ACID BASE IMBALANCE

AND THE ABG

 DEFINITIONS

Acid is defined as any chemical substance that can donate a hydrogen ion (H+).

When an acid releases a proton, it is converted to the conjugate base.

HA  H+ + A-

Base is defined as any chemical substance that can accept a hydrogen ion.(H+)

When a base binds a proton, it is converted to the conjugate acid.

B + H+ BH+
 pH

The pH of a solution refers to the activity or

potency of H+.

pH = minus log of the power of 10 of the

hydrogen ion concentration
-log 10 [H+].

The higher the pH number, the lower

the number of H+, and the less acidic
The pH of the body is controlled by three systems:

The chemical acid-base buffering by the body fluids that immediately

combine with acids or base to prevent excessive changes in pH.

The respiratory center which regulates the removal of volatile CO2 as a

gas in the expired air from the plasma and therefore also regulates
bicarbonate (HCO3-) from the body fluids via the pulmonary
circulation. This response occurs in minutes.

The kidneys which can excrete either acid or alkaline urine, thereby
adjusting the pH of the blood. This response takes place over hours
or even days, but represent a more powerful regulatory system.
 Buffers
• Solutes in an aqueous solution that are able to take up or release H + so that changes in pH are
minimized
• If we add a strong acid to a buffer, the buffer consumes most of the H and thereby buffers the pH ,
minimizing the H+ in solution.

HCl + B  H+ + Cl- + B(n)  HB(n+1) + Cl-

• Physiological buffers :
 Hemoglobin
 Plasma proteins
 Phosphate compounds
 Bone
 Bicarbonate/carbonic acid

.
Henderson-Hasselbalch Equation

HA  H+ + A-
 Carbonic Acid - Bicarbonate Buffer System

CA
• H2O + CO2 H2CO3 H+ + HCO3-
[H+][HCO3- ]
• Ka = [CO2]
-
[HCO3 ]
• pH = pKa + log
[CO2]
-
[HCO3 ]
• pH = 6.1 + log
0.03 x PCO2
 THE ROLE OF LUNGS AND KIDNEYS
IN ACID-BASE BALANCE
The ratio of HCO3- to CO2 was the important determinant of pH.
CO2 being controlled by the lungs is called the “respiratory”
component in acid-base physiology.
Bicarbonate being controlled by the kidneys is called the
“metabolic” or “renal” component.
In a normal person both the lung and kidney work to maintain
the 20:1 ratio
Since the pH of a CO2/HCO3- solution depends upon the ratio
of these tow buffer pairs, and because the lung control CO2 but
the kidney controls HCO3, the overall description of their
interaction might be described as
pH = k + KIDNEY / LUNG
(Not a real reaction equation, but rather a descriptive
relationship between the regulating components of ph in the
body)
Overview of Acid-Base Physiology
Lung and kidney help enhance the
homeostatic function of the buffers

CO2

[Kidney]
pH ~
~ [Lung]

HCO3- + H+

HCO3- H+ : Phosphoric
Nephrology & Hypertension LSUHSC
acid, NH4+ 10
 Acid Base Disorders : Terminology

• “ -EMIA”: describes a condition of the blood

• For describing blood pH problems we say:

 Acidemia: pH < 7.35

 Alkalemia: pH > 7.45

• Normal blood pH range is 7.35 - 7.45

• pH limits of 6.8 or 7.8 are incompatible with life

 Acid Base Disorders : Terminology

• “ -OSIS”: Describes a process

• Acidosis: Process producing acidemia (pH<7.35)

Either an excessive amount of acid or a decrease in
alkaline substances is the cause.

• Alkalosis: Process producing alkalemia (pH>7.45)

Either too many alkaline substances or not enough acid
substances.
 Acid Base Disorders : Terminology

• Compensation

– the physiologic metabolic (renal) and respiratory changes to

return the pH toward normal in response to a primary acidosis or
alkalosis.
 Acid Base Disorders : Terminology

• Simple disturbance
– only a single acid base process and its expected compensation
are present

• Mixed disturbance
– two or more primary acid base disturbances are present. The
arterial blood pH will depend on the direction and magnitude of
the disturbances.
 Simple Acid Base Disorders

Primary process Compensation

metabolic acidosis [HCO3] pCO2

metabolic alkalosis [HCO3] pCO2

respiratory acidosis pCO2 [HCO3]

respiratory alkalosis pCO2 [HCO3]

 Metabolic Acidosis
• Metabolic acidosis is a disorder with low plasma [HCO3-]
caused by a net gain of H+ or loss of HCO3-.

• If unopposed, it will result in acidemia.

• Criteria – pH<7.35; HCO3-< 22mEq/L; low pCO2

 Metabolic Acidosis
• Anion gap
• Hyperchloremic (normal anion gap)
– impaired acid excretion
– increased bicarbonate loss
– hydrogen ion gain
 Anion Gap Metabolic Acidosis

• The anion gap is an estimate of the relative abundance of the unmeasured anions.

• Used to determine if a metabolic acidosis is due to an accumulation of non-volatile

acids (e.g., lactic acid) or a net loss of bicarbo-nate (e.g., diarrhea)

• AG = [Na+] - [Cl-] - [HCO3-]

• Normal value: 10 ± 2 mmol/L

• Major unmeasured anions

– albumin
– phosphates
– sulfates
– organic anions
 Anion Gap

NORMAL METABOLIC ACIDOSIS

Hyperchloremic High Anion Gap

AG AG
AG
-
HCO3 - HCO3
HCO3-

Na+ Na+ Na+

- - -
Cl Cl Cl
 Corrected Anion Gap
160 Mg SO4
K
PO4 Albumin
ORGANIC ANIONS
Ca ALBUMIN
Corrected AG
120 HCO3

AG + 2.5 x
mEq/L

(4.4 – albumin in
80 gm/dl)
Na Cl

40
Each g/dl decrease
in albumin
underestimates
0 the AG by 2.5
CATIONSANIONS
20
 Causes of High Anion Gap Metabolic
Acidosis
Type Increased Anions
• diabetic ketoacidosis -- hydroxybutyrate,acetoacetate
• alcoholic ketolactic hydroxybutyrate,
acidosis acetoacetate, lactate
• lactic acidosis lactate
• renal failure phosphate, sulfate, organic
• Toxins anions
– methanol formate, lactate
– ethylene glycol oxalate, glycolate
– salicylate ketoacids, lactate, salicylate
– paraldehyde organic anions
 Causes of Hyperchloremic
(Normal anion gap) Metabolic Acidosis
• Impaired renal acid excretion
– renal failure
– classic distal RTA (type I)
– hyperkalemic distal RTA (type IV)
• Renal bicarbonate loss
– proximal RTA (type II)
– carbonic anhydrase inhibitors
– therapy of diabetic ketoacidosis
• Gastrointestinal bicarbonate loss
– diarrhea
– pancreatic drainage
– ureteral diversion
• Acid gain
– hyperalimentation fluids
– ammonium chloride ingestion
 Clinical manifestations

– Abdominal pain / Headache

– Negative ionotropic effect
– Resistance to catecholamines
– Predisposition to cardiac arrhythmias
– Stimulation of inflammatory cytokines
– Decreased tissue perfusion and oxygen delivery
– Abnormal glucose regulation
– Increased cellular apoptosis
– Hyperventilation
– Hyperkalemia / Hyperphosphatemia
 Metabolic Acidosis: Compensation

• Acidemia (low pH) triggers respiratory compensation

• Winters’ formula

pCO2 = 1.5 x [HCO3-] + 8 ± 2

 CO2
HYPER VENTILATION

compensation LOW HCO3

pH
LOWHCO
pH changes
3
pH in same direction
LOW pCO2 (compensated)
HCO3

Low Primary lesion

Alkali METABOLIC ACIDOSIS
 Δ AG – Δ HCO3-
• AG = [Na+] - [Cl- + HCO3- ]

• The change in anion gap (Increase anions that we do not

measure) should be equal to the drop in bicarbonate

• If the bicarbonate drops more than the change in anion

gap you have an associated NAGMA.

• If the bicarbonate does not drop as much as the change

in anion gapassociated Metabolic Alkalosis
 Metabolic Acidosis: Treatment
Treatm

• Treat underlying cause

• Alkali replacement
– Acute metabolic acidosis
• indicated when is pH less than ~7.15 or HCO3 <10 mEq/L
• goal is to raise serum [HCO3] to ~15mmol/L
• bicarbonate dose =
(0.3 x BE x Body wt.) / 2
Half correction is done within half hr & rest is given in slow
correction over 4 hrs and ABG is repeated.
– Chronic metabolic acidosis
• goal of treatment is to prevent long term sequelae
• serum [HCO3] should be normalized
 METABOLIC ALKALOSIS

• Metabolic alkalosis is a disorder with high plasma

[HCO3-] caused by a net gain of HCO3- or loss of H+.

• If unopposed, it will result in alkalemia.

• Criteria – pH >7.45; HCO3->26 mEq/L

28
 Metabolic Alkalosis
GENERATION PHASE: Due to acid loss or alkali gain.

• Acid loss • Alkali gain

– renal acid losses – bicarbonate administration
• diuretic therapy – milk alkali syndrome
• mineralocorticoid – infusion of organic anions
excess • citrate
• Cushing’s syndrome • acetate
• severe potassium • lactate
depletion – rapid correction of chronic
• Bartter’s syndrome hypercapnia
• Liddle’s syndrome
– gastrointestinal losses
• gastric acid loss
• chloride diarrhea
 Metabolic Alkalosis
MAINTENANCE PHASE: Prevents the excretion of the extra HCO3,
leading to its retention and hence the alkalosis.
• Decreased GFR
– renal failure
• Increased proximal HCO3- reabsorption
– chloride depletion
• Increased distal tubular H+ secretion
– mineralocorticoid excess
– hypokalemia
 CHRONIC METABOLIC ALKALOSIS
• Respiratory compensation begins within the first hour and is complete by 12
to 24 hours.

• Clinical manifestations
Dizziness
Lethargy
Tetany (Hypocalcemia)
Decreased respirations
Atrial tachycardia and other dysrhythmias
Paralytic ileus
Hypoxemia
Seizures, coma

31
 CHRONIC METABOLIC ALKALOSIS

Alkalemia (high pH) triggers respiratory

compensation

[H+] = 24 x PCO2 / [HCO3-]

10 mEq/L  HCO3  6 mmHg  PCO2

Expected PaCO2 = (0.7× HCO3) + ( 21 ± 2 )
MAX PCO2 = 55-60 mmHg
32
 DIFFERENTIAL DIAGNOSIS OF
METABOLIC ALKALOSIS USING URINE Cl
Low Urine [Cl-]<20meq Normal Urine [Cl-]>20meq
Chloride Responsive Chloride Resistent
Vomiting Mineralocorticoidism
NG suction RAS, aldosteronism
11-bDH deficiencies
Diuretics (late)

Posthypercapnia Diuretics (early)

Bartter and Gitelman ds
Cystic fibrosis
Severe K+ depletion
Milk-Alkali Syndrome

33 Nehrology &
Hypertension LSUHSC
 CO2 HYPO VENTILATION

compensation
HIGH HCO3
pH

HIGH pH CHANGES
BICARB
pH in same direction

HIGH pCO2 (compensated)

HCO3

High Primary lesion

Alkali METABOLIC ALKALOSIS
 Metabolic Alkalosis: Treatment

• Saline responsive
– intravascular volume expansion with normal saline
– potassium repletion

• Saline resistant
– potassium repletion
– mineralocorticoid antagonists
– acetazolamide
 RESPIRATORY ACIDOSIS

• Respiratory acidosis is a disorder with high PCO2 caused by

reduced CO2 elimination (or hypoventilation).
• If unopposed, it will result in acidemia

• Criteria - pH<7.35; PaCO2>45mmHg

• Causes
 Impaired alveolar gas exchange
 Obstructive airway disease
 Disorders of the respiratory muscles and chest wall
 Inhibition of medullary respiratory center

36
 RESPIRATORY ACIDOSIS

[H+] = 24 x PCO2
[HCO3-]

Renal Compensation begins in 6 -12 hours and is fully developed in a

few days.

ACUTE RESPIRATORY ACIDOSIS : before renal compensation

begins
10 mmHg  PCO2  1 mEq/L  HCO3 [ MAX HCO3 = 30-32 mEq/L]
EXPECTED pH = 7.4 – [ 0.008 × ( PaCO2 - 40 )]

CHRONIC RESPIRATORY ACIDOSIS : after renal compensation is

fully developed
10 mmHg  PCO2  4 mEq/L  HCO3 [ MAX HCO3 = 45mEq/L] 37
 BICARB CO 2 CHANGES
pH in opposite direction

compensation
HIGH pCO2
pH

LOW pH

HIGH HCO3 (compensated)

CO 2

High Primary lesion

CO2 Respiratory acidosis
 RESPIRATORY ALKALOSIS
• Respiratory alkalosis is a disorder with low PCO2 caused by increased CO2
elimination (or hyperventilation).
• If unopposed, it will result in alkalemia
• Criteria – pH > 7.45; PaCO2< 35mmHg
• Causes
– Fear
– Pain
– Fever
– Early salicylate intoxication
– Hypoxemia
– Central nervous system tumors and stimulation of medullary respiratory
centers
– Mechanical ventilation
– Pregnancy

39
 Clinical Manifestations

– Lightheadedness
– Paresthesia
– Decreased concentration
– Tachycardia and other dysrhythmias
– Tetany

40
 RESPIRATORY ALKALOSIS

[H+] = 24 x PCO2
[HCO3-]

• ACUTE RESPIRATORY ALKALOSIS: before the renal

compensation begins
10 mmHg  PCO2  2 mEq/L  HCO3 MIN HCO3 = 18 mEq/L
EXPECTED pH = 7.4 + [ 0.008 × ( 40 - PaCO2)]

• CHRONIC RESPIRATORY ALKALOSIS: after the renal

compensation is fully developed
10 mmHg  PCO2  4 mEq/L  HCO3 MIN HCO3 = 12-15 mEq/L
EXPECTED pH = 7.4 + [ 0.003 × (40 -PaCO2 )]
Nephrology & Hypertension LSUHSC 41
 BICARB CO 2 CHANGES
pH in opposite direction

compensation
LOW pCO2
pH

HIGH pH

LOW HCO3 (compensated)

CO 2

Low Primary lesion

CO2 Respiratory alkalosis
Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit

Full compensation
Partial compensation
No compensation…. (uncompensated)

BUT never overshoots,

If a overshoot pH is there,
Take it granted it is a MIXED disorder
Time course of buffering, respiratory
Compensation/renal excretion of an acid load
H+
Load Distribution
and extra-
Cellular Cell
buffering buffering
100
Respiratory
Renal H+
compensation
secretion

50

0 6 12 24 72
Hours 45
Introduction to Procedures:
The Arterial Blood Gas
 Information Obtained from an ABG:

• Acid base status

• Oxygenation
– Dissolved O2 (pO2)
– Saturation of hemoglobin

• CO2 elimination

• Levels of carboxyhemoglobin and methemoglobin

 pH

PO2 HCO3

PCO2
 Indications:

• Assess the ventilatory status, oxygenation and acid base status

• Assess the response to an intervention
• An arterial line is established if there is a need of multiple ABGs.

Contraindications:

Bleeding diathesis
AV fistula
Severe peripheral vascular disease, absence of an arterial pulse
Infection over site
 SaO2 : ABG v/s Pulse oximetry

• ABG machine calculates O2 saturation based on pH, PaCO2,temp,by

using normal adult O2 dissociation curve
• O2 dissociation curve in presence of
1) fetal Hb ,low 2,3 DPG……curve shifts Left
2)sickle cell anaemia, chronic hypoxia, cyanotic Heart
disease chronic asthama, high altitude…. curve
shifts to the Right.
And ABG machine becomes inaccurate
 ABG v/s Pulse oximetry
Pulse oximetry uses light absorption at two wavelengths to determine
hemoglobin saturation
• Advantages: • Disadvantages:

 Noninvasive  Pulse oximetry does not assess

 Portability ventilation (pCO2) or acid base status.
 Continuous monitoring
 Ease of use (no calibration)  Pulse oximetry becomes unreliable
 Rapidity when saturations fall below 70-80%.

 Technical sources of error (ambient or

fluorescent light, hypoperfusion, nail
polish, skin pigmentation)

 Pulse oximetry cannot interpret

methemoglobin or carboxyhemoglobin.
 Sample collection

• Which Artery to Choose?

 The radial artery is superficial, has collaterals and is easily compressed. It
should almost always be the first choice.
 Other arteries brachial , ulnar, dorsalis pedis, femoral can also be used.
 When using radial/ulnar arteries, the patency should be confirmed using
modified allen’s test.
• Syringes which can be used:
 Glass-
 Impermeable to gases
 Expensive and impractical
 Plastic-
 Somewhat permeable to gases
 Disposable and inexpensive
 Sample Collection

Heparin

 Just 0.2 mL of sodium (lithium) heparin (1,000 IU/mL) added to 5 mL of

blood will give a final heparin concentration of 40 IU/mL blood, sufficient for
anticoagulation.

Problems with heparin:

 Dilutional effect if <2-3 ml of blood collected.

 Sodium (and lithium) heparin binding of calcium reduces the ionized calcium
concentration, the magnitude of the reduction being directly proportional to
the heparin concentration. Not seen with zinc heparin.
 Performing the Procedure:
• Put on gloves
• Prepare the site
– Drape the bed
– Cleanse the radial area with a alcohol
• Position the wrist (hyper-extended, using a rolled up towel if necessary)
• Palpate the arterial pulse and visualize the course of the artery.
• If you are going to use local anesthetic, infiltrate the skin with 2% xylocaine.
• Line the needle up with the artery, bevel side up.
• Enter the artery and allow the syringe to fill spontaneously.
• Withdraw the needle and hold pressure on the site.
• Protect needle
• Remove any air bubbles
• Gently mix the specimen by rolling it between your palms
• Place the specimen on ice and transport to lab immediately.
 The Arterial Blood Gas (ABG)

pH, pCO2, pO2 – Measured directly

HCO3-, O2 saturation (usually) – Calculated from pH,
pCO2, and pO2
----XXXX Diagnostics-----

Blood Gas Report

328 03:44 Feb 5 2006
Pt ID 3245 / 00

Measured 37.0 0C
pH 7.452 Measured values…
pCO2 45.1 mm Hg
pO2 112.3 mm Hg most important
Corrected 38.6 0C
pH 7.436
pCO2 47.6 mm Hg Temperature Correction :
pO2 122.4 mm Hg Is there any value to it ?
Calculated Data

HCO3 act 31.2 mmol / L

HCO3 std 30.5 mmol / L Calculated Data :
BE
BEecf
6.6
7.9
mmol / L
mmol / L
Which are useful one?
BB 26 mmol / L
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78

Entered Data Entered Data :

Temp 38.6 0C
FiO2 30.0 % Important
ct Hb 10.5 gm/dl

Electrolytes
Na
K
Cl
iCa
 Normal Arterial Blood Gas Values*

Parameter Normal value

• pH • 7.35-7.45
• H+
•
• 40nmol/L
PaCO2
• 35-45 mm Hg
• PaO2
•
• 70-100 mm Hg**
SaO2
• HCO3- • 93-98%
• %MetHb
•
• 22-26 mEq/L
%COHb Base excess
• CtO2 • <2.0%
• <3.0%
* At sea level, breathing ambient air
* Age-dependent • -2.0 to 2.0 mEq/L
ABG is incomplete without : Hb & FiO2 • 16-22 ml O2/dl
 The Key to Blood Gas Interpretation:
4 Equations, 3 Physiologic Processes
Equation Physiologic Process

1) PaCO2 equation Alveolar ventilation

2) Alveolar gas equation Oxygenation
3) Oxygen content equation Oxygenation
4) Henderson-Hasselbalch equation Acid-base balance
 Oxygenation
-----XXXX Diagnostics- ---- Parameters: /limitations
Blood Gas Report
328 03:44 Feb 5 2006
Pt ID 3245 / 00 O2 Content of blood:
Measured 37.0 0C (Hb x1.34x O2 Sat + 0.003x Dissolved O2 )
pH 7.452
pCO2 45.1 mm Hg Remember Hemoglobin
pO2 112.3 mm Hg

Corrected 38.6 0C
pH 7.436 Oxygen Saturation:
pCO2 47.6 mm Hg
pO2 122.4 mm Hg ( remember this is calculated …error prone)
Calculated Data

HCO3 act 31.2 mmol / L

Alveolar / arterial gradient:
HCO3 std
BE
30.5
6.6
mmol / L
mmol / L
( classify respiratory failure)
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L Arterial / alveolar ratio:
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78 Proposed to be less variable
Entered Data Same limitations as A-a gradient
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl
 How much oxygen is in the blood?
PaO2 vs. SaO2 vs. CtO2
OXYGEN PRESSURE: PaO2OXYGEN
• pO2 is the oxygen partial pressure (or tension) in a gas phase in equilibrium with the blood. High and low pO2
values of arterial blood indicate hyperoxemia and hypoxemia, respectively.
• pO2(a) is an indicator of the oxygen uptake in the lungs.
• pO2(a) reference range (adult): 83-108 mmHg. FiO2 × 5 = PaO2.

SATURATION: SaO2
• sO2 is called oxygen saturation and is defined as the ratio between the concentrations of O2Hb and HHb + O2Hb:

• sO2(a) normal range (adult): 95-99 % )

• sO2(a) is the percentage of oxygenated hemoglobin in relation to the amount of hemoglobin capable of carrying
oxygen.

OXYGEN CONTENT: CtO2

• ctO2 is the concentration of the total oxygen in the blood. ctO2 is the sum of the concentration of hemoglobin-
bound oxygen and the concentration of physically dissolved oxygen.
• CtO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
• The oxygen content of the blood is an expression of the oxygen transport status of the blood
• normal range: male: 8.4-9.9 mmol/L (18.8-22.3 mL/dL) female: 7.1-8.9 mmol/L (15.8-19.9 mL/dL)
 Alveolar Gas Equation

• PAO2 = PIO2 - 1.2 (PaCO2)*

where PAO2 is the average alveolar PO2,and PIO2 is the partial pressure of
inspired oxygen in the trachea.

• PIO2 = FIO2 (PB – 47 mm Hg)

FIO2 is fraction of inspired oxygen

PB is the barometric pressure
47 mm Hg is the water vapor pressure at normal body temperature.
 P(A-a)O2
• P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen.
• It is commonly called the “A-a gradient.”
• It results from gravity-related blood flow changes within the lungs (normal
ventilation-perfusion imbalance).
• PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure.
• PaO2 is always measured, on an arterial blood sample in a ‘blood gas
machine’.
• Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it
increases with age).
• A higher than normal P(A-a)O2 means the lungs are not transferring oxygen
properly from alveoli into the pulmonary capillaries.
• Helps in classification of respiratory failure into its 2 types. It is wide in type 1
and normal in type 2 respiratory failure.
 -----XXXX Diagnostics-----

Blood Gas Report

328 03:44 Feb 5 2006
Pt ID 3245 / 00

Measured 37.0 0C Bicarbonate is calculated on

pH 7.452
pCO2
pO2
45.1
112.3
mm Hg
mm Hg
the basis of the
Corrected 38.6 0C Henderson equation:
pH 7.436
pCO2 47.6 mm Hg
pO2 122.4 mm Hg
+ -
Calculated Data [H ] = 24 pCO2 / [HCO ]
3
HCO3 act 31.2 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78

Entered Data
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl
-----XXXX Diagnostics----- Standard Bicarbonate:
•Plasma HCO3 after equilibration
Blood
328
Gas
03:44
Report
Feb 5 2006
to a PCO2 of 40 mm Hg
Pt ID 3245 / 00 • reflects non-respiratory acid base
Measured
pH 7.452
37.0 0C change
pCO2 45.1 mm Hg Base Excess: Actual Base Excess :
pO2 112.3 mm Hg
- D base to normalise HCO3 (to 24) with PCO2
Corrected 38.6 C
0

pH 7.436 at 40 mm Hg. “Base excess” is the absolute

pCO2
pO2
47.6
122.4
mm Hg
mm Hg
deviation (in mmol/L) of the buffer base amount
from the normal level in blood.
Calculated Data
- reflects metabolic part of acid base D.
HCO3 act 31.2 mmol / L
HCO3 std 30.5 mmol / L
BE 6.6 mmol / L
BE ecf 7.9 mmol / L Base excess (Ecf): Standard BE: base excess in
BB 26 mmol / L the total extracellular fluids of which blood is
O2 ct 15.8 mL / dl
O2 Sat 98.4 % 1/3. It is an estimate more representative of in
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg  vivo base excess than is BE.
pO2 (a/A) 0.78

Entered Data BB :Buffer base : represents the blood’s total

Temp 38.6 0C
FiO2 30.0 % buffer capacity, comprising the bicarbonate,
ct Hb 10.5 gm/dl hemoglobin, plasma protein, and phosphate
buffer systems. The normal buffer base level is
48 ± 2 mmol/L.
7 steps to analyze ABG
1. Consider the clinical settings! Anticipate the disorder
2. Look at pH?
3. Who is the culprit ?...Metabolic / Respiratory
4. If respiratory…… acute and /or chronic
5. If metabolic acidosis,
Anion gap ↑ed and/or normal or both?
6. Is more than one disorder present?
7. Correlate clinically
Look at the pH
Is the patient acidemic pH < 7.35
or alkalemic pH > 7.45

If pH = 7.4 …… Normal
Mixed
or Fully compensated
HCO3…… METABOLIC
HCO3 = Base
> 26 ….. Met. Alkalosis Normal…22-26

< 22 ……Met. Acidosis

PCO2 ……RESPIRATORY CO2 = ACID

> 45 …… Resp. Acidosis Normal…35-45

< 35 …… Resp. Alkalosis

If there is a primary Respiratory disturbance,
is it acute ?

.08 change in pH ( Acute )

10 mm EXPECTED pH = 7.4 – [ 0.008 × ( PaCO2 - 40 )]
Change =.03 change in pH (Chronic)
PaCO2 EXPECTED pH = 7.4 – [0.003 × ( PaCO2 - 40)]

Remember………… relation of CO2 and pH

 pH

Acute change .08

Chronic change .03

 RESPIRATORY disorders…
Expected HCO3 for a Change in CO2 ......... 1 2 3 4

Acidosis…. (expected) HCO3 = 0.1 x ∆ CO2

Acute respiratory
Alkalosis…. (expected) HCO3 = 0.2 x ∆ CO2

Acidosis…. (expected) HCO3 = 0.35 x ∆ CO2

Chronic respiratory
Alkaosis…. (expected) HCO3 = 0.4 x ∆ CO2
If it is a primary Metabolic disturbance,
whether respiratory compensation appropriate?
For metabolic acidosis:

Remember If :
Expected PCO2 = (1.5 x [HCO3]) + 8 + 2
(Winter’s equation)

CO is equal to
Suspect .............
2
actual PaCO2 is more than expected
For metabolic alkalosis:
Last two digits
additional...respiratory acidosis
Expected PCO2 = 6 mm… for 10 mEq. rise in
actual PaCO2 is less than expected
Bicarb.
of pH
additional...respiratory
………UNCERTAIN COMPENSATION alkalosis
If metabolic acidosis is there
How is anion gap ? Is it wide ...
- -
Na - (Cl + HCO3 ) = Anion Gap usually <12

If >12, Anion Gap Acidosis : M ethanol

U remia
D iabetic Ketoacidosis
P araldehyde
I nfection
L actic acid
E thylene Glycol
S alicylate
Step 6…
-- Clinical history
-- pH normal, abnormal PCO2 n HCO3
-- PCO2 n HCO3 moving opposite directions
-- Degree of compensation for primary
disorder is inappropriate
-- Find Delta Gap
Equivalent rise of AG and Fall of HCO3……
….Pure Anion Gap Metabolic Acidosis
Discrepancy…….. in rise & fall
+ Non AG M acidosis, + M Alkalosis
Delta gap = HCO3 + ∆ AG
Delta Gap = 24….Pure AG acidosis
 < 24 = non AG acidosis (+ AG M Acidosis)
 > 24 = metabolic alkalosis (+ AG M Acidosis)
Let’s Practice
 Sample Problem # a

• 9 year old with h/o of asthma, audibly wheezing x 1

week, has not slept in 2 nights; presents sitting up and
using accessory muscles to breath with audible wheezes

• pH: 7.51
• pCO2: 25 mmHg
• pO2 35 mmHg
• HCO3: 22 mEq/L
• BE: -2 mEq/L
 Sample Problem # a

• pH is > 7.45 : alkalosis

• pCO2 <40 : primary respiratory disorder
• Compensation : HCO3 should decrease by 6 mEq/L ( =18 mEq/L)
• Acute:10 mmHg  PCO2  2 mEq/L  HCO3
• Chronic:10 mmHg  PCO2  4 mEq/L  HCO3

• Uncompensated respiratory alkalosis with severe hypoxia due to

asthma exacerbation
 Sample Problem # b

40 yo man admitted with RR of 30, Na+ 142,

K+ 3.6, Cl- 100, HCO3- 12, pH 7.28, pCO2 26
 Sample Problem # b

• pH is < 7.35 : Acidosis

• bicarbonate is low ( <24) : metabolic acidosis

• Anion Gap : [Na] – [Cl + HCO3 ]

142 – [ 100 + 12] = 30 : High anion gap met acidosis
• Is there compensation?
pCO2exp = [12 x 1.5] +8 + 2 = 26 + 2 : Yes, this is a simple disorder
.
• So this is a case of high anion gap metabolic acidosis with
appropriate respiratory compensation.
 Sample Problem # c

• An ill-appearing alcoholic male presents with nausea

and vomiting.
– ABG - 7.4 / 41 / 85 / 22
– Na- 137 / K- 3.8 / Cl- 90 / HCO3- 22
 Sample Problem # c

• pH is normal (7.4) and pCO2 (41) and HCO3 (22) moving in

opposite directions : Mixed Disorder
• Anion Gap = 137 - (90 + 22) = 25
 anion gap metabolic acidosis
• Winters Formula = 1.5(22) + 8  2
= 39  2
 compensated
• Delta Gap = 25 - 10 = 15
15 + 22 = 37
 metabolic alkalosis
 Sample Problem #1

• A 60 year old admitted with gluteal abscess ; known

diabetic.
ABG
pH 7.18
pCO2 18
HCO3 9
Na 138
K 4.1
Cl 110
AG 23.1
 Sample Problem # 2
• A 50 year old with chronic renal failure : Smoker.

ABG
pH 7.1
PaCO2 50
HCO3 15
Na 140
K 5
Cl 105
AG 23
 Sample Problem # 3

• A 35 year old, collapsed on physical exertion was brought to hospital.

ABG
pH 6.99
PaCO2 34
HCO3 8
Na 141
K 6
Cl 105
 Sample Problem # 4

• A 70 kg healthy male had acute airway obstruction

during induction of anaesthesia.

ABG
pH 7.1
PaCO2 70
HCO3 21
 Sample Problem # 5

• A 56 year old male patient, with COPD having resting

pCO2 of 70 sustains perioperative myocardial infarction,
BP is 80/60 mm Hg, is sweating, cool and clammy.

ABG
pH 7.1
PaCO2 70
HCO3 21
 Sample Problem # 6

• A 23 year old woman with rheumatoid arthritis increased her dose

of salicylates because of a flare-up. She then developed
epigastric pain and vomited frequently for 2 days. She went to the
local hospital, where the following blood results were obtained.

ABG
pH 7.70
H+ 20 nmol / L
PaCO2 25
AG 17 meq / L
 Sample Problem # 7

• Consider the following values in a patient who complains

of diarrhoea and vomiting.
ABG
Na 140
K 2.3
Cl 103
HCO3 25
H 40 nmol / L
PaCO2 40 mm Hg
AG 12 mEq / L
 Sample Problem # 8

• An insulin dependent diabetic patient with several days of

vomiting developed diabetic ketoacidosis. His ABG was :
pH 7.18
PaCO2 38
PaO2 70
HCO3 15
Na 140
K 5
Cl 90
 Sample Problem # 9

• A 17 year old 48 kg woman with known IDDM entered

the emergency with kussmaul breathing and an irregular
pulse. Room air ABG :
pH 7.05
PaCO2 12
PaO2 108
HCO3 5
BE - 30
 Sample Problem # 10

• A 66 year old woman with a history of COPD entered the

emergency in respiratory distress with pulmonary rales. A
presumptive diagonosis of pulmonary oedema was made.
Room air ABG :
pH 7.10
PaCO2 25
PaO2 40
HCO3 8
BE - 20
 Sample Problem # 11

• A 17 year old girl with severe kyphoscoliosis entered the

hospital with pneumonia.

ABG
pH 7.37
PaCO2 25
PaO2 70
HCO3 14
BE -7