Arterial blood gas analysis & interpretation egh nsg.forum-palestine.com

Arterial Blood GasArterial Blood Gas
Analysis & interpretationAnalysis & interpretation
Mohammed A. El-haj MPH
07/12/2011

What is an ABG?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?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

LogisticsLogistics
 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 BalanceAcid 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 BalanceAcid 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 valuesNormal values
Uncompensated
acidosis
pH
.7 35–.7 45
Uncompensated
alkalosis
Respiratory
alkalosis
CO2
35-45
Respiratory
acidosis
Metabolic
acidosis
HCO3
23-27
Metabolic
alkalosis

CompensationCompensation
7.4
7.35 7.45
Partial compensated Partial

Respiratory AcidosisRespiratory Acidosis
↓pH, ↑CO2,↓Ventilation
Causes
– CNS depression
– Pleural disease
– COPD/ARDS
– Musculoskeletal disorders
– Compensation for metabolic alkalosis

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 AlkalosisRespiratory 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

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 AcidosisMetabolic 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 Winter’s Formula
PCO2 = 1.5(HCO3) +8 ± 2

The CausesThe 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 AlkalosisMetabolic Alkalosis
 ↑pH, ↑HCO3
 ↑PCO2by 0.7 for every 1mEq/L ↑ in HCO3
 Causes
– Vomiting
– Chronic diarrhea
– Hypokalemia
– Renal Failure

Mixed Acid-Base DisordersMixed 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 analysisThe 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 problemSample 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)

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

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)

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)

pH 7.37
PCO2 33
HCO3 18
 Metabolic acidosis
 Fully compensated

pH 7.36
PCO2 62
HCO3 34
PO2 70
O2 sat. 90%
 Respiratory acidosis
 Fully compensated
 E.g. COPD

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

hypoxemiahypoxemia
Conditions causing V/Q (Ventilation
perfusion) miss match
1. Shunt: loss of alveolar surface area
2. Dead space
3. Diffusion defect

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

Danger a headDanger a head
( Hypoxemia causing fatigue and 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)
Respiratory
Alkalosis
Normal ABG Respiratory
Acidosis

Case 1Case 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 Chem : Na+
137
PCO2 60 K+
4.5
HCO3
-
26 Cl-
100
PO2 55 HCO3
-
25

Case 2Case 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.
135
PCO2 34 K+
5.1
HCO3
-
18 Cl-
110
PO2 92 HCO3
-
16
Cr 1.4
Urine pH: 5.0

Case 3Case 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.
133
PCO2 28 K+
3.9
HCO3
-
21 Cl-
102
PO2 52 HCO3
-
22

DefinitionsDefinitions
 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)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)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 OH-
concentration when added to water.
Strength of acids or bases refers to their ability to
donate and accept H+ ions respectively.

Importance of acid-base balanceImportance 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 CALCULATIONSACID-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)
7 100
7.1 80
7.2 63
7.3 50
7.36 44
7.4 40
7.44 36
7.5 32
7.6 25
7.7 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 pHRegulation of pH
• *Buffer systems - very rapid (seconds),
incomplete
• *Respiratory responses - rapid (minutes),
incomplete
• *Renal responses - slow (hours to days),
complete

BackgroundBackground
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 AcidPrimary Abnormality in Acid
Base DisordersBase Disorders
Acidosis Alkalosis
Respiratory ↑ pCO2
Metabolic
H+
+ H+
CO3
-
⇔ H2CO3 ⇔ H2O + CO2

Acidosis Alkalosis
Respiratory ↑ pCO2 ↓ pCO2
Metabolic
H+
+ H+
CO3
-
⇔ H2CO3 ⇔ H2O + CO2

Acidosis Alkalosis
Metabolic ↓ H+
CO3
-
H+
+ H+
CO3
-
⇔ H2CO3 ⇔ H2O + CO2

Acidosis Alkalosis
Metabolic ↓ H+
CO3
- ↑ H+
CO3
-
H+
+ H+
CO3
-
⇔ H2CO3 ⇔ H2O + CO2

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

Metabolic Acidosis
Metabolic Alkalosis ↑ ↑

Metabolic Acidosis
Metabolic Alkalosis ↑ ↑ ↑

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis ↓ ↑
Chronic Respiratory Acidosis ↓ ↑

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Acidosis ↓ ↑ ↑
Chronic Respiratory Acidosis ↓ ↑ ↑↑

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Alkalosis ↑ ↓
Chronic Respiratory Alkalosis ↑ ↓

Metabolic Acidosis
Metabolic Alkalosis
Acute Respiratory Alkalosis ↑ ↓ ↓
Chronic Respiratory Alkalosis ↑ ↓ ↓↓

Metabolic Acidosis ↓ ↓ ↓
Metabolic Alkalosis ↑ ↑ ↑
Acute Respiratory Acidosis ↓ ↑ ↑
Chronic Respiratory Acidosis ↓ ↑ ↑↑
Acute Respiratory Alkalosis ↑ ↓ ↓
Chronic Respiratory Alkalosis ↑ ↓ ↓↓

CompensationCompensation
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 AcidCompensated Abnormality in Acid
Acidosis Alkalosis
1° Respiratory
Compensation
↑ pCO2 ↓ pCO2
1° Metabolic
Compensation
↓ H+
CO3
-
↑ H+
CO3
-
↑ H+
CO3
-
↓ H+
CO3
-
↑ pCO2
↓ pCO2
H+
+ H+
CO3
-
⇔ H2CO3 ⇔ H2O + CO2

Compensation (Continued)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

*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)
33222 HCOHCOHCOOH +↔↔+ +

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
*¼ 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 HCO3-
filtration
 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 CompensationRenal & 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
Chronic
↑PaCO2 3.5 meq ↑ HCO3 per 10 mm
↑PaCO2
Respiratory alkalosis:
Acute
↓PaCO2 2 meq ↓HCO3 per 10mm ↓ PaCO2
Chronic

SUMMARY OF SIMPLE ACID-BASE DISORDERS ANDSUMMARY OF SIMPLE ACID-BASE DISORDERS AND
COMPENSATIONCOMPENSATION
Primary Acid-
Base Disorder
Primary
Defect
Effect
on
pH
Compensatory
Response
Expected Range of
Compensation
Limits of
Compensatio
n
Respiratory
Acidosis
Hypoventilati
on (↑PCO2)
↓ HCO3-
Generation
↑ [HCO3-] =
1-4 mEq/L for each 10
mm Hg ↑ PCO2
[HCO3-] =
45 mEq/L
Respiratory
Alkalosis
Hyperventilati
on (↓PCO2)
↑ HCO3-
Consumption
↓ [HCO3-] =
2-5 mEq/L for each 10
mm Hg ↓ PCO2
[HCO3-] =
12-15 mEq/L
Metabolic
Acidosis
Loss of
HCO3- or
gain of H+(↑
HCO3-)
↓ Increase in
Ventilation
(↓PCO2)
PCO2 =
1.5[HCO3-] + 8
PCO2 =
12-14 mm
Hg
Metabolic
Alkalosis
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 OFGENERAL ASPECTS OF
ACID-BASE DISORDERSACID-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 intra-
cellular 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 DIAGNOSEDATA REQUIRED TO DIAGNOSE
ACID-BASE DISORDERSACID-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 LABORATORYNORMAL LABORATORY
VALUESVALUES
Arterial Blood Gas:
pH 7.35-7.45
[H+] 35-45 nmol/L or neq/L
PCO2 35-45 mm Hg
[HCO3-] 22-26 mmol/L or mEq/L
Plasma Electrolytes
[Na+] 135-145 mEq/L
[K+ ] 3.5-5.0 mEq/L
[Cl-] 96-109 mEq/L
[total CO2] 24-30 mEq/L

SIMPLE ACID-BASE DISORDERSSIMPLE 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 AcidosisMetabolic 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 GapAnion 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 whichUnmeasured anions which
accumulateaccumulate 
Anion Gap AcidosisAnion Gap Acidosis
Lactate
Ketones
Sulfates and phosphates
Other organic acids

Lactic AcidosisLactic Acidosis
Fundamentally what causes a lactic
acidosis?
Answer: Anaerobic metabolism

The differential diagnosis ofThe differential diagnosis of
Lactic AcidosisLactic 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 Murphy’s law: “Whatever can go
wrong will go wrong!” (i.e. take each step
in oxygen absorption and distribution—any
one of them can go away and cause lactic
acidosis.)

The differential diagnosis ofThe differential diagnosis of
Lactic Acidosis (2)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

KetoAcidosisKetoAcidosis
Occurs whenever the cells are unable to
utilize glucose

KetoAcidosisKetoAcidosis
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
NonAnion Gap
Acidosis
Ketoacidosis
Uremic
Acidosis
Lactic
Acidosis
Organic
Acidosis
Lung Disease
CO poisening
Shock (cardiogenic)
Septic shock
Focal vascular
obstruction
Cyanide poisening
DKA (Type 1)
Starvation
Alcoholic

Other anion gap acidosisOther 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
NonAnion Gap
Acidosis
Ketoacidosis
Uremic
Acidosis
Lactic
Acidosis
Organic
Acidosis
Lung Disease
CO poisening
Shock (cardiogenic)
Septic shock
Focal vascular
obstruction
Cyanide poisening
DKA (Type 1)
Starvation
Alcoholic
Methanol
Ethylene Glycol
Salicylate
intoxication

Non-anion gap metabolicNon-anion gap metabolic
acidosisacidosis
↑ Bicarbonate loss
 Diarrhea
 Severe Burns
 Urinary loss (renal tubular acidosis)

Metabolic
Acidosis
Anion Gap
Acidosis
NonAnion Gap
Acidosis
Ketoacidosis
Uremic
Acidosis
Lactic
Acidosis
Organic
Acidosis
Lung Disease
CO poisening
Shock (cardiogenic)
Septic shock
Focal vascular
obstruction
Cyanide poisening
DKA (Type 1)
Starvation
Alcoholic
Methanol
Ethylene Glycol
Salicylate
intoxication
Diarrhea
Burns (severe)
RTA

Clinical ManifestationClinical Manifestation
 Headache
 Confusion
 Drowsiness
 ↑ RR and depth
 Nausea and vomiting
 Peripheral vasodilation and decreased Cardiac
output (pH ↓7 )
 ↓BP
 Hyperkalemias

Metabolic Acidosis: TreatmentMetabolic Acidosis: Treatment
Treat underlying cause
Alkali replacement
– Acute metabolic acidosis
 indicated when is pH less than ~7.15
 goal is to raise serum [HCO3] to ~15mmol/L
 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 [HCO3] should be normalized

Metabolic AlkalosisMetabolic Alkalosis
Generation
Maintenance

Metabolic Alkalosis:Metabolic Alkalosis:
GenerationGeneration
Acid loss
– renal acid losses
 diuretic therapy
 mineralocorticoid
excess
 Cushing’s syndrome
 severe potassium
depletion
 Bartter’s syndrome
 Liddle’s syndrome
– gastrointestinal
losses
 gastric acid loss
 chloride diarrhea

Metabolic Alkalosis:Metabolic Alkalosis:
GenerationGeneration
Alkali gain
– bicarbonate administration
– milk alkali syndrome
– infusion of organic anions
 citrate
 acetate
 lactate
– rapid correction of chronic hypercapnia

Metabolic Alkalosis: MaintenanceMetabolic Alkalosis: Maintenance
Decreased GFR
– renal failure
Increased proximal HCO3
-
reabsorption
– chloride depletion
Increased distal tubular H+
secretion
– hypokalemia

Metabolic Alkalosis: TreatmentMetabolic Alkalosis: Treatment
Saline responsive
– intravascular volume expansion with normal
saline
– potassium repletion
Saline resistant
– potassium repletion
– mineralocorticoid antagonists
– acetazolamide

Think “Murphy’s Law” again
From Brain to alveolus, many problems can
cause hypoventilation  ↑ PaCO2  ↓pH
(Respiratory acidosis)

 Brain
 Spinal Cord
 Peripheral Nerve
 NeuroMuscular Junction
 Lung and Pleural disease
 Stroke
 Drug Intoxication
 C spine injury,
 Guillan Barre
 Myasthenia Gravis
 Asthma, COPD,
ARDS, etc

Clinical ManifestationClinical Manifestation
 Hypercapnia
 ↑Pulse
 ↑RR
 ↑BP
 Mental cloudiness
 Feeling of fullness in the head
 ↑ICP
 Headache
 Hyperkalemia

Hyperventilation  ↓PaCO2  ↑ pH
Etiologies
– Fever
– Pain
– Anxiety
– Pulmonary disease
– Sepsis
– Salicylate intoxication
– Neurologic disorders

MIXED ACID-BASE DISORDERSMIXED ACID-BASE DISORDERS
Mixed acid-base disorders include all
combinations of 2-3 simple acid base
disorders.
One must be able to recognize mixed acid-
base 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 toSummary of the Approach to
ABGsABGs
1. Check the pH
2. Check the pCO2
3. Select the appropriate compensation formula
4. Determine if compensation is appropriate
5. Check the anion gap
6. If the anion gap is elevated, check the delta-delta
7. If a metabolic acidosis is present, check urine pH
8. Generate a differential diagnosis

Putting it TogetherPutting it Together

What is the clinical picture?
Generate hypothesis!
What is the pH?
Acidemia Alkalemia
Check HCO3- & PaCO2
Is it respiratory or metabolic?
Check: Is compensation appropriate?
Check Anion Gap
Reach Final Diagnosis
Step 1
Step 2
Step 3
Step 4
Step 5
Step 6

Case 1Case 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 Chem 7: Na+
137
PCO2 60 K+
4.5
HCO3
-
26 Cl-
100
PO2 55 HCO3
-
25

Case 2Case 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.
135
PCO2 34 K+
5.1
HCO3
-
18 Cl-
110
PO2 92 HCO3
-
16
Cr 1.4
Urine pH: 5.0

Case 3Case 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.
133
PCO2 28 K+
3.9
HCO3
-
21 Cl-
102
PO2 52 HCO3
-
22

pH7.34pH7.34, PaCO2 60 , HCO3- 31, 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
Acute
↑PaCO2 1 meq ↑ HCO3 per 10 mm ↑PaCO2
Chronic
↑PaCO2 3.5 meq ↑ HCO3 per 10 mm
↑PaCO2
Acute
Chronic

Case 1Case 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: AnswerCase 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 2Case 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? What’s with the urine sodium?
 Answer: Metabolic alkalosis. Correct with NaCL

Case 3Case 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 (continuedCase 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?

Who gets your last ICU bed?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

Arterial punctureArterial puncture

Problems of taking arterialProblems of taking arterial
blood samplesblood 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

‫لحسن‬ ‫را‬ً ‫شك‬
‫استماعكم‬

Arterial blood gas analysis & interpretation egh nsg.forum-palestine.com

Arterial blood gas analysis & interpretation egh nsg.forum-palestine.com

Recomendados

Recomendados

Más contenido relacionado

Último

Último (20)

Destacado

Destacado (20)

Arterial blood gas analysis & interpretation egh nsg.forum-palestine.com