Acid Base Balance & Disorders - Part I

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Acid-Base Balance & Disorders . Part I . Normal Acid Base Balance & Metabolic Acid Base Disorders:

Acid-Base Balance & Disorders . Part I . Normal Acid Base Balance & Metabolic Acid Base Disorders Presented By Mohammed Abdel Gawad

Acid Base Balance & Disorders:

Acid Base Balance & Disorders Normal Acid Base Balance Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Mixed Acid Base Disorders ABG Interpretation 2 Part I Part II

pH:

pH Power of hydrogen Potential of hydrogen 3 pH Scale

Threats to pH:

4 Lactic acid Sulphuric acid Carbonic acid Phosphoric acid Threats to pH 1. Volatile acids: Carbon dioxide: 2. Fixed-non volatile acids: a- Sulphuric acid: an end product of the oxidation of sulphur containing aminoacids , methionine and cysteine . b- phosphoric acid: formed in the metabolism of phospholipids, nucleic acids, phosphorproteins and phosphoglycerides . 3. Organic acids: Lactic acid, acetoacetic acid and B-OH-butyric acid formed during the metabolism of carbohydrates and fats.

Defense against changes in H+ concentration:

Defense against changes in H + concentration I. Acid-base buffer systems in body fluids , within seconds. II. The respiratory system , within minutes. III. The kidneys , within hours. 5 Acid Base Acid Acid Base Base Buffer Weak Acid + Strong Base or Weak Base + Strong Acid A. The bicarbonate buffer system B- The phosphate buffer system C- The protein buffer system

I-acid-base buffers A. The bicarbonate buffer system :

I-acid-base buffers A. The bicarbonate buffer system consists of a mixture of: carbonic acid (H 2 CO3) and sodium bicarbonate (NaHCO3) in the same body fluid. When a strong acid, as hydrochloric acid, is added: When a strong base, as sodium hydroxide, is added: It is the most important buffer system in the body because: 1- present in all the body fluids, both ECF & ICF. 2- concentration of its components (CO2 & HCO3)can be independently regulated 6 HCl + NaHCO3 H2CO3 + NaCl NaOH + H2CO3 NaHCO3 + H2O

Defense against changes in H+ concentration:

Defense against changes in H + concentration I. Acid-base buffer systems in body fluids , within seconds. 7 A. The bicarbonate buffer system B- The phosphate buffer system C- The protein buffer system

I- acid-base buffers B- The phosphate buffer system: :

I- acid-base buffers B- The phosphate buffer system: composed of: more effective in ICF than in ECF: The total concentration of phosphate is much greater in ICF than ECF. also effective in buffering the tubular fluid in the kidneys because: Phosphate becomes greatly concentrated in the tubular fluid due to the reabsorption of water in excess of phosphate. 8

Defense against changes in H+ concentration:

Defense against changes in H + concentration I. Acid-base buffer systems in body fluids , within seconds. 9 A. The bicarbonate buffer system B- The phosphate buffer system C- The protein buffer system 1- proteins of cells and plasma 2- haemoglobin

I- acid-base buffers C- The protein buffer system :

I- acid-base buffers C- The protein buffer system 1) Proteins of the cells and the plasma: 10

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11 CO 2 Red Blood Cell Systemic Circulation H 2 O H + HCO 3 - carbonic anhydrase Plasma CO 2 CO 2 CO 2 CO 2 CO 2 CO 2 CO 2 Click for Carbon Dioxide diffusion + + Tissues H + Cl - Hb H + is buffered by Hemoglobin I-acid-base buffers C- Protein buffer system 2) Haemoglobin Tissue side

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12 Red Blood Cell Pulmonary Circulation CO 2 H 2 O H + + + HCO 3 - Cl - Alveolus Plasma CO 2 CO 2 H 2 O Hb Lung side

Defense against changes in H+ concentration:

Defense against changes in H + concentration I. Acid-base buffer systems in body fluids , within seconds. II. The respiratory system , within minutes. III. The kidneys , within hours. 13

II- Respiratory regulation of acid-base balance :

II- Respiratory regulation of acid-base balance 14

Defense against changes in H+ concentration:

Defense against changes in H + concentration I. Acid-base buffer systems in body fluids , within seconds. II. The respiratory system , within minutes. III. The kidneys , within hours. 15 Reabsorption (reclamation) of the filtered bicarbonate by proximal tubules. 2. Generation of new bicarbonate A- ammonia B- phosphate

1- Reabsorption (Reclamation)of the filtered bicarbonate - PCT:

1- Reabsorption (Reclamation)of the filtered bicarbonate - PCT 16

2. Generation of new bicarbonate A- ammonia (PCT & DCT) :

2. Generation of new bicarbonate A- ammonia (PCT & DCT) 17

2. Generation of new bicarbonate B- phosphate (DCT):

2. Generation of new bicarbonate B- phosphate (DCT) 18

Anion Gap:

Anion Gap 19 Normocholeremic Hypercholeremic

PowerPoint Presentation:

pH Scale

Normal Values:

Co2 is an acid While HCO3 is a base Normal Values Parameter Normal value pH 7.35 – 7.45 PCO2 35 – 45 mmHg HCO3 22- 26 mEq /L

Classification of Acid-basic Disorders:

Classification of Acid-basic Disorders pH PCO2 HCO3 Metabolic Acidosis ↓ ↓ (compensation) ↓ (1ry disorder) Metabolic Alkalosis ↑ ↑ (compensation) ↑ (1ry disorder) Respiratory Acidosis ↓ ↑ (1ry disorder) ↑ (compensation) Respiratory Alkalosis ↑ ↓ (1ry disorder) ↓ (compensation) 22

Henderson–Hasselbalch equation:

Henderson– Hasselbalch equation 24 pH = log 1 / H +

Acid Base Balance & Disorders:

Acid Base Balance & Disorders Normal Acid Base Balance Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Mixed Acid Base Disorders ABG Interpretation 25 Part I Part II

I- Approved metabolic acidosis: :

I- Approved metabolic acidosis: pH < 7.35 HCO3 < 22 mEq /L PCO2 < 35 mmHg (compensation) for each 1 ↓ HCO3 → 1.2 ↓ CO2 or Δ ↓ P co 2 = 1.2 x ΔHCO3 In absence of full compensation, this is called: A- partial compensation or better called: B- mixed metabolic & respiratory acidosis: as the lung not washing enough CO2 as needed, which mean that it is actually accumulating CO2 even if the PCO2 is lower than normal. 26 II- Expected compensation:

III- Calculate Anion Gap:

III- Calculate Anion Gap Equations: AG = (Na + K) – ( Cl + HCO3) = 12 ± 4 mmol /l or AG = (Na) – ( Cl + HCO3) = 12 ± 2 mmol /l Corrected Anion Gap: anion gap is decreased by 4 mmol /l for each 1 g/dl decrease in the serum albumin concentration below normal. The result: Wide (high) anion gap metabolic acidosis or Non (normal) anion gap metabolic acidosis 27

PowerPoint Presentation:

High AG acidosis • • • • • • • • K U S S M A L E Ketoacidosis (starvation, DM, alcohol) Uremia Sepsis Salicylate & other drugs e.g.paraldhyde Methanol Alcohol (Ethanol) Lactic acidosis Ethylene glycol 28 Wide Anion Gap Causes Normocholeremic

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29 4- uretrosigmoid-ostomy Non Anion Gap Causes Hypercholeremic

To remember:

To remember I- Approved Metabolic Acidosis II- Calculate Compensation III- Calculate Anion Gap IV- a- if high anion gap → calculate delta gap b- if normal anion gap → calculate urinary AG 30

IV- a- if high anion gap → calculate delta gap :

IV- a- if high anion gap → calculate delta gap ∆ Gap = ∆AG / ∆HCO3 > 1 = high AG metabolic acidosis mixed with metabolic alkalosis < 1 = high AG metabolic acidosis mixed with non AG metabolic acidosis = 1 = simple high AG metabolic acidosis 31 Ketoacidosis Uremia Sepsis Salicylate & other drugs Methanol Alcohol (Ethanol) Lactic acidosis Ethylene glycol AG HCO3 Cl 12 24

:

32 NH4Cl IV- b- if normal anion gap → calculate urinary AG 4- uretrosigmoid-ostomy urine AG = u[Na + K] – u[ Cl ] If – ve : so the loss is non renal If zero or + ve : so the loss is renal N.B. Normally it is + ve ranging from +30 to +50 mmol /L

To remember:

To remember I- Approved Metabolic Acidosis II- Calculate Compensation III- Calculate Anion Gap IV- a- if high anion gap → calculate delta gap b- if normal anion gap → calculate urinary AG 33

PowerPoint Presentation:

34 Metabolic Acidosis Treatment Treatment of metabolic acidosis usually involves either sodium bicarbonate or citrate: A- Sodium bicarbonate: orally as tablets or powder or given intravenously as a 1- hypertonic sodium bicarbonate bolus or 2- an isotonic sodium bicarbonate infusion (adding three ampules of sodium bicarbonate (50 mmol /amp) to a liter of 5% dextrose in water (D5W) solution. B- Sodium Citrate: orally as a liquid, as sodium citrate, potassium citrate, or citric acid and as a combination of these. Oral citrate therapy should not be combined with medications that include aluminum.

Bicarbonate Deficit – Equation 1:

Bicarbonate Deficit – Equation 1 35

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36 Bicarbonate Deficit – Equation 2

Bicarbonate Administration:

Bicarbonate Administration 37 Koda -Kimble et al: Replace 50% over 3 to 4 hours the reminder over 24 hours. Once the pH is 7.2 - 7.25, the serum [HCO3-] should not be increased by more than 4 to 8 Eq /L over 6 to 12 hours to avoid the risks of over- alkalinization (paradoxical CNS acidosis; decreased affinity of hemoglobin for oxygen leading to tissue hypoxia and lactic acid production; sodium overload; and hypokalemia ).

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38 Renal Tubular Acidosis

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Proximal Tubule Reabsorption : HCO3- (90%) calcium glucose Amino acids NaCl , water Secretion: H+ Distal Tubule Na+ reabsorbed molar competition between H+ and K+ excretion under effect of aldosterone 39 Renal Tubular Acidosis cont. Normal Tubules Transport

Functions of DCT & Collecting Duct:

Functions of DCT & Collecting Duct 40 Aldosteron

Renal Tubular Acidosis - Types:

Renal Tubular Acidosis - Types Type 2 RTA Type 1 RTA Type 4 RTA 41

Type 1 RTA (classical distal RTA – Hypokalemic RTA):

Distal defect  A- impaired H+ secretion ( secretory defect) Or B- defect in the basolateral anion exchanger AE1 → abnormally permeable distal tubule → resulting in increased backleak of normally secreted H+ (gradient defect) Net result A- H+ builds up in blood (acidosis) B- Urine pH > 5.5 C- K+ secreted instead of H+ ( hypokalemia ) D- The subsequent metabolic acidosis → stimulates reabsorption of bone matrix to release the calcium alkali salts present in bone. 42 Type 1 RTA (classical distal RTA – Hypokalemic RTA) Site of defect ❶ ❷

Type 1 RTA - Presentation:

Growth retardation Bone disease Kidney stones Intermittent muscle weakness ( hypokalemia ) Progressive renal failure as a result of: a- underlying disease a- hypokalemia induced interstitial fibrosis. 43 Type 1 RTA - Presentation

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44

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45

Type 1 RTA - When to suspect ? :

Type 1 RTA - When to suspect ? Type 1 RTA should be suspected in a patient with: a non anion gap metabolic acidosis & hypokalemia & urine pH above 5.5 in the setting of systemic acidosis & UAG value ≥ zero. 46

Type 1 RTA Causes:

Type 1 RTA Causes 47

Type 1 RTA - Treatment:

Type 1 RTA - Treatment Treat the cause. Alkali replacement: 1-3mmol/kg/day bicarbonate Potassium replacement if hypokalemia 48

Renal Tubular Acidosis - Types:

Renal Tubular Acidosis - Types Type 2 RTA Type 1 RTA Type 4 RTA 49

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Aldosterone deficiency or distal tubule resistance to aldosterone  impaired function of Na+/K+-H+ exhange mechanism  Decreased H+ and K+ secretion  plasma buildup of H+ and K+ 50 Defect in aldosteron action Type 4 RTA ( Hyperkalemic Distal RTA)

Distal Renal Tubular Acidosis:

Distal Renal Tubular Acidosis Type 1 RTA LOW serum K+ Type 4 RTA HIGH serum K+ 51

Type 4 RTA:

Type 4 RTA Urine pH: Variable 52

Type 4 RTA Causes:

Type 4 RTA Causes 53

Type 4 RTA - Treatment:

Type 4 RTA - Treatment 1- treat the cause 2- if due to hypoladosteronism : Give fludrocortisone 0.1 mg/d 3- if secondary to drugs (ACEI, Spironolactone ): Advice low K diet Mineralocorticoides of no significance to avoid Na retension . 4- Loop & thiazide diuretics 5- NaHCO3 for acidosis & hyperkalemia (but watch overload & worsening HTN) 54

Renal Tubular Acidosis - Types:

Renal Tubular Acidosis - Types Type 2 RTA Type 1 RTA Type 4 RTA 55

Type 2 RTA (Proximal RTA):

Type 2 RTA (Proximal RTA) Urine pH: Decreased reabsorption of HCO3  HCO3- wasting  Urine pH high initially then  the filtered bicarbonate load decreases to the point at which the proximal tubule is able to reabsorb sufficient filtered bicarbonate. When this process occurs, no further bicarbonate is lost in the urine, net acid excretion normalizes, and a new steady-state serum bicarbonate concentration develops, albeit at a lower than normal level  Urine pH < 5.5 56

PowerPoint Presentation:

Hypokalemia : Renal NaHCO3 losses → intravascular volume depletion → activates RAS system → increased distal nephron Na+ reabsorption & increased K+ secretion. In the steady state , when virtually all the filtered HCO3− is reabsorbed in the proximal and distal nephron , renal potassium wasting is less and the degree of hypokalemia tends to be mild. 57 Type 2 RTA (Proximal RTA)

Type 2 RTA (Proximal RTA) - Bone :

Type 2 RTA (Proximal RTA) - Bone Osteomalacia can develop as a result of: A- chronic hypophosphatemia if Fanconi syndrome is present. B- deficiency in the active form of vitamin D. 58

Type 2 RTA (Proximal RTA) – When to suspect ? :

Type 2 RTA (Proximal RTA) – When to suspect ? Proximal RTA should be suspected in a patient with: a normal anion gap acidosis & hypokalemia & intact ability to acidify the urine to below 5.5 while in a steady & UAG ≥ zero. ± other proximal tubular dysfunction, such as euglycemic glycosuria , hypophosphatemia , hypouricemia , and mild proteinuria . 59

Type 2 RTA Causes:

Type 2 RTA Causes 60

Type 2 RTA - Treatment:

Type 2 RTA - Treatment A problem we face: Administration of alkali → increases the serum bicarbonate concentration, → increases urinary bicarbonate losses → increases distal sodium load → increased circulating plasma aldosterone , → increased renal potassium wasting. As a result, substantial amounts of alkali, often in the form of a potassium bicarbonate required to prevent worsening hypokalemia . Alkali therapy: KHCO3 1.5 – 3 g/d in 3 divided doses. Vit D in infants 61

Type 3 RTA?:

Type 3 RTA? Very rare Used to designate mixed dRTA and pRTA of uncertain etiology Now describes genetic defect in Type 2 carbonic anhydrase (CA2), found in both proximal, distal tubular cells and bone 62

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66

Acid Base Balance & Disorders:

Acid Base Balance & Disorders Normal Acid Base Balance Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Mixed Acid Base Disorders ABG Interpretation 67 Part I Part II

I- Approved metabolic alkalosis: :

I- Approved metabolic alkalosis: pH > 7.45 HCO3 > 26 mEq /L PCO2 > 45 mmHg (compensation) for each 1 ↑ HCO3 → 0.7 ↑ CO2 or Δ ↑ P co 2 = 0.7 x ΔHCO3 In absence of full compensation, this is called: A- partial compensation or better called: B- mixed metabolic & respiratory alkalosis: as the lung can not retain enough CO2 as needed, which mean that it is actually washing CO2 even if the PCO2 is higher than normal. 68 II- Expected compensation:

III- Causes :

III- Causes A- Chloride Depletion (urine Cl < 10 mEq /L) B- Corticosteroid & Apparent Corticosteroid Induced (chloride resistant) (urine Cl > 10 mEq /L) C- Alkali Administration or Ingestion 69

A- Chloride Depletion (urine Cl < 10 mEq/L):

A- Chloride Depletion (urine Cl < 10 mEq /L) 70

B- Corticosteroid & Apparent Corticosteroid Induced (chloride resistant) (urine Cl > 10 mEq/L):

B- Corticosteroid & Apparent Corticosteroid Induced (chloride resistant) (urine Cl > 10 mEq /L) 71

C- Alkali Administration or Ingestion:

C- Alkali Administration or Ingestion 72

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73

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74 Metabolic Alkalosis Treatment 1- Treat the cause 2-

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75 To Be Continued …. Part II …. Thank You

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