Acid Base disorders.ppt
- 1. ACID- BASE DISORDERS Akram Fayed, MD Fellow, Surgical ICU Division of Critical Care Medicine Department of Anesthesia University of Iowa Hospitals and Clincs
- 2. Respiratory Metabolic Acidosis Respiratory Metabolic Alkalosis Acid- Base Disorders
- 3. Metabolic Acidosis Characterized by a primary decrease in bicarbonate concentration and a compensatory decrease in CO2. Occurs from: 1. Loss of bicarbonate through the kidneys or the bowel. 2. Addition of H+: A. Physiological ( normal metabolism). B. Pathological ( Lactic acidosis and Diabetic ketoacidosis). 3. Reduced renal ability to excrete an acid load.
- 4. Metabolic Acidosis Has deleterious effects on: 1. Myocardium. 2. Blood vessels. 3. Central nervous system. 4. Diaphragmatic functions. Anion Gap: The difference between measured cations and anions. Normal: {Na}+ – { Cl}- + {HCO3}- = 8- 14 meq/ L
- 5. Metabolic Acidosis Etiologies of Normal- Anion- Gap Metabolic Acidosis: Gastrointestinal loss of bicarbonate Diarrhea Urinary diversion Small bowel, Pancreatic, or bile drainage (fistulas, drains) Cholestyramine Renal loss of bicarbonate Renal tubular acidosis Recovery phase of DKA Renal insufficiency Posthypocapneic Acidifying substances HCl, NH4Cl, MgCl2
- 6. Metabolic Acidosis Etiologies of Increased- Anion Gap Metabolic Acidosis: Ketoacidoses Diabetic Alcoholic Starvation Lactic Acidosis Uremia Toxins Ethylene Glycol Methanol Salicylate Paraldehyde
- 7. Metabolic Acidosis Management: All medications and other substances contributing to the acidosis should be withdrawn, if possible. In normal anion gap acidosis with an ongoing loss of HCO3, bicarbonate therapy is indicated in amounts equal to losses. Bicarbonate is not effective in DKA ( rebound alkalemia). Alcoholic KA responds rapidly to glucose infusion. Starvation KA is easily controlled with nutritional support.
- 8. Metabolic Acidosis Management: Salicylate overdose responds to alkaline diuresis and, if severe, with hemodialysis Methanol and ethylene glycol poisoning, if severe and associated with metabolic acidosis, should be treated with Ethanol infusion Ethanol competitively inhibits metabolism to toxic products via alcohol dehydrogenase If acidosis remains severe, hemodialysis should be done
- 9. Metabolic Alkalosis Primary increase in bicarbonate concentration and a compensatory increase in carbon dioxide Results from: 1. Elevation of serum bicarbonate concentrations usually due to acid loss from the stomach or the kidneys 2. Stimulus for bicarbonate reabsorption due to: A. Hypovolemia with a chloride deficit B. Hypokalemia C. Increased mineralocorticoid activity
- 10. Metabolic Alkalosis Etiologies of Metabolic Alkalosis: Chloride- responsive Renal H+ loss Diuretic therapy Posthypercapnia Penicillin, Ampicillin, Carbenicillin therapy Gastrointestinal H+ losses Vomiting Nasogastric suction Villous adenoma Alkali administration Bicarbonate Citrate in blood products Acetate in Parenteral nutrition
- 11. Metabolic Alkalosis Etiologies of Metabolic alkalosis: Chloride Resistant Increased mineralocorticoids activity Primary aldosteronism Cushing’s syndrome Drugs with mineralocorticoid activity Profound hypokalemia Refeeding Parathyroid disease Hypercalcemia
- 12. Metabolic Alkalosis Management: Replacement of diuretic- induced potassium losses with KCl Minimization of Nasogastric suction and use of H2 blockers with prolonged Nasogastric suction Avoid rapid decreases in PaCO2 patients with COPD Adequate Chloride must be provided in those cases associated with volume and chloride deficit
- 13. Metabolic Alkalosis Management: In volume overload with metabolic alkalosis: 1. Acetazolamide ( reduces bicarbonate) 2. Continuous arteriovenous hemodialysis, which removes bicarbonate in proportion to its concentration in plasma, and fluid replacement with a lesser volume of bicarbonate- free NaCl Rapid correction: Indicated at a pH of 7.6 with arginine hydrochloride, ammonium chloride, and hydrochloric acid
- 14. Respiratory Acidosis Primary increase in PaCO2 and a compensatory increase in the bicarbonate concentration Respiratory acidosis occurs when alveolar ventilation is decreased relative to CO2 production Decrease in alveolar ventilation results from a decrease in minute ventilation, or from an increase in dead space without a compensatory rise in minute ventilation A rise in CO2 production will not produce hypercapnia unless ventilation does not increase appropriately
- 15. Respiratory Acidosis This develops in patients with near maximal ventilation or with fixed mechanical ventilation In acute respiratory acidosis, tissue buffers can increase HCO3 level only by 4 to 5 meq/L so, acidemia is usually severe In chronic respiratory acidosis, increase renal reabsorption of bicarbonate buffers the acidosis, so acidosis is less severe even with marked hypercapnia
- 16. Respiratory Acidosis Etiologies of Respiratory Acidosis: Inhibition of repsiratory control Drugs ( narcotics, sedatives, anesthetics) Sleep apnea CNS lesions Myxedema Cerebral Edema Status asthmaticus Compensation for metabolic acidosis Disorders of the chest wall Kyphoscoliosis Morbid obesity Burns
- 17. Respiratory Acidosis Etiologies of Respiratory Acidosis: Neuromuscular disease Myasthenia gravis Guillian- Barre syndrome Poliomyelitis Botulism Severe hypophosphatemia Severe hypokalemia Myopathy Multiple sclerosis Periodic paralysis Spinal cord injury
- 18. Respiratory Acidosis Etiologies of Respiratory Acidosis: Upper airway obstruction Obstructive sleep apnea Laryngospasm Foreign body Tracheal stenosis Disorders of the lung COPD Asthma Severe Pneumonia Pulmonary Edema Pneumothorax ARDS
- 19. Respiratory Acidosis Management: Aimed at reversing the disorders that led to decreased alveolar ventilation All factors leading to respiratory acidosis should be corrected: Increasing minute ventilation Decreasing dead space Decreasing CO2 production
- 20. Respiratory Acidosis Management: Narcotic overdose can be reversed with Naloxon Aggressive correction is needed in neurologic injuries, as acidemia can increase cerebral blood flow and intracranial pressure with a deleterious effects Permissive hypercapnia is allowed in ARDS to avoid the risk of barotrauma
- 21. Respiratory Alkalosis Primary reduction in PaCO2 when alveolar ventilation is increased relative to CO2 production A secondary, compensatory, two- phase reduction in bicarbonate level occurs with: 1. Small acute decrease owing to tissue buffers 2. A large chronic decrease due to renal acid excretion and an increase in renal bicarbonate excretion
- 22. Respiratory Alkalosis Etiologies of respiratory alkalosis: Hypoxia High altitude Pulmonary disease Decreased Fio2 Profound anemia Pulmonary disorders Pneumonia Pulmonary embolism Restrictive lung disease Pulmonary edema Pneumothorax Pleural effusion
- 23. Respiratory Alkalosis Etiologies of respiratory alkalosis: Mechanical Ventilation Increased CNS respiratory dirve Anxiety and pain Voluntary hyperventilation CNS disease ( CVA, Tumors, Infection, Trauma) Fever Sepsis and endotoxin Drugs ( Salicylate, Catecholeamines, progesterone) Hyperthyroidism Liver disease Pregnancy Exercise Epinephrine
- 24. Respiratory Alkalosis Management: Treatment of the underlying cause of hyperventilation Alkalemia from respiratory alkalosis does not require therapy unless superimposed on a metabolic alkalosis, sedation is then indicated In sepsis, a significant portion of cardiac output can go to the respiratory muscles, intubation and muscle relaxation can be used to control hyperventilation and redirect blood flow to more important organs
- 25. Acid- Base Interpretation Any measurement that falls outside the following ranges is considered to be abnormal: pH= 7.36 to 7.44 PaCO2 = 36 to 44 mmHg HCO3 = 22 to 26 mmHg Rule 1: A primary metabolic acid- base disorder is present if the pH is abnormal and the pH and PaCO2 change in the same direction
- 26. Acid- Base Interpretation Rule 2: A superimposed respiratory acid- base disorder is present if any of the following conditions are satisfied 1. The measured PaCO2 is normal. 2. The measured PaCO2 is higher than the expected PaCO2 ( denotes superimposed respiratory acidosis) 3. The measured PaCO2 is less than the expected PaCO2 ( denotes a superimposed respiratory alkalosis)
- 27. Acid- Base Interpretation Rule 3: A primary respiratory acid- base disorder is present if the PaCO2 is abnormal and the PaCO2 and pH change in opposite Directions Rule 4: A mixed (acidosis and alkalosis) acid- base disorder is present if the PaCO2 is abnormal and the pH is unchanged or normal, or if the pH is abnormal and the PaCO2 is unchanged or normal
- 28. Acidemia If the pH is below 7.36, check the PaCO2 and proceed as follows: A low or normal PaCO2 indicates a primary metabolic acidosis. The difference between the measured and expected PaCO2 is then used to identify a superimposed respiratory disorder. A high PaCO2 indicates a primary respiratory acidosis. The change in pH is then used to determine whether the disorder is acute or chronic.
- 29. Alkalemia If the pH is above 7.44, check the PaCO2 and proceed as follows: A normal or high PaCO2 indicates a primary metabolic alkalosis. A comparison of the measured and expected PaCO2 is then used to identify an associated respiratory disorder. A low PaCO2 indicates a primary respiratory alkalosis. The change in pH is then used to determine whether the disorder is acute or chronic, or whether a superimposed metabolic disorder is present.
- 30. Normal pH If the arterial pH is unchanged or normal, the PaCO2 should be checked: A high PaCO2 indicates a mixed respiratory acidosis- metabolic alkalosis. A low PaCO2 indicates a mixed respiratory alkalosis- metabolic acidosis. A normal pH combined with a normal PaCO2 is not absolute evidence against an acid- base disorder because a metabolic acidosis coexisting with a metabolic alkalosis can be accompanied by a normal pH and PaCO2.
- 31. Expected Changes In Acid- Base Disorders Primary Disorder Expected Changes Metabolic Acidosis PaCO2= 1.5* HCO3+(8±2) Metabolic Alkalosis PaCO2= 0.7* HCO3+(21±2) Acute Respiratory Acidosis ΔpH= 0.008 * (PaCO2-40) Chronic Respiratory Acidosis ΔpH= 0.003 * (PaCO2-40) Acute Respiratory Alkalosis ΔpH= 0.008 * (40- PaCO2) Chronic Respiratory Alkalosis ΔpH= 0.017 * (40- PaCO2)
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- 36. Respiratory Metabolic Acidosis Respiratory Metabolic Alkalosis Acid Base Disorders