abg.2 arterial blood gas analysis and example interpretation

Arterial Blood Gas Analysis …..1SAMIR EL ANSARYICU PROFESSOR AIN SHAMSCAIRO

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Existing approaches to acid base balance:

Henderson-Hasselbalch EquationCopenhagen approachBoston approachStewart approach

To provide Bedside approach to ABG analysis

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Copenhagen approach

Acid-base disorders are classified as being of

Respiratory origin (primary change in pCO2)

or of

Metabolic origin (primary change in fixed acids)

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Copenhagen approach

•Respiratory disorders are quantified by pCO2

•Metabolic disorders are quantified by the amount of excess fixed acids (the ‘metabolic

acids’)

Often there may be more than one type involved. It is difficult to predict which one it is and it is not feasible to

measure all of them.

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Copenhagen approach

The magnitude of the metabolic disorder (in the ECF)

can be quantified indirectly by the amount of change in the

[HCO3]

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Boston Approach

This approach is based on actual whole body titrations rather than on blood samples in a machine.

The aim has been to determine the magnitude of the compensation that occurs to graded degrees of acid-base disturbance.

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Stewart’s physicochemical approach

• Henderson–Hasselbalch equation fails to consider all the factors influencing

hydrogen ion concentration

• And is insufficient to explain complex metabolic abnormalities of acid–base

physiology

1970

Stewart’s physicochemical approach

Based on 3 principles:

• Electrochemical neutrality

• Conservation of mass

• Law of mass action

1970

pH is dependent on other ions in solution not just H+ and HCO3-- There are dependent and independent variables :

Dependent:-H+ - OH- - HCO3- - CO32-

Independent:-PaCO2Total of weak non-volatile acidsSID {Strong Ion Difference }

Stewart Equation

A strong ion = an ion that totally dissociates at a given pH

SID = strong cations – strong anions

SID = (Na+ + K+ + Ca2+ +Mg2+) – (Cl- - other anions)

Modified SID(Na+ + K+) – Cl-

Henderson-Hasselbalch Equation

The starting point is the Henderson Equation

Based on application of law of mass action on reaction of CO2 with

water

[H+] x [HCO3-] = K x [CO2] x [H2O]

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Hasselbalch modified Henderson's elegant idea

Regarding the water concentration as constant and taking logarithms of the

remaining components. This resulted in the Henderson-Hasselbalch

Equation:

pH = pK + log ( [HCO3-] / [CO2] )

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Kassirer-Bleich equation

H+ = 24 × Pco2/HCO3 −

This equation illustrates that acid-base balance depends on the ratio of Pco2 and HCO3 −

Not on the absolute value of either one alone.

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1. Is patient acidemic or alkalemic?2. Is primary disorder respiratory or metabolic?3. If respiratory, is it acute or chronic?4. If metabolic acidosis is there an anion gap? is there an osmolar gap?

ABG Interpretation

5. Is there appropriate compensation? if no, what is the second disorder?

6. IN THE SETTING OF AG METABOLIC ACIDOSIS, is there another problem? what is the delta gap?

ABG Interpretation

Are the data consistent?

The Henderson Equation

[ ] −+ ×=

3

2

24HCO

PaCOH

Convert [H+] to pH

• Subtract calculated [H+] from 80; this gives the last two digits of a pH beginning with 7

• example: calculated [H+] of 24 converts to pH of (80-24)~7.56

• example: calculated [H+] of 53 converts to pH of (80-53)~7.27

• Refer to table for more precise conversion, or if

Calculated [H+] exceeds 80

Relationship between [H+] & pH

pH [H+] pH [H+]

7.807.75

1618

7.307.25

5056

7.707.65

2022

7.207.15

6371

7.607.55

2528

7.107.00

7989

7.507.45

3235

6.956.90

100112

7.407.35

4045

6.856.80

141159

HCO3- (bicarbonate)

SB (standard bicarbonate) AB (actual bicarbonate)

SBThe contents of HCO3

- of serum of arterial blood

{ at 37 , PaCO2 40mmHg, SaO℃ 2 100%.}

Normal: 22-27mmol/L Mean: 24mmol/L

AB The contents of HCO3

- in actual condition.

In normal person

AB=SB

AB and SB are parameters to reflect

metabolism, regulated by kidney

Difference of AB-SB can reflect the respiratory affection on serum HCO3

-

Respiratory acidosis: AB > SB Respiratory alkalosis: AB < SB

Metabolic acidosisAB ＝ SB < Normal

Metabolic alkalosis AB = SB > Normal

Base Excess

∆base to normalise HCO3 (to 24) with PaCO2 at 40 mm Hg

HCO3-

Hemoglobin Plasma proteins HPO42- (phosphate)

Buffer bases （ BB)Buffer base is a measure of the concentration of all the

buffers present in either plasma or blood.

Normal: 45-55mmol/L mean: 50mmol/L

SignificanceMetabolic acidosis: BB

Metabolic alkalosis: BB

Buffer bases （ BB)

Regulation of Acid-basic Balance

Chemical bufferDielectric changes of incells and

excells

H+---K+ HCO3- ---Cl-

Physiology regulation through

lung and kidney

Classification of Acid-basic Disorder

Complementary: PH is normal

Dis-complementary: PH is abnormal.

Oxygenation parameters

PaO2

Normal: 95-100mmHg

PaO2=100mmHg - (age×0.33) ±5mmHg

Hypoxia

Mild: 80-60mmHgMODERATE

60-40mmHgSevere: <40mmHg

SaO2

0.95-0.98

Not sensitive

PaCO2

35-45mmHg (4.7-6.0kPa)

Mean: 40mmHg

PA-aO2

Gas exchange

Normal: 15-20mmHg

(<30mmHg in the old)

CaO2 19-21 mmol/L

PvO2

Mixed venous oxygen pressure

35-45mmHg

Mean: 40mmHg

Significance

Pa-vO2 is to reflect the tissue absorbing oxygen

O2 Content of blood:Hb. x O2 Sat + Dissolved O2

(Don’t forget hemoglobin)

Oxygen Saturation: reported as ABG report( Derived from oxygen dis. curve not a measured value )

Alveolar / arterial gradient:( Useful … to classify respiratory failure )

Oxygenation Indices

0 10 20 30 40 50 60 70 80 90 100 PaO2

20

40

60

80

100

Rt. Shift

Normal arterio/venous difference

Shift of the curve ……changes saturation for a given PaO2

Normal

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Oxygen delivered to tissues

with normally placed curve

Delivered oxygen with Rt. Shift curve

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Alveolar-arterial DifferenceInspired O2 = 21 % piO2 = (760-45) x . 21 = 150 mmHg

O2

CO2

palvO2 = piO2 – pCO2 / RQ

= 150 – 40 / 0.8= 150 – 50 = 100 mm Hg

PaO2 = 90 mmHg

palvO2 – partO2 = 10 mmHg One click and wait

Alveolar- arterial Difference

O2

CO2

Oxygenation Failure WIDE GAPpiO2 = 150pCO2 = 40

palvO2= 150 – 40/.8=150-50

=100

PaO2 = 45

= 100 - 45 = 55

Ventilation Failure NORMAL GAPpiO2 = 150

pCO2 = 80

palvO2= 150-80/.8 =150-100

= 50PaO2 = 45

= 50 - 45 = 5 PAO2 (partial pres. of O2. in the alveolus.)

= 150 - ( PaCO2 / .8 )760 – 45 = 715 : 21 % of 715 = 150

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20 × 5 = 100

Expected PaO2

FiO2 × 5 = PaO2

Normal situation

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The Blood Gas Report: normals…

pH 7.40 + 0.05PaCO2 40 + 5 mm HgPaO2 80 - 100 mm Hg

HCO3 24 + 4 mmol/L

O2 Sat >95Always mention and see FIO2

The essentials

HCO3

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5The

Steps forSuccessfulBlood Gas

Analysis

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Step 2 Who is responsible for this change in pH ( culprit )? CO2 wil l change pH in opposite direction Bicarb. wil l change pH in same directionAcidemia: With HCO3 < 24 mmol/L = metabolic

With PCO2 >40 mm hg = respiratory

Alkalemia: With HCO3 >24 mmol/L = metabolicWith PCO2 <40 mm Hg = respiratory

Step 1Look at the pHIs the patient acidemic pH < 7.40or alkalemic pH > 7.40

Step 3I f there is a primary respiratory

disturbance, is it acute ?

.08 change in pH ( Acute )

.03 change in pH ( Chronic )

10 mm Change PaCO2

=

Primary lesion

Compensation

pH

Bicarbonate

PaCO2

METABOLIC ACIDOSIS

HYPER VENTILATION

BICARB CHANGES pH in same direction

Low Alkali

Three clicks

Primary lesion

Compensation

pH

Bicarbonate

PaCO2

METABOLIC ALKALOSIS

HYPO VENTILATION

BICARB CHANGES pH in same direction

High Alkali

Three clicks

Primary lesion

compensation

pH

PaCO 2

BICARB

Respiratory acidosis

CO 2 CHANGES pH in opposite direction

HighCO2

Three clicksWait for red circle

Primary lesion

compensation

pH

PaCO 2

BICARB

Respiratory alkalosis

PaCO 2 CHANGES pH in opposite direction

LowPaCO2

Three clicksWait for red circle

Primary disorder Formula

Metabolic acidosis ↓PCO2 = 1.2 x ↓[HCO3-]

Metabolic alkalosis ↑PCO2 = 0.7 x ↑[HCO3-]

Respiratory acidosis

Acute ↑[HCO3-] = 0.1 x ↑PCO2

Chronic ↑[HCO3-] = 0.4 x ↑PCO2

Respiratory alkalosis

Acute ↓[HCO3-] = 0.2 x ↓ PCO2

Chronic ↓[HCO3-] = 0.5 x ↓ PCO2

Step 4 : Degree of compensation

Suspect i f . .. . .. .. . .. .. actual PaCO2 is more than

expected : addit ional …respiratory acidosis

actual PaCO2 is less than expected : addit ional …respiratory alkalosis

Step 4 : cont.I f there is metabolic acidosis, is there a wide anion gap ?

Na - (Cl -+ HCO3-) = Anion Gap usually < 12

If >12, Anion Gap Acidosis : M ethanolU remiaD iabetic KetoacidosisP araldehydeI nfection (lact ic acid)E thylene GlycolS alicylate

Common pediatric causes

1) Lactic acidosis2) Metabolic

disorders3) Renal fai lure

Step 4: Which type?

• Check anion gap (AG): If AG is high• High AG metabolic acidosis is present• If metabolic acidosis is diagnosed:

Check ↑AG / ↓[HCO3-]

• <1 : High AG Met. Acid + normal AG Met. Acid.

• 1-2 : High AG Met. Acid

• >2 : High AG Met. Acid. + Met. Alk.

• If metabolic acidosis is not diagnosed:• High AG Met. Acid. + Met. Alk.

1. Normal gap 2. Increased gap

1. Renal “HCO3” losses

2. GI “HCO3” losses

Proximal RTA Distal RTA

Diarrhea

1. ↑ Acid prod

2. ↓ Acid elimination

LactateDKAKetosisToxinsAlcoholsSalicylatesIron

Renal disease

Metabolic acidosis and the anion gap

5 th step

Clinical correlation

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HCO3 META.pH

PaCO2 pH RESP.

Same direction

Opposite direction

Same direction

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PaCO2 of 10 pH

Acute change .08

Chronic change .03

Com

pensation

Considered complete when the pH returns

to normal range

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CO

MP

EN

SA

TIO

N LIM

ITS

METABLIC ACIDOSISPaCO2 = Down to 10 ?

METABOLIC ALKALOSISPaCO2 = Maximum 6O

RESPIRATORY ACIDOSISBICARB = Maximum 40

RESPIRATORY ALKALOSISBICARB = Down to 10

Blood Gas Report

Measured 37.0o

CpH 7.523PaCO2 30.1 mm HgPaO2 105.3 mm Hg

Calculated DataHCO3 act 22 mmol / L

O2 Sat 98.3 %PO2 (A - a) 8 mm Hg ∆PO2 (a / A) 0.93

Entered DataFiO2 21.0 %

Case 1

16 year old female withsudden onset of dyspnea.

No Cough or Chest Pain

Vitals normal but RR 56,anxious.

Acute respiratory alkalosis And why acute ?

Case 2 6 year old male with progressive respiratory distress

Muscular dystrophy .

Blood Gas Report

Measured 37.0o

CpH 7.301PaCO2 76.2 mm HgPaO2 45.5 mm Hg

Calculated DataHCO3 act 35.1 mmol / L

O2 Sat 78 %PO2 (A - a) 9.5 mm Hg ∆PO2 (a / A) 0.83

Entered DataFiO2 21 %

pH <7.35 :acidemia

Res. Acidemia : High PaCO2 and low pH

HypoxemiaNormal A-a gradient

CO2 =76-40=36Expected pH for ( Acute ) = .08 for 10Expected ( Acute ) pH = 7.40 - 0.29=7.11Chronic resp. acidosis

Hypoventilation

Chronic respiratory acidosisWith hypoxia due to hypoventilation

Five clicks

Case 38-year-old male asthmatic;3 days of cough, dyspneaand orthopnea notresponding to usualbronchodilators.

O/E: Respiratory distress;suprasternal and intercostal retraction;tired looking; on 4 L NC.

pH <7.35 ; acidemia

PaCO2 >45; respiratory acidemia

piO2 = 715x.3=214.5 / palvO2 = 214-49/.8=153 Wide A / a gradient

Hypoxia

WITH INCREASE IN CO2 BICARB MUST RISE ?Bicarbonate is low……… Metabolic acidosis + respiratory acidosis

30 × 5 = 150

CO2 = 49 - 40 = 9Expected pH ( Acute ) = 9/10 x 0.08 = 0.072Expected pH ( Acute ) = 7.40 - 0.072 = 7.328Acute resp. acidosis

8-year-old male asthmatic with resp. distress Six clicks

Case 4 8 year old diabetic with respi. distress fatigue and loss of appetite.

Blood Gas Report

Measured 37.0o

CpH 7.23PaCO2 23 mm HgPaO2 110.5 mm Hg

Calculated DataHCO3 act 14 mmol / L

O2 Sat %PO2 (A - a) mm Hg ∆PO2 (a / A)

Entered DataFiO2 21.0 %

pH <7.35 ; acidemia

HCO3 <22; metabolic acidemia

Last two digits of pHCorrespond with co2

If Na = 130, Cl = 90Anion Gap = 130 - (90 + 14)

= 130 – 104 = 26

Three clicks

Blood Gas Report

Measured 37.0o

CpH 7.46PaCO2 28.1 mm HgPaO2 55.3 mm Hg

Calculated DataHCO3 act 19.2 mmol / L

O2 Sat %PO2 (A - a) mm Hg ∆PO2 (a / A)

Entered DataFiO2 24.0 %

Case 5 : 10 year old child with encephalitis

pH almost within normal rangeMild alkalosis

PaCO2 is low , respiratorylow by around 10 ( Acute ) by .08 (Chronic ) by .03

BICARBINATURIA

Bicarb looks low ?Is it expected ?

Four clicks

Case #6:• A 4 year old with chronic renal failure

presents to the pedes ER with history of increasing azotemia, weakness, and lethargy.

• Exam reveals the patient to be modestly hypertensive, and tachypneic. Labs reveal BUN=100, and Creatinine=8.

• How can we tell if an acid-base disorder is present?

Case #6:

• Steps 1&2: must know pH, PaCO2, HCO3

• pH=7.37, PaCO2=22, and HCO3=12

• Step 3: are the available data consistent?

[ ] −+ ×=

3

2

24HCO

PaCOH

Case #6:

• [H+]=44, equates to pH~7.36; data are thus consistent

• What is the primary disorder?

• “_________Acidosis”

• Which variable (PaCO2, HCO3) is deranged in a direction consistent with acidosis?

• Primary disorder is “Metabolic Acidosis”

Is compensation appropriate?• HCO3 is decreased by 12 mmoles/l

• PaCO2 should decrease by 1 to 1.5 times the fall in HCO3; expect PaCO2 to decrease by 12-18 mm Hg or be between 22-28 mm Hg

• Since PaCO2 is 22 mm Hg, compensation is appropriate, and the data are consistent with a simple metabolic acidosis with respiratory compensation

• If the data are consistent with a simple disorder, it does not guarantee that a simple disorder exists; need to examine the patient’s history

• When compensatory responses do not lie within the accepted range, by definition a

combined disorder exists.

Case #7:

• A 15 year old female is brought to the pedes ER in an obtunded state.

• Per her family, patient history is notable for progressive weakness over two months.

Case #7:

• A recent “complete physical” demonstrated decreased DTRs symmetrically, without other abnormal findings.

• Exam shows shallow, tachypneic respiratory effort.

Case #7: Steps 1, 2, and 3

• What baseline information is required?

• PaCO2=40 mm Hg, HCO3=7, pH=6.88

• Are the data internally consistent?

[ ] −+ ×=

3

2

24HCO

PaCOH

Case #7:

• [H+]~140, which equates to a pH~6.85, so data are internally consistent

• What is the primary disturbance?

• “___________ Acidosis”

• Which variable is deranged in a direction which is consistent with acidosis?

• PaCO2 WNL, “Metabolic Acidosis”

Is compensation appropriate?• Metabolic Acidosis

• PaCO2 should fall by 1 to 1.5 mm Hg x the fall in plasma [HCO3]

• HCO3 decreased by 17, so we expect PaCO2 to be decreased by 17-26

• PaCO2 WNL; since PaCO2 inappropriately high, there is a combined metabolic acidosis and respiratory acidosis

Case #8:

• A 16 year old male with sickle cell anemia, hemochromatosis, & subsequent cirrhosis, presents with a several day history of emesis.

• At presentation to the pedes ER, he is hypotensive, orthostatic, and confused.

• What acid-base disorders might be anticipated based on the above information?

Case #8:

• 16 yo male with sickle cell anemia, hemo-chromatosis, & subsequent cirrhosis, and several days of emesis. In the pedes ER, he is hypotensive, orthostatic, and confused.

• Emesis-loss of H+ (HCl)-metabolic alkalosis

Case #8:

• Orthostatic hypotension-?

• lactic acidosis

Case #8:

• SCD-decreased O2 delivery-?

• Lactic acidosis

Case #8:

• Cirrhosis

Decreased lactate metabolism

Case #8:• What baseline information is available?

• pH=7.55, PaCO2=66

• ‘lytes: Na+=166, K+=3.0, Cl-=90, HCO3=56

• Are the data internally consistent?

[ ] −+ ×=

3

2

24HCO

PaCOH

Case #8:

• [H+]~28, equates to pH~7.55; consistent

• What is the primary abnormality?

• “_________ Alkalosis”

• PaCO2↑ed, HCO3 ↑ed, therefore…….

• “Metabolic Alkalosis” presumed due to emesis

• Is compensation appropriate?

Case #8:• Metabolic Alkalosis

• PaCO2 should rise by .25 to 1 mm Hg x the rise in plasma [HCO3]

• HCO3 ↑ed by 32; PaCO2 should ↑ by 8-32

• PaCO2 ↑ed by 26, so compensation appears appropriate

• What about multiple risk factors for lactic acidosis?

Case #8:• Could there be a concealed lactic acidosis?

• What is the anion gap?

• Na+- (Cl- + HCO3), normally 12-14

• Anion gap here is 166 - (90 + 56) = 20

∀ ↑ed anion gap implies metabolic acidosis

• Combined metabolic alkalosis & metabolic acidosis therefore present

• Always calculate the anion gap• Often it is the only sign of an occult

metabolic acidosis

• Acidotic patients partially treated with HCO3

• Acidotic patients with emesis

IN

• Always calculate the anion gap

May be the only sign of metabolic acidosis “concealed” by concomitant

acid-base disorders

Occult metabolic acidosis post-Rx:

Normal Ketoacidosis Post-RXNa+ 140 140 148Cl- 105 105 98HCO3 25 10 25ketones 0 15 15AG 10 25 25pHPaCO2

7.4040

7.3031

7.4040

Causes of Anion Gap Acidosis• Endogenous acidosis

• Uremia (uncleared organic acids)

• Ketoacidosis, Lactic acidosis (increased organic acid production), Rhabdomyolosis

• Exogenous acidosis

• Ingestions: salicylate, iron; paraldehyde use

• Other Ingestions

• Methanol toxicity, Ethylene Glycol toxicity

Anion Gap:Based on the concept of

electroneutrality

Available cations =

Available anions

Anion Gap:

UA-UCAnion Gap

Na+ - (Cl-+HCO3-)

12 to 14

Anion Gap:

Serum albumin contributes ~1/2 of the

total anion “UA” pool

Anion Gap:

1gm/dl in serum albumin

Anion gap by

3 mEq/L

Anion Gap:

• Therefore an anion gap of 12 mEq/L is corrected to 17-18 mEq/L when the

serum albumin is half of normal

Case #9:

• A 3 year old is brought to the pedes ER at ~3am, stuporous and tachypneic. History is remarkable for his parents having cleaned out their medicine cabinet earlier that day.

Case #9:

• An ABG and electrolytes have been

•Accidentally drawnby the nurse.

Case #9:

• Available data: pH=7.53, PaCO2=12; Na+=140, K+=3.0, Cl-=106, HCO3=10

• Are the data internally consistent?

[ ] −+ ×=

3

224HCO

PaCOH

Case #9:• [H+]~29, so pH~7.51; data consistent

• What is the primary disturbance?

• “__________ Alkalosis”

• Which variable (PaCO2, HCO3) is deranged in a direction consistent with alkalosis?

∀ ↓ed PaCO2, ↓ed HCO3; so “Respiratory Alkalosis”

Case #9:• Is compensation appropriate?

• Acute respiratory alkalosis

• Plasma [HCO3] should fall by ~1-3 mmole/l for each 10 mm Hg decrement in PaCO2, usually not to less than 18 mmoles/l

• PaCO2 ↓ed by ~30 mm Hg; HCO3 should fall by 3-9 mmole/l; HCO3 ↓ is too great, so superimposed metabolic acidosis

Case #9:• What is the anion gap?

• 140 - (106 + 10) = 24; elevated anion gap consistent with metabolic acidosis

• What is the differential diagnosis?

• Combined (true) respiratory alkalosis and metabolic acidosis seen in sepsis, or salicylate intoxication

Case #10:

• A 5 year old with Bartter’s Syndrome is brought to clinic, where she collapsed.

• She has recently been febrile, but history is otherwise unremarkable.

• pH=6.9, PaCO2=81; Na+=142, K+=2.8, Cl-

=87, HCO3=16

Case #10:

• Are the data consistent?

• [H+]=122, pH~6.9; data are consistent

[ ] −+ ×=

3

224HCO

PaCOH

Case #10:• What is the primary disturbance?

• “_________ Acidosis”

• Which variable (PaCO2, HCO3) is deranged in a direction consistent with acidosis?

• Both; pick most abnormal value--

• “Respiratory Acidosis”

• Is compensation appropriate?

Case #10:• Acute Respiratory Acidosis

• Plasma [HCO3] should rise by ~1mmole/ for each 10 mm Hg increment in PaCO2

• Since HCO3 is inappropriately depressed, compensation is not appropriate, and there is a concomitant metabolic acidosis as well

• What is the anion gap?

• AG=39, confirms metabolic acidosis

Case #10:

• Combined Respiratory Acidosis and Metabolic Acidosis; are there other disorders present?

• What about the dx of Bartter’s Syndrome?

• Bartter’s Syndrome characterized by

hypokalemic metabolic alkalosis• Does this patient have a concealed metabolic

alkalosis?

Case #10:• Anion gap is 39, or 25-27 greater than

normal

• Typically, increases in anion gap correlate with decreases in HCO3

• Assuming a 1:1 relationship, as anion gap increases by 25, HCO3 should fall by 25

• Starting HCO3 must have been 16 + 25 = 41

Case #10:

• Therefore, starting HCO3 was ~41 mmol/l, consistent with expected chronic metabolic alkalosis.

• This metabolic alkalosis was “concealed” by the supervening profound metabolic and respiratory acidoses

Case #10:

• Final diagnosis

Metabolic alkalosis, metabolic acidosis, & respiratory acidosis

Rule

Mixed Acid-Base Disorders

Coexistant metabolic acidosis and metabolic alkalosis may occur.

Always check the change in the anion gap vs. decrement in bicarbonate to rule out

a concealed metabolic disorder.

Delta Ratio

• The increase in Anion Gap / the decrease in HCO3-

• Indicates what has happen to the denominator (HCO3-)

Delta Ratio

• Used in RAGMA to see whether change in HCO3- is appropriate

• Normal value = 1 to 1.5

• If normal there is only one pathology (uncomplicated RAGMA)

Delta Ratio

• Interpretation

• < 0.4 - hyperchloraemic normal anion gap acidosis

• 0.4 - 0.8 - consider combined high AG & normal AG acidosis

• BUT note that the ratio is often < 1 in acidosis associated with renal failure

Delta Ratio

• 1 – 2 - usual for uncomplicated high-AG acidosis (lactic acidosis: average value 1.6 ) { DKA: around 1 }

• > 2 - a high delta ratio an elevated bicarbonate at onset of the metabolic acidosis pre-existing metabolic alkalosis or compensated respiratory acidosis.

Case #11:• A 3 year old toddler is brought to the ER at 3

am after being found unarousable on his bedroom floor, with urinary incontinence, bradycardiac.

• One amp of D50W and 0.1 mg of naloxone were given IV without response.

• Vital signs are stable; respiratory effort is regular, but tachypneic.

• He is acyanotic.

Case #11:• Initial lab studies (lytes, ABG & urine tox

screen) are sent. Initial dextrostick is >800.

• Initial available data are:

• Na+=154, K=5.6, Cl=106, HCO3=5, BUN=6 creatinine=1.7, glucose=804, PO4=12.3, Ca+

+=9.8, NH4=160, serum osms=517

• pH=6.80, PaCO2=33, PaO2=298

Case #11:• What is the primary disturbance?

• ________ Acidosis

• Metabolic Acidosis

• Is compensation appropriate?

• No; PaCO2 level is inappropriately high

• Are other disorders present?

• Respiratory acidosis (due to evolving coma)

Case #11:

• What is our differential thus far?• Anion gap vs. non-anion gap metabolic acidosis• DKA, lactic acidosis, renal failure, ingestion

• The urine tox screen comes back negative• What does urine tox screen actually screen for?

• The patient’s IV falls out.

• He then has a seizure, is incontinent of urine.

Case #11:

• What is the calculated serum osmolality, and does an osmolal gap exist?

• 2(Na) + BUN/2.8 + Glucose/18• Calculated=355, Measured=517

• What is the most likely diagnosis?

• How can this be confirmed definitively?• Review of urinanalysis

• Serum ethylene glycol level

Case #11:

Anion gap metabolic acidosis

Osmolal gap

Methanol, ethylene glycol

ethyl alcohol, isopropyl alcohol

You CAN have a respiratory problem and a metabolic problem (and even a secondary

metabolic problem on top of that)

look at delta gap Anion gap delta versus Bicarb delta

Normally in AG Met Acidosisthe number of anions above 14 should equal the number of bicarb below 24

(Calculated anion gap - 14) versus (24 - measured HCO3)

If Bicarb delta is less than the Anion gap delta

Metabolic alkalosis as well

If Bicarb delta is more than the Anion gap delta

Non AG metabolic acidosis as well

Most common AG met acidosis: ketoacidosis, lactic acidosis, ASA

(IF ruled out investigate toxic alcohols)

ASA not only results in AG met acidosis but also Resp alkalosis

A low glucose does not rule out ketoacidosis

Look out for starvation, dehydration, alcohol

Consider cyanide and carbon monoxide in inhalation and burn

victims

Don’t be fooled by normal Osat and PaO2 - Carbon monoxide needs

Carboxyhemoglobin

Isoniazid antidote is vit b6...think about it in refractory seizures (esp

high risk TB populations)

Reduced arterial-venous oxygen sat difference (<10%) suggests cyanide

toxicity

Cyanide antidote is induced methemaglobinemia

Ethylene glycol or methanol antidote is etoh or Fomepizole

Ethylene glycol in urine will fluoresce using a Wood’s lamp

Calcium oxalate crystals in urine are sign of possible ethylene glycol

ingestion

Most common loss of bicarb by GI {Diarrhea}

or kidneys{ Tubular acidosis or renal failure }

Metabolic Alkalosis - Saline Responsive

Either loss of H+ or contraction (volume contraction around constant HCO3)

Urine Cl <10 Gastric suctionVomiting Diuretics

Give Saline, gets better

Metabolic Alkalosis - Non Saline ResponsiveRetention of HCO3 associated with mineralcorticoid excessUrine Cl >20 Hyper aldosteronismExogenous steroids AdenocarcinomoaBartter’s syndrome

Cushing’s syndrome

RAGMA{Raised anion gap metabolic acidosis }

look for lactate, calculate Delta ratio, Stewart Equation

When to calculate what ?

NAGMA{Normal anion gap metabolic acidosis }

Calculate Urinary anion gapStewart Equation

Osmolar gap

When to calculate what ?

Osmolar Gap The osmolality is measured in lab

Calculated osmolarity(2 x [Na+]) + [glucose]/18 + [urea]/2.8

Osmolality {from lab.} – Osmolarity {calculated}An osmolar gap > 10 mOsm/l is often stated to

be abnormal

Osmolar Gap

SignificanceIndirect evidence for the presence of an

abnormal solute which is present in significant amounts.

Ethanol, methanol & ethylene glycol -> will cause an elevated osmolar gap.

Urinary Anion Gap {UAG}

[Na+]+ [K+] - [Cl-]

Clinical UseDifferentiate between GIT and renal

causes of a hyperchloraemic metabolic acidosis

The decreased PaO2 causes us to increase our minute ventilation resulting in a lower PaCO2.

In order that pH remain within normal limits, the kidneys excrete HCO3

- to compensate for the low PaCO2

So ABG values are slightly different than textbook sea level values

Blood Gas values { High altitudes }

The pH may be very low, i.e. < 7.00Since both a metabolic acidemia

(anaerobic metabolism, lactic acidemia)

And a respiratory acidemia (inadequate ventilation) will be causing the pH to fall.

In a code situation

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Remember that COPD patients may ‘normally’ have a %HBO2 in the 88% range.

THANK YOUSAMIR EL ANSARY

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