Diagnosis and treatment of acid base disorders(1)

diagnosis and treatment of acid base disorders

1. DIAGNOSIS AND TREATMENT OF ACID BASE DISORDERS

2. Why pH is important ? Precise regulation of the pH in a narrow range of 7.35-7.45 is essential. pH is vital for normal cellular enzymatic reactions and for normal ionic concentration. Extreme ranges of pH (<7.2 or >7.5) are potentially life threatening (for eg cardiac arrhythmias )as can cause disruption of many vital cellular enzymatic reactions and physiological processes. Buffering: the concentration of free hydrogen is controlled by buffers which acts as hydrogen sponge. When H conc is low (high pH) , hydrogen sponges release hydrogen and increase the free H conc. When H conc is high (low pH), hydrogen sponges engulf the free hydrogen and decrease the free H conc. The major Hydrogen buffers are Bicarbonate, phosphate ,hemoglobin and bone.

3. Acid base terminology 1/3 Clinical terminology Criteria Normal pH 7.4 (7.35-7.45) Acidemia pH < 7.35 Alkalemia pH > 7.45 Normal PaCO2 40 (35- 45 ) mm of Hg Respiratory acidosis (failure) PaCO2 > 45 mm Hg and low pH Respiratory alkalosis (hyperventilation) PaCO2 < 35 mm Hg and high pH Normal HCO3 24 (22- 26 ) mEq /L Metabolic Acidosis HCO3 < 22 mEq /L and low pH Metabolic Alkalosis HCO3 > 26 mEq /L and high pH

4. Acid base terminology 2/3 pH: pH signifies free hydrogen ion concentration. pH is inversely related to H ion concentration. Increase in pH means H ion is decreasing. Decrease in pH means H ion is Increasing. Acid: A substance that can “donate” H ion or when added to solution raises H ion ( ie . Lowers pH) Base: A substance that can accept H ion or when added to solution lowers H ion ( ie . Raises pH) Anion: An ion with negative charge is anion ( ie . Cl, HCO3) Cation: An ion with positive charge is cation ( ie . Na, K, Mg) If cation and anion is confusing Anion “n” –negative charge. Cation “t” – Positive (+) charge.

5. Acid base terminology 3/3 Acidemia and alkalemia : The “- aemia ” is the same suffix found in anemia . It means “blood”. Acidemia : means “acid blood” refers to a blood pH below normal (pH < 7.35) and increased H ion concentration. Alkalemia : means “alkaline blood” refers to a blood pH above normal (pH > 7.35) and decrease H ion concentration. Acidosis : Abnormal process or disease which reduce pH due to increase in acid or decrease in alkali is called acidosis. Alkalosis : Abnormal process or disease which increases pH due to decrease in acid or increase in alkali is called alkalosis.

6. Basic Concepts : Hydrogen Ion Concentration and pH The hydrogen ion concentration [H 1 ] in extracellular fluid is determined by the balance between the partial pressure of carbon dioxide (PCO 2 ) and the concentration of bicarbonate (HCO 3 ) in the fluid. This relationship is expressed as follows( The Henderson Equation ) Using a normal arterial PCO 2 of 40 mm Hg and a normal serum HCO 3 concentration of 24 mEq /L, the normal [ H+] in arterial blood is 24 × (40/24) = 40 nEq /L.

7. Respiratory regulation By excreting volatile acids, lung regulates PaCO2. Normally CO2 production and excretion are balanced which maintain CO2 at 40 mm hg. When rate of CO2 production increases it will stimulate PaCO2 sensitive chemoreceptors at central medulla with resultant rise in rate and depth of breathing. This hyperventilation will maintain PaCO2 at normal range.

8. When the respiratory regulation falls what will be the consequences ? If the underlying disorder (respiratory or CNS) causes hypoventilation, CO2 excretion is reduced. Retained PaCO2 (hypercapnia) causes fall in pH leading to respiratory acidosis. If the underlying disorder causes inappropriately high hyperventilation, CO2 is washed out. Low PaCO2 ( hypocapnia ) causes rise in pH leading to respiratory alkalosis . Hypoventilation= Hypercapnia= Respiratory Acidosis Hyperventilation = Hypocapnia = Respiratory Alkalosis

9. Renal regulation The role of kidney is to maintain plasma HCO3 concentration and there by pH regulation. The kidneys regulate HCO3 by: Excretion of H ions by tubular secretion. Reabsorption of filtered bicarbonate ions. Production of new HCO3 ions.

10. How kidney responds to metabolic ABD and regulate HCO3 ? In response to acid load, normal kidneys are able to increase net acid excretion greatly. Increased excretion of H ions along with regeneration of HCO3 will correct plasma HCO3 to normal range. When there is primary increase in plasma HCO3 ,there will be increase renal excretion of HCO3 in urine.

11. When does metabolic regulation falls ? Metabolic acidosis occurs when excess HCO3 is lost (diarrhea) , acids are added (DKA/lactic acidosis)/ Salicyclate overdose or bicarbonate is not generated (renal failure ). Metabolic alkalosis occurs when excess H ion is lost (vomiting), or renal bicarbonate excretion fails (hypovolemia).

12. one feature of metabolic disorders with respiratory is that the pH, bicarbonate and PCO2 all changes in the same direction.

13. In respiratory acid-base disorders, the pH changes in the opposite direction as the change in bicarbonate and PCO2.

14. THOUGH SECONDARY RESPONSES SHOULD NOT BE CALLED “COMPENSATORY RESPONSES” BECAUSE THEY DO NOT COMPLETELY CORRECT THE CHANGE PRODUCED BY PRIMARY ACID BASE DISORDER.

15. Compensation Disorder Expected compensation Metabolic Acidosis Expected PaCO2= HCO3 X 1.5 + 8 Metabolic Alkalosis Rise in PaCO2 = Rise in HCO3 X 0.75 Respiratory Acidosis Rise in HCO3 = Rise in Paco2 X 0.1 Respiratory Alkalosis Fall in HCO3 = Fall in PaCo2 X 0.2

16. Characteristics of Primary acid-base disorders Basic disorder pH Primary change 2 nd change Metabolic Acidosis Low HCO3 Low PaCO2 decreased Metabolic Alkalosis High HCO3 High PaCO2 Increased Respi Acidosis Low PaCO2 High HCO3 Increased Respi Alkalosis High PaCO2 Low HCO3 decreased

17. High

18. Clinical conditions Clues to possible ABD Type CNS Coma (hypo/hyperventilation Respiratory Acidosis/alkalosis CVS Congestive heart failure Shock (decrease perfusion/lactic acid production) Respiratory Alkalosis Metabolic Acidosis/ Respiratory Alkalosis Respiratory Tachypnea (Co2 washout) Bradypnea (CO2 retention) Respiratory Alkalosis Respiratory Acidosis GI Vomiting (loss of H) Diarrhea (Loss of HCO3) Abdominal pain Metabolic alkalosis Metabolic Acidosis Respiratory Alkalosis

19. Clinical conditions Clues to possible ABD Type Renal Oliguria/ anuria Polyuria Metabolic Acidosis Metabolic Alkalosis Endocrine Myxedema ( bradypnea ) Hypertension (Na gain and H loss) Respiratory acidosis Metabolic alkalosis

20. Common mixed Acid base disorder Disorders Common causes Metabolic Acidosis Respi Acidosis ↓ pH, ↓ HCO3, ↑PCO2 Cardiac arrest (hypoventilation + lactic acidosis) Respi Alkalosis ↔pH, ↓HCO3, ↓ PCO2 Salicyclate intoxication Liver failure with hyperventilation Metabolic Alkalosis Respi Acidosis ↔ pH, ↑ HCO3, ↑ PCO2 COPD with diuretics Respi Alkalosis ↑pH, ↑ HCO3, ↓PCO2 Pneumonia with vomiting

21. Evaluation and investigations History and examination : Careful history and examination can provide clue for underlying clinical disorders. Diarrhea or ketoacidosis  metabolic acidosis Presence of Kussmaul’s breathing  Metabolic acidosis. 12/21/2015

22. Basic investigations are essential as they may provide clue for underlying disorders. Most useful investigations are serum sodium, potassium, chloride, Hco 3 and anion gap. Other relevant investigations are CBC, urine examination, urine electrolytes, blood sugar, renal function test etc. Primary investigations 12/21/2015

23. Indications for ABG Critical and unstable patients where significant acid base disorder is suspected. If history, examination and serum electrolytes suggest severe progressive acid base disorders. Sick patient with significant respiratory distress, secondary to acute respiratory diseases or exacerbation of chronic respiratory diseases 12/21/2015

24. If pH and PaCO2 changes in same direction, the primary disorder is metabolic and if they change in opposite direction ,the primary disorder is respiratory. S tep II: determine the primary disorder Chemical change Primary disorder Compensation pH Low HCO3- Metabolic acidosis Respiratory alkalosis low pH High HCO3- Metabolic alkalosis Respiratory acidosis High pH High PaCO2 Respiratory acidosis Metabolic alkalosis Low pH Low PaCO2 Respiratory alkalosis Metabolic acidosis High pH

25. Normal pH is 7.4 Calculate the change in pH (from 7.4) A. in acute respiratory disorder (acidosis / alkalosis) change in pH = 0.008 X [PaCO2 -40] expected pH = 7.4 +/-change in pH B. in chronic respiratory disorder (acidosis/alkalosis) change in pH = 0.003 X [PaCO2 -40 ] expected pH = 7.4 +/- change in pH Compare the pH on ABG if pH on ABG is close to A, it is acute disorder if pH on ABG is close to B, it is chronic disorder S tep III: if primary disorder is respiratory, determine acute / chronic disorder

26. Unmeasured Anions Unmeasured Cation Albumin: 15 mEq/L Calcium: 5 mEq/L Organic Acids: 5 mEq/L Potassium: 4.5 mEq/L Phosphate: 2 mEq/L Magnesium: 1.5 mEq/L Sulfate: 1 mEq/L Total UA: 23 mEq/L Total UC: 11 mEq/L Anion AG = UA – UC = 12 mEq/L D etermination of anion gap Adjusted AG = calculated AG + 2.5 X [4 – S.albumin gm%]

27. Pneumonic Causes M Methanol U Uremia D Diabetic ketoacidosis P Paraldehyde I Isoniazid / iron L Lactate E Ethanol, ethylene glycol R Rhabdomyolysis / renal failure S Salicylate / sepsis C auses of a raised AG metabolic acidosis

28. Pneumonic Causes H Hyper alimentation A Acetazolamide R Renal tubular acidosis D Diarrhea U Uremia (acute) P Post ventilation hypocapnia C auses of a non – AG metabolic acidosis

29. Check urinary AG in non-AG metabolic acidosis U Na + U K – U Cl Normal : negative Non-renal loss of bicarbonate [diarrhea] : negative Renal loss of bicarbonate[ RTA / H+ excretion] : positive Urinary AG

30. In less obvious cases, the coexistence of two metabolic acid-base disorders may be apparent by calculating the difference between the change in AG [delta AG] and the change in serum HCO3- [delta HCO3-]. e.g. Diabetic ketoacidosis This is called the Delta gap or gap –gap. Step VI I : for an increased anion gap metabolic acidosis; are there other disorders

31. Delta gap = delta AG – delta HCO3- Where delta AG = patient’s AG – 12 mEq/L Delta HCO3- = 24 mEq/L – patient’s HCO3- Normally the delta gap is zero : AG acidosis A positive delta gap of more than 6 mEq/L : metabolic alkalosis and/or HCO3- retention. The delta gap of less than 6 mEq/L : Hypercholremic acidosis and/or HCO3- excretion. D elta Gap

32. GENERATION OF M.AKL FACTORS EX I. LOSS OF ACID FROM ECS A. LOSS OF GASTRIC ACID VOMITING B. LOSS OF ACID IN URINE PRIMARY ALDOSTERONISM+DIURETIC C. SHIFT OF ACID INTO THE CELL POTASSIUM DEFICIENCY D. LOSS OF ACID INTO THE STOOL CONGENITAL CHLORIDE LOSING DIARRHEA II. EXCESSIVE BICARBONATE LOAD A. ABSOLUTE ORAL /PARENTRAL HCO3 MILK ALKALI SYNDROME CONVERSION OF SALTS OF ORGANIC ACIDS INTO HCO3 LACTATE/CITRATE/ACETATE ADMINSTRATION B. RELATIVE NaCO3 DIALYSIS III.POST HYPERCAPNEIC STATES Correction (e.g., by mechanical ventilatory support) of chronic hypercapnia

33. Metabolic alkalosis is associated with hypokalemia , ionized hypocalcemia , secondary ventricular arrhythmias, increased digoxin toxicity, and compensatory hypoventilation ( hypercarbia ), although compensation rarely results in Paco 2 >55 mm Hg Alkalemia may reduce tissue oxygen availability by shifting the oxyhemoglobin dissociation curve to the left and by decreasing cardiac output.

34. In patients in whom arterial blood gases have not yet been obtained, serum electrolytes and a history of major risk factors, such as vomiting, nasogastric suction, or chronic diuretic use, can suggest metabolic alkalosis. Total CO 2 -should be about 1.0 mEq /L greater than [HCO 3 - ] on simultaneously obtained arterial blood gases. If either calculated [HCO 3 - ] on the arterial blood gases or “CO 2 ” on the serum electrolytes exceeds normal (24 and 25 mEq /L, respectively) by >4.0 mEq /L, either the patient has a primary metabolic alkalosis or has conserved bicarbonate in response to chronic hypercarbia .

35. Classification of metabolic alkalosis

36. TREATMENT Etiologic therapy- expansion of intravascular volume or the administration of potassium. Infusion of 0.9% saline will dose-dependently increase serum [ Cl - ] and decrease serum [HCO 3 - ]. Nonetiologic therapy - acetazol -amide (a carbonic anhydrase inhibitor that causes renal bicarbonate wasting ), (5-10mg/kg iv/po) infusion of [H + ] in the form of ammonium chloride, arginine hydrochloride, or 0.1 N hydrochloric acid (100 mmol /L), or dialysis against a high-chloride/low bicarbonate dialysate . 0.1 N hydrochloric acid most rapidly corrects life-threatening metabolic alkalosis but must be infused into a central vein; peripheral infusion will cause severe tissue damage.

37. Infusion rate 0.2mEq/l/hr

38. METABOLIC ACIDOSIS hypobicarbonatemia (<21 mEq /L) an acidemic pH (<7.35) Metabolic acidosis occurs as a consequence of- endogenous or exogenous acid loads abnormal external loss of bicarbonate. Approximately 70 mmol of acid metabolites are produced, buffered, and excreted daily; - 25 mmol of sulfuric acid from amino acid metabolism, 40 mmol of organic acids, and phosphoric and other acids. Extracellular volume in a 70-kg adult contains 336 mmol of bicarbonate buffer (24 mEq /L × 14 L of extracellular volume). Glomerular filtration of plasma volume necessitates reabsorption of 4,500 mmol of bicarbonate daily, of which 85% is reabsorbed in the proximal tubule, 10% in the thick ascending limb, and the remainder is titrated by proton secretion in the collecting duct

39. Calculation of the anion gap [(Na + - ([ Cl - ] + [HCO 3 - ])] distinguishes between two types of metabolic acidosis The anion gap - normal (<13 mEq /L.) In metabolic acidosis associated with a high anion gap, bicarbonate ions are consumed in buffering hydrogen ions, while the associated anion replaces bicarbonate in serum. Because three quarters of the normal anion gap consists of albumin, the calculated anion gap should be corrected for hypoalbuminemia Corrected AG = AG+2.5x(4.5-albumin in g/dl)

40. DIFFERENTIAL DIAGNOSIS OF M.AC ELEVATED A.G NORMAL A.G THREE DISEASES RENAL TUBULAR ACIDOSIS UREMIA DIARRHEA KETOACISOSIS CARBONIC ANHYDRASE INHIBITOR LACTIC ACIDOSIS URETERAL DIVERSION TOXINS EARLY RENAL FAILURE METHANOL HYDRONEPHROSIS ETHYLENE GLYCOL HCL ADMINISTRATION SALISYLATES CHLORIDE ADMINISTRATION PARALDEHYDE

41. METABOLIC ACIDOSIS CAUSES Decrease myocardial contractility, increase pulmonary vascular resistance, and decrease systemic vascular resistance.

42. ANESTHETIC IMPLICATION A patient with hyperchloremic metabolic acidosis may be relatively healthy, those with lactic acidosis, ketoacidosis , uremia, or toxic ingestions will be chronically or acutely ill. Preoperative assessment should emphasize volume status and renal function. If shock has caused metabolic acidosis,- direct arterial pressure monitoring preload may require assessment via echocardiography or pulmonary arterial catheterization. Intraoperatively , one should be concerned about the possibility of exaggerated hypotensive responses to drugs and positive pressure ventilation. In planning intravenous fluid therapy, consider that balanced salt solutions tend to increase [HCO 3 - ] (e.g., by metabolism of lactate to bicarbonate) and pH and 0.9% saline tends to decrease [HCO 3 - ] and pH

43. TREATMENT The treatment of metabolic acidosis consists of the treatment of the primary pathophysiologic process, that is, hypo-perfusion, hypoxia, and if pH is severely decreased, administration of NaHCO 3 - . Hyperventilation, although an important compensatory response to metabolic acidosis, is not definitive therapy for metabolic acidosis.

44. The initial dose of NaHCO 3 can be calculated as: NaHCO 3 ( mEq /L)= WT( kgs )x 0.3(24mEq/L-actual HCO3) / 2 0.3 = the assumed distribution space for bicarbonate and 24 mEq /L is the normal value for [HCO 3 - ] on arterial blood gas determination. The calculation markedly underestimates dosage in severe metabolic acidosis. In infants and children, a customary initial dose is 1.0 to 2.0 mEq /kg of body weight.

45. DILUTIONAL ACIDOSIS It occurs when the plasma bicarbonate concentration is decreased due to extracellular volume expansion with solutions(NS, albumin) that contain neither acid nor alkali. A hyperchloremic metabolic acidosis may accompany large volume infusion of isotonic saline I/O complicated with blood loss and extensive tissue dissection.

46. RESPIRATORY ALKALOSIS hypocarbia (Paco 2 ≤35 mm Hg) alkalemic pH (>7.45), results from an increase in minute ventilation that is greater than that required to excrete metabolic CO 2 production. respiratory alkalosis may be a sign of pain, anxiety, hypoxemia, central nervous system disease, or systemic sepsis, the development of spontaneous respiratory alkalosis in a previously normocarbic patient requires prompt evaluation . Respiratory alkalosis, like metabolic alkalosis, may produce hypokalemia , hypocalcemia , cardiac dysrhythmias , bronchoconstriction , and hypotension, and may potentiate the toxicity of digoxin . In addition, both brain pH and cerebral blood flow are tightly regulated and respond rapidly to changes in systemic pH.Doubling minute ventilation reduces Paco 2 to 20 mm Hg and halves cerebral blood flow; conversely, halving minute ventilation doubles Paco 2 and doubles cerebral blood

47. TREATMENT Treatment of respiratory alkalosis per se is often not required. The most important steps are recognition and treatment of the underlying cause. For instance, correction of hypoxemia or hypoperfusion -induced lactic acidosis should result in resolution of the associated increases in respiratory drive. Preoperative recognition of chronic hyperventilation necessitates intraoperative maintenance of a similar Paco 2.

48. RESPIRATORY ACIDOSIS hypercarbia (Paco 2 ≤45 mm Hg) low pH (<7.35), occurs because of a decrease in minute alveolar ventilation (V A ), an increase in production of carbon dioxide (V CO2 ) or both, from the equation: PaCO2=k x VCO2 / VA where K = constant Respiratory acidosis - acute, without compensation by renal [HCO 3 - ] retention chronic , with [HCO 3 - ] retention offsetting the decrease in Ph.

49. CAUSES A reduction in V A may be due to an overall decrease in minute ventilation (V E ) or to an increase in the amount of wasted ventilation (V D ), according to the equation; VA= VE-VD Decreases in V E – central ventilatory depression by drugs or central nervous system injury. airway obstruction neuromuscular dysfunction. Increases in V D – with chronic obstructive pulmonary disease, pulmonary embolism, and most acute forms of respiratory failure. V CO2 may be increased by sepsis, high-glucose parenteral feeding, or fever

50. ANESTHETIC IMPLICATION Patients with chronic hypercarbia due to intrinsic pulmonary disease require careful preoperative evaluation. The ventilatory restriction imposed by upper abdominal or thoracic surgery may aggravate ventilatory insufficiency after surgery. Administration of narcotics and sedatives, even in small doses, may cause hazardous ventilatory depression. Preoperative evaluation should consider direct arterial pressure monitoring and frequent intraoperative blood gas determinations, as well as strategies to manage postoperative pain with minimal doses of systemic opioids .

51. Intraoperatively , a patient with chronically compensated hypercapnia should be ventilated to maintain a normal pH. Inadvertent restoration of normal V A may result in profound alkalemia . Postoperatively, prophylactic ventilatory support may be required for selected patients with chronic hypercarbia Epidural narcotic administration may provide adequate postoperative analgesia while limiting depression of ventilatory drive.

52. TREATMENT The treatment of respiratory acidosis depends on whether the process is acute or chronic. Acute respiratory acidosi s – require mechanical ventilation unless a simple etiologic factor (i.e., narcotic overdosage or residual muscular blockade) can be treated quickly. Bicarbonate administration rarely is indicated unless severe metabolic acidosis is also present or unless mechanical ventilation is ineffective in reducing acute hypercarbia . chronic respiratory acidosis is rarely managed with ventilation but rather with efforts to improve pulmonary function.

53. Changes of [HCO 3 - ] and pH in Response to Acute and Chronic Changes in Paco 2 Decreased PaCO 2 pH increases 0.10 per 10 mm Hg decrease in PaCO 2 [HCO 3 - ] decreases 2 mEq /L per 10 mm Hg decrease in PaCO 2 pH will nearly normalize if hypocarbia is sustained [HCO 3 - ] will decrease 5 to 6 mEq /L per 10 mm Hg chronic ↓ in PaCO 2 a Increased PaCO 2 pH will decrease 0.05 per acute 10 mm Hg increase PaCO 2 [HCO 3 - ] will increase 1.0 mEq /L per 10 mm Hg increase PaCO 2 pH will return toward normal if hypercarbia is sustained [HCO 3 - ] will increase 4–5 mEq /L per chronic 10 mm Hg increase in PaCO 2

54. Consequences of acidosis

55. Consequences of alkalosis