Carbon monoxide Poisoning imp on respiratory systemacts.pptx

The presentation describes carbon monoxide gas harmful and potentially lethal effects on human respiratory system and its connections with the brainstem

1. Carbon monoxide Poisoning

2. Scenario 40 years old Ahmed returned to his apartment in the cold winter night. He turned on his heater and shut all the windows. After sleeping for 2 hours, he woke up and noticed that his vision became progressively blurred. When he got up he became disoriented and fell down. His friend found him unconscious and hyperventilating with a reddish complexion. He immediately took him out of the house and called for an ambulance. The doctor made a diagnosis of “CO poisoning” based upon history and examination. Ahmed was treated with hyperbaric oxygen therapy.  

3. Learning Objectives Dynamics of oxygen transport by the blood. Understanding the oxygen- Hb dissociation curve and effect of CO on this curve. Forms of transport of respiratory gases in blood including O2, CO2, CO and Nitrogen. Learning the physiological basis of treatment with hyperbaric oxygen. Compare the skin color of the patient in cyanosis, CO poisoning and methemoglobinemia Pathophysiology of CO poisoning. Relate the symptoms to CO poisoning . (Clinical) Which complex protein of electron transport chain is inhibited by carbon monoxide? why is oxygen carrying capacity is reduced in carbon monoxide poising?

4. Symptoms of CO Poisoning Blurred vision Disorientation dizziness Unconsciousness Hyperventilation Reddish complexion

5. Physiological CO is toxic because it reacts with Hb to form CARBOXY Hb ( bright red colour ) Hb affinity for CO is 250 times > O 2 It competes with O2 to react with Hb Once carboxyHb is formed ,it librates CO very slowly Dissociation curve of remaining HbO2 shifts to left.

6. Although the oxygen content of blood is greatly reduced , P02 remains normal so cherry red colour of COHb is visible in the skin. It is dangerous because the brain is one of the first organs affected by lack of oxygen, the person may become disoriented and unconscious before becoming aware of the danger.

7. Effect of CO on O2 – Hb dissociation curve curve curve

8. Treatment Administer hyperbaric oxygen. Oxygen at high alveolar pressure can displace carbon monoxide rapidly from its combination with hemoglobin. The patient can also benefit from simultaneous administration of 5 % CO2 which strongly stimulates the respiratory center, which increases alveolar ventilation and reduces the alveolar CO. With intensive O2 and CO2 therapy, CO can be removed from the blood

9. Compare skin colour Cyanosis:- bluish CO poisoning:- cherry red Methemoglobinemia :- bluish Here Hb contain Ferric form of iron.

10. Transport of oxygen from alveoli to pulmonary capillaries Alveolar PO 2 104mmHg  Pulmonary capillary PO 2 40mmHg This great difference of pressure allows rapid uptake of oxygen by the pulmonary blood. PO 2 becomes equal before blood has passed more than one third of the distance through the capillary.

11. Transport of Oxygen in the Arterial blood 98% of blood entering the left atrium  PO 2 104 mmHg 2% has passed from the aorta through the bronchial circulation and is not exposed to lung air, this is called “shunt flow” (it is shunted past the gas exchange area) Shunt flow PO 2 is 40mmHg as that of normal venous blood This “venous admixture of blood” causes the PO 2 of aortic blood to fall to 95mmHg

12. (Important graph)

13. Diffusion of Oxygen from the Peripheral Capillaries into the Tissue Fluid When the arterial blood reaches the peripheral tissues, its PO 2 in the capillaries is still 95 mm Hg while the PO 2 in the interstitial fluid that surrounds the tissue cells averages only 40 mm Hg Thus, there is a tremendous initial pressure difference that causes oxygen to diffuse rapidly.

14. Diffusion of oxygen from the peripheral capillaries into the tissue cells The normal intracellular PO 2 ranges from as low as 5 mm Hg to as high as 40 mm Hg, averaging 23 mm Hg. Because only 1 to 3 mm Hg of oxygen pressure is normally required, even this low intracellular PO 2 of 23 mm Hg is more than adequate and provides a large safety factor.

15. Diffusion of oxygen from the peripheral capillaries into the tissue fluid and cells

16. Forms of transport O 2  97 % bound to Hb in RBCs 3 % dissolved in water of blood and cells N 2  At sea level, 1 litre of N2 is dissolved in the entire body. Slightly less than one half is dissolved in H2O of the body and rest is dissloved in the fat. N2 is 5 times more soluble in fat.

17. Forms of transport CO 2 a) 70 % transported from tissues to the lungs in reversible combination of CO2 with H2O in RBCs b) 30 % carbaminoHb in combination with amino radicals of Hb molecule loose bond c) Plasma proteins in tissue capillaries also carry little amount of CO2.

18. Physiological basis for hyperbaric O 2 Breathing 100% oxygen while under increased atmospheric pressure.  Although only a fractional increase in oxyhaemoglobin occurs, there is a many-fold increase in oxygen dissolved in the plasma. This provides extra available oxygen for the tissues and because of the high partial pressure at which the oxygen is dissolved, causes a diffusion gradient from plasma to tissues.

19. Allows oxygen to cross the blood brain barrier effortlessly Stimulates the growth of new capillaries (tiny blood vessels) which allows circulation to be restored or improved, and this reduces or eliminates  hypoxia  in affected areas.  Stimulates  the immune response  Has potent anti-inflammatory effects

20. Q. which complex protein of electron transport chain is inhibited by carbon monoxide? A.Complex 4 of cytochrome oxidase enzyme gets inhibited by carbon monoxide leading to formation of reactive oxygen species and lack of production of ATP. Q.Why is oxygen carrying capacity is reduced in carbon monoxide poising? A. Carbon monoxide has got greater affinity of binding with hemoglobin than oxygen which further prevents the RBC from carrying oxygen around the body leading to hypoxia of body cells.