ACID BASE BALANCE & ARTERIAL BLOOD GAS ANALYSIS

ARTERIAL BLOOD GAS ANALYSIS
Life is a struggle, not against sin, not against Money
Power . . But against hydrogen ions.
--H.L. Mencken
PRESENTOR:DR.ABHINAV KUMAR
MODERATOR: DR.PRASANNA KUMAR

OVERVIEW
• Physiology of acid base status
• Types of acid base disturbances
• Treatment
• Interpretation of ABG

BASIC TERMINOLOGY
• pH: measures the degree of acidity. It is negative
logarithm of hydrogen ion concentration
• Normal systemic arterial pH is between 7.35 and
7.45
• Acid : is defined as compound which dissociates to
form hydrogen ion in solution
• Base : A compound that combines with hydrogen
ion in solutions

ACIDS
• Acids can be defined as a proton (H+) donor
• Hydrogen containing substances which
dissociate in solution to release H+
4
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ACIDS
5
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ACIDS
6

ACIDS
• Physiologically important acids include:
• Carbonic acid (H2CO3)
• Phosphoric acid (H3PO4)
• Pyruvic acid (C3H4O3)
• Lactic acid (C3H6O3)
• These acids are dissolved in body fluids
7
Lactic acid
Pyruvic acid
Phosphoric acid

BASES
• Bases can be defined as:
• A proton (H+) acceptor
• Molecules capable of accepting a hydrogen ion
(OH-)
8
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BASES
(OH-)
9
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BASES
(OH-)
10

BASES
• Physiologically important bases include:
• Bicarbonate (HCO3
- )
• Biphosphate (HPO4
-2 )
11
Biphosphate

pH SCALE
• Pure water is Neutral
• ( H+ = OH- )
• pH = 7
• Acid
• ( H+ > OH- )
• pH < 7
• Base
• ( H+ < OH- )
• pH > 7
• Normal blood pH is 7.35 - 7.45
• pH range compatible with life is 6.8 - 8.0
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OH-
OH-
OH-
OH-
OH-
OH-
H+
H+
H+
H+
OH-
OH-
OH-
OH-OH-
H+
H+
H+
H+
OH-
OH-
OH-
H+
H+
H+
H+
H+
H+
H+
ACIDS, BASES OR NEUTRAL???
1
2
3

pH SCALE
• pH equals the logarithm (log) to the base
10 of the reciprocal of the hydrogen ion
(H+) concentration
• H+ concentration in extracellular fluid (ECF)
13
pH = log 1 / H+ concentration
4 X 10 -8 (0.00000004)

pH SCALE
• Low pH values = high H+ concentrations
• H+ concentration in denominator of formula
• Unit changes in pH represent a tenfold change in
H+ concentrations
• Nature of logarithms
14
pH = log 1 / H+ concentration
4 X 10 -8 (0.00000004)

pH SCALE
• pH = 4 is more acidic than pH = 6
• pH = 4 has 10 times more free H+ concentration
than pH = 5 and 100 times more free H+
concentration than pH = 6
15
ACIDOSIS ALKALOSISNORMAL
DEATH DEATH
Venous
Blood
Arterial
Blood
7.3 7.57.46.8 8.0

EFFECTS OF pH
• The most general effect of pH changes are on
enzyme function
• Also affect excitability of nerve and muscle
cells
16
pH
pH
Excitability
Excitability

ACID-BASE BALANCE
•Acid - Base balance is primarily concerned
with two ions:
• Hydrogen (H+)
• Bicarbonate (HCO3
- )
18H+ HCO3
-

19
ACIDOSIS / ALKALOSIS
•Acidosis
• A condition in which the blood has too much
acid (or too little base), frequently resulting in
a decrease in blood pH
•Alkalosis
• A condition in which the blood has too much
base (or too little acid), occasionally resulting
in an increase in blood pH

ACIDOSIS / ALKALOSIS
• pH changes have dramatic effects on normal cell
function
• 1) Changes in excitability of nerve and muscle
cells
• 2) Influences enzyme activity
• 3) Influences K+ levels
20

CHANGES IN CELL
EXCITABILITY
• pH decrease (more acidic) depresses the
central nervous system
• Can lead to loss of consciousness
• pH increase (more basic) can cause over-
excitability
• Tingling sensations, nervousness, muscle
twitches
21

INFLUENCES ON ENZYME
ACTIVITY
• pH increases or decreases can alter the shape of
the enzyme rendering it non-functional
• Changes in enzyme structure can result in
accelerated or depressed metabolic actions
within the cell
22

INFLUENCES ON K+ LEVELS
• When reabsorbing Na+ from the filtrate of the
renal tubules K+ or H+ is secreted (exchanged)
• Normally K+ is
secreted in much
greater amounts
than H+
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K+
K+K+K+K+K+K+
Na+Na+Na+Na+Na+Na+
H+

INFLUENCES ON K+ LEVELS
• If H+ concentrations are high (acidosis) than H+ is
secreted in greater amounts
• This leaves less K+ than usual excreted
• The resultant K+ retention can affect cardiac
function and other systems
24
K+K+K+
Na+Na+Na+Na+Na+Na+
H+H+H+H+H+H+H+
K+K+K+K+K+

Acidemia is present when blood pH <7.35
Alkalemia is present when blood pH >7.45
Acidosis is a process which tends to acidify body
fluids (lower plasma bicarbonates) and if unopposed
will lead to a fall in pH
Alkalosis is a process which tends to alkalinize body
fluids (raise plasma bicarbonates) and if unopposed
will lead to an alkalemia

Importance of hydrogen Ion
concentration
• Needed for maintaining intracellular PH: Cellular Viability,
metabolism, enzyme function
• Change in PH alters the degree of ionization of protein, affects
its function. At more extreme H+ ion conc. Proteins structure
gets completely disrupted
• Disturbance in PH results in abnormal respiratory and cardiac
function ,derangement in blood clotting and drug metabolism

Intracellular PH is difficult to measure & varies with cells
Skeletal muscle pH 6.9-7.2
Cardiac muscle pH 7.0-7.4
Liver cell pH 7.2
Brain cell pH 7.1

The ultimate pH of the body will depend on
• The amount of acid produced
• The buffering capacity of the body,
and
• The rate of acid excretion by the lungs and
kidneys

Production of hydrogen Ions
a) Non volatile acids
Metabolism generates H+ small amounts (40-80
mmol/24h) from oxidation of amino acids and
anaerobic metabolism of glucose to lactic acid and
pyruvic acid
Excreted by kidney

b) Volatile acids
• Far more acid produced as a result of CO2 release
from aerobic metabolism -15000 mmol / day
• CO2 produced as a result of cellular respiration,
reacts with water to from carbonic acid (H2CO3)
which dissolves in to H+ and bicarbonate (HCO3)
• Co2 + H2O H2CO3 HCO3 + H+
• Excreted by lungs

ACID-BASE REGULATION
• Chemical Buffers
• The body uses pH buffers in the blood to guard against sudden changes in
acidity
• A pH buffer works chemically to minimize changes in the pH of a solution
32
Buffer

BUFFERS
• Buffers are substances that can absorb or donate H+ so that
changes in the free H+ concentration are minimized
Extracellular buffers 40-45%
• Bicarbonate / carbonic acid buffer system
• Inorganic phosphates
• Plasma proteins
Intracellular and Bone buffers 55-60%
• Proteins – Albumin, plasma proteins
• Organic and Inorganic phosphates
• Hemoglobin – deoxy Hb has strongest affinity for both CO2 and H+
• Bone

PROTEIN BUFFER SYSTEM
• Most important
intracellular buffer (ICF)
• The most plentiful buffer
of the body
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PROTEIN BUFFER SYSTEM
35
-
-
-
- - - -
-
-
-
-
-
-
--------
-
---
-
-
-
-
- - - -
+
+
++
+
+
+
+
+
+
+
+
+
++ +
+
+
+
+
+
+
+ +
+
OH-
OH-
OH-
OH- OH- OH-
OH-
OH-
OH-OH-
OH-
OH-
H+
H+
H+
H+ H+ H+
H+
H+
H+
H+
H+
H+
H+
H+H+
H+H+H+H+H+H+

Carbonic Acid / Bicarbonate Buffer system
• Most important extra cellular buffer
• In RBC it buffers metabolic CO2
• It provides a substrate for acid secretion in the kidneys
• Its buffering capacity is potentiated by its being an open
system allowing respiration to independently modulate CO2

BICARBONATE BUFFER
SYSTEM
• 3) Bicarbonate Buffer System
• Predominates in extracellular fluid (ECF)
HCO3
- + added H+ H2CO3
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HCO3
-
H2CO3

Buffers in Urine
• Phosphate HPO4
-2 & ammonia NH3
• HPO4
-2 freely filtered by the glomerulus, in tubule it combines
with H+ to form H2PO4 & excreted
• NH3 produced in renal tubular cell by action of enzyme
glutaminase on glutamine
• Enzymes acts optimally in Acidic PH than normal
• NH3 combines with H+ to form the NH4+, being ionized
doesn’t pass back and NH4+ is lost is urine along Cl

ACIDIFICATIONOFURINEBYEXCRETIONOFAMMONIA
39
Capillary Distal Tubule Cells
Tubular urine to
be excreted
NH2
H+
NH3
NH2
H+
NH3
WHAT
HAPPENS
NEXT?

ACIDIFICATIONOFURINEBYEXCRETIONOFAMMONIA
40
Capillary Distal Tubule Cells
Tubular Urine
NH3
Na+ Cl-+
H2CO3HCO3
- +
NaCl
NaHCO3
Click Mouse to Start
Animation
NaHCO3
NH3Cl-
H+
NH4Cl
Click Mouse to See
Animation Again
Notice the
H+ - Na+
exchange to
maintain
electrical
neutrality
Dissociation of
carbonic acid

• Hydrogen Ion Homeostasis
The maintenance of hydrogen ion homeostasis is by 3
mechanisms
1.Control of CO2 by the respiratory centre & lungs
• CO2 is responsible for majority of hydrogen ion
production by its metabolism
• Respiratory system single most important organ system
involved in the control of hydrogen ion
• If alveolar ventilation falls the PaCO2 rises

ACID-BASE REGULATION
• Respiratory Regulation
• Carbon dioxide is an important by-product of metabolism and is
constantly produced by cells
• The blood carries carbon dioxide to the lungs where it is exhaled
CO2CO2 CO2
CO2 CO2
CO2
Cell
Metabolism

 Therefore relative small changes in ventilation will
have profound effect on hydrogen ion concentration
and PH
 An acute rise in PCO2 of 1KPA results in a 5.5 nmol/L
rise in the hydrogen ion conc. and resulting fall in PH
 Control of ventilation is brought by PCO2, which
produces decline in blood & CSF PH

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CO2
CO2
Red Blood Cell
Systemic Circulation
CO2 H2O H+ HCO3
-+ +
HCO3
-
Cl-
(Chloride Shift)
CO2 diffuses into plasma and into RBC Within RBC,
the hydration of CO2 is catalyzed by carbonic
anhydrase
Bicarbonate thus formed diffuses into plasma
carbonic
anhydrase
Tissues
Plasma
CARBONDIOXIDEDIFFUSION

45
CO2
Red Blood Cell
Systemic Circulation
H2O
H+ HCO3
-
carbonic
anhydrase
Plasma
CO2 CO2
CO2 CO2 CO2 CO2
CO2
Click for Carbon
Dioxide diffusion
+ +
Tissues
H+
Cl-
Hb
H+ is buffered by
Hemoglobin
CARBON DIOXIDE DIFFUSION

• This mechanism depends on carbonic anhydrase which is in
the tubule and H+ secretion from cell in to the lumen in
exchange for the sodium filtered with the bicarbonate
(b)Renal excretion of H+
• Most of the dietary H+ ions come from sulphur containing
amino acids and are excreted in distal nephrons by proton
pump H+ ATPase
• Two buffer systems are important in acid excretion:
titratable acids such as phosphates and ammonia

Phosphate Buffer
• Phosphate in the form of monohydrogen phosphate ion in
the glomerular filtrate, accepts H+ formed by carbonic
anhydrase mechanism to become dihydrogen phosphate,
bicarbonate generation can then continue.

PHOSPHATE BUFFER SYSTEM
• 1) Phosphate buffer system
Na2HPO4 + H+ NaH2PO4 + Na+
• Most important in the intracellular system
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H+ Na2HPO4+
NaH2PO4Click to
animate
Na++

• Alternately switches Na+ with H+
49
H+ Na2HPO4+
NaH2PO4Click to
animate
Na++
Disodium hydrogen phosphate

• Phosphates are more abundant within the cell and are rivaled as
a buffer in the ICF by even more abundant protein
50
Na2HPO4
Na2HPO4
Na2HPO4

Acid base balance
• Acid base homeostasis is essential for normal cellular
function
• The pH is maintained within a very narrow range by the
interaction of
Blood buffers Occurs in seconds to mins
Lungs Occurs in 1 to 15 minutes
Kidneys Occurs in hours to days

Calculation of pH
203.0
log10.6 3
PaCO
HCO
pH




ACIDOSIS/ALKALOSIS
• Metabolic refers to a disorder that results from primary
alteration in [H+] or [HCO3]
• Respiratory refers to a disorder that result from a
primary alteration in PaCO2 due to altered CO2
elimination

Metabolic Acidosis
• Primary Defect : Fall in HCO3. Accumulation of
metabolic acids (non-carbonic) caused by:
• Excess acid production which overwhelms renal capacity for
excretion. e.g. Diabetic ketoacidosis.
• Loss of alkali. Leaves un-neutralized acid behind. e.g.
Diarrhea
• Renal excretory failure: Normal total acid production in face
of poor renal function. e.g. Chronic renal failure

CONTD…
• Compensatory Change:
• Tissues and RBC act to increase serum HCO3 by
exchanging intracellular Na and K for extracellular H+.
Acts to raise serum HCO3 and K
• Increased pulmonary ventilation. Fall in PCO2 brings
pH back toward normal

CLINICAL FEATURES OF
METABOLIC ACIDOSIS
Pulmonary- Kussmaul breathing
Cardiac -Arrythmias, Hypotension
CNS -headache,confusion,lethargy,coma
Glucose intolerance
Non specific-
anorexia,nausea,vomiting,muscle weakness

Types – Two major Clinical Categories of metabolic Acidosis are
High anion Gap Acidosis
Normal Anion Gap or Hyperchloremic Acidosis

ANION GAP
• It represents conc of all unmeasured anions is plasma
• AG is calculated by formula AG= Na+ - (CI + HCO3)
• Normal range is 10 -12 mmol/L
• Negatively changed proteins account for 10% plasma anions
• Acid Anions (Eg: Lactate, acetoacetate, sulphate) produced
during metabolic acidosis not measured as a part of
biochemical profile

USE OF ANION GAP
• Signals presence of metabolic acidosis
• Help differentiate causes of metabolic acidosis
• Assessing the biochemical severity of acidosis and follow
response to treatment

Problems with AG
• Calculated by measuring only 3 ions
• Errors with AG is much higher than that of single electrolyte
determination
• If AG>30mmol/L invariably means metabolic acidosis is
present
• If AG range 20 – 291/3 of these patients may not have
metabolic acidosis
• Significant lactic acidosis may be associated with normal AG

LACTIC ACIDOSIS
• An increase in plasma L-lactate may be
secondary to poor tissue perfusion (type A)
circulatory insufficiency or to aerobic disorders (B)
• D-Lactic acid acidosis,associated with
jejunoileal bypass
short bowel syndrome
intestinal obstruction
• due to formation of D-lactate by gut bacteria

TREATMENT
• The underlying condition that disrupts lactate metabolism
must first be corrected
• Alkali therapy is generally advocated for acute, severe
acidemia (pH < 7.15) to improve cardiac function and lactate
utilization.
• A reasonable approach is to infuse sufficient NaHCO3 to raise
the arterial pH to no more than 7.2 over 30–40 min.

Ketoacidosis
Diabetic Ketoacidosis (DKA)
• increased fatty acid metabolism and the accumulation of
ketoacids.
• relationship between the AG and HCO3
– is ~1:1 in DKA but may
decrease in the well-hydrated patient with preservation of
renal function.
• insulin prevents production of ketones, bicarbonate therapy is
rarely needed except with extreme acidemia (pH < 7.1),

Alcoholic Ketoacidosis (AKA)
• usually associated with binge drinking, vomiting, abdominal
pain, starvation, and volume depletion.
• glucose concentration is variable, and acidosis may be
severe because of elevated ketones, predominantlyβ –
hydroxybutyrate.
• mixed acid-base disorders are common in AKA
• IV administration of saline and glucose (5% dextrose in
0.9% NaCl).

OSMOLAR GAP
• Plasma osmolality is calculated according to the following
expression:
Posm = 2Na+ + Glu/18 + BUN/2.8.
• When the measured osmolality exceeds the calculated
osmolality by >15–20 mmol/kg H2O
Either the serum sodium is spuriously low,
osmolytes other than sodium salts, glucose, or urea have
accumulated in plasma.
• Mannitol, Radiocontrast media,ethanol, methanol, and
acetone

Drug- and Toxin-Induced Acidosis
• Salicylates
• Alcohols
Three alcohols may cause fatal intoxications:
ethylene glycol
methanol
isopropyl alcohol
All cause an elevated osmolal gap, but only the first
two cause a high-AG acidosis.

Renal Failure
• Hyperchloremic acidosis of moderate renal insufficiency is
eventually converted to the high-AG acidosis of advanced
renal failure.
• Uremic acidosis is characterized, therefore, by a reduced rate
of NH4
+ production and excretion, primarily due to decreased
renal mass.
• [HCO3
–] rarely falls to <15 mmol/L, and the AG is rarely >20
mmol/L.
• The acid retained in chronic renal disease is buffered by
alkaline salts from bone.

TREATMENT
• Both uremic acidosis and the hyperchloremic acidosis of renal
failure require oral alkali replacement to maintain the [HCO3
–]
between 20 and 24 mmol/L.
• Accomplished with relatively modest amounts of alkali (1.0–
1.5 mmol/kg body weight per day). Sodium citrate (Shohl's
solution) or NaHCO3 tablets (650-mg tablets contain 7.8 meq)
are equally effective alkalinizing salts.
• When hyperkalemia is present, furosemide (60–80 mg/d)
should be added.

Urine Electrolytesin MetabolicAcidosis
Urine Anion Gap = (U. Na+ + U. K+ )– U. Cl-
In Metabolic Acidosis:
Positive Urine AG suggests distal Renal Tubular Acidosis
Negative Urine AG suggests non-renal cause for
Metabolic Acidosis

TREATMENT
• Specific treatment against underlying cause
• Severe academia 7.10/7.0 warrants treatment with
alkali

GOALS OF
BICARBONATE USE
Definite use of IV bicarb in
1) Renal failure
2) Hyperkalemia
3) Acidosis in diarrhoea
4) RTA
Definite use : if pH<7.10/7.20
Others like: DKA pH<7.0

• Bicarbonate deficit is estimated by
0.5 × body weight(24-HCO3)
• Severe acidosis (pH <7.20) warrants the intravenous
administration of 50 to 100 meq of NaHCO3, over 30
to 45 min, during the initial 1 to 2 hrs of therapy
• Goal is to increase the [HCO3-] to 10 meq/L and the
pH to 7.15, not to increase these values to normal

BASE EXCESS
• Is a calculated value estimates the metabolic component
of an acid based abnormality.
• It is an estimate of the amount of strong acid or base
needed to correct the met. component of an acid base
disorder (restore plasma pH to 7.40at a Paco2 40 mmHg)

Formula
• With the base excess is -10 in a 50kg person with
metabolic acidosis mM of Hco3 needed for correction is:
= 0.3 X body weight X BE
= 0.3 X 50 X10 = 150 mM

SIDE EFFECTS
 Hypernatraemia
 Hyperosmolality
 Volume overload
 Rebound alkalosis
 Hypokalaemia
 CSF acidosis
 Hypercapnia

Respiratory Acidosis
• Primary Defect:
• Decrease in pulmonary clearance of CO2 (Increase in PCO2)
• Acute (<24 hrs): Buffering by tissue and RBC to increase HCO3. Rarely
more than 4 mEq
• Chronic (>72 hrs): Stimulation of renal tubular secretion of H+ thus
synthesizing more HCO3. Chloride is lost along with NH4+

CAUSES
1. CENTRAL
• a. Drugs – Anesthetics, morphine, sedatives
• b. Stroke
• c. Infection
2. AIRWAY
• a. Obstruction
• b. Asthma
3.Parenchyma
• a.emphysema,
• b.pneumoconiosis
• c.Bronchitis,
• d.ARDS

4. Neuromuscular
• a. Poliomyelitis
• b. myasthenia
• c. muscular dystrophies
5. Miscellaneous
• obesity
• hypoventilation

CLINICAL FEATURES
• Vary according to the
severity
duration of the respiratory acidosis
underlying disease
whether there is accompanying hypoxemia
• A rapid increase in PaCO2 may cause anxiety,
dyspnea, confusion, psychosis, and hallucinations
and may progress to coma

• Lesser degrees of dysfunction in chronic hypercapnia
include
sleep disturbances
loss of memory
daytime somnolence
personality changes
impairment of coordination
tremor, myoclonic jerks, and asterixis
• Headaches and other signs that mimic raised
intracranial pressure, such as papilledema, abnormal
reflexes, and focal muscle weakness, are due to
vasoconstriction secondary to loss of the vasodilator
effects of CO2

TREATMENT
ACUTE – Bronchodilators
Mechanical ventilation
Antibiotics
CHRONIC – Oxygen long term
Nasal continous PAP
Increase respiratory muscle function
Drugs – doxapram, methylphenidate,
caffeine

Metabolic Alkalosis
(Rise in serum bicarbonate)
• Primary Defect:
• New HCO3 must be added from renal or extrarenal sources,often
assoc with hypochloremia,hypokalemia
• Compensatory change:
• Tissues and RBC exchange intracellular H+ for extracellular Na+
and K+
• Hypoventilation and elevation of PCO2 (Maximal PCO2 rarely
excedes 55 mmHg)

PATHOGENESIS
Metabolic alkalosis occurs as a result of
net gain of [HCO3-]
loss of nonvolatile acid (usually HCl by vomiting) from
the extracellular fluid
Since it is unusual for alkali to be added to the body, the
disorder involves 2 stages
1. Generative stage  loss of acid usually causes alkalosis
2. Maintenance stage  kidneys fail to compensate by
excreting HCO3- because of volume contraction, a low
GFR, or depletion of Cl- or K+

CAUSES
• SALINE RESPONSIVE
(URINE CL<20mEq/L)
Vomiting
Gastric aspiration
Diuretics
Hypercapnia correction
NaHco3 infusion
Multiple transfusions
• SALINE RESISTANT
(URINE CL>20mEq/L)
Hyperaldosteronism
Cushing syndrome
Bartter’s syndrome
Severe k+ depletion

CLINICAL FEATURES
CNS: similar to those of hypocalcemia symptoms
light headache
mental confusion
obtundation
predisposition to seizures
paresthesia
muscular cramping,tetany
CVS: Arrythmias, Hypotension
RS : Hypoxia in preexisting lung disease
Others: Weakness,muscle cramps

SIMPLE METABOLIC ALKALOSIS
• Most common acid base disorder in hospitalised
patients
• pH >7.65 – 80% mortality
• Occurs only in the presence of one of the
bicarbonate retaining mechanisms
• Chloride depletion
• Potassium depletion (+/- hypertension)
• Base loading (multiple blood transfusions)

TREATMENT
• Treat the underlying cause
• Stop diuretics, nasogastric aspiration and steroid
use
• Correct ECF volume deficit with normal saline
• H2 receptor blockers in case of prolonged vomiting
in order to reduced H+ loss

saline responsive cases
• Chloride replacement is main stay
• Cl deficit= 0.2× wt (kg)× (normal cl-actual cl)
• Can be given as Nacl,Kcl,.1N Hcl
• Hydrochloric acid is administered when there is
an immediate need for correction of pH

SALINE RESISTANT
• Treat the underlying cause
• Correct the potassium deficit
• acetazolamide

RESPIRATORY ALKALOSIS
• Primary Defect:
• Fall in PCO2 due to abnormally rapid or deep
respiration, when the CO2 transport capacity of the
pulmonary alveoli is relatively normal
• Acute (<24 hrs): Buffering by tissue and RBC to lower
HCO3. Rarely to less than 18 mEq/L
• Chronic (>72 hrs): Impairs kidney's ability to excrete
acid thus lowering HCO3. If more than 2 weeks, pH
may return to normal

CAUSES
• CNS stimulationCVA, meningitis, encephalitis,
tumor, trauma
• HypoxaemiaHigh altitude, pneumonia, severe
Anemia, Aspiration
• Drugs or HormonesPregnancy, Progesterone,
Salicylates
• Stimulation of chest receptorsHemothorax, flail
chest, cardiac failure, pulmonary embolism
• Miscellaneous; Septicemia, hepatic failure,
mechanical hyperventilation, heat exposure

CLINICAL FEATURES
• CNS: Reduced cerebral blood flow as a consequence
of a rapid decline in PaCO2 may cause
dizziness
mental confusion
seizures, even in the absence of hypoxemia
• CVS: Minimal but in anesthetized or mechanically
ventilated patient ,cardiac output and blood pressure
may fall because of the depressant effects of
anesthesia and positive-pressure ventilation on heart
rate, systemic resistance, and venous return. Cardiac
arrhythmias may occur

TREATMENT
Doesn’t need any treatment unless PH > 7.5
-Relief of hypoxia by person coming down from high
altitude, administration of oxygen
-Re breathing into a non compliant bag as long as
hyperventilation exists
- Treatment of anxiety
-If respiratory alkalosis complicates ventilator
management, changes in dead space, tidal volume,
and frequency can minimize the hypocapnia

ASSESSMENT OF PATIENT’S ACID
BASE STATUS – INTERPRETATION OF
ARTERIAL BLOOD GAS (ABG)

Dictums in ABG Analysis
• Dictum 1:
Primary change & Compensatory
change always occur in the same
direction.

Calculation of Compensation
Primary
disorder
Formula for calculation of
compensation
Metabolic
acidosis
Δ PaCO2 = 1.2 × Δ HCO3
Metabolic
alkalosis
Remember: The formula calculates the change in the
compensatory parameter.

Primary disorder Formula for calculation of
compensation
Acute Respiratory
acidosis
Δ HCO3 = 0.1 × Δ PaCO2
Chronic Respiratory
acidosis
Acute Respiratory
alkalosis
Chronic Respiratory
alkalosis

1.2
0.7
0.1 0.3
0.2 0.5
Compensation Formula Simplified
Acute Chronic
Metabolic
Respiratory
Acidosis
Alkalosis
Acidosis
Alkalosis

• Dictum 2:
• pH and Primary change in the same direction suggests a
metabolic problem
• pH and Primary change in the opposite direction
suggests a respiratory problem

pH HCO3 PaCO2 Primary disorder
↓ ↓ ↓ Metabolic acidosis
↑ ↑ ↑ Metabolic alkalosis
↓ ↑ ↑ Respiratory acidosis
↑ ↓ ↓ Respiratory
alkalosis
= indicates compensatory change

• Dictum 3:
• Renal and pulmonary compensatory mechanisms return pH
towards but rarely to normal
• A normal pH in the presence of changes in PCO2 or HCO3
suggests a mixed acid-base disorder

CLUES TO MIXED ACID BASE
DISORDER
• A normal PH in the presence of changes in Pco2 or Hco3
suggests a mixed acid base disorder
• PaCo2 & HCo3 deviating in opposite direction
• PH change in the opposite direction of known primary (
dominate ) acid base disorder

Steps in the Evaluation of
Acid-Base Disorders
1. Comprehensive history and physical examination.
2. Evaluation of simultaneously performed arterial
blood gas and electrolyte profile
3. Assess The Accuracy/Internal Consistency of the
parameters by comparing measured and calculated
HCO3
−
Henderson-
Hesselbach equn.
  


3
2
24
HCO
PaCO
H

Step 4. Identify the Dominant Disorder
pH HCO3 PaCO2 Primary disorder
↓ ↓ ↓ Metabolic acidosis
↑ ↑ ↑ Metabolic alkalosis
↓ ↑ ↑ Respiratory acidosis
↑ ↓ ↓ Respiratory
alkalosis
= indicates compensatory change

Step5. Checkif the compensatoryresponseis
appropriateor not.
If the compensation is not appropriate, suspect a second (and
perhaps a triple) acid-base disorder.

Disorder pH Primary
change
Compensatory
Response
Equation
Metabolic
Acidosis
  [HCO3
-]  PCO2 ΔPCO2  1.2  ΔHCO3
Metabolic
Alkalosis
  [HCO3
-]  PCO2 ΔPCO2  0.7  ΔHCO3
Respiratory
Acidosis
  PCO2  [HCO3
-] Acute:
ΔHCO3
-  0.1  ΔPCO2
Chronic:
ΔHCO3
-  0.3  ΔPCO2
Respiratory
Alkalosis
  PCO2  [HCO3
-] Acute:
ΔHCO3
-  0.2  ΔPCO2
Chronic:
ΔHCO3
-  0.5  ΔPCO2

Step 6: Calculate the “gaps”
Anion gap = Na+ − ( Cl- + HCO3
-)
Δ AG = (Anion gap − 12)
Δ HCO3 = (24 − HCO3)
Note: Add Δ AG to measured HCO3
- to obtain bicarbonate level that would
have existed if the high AG metabolic acidosis were to be absent.
Δ AG = Δ HCO3-, then Pure high AG Met. Acidosis
Δ AG > Δ HCO3-, then High AG Met Acidosis + Met. Alkalosis
Δ AG < Δ HCO3-, then High AG Met Acidosis + HCMA

Common clinical states and associated acid-base disorders
Clinical state Acid-base disorder
Renal failure Metabolic acidosis
Vomiting Metabolic alkalosis
Severe diarrhea Metabolic acidosis
Cirrhosis Respiratory alkalosis
Hypotension Metabolic acidosis
COPD Respiratory acidosis
Sepsis Respiratory alkalosis, metabolic acidosis
Pulmonary embolus Respiratory alkalosis
Pregnancy Respiratory alkalosis
Diuretic use Metabolic alkalosis

NormalValuesforMajor Acid-Basevariables
• S Na = 135 – 145 mEq/L
• S K = 3.5 – 5.5 mEq/L
• S Cl = 97 – 110 mEq/L
pH H+
nanoEq/L
PaCO2
mmHg
HCO3
–
mEq/L
Arterial 7.37 – 7.43 37 – 43 36 – 44 22 – 26
Venous 7.32 – 7.38 42 – 48 42 – 50 23 – 27

Case 1
• A 50 yr old man presented with history of
progressive dyspnoea with wheezing for 4 days.
• He also had fever, cough with yellowish
expectoration.
• He had increased sleepiness for 1 day.
• On examination, he was tachypnoeic, pulse-
100/min, BP-160/96, central cyanosis +, drowsy,
asterixis +, RS – B/L extensive wheezing +.
• CXR- hyperinflated lung fields with tubular heart.

Case 1: Laboratory data
• ABG:
pH 7.30
PaCO2 60 mmHg
HCO3 28 mEq/L
PaO2 68 mm Hg
• Serum Electrolytes:
Na 136 mEq/L
K 4.5 mEq/L
Cl 98 mEq/L
• Evaluate the acid-base disturbance(s)?

Case 1: Solution
• Dominant disorder is Respiratory Acidosis (pH 7.30,
PaCO2 60 mmHg,HCO328 mEq/LPaO2,,68 mm Hg)
• Compensation formula:
= 0.3 × 20
= 6
HCO3 = 24 + 6 = 30
Compensation is appropriate.
• Anion Gap = 138 – (98 + 28)
= 10
AG is normal.

Case 2
• A 15 yr old juvenile diabetic presents with
abdominal pain, vomiting, fever & tiredness for 1
day. He had stopped taking insulin 3 days ago.
Examination revealed tachycardia, BP- 100/60,
dehydration+, abdominal examination normal.
• ABG:
pH 7.31
PaCO2 26 mmHg
HCO3 12 mEq/L
PaO2 92 mm Hg
• Evaluate the acid-base disturbance(s)?
Serum Electrolytes:
Na 140 mEq/L
K 5.0 mEq/L
Cl 100 mEq/L

Case 2: Solution
• Dominant disorder is Metabolic Acidosis
(pH7.31,HCO3 12,Paco26)
= 1.2 × 12
= 14.4
PaCO2 = 40 – 14 = 26
• Anion Gap = 140 – (100 + 12)
= 28
AG is high.

Case 2: Solution
• Δ AG = 28 – 12
= 16
• Δ HCO3 = 24 – 12
= 12
• Δ AG > Δ HCO3
-
• Final Diagnosis:
High AG Met. Acidosis + Met. Alkalosis

Case 3
• acid-base status of a 35-year-old man with history
of chronic renal failure treated with high dose
diuretics admitted to hospital with pneumonia and
the following lab values:
ABG Serum Electrolytes
pH 7.52 Na+ 145 mEq/L
PaCO2 30 mm Hg K+ 2.9 mEq/L
PaO2 62 mm Hg Cl- 98 mEq/L
HCO3
- 21 mEq/L

Case 3: Solution
• Dominant disorder is Respiratory Alkalosis (pH 7.52,
PaCO2 30 mm Hg,PaO2 62 mm Hg, HCO3
- 21 mEq/L)
= 0.2 × 10
= 2
HCO3 = 24 – 2 = 22
• Anion Gap = 145 – (98 + 21)
= 26
AG is very high suggestive of metabolic acidosis.

Case 3: Solution
• Δ AG = 26 – 12
= 14
• Δ HCO3 = 24 – 21
= 3
• Δ AG > Δ HCO3
-
High AG Met Acidosis + Met. Alkalosis
• Final Diagnosis:
Respiratory Alkalosis +
High AG Metabolic Acidosis +
Metabolic Alkalosis

EQUIPMENT
Blood gas kit OR
• 1ml syringe
• 23-26 gauge needle
• Stopper or cap
• Alcohol swab
• Disposable gloves
• Plastic bag & crushed ice
• Lidocaine (optional)
• Vial of heparin (1:1000)
• Par code or label
124
A.
Y.
T

Preparatoryphase:
• Record patient inspired oxygen concentration
• Check patient temperature
• Explain the procedure to the patient
• Provide privacy for client
• If not using hepranized syringe , hepranize the needle
• Perform Allen's test
• Wait at least 20 minutes before drawing blood for ABG
after initiating, changing, or discontinuing oxygen
therapy, or settings of mechanical ventilation, after
suctioning the patient or after extubation.
A.
Y.
T

ALLEN’S TEST
It is a test done to determine that collateral
circulation is present from the ulnar artery in
case thrombosis occur in the radial
126
A.
Y.
T

Sites for obtaining abg
• Radial artery ( most common )
• Brachial artery
• Femoral artery
Radial is the most preferable site
used because:
• It is easy to access
• It is not a deep artery which
facilitate palpation, stabilization
and puncturing
• The artery has a collateral blood
circulation
127
A.
Y.
T

Performancephase:
• Wash hands
• Put on gloves
• Palpate the artery for maximum pulsation
• If radial, perform Allen's test
• Place a small towel roll under the patient wrist
• Instruct the patient to breath normally during the test
and warn him that he may feel brief cramping or
throbbing pain at the puncture site
• Clean with alcohol swab in circular motion
• Skin and subcutaneous tissue may be infiltrated with
local anesthetic agent if needed
128
A.
Y.
T

• Insert needle at 45 radial ,60
brachial and 90 femoral
• Withdraw the needle and apply
digital pressure
• Check bubbles in syringe
• Place the capped syringe in the
container of ice immediately
• Maintain firm pressure on the
puncture site for 5 minutes, if
patient has coagulation
abnormalities apply pressure for
10 – 15 minutes
129
A.
Y.
T

Followup phase:
• Send labeled, iced specimen to the lab immediately
• Palpate the pulse distal to the puncture site
• Assess for cold hands, numbness, tingling or discoloration
• Documentation include: results of Allen's test, time the
sample was drawn, temperature, puncture site, time
pressure was applied and if O2 therapy is there
• Make sure it’s noted on the slip whether the patient is
breathing room air or oxygen. If oxygen, document the
number of liters . If the patient is receiving mechanical
ventilation, FiO2 should be documented
130
A.
Y.
T

Precautions in arterial sampling
• Steady state of ventilatory parameters.
• If no pulmonary disease – steady state reached in 10min
• If pulmonary disease – steady state reached in 20 – 30
min
• Anaerobic collection
• Avoid excess heparin
• may in itself reduce pH; 0.05 ml of heparin per 1 ml of
blood (<1:20)
• No delay in processing (or cool to 4°C)
• Can be refrigerated for a maximum of 1 hrs

REFERENCES
• WASHINGTON MANUAL OF CRITICAL CARE
• WASHINGTON MANUAL OF MEDICAL
THERAPEUTICS
• HARRISONS PRINCIPLE OF INTERNAL MEDICINE
• JOURNAL OF CRITICAL CARE
• ICU BOOK, PAUL MARINO

It’s not magic understanding ABG’s,
it just takes a little practice!

ACID BASE BALANCE & ARTERIAL BLOOD GAS ANALYSIS

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