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ACID BASE EQUILIBRIUM, CLINICAL CONCEPTS AND ACID BASE DISORDERS Dr Sajith Damodaran University College of Medical Sciences & GTB Hospital, Delhi.

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Presentation on theme: "ACID BASE EQUILIBRIUM, CLINICAL CONCEPTS AND ACID BASE DISORDERS Dr Sajith Damodaran University College of Medical Sciences & GTB Hospital, Delhi."— Presentation transcript:

1 ACID BASE EQUILIBRIUM, CLINICAL CONCEPTS AND ACID BASE DISORDERS Dr Sajith Damodaran University College of Medical Sciences & GTB Hospital, Delhi

2 Homeostasis The Interstitial Fluid is the environment of the cells, and life depends on the constancy of this internal sea. Homeostatic Mechanisms : Maintain within a narrow range.  Tonicity  Volume  Specific ion concentration Defence of Tonicity –( mOsm/L)  Vasopressin secretion  Thirst Mechanism Increased Osmolality of ECF Thirst Increased Vasopressin Secretion Increased Water IntakeWater Retention Dilution of ECF Increased Osmolality of ECF Thirst Increased Vasopressin Secretion Increased Water IntakeWater Retention Dilution of ECF Inhibitory

3 Homeostasis Defence of Volume:  ECF Na + - Most important  Renin-Angiotensin- Aldosterone System  Vasopressin Secretion: Volume stimuli override osmotic regulation  ANP & BNP Angiotensinogen Renin Angiotensin I ACE Angiotensin II AldosteroneVasopressin Adrenal Cortex Brain Kidney Na Retention Water Retention Blood Vessel Vasoconstriction Thirst

4 Homeostasis Defence of Specific Ionic Concentration:  Glucose  Na + & K +  Ca ++ - Mainly by Parathyroid & Calcitonin  Mg ++ - Incompletely understood mechanisms Also dependent on H + ion pH is maintained within a narrow range.

5 Acid Base Equilibrium What is Acid Base Equilibrium About? ? Buffers? Fixed Cation? Base Excess/ Deficit? Anion Gap?

6 Acid Base Equilibrium Acid Base Equilibrium is all about Maintenance of H + ion concentration of the ECF. Source of H + ion in Body: CO 2 from metabolism H + load from AA metabolism Strenuous Exercise  Lactic Acid Diabetic KA Ingestion of NH 4 Cl, CaCl 2 Failure of Kidneys to Excrete PO4 --, SO4 --

7 Some Basic Chemistry Definitions: Arrhenius:  Acid: H + Donor in Solution  Base: OH - donor in Solution Browsted and Lowry:  Acid: Proton Donor  Base: Proton Acceptor H 2 0 can be both

8 Some Basic Chemistry Simple Rule of Thumb: Acid  Higher conc. Of H + ion Base  Lower conc. Of H + ion Strong Acid/Base  Dissociates completely and irreversibly Weak Acid/Base  Dissociates partially and reversibly Strong Electrolyte: Dissociates completely in solution at physiological pH Eg: NaCl, KCl Weak Electrolyte: Dissociates incompletely in solution at physiological pH Eg: CO 2 – HCO 3 - System, Proteins

9 Some Basic Chemistry pH (Puissant of Hydrogen): Negative logarithm of H + ion concentration to the base of 10 Why pH?  Normal H + ion conc: meq/L or 40nEq/L or 4x10 -9 mol/L  pH converts to decimal numbers & takes away negative sign.  Normal pH:  Normal H + Conc: mEq/L – mEq/L

10 Some Basic Chemistry Pitfalls: Non-linear Negative Logarithmic scale  pH Decreases as [H + ] increases.  Each unit change in pH from 7 represents 10 fold change in H + ion conc. Eg: At pH 4, there are 10 times as much H + than at pH 5, & 100 times as at pH 6  Same numeric change in different portions of the pH scale implies vastly different nanomolar change in H + ions Eg: pH 5  6 => 100 times greater change in ionic conc than when pH 7  8  Body H + ion conc is not as tightly controlled as the other ion, though the pH scale implies so.

11 Some Basic Chemistry Water (H 2 O) Water dissociates, but to a very low extent. H 2 O H + + OH - But, a glass of water has a billion times more H 2 O than H + & OH - At equilibrium: [H + ] [OH - ] = Kw[H 2 O] {Kw(Dissociation constant of water) changes with temperature} Or, [H + ] [OH - ] = Kw’ pH of Water: Since at neutral pH, [H + ] = [OH - ] [H + ] = ROOT (Kw’)  Acidic solution, [H + ] > ROOT (Kw’), Basic sol, [H + ] < ROOT(Kw’)  pH changes with temperature

12 Acid Base Equilibrium: Solutions: When substances are added to water, 3 simple rules have to be satisfied at all time: 1. Electrical Neutrality 2. Mass conservation 3. Dissociation Equilibrium ECF is a complex solution with strong ions, weak ions and CO 2 dissolved in water.

13 Acid Base Equilibrium: CO 2 in Water:  Can Dissolve in water  Can form - Carbonic Acid  - Bicarbonate ion  - Carbonate ion CO 2(gas) CO 2(dissolved) Rate of Forward Reaction = K f * PCO 2 Rate of Reverse reaction = K r *[CO 2(dissolved) ] => [CO 2(dissolved) ] = K f /K r *PCO 2 K f /K r = SCO 2 (Solubility of CO 2 ) = 0.03mEq/L/mm Hg at 37 0 C } All these reactions have equilibrium Constants and can be solved at equilibrium.

14 Acid Base Equilibrium: CO 2 + H 2 O H 2 CO 3 => [CO 2 ][H 2 O] = K*[H 2 CO 3 ] => [H 2 CO 3 ] = K’*PCO 2 H 2 CO 3 H + + HCO 3 - Henderson Equation: [H + ] = K 1 [H 2 CO 3 ]/[HCO 3 - ] Modified Henderson Equation: [H + ][HCO 3 - ] = K 2 [CO 2 ][H 2 O] [H + ][HCO 3 - ] = K 3 [CO 2 ] [H + ] = K*PaCO 2 /[HCO 3 - ]

15 Acid Base Equilibrium: The Henderson-Hasselbalch Equation: CO 2 + H 2 O H + + HCO 3 - => [H + ] = K’a * [CO 2 ]/[HCO 3 - ] Rearranging: =>1/[H + ] = 1/K’a*[HCO 3 - ]/[CO 2 ] Taking Logarithm on both sides & Rearranging: => pH= pK’a + log 10 [HCO 3 - ]/0.03*PCO 2 Significance:  Includes components of both Met & Resp Acid base disorders  Value of any one variable can be determined if other two known. Mostly HCO 3 - is calculated  pH determined by ratio of [HCO 3 - ]/PCO 2. Maintained at 20. Increase=> alkalosis, Decrease => Acidosis

16 Clinical Concepts: The Stewart Approach  Dissociation equations can be solved mathematically.  When the equations are solved-  Independent Variables: SID, [A tot ] & PaCO 2  Constants : Dissociation constants  Dependent Variables: [H + ], [OH - ], [HCO3 - ], [CO3 2- ], [A + ], [HA], [H 2 CO 3 ], [CO 2 dissolved ]

17 Clinical Concepts: The Stewart Approach  Dissociation equations can be solved mathematically.  When the equations are solved-  Independent Variables: SID, [A tot ] & PaCO 2  Constants : Dissociation constants  Dependent Variables: [H + ], [OH - ], [HCO3 - ], [CO3 2- ], [A + ], [HA], [H 2 CO 3 ], [CO 2 dissolved ]

18 Clinical Concepts: The Stewart Approach SID: Strong Ion Difference – ([Na + ] + [K + ] + [Ca ++ ] + [Mg ++ ]) – [Cl - ]+ [other Strong Anions]  Normal: 40-44mEq/L with normal protein levels  Change from normal is equivalent to SBE  Dehydration: Increases SID ==> Alkalosis  Dilution, Organic Acids, Hyperchloremia : Decreases SID ==> Acidosis [A tot ]: Total Amount of Weak Acid in Solution  Albumin is the most important weak electrolyte in plasma.  Other weak acids are Inorganic Phosphates, Plasma proteins.  Hypoproteinemia: Alkalosis  Renal Failure: Accumulation of Phosphate: Acidosis

19 Clinical Concepts: Base Excess: Amount of Acid or Alkali required to return plasma in vitro to normal pH under standard conditions. Standard BE: BE calculated for Anaemic Blood (Hb = 5Gm%).  Since Hb effectively buffers plasma & ECF to a large extent.  Quantity of Acid or Alkali required to return plasma in-vivo to a normal pH under standard conditions Anion Gap:  AG = [Na + ] + [K + ] - {[HCO 3 - ] + [Cl - ]}  Normal Value: 8-12mEq/L,  Unmeasured Anion: Albumin, Phosphate, sulphate, organic anions  AG decreases by 2.5mEq/L for every 1mEq/L decrease in Plasma albumin  AG>16 ==> Ketones, lactate, salicylate, antifreeze, methanol

20 Clinical Concepts: Acid Base Equilibrium:  Elimination of Acid  Recovery/Regeneration of Base Mechanisms that keep pH stable  Buffering  Compensation  Correction

21 Clinical Concepts: Buffers: Definition: A substance that can bind or release H + ions in solution, thus keeping the pH of the solution relatively constant despite addition of large amounts of acid or base. For Buffer HA, HA H + + A - pH = pK a + log [A - ]/[HA]  When [A - ] = [HA], pH= pK, buffering capacity is maximum.  Ideal body buffer has pK a between 6.8 and 7.2

22 Clinical Concepts: Most buffers are weak acids (Hbuffer) & their Na Salts (Nabuffer)  Strong Acids Buffered by NaBuffer HCl + NaBuffer H + + Cl - +Na + + Buffer Hbuffer + NaCl  Strong Bases buffered by Hbuffer NaOH + H Buffer Na + + OH - + H + + Buffer NaBuffer + H 2 O Buffer Effectiveness Depends on:  Quanitity  H 2 CO 3 /HCO Most important Extracellular Buffer  Protein Buffers – Most improtant Intracellular Buffer  pK a – Buffering capacity maximum when pH=pK a  Function well within 1 pH unit. (Eg: HCO )

23 Clinical Concepts: Buffers in ECF:  Carbonate-Bicarbonate Buffer53%  Plasma (35%)  Erythrocyte(18%)  Hemoglobin35%  Plasma Proteins7%  Organic & Inorganic Phosphates5% Buffers in ICF:  Intracellular Proteins  H 2 PO 4 -HPO 4 - system Intracellular buffers are responsible for ~85% buffering in Met. Acidosis and ~35% in met alk and almost complete buffering in respiratory acidosis and alkalosis

24 Clinical Concepts: Bicarbonate Buffer: HCl + NaHCO 3 - NaCl + H 2 CO 3 NaCl + H 2 O + CO 2  useful only for metabolic acid Hb System:  Both Respiratory & Metabolic Acid in ECF  Forms Carbamino compounds with CO 2  Buffers H + directly CO 2 + H 2 O H 2 CO 3 + KHb HHb + KHCO 3  HCO 3 - diffuses out & Cl - diffuses into cells – Chloride shift  pKa – 6.8

25 Clinical Concepts: Protein Buffer:  Predominant Intracellular Buffer – Large total concentration  pK = 7.4  AA have Acidic & Basic Free radicles. COOH + OH - COO - + H 2 O. NH 3 OH + H + NH 3 + H 2 O Phosphate Buffer:  pK = 6.8  Predominantly Intracellular  Also in renal tubular HCl + Na 2 HPO 4 NaH 2 PO 4 + NaCl NaOH + NaH 2 PO 4 Na 2 HPO 4 + H 2 O

26 Clinical Concepts: Compensation: Pulmonary Compensation H + + HCO 3 - H 2 CO 3 CO 2 + H 2 O  H + acts on medullary centres.  Increased PaCO 2 stimulates ventiallation  Metabolic Acidosis – Increased Ventillation  Metabolic Alkalosis – Depression of Ventillation But, limited because Hypoxic stimulus can override Hypercapnia

27 Clinical Concepts: Renal Compensatoin: Mechanisms: 1. Reabsorption of filtered HCO 3- ( mEq/d) 2. Generation of fresh bicarbonate 3. Formation of titrable acid – (1mEq/Kg/d) 4. Excretion of NH4 + in urine

28 PERITUBULAR BLOOD RENAL TUBULAR CELL GLOMULAR FILTRATE HCO H + CO 2 HCO H + HCO H + HCO 3 - Na + HPO 4 2- Na + NH 3 Na + H 2 CO 3 CO 2 + H 2 O H2OH2O H 2 PO 4 - NH NaHCO 3 2. NaHCO 3 3. NaHCO 3 MAJOR RENAL MECHANISMS RESPONSIBLE FOR H + EXCRETION/HCO 3 - RETENTION CO 2 can be obtained from blood or the tubular fluid Glutamine CO 2 CA

29 Clinical concepts: Compensation Prediction of Compensatory Responses on Simple Acid Base Disorders DisorderPrediction of Compensation Metabolic AcidosisPaCO 2 = (1.5 x HCO 3 - ) + 8 Or PaCO 2 will 1.25mm Hg per mmol/L in [HCO 3 - ] Or PaCO 2 = [HCO 3 - ] + 15 Metabolic AlkalosisPaCO 2 will 0.75 mm Hg per mmol/L in [HCO 3 - ] Or PaCO 2 will 6mm Hg per 10 mmol/l in [HCO 3 - ] Or PaCO 2 = [HCO 3 - ] + 15 Respiratory Alkalosis Acute[HCO 3 - ] will 2mmol/L per 10 mmHg in PaCO 2 Chronic[HCO 3 - ] will 4mmol/L per 10 mmHg in PaCO 2 Respiratory Acidosis Acute[HCO 3 - ] will 1mmol/L per 10 mmHg in PaCO 2 Chronic[HCO 3 - ] will 4mmol/L per 10 mmHg in PaCO 2 DisorderPrediction of Compensation Metabolic AcidosisPaCO 2 = (1.5 x HCO 3 - ) + 8 Or PaCO 2 will 1.25mm Hg ( ) per mmol/L in [HCO 3 - ] Or PaCO 2 = [HCO 3 - ] + 15 Metabolic AlkalosisPaCO 2 will 0.75 ( ) mm Hg per mmol/L in [HCO 3 - ] Or PaCO 2 will 6mm Hg per 10 mmol/l in [HCO 3 - ] Or PaCO 2 = [HCO 3 - ] + 15, Max – 55mmHg Respiratory Alkalosis Acute[HCO 3 - ] will 2mmol/L per 10 mmHg in PaCO 2 Chronic[HCO 3 - ] will 4mmol/L per 10 mmHg in PaCO 2 Respiratory Acidosis Acute[HCO 3 - ] will 1mmol/L per 10 mmHg in PaCO 2 Chronic[HCO 3 - ] will 4mmol/L per 10 mmHg in PaCO 2

30 Acid-Base Nomogram:

31 Clinical concepts: Effect of Temp:  pH rises 0.015/ 0 C drop in temp Effect of PaCO 2 on pH:  pH changes by 0.08/10mm Hg change in PaCO 2 Effect of change of [HCO 3 - ] on pH:  pH changes by 0.1/ 6 mEq change in [HCO 3 - ]

32 Clinical Concepts: Effect of Electrolytes in Buffering:  Potassium Ion: Intracellular  Hypokalemia - K + Moves out  H + moves in - K + & HCO 3 - reabsorption, H + Excretion  Sodium Ion  Hyponatremia -- Na + & HCO 3 - reabsorption & H + excretion

33 Clinical Concepts: Role of Bones:  Exchange of Extracellular H + for Na + & Ca ++  Acid load  Demineralise Bones  Alkaline load  Deposition of CO 3 2- in Bones Time Course of Buffering:  Plasma HCO > Immediate  Interstitial HCO > Min  Intracellular Proteins & Bones ----> 2-4 Hours

34 Acid Base Disorders Acidosis/Alkalosis: Any process that tends to increase/decrease pH  Metabolic: Primarily affects Bicarbonate  Respiratory: Primarily affects PaCO 2 Acidemia/Alkalemia: Net effect of all primary and compensatory changes on arterial blood pH.

35 Acid Base Disorders The primary disorders:  Metabolic Acidosis  Metabolic Alkalosis  Respiratory Acidosis  Acute  Chronic  Respiratory Alkalosis  Acute  Chronic DisorderPrimary Change Compensatory Change Metabolic Acidosis HCO 3 _ PaCO 2 Metabolic Alkalosis HCO 3 _ PaCO 2 Respiratory Acidosis PaCO 2 HCO 3 _ Respiratory Alkalosis PaCO 2 HCO 3 _

36 Acidosis:Clinical Effects CVS: Combination of Effects of Direct depression and Catecholamine stimulation Heart Rate: Initial Increase then Decrease Rhythm: Increased Atrial & Ventricular Dysrrhythmias  Due to Changes in S K +  Lower threshold for VF Contractility: Increased contractility. Depression if pH<7.0 Cardiac Output: Increased  Increased Catecholamines,  Decreased Arterial tone,  Increased Venous Tone  At <7.0, Decreased d/t direct depressant effects  CCF d/t Increased venous tone.

37 Acidosis:Clinical Effects Vascular Effects:  Direct Vasodilatation  Vasoconstriction d/t Catecholamines  Respiratory: Vasodilatation predominates  Metabolic: Vasoconstriction Splanchnic & Renal Vasoconstriction Variable effects on Coronary, Cutaneous, Uterine  BP doesn’t change till extremes imbalance  Hypotension occurs when pH falls below 7.0

38 Clinical Effects of Acidosis: Respiratory System:  Minute Ventilation: TV RR  Twice more for RA than MA  Airway Resistance:  Direct: Decrease by Smooth muscle relaxation  Indirect: Increased by Vagal Tone Vagal Effect predominates: Increased WoB  Pulmonary Vasculature:  Vasoconstriction  Enhanced HPV  Right shift of ODC:  But tissue hypoxia can occur due to hypotension

39 Clinical Effects of Acidosis: GI System:  Variable effects in splanchnic BF Renal System  Vasoconstriction Uteroplacental:  CO 2 freely diffuses  HCO 3 - slowly over hours  Similar effects in Fetal systems Electrolytes:  Calcium: Increased Free Ca ++  Potassium: Increased S K +

40 Clinical Effects of Acidosis: NeuroEndocrine:  CBF (by PaCO 2 )  Mental Changes: CNS Depression  More with RA  Decreased Body Temp  Impaired central regulation  Cutaneous vasodilatation  Decreased Cellular Metabolism  Increased secretion of catecholamines

41 Clinical Effects of Acidosis: EffectDirectIndirectClinical Cerebral blood flow+++ Heart rate-++ Cardiac inotropy-+0 Systemic arterial tone-+- Systemic venous tone+++ Pulmonary artery tone+++ Airway tone-++ Uterine blood flow+-0 Renal blood flow+-- Ionised calcium+0+ Serum potassium+0+

42 Respiratory Acidosis: Primary Increase in PaCO 2 Cause: Production/ Elimination  Produced by:  Carbohydrate and fat metabolism,  muscle activity,  body temp  thyroid hormone activity  Elimination by Lungs.  Immense capacity  CO2 - ventilation compromised

43 Respiratory Acidosis: Causes: Alveolar Hypoventilation  CNS Depression  Drugs  Cerebral Ischemia/trauma  Sleep Disorders  Pickwickian Syndrome  Neuromuscular Disorders  Neuropathy  Myopathy  Chest Wall Abnormality  Kyphoscoliosis  Flail Chest  Pleural Abnormality  Pneumothorax  Pleural Effusion  Airway Obstruction  FB/Tumor  COPD/Sever Asthma  Parenchymal Lung Disease  Pul edema/embolus  Pneumonia  ILD  Ventilator Dysfunction

44 Respiratory Acidosis: Causes Contd… Increased CO 2 Production:  Large Carbohydrate meal  Malignant Hyperthermia  Intensive shivering  Prolonged seizures  Thyroid Storm  Extensive Burns

45 Respiratory Acidosis: pH – 7.36 PaCO 2 – 64 HCO pH is acidic, but normal PaCO 2 > 40 => Resp Acidosis Compensation expected: HCO 3 - = 24 + (64-40) x 0.1 = = 26.4 or 24 + (64-40) x 0.4 = = 33.6 Diagnosis: Chronic Respiratory Acidosis

46 Metabolic Acidosis: Causes: Increased Anion Gap  Increased Production of Endogenous Acid  Ketoacidosis- DM, Starvation  Lactic Acidosis  Mixed- NKHC, Alcoholic  Abnormal AA Met.  CRF  Ingestion of Toxins  Salicylate  Methanol  Ethylene Glycol  Paraldehyde, Toluene, Sulphur  Rhabdomyolysis

47 Metabolic Acidosis: Causes Contd… Normal AG(Hyperchloremic)  GI Loss of HCO 3 -  Diarrhea  Fistula- Pancreatic, Biliary, Small Intestinal  Ureterosigmoidostomy  Obstructed Bowel Loop  Cholestrylamine, CaCl 2, MgSO 4  Renal Loss of Bicarb  RTA  CA Inhibitors  Hypoaldosteronism  Dilutional-  Bicarb free fluid  TPN  Increased Intake of Cl containing Acids –  NH 4 Cl, Lysine hydrochloride, Arginine Hydrochloride

48 Metabolic Acidosis:  pH – 7.36  PaCO 2 – 26  HCO  BE pH – Acidic but normal PaCO 2 – Decreased => Not Respiratory HCO Decreased => Metabolic Acidosis Compensation expected: 40 - (24-13)x1.25 = = Diagnosis: compensated Metabolic Acidosis

49 Treatment: Alkali Therapy:  Indications  Normal AG (Hyperchloremic Acidosis)  Slightly elevated AG (Mixed Hyperchloremic & AG Acidosis)  AG due to Non Metabolisable Anion (Renal Failure) Goal: To slowly increase plasma HCO 3 - to mmol/L  AG Acidosis due to Accumulation of Organic metabolizable anion, if pH< 7.2 Goal: pH to 7.15, Plasma HCO 3 - ~10mmol/L  Either orally (NaHCO 3 / Shohl’s solution) or IV (NaHCO 3 )  Carbicarb, THAM Acute Respiratory AcidosisChronic Respiratory Acidosis Correction of the cause Restoration of Adequate vent – Mechanical ventillation Difficult to Correct Measure to Improve lung function

50 Treatment: Problems with Bicarbonate Therapy  Cardiac Arrest: Both MA & RA  50mL NaHCO 3 Releases 200 mL CO 2  Bicarb corrects MA but worsens RA  Intracellular Acidosis  COP increase maybe due to increased intravascular vol  CSF Acidosis  Increased Plasma Osmolarity (3 mmol/50mL)  Extracellular alkalosis - ODC to Left - Decreased Tissue Oxygenation  Rebound Alkalosis  Decreased Ca > Myocardial depression

51 Acidosis: Anaesthetic Considerations:  Potentiation of depressant effects of sedatives and anaesthetic agents  Exaggerated circulatory depressant effects  more pronounced with agents that rapidly decrease symp tone  Increased opioid penetration into brain  basic drugs  increased non ionised form  Increased arrhytmogenicity of halothane  Respiratory Acidosis augments NDMR  delayed reversal  Succinyl Choline  increases Serum K + further

52 Alkalosis: Physiologic Effects: 1. Left shift of ODC 2. Hypokalemia 3. Low ionised Ca++ 4. Decreased CBF 5. Depressed Ventilatoin 6. Respiratory Alkalosis  Bronchoconstriction  Decreased PVR EffectDirectIndirectClinical Cerebral BF-0- Heart rate000 Cardiac inotropy000 Systemic Art tone+0+ Syst venous tone000 PA tone0-- Airway tone+-+ Uterine BF-0- Renal BF000 Ionised Ca Serum Potassium-0-

53 Respiratory Alkalosis: Primary Decrease in PaCO 2 Causes:  Central Stimulation  Pain  Anxiety  Ischemia  Tumor  Infection  Fever  Drugs: Salicylates, Progesterone, Doxapram  Peripheral Stimulation  Hypoxemia  High Altitude  Pulmonary Disease: CHF, NCPE, PE, Asthma  Severe Anemia  Unknown  Sepsis, Metabolic Enceph  Iatrogenic:  Ventilator Induced

54 Respiratory Alkalosis:  pH – 7.5  PaCO 2 – 35  HCO pH – Alkalemia PaCO 2 – Decrease => Respiratory Alkalosis Expected Compensation: 24-(40-35)x0.2 = 23 or 24-(40-35)x0.4 = 22 Diagnosis: Chronic Respiratory Alakalosis

55 Respiratory Alkalosis: Treatment:  Treatment of Underlying cause  Ventilator adjustments  Reassurance, Rebreathing from paper bag

56 Metabolic alkalosis: Causes: ECF Contraction, Normotension, K + Deficiency & 2 0 Hyperreninemic Hyperaldosteronism  Gastrointestinal  Vomiting  NG suction  Villous Adenoma  Renal  Diuretics  Mg ++ Deficiency  Chronic Hypokalemia  Hypercalcemia/Hyperpara.  Post Hypercapnic State  Barter’s syndrome  Sweat  Cystic Fibrosis

57 Metabolic alkalosis: Causes: ECF Expansion, Hypertension, K + Deficiency & Mineralocorticoid Excess  High Renin  Renal Artery Stenosis  Accelerated HTN  Low Renin  Primary Aldosteronism  Adrenal Enzyme defects  Cushing’s Syndrome  Other  Liquorice Exogenous HCO - Loads:  Massive Blood Transfusion  Acetate containing colloids  Alkali therapy + Renal Failure  Milk-Alkali Syndrome

58 Metabolic Alaklosis:  pH – 7.58  PaCO 2 – 48  HCO  BE pH – Alkalemia PaCO 2 – Increased => Not Respiratory HCO Increased => Metabolic Acidosis Expected Compensatoin: 40+(44-24)x0.8 = 56 Diagnosis: Partially compensated Metabolic Alkalosis

59 Metabolic Alkalosis: Treatment:  Correction of underlying stimulus for HCO 3 - generation:  Correction of cause of 1 0 Hyperaldosteronism  Reduction of Gastric secretions: H 2 Blockers, PPI  Reduction of Renal loss of H + : Discontinue Diuretics  Remove factors that sustain HCO 3 - Reabsorption  ECF contraction – NaCl administration  K + deficiency – KCl administration  Acetazolamide  But can cause K + loss  Dilute HCl (0.1N HCl)  Oral NH 4 Cl

60 Alkalosis: Anaesthetic considerations:  Increased protein binding of opioids  prolonged respiratory depression  Decreased cerebral blood flow  Cerebral Ischemia  Atrial and Ventricular dysrhythmias  with hypokalemia  Potentiation of NDMR  due to hypokalemia

61 Acid Base Disorders:  PO 2 – 90.6  PCO 2 – 53.8  pH –  K  Na  HCO 3 - (A) – 37.7  HCO 3 - (S) – 34.3  BE – 13.9  SBE – 14.1  SO 2 – 97.3 pH – Alkalemia PCO 2 – Increased => Metabolic Alkalosis Expected Compensation: PaCO 2 = 40+(13.7x0.75) = 50.2 Body never overcompensates Diagnosis: Metabolic Alkalosis + Respiratory Acidosis

62 Summary:  Acid Base Homeostasis is all about maintenance of normal H + concentration.  Changes in acid base status of ECF have profound and often unpredicatble clinical and laboratory effects, more so during anaesthesia.  pH scale is a negative logarithmic scale with it’s inherent counterintutive results.  The three independent variables which affect acid base status are SID, [A tot ] & PaCO 2.  SBE as a measure for Metabolic acid base disturbance is most accurate and clinically validated.  Anion gap must always be calculated, and effect of Plasma Albumin considered to decipher more accurately the complex acid-base disorders in critically ill patients.  Bicarbonate therapy must be used with caution in view of it’s various deleterious effects.

63 References:  Miller’s Anesthesia, 7 th Edition  Wylie And Churchill Davidson’s A Practice of Anaesthsia, 7 th Edition  Morgan Michael &  Clinical Application of Blood Gases, Shapiro, 5 th Edition  Harrison’s Principles of Internal Medicine, 16 th Edition  Ganong’s Review of Medical Physiology, 20 th Edition  ‘Acid-Base tutorial. Prof. Alan W Grogono, MD, FRCA  A Basic Approach to body pH m m

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