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ACID BASE EVALUATION:

Nauman Tarif, MD
Associate Professor SIMS

ACIDS AND BASES


Using the definitions proposed by Bronsted
An acid is a substance that can donate H+ ions A base is a substance that can accept H+ ions

H2CO3

<>

H+ + HCO3H+ + ClH+ + NH3

HCl <> NH4+ <>

H2PO4- <> H+ + HPO42Acid Base

pH
What is pH ? P French word Pvissance (power) Meaning power of hydrogen Def: -ve log of [H+] conc. i.e.minus no. to which 10 must be raised to get that no.

pH Scale
7 (neutral) | 0 --------------------------------------------------14 | alkaline 7.40(Blood)
pH< 7.35 Acidosis

pH > 7.45 Alkalosis

Acid-Base Disorders
Blood PH 7.4 H+ = 40 x 10-9 = 40 nmol/L

Acids
H+ ions or proton donor Two types of acids are formed by metabolic processes
Volatile acids: liquid gas. CO2 eliminated by lungs.
CO2 + H2O H2CO3 H+ + HCO3

Nonvolatile or fixed acids: are eliminated by the kidneys


Examples: SO4, PO4, lactic acid, ketoacids

The non-volatile portion is trivial when compared to the volatile CO2.About 50-100

H+ is maintained within narrow limits. Normal Level approx.40 nanomol/L Low Conc. Essential for normal cellular fxn. Changes in the H+ conc., proteins gain or lose H+ ions. resulting in: alteration in charge distribution molecular configuration protein function

pH change Regulation
The body constantly produces acids through metabolism These acids must be constantly eliminated from the body Buffers Chemical substance that prevents large changes in pH Ventilation Can handle ~75% of most pH disturbances Renal regulation of H+ & HCO3slow but very effective

Acid-Base Load
Addition from extrinsic source:
Infusions [eg HCl, NH4Cl]

Intrinsic sources:
Acid generation: ketoacidosis, Lactic acidosis Acid loss: Vomiting Base loss: Diarrhea

HENDERSON-HASSELBACH EQUATION HA H+ + ALaw of Mass Action: at Equilibrium reactions are equal

pH = pKa + log base acid


When ph and pKa are equal: 50% exists as Base & 50% as Acid
Strong Acid: Completely ionized at ph= 7.4

weak acids, are able to take up or release H+ so that changes in the free H+ concentration are minimized

HPO4 (2-) + H+

<>

H2PO4-

pKa= 6.8

pH =

[HPO4-] PKa [H2PO4 (2-) ] = 160 nanomol/L (pH=6.80)

10 = 160 x 10
pKa= 6.8

At pH=7.4 [HPO4-] : [H2PO4-]:

80% 20%

Addition of Acid: Large changes in H+ concentration are prevented by:

Buffering

HCl + Na2HPO4

>

NaCl + NaH2PO4

It was possible because the Na2HPO4 can be ionized as pk is close to the physiological Ph 7.4 pK= 6.8 and so can bind the H ions and make a weaker acid and thus nullify the effect of HCL

If all H+ taken up by HPO4 then [HPO4-] [H2PO4 (2-) ] H+ 12 = 6.8 x = 240 nanomol/L (pH =6.62) 8

If No Buffer

pH = 2.7

[CO2]dis + H2O

<> H2CO3 <> H+ + HCO3-

At Physiological pH

Ka

[H+] [HCO3-] = [CO2]dis [H2O]

[H+] [HCO3-] K'a = [CO2]dis

pKa x [CO2]dis pH = [HCO3-]

pH =

PCO2 24 x [HCO3-]

Buffer
There are four main buffer systems in the body:
Bicarbonate buffer system. (the MAIN one) 64% NaHCO3 H2CO3 CO2 Hemoglobin buffer system. 29% HbO2- HHb Protein buffer system. 6% Pr- HPr Phosphate buffer system. 1% Na2HPO4 NaHPO4

Open buffer system


Expired Gas
[CO2]dis + H2O

Add Acid
<> H2CO3 <> H+ + HCO320:1

At physiologic pH of 7.4: HCO3 : H+

Primary and Secondary Disorders


Primary:
Respiratory: Acidosis

Alkalosis
Metabolic: Acidosis

Alkalosis Secondary:
Respiratory: Acidosis

Alkalosis
Metabolic: Acidosis

Alkalosis

Two classes of acids are physiologically important:


Carbonic acid (H2CO3) & non-carbonic acids.

Metabolism of carbohydrates and fats results in the generation of approximately 15,000 mmol of CO2/Day

CO2 + H2O H2CO3 H+ + HCO3

This is prevented by the loss of CO2 via Via lungs

Noncarbonic acids:
Primarily derived from the metabolism of proteins

CO2 + H2O

<> H2CO3

<> H+ + HCO3 HCO3-

At Physiological pH

H2CO3 : HCO3= 1 : 6800

H2CO3 : PCO2= 1: 340

The primary intracellular buffers are organic and inorganic phosphates, and,

proteins,

in the erythrocyte, hemoglobin (Hb-):

H+ + Hb- HHb H+ + Pr- HPr

H+ + Hb- HHb

H+ + Pr- HPr

Bone: Important site of acid and base buffering Exchange for surface Na+ and K+, Dissolution of bone mineral Release of buffer compounds: NaHCO3 & KHCO3 initially Then CaCO3 and CaHPO4, This buffering reaction appears to be initiated in part by the fall in the plasma HCO3concentration

Methionine

>

glucose + urea + SO4(2-) + 2 H+


glucose (or CO2) + urea + H+

Arginine+ > R-H2PO4 + H2O

>

ROH + 0.8 HPO42- / 0.2 H2PO4- + 1.8 H+

Increasing the pH/ Alkalosis/ Decreasing H+

Glutamate- + H+ Citrate- + 4.5 O2 Lactate- + H+

> >

glucose + urea 5 CO2 + 3 H2O + HCO3-

>

glucose + CO2

Increasing the pH/ Alkalosis/ Decreasing H+

Glutamate- + H+ Citrate- + 4.5 O2 Lactate- + H+

> >

glucose + urea 5 CO2 + 3 H2O + HCO3-

>

glucose + CO2

Renal Actions
(1)Reabsorption of the filtered HCO3(1)Excretion of the 50 to 100 meq of H+ produced per day

A normal subject GFR: 180 L/day (125 mL/min) plasma HCO3- concentration of 24 meq/L filters & then must reabsorb approximately 4300 meq of HCO3- each day

The lowest urine pH that can be achieved in humans is 4.5. Almost 1000 times (3 log units) more acid than the extracellular pH, Still extremely low free H+ concentration of less than 0.04 meq/L.

Secretion of each H+ ion is associated with the generation of one HCO3- ion in the plasma.

steady state, the net amount of H+ excreted is equal to the normal H+ load of 50 to 100 meq/day This value can exceed 300 meq/day (primarily due to enhanced NH4+ excretion) if acid production is increased

Secretion of each H+ ion is associated with the generation of one HCO3- ion in the plasma.

Proximal Tubular Cell


Renal Tubular Acidosis: Proximal RTA
Na+
HCO3 + H+ H2O H+ OH + CO2 CA 3HCO3 HCO3

Na+
H2O + CO2 2K Na K AtPase 2K

3Na+
Tubular Lumen Blood

Distal acidification
H+ secretion in the distal nephron primarily occurs in the intercalated cells in the cortical collecting tubule and in the cells in the outer and inner medullary collecting tubules

-Intercalated Cells of Cortical Collecting Collecting Tubule


Renal Tubular Acidosis: Distal RTA
H-ATPase H2O H+ H+ OH CA HCO3 HCO3 Cl H+ K Tubular Lumen H+ Cl K Blood Cl

-Intercalated Cells of Cortical Collecting Collecting Tubule


H-ATPase OH CA HCO3 HCO3 H2O H+ H+

Cl

Cl

Cl

Tubular Lumen

Blood

AMMONIUM EXCRETION

Glutamine <>

<>

NH4+ + glutamate-

NH4+ + alpha-ketoglutarate(2-)

Metabolic Acidosis
Clinical Features: a. Peripheral resistance b. Myocardial contractility - BP - pulm. odema - Hypoxia vent. Fib. c. Kussmaul breathing d. Ch Acidosis.Bone changes (RTA) (CRF)

Acidosis
So what kind of metabolic acidosis is it? Loss of HCO3 or gain of intrinsic or extrinsic Acids Calculate anion gap: 8-16(normal)

Anion Gap [AG]


Na= 139 Cl= 103 HCO3=24

AG =

[+VE] [-VE] Ca, Mg, K= So4 , PO3 Na - [Cl+HCO3] = 139 - [103+ 24] = 139 - 127 = 12

What is AG of 12 ? All charges POSITIVE = Negative

Some other [ ve] charges that we could not estimate from our lab These [ ve] charges are for Albumin

Causes of High AG MA:


M U D P I L E S Methanol Uremia DKA Paraldehyde Isopropyl Alcohol Lactic Acidosis Ethylene Glycol ASA [Formate] [SO4, Pho3, other] [Acetoacetate, -OH Butyrate] [unknown/Acetic Acid] [Lactate] [Lactate] [Oxalate, Glycolate] [Lactate & Ketoacids]

Buffer
There are four main buffer systems in the body:
Bicarbonate buffer system. (the MAIN one) 64% NaHCO3 H2CO3 Hemoglobin buffer system. 29% HbO2- HHb Protein buffer system. 6% Pr- HPr Phosphate buffer system. 1% Na2HPO4 NaHPO4

Osmolal Gap: Addition of solute the P Osmolality Calculated Osmol = 2 x Na + Urea + Glucose= mmol/L
Measured Osmol - Calculated Osmol = < 20 [Nml]

Causes of Osmol Gap


Ethanol Methanol Ethylene Glycol Isopropyl Alcohol

Basic Rules of the game AG, CO2, HCO3, pH


1: PH=7.4 CO2 =40 HCO3 =24 2: HCO3 < 13 Definitely Metabolic Acidosis 3: Anion Gap [AG] AG >20 Metabolic Acidosis Definitely AG 12-20 MA Or MAlk Metabolic Acidosis 1. Last 2 digits of pH 7.25: CO2 = 25 2. Expected PCO2 = HCO3 X 1.2 [Limit: Max PCO2 10 mm of Hg]

Acid Base Evaluation: Summary Nauman Tarif, MD


Metabolic Alkalosis Expected PCO2 = 0.7 X HCO3 24-36 hrs for respiratory compensation Limit: Max PCO2 55 mm of Hg Osmolal Gap: Addition of solute will the plasma Osmolality Measured Osmolality - Calculated Osmolality = Nml < 20 Calculated Osmolality=2Na + Urea + Glucose= All in mmol/L Acute Respiratory Alkalosis 10 PCO2 = 2 HCO3 , 5-10 minutes for Compensation Max : 18 meq/L Chronic Respiratory Alkalosis 10 PCO2 = 4 HCO3 2-3 Days for Metabolic Compensation Max : 14 meq/L IF YOU FOLLOW THE RULES Mixed Acid Base Disorder evaluation is easy! Clinical Picture AG, HCO3, PCO2, pH, Osmolal Gap

12-24 Hours for compensation

Acute Respiratory Acidosis


10 PCO2 = by 1 HCO3 5-10 minutes for Compensation Max : 30 meq/L Chronic Respiratory Acidosis 10 PCO2 = 4 HCO3- [ Chronic RA] 5-10 Days for Metabolic Compensation Max : 45 meq/L

AG / HCO3 = 1-1.6

Primary Disorder
Acidosis or Alkalosis
If it is Respiratory then Renal [metabolic] compensation
Respiratory Disorders: Breathe Too MUCH! Respiratory Alkalosis

H+ + HCO3 H2CO3 H2O + CO2 Breathe Too LESS! Respiratory Acidosis

H2O + CO2 H2CO3 H+ + HCO3

Metabolic Disorders Add Acid or Lose HCO3 Add Alkali or Lose Acid Metabolic Acidosis Metabolic Alkalosis

If it is Metabolic then Respiratory compensation

Compensatory responses will not bring the pH to normal; always close towards normal.

In the presence of NORMAL pH


Abnormal CO2 or HCO3

IT IS A MIXED Disorder! AT least 2 primary disorders

Human environment is Dynamic !

PulmonaryEmbolus RespiratoryAlkalosis Shock Pulmonaryedema RenalFailure Sepsis COPD DiureticUse Cirrhosis Metabolicacidosis RespiratoryAlkalosis MetabolicAcidosis RespAlk+MetAcid Respiratoryacidosis MetabolicAlkalosis RespiratoryAlkalosis

42 y/o male found unconsciuos in the desert [lost his way for the last 2 days] with an empty bottle BP & bilateral chest crepts AG PCO2 144 -[97+10]= 37 35 HAGMA

14 X 1.2 = 16.8 , [40-17 = 23 ] Here PCO2 is 35

So PCO2 should be 25

So Something is keeping the PCO2 RA

In an unconscious pt with no clear cut history and MA MUST Exclude: Ingestion [empty bottle!] Gap: Osmolal Gap Measured - Calculated Osmolality > 20 [Ingestion] Methanol, Ethylene Glycol and Isopropyl Alcohol Osmolal gap = 29 MSU : CaOxalate Crystals

Ethylene Glycol Intoxication

Gap of the Gaps Delta AG : Delta HCO3 37-12 : 24-10 25 : 14 1. 8 : 1 [ >1.6]

So Something is keeping the HCO3 MAlk He apparently had Vomiting after ingestion of EthGlycol HAGMA + RA + MAlk

pH 7.28

Management Guidelines:
1. Treat the Clinical state 2. Metabolic Acidosis: pH to 7.2 & HCO3 >10 [Prevent CVS Instability] 3. Metabolic Alkalosis Fluid for Cl responsive Acetazolamide IV HCL, NH4Cl, ArgHCl 4. Respiratory Acidosis : 5. Respiratory Alkalosis

Management Guidelines:
1. Treat the Clinical state 2. Metabolic Acidosis: pH to 7.2 & HCO3 >10 [Prevent CVS Instability] 3. Metabolic Alkalosis Fluid for Cl responsive Acetazolamide IV HCL, NH4Cl, ArgHCl 4. Respiratory Acidosis : 5. Respiratory Alkalosis