Acid base disturbance(definitin,mechanism).pptx

This lecture discusses the mechanism of acide-base balance

1. Acid – base balance A.Prof: Abdul Kareem Alkhawlani

2. Acid – base balance -The pH(-ve logarithm of H+ concentration) and is widely used in medicine. - Normal arterial blood pH range from 7.36 to 7.44 (7.4 +- 0.04) - Many of the body‘s metabolic and physiologic functions are pH dependent, or pH sensitive. - PH of blood &body fluids (extra and intra cellular) is stabilized within these limits despite of addition of acid (through oxidative metabolism of protein ,fat and carbohydrate) or alkali.

3. -Wide fluctuation in H +concentration are prevented by the presence of several PH buffers. The buffers are weak acids that exist in equilibrium with the corresponding base, at physiological PH.as well a s by respiratory and renal mechanisms. -Phosphate , ammonia, proteins including Hb, and bone, all provide PH buffering capacity but the major PH buffer in the blood is the bicarbonate / carbonic acid system . -Pa CO2 is used to represent concentration of acid in system. -Concentration of base in system can be determined by measuring HCO3 – concentration.

4. -Plasma bicarbonate ,CO2 concentration, and PH are chemically related to one another by the Henderson-Hassel Balch equation PH= pka+log (base/acid ) Pka (constant)=6.1 for carbonic acid The equation represent a very important relationship. It predicts that the ratio of HCO3 – to dissolved CO2 ,determines blood PH. -The buffer system is of physiologic importance because both pulmonary and renal mechanisms for regulation PH, work by adjusting this ratio.

5. - The PaCO2 can be modified rapidly by changes in respiratory minute ventilation, while plasma HCO3 can be altered by regulating its excretion by the kidneys. - Clinical disturbance of acid-base metabolism classically are defined in terms of the HCO3- /CO2 buffer system. - Rise or fall in HCO3-(22-30mmol/L) are termed metabolic alkalosis or acidosis, respectively. Rise or falls in PCO2 (36-46mmHg)are termed respiratory acidosis or alkalosis respectively.

6. The 1ry changes in the 4 simple acid-base disturbance as follow .

7. Acid –base disturbance: may be either: 1-Simple : presenting as isolated metabolic acidosis or alkalosis or respiratory acidosis or alkalosis. 2-Mixed : denoting independently co-existing disorders.

8. Simple acid-base disturbance 1-Metabolic acidosis: Which is characterized by primary decrease of plasma bicarbonate concentration. The resulting decrease in arterial PH stimulate ventilation to decrease Paco2 and returns PH towards normal. 2-Metabolic alkalosis : Which is characterized by primary increase in plasma bicarbonate concentration. The elevated arterial PH depresses ventilation and this elevates Paco2 and return toward normal.

9. 3-Respiratory acidosis: Which is characterized by primary retention of CO2 and elevation of Paco2. The depressed arterial PH enhance renal retention of bicarbonate. 4-Respiratory alkalosis: Which is characterized by primary washout of CO2 and consequently decrease of Paco2. The elevated arterial PH enhances renal bicarbonate excretion.

10. Mixed acid-base disorders Any combination of simple acid-base disorders can co-exist except combined respiratory acidosis and alkalosis. The patient is either hypo ventilating or hyperventilating for example patient with pulmonary disease may not respond to metabolic acidosis with appropriate hyperventilation. The result in the production of combined metabolic and respiratory acidosis which can lead to severe acidaemia, and poor prognosis. Even a triple acid-base disturbance may occur for example patient with alcoholic ketoacidosis may develop added metabolic alkalosis due to vomiting and respiratory alkalosis due to hyperventilation of hepatic dysfunction.

11. Metabolic acidosis - This may develop as a result of accumulation of any acid other than carbonic acid or loss of bicarbonate. - It is evaluation is facilited by calculating the anion Gap. - The normal cation as Na+, K+ ,Ca+ and MG2+ - The normal anions as Hco3- ,cl- ,ph, and sulfate. - The sum of cation and anion are equal Anion gap= {Na +K} – {HCO3+Cl } -Normally it equals 10-12 mmol/L A etiology: MA may be associated with either: A-Normal AG: When it results from loss of bicarbonate, there disorders are termed hyperchloremic acidosis. B-High anion gap : When it result from retention of unmeasured anion whether endogenous or exogenous.

12. The causes of metabolic acidosis include: A- Normal AG metabolic acidosis (hyperchloraemic acidosis): 1-Increased gastro-intestinal bicarbonate loss: a-Diarrhea b-Ileostomy c- Uretero - sigmoidostomy 2-Increase renal bicarbonate loss: a- Proximal RTA (type 2) b-Acetazolamide c-Hyperparathyroidism d-Tubular damage e.g.: drugs, Para proteins. 3- Decrease renal H+ execration: a-Distal RTA (type I) b-Type 4 RTA+ Hyperkalemia 4-Increased chloride production: a-Ammonium chloride ingestion b-Increased catabolism of lysine or arginine.

13. B-High AG metabolic acidosis: 1-Endogenous: a-Lactic acidosis. b-Ketoacidosis : DM, starvation, alcoholic. c-Renal failure (acute & chronic) 2-Exogenuous: a-Salicylate. b-Methanol. c-Ethylene glycol.

14. Pathophysiology: 1-Fall in plasma PH: a-Stimulate ventilation (kussmaul’s respiration) b-Depressed cardiac contractility c-Peripheral arterial vasodilation d- Venoconstrication c-Depressed CNS f-Glucose intolerance g- K+ loss from the cells which may lead to K+ deficiency if renal function is normal, a hyperkalaemia if renal im pairment.

15. 2-Diarrhoea : Causes loss of large quantities of bicarbonate . metabolic acidosis develops a long with volume depletion. Despite acidosis the urine PH remains above 5.5 because acidosis and the associated hypokalemia increase the renal synthesis and excretion of ammonia . 3-Lactic acidosis : Two type recognize: a- Type A due to lack of O2 in tissue in case of shock , heart failure , a sever anemia . b- Type B: due to increase production or decrease hepatic metabolism of lactate, in case of hepatic failure , DM , metformin ingestion.

16. 4- Alcoholic ketoacidosis : M ay develop in chronic alcoholic when alcohol consumption is abruptly diminished . typically Glucose concentration is low or normal, triglyceride, cortisol are increased. Hypokalemia . 5 -Salicylate intoxication: in adult cause a high AG MA. Lactic and ketoacid production is increased by direct effect of the drug interfering with carbohydrate , fat and protein metabolism. Respiratory alkalosis may be associate due to central stimulation of the respiratory center.

17. Clinical pictures: 1-Hyperventilation manifesting by deep ,sighing, and rapid ( kussmaul ’s respiration). 2-Cardiovascular dysfunction may manifest with hypotension ,arrhythmias and pulmonary edema. 3-Cerebral dysfunction may result in confusion and convulsions. 4-Mainfestation of the underlying disorder. Investigations: a-Arterial blood gases: plasma PH, bicarbonate , Paco2 are all decreased . b-AG may be normal or elevated according to the underlying case. c- Hypokalemia may develop.

18. Treatment : 1- Treatment of the underlying cause: a-For lactic acidosis O2 delivery to tissue should be maximized . b-For salicylate intoxication : gastric lavage with isotonic saline ,induction of alkaline diuresis by sodium bicarbonate or acetazolamide . Hypokalemia should be corrected. H emodialysis is needed in severe case and if renal failure develop. 2-Alkali therapy : with oral or IV sodium bicarbonate . this usually reserved for patient with severe acidosis ( PH <7.0) and normal AG. The aim is to raise plasma bicarbonate concentration to about 20 mml/L.

19. Metabolic alkalosis This may develop as a result of gain of bicarbonate or loss of non-volatile acid ( usually HCL by vomiting ) from the extracellular fluid. Etiology : -For bicarbonate to be added to the extracellular fluid, it may be either administered exogenously as ( acute alkali administration or milk alkali sy ) or synthesized endogenously mainly by the kidney.

20. The kidney retains HCO3 or a result of two mechanism. a-Contraction of extracellular fluid is commonly associated with CL- deficiency , K+ deficiency and decreased in GFR. These factors enhance Proximal tubule HCO3 reabsorption And evoke secondary hyperaldasteronism which stimulate H+ secretion by the collecting tubule which result in alkalosis. b- Autonomous hyperaldosteronism which is commonly associated with extracellular fluid volume expansion and hypokalemia in primary hyperaldestonism, Cushing sy ,and liddle s sy .

21. Pathophysiology: 1-Arise in plasma PH result in: a-Depression of ventilation. b-Cardiac arrhythmias. c-Depression of CNS function. d- Tetany and increase in neuromuscular irritability (due to decrease in ionized calcium ). Clinical picture: - There is no specific symptoms or sign of metabolic alkalosis ,however severe case may result in cardiac arrhythmia, hypoventilation, mental confusion , seizure and rarely tetany .

22. Investigation : 1-Arterial blood gases and plasma electrolytes. Plasma PH, HCO3 ,Paco2, are all increased. Hypokalemia , hypophosphatemia are associated . 2-Urinary chloride concentration is useful in distinguishing alkalosis due to volume contraction from that due to primary mineralocorticoid excess. In the former state the urinary chloride is less than 10 mmol/ L,whil In the primary mineralocorticoid excess, the urinary chloride above 20 mmol/L.

23. Treatment : 1-Treatment of the underlying cause . 2-Correction of the extracellular fluid volume by 0.9 % Nacl to be given at rate to correct hypotension &tachycardia . 3-Correction of the associated ↓K . 4-In severe case dilute (0.1 N) Hcl or laysine hydrochloride, arginine hydrochloride are given . 5-If renal function, is impaired hemodialysis, may indicated.

24. Respiratory acidosis It result from rise in Paco2 as a result of alveolar hypoventilation. Etiology : 1-CNS: depression of RC: Narcotics ,head injury or high o2 inhalation. 2-Impaired in ventilating mechanisms :respiratory muscle paralysis. 3-Lung disease : COLD, sever pneumonia, pulmonary edema. 4-Largngeal or tracheal obstruction.

25. Pathophysiology: - Arise in Paco2 is compensated by elevation of Hco3+ due to stimulation of the kidney to regenerate Hco3+. Clinical picture : 1-In acute cases a rapid rise in Paco2 may cause dyspnea , confusion , hallucinations and coma. 2-In chronic case, sleep disturbance, memory loss , impaired in co-ordination . 3-Because of co2 is a cerebral vasodilatation headache occur, dilated retinal vessels and papilledema may occur.

26. Investigation: 1-Arterial blood gases reveal elevation Paco2 and Hco3- and depressed in PH. Treatment : 1-Treatment the cause. 2-bronchodilator. 3-mechanical ventilation.

27. Respiratory alkalosis It results from reduction of Paco2 due to alveolar hyperventilation. It is the commonest acid-base disturbance in critically ill patients. Etiology: 1-Primary CNS stimulation . a-Functional : hysterical hyperventilation Sy. b-Organic brain disease: head injury, tumor, encephalitis. c-Drugs : salicylates, catecholamine, analeptics. d-Others : fever ,gram -ve septicemia , liver failure , pregnancy 2-Peripheral chemoreceptor stimulation: hypoxemia. 3-Intra thoracic receptor stimulation -Pulmonary embolism. -Pneumonia.

28. Pathophysiology: A fall in Paco2 is compensated by a variable decrease in plasma bicarbonate concentration initially as a result of consumption by cellular buffers , and after 2-6 hours by decrease renal ammonium and titrable acid excretion and decrease bicarbonate reabsorption. Clinical pictures: 1-CNS manifestation due to ↓ cerebral blood flow , dizziness, confusion, and seizures. 2-↓In ionized ca+2 resulting in tetany and muscle cramp. 3-Cardiovasular manifestation: arrhythmias and occasionally HTN.

29. Investigation: Arterial blood gases & electrolytes reveal of :Paco2 , plasma bicarbonate decrease and increase of PH. plasma K is often reduced and Cl - increased . Treatment: 1-Treatment the cause. 2-Reassurance. 3-Rebreathing in a paper bag. 4-Sedation in hysterical.

30. Thank you for listening