Interpretation of the Arterial Blood Gas Analysis

DM SEMINARDr. Vishal Golay

2/11/2011

Overview of the discussion• Basics of acid-base balance.

• Role of kidneys in acid-base homeostasis.

• Step-wise approach in diagnosis of acid-base disorders.

• Some practical examples.

Basic terminology • pH – signifies free hydrogen ion concentration. pH is inversely

related to H+ ion concentration.

• Acid – a substance that can donate H+ ion, i.e. lowers pH.

• Base – a substance that can accept H+ ion, i.e. raises pH.

• Anion – an ion with negative charge.

• Cation – an ion with positive charge.

• Acidemia – blood pH< 7.35 with increased H+ concentration.

• Alkalemia – blood pH>7.45 with decreased H+ concentration.

• Acidosis – Abnormal process or disease which reduces pH due to increase in acid or decrease in alkali.

• Alkalosis – Abnormal process or disease which increases pH due to decrease in acid or increase in alkali.

Endogenous sources of acid.

Daily production ~ 1 mEq of H+/kg/day• Sulfuric acid ( from S containing AA)• Organic acids (from intermediary metabolism)• Phosphoric acid ( hydrolysis of PO4 containing

proteins)• Hydrochloric acid (from metab of cationic AA-

Lysine, Arg, Histidine)

pH in humans is tightly regulated between 7.35-7.45.

Renal regulatory responses

Respiratory

regulatory responses

Chemical Buffers

Buffers• Buffers are chemical systems which either

release or accept H+ and minimize change in pH induced by an acid or base load.

• First line of defense blunting the changes in [H+]

A buffer pair consists of: A base (H+ acceptor) & An acid (H+ donor)

Buffers continued……

Extracellular buffers:

• HCO3¯/H2CO3• HPO4²¯/H2PO4• Protein buffers

Intracellular buffers:•Hb•Proteins•Organophosphate compounds•Bone apatite

Examples:

HPO42- + (H+)↔H2 PO4

-

H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-

Respiratory regulation

• 2nd line of defense

• 10-12 mol/day CO2 is accumulated and is transported to the lungs as Hb-generated HCO3 and Hb-bound carbamino compounds where it is freely excreted.

H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-

• Accumulation/loss of Co2 changes pH within minutes

Respiratory regulation contd…..

• Balance affected by neurorespiratory control of ventilation.

• During Acidosis, chemoreceptors sense ↓pH and trigger ventilation decreasing pCO2.

• Response to alkalosis is biphasic. Initial hyperventilation to remove excess pCO2 followed by suppression to increase pCO2 to return pH to normal

Renal Regulation

• Kidneys are the ultimate defense against the addition of non-volatile acid/alkali.

HA + NaHCO3↔H2 O + CO2 + NaA

Addition of Acid causes loss of HCO3¯

• Kidneys play a role in the maintenance of this HCO3¯ by:– Conservation of filtered HCO3 ¯– Regeneration of HCO3 ¯

Net Acid Excretion(NAE)

• Kidneys balance nonvolatile acid generation during metabolism by excreting acid.

• Each mEq of NAE corresponds to 1 mEq of HCO3 ¯ returned to ECF.

• NAE has three components: 1. NH4⁺ .2. Titrable acids. (acid excreted that has titrated urinary

buffers)3. Bicarbonate.

NAE= NH4⁺ + TA-HCO3¯

75-80% HCO3 is absorbed in the proximal tubule.

Ammonium excretion

2 2

Interpreting acid-base disorders

Normal ABG valuespH 7.35 - 7.45

PaCO2 35 - 45 mm Hg

PaO2 70 - 100 mm Hg

SaO2 93 - 98%

HCO3¯ 22 - 26 mEq/L

%MetHb < 2.0%

%COHb < 3.0%

Base excess -2.0 to 2.0 mEq/L

----- XXXX Diagnostics ------

Blood Gas Report248 05:36 Jul 22 2000Pt ID 2570 / 00

Measured 37.0o

CpH 7.463pCO2 44.4 mm HgpO2 113.2 mm Hg

Corrected 38.6o

CpH 7.439pCO2 47.6 mm HgpO2 123.5 mm Hg

Calculated DataTPCO2 49HCO3 act 31.1 mmol / LHCO3 std 30.5 mmol / LBE 6.6 mmol / LO2 CT 14.7 mL / dlO2 Sat 98.3 %ct CO2 32.4 mmol / LpO2 (A - a) 32.2 mm HgpO2 (a / A) 0.79

Entered DataTemp 38.6 oCct Hb 10.5 g/dlFiO2 30.0 %

-----XXXX Diagnostics-----

Blood Gas Report328 03:44 Feb 5 2006Pt ID 3245 / 00

Measured 37.0 0CpH 7.452 pCO2 45.1 mm HgpO2 112.3 mm Hg

Corrected 38.6 0CpH 7.436pCO2 47.6 mm HgpO2 122.4 mm Hg

Calculated Data

HCO3 act 31.2 mmol / LHCO3 std 30.5 mmol / LB E 6.6 mmol / LO2 ct 15.8 mL / dlO2 Sat 98.4 %ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78

Entered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl

Measured values…most important

Temperature Correction :Is there any value to it ?

Calculated Data :Which are useful one?

Entered Data :Important

Measured values should be consideredAnd

Corrected values should be discarded

Bicarbonate is calculated on the basis of the Henderson equation:

[H+] = 24 pCO2 / [HCO3-]

Act Bicarbonate: -----XXXX Diagnostics-----

Blood Gas Report328 03:44 Feb 5 2006Pt ID 3245 / 00

Measured 37.0 0CpH 7.452 pCO2 45.1 mm HgpO2 112.3 mm Hg

Corrected 38.6 0CpH 7.436pCO2 47.6 mm HgpO2 122.4 mm Hg

Calculated Data

HCO3 act 31.2 mmol / LHCO3 std 30.5 mmol / LB E 6.6 mmol / LO2 ct 15.8 mL / dlO2 Sat 98.4 %ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78

Entered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl

-----XXXX Diagnostics-----

Blood Gas Report328 03:44 Feb 5 2006Pt ID 3245 / 00

Measured 37.0 0CpH 7.452 pCO2 45.1 mm HgpO2 112.3 mm Hg

Corrected 38.6 0CpH 7.436pCO2 47.6 mm HgpO2 122.4 mm Hg

Calculated Data

HCO3 act 31.2 mmol / LHCO3 std 30.5 mmol / LB E 6.6 mmol / LO2 ct 15.8 mL / dlO2 Sat 98.4 %ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78

Entered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl

Standard Bicarbonate:Plasma HCO3 after equilibrationto a PCO2 of 40 mm Hg

: reflects non-respiratory acid base change: does not quantify the extent of the buffer base abnormality : does not consider actual buffering capacity of blood

Base Excess: D base to normalise HCO3 (to 24) with PCO2 at 40 mm Hg(Sigaard-Andersen)

: reflects metabolic part of acid base D: no info. over that derived from pH, pCO2 and HCO3: Misinterpreted in chronic or mixed disorders

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1. Consider the Clinical Setting.2. Obtain ABG and Electrolyte values

simultaneously.3. Verify the ABG values.4. Identify the nature of the disturbance.5. Calculate the Anion gap in case of MA.6. Assess ∆AG, ∆ HCO3, ∆Cl & ∆Na7. Detecting mixed disorders.8. Clinical correlation

Steps 1 & 2 • Basic clinical scenario gives an idea about the

type of the underlying disorder.

• ABG samples should be taken properly.

• Excess of heparin should be avoided during sampling.

Sampling for ABG analysis Perform Allen’s test.

Clean the site.

Use 21 gauze needle with syringe.

Flush syringe and needle with heparin.

Enter skin at 45° angle

Obtain 2-4ml blood without aspiration. Avoid suction of syringe .

If sample contains any air bubble, tap it to the surface and push it out of the syringe. Air bubbles can lead to increase in PaO2 and decrease in

PaCO2.

Apply firm pressure at punctured site.

Special mention

1. Specimens held at room temperature must be analyzed within 10-15 minutes of drawing; iced

samples should be analyzed within 1 hour.

2. The PaO2 of samples drawn from subjects with elevated white cell counts may decrease very rapidly.

Immediate chilling is necessary.

Indications for performing an ABG analysis

• The need to evaluate the adequacy of ventilatory (PacO2)

acid-base (pH and PaCO2), and oxygenation (PaO2 and SaO2) status, and the oxygen-carrying capacity of blood (PaO2, HbO2,

Hbtotal, and dyshemoglobins).

• The need to quantitate the patient's response to therapeutic intervention and/or diagnostic evaluation (eg, oxygen therapy, exercise testing)

• The need to monitor severity and progression of a documented disease process.

Steps 2 Verify the ABG values.

• The values should be checked for internal consistency.

• In ABG samples, pH and PaCO2 are measured and HCO3 calculated by the HH equation.

• Simultaneously measured plasma HCO3 should be within ±2-3 mmol/L of each other.

Steps 3 continued…….

• Most ABG reports do not give HCO3. It can be calculated indirectly from pH an PaCO2 values.

Normal [H+] 40 nmol/L first 2 decimals of pH value.

• Thus, HCO3 can now be calculated from [H+] and PaCO2 using the Henderson equation.

For every 0.1 decrease in pH, [H+] increases by 10nmol/L

[H+]=24 (PaCO2/ [HCO3])

Step 3 Identify the disorder • Take a look at the pH, as it directs towards the

principal disorder.

< 7.35

• Acidosis>7.4

5• Alkalosis7.35-

7.45

• Normal• Mixed disorder

PCO2

pH

HCO3

HCO3 •Metabolic Disorder

PaCO2 •Respiratory Disorder

During compensation HCO3¯ & PaCO2 move in the same direction

Compensatory changes (Respiratory disorders).Primary disorder

Primary defect

Compensatory response

Expected Compensation Limits of compensation

Respiratory acidosis

↑ PCO2 ↑ HCO3 Acute:+ 1 Meq/L ↑ HCO3 for each ↑ PCO2 of 10mmHg

[HCO3]=38 Meq/L

Chronic:+4 Meq/L ↑ HCO3 for each ↑ PCO2 of 10mmHg

[HCO3]=45 Meq/L

Respiratory Alkalosis

↓ PCO2 ↓ HCO3 Acute:-2Meq/l ↓ in HCO3 for each ↓ in PCO2 of 10mmHg

[HCO3]=18 Meq/L

Chronic:-5 Meq/L ↓ in HCO3 for each ↓ in PCO2 of 10mmHg

[HCO3]=15 mEq/L

1 4 2 5

Compensatory changes (Metabolic disorders).Primary disorder

Primary defect

Compensatory response

Expected Compensation Limits of compensation

Metabolic acidosis

↓ HCO3 ↓ PCO2 PCO2=1.5[HCO3] + 8 ± 2PCO2= last 2 digits of pH X 100PCO2= 15+ [HCO3]

PCO2=15mmHg

Metabolic Alkalosis

↑ HCO3 ↑ PCO2 PCO2= + 0.6 mmHg for Δ [HCO3] of 1 mEq/LPCO2=15+ [HCO3]

PCO2=55mmHg

Remember…….Respiratory compensation

is always FAST …12-24 hrsMetabolic compensation

is always SLOW...5 -7 days

Body’s physiologic response to Primary disorder in order to bring pH towards NORMAL limitBody’s physiologic response to Primary disorder in order to bring pH towards NORMAL limit

Full compensationPartial compensationNo compensation…. (uncompensated)

Full compensationPartial compensationNo compensation…. (uncompensated)

BUT never overshoots, If a overshoot pH is there, Take it granted it is a MIXED disorder

BUT never overshoots, If a overshoot pH is there, Take it granted it is a MIXED disorder

Step 5 Anion Gap

• Normal range is 10 ± 2 mEq /L

• It represents unmeasured anions. These unmeasured anions can be;– Anionic proteins– SO4, PO4, organic anions– Acid anions (acetoacetate, lactate, uremic anions)

AG= Na⁺ – (Cl¯ + HCO3¯)

• Anion gap can increase either due to:– Increase in the unmeasured anions.– Decrease in the unmeasured cations ( hypocal,

hypomag)

• Anion gap may decrease due to:– Increase in unmeasured cations (Ca, Mg, K)– Addition of abnormal cations (Li)– Decrease in albumin ( each 1g/dl decrease of alb

decrease AG by 2.5 mEq/L)

Step 6 & 7 Detecting mixed disorders

Clues to the presence of a mixed disorder.• Clinical history

• pH normal, abnormal PCO2 n HCO3

• PCO2 n HCO3 moving opposite directions

• Acid Base map (Flenley Nomogram)• Degree of compensation for primary disorder is

inappropriate• Find Delta Gap

Flenley Nomogram

• Compensation in excess points towards a mixed disorder.

• Example: In a case of primary metabolic acidosis, HCO3=12 Expected compensated PCO3 will be 24-28 (PCO2=1.5XHCO3 + 8 ± 2)If, PCO2 is < 24, Metabolic acidosis + Respiratory AlkalosisIf, PCO2 is > 28, Metabolic acidosis + Respiratory Acidosis

Δs for metabolic acidosis

• Every increase in unmeasured anion (Δ AG), should be met with similar decrease in HCO3 (Δ HCO3).

• Thus, Δ AG= Δ HCO3 in a case of simple AG metabolic acidosis

• However, If, Δ AG is > Δ HCO3= AG Metabolic acidosis +

Metabolic alkalosis

Delta gap

Delta ratio =∆AG/ ∆HCO3 = (observed AG-12)/ (24- obs HCO3) • <1 =High anion gap & normal AG acidosis• 1-2= Pure anion gap metabolic acidosis• >2 = High anion gap acidosis with concurrent

metabolic alkalosis

Significance of Δ Cl

• Normally the values of Cl change according to the hydration stature or Na

• If this proportional change is absent, then it indicates an acid base disorder.

If there is a disproportionate decrease of Cl= Metabolic alkalosis or Respiratory acidosis

If there is a disproportionate increase of Cl= Metabolic acidosis or Respiratory alkalosis

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1. Consider the Clinical Setting.2. Obtain ABG and Electrolyte values

simultaneously.3. Verify the ABG values.4. Identify the nature of the disturbance.5. Calculate the Anion gap in case of MA.6. Assess ∆AG, ∆ HCO3, ∆Cl & ∆Na7. Detecting mixed disorders.8. Clinical correlation

Interpretation with examples

Clinical examples

Example 1

• A 19 year old pregnant insulin dependent diabetic patient was admitted with a history of polyuria and thirst. She now felt ill and presented to hospital. There was a history of poor compliance with medical therapy.

• She was afebrile. Chest was clear. Circulation was adequate. Urinalysis: 2+ ketones, 4+ glucose.

• Na+ 136, K+ 4.8, Cl- 101, pH 7.26, pCO2 16 mmHg, pO2 128 mmHg, HCO3 7.1 mmol/l

• Clinical possibilities:– Diabetic ketoacidosis– Lactic acidosis– Hyperchloremic metabolic acidosis– Respiratory acid-base disturbances

• Check the internal validity of the report. Observed HCO3 report= 7.1, calculated HCO3= 7

• Look at the pH: 7.26• Then find the primary disorder: Low HCO3 along

with low pCO2 suggests a METABOLIC disorder.

ACIDOSIS

CORRECT

• Check for compensation: compensation for metabolic acidosis brings pCO2 to 16.5-20.6 mmHg. Thus the acidosis is

by respiratory regulation and there is • Anion Gap= 136-(101+7.1)=28.1• ∆AG=27.9-12=15.9, ∆HCO3=24-7.1=14.9• Delta ratio=15.9/14.9=1.07

• Na is normal with low Cl (NO HYPERCHLOREMIA)FINAL ABG DIAGNOSISPURE ANION GAP

METABOLIC ACIDOSIS (Etiology, DKA)

PURE ANION GAP ACIDOSIS

HIGH ANION GAP acidosis

NO MIXED disorder.

FULLY COMPENSATED

Example 2

• A 60 year old woman was admitted with lobar pneumonia. She was on a thiazide diuretic for 9 months following a previous admission with congestive cardiac failure. The admission arterial blood results were:

• pH 7.64• pCO2 32 mmHg• pO2 75 mmHg• HCO3 33 mmol/l• K+ 2.1 mmol/l

• Clinical possibilities:– Severe hypokalemis to be corrected immediately– Respiratory acidosis (respiratory failure)– Respiratory alkalosis (dyspnea)– Metabolic alkalosis (diuretics)

• Look at the pH: 7.64• Then find the primary disorder: Low pCO2 along

with high HCO3 suggests aMIXED ALKALOSIS.

ALKALOSIS

Check for compensation: • Considering Chronic respiratory alkalosis, expected

HCO3 is 20mEq/l on maximal compensation. Observed value is much higher so a Metabolic alkalosis should be present.

• Considering Metabolic alkalosis, predicted pCo2 after compensation is 43mmHg. The observed value is much lower so a respiratory alkalosis should be present.

FINAL ABG DIAGNOSISMIXED METABOLIC & RESPIRATORY ALKALOSIS

Ph 6.99

PCo2 10.5 mmHg

P02 111 mmHg

BE -29 mmol/L

HCo3 2.6

Tco2 45

SO2 95

Na+ 138 mmol/L

K+ 4.2 mmol/L

iCa+ 1.06 mmol/L

Hb 12.6 g/dl

For the audience

Expected fall in PCO2

=(1.5 x HCO3)+8 = (1.5 x 2.6) +8±2 = 9.9 to 13.9 Thus the compensation is within limits and the diagnosis is

COMPENSATED METABOLIC ACIDOSIS

For the audience

Primary dis- Respiratory alkalosis.For acute Resp. alkalosis---Expected HCO3 = 24- 2(40-19)/10

= 19.8but actual HCO3=13.5 which is less then the expected.

So it is mixed disorder with Respiratory alkalosis with

Metabolic acidosis

“Understanding ABG is not magic but an art learned by continued practice”

THANK YOU