of carbon dioxide inhalation .
Co2 concentration Clinical features
Upto 2% No physical uneasiness
2-5 % Respiratory rate increase & deep
breathing
5-10 % Headache , dizziness,confusion ,
nausea ,dyspnoea
>10 % Tachycardia , increased HR ,
increased BP
20-30 % Fall nin respiratory minute volume ,
convulsions
40-50 % Paralysis of respiratory centers

39. TREATMENT
• Administer oxygen
• Supportive treatment

40. POST MORTEM FINDINGS
• Cyanosis
• Froth at mouth or nostrils
• Congestion
• Petechial haemorrhages

41. METHYL ISOCYNATE
• Stable liquid below 27c, gaseous at 31c
• Highly volatile n inflammable
• Used in manufacture of carbamate pesticides, adhesives n plastic
• The Bhopal disaster was an industrial disaster that occurred in the city of Bhopal
(1984)A pesticide plant released 40 tones of methyl isocyanate (MIC) gas.

42. MECHANISM OF ACTION
• Causes carbamylation at biochemical level
• Irritant action on skin , eyes & mucous membrane

43. CLINICAL FEATURES
• Lacrimation chest pain
• Irritation of eyes hemoptysis
• Blurring of vision pulmonary edema
• Photophobia convulsions
• Corneal ulceration coma
• Cough death
• Dyspnea
• Dermal- erythema, rashes

44. MANAGEMENT
• Decontamination of skin & eyes
• Oxygen administration
• Bronchodilators & steroids
• Supportive treatment

45. POST MORTEM FINDINGS
• Signs of asphyxia
• Pulmonary edema ( increased weight of lung 2-3 times normal )
• Cerebral edema
• Visceral congestion

46. PHOSGENE
• colourless gas,
• heavier than air,
• odour of freshly-cut hay.
• it is hydrolysed in the body to hydrochloric acid which produces a systemic
inflammatory response .
• Also stimulates the synthesis of lipoxygenase-derived leukotrienes causing pulmonary
oedema.
• it increases pulmonary vascular permeability, leading to increased fluid accumulation in
the interstitial and alveolar compartments