acid base balance & abg interpretation,dept of anesthesiology,jjmmc,davangere

DEPARTMENT OF ANESTHESIOLOGYJJMMC, DAVANGERE.SEMINAR ON ACID BASE BALANCE AND ABG ANALYSIS

CHAIR PERSON PRESENTED BY

Dr.RAVI.R Dr.GOPAN.G

PROFESSOR

DATE:14-6-2013

Over view

1. Basics concepts

2. History ;approaches

3. Acid base disorders &regulation

4. Treatment

5. interpretation

In pure water at 25°C, the [H+] and [OH-] are 1 × 10-7

mmol/L.

A solution is considered acidic if the concentration of hydrogen ions exceeds that of hydroxyl ions.

A solution is considered alkaline if the hydroxyl ion concentration exceeds the hydrogen ion concentration.

H2O ↔ H+ + OH-

Basic concepts

Physical Chemistry of Water

• pH -the negative logarithm of the hydrogen ion concentration

• pH for pure water is 7.0

•Physiologic pH, for the ECF, is 7.4, which is alkaline.

•Henderson Hasselbalch equation : pH = pK + log [HCO3

-]/αPaCO2

Cont’dBASIC CONCEPTS

•A substance is an acid if, when added to a solution, it brings about an increase in the hydrogen ion concentration of the solution

•A substance is a base if, when added to a solution, it brings about a decrease in the hydrogen ion concentration of the solution

Definitions: Acid & Base

•Consequently, strong cations—Na+, K+, Ca2+, Mg2+—act as Arrhenius bases (because they drive hydroxyl out of, and hydrogen into, solution, to maintain electric neutrality)

• Strong anions—Cl-, LA-, ketones, sulfate and formate—act as Arrhenius acids

• Bicarbonate

•Haemoglobin

• Plasma proteins

• Phosphate

Minimise the change in pH

BUFFER

• tools that have evolved over the past 50 years

•None are entirely accurate, and each has a dedicated group of followers

• Textbooks and clinical practice have tended to overestimate the importance of isolated changes in hydrogen or bicarbonate ion concentration

•Clinical significance of acid-base balance is determined by the underlying cause, rather than the serum concentration of hydrogen and hydroxyl ions

Analytic Tools Used in Acid-Base Chemistry

Carbon Dioxide–Bicarbonate (Boston) Approach

• Siggard Andersen developed the concept base deficit/excess

•Base deficit/excess : Defined as the amount of strong acid or base required to return pH to 7.4, assuming a PCO2 of 40 mm Hg and temperature of 38°C

•Current algorithms for computing the standardized base excess (BE for ECF) are derived from the Van Slyke equation• SBE = 0.9287 [HCO3

- - 24.4 + (PH – 7.4)]

• Ref:Miller’s anesthesia 7th edition Pg:1564

Base Deficit/Excess (Copenhagen) Approach

• proposed “whole-blood buffer base”

• The sum of the bicarbonate and the nonvolatile buffer ions

(serum albumin, phosphate, and hemoglobin)

• [Na+] + [K+] - [Cl-] = 48-49 mmol/L

•Buffer base increases in metabolic alkalosis and decreases in metabolic acidosis.

Cont’d

Acid-base nomogram using the Copenhagen approach (Crit Care Med26:1173-1179,1998)

•Developed by Emmett and Narins•Anion gap = [Na+ + K+ - (Cl- + HCO3

-)]

• Sum of the difference in charge of the common extracellular ions reveals an unaccounted for “gap” of -10 to -12 mEq/L

• Anion gap is based on the law of electric neutrality

Anion Gap Approach

Concept of anion gap

•Most critically ill patients are hypoalbuminemic, and many are also hypophosphatemic

•Consequently, the gap may be normal in the presence of unmeasured anions

•Anion gap corrected for albumin = calculated anion gap + 2.5 ( Normal albumin in gm/dL – observed albumin in gm/dL )

• Second weakness with this approach is the use of bicarbonate in the equation

Failure of Anion-Gap approach

• Electric neutrality

•Dissociation equilibriums

•Mass conservation

Determined the hydrogen ion concentration of ECF , by applying laws of :

Stewart Approach

• Small advance from the “anion gap” approach

•Proposed “SIG”

• SIG = Apparent SID –Effective SID(UMA)

•Normal “SIG” is 8 ± 2 mEq/L

•Apparent SID = ([Na+]+ [K+]+ [Mg2+]+ [Ca2+]) - [Cl-]) • Effective SID = [HCO3

-] + [charge on albumin] + [charge on Pi]

Stewart-Fencl Approach

“ANION GAP” Vs “SIG”

• The strong ion difference (SID)

• The total concentration of weak acids (ATOT).

• The PaCO2

Only three factors independently affect acid-base balance

• ([Na+] – [Cl-]) + ([H+] – [OH-]) = 0• [H+] = √Kw’ +([Na+] – [Cl-])2 /4-([Na+] –[Cl-]) /2

• [OH-] = √Kw’ +([Na+] – [Cl-])2 /4-([Na+] –[Cl-]) /2

• hydrogen and hydroxyl concentrations are determined by the KW′ and the difference in charge between sodium and chloride

• Dissociate completely.

• Strong ions in the ECF are Na+,K+,Mg2+,Ca2+,SO42- and

Cl-

STRONG ANIONS

• The sum total of the charges imparted by strong cations minus the charges from strong anions.

• SID=([Na+]+[K+]+[Ca2+]+[Mg2+]) – ([Cl-]+[A-])

=40-44 mEq

(1)STRONG ION DIFFERENCE

Effect of changes in SID on hydrogen and hydroxyl ion concentration.  ( Can J Physiol Pharmacol 61:1444-1461, 1983.)

•weak acids are partially dissociated compounds

•Albumin and phosphate

• Stewart used the term “ATOT” to represent the total concentration of weak anions

(2)Weak Acid “Buffer” Solutions

• Exists in four forms: CO2 [dissolved CO2(d)], carbonic acid (H2CO3), bicarbonate ions (HCO3

-), and carbonate ions (CO32-).

• The concentration of CO2 in ECF is determined by tissue production and alveolar ventilation.

•As CO2 increases HCO3- also increases.

(3)Carbon Dioxide

LAWS EQUATIONS

Water dissociation equilibrium [H+] × [OH-] = Kw’

Weak acid dissociation equilibrium

[H+] × [A-] = KA × [HA]

Conservation of mass for weak acids

[HA] + [A-] = [ATOT]

Bicarbonate ion formation equilibrium

[H+] × [HCO3-] = KC × PCO2

Carbonate ion formation equilibrium

[H+] × [CO32-] = K × [HCO3

-]

Electric neutrality [SID] + [H+] - [HCO3-] - [A-] -

[CO32-] - [OH-] = 0

Stewart combined six derived equations to solve for [H+]:

• [ SID ] + [ H+ ] – KC ×PC/[H+] – KA - [ATOT]/(KA + [H+]) –K × KCPC/[H+]2 – KW’/[H+] =0

• [ H+ ] is a function of SID, ATOT, PCO2

• [H+] , [OH-] and [HCO3-] are dependent and

cannot independently influence acid-base balance

Although the above-listed equations look simple, they require fourth-order polynomials for solution. This is impossible without computer technology

•Alterations in arterial carbon dioxide (PaCO2) tension—respiratory acidosis or alkalosis

• Alterations in blood chemistry—metabolic acidosis or alkalosis.

Acid-Base Abnormalities Classification

Terminology of Acid-Base Disorders

The definitions of the terms used to describe acid-base disorders are suggested by the Ad-Hoc Committee of the New York Academy of Sciences in 1965

Simple (Acid-Base) Disorders  are those in which there is a single primary aetiological acid-base disorder

Mixed (acid-Base) Disorders are those in which two or more primary aetiological disorders are present simultaneously.

• neurologic injury (e.g., stroke, spinal cord injury, botulism, tetanus)

• toxic suppression of the respiratory center (e.g., opioids, barbiturates, benzodiazepines)

• neuromuscular disorders (e.g., Guillain-Barré syndrome, myasthenia gravis)

•flail chest, hydro-hemo-pneumothorax, pulmonary edema, and pneumonia.

Acute respiratory acidosis:

Acid-Base Disturbances in the Emergency Setting

• anxiety, central respiratory stimulation (as occurs early in salicylate poisoning)

• excessive artificial ventilation

Acute metabolic acidosis

• severe diarrhea,renal tubular acidosis

•Dilutional acidosis

• lactic acidosis, renal acidosis, ketoacidosis

Acute respiratory alkalosis Cont’d

•Respiratory acidosis : narcosis, incomplete reversal of neuromuscular blockade

•Respiratory alkalosis : anxiety

•Metabolic acidosis : Hypoperfusion,Hypotonic fluid administration & Hyperchloremia

•Metabolic alkalosis : Massive blood transfusion & nasogastric suctioning

Acid-Base Disturbances Commonly Seen Perioperatively

• hypoalbuminemia (imp)

• metabolic alkalosis that can mask significant lactic acidemia

• Mechanical ventilation increases the circulating volume of antidiuretic hormone-dilutional acidosis

• Nasogastric suctioning causes chloride loss, diarrhea leads to sodium and potassium loss

• Surgical drains placed in tissue beds will remove fluids with varying electrolyte concentrations

Acid-Base Disturbances in Critical Illness

•Respiratory acidosis occurs when there is an acute increase in PaCO2 principally resulting from respiratory failure

•Cyanosis, vasodilation, and narcosis

•Respiratory alkalosis occurs when there is an acute decrease in PaCO2 as a result of hyperventilation

• Light headedness, visual disturbances, dizziness, and hypocalcemia

Respiratory Acid-Base Abnormalities

•Associated with alterations in transcellular ion pumps and increased ionized calcium

•Vasodilation, diminished muscular performance (particularly myocardial), and arrhythmias

•Oxyhemoglobin dissociation curve shifts rightward to increase oxygen offload into the tissues

Metabolic acidosis

• In dysoxia and states of severe stress, lactate is produced

• In diabetic-ketoacidosis—β-hydroxybutyrate and acetoacetate—are produced• In severe renal failure, SO4

2- and PO43- (“fixed

renal acids”) are not excreted, causing acidosis

• Severe metabolic acidosis is associated with increased SIG(UMA)

METABOLIC ACIDOSIS

• In dilutional & hyperchloremic acidosis relative ratio of cations to anions decreases(relative increase of anions).

• In contraction alkalosis relative ratio of cations to anions increases

•Doberer etal : acidosis develops because of dilution of HCO3

- (HCO3- in the blood is

a"closed system") without there being a dilution of acid in the form of CO2 gas (which due to its ability to be exhaled can be considered an "open system").

Dilutional acidosis , hyperchloremic acidosis and contraction alkalosis

•Hypoalbuminemia decreases ATOT, increases SID and is associated with metabolic alkalosis.

• SID=([Na+]+[K+]+[Ca2+]+[Mg2+]) – ([Cl-]+[A-])

• The presence of hypoalbuminemia may mask the detection of acidosis caused by unmeasured anions

HYPOALBUMINEMIA

Abnormalities Acidosis Alkalosis

Respiratory Increased PCO2 Decreased PCO2

Metabolic    

 Abnormal SID    

  Caused by water excess or deficit

Water excess = dilutional Water deficit = contraction

  ↓ SID +↓[Na+] ↑ SID ↑[Na+]

  Caused by electrolytes

Chloride excess Chloride deficit

   Chloride (measured)

↓ SID ↑[Cl-] ↑ SID +↓[Cl-]

   Other (unmeasured) anions, such as lactate and keto acids

↓ SID ↑[UMA-] —

 Abnormal ATOT    

  Albumin [Alb] ↑[Alb] (rare) ↓[Alb]

  Phosphate [Pi] ↑[Pi]  

Stewart approach for Acid-Base Disturbances

• The major source of acid in the body is CO2

• Excreted by the lungs

•Only 20 to 70 mEq of hydrogen ions are excreted through the kidney each day•CO2 is buffered directly by hemoglobin and by plasma proteins

Respiratory failureRegulation of Acid-Base Balance in

•Once Hemoglobin, becomes overwhelmed Kidney excretes an increased chloride load using NH4

+, a weak cation, for electrochemical balance

• “Metabolic compensation”

Acid base regulation in respiratory failure contd

•Metabolic acid is buffered principally by increased alveolar ventilation , bicarbonate(imp), plasma proteins & phosphate • coupling of bicarbonate and H2O produces CO2 that is excreted through the lungs via an increase in alveolar ventilation

•Chloride is preferentially excreted by the kidney

Acid base regulation in metabolic disorder

Compensation

A patient can be uncompensated, partially compensated, or fully compensated

When an acid-base disorder is either uncompensated or partially compensated, the pH remains outside the normal range

In fully compensated states, the pH has returned to near normal range

Body never overcompensates

 Correct Terminology for Compensatory Responses

According to the Ad-Hoc Committee , Secondary or compensatory responses should NOT be designated as acidosis or alkalosis.

Eg: A patient with diabetic ketoacidosis and compensatory Kussmaul respirations should be described as having a 'metabolic acidosis with compensatory hyperventilation’

The use of the term ‘secondary respiratory alkalosis’ in this case would be wrong

• Lactic acidosis is treated with volume resuscitation and source control.

•Diabetic ketoacidosis is treated with volume resuscitation and insulin.

•Renal acidosis is treated with dialysis

•Occasionally,treatment with intravenous sodium bicarbonate is necessary

• (base excess × weight in kg)÷3

METABOLIC ACIDOSIS

TREATMENT AND CORRECTION

• A severe deficit (HCO3- < 10-12 mEq/L and pH<7.2) should be corrected with sodium bicarbonate

• Useful if the acidosis is due to inorganic acids

• It is recommended that 50% of total deficit be given over 3 to 4 hours. 7.5% NaHCO3

- contains 0.9 mEq/ml• The usual initial target((desired HCO3- concentration): 10 - 12 mEq/L, which should bring the blood pH to ~7.20

• IV-push administration should be reserved for CPR

Ref:Koda-Kimble M, Young LY, et al. Handbook of Applied Therapeutics. Lippincott Williams & Wilkins, 2006. P10.3(1104).

When and how to correct

•Key to managing acid-base disturbances lies not in altering acid-base balance, but rather in correcting the underlying defect

• Sodium bicarbonate is administered as an 7.5/8.4% hypertonic solution and has a plasma-expanding effect that can lead to a dilutional acidosis and increases PaCO2 as well

•Over-alkalinization causes decreased affinity of hemoglobin for oxygen leading to tissue hypoxia and lactic acid production ,Sodium overload and hypokalemia.

Use of sodium bicarbonate boluses or infusions is controversial

• Treat the primary cause.

• Potassium and magnesium should be replaced.

• Dilute hydrochloric acid can be given orally or intravenously.

• Acetazolamide can be considered.

METABOLIC ALKALOSIS

TREATMENT AND CORRECTION

• Increase alveolar ventilation.

•Associated hypophosphatemia should be monitored.

RESPIRATORY ALKALOSIS

•Decrease in alveolar ventilation

•Hypoxaemia is an important cause of respiratory alkalosis.

•Administration of oxygen in sufficient concentrations and sufficient amount is essential.

RESPIRATORY ACIDOSIS

TREATMENT AND CORRECTION

How to take an ABG Sample?

1. Site of puncture

2. Equipment required

3. Expel air bubbles

4. Keep sample in ice

5. Patient’s inspired oxygen concentration

ABG Sampling.mp4

• pH = 7.36 to 7.44

•PCO2 = 36 to 44 mmHg

•HCO3 = 22 to 26 mEq/L

•PaO2 = 80 to 100 mmHg

• SaO2 = 94 to 100 %

•Base excess = -2 to +2 mEq/L

NORMAL VALUES

• Stage I: Identify the Primary Acid-Base Disorder

• Rule 1: An acid-base abnormality is present if either the PaCO2 or the pH is outside the normal range

• Rule 2: If both change in the same direction, the primary acid-base disorder is metabolic, and if both change in opposite directions, the primary acid-base disorder is respiratory (ROME)

• Example: Consider a patient with an arterial pH of 7.23 and a PaCO2 of 23 mm Hg

• primary metabolic acidosis

A Stepwise Approach to Acid-Base Interpretation

•Rule 3: If either the pH or PaCO2 is normal, there is a mixed metabolic and respiratory acid-base disorder (one is an acidosis and the other is an alkalosis). If the pH is normal, the direction of change in PaCO2 identifies the respiratory disorder, and if the PaCO2 is normal, the direction of change in the pH identifies the metabolic disorder

• Example: Consider a patient with an arterial pH of 7.4 and a PaCO2 of 55 mm Hg

•mixed respiratory acidosis and metabolic alkalosis

•Metabolic acidosis Expected PaCO2 = (1.5 × HCO3) + (8 ± 2)

•Metabolic Alkalosis

Expected PaCO2 = (0.7 × HCO3) + (21 ± 2)

Stage II: Evaluate Compensatory Responses (winter’s formula)

Disorder Acute Chronic

Resp. Acidosis pH decreases by 0.08

HCO3- increases by 1

pH decreases by 0.03

HCO3- increases by 4

Resp. Alkalosis pH increases by 0.08

HCO3- decreases by 2

pH increases by 0.03

HCO3- decreases by 5

Compensation for 10 mmHg change in PaCO2 in respiratory disturbances

•Rule 4: If there is a primary metabolic acidosis or alkalosis, use the measured serum bicarbonate concentration to identify the expected PaCO2

• Example: Consider a patient with a PaCO2 of 23 mm Hg, an arterial pH of 7.32, and serum HCO3 of 15 mEq/L.

• (1.5 × 15) + (8 ±2) = 30.5 ± 2 mm Hg.

primary metabolic acidosis with a superimposed respiratory alkalosis

• Example: Consider a patient with a PaCO2 of 23 mm Hg and a pH of 7.54

7.40 + [0.008 × (40 - 23)] =7.54

acute respiratory alkalosis

If the measured pH was higher than 7.55

a superimposed metabolic alkalosis

Rule 5: If there is a respiratory acidosis or alkalosis, use the PaCO2 to calculate expected pH

• The anion gap helps to classify met.acidosis

• The normal value is 12 ± 4 mEq/L

•High AG : lactic,ketoacidosis,ESRF,methanol

•Normal AG : diarrhea,saline infusion,RTA

• In hypoalbuminemia AG should be corrected

ANION GAP

Stage III: Use The “Gaps” to Evaluate MetabolicAcidosis

• High AG metabolic acidosis, the gap-gap (AG Excess/HCO3 deficit) ratio is unity (=1)

• Hyperchloremic acidosis, the ratio (AG excess/∆HCO3 ) falls below unity (< 1)

• Therefore, in the presence of a high AG metabolic acidosis, a “gap-gap” (AG excess/∆HCO3)ratio of less than 1 indicates the co-existence of a normal AG metabolic acidosis

• In the presence of a high AG metabolic acidosis, a gap-gap (AG excess/∆HCO3 ) ratio of greater than 1 indicates the co-existence of a metabolic alkalosis.

The “Gap-Gap” ratio

• CASE 1: A 20 year old man is brought to the emergency room with a history of consumption of a bottle of pills.

• pH = 7.35• PaCO2 = 15 mmHg

•HCO3- = 8 mmolL-1

•Na+ = 140 mmolL-1

• K+ = 3.5 mmolL-1

• Cl - = 104 mmolL-1

• Step 1: Evaluate pH and narrow down to two possible processes

• pH < 7.36 Acidosis (metabolic or respiratory)

• Step 2: Evaluate the PaCO2 and narrow down to one definitive process

PaCO2 < 40 mmHg ( metabolic acidosis is present)

• Step 3: Apply the formula for metabolic acidosis Predicted PaCO2 = 1.5 (HCO3

-) + 8

= 20mmHg Actual PaCO2 = 15 mmHg

• Step 4: Determine if any other processes are present

The actual PaCO2 is less than the predicted Respiratory alkalosis

Diagnosis: Mixed metabolic acidosis + Respiratory alkalosis

• Step 5: Evaluate anion gap

Anion gap = 140 - (104 + 8) = 28 (↑)

• Step 6: Evaluate gap-gap ratio

Delta gap= (28 - 12) / (24 - 8)= 16/16= 1

•Conclusion: Combined high anion gap metabolic acidosis and Respiratory alkalosis

• A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhea. Electrolyte results: Na+ 134, K+ 2.9, Cl- 108, HCO3- 16, BUN 31, Cr 1.5.

• ABG: pH 7.31     pCO2 33 mmHg          HCO3 16   pO2   93 mmHg

• Based on the clinical scenario, likely acid base disorders in this patient are:

•Normal anion gap acidosis from diarrhea or

• Elevated anion gap acidosis secondary to lactic acidosis as a result of hypovolumia and poor perfusion.

Case 2

•  Look at the pH.      The pH is low, (less than 7.35) therefore by definition, patient is acidemic.

• pH & pCO2 change in same direction(decrease)-metabolic acidosis

•  Is compensation adequate?

• Calculate the estimated PCO2.   Using Winter's formula; PCO2 = 1.5 × [HCO3-]+ 8 ± 2 = 1.5 ×16 + 8 ± 2 = 30-34.

• Calculate the anion gap    The anion gap is Na - (Cl + HCO3-) = 134 -(108 + 16) = 10     Since gap is less than 16, it is therefore normal

• Since the actual PCO2 falls within the estimated range, we can deduce that the compensation is adequate and there is no seperate respiratory disorder present.

•Assessment: Normal anion gap acidosis with adequate compensation most likely secondary to severe diarrhea.

• 1) Is the "pH“ normal?

• 2) Is the "CO2“ normal?

• 3) Is the "HCO3“ normal?

• 4) Apply “ROME”

• 5) Look for compensation

• 6) Are the "pO2“ and the "O2“ saturation normal?

The '6‘ Easy Steps to'ABG'Analysis

• pH normal, PCO2 increased

•Mixed disorder.

• Primary Respiratory acidosis

• Compensatory response?

• 7.4 – (0.003×20)• [HCO3

-] to be increased by 4

•Respiratory acidosis with

metabolic alkalosis

•Conclusion

• The use of physical chemistry principles permits a better explanation of acid-base balance and provides tools to apply to a wide variety of clinical situations. This does not suggest that the “traditional” approach is incorrect. There is currently no clear strategy to determine which of the ‘modern’ approaches, the Stewart approach or the bicarbonate-centred approach , is the correct one.

•Miller’s anesthesia 7th edition

• The ICU book 3rd edition Paul L Marino

•A practice of Anesthesia 7th edition Wylie

• Lee’s synopsis of Anaesthesia 13th edition

•Anaesthesia CME programme 2011 Mysuru

•A simple guide to blood gas analysis Peter Driscoll

•www.acid-base.com

•www.acidbasedissorders.com

Bibliography