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Acid Base Equilibrium, Clinical Concepts and Acid Base Disorders

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1 Acid Base Equilibrium, Clinical Concepts and Acid Base Disorders
Dr Sajith Damodaran University College of Medical Sciences & GTB Hospital, Delhi

2 Increased Osmolality of ECF
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 Intake Water 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 Aldosterone Vasopressin Thirst Adrenal Cortex Brain Blood Vessel Vasoconstriction Kidney Na Retention Water Retention

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 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: mEq/d 12500 mEq/d H+ load from AA metabolism CO2 from metabolism H+ ion Failure of Kidneys to Excrete PO4--, SO4-- Ingestion of NH4Cl, CaCl2 Diabetic KA Strenuous Exercise Lactic Acid

7 Some Basic Chemistry Definitions: Arrhenius: Browsted and Lowry:
Acid: H+ Donor in Solution Base: OH- donor in Solution Browsted and Lowry: Acid: Proton Donor Base: Proton Acceptor H20 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: CO2 – HCO3- 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 (H2O)
Water dissociates, but to a very low extent. H2O <====>H+ + OH- But, a glass of water has a billion times more H2O than H+ & OH- At equilibrium: [H+] [OH-] = Kw[H2O] {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: Electrical Neutrality Mass conservation Dissociation Equilibrium ECF is a complex solution with strong ions, weak ions and CO2 dissolved in water.

13 Acid Base Equilibrium:
CO2 in Water: Can Dissolve in water Can form - Carbonic Acid - Bicarbonate ion - Carbonate ion CO2(gas) <====> CO2(dissolved) Rate of Forward Reaction = Kf * PCO2 Rate of Reverse reaction = Kr *[CO2(dissolved) ] => [CO2(dissolved)] = Kf /Kr *PCO2 Kf /Kr = SCO2 (Solubility of CO2 ) = 0.03mEq/L/mm Hg at 370 C } All these reactions have equilibrium Constants and can be solved at equilibrium.

14 Acid Base Equilibrium:
CO2 + H2O <====> H2CO3 =>[CO2][H2O] = K*[H2CO3] => [H2CO3] = K’*PCO2 H2CO3 <====> H+ + HCO3- Henderson Equation: [H+ ] = K1 [H2CO3]/[HCO3- ] Modified Henderson Equation: [H+ ][HCO3- ] = K2 [CO2][H2O] [H+ ][HCO3- ] = K3 [CO2] [H+] = K*PaCO2/[HCO3-]

15 Acid Base Equilibrium:
The Henderson-Hasselbalch Equation: CO2 + H2O <====> H+ + HCO3- => [H+] = K’a * [CO2]/[HCO3-] Rearranging: =>1/[H+] = 1/K’a*[HCO3-]/[CO2] Taking Logarithm on both sides & Rearranging: => pH= pK’a + log10[HCO3-]/0.03*PCO2 Significance: Includes components of both Met & Resp Acid base disorders Value of any one variable can be determined if other two known. Mostly HCO3- is calculated pH determined by ratio of [HCO3-]/PCO2 . 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, [Atot] & PaCO2 Constants : Dissociation constants Dependent Variables: [H+], [OH-], [HCO3-], [CO32-], [A+], [HA], [H2CO3], [CO2 dissolved]

17 Clinical Concepts: The Stewart Approach
Dissociation equations can be solved mathematically. When the equations are solved- Independent Variables: SID, [Atot] & PaCO2 Constants : Dissociation constants Dependent Variables: [H+], [OH-], [HCO3-], [CO32-], [A+], [HA], [H2CO3], [CO2 dissolved] Dependent Variables can only be changed by changing the independent variables!!!

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 [Atot]: 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+] - {[HCO3-] + [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 Causes of Low AG Increased unmeasured cations – Ca, Mg Addition of abnormal cations Li Decreased Alb Altered charge in Alb d/t acidosis Hpyervisocity, severe hyperlipidemia – underestimation of Na & Cl in lab. In a mixed disorder like Malk f/b M Acidosis, the HCO3- & pH would be normal, but AG will be raised.

20 Clinical Concepts: Acid Base Equilibrium: Elimination of Acid
Recovery/Regeneration of Base Mechanisms that keep pH stable Buffering Compensation Correction Components of Acid Base Equlibrium: Elemination of Acid Recovery/Regeneration of Base Mechanisms that keep pH stable Buffering: Chemical buffers in body to immediately minimise the change in pH Compensation: Attempt to restore [HCO3- ]/PaCO2 ratio to normal by alteration of non deranged value Correction: Rearranging homeostasis by correcting primary metabolic derangement

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 = pKa + log [A-]/[HA] When [A-] = [HA], pH= pK, buffering capacity is maximum. Ideal body buffer has pKa between 6.8 and 7.2

22 Clinical Concepts: Quanitity pKa
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 + H2O Buffer Effectiveness Depends on: Quanitity H2CO3 /HCO3- - Most important Extracellular Buffer Protein Buffers – Most improtant Intracellular Buffer pKa – Buffering capacity maximum when pH=pKa Function well within 1 pH unit. (Eg: HCO ) Hbuffer is a weak acid. So less H+ is realsed in solution as compared to HCl which is a strong acid If no buffer were there, OH from NaOH would combine with H+ n reduce its concentration thus raising pH. But NaBuffer is a weak base, n less OH is released in solutiong.

23 Clinical Concepts: Buffers in ECF: Carbonate-Bicarbonate Buffer 53%
Plasma (35%) Erythrocyte(18%) Hemoglobin 35% Plasma Proteins 7% Organic & Inorganic Phosphates 5% Buffers in ICF: Intracellular Proteins H2PO4-HPO4- 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: useful only for metabolic acid
HCl + NaHCO3- <==>NaCl + H2CO3<==>NaCl + H2O + CO2 useful only for metabolic acid Hb System: Both Respiratory & Metabolic Acid in ECF Forms Carbamino compounds with CO2 Buffers H+ directly CO2 + H2O <====>H2CO3 + KHb <====> HHb + KHCO3 HCO3- diffuses out & Cl- diffuses into cells – Chloride shift pKa – 6.8 CO2 combines with terminal AA of Hb to form Carbamino compounds % of total co2 transport in bld. Co2 in RBC forms cabonic acid by CA n breaks down to H+ & OH-. The H+ is buffered by HHb. CO3- diffuses out and cl- comes in. Thus most of the change happens in plasma. Imidazole groups of Histidine residues in Hb act as buffer. 38 His residues in Hb.

25 Clinical Concepts: Protein Buffer:
Predominant Intracellular Buffer – Large total concentration pK = 7.4 AA have Acidic & Basic Free radicles .COOH + OH- <====> COO- + H2O .NH3OH + H+ <====> NH3 + H2O Phosphate Buffer: pK = 6.8 Predominantly Intracellular Also in renal tubular HCl + Na2HPO4 <====> NaH2PO4 + NaCl NaOH + NaH2PO4 <====> Na2HPO4 + H2O

26 H+ + HCO3-<====> H2CO3 <====>CO2 + H2O
Clinical Concepts: Compensation: Pulmonary Compensation H+ + HCO3-<====> H2CO3 <====>CO2 + H2O H+ acts on medullary centres. Increased PaCO2 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:
Reabsorption of filtered HCO3- ( mEq/d) Generation of fresh bicarbonate Formation of titrable acid – (1mEq/Kg/d) Excretion of NH4+ in urine

28 MAJOR RENAL MECHANISMS RESPONSIBLE FOR H+ EXCRETION/HCO3- RETENTION
PERITUBULAR BLOOD RENAL TUBULAR CELL GLOMULAR FILTRATE Glutamine HCO3- + H+ CO2 HCO3- Na+ HPO42- Na+ NH3 Na+ H2CO3 NaHCO3 CO2 + H2 O CO2 H2PO4- NaHCO3 CA NH4+ NaHCO3 H2O H2PO4- NH4+ CO2 can be obtained from blood or the tubular fluid

29 Prediction of Compensation Prediction of Compensation
Clinical concepts: Compensation Prediction of Compensatory Responses on Simple Acid Base Disorders Disorder Prediction of Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3- ) + 8 Or PaCO2 will mm Hg ( ) per mmol/L in [HCO3- ] PaCO2 = [HCO3- ] + 15 Metabolic Alkalosis PaCO2 will ( ) mm Hg per mmol/L in [HCO3- ] PaCO2 will 6mm Hg per 10 mmol/l in [HCO3- ] PaCO2 = [HCO3- ] + 15, Max – 55mmHg Respiratory Alkalosis Acute [HCO3- ] will 2mmol/L per 10 mmHg in PaCO2 Chronic [HCO3- ] will 4mmol/L per 10 mmHg in PaCO2 Respiratory Acidosis [HCO3- ] will 1mmol/L per 10 mmHg in PaCO2 Disorder Prediction of Compensation Metabolic Acidosis PaCO2 = (1.5 x HCO3- ) + 8 Or PaCO2 will mm Hg per mmol/L in [HCO3- ] PaCO2 = [HCO3- ] + 15 Metabolic Alkalosis PaCO2 will mm Hg per mmol/L in [HCO3- ] PaCO2 will 6mm Hg per 10 mmol/l in [HCO3- ] Respiratory Alkalosis Acute [HCO3- ] will 2mmol/L per 10 mmHg in PaCO2 Chronic [HCO3- ] will 4mmol/L per 10 mmHg in PaCO2 Respiratory Acidosis [HCO3- ] will 1mmol/L per 10 mmHg in PaCO2

30 Acid-Base Nomogram:

31 Clinical concepts: Effect of Temp: pH rises 0.015/0C drop in temp
Effect of PaCO2 on pH: pH changes by 0.08/10mm Hg change in PaCO2 Effect of change of [HCO3-] on pH: pH changes by 0.1/ 6 mEq change in [HCO3-] This is because CO2 is more soluble as blood cools and thus PCO2 drops.(4.5%/degree) Hb accepts more H+ when cooled.

32 Clinical Concepts: Effect of Electrolytes in Buffering:
Potassium Ion: Intracellular Hypokalemia - K+ Moves out  H+ moves in - K+ & HCO3- reabsorption, H+ Excretion Sodium Ion Hyponatremia -- Na+ & HCO3- reabsorption & H+ excretion Extra HCO3- in Blood  Extracellular Metabolic Alkalosis & Intracellular Metabolic Acidosis

33 Clinical Concepts: Role of Bones:
Exchange of Extracellular H+ for Na+ & Ca++ Acid load  Demineralise Bones Alkaline load  Deposition of CO32- 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 PaCO2 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 Disorder Primary Change Compensatory Change Metabolic Acidosis HCO3_ PaCO2 Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis

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. Resp Acidosis due to volatile agents. Causes increased arrhythmogenicity in patients with CVS & RS

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: CO2 freely diffuses HCO3- slowly over hours Similar effects in Fetal systems Electrolytes: Calcium: Increased Free Ca++ Potassium: Increased S K+ Increased free Ca due to displacement from Neg binding sites on alb As H+ shifts intracellularly, K+ shift extracellularly For every 0.1 unit change in pH, K changes 0.6. But this is non linear.

40 Clinical Effects of Acidosis:
NeuroEndocrine: CBF (by PaCO2) Mental Changes: CNS Depression More with RA Decreased Body Temp Impaired central regulation Cutaneous vasodilatation Decreased Cellular Metabolism Increased secretion of catecholamines Physiologic Effects of Acidemia: Direct depressant effects Secondary effects due to sympathoadrenal activation Myocardial Depression  Hypotension Smooth muscle depression  Hypotension Right shift of ODC But tissue hypoxia due to hypotension Decreased responsiveness to endogenous and exogenous catecholamines Progressive Hyperkalemia. K+ increases 0.6 mEq/L for each 0.10 decrease in pH Decreased threshold for Ventricular Fibrillation CNS depression: Due to Respiratory Acidosis

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

42 Respiratory Acidosis:
Primary Increase in PaCO2 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 CO2 Production: Large Carbohydrate meal Malignant Hyperthermia Intensive shivering Prolonged seizures Thyroid Storm Extensive Burns

45 Respiratory Acidosis:
pH – 7.36 PaCO2 – 64 HCO pH is acidic, but normal PaCO2 > 40 => Resp Acidosis Compensation expected: HCO3- = 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 Any Acidosis that can’t be explained by Respiratory component is due to Metabolic Acids. Primary Mechanisms: Consumption of HCO3- by non-volatile acid Renal wasting of HCO3- Rapid Dilution of ECF with Bicarb. Free fluid

47 Metabolic Acidosis: Causes Contd…
Normal AG(Hyperchloremic) GI Loss of HCO3- Diarrhea Fistula- Pancreatic, Biliary, Small Intestinal Ureterosigmoidostomy Obstructed Bowel Loop Cholestrylamine, CaCl2, MgSO4 Renal Loss of Bicarb RTA CA Inhibitors Hypoaldosteronism Dilutional- Bicarb free fluid TPN Increased Intake of Cl containing Acids – NH4Cl, Lysine hydrochloride, Arginine Hydrochloride

48 Metabolic Acidosis: pH – 7.36 PaCO2 – 26 HCO3- - 13 BE - -11
pH – Acidic but normal PaCO2 – Decreased => Not Respiratory HCO3- - Decreased => Metabolic Acidosis Compensation expected: 40 - (24-13)x1.25 = = 26.25 Diagnosis: compensated Metabolic Acidosis

49 Treatment: Alkali Therapy: Indications
Acute Respiratory Acidosis Chronic Respiratory Acidosis Correction of the cause Restoration of Adequate vent – Mechanical ventillation Difficult to Correct Measure to Improve lung function 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 HCO3- to mmol/L AG Acidosis due to Accumulation of Organic metabolizable anion, if pH< 7.2 Goal: pH to 7.15, Plasma HCO3- ~10mmol/L Either orally (NaHCO3 / Shohl’s solution) or IV (NaHCO3) Carbicarb, THAM Depends on severity and rate of onset. Acute: Reversal of underlying cause Restoration of adequate ventillation – Mechanical ventillation Chronic: Difficult to correct. Measures to improve lung function Carbicarb: This compound has an equimolar concentration of NaHCO3 - and sodium carbonate. Because carbonate is a stronger base, it buffers H+ in preference to HCO3 -, resulting in the generation of HCO3 - rather than CO2. This drug is not available in the United States. THAM is a sodium-free alkalizing solution containing 0.3N tromethamine. It buffers acids and limits the generation of CO2 and has been used in some clinical situations to treat severe metabolic acidosis. Major adverse effects include hyperkalemia and hypoglycemia, and the drug should not be used in patients with oliguria or poor renal function. This drug is not used widely in the United States.

50 Treatment: Problems with Bicarbonate Therapy
Cardiac Arrest: Both MA & RA 50mL NaHCO3 Releases 200 mL CO2 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: Left shift of ODC Hypokalemia
Low ionised Ca++ Decreased CBF Depressed Ventilatoin Respiratory Alkalosis Bronchoconstriction Decreased PVR Effect Direct Indirect Clinical Cerebral BF - Heart rate Cardiac inotropy Systemic Art tone + Syst venous tone PA tone Airway tone Uterine BF Renal BF Ionised Ca++ Serum Potassium

53 Respiratory Alkalosis: Primary Decrease in PaCO2 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 Usually d/t alveolar hyperventilation.

54 Respiratory Alkalosis:
pH – 7.5 PaCO2 – 35 HCO pH – Alkalemia PaCO2 – 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 & 20 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 Primary decrease in Bicarb

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 PaCO2 – 48 HCO3- - 44 BE - +19
pH – Alkalemia PaCO2 – Increased => Not Respiratory HCO3- - 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 HCO3- generation: Correction of cause of 10 Hyperaldosteronism Reduction of Gastric secretions: H2 Blockers, PPI Reduction of Renal loss of H+ : Discontinue Diuretics Remove factors that sustain HCO3- Reabsorption ECF contraction – NaCl administration K+ deficiency – KCl administration Acetazolamide But can cause K+ loss Dilute HCl (0.1N HCl) Oral NH4Cl

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: PO2 – 90.6 PCO2 – 53.8 pH – 7.484 K+ - 3.7
Na HCO3- (A) – 37.7 HCO3- (S) – 34.3 BE – 13.9 SBE – 14.1 SO2 – 97.3 pH – Alkalemia PCO2 – Increased => Metabolic Alkalosis Expected Compensation: PaCO2 = 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, [Atot] & PaCO2. 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, 7th Edition
Wylie And Churchill Davidson’s A Practice of Anaesthsia, 7th Edition Morgan Michael & Clinical Application of Blood Gases, Shapiro, 5th Edition Harrison’s Principles of Internal Medicine, 16th Edition Ganong’s Review of Medical Physiology, 20th Edition ‘Acid-Base tutorial. Prof. Alan W Grogono, MD, FRCA A Basic Approach to body pH m

64 Thank You


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