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Acute Aspirin Overdose Relationship to the Blood Buffering System biochem

Acute Aspirin Overdose Relationship to the Blood Buffering System Focus concept The response of the carbonic acid/bicarbonate buffering system to an overdose of aspirin is Prerequisites Principles of acids and bases, including pK, and the Henderson-Hasselbalch equation. The carbonic acid bicarbonate blood buffering system. Background You are an emergency room physician and you have just admitted a patient, a 23-year-old female, who had been hospitalized for psychiatric treatment for the past six months. She was out on a day pass when she was brought to the emergency room around 9 pm. The patient was disoriented, had trouble speaking, and was suffering from nausea and vomiting. She was also hyperventilating. The patient admitted to taking an entire bottle of aspirin, which contained 250 tablets. The patient said that she took the tablets around 7 pm that evening. You draw blood from the patient and the laboratory performs the analyses shown in Table 1.. The patient is experiencing mild respiratory alkalosis. Table 1.1: Arterial blood gas concentration in Patient, twe hours Patient, ten hours after aspirin ingestion Normal values after aspirin ingestion 35-45 mm Hy 9 Pco HCO 18 mM 21 mM 22-26 mM 75-100 mm Hg 43 mm Hg 113 mm Hg Po pH 7.44 7.55 7.35-7.45 Blood salicylate 57
In the emergency room, the patient is given a stomach lavage with saline and two doses of activated charcoal to adsorb the aspirin. Eight hours later, nausea and vomiting became severe, and her respiratory rate increased; she was in severe respiratory alkalosis, and further treatment was required. You carry out a gastric lavage at pH = 8.5 and administer further activated charcoal treatments, one every 30 minutes. A bicarbonate drip was required to prevent the blood bicarbonate concentration from dropping below 15 mM. After 12 hours, blood salicylate concentrations began to decrease. The patient's blood pH begins to drop around 24 hours after the aspirin ingestion and finally returned to normal at 60 hours after the ingestion, although salicylate concentrations did not fall to zero until about 80 hours after aspirin ingestion.

Determine the ratio of HCO3- to H2CO3 in the patient’s blood 10 hours after aspirin ingestion. How does this  compare  to  the  ratio  of  HCO3-  to  H2CO3  in  normal  blood?  Can  the  H2CO3/  HCO3-  system  work effectively as a buffer in this patient under these conditions? Explain?

 

Sixty  hours  after  aspirin  ingestion,  the  patient’s  blood  pH  returned  to  normal  (pH  =  7.4).  But  what mechanism(s) was the patient’s blood pH return to normal?


Are there other substances in the blood that can serve as buffers?



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Sixty hours after aspirin ingestion, the patient’s blood pH returned to normal (pH = 7.4). But what mechanism(s) was the patient’s blood pH return to normal?

Acetylsalicylic acid or aspirin which is monoprotic organic acid (pH 4.57) and less acidic in comparison to the salicylic acid due to the replacement of an acidic group phenol by ester in acetylsalicylic acid or aspirin. Therefore, after ingestion of aspirin pH of the blood is imbalanced As the salicylate is removed, the stimulus of salicylate-induced hyperventilation also decreases. After 60 hours, the concentration is decreased to a minimal amount, and in the basic blood OH and H+ combine to form water. Depletion of H+ ions lead to shift in the reaction equilibrium, which in turn leads to H2CO3 depletion and hence CO2 depletion. The breaths are shallow and which result in greater concentration of CO2 and hence more H- ions thus bringing back the pH to normal

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