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Arterial Blood Gases ------------(sami).ppt
1. Acid – Base Balance
And Blood Gases
Prof. Dr. Sami El Shimi
Professor of Pediatrics,
Head of Neonatology Unit
Faculty of Medicine, Ain Shams University.
2. 1. Idea about ABG
(importance, values, pitfalls).
2. How to analyze ABG reading.
3. How to correct any defer by different
therapies.
Goals
3. Why measuring Blood Gases?
Evaluation of:
• Adequacy of Ventilation.
• Oxygenation.
• Acid Base status.
• Assess the response to an intervention.
5. Acids
Substance containing 1 or more H+ ions
(protons) that can be liberated into solution.
• Two types of acids are formed by metabolic
processes
– Volatile acids: liquid ↔ gas. CO2 eliminated by lungs.
• CO2 + H2O ↔H2CO3 ↔ H+ + HCO3
-
– Nonvolatile or fixed acids: cannot be converted to a gas
and subsequently must be converted or eliminated by the
kidneys
• Examples: SO4, PO4, lactic acid, ketoacids
• The non-volatile portion is trivial when compared to the volatile
H2co3.
6. Bases
Substance that can capture or combine
with hydrogen ions to form a salt
• A proton acceptor
• Example: HCO3
- (bicarbonate)
7. Buffers
Chemical substance that minimizes the pH
change in a solution caused by the addition of
either an acid or base.
• There are four main buffer systems in the body:
– Bicarbonate buffer system. (the MAIN one) 64%
• NaHCO3 ↔ H2CO3
– Hemoglobin buffer system. 29%
• HbO2
- ↔ HHb
– Protein buffer system. 6%
• Pr- ↔ HPr
– Phosphate buffer system. 1%
• NaH2PO4 ↔ NaHPO4
8. Regulation of Extracellular Fluid pH
Acids and bases continually enter the body via breakdown
of ingested substances, normal body metabolism,
IVF’s, etc.
• Compensation must occur to keep the pH normal.
• Three cooperative mechanisms exist:
– Buffer systems:
• Immediate (HCO3
-)
– Respiratory control: CO2 elimination or retention.
• Rapid (minutes)
– Renal regulation: Bicarbonate level regulation.
• Slow (hours to days).
• Kidneys can excrete H+ and/or retain/reabsorb HCO3
- as
needed.
9. • The symbol used to measure the
hydrogen ion (H+) concentration (results
from the byproducts of metabolism).
• As the H+ concentration increases, the
pH decreases (acidosis)
• As the H+ concentration decreases, the
pH increases (alkalosis).
PH
12. To keep Blood pH value normal
• There should be a balance between
acids, which results from the
byproducts of metabolism,
• and the body’s buffer systems.
13. For example:
• if the carbon dioxide is not excreted
effectively by the lungs, it combines
with water to form carbonic acid, which
leads to an excess of hydrogen ions
and the development of acidemia.
16. • PH abnormalities resulting from abnormal
PaCO2 are considered respiratory in
origin.
• Any abnormalities in HCO3
- are
considered metabolic in origin.
• Base excess (BE)
reflects the concentration & function of
buffer system.
21. • Acidemia is a PH below normal < 7.35.
• Alkalemia is a PH above normal >7.45.
• Acidosis is a pathological process
that causes an increase in H+ ion
concentration
• Alkalosis is a pathological process
that causes a decrease in H+ ion
concentration
22. Acidemia & Alkalemia
indicated the PH abnormality
Acidosis & Alkalosis indicate
the pathological process that
is taking place
23. DEFINITIONS
• Respiratory Acidosis –
occurs when carbon dioxide is not
promptly vented by the lungs and
carbon dioxide combines with
bicarbonate to form carbonic acid
24. DEFINITIONS
• Metabolic Acidosis –
occurs when a disorder adds acid to
the body or causes alkali to be lost
faster than the buffer system (lungs
or kidneys) can regulate the load.
29. low pH (Acidosis)
• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3
-
low bicarbonate
Metabolic acidosis
Gain of
H+ ion
Decreasd
tissue
perfusion
Sepsis,
Renal
failure
Loss of base
Renal tubular acidosis
Diarrhea
high PCO2
Respiratory acidosis
CNS depression –
maternal narcotics during
labor, asphyxia, severe
intracranial bleeding,
neuromuscular disorder,
CNS dysmaturity (apnea
or prematurity)Obstructed
airways,meconium aspir.
Don’t forget
PH∞ HCO3
- /
PaCO2
Gain of
H+ ion
30. High pH (Alkalosis)
High
bicarbonate
Metabolic
Alkalosis
Loss of H+ ion Adding a base
Gastric suctioning
Severe vomiting
Diuretic therapy
Iatrogenic (gave too much
HCO3)
Exchange transfusion
low PCO2
Respiratory
Alkalosis
Iatrogenic (mechanical
ventilation)
Hypoxemia
CNS irritation (pain)
Loss of H+ ion
Don’t forget
PH∞ HCO3
- /
PaCO2
• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3
-
31. Normal Neonatal Arterial Blood Gas
Values
• pH 7.35 - 7.45
• PaCO2 35 - 45 mm Hg
• PaO2 50 - 70 mm Hg (term infant)
45 - 65 mm Hg (preterm infant)
• HCO3 20 - 28 mEq/liter
• Base Excess -2 - + 2 mEq/liter
• O2 saturation 92 - 94 %
32. Important rules to analyze ABGs
• Rule 1
To
diagnose
respiratory
component
• Rule 2
To
diagnose
metabolic
component
34. Rule 1
Any increase or decrease in
Pco2 by 10mmhg Change in PH by 0.08
If we find accurate result for
the equation so the disorder
is purely respiratory
Ex: Pco2 50 mmHg (n. 40) so:
PH=7.40 – 0.08 = 7.32
36. Rule 2
Any increase or decrease in
HCO3 by 10 mmhg Change in PH by
0.15
Ex: HCO3 32 mmHg (n. 22) so:
PH = 7.40 + 0.15 = 7.55
If we find accurate result for
the equation so the disorder
is purely metabolic
38. Rule 3
Base Excess/Deficit
• It is an empirical expression which
approximates the amount of acid or base
which would be needed to titrate one liter
of blood back to normal PH 7.4
39. What is base excess?
Any increase or decrease in
HCO3 by 10 mmhg Change in PH by 0.15
(?) Needed amount to
titrate one liter of blood by 0.01
Change in PH
So needed amount to titrate one liter of blood
= 2/3 cc of 8.4% NaHco3
But bicarbonate is mainly in extracellular fluid
(around 1/3 body wt.)
so correction needed = (BW x 0.3 x BE)
0.0000397mEq/L =7.4
41. Example of BE
• If PCO2= 50 & pH= 7.26
• If PCO2 10 pH should be 7.32
(according to rule 1)
• But pH is 7.26 (difference of 0.06)
• Thus There is a base deficit of 4 mEq/L
(6x2/3) amount of 8.4% NaHCO3 needed to
titrate 1 ml of blood from 7.39 to 7.4 .
• There is both
Respiratory
acidosis
Metabolic
acidosis
42. Compensation
• Compensation occurs in response
to a primary disturbance in acid-base
equilibrium leading to correcting
gradually the change in PH
• Compensation is a change in the
system not originally affected by the
primary disturbance.
43. Acid-Base Imbalances, &Compensation
Disorder
Primary
Compon
ent
Affected
Compensatory Effect Correction
Metabolic
Acidosis
pH < 7.35
HCO3 PCO2
Hyperventilation Give
bicarbonate
and treat the
cause
Respiratory
Acidosis
pH < 7.35
PCO2 HCO3
by the retention of
bicarbonate as
a result of
adjustment in
renal function
or assist
ventilation
Don’t forget
PH∞ HCO3
- /
PaCO2
44. Disorder Primary
Compon-
ent
Affected
Compensatory
Effect Correction
Metabolic
Alkalosis
pH >
7.45
HCO3
PCO2
by hypoventilation to
diminish the
elimination by CO2.
Give KCl
Stop diuretics
Treat cause
Respiratory
Alkalosis
pH >
7.45
PCO2
HCO3
by the kidneys
increasing their
secretion of
bicarbonate to restore
the
bicarbonate/carbonic
acid ratio to normal
Attempt to
stop
hyperventil-
ation
Don’t forget
PH∞ HCO3
- /
PaCO2
Acid-Base Imbalances &Compensation
45. Acid Base status Interpretation
• Interpretation of blood gas data should
follow a logical pattern:
• Initially evaluate the pH to determine if an
acidemia or alkalemia is present.
• Then evaluate
– The respiratory parameter (PaCO2) and
– The metabolic parameter (HCO3
-)
• to determine if the acidemia or alkalemia
is respiratory or metabolic in origin.
47. Appropriate Compensation during simple Acid-Base disorders
EXPEDTED COMPENSATION
DISORDER
Pco2= 1.5X(Hco3) + 8
METABOLIC
ACIDOSIS
Pco2 increases by 7 mmHg for each 10 mEq/L in serum Hco3
METABOLIC
ALKALOSIS
Hco3 increase by 1 for each 1o mmHg increase in Pco2
Hco3 increase by 3.5 for each 1o mmHg increase in Pco2
RESPIRATORY
ACIDOSIS
Acute
Chronic
Hco3 falls by 2 for each 1o mmHg decrease in Pco2
Hco3 falls by 4 for each 1o mmHg decrease in Pco2
RESPIRATORY
ALKALOSIS
Acute
Chronic
48. Acidemia
Derceased
HCO3
Increased
PCO2
Metabolic Acidosis Respiratoy Acidosis
High
PCO2
Mixed
metabolic
acidosis
&
Resp.
acidosis
Expected
PCO2
Simple
metabolic
acidosis
Low
PCO2
Mixed
metabolic
acidosis
&
Resp.
alkalosis
High
HCO3
Mixed
resp.
acidosis
&
Metabolic
alkalosis
Expected
HCO3
Simple
resp.
acidosis
Low
HCO3
Mixed
resp.
acidosis
&
Metabo-
lic
acidosis
49. Mixed acid-base disorders
Two or more simple acid-base disorders coexist
• Metabolic acidosis +
Respiratory Acidosis
– pH usually very low
– Pa CO2 too high
– HCO3
- too low
• Metabolic Alkalosis +
Respiratory Alkalosis
– pH usually very high
– Pa CO2 too low
– HCO3
- too high
• Metabolic Acidosis +
Respiratory Alkalosis
– pH may be near normal
– Pa CO2 too low
– HCO3
- too low
• Metabolic Alkalosis +
Respiratory Acidosis
– pH may be near normal
– Pa CO2 too high
– HCO3
- too high
50. Example
• In a patient with primary metabolic acidosis with s
Hco3 10mEqL
• The expected resp. compensation of PCo2 :
(1.5(sHco3)+8 ± 2 )
• So = 23±2
• If we found Pco2 > 25 : means concurrent resp.
acidosis is present(the Pco2 is higher than expected)
• This means that the patient may have a process of
resp. acidosis despite Pco2 is less than normal (35-
45)
51. • The clinical picture can become
complex if abnormalities exist in
both systems simultaneously.
• A review of:
infant’s clinical statues,
treatment
measures
previous blood
gas values,
52. The following steps can be used
as a systematic way of evaluating
parameters in neonatal blood gases:
1. Assess pH
2. Assess respiratory component
3. Assess metabolic component
4. Assess compensation status
5. Complete the acid-base classification
6. Formulate a plan
53. Anion Gap (AG)
• AG is a measure of the relative abundance of unmeasured
anions.
• Used to evaluate patients with metabolic acidosis.
• High AG metabolic acidosis is due to the accumulation of [H+]
plus an unmeasured anion in the ECF.
– Most likely caused by organic acid accumulation or renal failure with
impaired [H+] excretion.
• Normal AG metabolic acidosis is caused by the loss of HCO3
-
which is counterbalanced by the gain of Cl- (measured cation)
to maintain electrical neutrality.
– Most likely caused by HCO3
- wasting from diarrhea or
urinary losses in early renal failure.
54. Determinants of the Anion Gap
AG= UA - UC = [Na+]-([Cl-] + [HCO3
-])
Unmeasured Anions
Proteins (15 mEq/L)
Organic Acids (5 mEq/L)
Phosphates (2 mEq/L)
Sulfates (1mEq/L)
UA = 23 mEq/L
Unmeasured Cations
Calcium (5 mEq/L)
Potassium (4.5 mEq/L)
Magnesium (1.5 mEq/L)
UC = 11 mEq/L
55. Common Causes of Metabolic Acidosis
Increased Anion Gap
(Excess +ve charges (H))
(Think…”MUDPILES”)
• D-lactic acidosis
• Methanol intoxication*
• Uremic acidosis (advanced renal failure)
• Paraldehyde intoxication
• Iron overdose
• L-lactic acidosis*
• Ethylene glycol intoxication*
• Salicylate intoxication
*Denotes most common
56. Common Causes of Metabolic Acidosis
Normal anion gap
(No excess +ve charges(H) but loss of Hco3)
• Mild to moderate renal failure*
• Gastrointestinal loss of HCO3
- (acute
diarrhea)*
• Type I (distal) renal tubular acidosis
• Type II (proximal) renal tubular acidosis
• Ketones lost in urine
*Denotes most common
58. Oxygen Parameters
• Hypoxemia refers to a lower than
normal arterial PO2, and
• hypoxia refers to inadequate oxygen
supply to the body tissue.
59. • Arterial oxygen content is the sum of
dissolved and hemoglobin bound oxygen in
100 ml blood
• Oxygen capacity : O2 carried by 100ml blood
when it is fully saturated
• Saturation of O2 : % of hemoglobin bound to
oxygen (%)
(O2 content / O2 capacity x. 100)
60. Arterial oxygen content
is the sum of
hemoglobin
bound
oxygen in
100 ml
blood
oxygen
dissolved
in
plasma
61. Oxygen content (ml/100 ml of blood)
= (1.37 x Hb )x SaO2) + (0.003 x PaO2)
Where:
1.37 = Milliliters of oxygen bound to 1 g of
hemoglobin at 100 percent saturation(%)
0.03 = Solubility factor of oxygen in plasma (ml/mm Hg)
63. Cao2= (1.37 x Hb )x SaO2) + (0.003 x PaO2)
• Cao2= (1.37 x 14gdl )x 92%) + (0.003 x 60mmhg)
•Cao2= (17.6 ml) + (0.1 ml)
•Cao2= (99%) + (1%)
In premature
In Infant with IVH & Hb content. Drops to 10.5 g/dl
• Cao2= (1.37 x 10.5gdl )x 92%) + (0.003 x 60mmhg)
•Cao2= (13.3 ml) + (0.1 ml) =13.4
•Thus without change in PaO2 & SaO2 a 25% drop in
Hb concent. reduces the O2 content by 24%
64. • This concept is important to remember
when taking care of infant with resp.
disease
• Hb level should be monitored & if low
rapid correction to keep adequate level
of oxygenation
65. Once loaded with oxygen, in the lungs the
blood should reach the tissues to transfer
oxygen to the cells.
Oxygen delivery to the tissue depends
on cardiac output (CO) and arterial
oxygen content (CaO2) :
68. The key concept is that when
assessing a patient’s oxygenation,
more information than just PaO2 and
SaO2 should be considered.
PaO2 and SaO2 may be normal,
but if hemoglobin concentration is low
or cardiac output is decreased, oxygen
delivery to the tissue is decreased.
69. The force that loads hemoglobin with
oxygen in the lungs and unloads it in
the tissues is the difference in partial
pressure of oxygen. In the lungs
alveolar oxygen partial pressure is
higher than capillary oxygen partial
pressure so that oxygen moves to the
capillaries and binds to the
hemoglobin.
70.
71. In tissue partial pressure of
oxygen is lower than that of the
blood, so oxygen moves from
hemoglobin to the tissue.
72.
73. Several factors can affect the affinity of
hemoglobin for oxygen
• The relationship between partial
pressure of oxygen and hemoglobin is
referred to as the oxyhemoglobin
dissociation curve.
75. • Alkalosis,
hypothermia,
hypocapnia, and
decreased levels of
2, 3-
diphosphoglycerate
(2, 3 DPG) increase
the affinity of
hemoglobin for
oxygen.
• Shift to left
• Acidosis, hyperthermia,
hypercapnia and
increased 2, 3 DPG
have the opposite effect,
decreasing the affinity of
hemoglobin for oxygen.
This is referred to as
hemoglobin dissociation
curve shifting to the
right.
76. • This characteristic of hemoglobin
facilitates oxygen loading in the lung
and unloading in the tissue where the
pH is lower and the PaCO2 is higher
77. • . Fetal hemoglobin, which has a higher
affinity for oxygen than adult
hemoglobin, is more fully oxygenated at
lower PaO2 values. This high affinity is
represented by a left shift on the curve
of dissociation of hemoglobin.
78.
79. Oxyhemoglobin Dissociation Curve
The curve is of sigmoidal shape and relates
oxygen content to the partial pressure of oxygen
in the blood. Percent of oxygen saturation is on
the y-axis, and pO2 pressure is on the x-axis,
expressed in mmHg.
80. Why an ABG instead of Pulse
oximetry?
• Pulse oximetry uses light absorption
at two wavelengths to determine
hemoglobin saturation.
• Pulse oximetry is non-invasive and
provides immediate and continuous
data.
81.
82. Why an ABG instead of Pulse
oximetry?
• Pulse oximetry does not assess ventilation
(pCO2) or acid base status.
• Pulse oximetry becomes unreliable 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.
83. Errors in Blood Gas Measurement
• During collection and analysis of blood
gases, the clinician should be aware of the
following potential sources of error:
Temperature – blood gas machines
report results for 37° C. Hypo or
hyperthermia can alter true arterial gas
values.
Hemoglobin – calculated oxygen
saturations are based on adult
hemoglobin, not on fetal or mixed
hemoglobins.
84. Errors(cont.)
Dilution – heparin in a gas sample will
lower the PCO2 and increase the base
deficit without altering the pH.
Air bubbles – room air has a PCO2
close to 0 and a partial pressure of oxygen
of 150. Therefore, air bubbles in the
sample will decrease the PCO2 and
increase the PO2 unless the PO2 is greater
than 150.
85. • Steady state. Ideally, blood gases
should measure the infant’s
condition in a state of equilibrium.
• After changing ventilator settings or
disturbing the infant, a period of 20
to 30 minutes should be allowed for
arterial blood chemistry to reach a
steady state. This period will vary
from infant to infant.
86. Capillary Blood Gas Sampling for
Neonatal
• Capillary blood gas (CBG) samples may be
used in place of samples from arterial
punctures or indwelling arterial catheters to
estimate acid-base balance (pH) and adequacy
of ventilation (PaCO2).
• Capillary PO2 measurements are of little value
in estimating arterial oxygenation.
87. Capillary sampling may be performed by
trained health care personnel in
• 1 Acute care hospitals,
• 2 Clinics,
• 3 Physician offices,
• 4 Extended care facilities,
• 5 Homes.
88. Capillary blood gas sampling is indicated
when
Arterial blood gas analysis is indicated but arterial
access is not available.
Noninvasive monitor readings are abnormal:
transcutaneous values, end-tidal CO2, pulse oximetry.
Assessment of initiation, administration, or change in
therapeutic modalities (ie, mechanical ventilation) is
indicated.
A change in patient status is detected by history or
physical assessment.
Monitoring the severity and progression of a documented
disease process is desirable.
89. Capillary punctures should not be performed
1. at or through the following sites
• posterior curvature of the heel, as the device may puncture the
bone
• Site of peripheral arteries.
• the fingers of neonates (to avoid nerve damage)
• previous puncture sites
• inflamed, swollen, or edematous tissues
• cyanotic or poorly perfused tissues
• localized areas of infection
90. Capillary punctures should not be performed (cont.)
2. on patients less than 24 hours old, due
to poor peripheral perfusion;
3. when there is need for direct analysis
of oxygenation;
4. when there is need for direct analysis
of arterial blood
92. Example1
3ds ♂ old is admitted to the hospital. He was diagnosed as
severe anoxia. His arterial blood gas values are reported as
follows:
pH 7.32
PaCO2 32
HCO3- 18
Don’t forget
PH∞ HCO3
- /
PaCO2
93. • pH 7.32 PaCO2 32 HCO3- 18
1. Assess the pH. It is low (normal 7.35-7.45); therefore
we have acidosis.
2. Assess the PaCO2. It is low. Normally we would
expect the pH and PaCO2 to move in
opposite directions, but this is not the case.
94. • pH 7.32 PaCO2 32 HCO3- 18
• Because the pH and PaCO2 are moving in the same
direction, it indicates that the acid-base disorder is
primarily metabolic.
• In this case, the lungs, acting as the primary acid-
base buffer, are now attempting to compensate by
“blowing off excessive C02”, and therefore increasing
the pH.
95. • pH 7.32 PaCO2 32 HCO3- 18
3. Assess the HCO3. It is low (normal 22-26).
We would expect the pH and the HCO3 - to
move in the same direction, confirming that
the primary problem is metabolic.
96. • pH 7.32 PaCO2 32 HCO3- 18
• What is your interpretation? Because there is
evidence of compensation (pH and PaCO2
moving in the same direction) and because the
pH remains below the normal range, we would
97. interpret this ABG result as a
• partially compensated
metabolic acidosis.
-
•pH ↓ PaCO2 ↓ HCO3 ↓
98. Example 2
2ds old♀ 34 wk is a patient with RDS being admitted in our NICU
. Her admission labwork
reveals an arterial blood gas with the following values:
pH 7.35
PaCO2 48
HCO3 - 28
99. • Follow the three steps:
• pH 7.35 PaCO2 48 HCO3 - 28
1.Assess the pH. It is within the normal range, but on
the low side of neutral (<7.40).
2. Assess the PaCO2. It is high (normal 35-45). We
would expect the pH and PaCO2 to move in
opposite directions if the primary problem is
respiratory.
100. • pH 7.35 PaCO2 48 HCO3 - 28
3. Assess the HCO3. It is also high (22-26).
Normally, the pH and HCO3 should move in the
same direction.
• Because they are moving in opposite directions,
it confirms that the primary acid-base disorder
is respiratory and that the kidneys are
attempting to compensate by retaining HCO3.
101. this ABG as a fully compensated respiratory acidosis.
• Because the pH has returned into the
low normal range, we would interpret
102. Example 3
IDM started to have RD after 4 ds in our intermediate care
neonatal unit . His initial arterial blood gas result is
as follows:
• pH 7.33 PaC02 62 HC03 35
103. pH 7.33 PaC02 62 HC03 35
1. Assess the pH. It is low (normal 7.35-7.45).
This indicates that an acidosis exists.
2. Assess the PaC02. It is high (normal 35-45).
The pH and PaC02 are moving in opposite
directions, as we would expect if the problem
were primarily respiratory in nature.
104. • pH 7.33 PaC02 62 HC03 35
3. Assess the HC03. It is high (normal 22-26).
• Normally, the pH and HC03 should move in the
same direction. Because they are moving in
opposite directions,
• it also confirms that the primary acid-base
disorder is respiratory in nature.
105. • In this case, the kidneys are attempting
to compensate by retaining HCO3 in
the blood in an order to return the pH
back towards its normal range.
106. • Because there is evidence of compensation
occurring (pH and HC03 moving in opposite
directions),
• and seeing that the pH has not yet been
restored to its normal range,
107. • we would interpret this ABG result as
a partially compensated respiratory
acidosis.
108. Example 4
5ds female admitted for ttt of a 26 bilirubin level in her
blood . Exchange transfusion was done . Here are the
last ABG results
• pH 7.43
• PaC02 48
• HC03 36
109. pH 7.43 PaC02 48 HC03 36
1.Assess the pH. It is normal,
but on the high side of
neutral (>7.40)
110. 2. Assess the PaC02. It is high (normal 35-45).
• Normally, we would expect the pH and PaC02
to move in opposite directions. In this case,
they are moving in the same direction
indicating that the primary acid-base disorder is
metabolic in nature.
• pH 7.43 PaC02 48 HC03 36
111. • In this case, the lungs, acting as the
primary acid-base buffer system, are
retaining C02 (hypoventilation) in order
to help lower the pH back towards its
normal range.
112. 3. Assess the HC03. It is high (normal 22-
26). Because it is moving in the same
direction, as ph
• we would expect, it confirms the primary
acid-base disorder is metabolic in
nature on the Alkalotic side.
• pH 7.43 PaC02 48 HC03 36
113. • What is your interpretation?
• Because there is evidence of
compensation occurring (pH and PaC02
moving in the same direction)
• and because the pH has effectively
been returned to within its normal
range,
114. • we would call this
fully compensated metabolic
alkalosis.
