Arterial Blood Gas

Analysis & interpretation

Mohammed A. El-haj MPH
07/12/2011

What is an ABG?
The

Components
pH / PaCO2 / PaO2 / HCO3 / O2sat / BE
Desired Ranges
pH - 7.35 - 7.45
PaCO2 - 35-45 mmHg
PaO2 - 80-100 mmHg
HCO3 - 21-27
O2sat - 95-100%
Base Excess - +/-2 mEq/L

Why Order an ABG?

Aids

in establishing a diagnosis
Helps guide treatment plan
Aids in ventilator management
Improvement in acid/base management
allows for optimal function of medications
Acid/base status may alter electrolyte levels
critical to patient status/care

Logistics
When

to order an arterial line - Need for continuous BP monitoring

Need for multiple ABGs
Where to place -- the options
Radial
Femoral
Brachial
Dorsalis Pedis
Axillary

Acid Base Balance

The

body produces acids daily

15,000 mmol CO2

50-100 mEq Nonvolatile acids

The

lungs and kidneys attempt to maintain

balance

Acid Base Balance

Assessment

of status via bicarbonate-carbon

dioxide buffer system
CO2 + H2O <--> H2CO3 <--> HCO3- + H+
pH = 6.10 + log ([HCO3] / [0.03 x PCO2])

Normal values
pH

Uncompensated
acidosis

7.45 7.35

Uncompensated
alkalosis

Respiratory
alkalosis

CO2
45 - 35

Respiratory
acidosis

Metabolic
acidosis

HCO3
27 - 23

Metabolic
alkalosis

Compensation
7.4

7.35
Partial

compensated

7.45
Partial

Respiratory Acidosis
pH,

CO2, Ventilation

Causes
CNS depression
Pleural disease
COPD/ARDS
Musculoskeletal disorders
Compensation for metabolic alkalosis

Respiratory Acidosis
Acute

vs Chronic

Acute - little kidney involvement. Buffering

via titration via Hb for example

pH by 0.08 for 10mmHg in CO2

Chronic - Renal compensation via synthesis

and retention of HCO3 (Cl to balance charges

hypochloremia)

pH by 0.03 for 10mmHg in CO2

Respiratory Alkalosis
pH,

CO2, Ventilation
CO2 HCO3 (Cl to balance charges
hyperchloremia)
Causes

Intracerebral hemorrhage
Salicylate and Progesterone drug usage
Anxiety lung compliance
Cirrhosis of the liver
Sepsis

Respiratory Alkalosis
Acute

vs. Chronic

Acute - HCO3 by 2 mEq/L for every 10mmHg

in PCO2
Chronic - Ratio increases to 4 mEq/L of HCO3
for every 10mmHg in PCO2
Decreased bicarb reabsorption and decreased

ammonium excretion to normalize pH

Metabolic Acidosis
pH,

HCO3
12-24 hours for complete activation of
respiratory compensation
PCO2 by 1.2mmHg for every 1 mEq/L
HCO3
The degree of compensation is assessed via
the Winters Formula
PCO2 = 1.5(HCO3) +8 2

The Causes
Metabolic Gap Acidosis

M - Methanol
U - Uremia
D - DKA
P - Paraldehyde
I - INH
L - Lactic Acidosis
E - Ehylene Glycol
S - Salicylate

Non Gap Metabolic Acidosis

Hyperalimentation
Acetazolamide
RTA (Calculate urine

anion gap)
Diarrhea
Pancreatic Fistula

Metabolic Alkalosis
pH,

HCO3

PCO2 by

0.7 for every 1mEq/L in HCO3

Causes
Vomiting
Chronic diarrhea
Hypokalemia
Renal Failure

Mixed Acid-Base Disorders

Patients

may have two or more acid-base

disorders at one time

Delta

Gap

Delta HCO3 = HCO3 + Change in anion gap

>24 = metabolic alkalosis

The six steps to ABGs

analysis
Look

at the pH if it is normal/acidotic/alkalotic
Look at the PaCO2 if it is normal/acidotic/alkalotic
Look at the HCO3 if it is normal/acidotic/alkalotic
If the pH match with the PCO2 or with the HCO3
If the value goes opposite direction of the pH
(determine the compensation).
Look at the Po2 and oxygen saturation

Sample problem
pH

7.49
PCO2 40
HCO3 28

Uncompensated metabolic alkalosis

Vomiting/dearrhea
In this example the Bicarb is
matching the pH
No compensation (Partial)

Sample problem
pH

7.10
PCO2 25
HCO3 7

Uncompensated metabolic acidosis

DKA/Dearrhea/shock/bleeding
/sepsis
In this example the Bicarb is
matching the pH
No compensation (Partial)
Severe metabolic acidosis

Sample problem
pH

7.42
PCO2 18
HCO3 11
PO2
150
O2 sat 99%

compensated respiratory alkalosis

This pt is hyperventilated for

too long (blowing off CO2)

Sample problem
pH

7.35
PCO2 60
HCO3 32
PO2
92
O2 sat 96%

No

need for correction

or treatment because
pH is normal
Compensation is
bringing the pH to the
side of 7.4 but doesn't
to the opposite side
(stop in 7.4)

Sample problem
pH

7.37
PCO2 33
HCO3 18

Metabolic

acidosis
Fully compensated

Sample problem
pH

7.36
PCO2 62
HCO3 34
PO2
70
O2 sat. 90%

Respiratory

acidosis
Fully compensated
E.g. COPD

Respiratory Alkalosis
Most

common causes of respiratory

alkalosis are:
1. Hypoxemia ( PaO2< 60mmHg and O2 sat.

<90% ). A low PO2 drives increased breathing

in spite of CO2 levels.
2. Anxiety
3. Pain

hypoxemia
Conditions

causing V/Q (Ventilation

perfusion) miss match
1. Shunt: loss of alveolar surface area
2. Dead space
3. Diffusion defect

Danger a head
Hypoxemia
Respiratory
alkalosis
Increased
W.O.B
Muscle
fatigue
Respiratory
Acidosis

Danger a head
( Hypoxemia causing fatigue and respiratory
acidosis)
Respiratory
Alkalosis

Normal ABG

Respiratory
Acidosis

In the path from respiratory alkalosis to

respiratory acidosis, the acid/base will
temporarily appear normal, however the Ve
(minute ventilation) will be increased (and
probably the W.O.B)

Case 1
A 26 year old man with unknown past medical history is brought in to the
ER by ambulance, after friends found him unresponsive in his apartment.
He had last been seen at a party four hours prior.
ABG:

pH
7.25
PCO2 60

Na+
K+

137
4.5

HCO3- 26

Cl-

100

PO2

HCO3-

25

55

Chem :

Case 2
A 67 year old man with diabetes and early diabetic nephropathy (without
overt renal failure) presents for a routine clinic visit. He is currently
asymptomatic. Because of some abnormalities on his routine blood
chemistries, you elect to send him for an ABG.
ABG:

Urine pH:

pH
7.35
PCO2 34
HCO3- 18
PO2 92

5.0

Chem :

Na+
K+
ClHCO3Cr

135
5.1
110
16
1.4

Case 3
A 68 year old woman with metastatic colon cancer presents to
the ER with 1 hour of chest pain and shortness of breath. She
has no known previous cardiac or pulmonary problems.
ABG:

pH
PCO2
HCO3PO2

7.49
28
21
52

Chem :

Na+
133
K+
3.9
Cl102
HCO3- 22

Definitions
Acidemia:

Blood pH < 7.35

Alkalemia: Blood pH > 7.45
Acidosis:is a process that will result in acidemia if left
unopposed.
Alkalosis:is a process that will result in alkalemia if left
unopposed
Metabolic refers to a disorder that results from a primary
alteration in [H+] or [HCO3-].
Respiratory refers to a disorder that results from a primary
alteration in PCO2 due to altered CO2 elimination.
Normal HCO3- 24 meq/L; Normal PCO2 40 mm Hg ;
Normal pH 7.35-7.45

Definitions (Continued)
PH: - is a negative logarithm of Hydrogen
ion concentration; and it is the initials of
these two wards (puiessence Hydrogen)
that mean the power of hydrogen

Definitions (Continued)
An acid: - is a hydrogen ion or proton donor, and a
substance which causes a rise in H+
concentration on being added to water.
A base: - is a hydrogen ion or proton acceptor, and
a substance which causes a rise in OHconcentration when added to water.
Strength of acids or bases refers to their ability to
donate and accept H+ ions respectively.

Importance of acid-base balance

The hydrogen ion (H+)concentration must

be precisely maintained within a narrow
physiological range

Small changes from normal can produce

marked changes in enzyme activity &
chemical reactions within the body

 Acidosis

- CNS depression, coma (pH ~

6.9)
Alkalosis - CNS excitability, tetany,
siezures
Hydrogen ion concentration is most
commonly expressed as pH (= negative
logarithm of the H+ concentration)

ACID-BASE CALCULATIONS
The

Henderson equation is easier to use, but

only applies when pH is between 7.2 and
7.6. For this equation, one must calculate
[H+] from pH. [H+] = 40 nEq/L when pH is
7.4. The [H+] increases 10 nEq/L for a 0.1
unit drop in pH.
Henderson Eq.
[H+] = 24 PCO2 / [HCO3-]

ph

H+ (nmol/l)

7
7.1
7.2
7.3
7.36
7.4
7.44
7.5
7.6
7.7

100
80
63
50
44
40
36
32
25
20

Normal pH:
Arterial

blood: 7.35 - 7.45

Venous blood, interstitial fluid: 7.35
Intracellular: 6.0-7.4 (average 7.0)

Regulation of pH

*Buffer systems - very rapid (seconds),

incomplete
*Respiratory responses - rapid (minutes),
incomplete
*Renal responses - slow (hours to days),
complete

Background
H+ + H+CO3- H2CO3 H2O + CO2
-Metabolic Disorders:
Affect HCO3-: (Normal 22-26 meq/L)

-Metabolic Acidosis

Acid neutralizes HCO3- H+CO3-, pH

-Metabolic Alkalosis

H+CO3- Production Drives Rxn to Right

H+ pH

Primary Abnormality in Acid

Base Disorders
Acidosis
Respiratory

Alkalosis

pCO2

Metabolic

H+ + H+CO3- H2CO3 H2O + CO2

Primary Abnormality in Acid

Base Disorders
Respiratory

Acidosis

Alkalosis

pCO2

pCO2

Metabolic

H+ + H+CO3- H2CO3 H2O + CO2

Primary Abnormality in Acid

Base Disorders
Respiratory
Metabolic

Acidosis

Alkalosis

pCO2

pCO2

H+CO3-

H+ + H+CO3- H2CO3 H2O + CO2

Primary Abnormality in Acid

Base Disorders
Respiratory
Metabolic

Acidosis

Alkalosis

pCO2

pCO2

H CO
+

H+CO3-

H+ + H+CO3- H2CO3 H2O + CO2

Simple Acid-Base Disorders:

Type of Disorder
Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis
Chronic Respiratory Acidosis
Acute Respiratory Alkalosis
Chronic Respiratory Alkalosis

pH PaCO2 [HCO3]

Simple Acid-Base Disorders:

Type of Disorder

pH PaCO2 [HCO3]

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis
Chronic Respiratory Acidosis
Acute Respiratory Alkalosis
Chronic Respiratory Alkalosis

Simple Acid-Base Disorders:

Type of Disorder

pH PaCO2 [HCO3]

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis
Chronic Respiratory Acidosis
Acute Respiratory Alkalosis
Chronic Respiratory Alkalosis

Simple Acid-Base Disorders:

Type of Disorder

pH PaCO2 [HCO3]

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis

Chronic Respiratory Acidosis

Acute Respiratory Alkalosis

Chronic Respiratory Alkalosis

Simple Acid-Base Disorders:

Type of Disorder

pH PaCO2 [HCO3]

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis

Chronic Respiratory Acidosis

Acute Respiratory Alkalosis

Chronic Respiratory Alkalosis

Simple Acid-Base Disorders:

Type of Disorder

pH PaCO2 [HCO3]

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis
Chronic Respiratory Acidosis
Acute Respiratory Alkalosis

Chronic Respiratory Alkalosis

Simple Acid-Base Disorders:

Type of Disorder

pH PaCO2 [HCO3]

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis
Chronic Respiratory Acidosis
Acute Respiratory Alkalosis

Chronic Respiratory Alkalosis

Simple Acid-Base Disorders:

Type of Disorder

pH PaCO2 [HCO3]

Metabolic Acidosis

Metabolic Alkalosis

Acute Respiratory Acidosis

Chronic Respiratory Acidosis

Acute Respiratory Alkalosis

Chronic Respiratory Alkalosis

Compensation
For

each acid-base disorder , there is a

compensatory response mediated by the
kidneys or the lungs that tends to bring the
pH back towards normal.
Compensation is never complete (i.e. pH
never returns to 7.4). Therefore if the pH <
7.4, the primary process is an acidosis. If the
pH > 7.4 the primary process is an alkalosis

Compensated Abnormality in Acid

Base Disorders

1 Respiratory
Compensation

Acidosis

Alkalosis

pCO2

pCO2

H+CO3-

1 Metabolic

H+CO3-

Compensation

pCO2

H+CO3 H+CO3-

pCO2
H+ + H+CO3- H2CO3 H2O + CO2

Compensation (Continued)
Formulas

predict normal compensation in

both acute and chronic conditions.
Inadequate compensation tells you that
something else is wrong!
Metabolic compensation takes time and is
more complete in chronic conditions than
acutely

Buffer Systems
A substance

that can prevent major

changes in the pH of body fluids by
removed or releasing hydrogen ions
,they can act quickly to prevent
excessive changes in hydrogen ion
concentration
Bicarbonate, phosphate and protein
buffering systems are the three major
buffering systems

Bicarbonate buffer system

*Primary extracellular buffer system (>50% of
extracellular buffering)
*Accurate assessment - readily calculated from
PCO2 and pH using available blood gas
machines
*Consists of carbonic acid (weak acid) and
bicarbonate


H
O

C
O

H
C
O

H
H
C
O
2223
3

*CO2 regulated by the lungs - rapidly

*HCO3- is regulated by the kidneys slowly
*Not powerful
*pKa = 6.1)the pK of a buffer system identifies the pH at
which the concentration of acid and base in that system is
equal)

Protein buffer system

*Most powerful
*75 % of all intracellular buffering
*Hemoglobin
-important extracellular buffer due to large
concentration of hemoglobin in blood
-buffering capacity varies with oxygenation
-reduced hemoglobin is a weaker acid than
oxyhemoglobin
-dissociation of oxyhemoglobin results in more base
available to combine w/ H+

Plasma protein
*acid buffer

*important intracellular buffer system

Phosphate buffer system

*H2PO4- and HPO42*important renal buffering system
*extracellular concentration, 1/12 that of
bicarbonate
*pKa = 6.8

*phosphate is concentrated in the renal

tubules

Respiratory Responses

occurs within minutes of alteration in pH due to

stimulation/depression of respiratory centers in the CNS
H+ acts directly on respiratory center in Medulla
Oblongata
alveolar ventilation increases/decreases in response to
changes in CO2
alveolar ventilation is inversely proportional to PaCO2
*2 x ventilation pH 7.4 to 7.63
* ventilation pH 7.4 to 7.0

incomplete response because as the change in alveolar

ventilation brings pH back towards normal, the stimulus
responsible for the change in ventilation decreases .

Renal Responses
the

kidneys regulate pH by either acidification or

alkalinization of the urine
complex response that occurs primarily in the
proximal renal tubules
with acidosis, rate of H+ secretion exceeds HCO3filtration
with alkalosis, rate of HCO3- filtration exceeds
H+ secretion
occurs over hours/days, and is capable of nearly
complete restoration of acid/base balance

Renal & Respiratory Compensation

Primary Disorder

Primary
change

Predicted Compensatory
Response

Metabolic acidosis

HCO3

1.2 PaCO2 per 1 meg HCO3

Metabolic Alkalosis

HCO3

.7 PaCO2 per 1meq HCO3

Respiratory acidosis:
Acute

PaCO2

1 meq HCO3 per 10 mm PaCO2

Respiratory acidosis:
Chronic

PaCO2

3.5 meq HCO3 per 10 mm

PaCO2
2 meq HCO3 per 10mm PaCO2

Respiratory alkalosis: PaCO2

Acute
Respiratory alkalosis: PaCO2
Chronic

4 meq HCO3 per 10mm PaCO2

SUMMARY OF SIMPLE ACID-BASE DISORDERS AND

COMPENSATION
Primary AcidBase Disorder
Respiratory
Acidosis

Primary
Defect

Effect
on
pH

Hypoventilati
on (PCO2)

Compensatory Expected Range of

Response
Compensation
HCO3Generation

Limits of
Compensatio
n

[HCO3-] =

[HCO3-] =
1-4 mEq/L for each 10 45 mEq/L
mm Hg PCO2

Respiratory
Alkalosis

Hyperventilati
on (PCO2)

HCO3Consumption

[HCO3-] =
2-5 mEq/L for each 10 12-15 mEq/L
[HCO3-] =

mm Hg PCO2
Metabolic
Acidosis
Metabolic
Alkalosis

Loss of
HCO3- or
gain of H+(
HCO3-)

Increase in
Ventilation
(PCO2)

PCO2 =
1.5[HCO3-] + 8

PCO2 =
12-14 mm
Hg

Gain of
HCO3- or loss
of H+
( HCO3-)

Decrease in
Ventilation
(PCO2 (

PCO2 =
0.6 mm Hg for each 1
mEq/L [HCO3-]

PCO2 =
55 mm Hg

GENERAL ASPECTS OF
ACID-BASE DISORDERS
A primary alteration in [H+], [HCO3-] or PCO2 results in
abnormal pH.
The body has several mechanisms to correct pH towards
the normal range.
-In the acute phase (minutes to hours), the extra- and intracellular buffer systems (most importantly the bicarbonate
system) minimize the pH changes.
- In the chronic phase (hours to days), renal or respiratory
compensation partially or completely restore pH towards
normal.
There are limits to both types of compensation.
Compensation does not result in over correction of pH.

DATA REQUIRED TO DIAGNOSE

ACID-BASE DISORDERS
An

arterial blood gas shows the blood pH, PCO2

and [HCO3-].
A chemistry panel shows the [total CO2], [Cl-],
[K+] and [Na+], [glucose], [BUN] and
[creatinine].
The [total CO2] is the sum of the measured [CO2]
+ [HCO3-]. Thus the [HCO3-] from the blood gas
and the [total CO2] from the electrolyte panel
usually are within 2 mEq/L. Otherwise the
measurements are in error or were taken at
different times.

NORMAL LABORATORY
VALUES
Arterial Blood Gas:
pH
[H+]
PCO2
[HCO3-]
Plasma Electrolytes
[Na+]
[K+ ]
[Cl-]
[total CO2]

7.35-7.45
35-45 nmol/L or neq/L
35-45 mm Hg
22-26 mmol/L or mEq/L
135-145 mEq/L
3.5-5.0 mEq/L
96-109 mEq/L
24-30 mEq/L

SIMPLE ACID-BASE DISORDERS

Simple

acid-base disorders have one primary

abnormality.
The four primary disorders are respiratory
acidosis, respiratory alkalosis, metabolic acidosis
and metabolic alkalosis.
Mixed acid-base disorders have more than one
abnormality. Two to three primary disorders can
be combined together to result in a mixed disorder.

Metabolic Acidosis
Secondary

to

Acid production or
H+CO3- loss
Characterized

by low serum H+CO3( by hyperventilation PCO2 HCO3- )

Divided into two categories:
Anion gap metabolic acidosis (High anion gap)
NonAnion gap metabolic acidosis (Normal anion
gap)

Anion Gap
The

anion gap (AG) represents the

difference between the major plasma
cations and anions ,and reflects usually
unmeasured anions such as sulfate.
Anion Gap = [Na+] - ( [H+CO3-] + [Cl-] )
Normal

14 +/- 2

 Why

does this help us in patients with metabolic

acidosis?
Secondary to

Acid production or
H+CO3- loss

In disorders associated with acid production there

anions accumulate anion gap whereas

In disorders associated with H+CO3- loss, there is no
accumulation of unmeasured anions and the anion gap
is normal

Unmeasured anions which

accumulate
Anion Gap Acidosis
Lactate
Ketones
Sulfates

and phosphates
Other organic acids

Lactic Acidosis
Fundamentally

what causes a lactic

acidosis?
Answer: Anaerobic metabolism

The differential diagnosis of

Lactic Acidosis
Lactic

acidosis occurs whenever the cells

are unable to utilize aerobic respiration: i.e.
whenever the cells are unable to obtain or
utilize oxygen
Consider Murphys law: Whatever can go
wrong will go wrong! (i.e. take each step
in oxygen absorption and distributionany
one of them can go away and cause lactic
acidosis.)

The differential diagnosis of

Lactic Acidosis (2)
Low

environmental O2
Inability to absorb O2
O2 unable to bind Hg
Unable to pump O2
Tissues unable to utilize
O2

High

altitude
Lung Disease
CO poisoning
Shock (cardiogenic)
Septic shock
Focal vascular obstruction
Cyanide poisoning

KetoAcidosis
Occurs

whenever the cells are unable to

utilize glucose

KetoAcidosis
Three

etiologies

Diabetic Ketoacidosis
Primarily in type 1 diabetes mellitus
Severe, life threatening
Often associated with precipitating illness
Starvation ketoacidosis
Mild acidosis
Alcoholic ketoacidosis
Mild acidosis

Metabolic
Acidosis

Anion Gap
Acidosis
Lactic
Acidosis
Lung Disease
CO poisening
Shock (cardiogenic)
Septic shock
Focal vascular
obstruction
Cyanide poisening

Ketoacidosis

DKA (Type 1)
Starvation
Alcoholic

NonAnion Gap
Acidosis
Uremic
Acidosis

Organic
Acidosis

Other anion gap acidosis

Uremia
Failure to excrete daily metabolic acid load
Accumulation of phosphates and sulfates

Organic

acidosis

Methanol
Ethylene Glycol
Salicylates

Metabolic
Acidosis

Anion Gap
Acidosis
Lactic
Acidosis
Lung Disease
CO poisening
Shock (cardiogenic)
Septic shock
Focal vascular
obstruction
Cyanide poisening

Ketoacidosis

DKA (Type 1)
Starvation
Alcoholic

NonAnion Gap
Acidosis
Uremic
Acidosis

Organic
Acidosis
Methanol
Ethylene Glycol
Salicylate
intoxication

Non-anion gap metabolic

acidosis

Bicarbonate loss
Diarrhea
Severe Burns
Urinary loss (renal tubular acidosis)

Metabolic
Acidosis
Anion Gap
Acidosis

NonAnion Gap
Acidosis
Diarrhea
Burns (severe)
RTA

Lactic
Acidosis
Lung Disease
CO poisening
Shock (cardiogenic)
Septic shock
Focal vascular
obstruction
Cyanide poisening

Ketoacidosis

DKA (Type 1)
Starvation
Alcoholic

Uremic
Acidosis

Organic
Acidosis
Methanol
Ethylene Glycol
Salicylate
intoxication

Clinical Manifestation
Headache
Confusion
Drowsiness

RR and depth
Nausea and vomiting
Peripheral vasodilation and decreased Cardiac
output (pH 7 )
BP
Hyperkalemias

Metabolic Acidosis: Treatment

Treat underlying cause
Alkali replacement
Acute metabolic acidosis
indicated when is pH less than ~7.15
goal is to raise serum [HCO ] to ~15mmol/L
3
bicarbonate dose =
0.5 x BW (kg) x{[HCO3]desired - [HCO3]actual}

Chronic metabolic acidosis

goal of treatment is to prevent long term sequelae
serum [HCO ] should be normalized
3

Metabolic Alkalosis
Generation
Maintenance

Metabolic Alkalosis:
Generation
Acid

loss

renal acid losses

diuretic therapy
mineralocorticoid
excess
Cushings syndrome
severe potassium
depletion
Bartters syndrome
Liddles syndrome

gastrointestinal

losses
gastric acid loss
chloride diarrhea

Metabolic Alkalosis:
Generation
Alkali

gain

bicarbonate administration
milk alkali syndrome
infusion of organic anions
citrate
acetate
lactate
rapid correction of chronic hypercapnia

Metabolic Alkalosis: Maintenance

Decreased

GFR

renal failure

Increased

proximal HCO3- reabsorption

chloride depletion

Increased

distal tubular H+ secretion

hypokalemia

Metabolic Alkalosis: Treatment

Saline

responsive

intravascular volume expansion with normal

saline
potassium repletion
Saline

resistant

potassium repletion
mineralocorticoid antagonists
acetazolamide

Respiratory Acidosis
Think

Murphys Law again

From Brain to alveolus, many problems can
cause hypoventilation PaCO2 pH
(Respiratory acidosis)

Respiratory Acidosis
Brain

Stroke
Drug

Spinal

Cord

Peripheral

Nerve
NeuroMuscular Junction
Lung and Pleural disease

Intoxication
C spine injury,
Guillan

Barre
Myasthenia Gravis
Asthma, COPD,
ARDS, etc

Clinical Manifestation
Hypercapnia
Pulse

RR
BP
Mental cloudiness
Feeling of fullness in the head
ICP
Headache
Hyperkalemia

Respiratory Alkalosis
Hyperventilation

PaCO2 pH

Etiologies
Fever
Pain
Anxiety
Pulmonary disease
Sepsis
Salicylate intoxication
Neurologic disorders

MIXED ACID-BASE DISORDERS

Mixed

acid-base disorders include all

combinations of 2-3 simple acid base
disorders.
One must be able to recognize mixed acidbase disorders. This can be accomplished
by examining the degree of compensation
and calculating an anion gap.
If the pH, PCO2 and [HCO3-] do not fit the
rules of compensation for a simple disorder,
one must hypothesize that there is a mixed
acid-base disorder (or hypothesize that there
is an error in the data).

 If

there is extreme acidemia or alkalemia,

one could hypothesize multiple acid-base
disorders that that are additive.
If there is a mild acidemia or alkalemia, or
pH is normal, particularly with an anion gap
one could hypothesize multiple acid-base
disorders that cancel each other out.

Summary of the Approach to

ABGs
1.
2.
3.
4.
5.
6.
7.
8.

Check the pH
Check the pCO2
Select the appropriate compensation formula
Determine if compensation is appropriate
Check the anion gap
If the anion gap is elevated, check the delta-delta
If a metabolic acidosis is present, check urine pH
Generate a differential diagnosis

Putting it Together

Step 1

What is the clinical picture?

Generate hypothesis!

Step 2

What is the pH?

Acidemia

Alkalemia

Step 3

Check HCO3- & PaCO2

Is it respiratory or metabolic?

Step 4

Check: Is compensation appropriate?

Step 5

Check Anion Gap

Step 6

Reach Final Diagnosis

Case 1
A 26 year old man with unknown past medical history is
brought in to the ER by ambulance, after friends found him
unresponsive in his apartment. He had last been seen at a
party four hours prior.
ABG: pH
PCO2
HCO3PO2

7.25
60
26
55

Chem 7:

Na+
K+
Cl-

137
4.5
100

HCO3- 25

Case 2
A 67 year old man with diabetes and early diabetic
nephropathy (without overt renal failure) presents for a
routine clinic visit. He is currently asymptomatic. Because
of some abnormalities on his routine blood chemistries, you
elect to send him for an ABG.
ABG: pH
PCO2
HCO3PO2
Urine pH:

5.0

7.35
34
18
92

Chem 7:

Na+
K+
ClHCO3Cr

135
5.1
110
16
1.4

Case 3
A 68 year old woman with metastatic colon cancer presents
to the ER with 1 hour of chest pain and shortness of breath.
She has no known previous cardiac or pulmonary problems.
ABG: pH
PCO2
HCO3PO2

7.49
28
21
52

Chem 7:

Na+
K+
ClHCO3-

133
3.9
102
22

pH7.34, PaCO2 60 , HCO3- 31

Primary Disorder

Primary
change

Predicted Compensatory
Response

Metabolic acidosis

HCO3

1.2 PaCO2 per 1 meg HCO3

Metabolic Alkalosis

HCO3

.7 PaCO2 per 1meq HCO3

Respiratory acidosis:
Acute

PaCO2

1 meq HCO3 per 10 mm PaCO2

Respiratory acidosis:
Chronic

PaCO2

3.5 meq HCO3 per 10 mm

PaCO2
2 meq HCO3 per 10mm PaCO2

Respiratory alkalosis: PaCO2

Acute
Respiratory alkalosis: PaCO2
Chronic

4 meq HCO3 per 10mm PaCO2

Case 1
A 52

y.o. man with COPD is admitted to the hospital

with a lower extremity cellulitis.
Hypothesis
Labs: Na+ 139, K+ 4.9, Cl- 98, HCO3- 31
ABG: pH 7.34, PaCO2 60, PaO2 69
Is he acidemic or alkalemic?
Is this metabolic (from sepsis) or respiratory (from
COPD)?
Is this acute or chronic? Why does that matter?

Case 1: Answer
A 52

y.o. man with COPD is admitted to the hospital

with a lower extremity cellulitis.
Labs: Na+ 139, K+ 4.9, Cl- 98, HCO3- 31
ABG: pH 7.34, PaCO2 60, PaO2 69
Why is he acidemic?
Is this metabolic (from sepsis) or respiratory (from
COPD)?
Is this acute or chronic? Why does that matter?
Dx: Chronic Respiratory Acidosis
Not from sepsis
No need for intubation or ICU care
Note AG 10

Case 2

A 45 y.o. man reports 6 days of persistent nausea and vomiting.

PE supine BP 100/60 pulse 105; Standing BP 85/55 pulse 125.
Neck veins are flat
Hypotheses?
Labs:
Na+ 140, K+ 2.2, Cl- 86, HCO3 42 BUN 80, Cr 1.9
ABG: pH 7.53, PaCO2 53, PaO2 82
Urine Na+ 2 meg/L

Acidemic or Alkalemic?
Metabolic or Respiratory?
What is his acid base disorder?
Why is he alkalemic?
How would you fix it? Whats with the urine sodium?
Answer: Metabolic alkalosis. Correct with NaCL

Case 3
79

y.o. woman with CC of abdominal pain

Patient c/o abdominal pain for 2 days. Pain is
moderately severe & diffuse, associated with
vomiting. She reports passing no bowel
movements or flatus for 2 days.
PE: Elderly appearing woman in moderate
distress; Vital signs T 38.5, RR 20, BP 115/60,
HR 95. Abdominal exam: absent bowel sounds,
diffusely distended, mild tenderness, without
rebound or guarding. Rectal FOBT negative

Case 3 (continued)
Labs:
WBC 18K, 82% neutrophils, 10% bands
HCT 37
Na 138, K 4.2 HCO3- 6 CL 106 BUN 45 Cr. 1.0

Glucose 110
ABG: pH 7.10, PaCO2 20mm Hg, PaO2 90
What

is her acid base disorder?

What does it tell you?

Metabolic
Acidosis
Anion Gap
Acidosis

NonAnion Gap
Acidosis
Diarrhea
Burns (severe)
RTA

Lactic
Acidosis
Lung Disease
CO poisening
Shock (cardiogenic)
Septic shock
Focal vascular
obstruction
Cyanide poisening

Ketoacidosis

DKA (Type 1)
Starvation
Alcoholic

Uremic
Acidosis

Organic
Acidosis
Methanol
Ethylene Glycol
Salicylate
intoxication

Who gets your last ICU bed?

75 y.o. WF with COPD with CC cough & SOB
R.A. ABG 7.35, PaC02 60, Pa02 48.
70 y.o. WM with COPD with CC purulent sputum,
SOB.

ABG on 4L 7.2, PaC02 60, Pa02 of 70

Step 1

What is the clinical picture?

Generate hypothesis!

Step 2

What is the pH?

Acidemia

Alkalemia

Step 3

Check HCO3- & PaCO2

Is it respiratory or metabolic?

Step 4

Check: Is compensation appropriate?

Step 5

Check Anion Gap

Step 6

Reach Final Diagnosis

Arterial puncture

Problems of taking arterial

blood samples
Bleeding
Vessel

obstruction
Infection

 Allen's

test. The radial and ulnar arteries are

occluded by firm pressure while the fist is
clenched. The hand is opened and the
arteries released one at a time to check their
ability to return blood flow to the hand