Abg.2 Arterial blood gas analysis and example interpretation

4,650 views 138 slides Mar 17, 2015
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About This Presentation

Arterial blood gas analysis and example interpretation


Slide Content

Arterial Blood Gas
Analysis …..1
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO

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No click

Existing approaches to acid
base balance:
Henderson-Hasselbalch Equation
Copenhagen approach
Boston approach
Stewart approach
To provide Bedside approach to
ABG analysis
No click

Copenhagen approach
Acid-base disorders are classified as
being of
Respiratory origin
(primary change in pCO2)
or of
Metabolic origin
(primary change in fixed acids)
No click

Copenhagen approach
•Respiratory disorders are quantified by
pCO2
•Metabolic disorders are quantified by the
amount of excess fixed acids (the ‘metabolic
acids’)
Often there may be more than one type involved.
It is difficult to predict which one it is and it is not feasible to
measure all of them.
No click

Copenhagen approach
The magnitude of the metabolic
disorder (in the ECF)
can be quantified indirectly by
the amount of change in the
[HCO3]

No click

Boston Approach
This approach is based on actual whole body
titrations rather than on blood samples in a
machine.
The aim has been to determine the magnitude
of the compensation that occurs to graded
degrees of acid-base disturbance.
No click

Stewart’s physicochemical
approach
•Henderson–Hasselbalch equation fails to
consider all the factors influencing
hydrogen ion concentration
•And is insufficient to explain complex
metabolic abnormalities of acid–base
physiology
1970

Stewart’s physicochemical
approach
Based on 3 principles:
•Electrochemical neutrality
•Conservation of mass
•Law of mass action
1970

pH is dependent on other ions in solution not
just H+ and HCO3-
- There are dependent and independent variables :
Dependent:
-H+ - OH- - HCO3- - CO32-
Independent:
-PaCO2
Total of weak non-volatile acids
SID {Strong Ion Difference }
Stewart Equation

A strong ion = an ion that totally
dissociates at a given pH
SID = strong cations – strong anions

SID = (Na+ + K+ + Ca2+ +Mg2+) – (Cl- -
other anions)

Modified SID
(Na+ + K+) – Cl-

Henderson-Hasselbalch
Equation
The starting point is the Henderson
Equation
Based on application of law of mass
action on reaction of CO2 with
water
[H
+
] x [HCO
3
-
] = K x [CO
2
] x [H
2
O]
No click

Hasselbalch modified
Henderson's elegant idea
Regarding the water concentration as
constant and taking logarithms of the
remaining components.
This resulted in the Henderson-Hasselbalch
Equation:
pH = pK + log ( [HCO
3
-
] / [CO2] )
No click

Kassirer-Bleich equation
H+ = 24 × Pco
2
/HCO
3



This equation illustrates that acid-base balance
depends on the ratio of Pco2 and HCO3 −
Not on the absolute value of either one alone.
No click

1. Is patient acidemic or alkalemic?
2. Is primary disorder respiratory or
metabolic?
3. If respiratory, is it acute or chronic?
4. If metabolic acidosis is there an anion
gap? is there an osmolar gap?
ABG Interpretation

5. Is there appropriate compensation?
if no, what is the second disorder?
6. IN THE SETTING OF AG
METABOLIC ACIDOSIS, is there
another problem? what is the delta gap?
ABG Interpretation

Are the data consistent?
The Henderson Equation
[ ]
-
+
´=
3
2
24
HCO
PaCO
H

Convert [H
+
] to pH
•Subtract calculated [H
+
] from 80; this gives the last
two digits of a pH beginning with 7
•example: calculated [H
+
] of 24 converts to pH
of (80-24)~7.56
•example: calculated [H
+
] of 53 converts to pH
of (80-53)~7.27
•Refer to table for more precise conversion, or if
Calculated [H
+
] exceeds 80

Relationship between [H
+
] & pH
pH [H
+
] pH [H
+
]
7.80
7.75
16
18
7.30
7.25
50
56
7.70
7.65
20
22
7.20
7.15
63
71
7.60
7.55
25
28
7.10
7.00
79
89
7.50
7.45
32
35
6.95
6.90
100
112
7.40
7.35
40
45
6.85
6.80
141
159

HCO
3
-
(bicarbonate)
SB (standard bicarbonate)
AB (actual bicarbonate)
SB
The contents of HCO
3
-
of serum of arterial
blood
{ at 37 , PaCO2 40mmHg, SaO

2
100%.}
Normal: 22-27mmol/L
Mean: 24mmol/L

AB
The contents of HCO
3
-
in actual
condition.
In normal person
AB=SB

AB and SB are parameters to
reflect
metabolism, regulated by kidney
Difference of AB-SB can reflect the
respiratory affection on serum HCO
3
-

Respiratory acidosis: AB > SB
Respiratory alkalosis: AB < SB
Metabolic acidosis
AB = SB < Normal
Metabolic alkalosis
AB = SB > Normal

Base Excess

Dbase to normalise HCO
3
(to 24)
with PaCO
2
at 40 mm Hg

HCO
3
-

Hemoglobin
Plasma proteins
HPO42- (phosphate)
Buffer bases(BB)
Buffer base is a measure of the concentration of all the
buffers present in either plasma or blood.

Normal: 45-55mmol/L
mean: 50mmol/L
Significance
Metabolic acidosis: BB
Metabolic alkalosis: BB
Buffer bases(BB)

Regulation of Acid-basic
Balance
Chemical buffer
Dielectric changes of incells and
excells
H
+
---K
+
HCO
3
-
---Cl
-
Physiology regulation through
lung and kidney

Classification of Acid-basic
Disorder
Complementary: PH is
normal
Dis-complementary: PH is
abnormal.

Oxygenation parameters
PaO
2

Normal: 95-100mmHg
PaO
2
=100mmHg - (age×0.33)
±5mmHg

Hypoxia
Mild: 80-60mmHg
MODERATE
60-40mmHg
Severe: <40mmHg

SaO2
0.95-0.98
Not sensitive
PaCO
2

35-45mmHg (4.7-6.0kPa)
Mean:
40mmHg

P
A-a
O
2
Gas exchange

Normal: 15-20mmHg
(<30mmHg in the old)
CaO2
19-21 mmol/L

PvO
2
Mixed venous oxygen pressure
35-45mmHg
Mean: 40mmHg
Significance
Pa-vO
2
is to reflect the tissue absorbing oxygen

O
2
Content of blood:
Hb. x O
2
Sat + Dissolved O
2
(Don’t forget hemoglobin)
Oxygen Saturation: reported as ABG report
( Derived from oxygen dis. curve
not a measured value )
Alveolar / arterial gradient:
( Useful … to classify respiratory failure )
Oxygenation
Indices

0 10 20 30 40 50 60 70 80 90 100 PaO
2
20
40
60
80
100
Rt. Shift
Normal arterio/venous difference
Shift of the curve ……changes saturation for a given PaO
2
Normal
No click
Oxygen delivered
to tissues
with normally placed curve
Delivered oxygen
with Rt. Shift curve

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Alveolar-arterial Difference
Inspired O
2
= 21 %
p
i
O
2
= (760-45) x . 21 = 150 mmHg
O
2
CO
2
p
alv
O
2
= p
i
O
2
– pCO
2
/ RQ
= 150 – 40 / 0.8
= 150 – 50 = 100 mm Hg
PaO
2
= 90 mmHg
p
alv
O
2
– p
art
O
2
= 10 mmHg
One click and wait

Alveolar- arterial Difference
O
2
CO
2
Oxygenation Failure
WIDE GAP
p
i
O
2
= 150
pCO
2
= 40
p
alv
O
2
= 150 – 40/.8
=150-50
=100
PaO
2
= 45
 = 100 - 45 = 55
Ventilation Failure
NORMAL GAP
p
i
O
2
= 150
pCO
2
= 80
p
alv
O
2
= 150-80/.8
=150-100
= 50
PaO
2
= 45
 = 50 - 45 = 5
PAO
2
(partial pres. of O
2
. in the alveolus.)
= 150 - ( PaCO
2
/ .8 )
760 – 45 = 715 : 21 % of 715 = 150
No click

20 × 5 = 100
Expected PaO
2

FiO
2
× 5 = PaO
2
Normal situation
No click

The Blood Gas
Report: normals…
pH 7.40 + 0.05
PaCO
2
40 + 5 mm
Hg
PaO
2
80 - 100 mm Hg
HCO
3
24 + 4 mmol/L
O2 Sat >95
Always mention and see
FIO2
The essentials
HCO3
No click

5
The
Steps for
Successful
Blood Gas
Analysis
No click

Step 2
Who is responsible for this change in pH ( culprit )?
 CO
2
will change pH in opposite direction
 Bicarb. will change pH in same direction
Acidemia: With HCO
3
< 24 mmol/L = metabolic
With PCO
2
>40 mm hg = respiratory
Alkalemia:With HCO
3
>24 mmol/L = metabolic
With PCO
2
<40 mm Hg = respiratory
Step 1
Look at the pH
Is the patient acidemic pH < 7.40
or alkalemicpH > 7.40

Step 3
If there is a primary respiratory
disturbance, is it acute ?
.08 change in pH ( Acute )
.03 change in pH ( Chronic )
10 mm
Change
PaCO
2
=

Primary lesion
Compensation
pH
Bicarbonate
PaCO
2
METABOLIC ACIDOSIS
HYPER VENTILATION
BICARB CHANGES
pH in same direction
Low
Alkali
Three clicks

Primary lesion
Compensation
pH
Bicarbonate
PaCO
2
METABOLIC ALKALOSIS
HYPO VENTILATION
BICARB CHANGES
pH in same direction
High
Alkali
Three clicks

Primary lesion
compensation
pH
PaCO
2
BICARB
Respiratory acidosis
CO
2
CHANGES
pH in opposite direction
High
CO
2
Three clicks
Wait for red circle

Primary lesion
compensation
pH
PaCO
2
BICARB
Respiratory alkalosis
PaCO
2
CHANGES
pH in opposite direction
Low
PaCO
2
Three clicks
Wait for red circle

Primary disorderFormula
Metabolic acidosis¯PCO
2
= 1.2 x ¯[HCO
3
-
]
Metabolic alkalosis­PCO
2
= 0.7 x ­[HCO
3
-
]
Respiratory acidosis
Acute ­[HCO
3
-
] = 0.1 x ­PCO
2

Chronic ­[HCO
3
-
] = 0.4 x ­PCO
2

Respiratory alkalosis
Acute ¯[HCO
3
-
] = 0.2 x ¯ PCO
2

Chronic ¯[HCO
3
-
] = 0.5 x ¯ PCO
2
Step 4 : Degree of compensation

Suspect if .............
actual PaCO
2
is more than
expected : additional …
respiratory acidosis
actual PaCO
2
is less than
expected : additional …respiratory
alkalosis

Step 4 : cont.
If there is metabolic acidosis, is there a wide anion gap ?
Na - (Cl
-
+ HCO
3
-
) = Anion Gap usually < 12
If >12, Anion Gap Acidosis :
M ethanol
U remia
D iabetic Ketoacidosis
P araldehyde
I nfection (lactic acid)
E thylene Glycol
S alicylate
Common pediatric
causes
1)Lactic acidosis
2) Metabolic
disorders
3) Renal failure

Step 4: Which type?
•Check anion gap (AG): If AG is high
•High AG metabolic acidosis is present
•If metabolic acidosis is diagnosed:
Check ­AG / ¯[HCO
3
-
]
•<1 : High AG Met. Acid + normal AG Met. Acid.
•1-2: High AG Met. Acid
•>2: High AG Met. Acid. + Met. Alk.
•If metabolic acidosis is not diagnosed:
•High AG Met. Acid. + Met. Alk.

1. Normal gap
2. Increased gap
1.Renal “HCO
3

losses
2. GI “HCO
3

losses
Proximal RTA
Distal RTA
Diarrhea
1. ­ Acid prod
2. ¯ Acid elimination
Lactate
DKA
Ketosis
Toxins
Alcohols
Salicylates
Iron
Renal disease
Metabolic acidosis and the anion gap

5 th step
Clinical correlation
No click

HCO3
META.pH
PaCO
2 pH RESP.
Same direction
Opposite direction
Same direction
No click

PaCO
2 of 10pH
Acute change .08
Chronic change .03

C
o
m
p
e
n
s
a
t
io
n
Considered complete
when the pH returns
to normal range
No click

C
O
M
P
E
N
S
A
T
I
O
N


L
I
M
I
T
S
METABLIC ACIDOSIS
PaCO2 = Down to 10 ?
METABOLIC ALKALOSIS
PaCO2 = Maximum 6O
RESPIRATORY ACIDOSIS
BICARB = Maximum 40
RESPIRATORY ALKALOSIS
BICARB = Down to 10

Blood Gas Report
Measured 37.0
o

C
pH 7.523
PaCO
2
30.1 mm Hg
PaO
2
105.3mm Hg
Calculated Data
HCO
3
act 22 mmol / L
O
2
Sat 98.3 %
PO
2
(A - a) 8 mm Hg D
PO
2
(a / A) 0.93
Entered Data
FiO
2
21.0 %
Case 1
16 year old female with
sudden onset of dyspnea.
No Cough or Chest Pain
Vitals normal but RR 56,
anxious.
Acute respiratory alkalosis
And why acute ?

Case 2 6 year old male with progressive respiratory distress
Muscular dystrophy .
Blood Gas Report
Measured 37.0
o

C
pH 7.301
PaCO
2
76.2 mm Hg
PaO
2
45.5 mm Hg
Calculated Data
HCO
3
act 35.1 mmol / L
O
2
Sat 78 %
PO
2
(A - a) 9.5 mm Hg D
PO
2
(a / A) 0.83
Entered Data
FiO
2
21 %
pH <7.35 :acidemia
Res. Acidemia : High PaCO
2
and low pH
Hypoxemia
Normal A-a gradient
 CO
2
=76-40=36
Expected  pH for ( Acute ) = .08 for 10
Expected ( Acute ) pH = 7.40 - 0.29=7.11
Chronic resp. acidosis
Hypoventilation
Chronic respiratory acidosis
With hypoxia due to hypoventilation
Five clicks

Case 3
8-year-old male asthmatic;
3 days of cough, dyspnea
and orthopnea not
responding to usual
bronchodilators.
O/E: Respiratory distress;
suprasternal and
intercostal retraction;
tired looking; on 4 L NC.
pH <7.35 ; acidemia
PaCO
2
>45; respiratory acidemia
p
i
O
2
= 715x.3=214.5 / p
alv
O
2
= 214-49/.8=153 Wide A / a gradient
Hypoxia
WITH INCREASE IN CO2 BICARB MUST RISE ?
Bicarbonate is low………
Metabolic acidosis + respiratory acidosis
30 × 5 = 150
 CO
2
= 49 - 40 = 9
Expected  pH ( Acute ) = 9/10 x 0.08 = 0.072
Expected pH ( Acute ) = 7.40 - 0.072 = 7.328
Acute resp. acidosis
8-year-old male asthmatic with resp. distress Six clicks

Case 4 8 year old diabetic with respi. distress fatigue and loss of appetite.
Blood Gas Report
Measured 37.0
o

C
pH 7.23
PaCO2 23 mm Hg
PaO2 110.5mm Hg
Calculated Data
HCO
3
act 14 mmol / L
O2 Sat %
PO2 (A - a) mm Hg D
PO2 (a / A)
Entered Data
FiO2 21.0 %
pH <7.35 ; acidemia
HCO3 <22; metabolic acidemia
Last two digits of pH
Correspond with co2
If Na = 130,
Cl = 90
Anion Gap = 130 - (90 + 14)
= 130 – 104 = 26
Three clicks

Blood Gas Report
Measured 37.0
o

C
pH 7.46
PaCO2 28.1 mm Hg
PaO2 55.3 mm Hg
Calculated Data
HCO
3
act 19.2 mmol / L
O2 Sat %
PO2 (A - a) mm Hg D
PO2 (a / A)
Entered Data
FiO2 24.0 %
Case 5 : 10 year old child with encephalitis
pH almost within normal range
Mild alkalosis
PaCO
2
is low , respiratory
low by around 10
( Acute ) by .08
(Chronic ) by .03
BICARBINATURIA
Bicarb looks low ?
Is it expected ?
Four clicks

Case #6:
•A 4 year old with chronic renal failure
presents to the pedes ER with history of
increasing azotemia, weakness, and
lethargy.
•Exam reveals the patient to be modestly
hypertensive, and tachypneic. Labs reveal
BUN=100, and Creatinine=8.
•How can we tell if an acid-base disorder is
present?

Case #6:
•Steps 1&2: must know pH, PaCO
2, HCO
3
•pH=7.37, PaCO
2
=22, and HCO
3
=12
•Step 3: are the available data consistent?
[]
-
+
´=
3
2
24
HCO
PaCO
H

Case #6:
•[H+]=44, equates to pH~7.36; data are
thus consistent
•What is the primary disorder?
•“_________Acidosis”
•Which variable (PaCO
2
, HCO
3
) is
deranged in a direction consistent with
acidosis?
•Primary disorder is “Metabolic Acidosis”

Is compensation appropriate?
•HCO
3
is decreased by 12 mmoles/l
•PaCO
2
should decrease by 1 to 1.5 times the
fall in HCO
3
; expect PaCO
2
to decrease by
12-18 mm Hg or be between 22-28 mm Hg
•Since PaCO
2
is 22 mm Hg, compensation is
appropriate, and the data are consistent with
a simple metabolic acidosis with respiratory
compensation

•If the data are consistent with a simple disorder,
it does not guarantee that a simple disorder
exists; need to examine the patient’s history
•When compensatory responses do not lie within
the accepted range, by definition a
combined disorder exists.

Case #7:
•A 15 year old female is brought to the
pedes ER in an obtunded state.
•Per her family, patient history is
notable for progressive weakness over
two months.

Case #7:
•A recent “complete physical”
demonstrated decreased DTRs
symmetrically, without other
abnormal findings.
•Exam shows shallow, tachypneic
respiratory effort.

Case #7: Steps 1, 2, and 3
•What baseline information is required?
•PaCO
2
=40 mm Hg, HCO
3
=7, pH=6.88
•Are the data internally consistent?
[]
-
+
´=
3
2
24
HCO
PaCO
H

Case #7:
•[H
+
]~140, which equates to a pH~6.85, so
data are internally consistent
•What is the primary disturbance?
•“___________ Acidosis”
•Which variable is deranged in a direction
which is consistent with acidosis?
•PaCO
2 WNL, “Metabolic Acidosis”

Is compensation appropriate?
•Metabolic Acidosis
•PaCO
2
should fall by 1 to 1.5 mm Hg x the fall
in plasma [HCO
3
]
•HCO
3
decreased by 17, so we expect PaCO
2

to be decreased by 17-26
•PaCO
2
WNL; since PaCO
2
inappropriately
high, there is a combined metabolic acidosis
and respiratory acidosis

Case #8:
•A 16 year old male with sickle cell
anemia, hemochromatosis, & subsequent
cirrhosis, presents with a several day
history of emesis.
•At presentation to the pedes ER, he is
hypotensive, orthostatic, and confused.
•What acid-base disorders might be
anticipated based on the above
information?

Case #8:
•16 yo male with sickle cell anemia, hemo-
chromatosis, & subsequent cirrhosis, and
several days of emesis. In the pedes ER,
he is hypotensive, orthostatic, and
confused.
•Emesis-loss of H
+
(HCl)-metabolic
alkalosis

Case #8:
•Orthostatic hypotension-?
• lactic acidosis

Case #8:
•SCD-decreased O
2
delivery-?
•Lactic acidosis

Case #8:
•Cirrhosis
Decreased lactate metabolism

Case #8:
•What baseline information is available?
•pH=7.55, PaCO
2
=66
•‘lytes: Na
+
=166, K
+
=3.0, Cl
-
=90, HCO
3
=56
•Are the data internally consistent?
[ ]
-
+
´=
3
2
24
HCO
PaCO
H

Case #8:
•[H+]~28, equates to pH~7.55; consistent
•What is the primary abnormality?
•“_________ Alkalosis”
•PaCO
2
­ed, HCO
3
­ed, therefore…….
•“Metabolic Alkalosis” presumed due to
emesis
•Is compensation appropriate?

Case #8:
•Metabolic Alkalosis
•PaCO
2
should rise by .25 to 1 mm Hg x the
rise in plasma [HCO
3
]
•HCO
3
­ed by 32; PaCO
2
should ­ by 8-32
•PaCO
2
­ed by 26, so compensation
appears appropriate
•What about multiple risk factors for
lactic acidosis?

Case #8:
•Could there be a concealed lactic acidosis?
•What is the anion gap?
•Na
+
- (Cl
-
+ HCO
3
), normally 12-14
•Anion gap here is 166 - (90 + 56) = 20
"­ed anion gap implies metabolic acidosis
•Combined metabolic alkalosis & metabolic
acidosis therefore present

•Always calculate the anion gap
•Often it is the only sign of an occult
metabolic acidosis
•Acidotic patients partially treated
with HCO
3
•Acidotic patients with emesis
IN

•Always calculate the anion gap
May be the only sign of metabolic
acidosis “concealed” by concomitant
acid-base disorders

Occult metabolic acidosis post-Rx:
NormalKetoacidosisPost-RX
Na
+
140 140 148
Cl
-
105 105 98
HCO3 25 10 25
ketones0 15 15
AG 10 25 25
pH
PaCO2
7.40
40
7.30
31
7.40
40

Causes of Anion Gap Acidosis
•Endogenous acidosis
•Uremia (uncleared organic acids)
•Ketoacidosis, Lactic acidosis (increased
organic acid production), Rhabdomyolosis
•Exogenous acidosis
•Ingestions: salicylate, iron; paraldehyde
use
•Other Ingestions
•Methanol toxicity, Ethylene Glycol toxicity

Anion Gap:
Based on the concept of
electroneutrality
Available cations
=
Available anions

Anion Gap:
UA-UC
Anion Gap
Na
+
- (Cl
-
+HCO
3-
)
12 to 14

Anion Gap:
Serum albumin
contributes ~1/2 of the
total anion “UA” pool

Anion Gap:
1gm/dl in serum
albumin
Anion gap by
3 mEq/L

Anion Gap:
•Therefore an anion gap of
12 mEq/L is corrected to
17-18 mEq/L when the
serum albumin is half of
normal

Case #9:
•A 3 year old is brought to the pedes
ER at ~3am, stuporous and
tachypneic. History is remarkable
for his parents having cleaned out
their medicine cabinet earlier that
day.

Case #9:
•An ABG and electrolytes have
been
•Accidentally drawn
by the nurse.

Case #9:
•Available data: pH=7.53, PaCO
2
=12;
Na
+
=140, K
+
=3.0, Cl
-
=106, HCO
3
=10
•Are the data internally consistent?
[]
-
+
´=
3
2
24
HCO
PaCO
H

Case #9:
•[H+]~29, so pH~7.51; data consistent
•What is the primary disturbance?
•“__________ Alkalosis”
•Which variable (PaCO
2
, HCO
3
) is deranged
in a direction consistent with alkalosis?
"¯ed PaCO
2
, ¯ed HCO
3
; so “Respiratory
Alkalosis”

Case #9:
•Is compensation appropriate?
•Acute respiratory alkalosis
•Plasma [HCO
3
] should fall by ~1-3
mmole/l for each 10 mm Hg decrement in
PaCO
2
, usually not to less than 18 mmoles/l
•PaCO
2
¯ed by ~30 mm Hg; HCO
3
should fall
by 3-9 mmole/l; HCO
3
¯ is too great, so
superimposed metabolic acidosis

Case #9:
•What is the anion gap?
•140 - (106 + 10) = 24; elevated anion
gap consistent with metabolic acidosis
•What is the differential diagnosis?
•Combined (true) respiratory alkalosis
and metabolic acidosis seen in sepsis,
or salicylate intoxication

Case #10:
•A 5 year old with Bartter’s Syndrome is
brought to clinic, where she collapsed.
•She has recently been febrile, but
history is otherwise unremarkable.
•pH=6.9, PaCO
2
=81; Na
+
=142, K
+
=2.8, Cl
-
=87, HCO
3
=16

Case #10:
•Are the data consistent?
•[H
+
]=122, pH~6.9; data are consistent
[]
-
+
´=
3
2
24
HCO
PaCO
H

Case #10:
•What is the primary disturbance?
•“_________ Acidosis”
•Which variable (PaCO
2
, HCO
3
) is
deranged in a direction consistent with
acidosis?
•Both; pick most abnormal value--
•“Respiratory Acidosis”
•Is compensation appropriate?

Case #10:
•Acute Respiratory Acidosis
•Plasma [HCO
3
] should rise by ~1mmole/ for each
10 mm Hg increment in PaCO
2
•Since HCO
3
is inappropriately depressed,
compensation is not appropriate, and there is
a concomitant metabolic acidosis as well
•What is the anion gap?
•AG=39, confirms metabolic acidosis

Case #10:
•Combined Respiratory Acidosis and
Metabolic Acidosis; are there other disorders
present?
•What about the dx of Bartter’s Syndrome?
•Bartter’s Syndrome characterized by
hypokalemic metabolic alkalosis
•Does this patient have a concealed metabolic
alkalosis?

Case #10:
•Anion gap is 39, or 25-27 greater than
normal
•Typically, increases in anion gap correlate
with decreases in HCO
3
•Assuming a 1:1 relationship, as anion gap
increases by 25, HCO
3
should fall by 25
•Starting HCO
3
must have been 16 + 25 = 41

Case #10:
•Therefore, starting HCO
3
was ~41 mmol/l,
consistent with expected chronic metabolic
alkalosis.
•This metabolic alkalosis was “concealed” by
the supervening profound metabolic and
respiratory acidoses

Case #10:
•Final diagnosis
Metabolic alkalosis, metabolic
acidosis, & respiratory acidosis

Rule
Mixed Acid-Base Disorders
Coexistant metabolic acidosis and
metabolic alkalosis may occur.
Always check the change in the anion gap
vs. decrement in bicarbonate to rule out
a concealed metabolic disorder.

Delta Ratio
•The increase in Anion Gap /
the decrease in HCO3-
•Indicates what has happen to
the denominator (HCO3-)

Delta Ratio
•Used in RAGMA to see whether
change in HCO3- is appropriate
•Normal value = 1 to 1.5
•If normal there is only one pathology
(uncomplicated RAGMA)

Delta Ratio
•Interpretation
•< 0.4 - hyperchloraemic normal anion
gap acidosis
•0.4 - 0.8 - consider combined high AG &
normal AG acidosis
•BUT note that the ratio is often < 1 in
acidosis associated with renal failure

Delta Ratio
•1 – 2 - usual for uncomplicated high-AG
acidosis (lactic acidosis: average value 1.6
) { DKA: around 1 }
•> 2 - a high delta ratio an elevated
bicarbonate at onset of the metabolic
acidosis pre-existing metabolic
alkalosis or compensated respiratory
acidosis.

Case #11:
•A 3 year old toddler is brought to the ER at 3
am after being found unarousable on his
bedroom floor, with urinary incontinence,
bradycardiac.
•One amp of D
50
W and 0.1 mg of naloxone
were given IV without response.
•Vital signs are stable; respiratory effort is
regular, but tachypneic.
•He is acyanotic.

Case #11:
•Initial lab studies (lytes, ABG & urine tox
screen) are sent. Initial dextrostick is >800.
•Initial available data are:
•Na
+
=154, K=5.6, Cl=106, HCO
3
=5, BUN=6
creatinine=1.7, glucose=804, PO
4
=12.3, Ca
+
+
=9.8, NH
4
=160, serum osms=517
•pH=6.80, PaCO
2
=33, PaO
2
=298

Case #11:
•What is the primary disturbance?
•________ Acidosis
•Metabolic Acidosis
•Is compensation appropriate?
•No; PaCO2 level is inappropriately high
•Are other disorders present?
•Respiratory acidosis (due to evolving coma)

Case #11:
•What is our differential thus far?
•Anion gap vs. non-anion gap metabolic acidosis
•DKA, lactic acidosis, renal failure, ingestion
•The urine tox screen comes back negative
•What does urine tox screen actually screen for?
•The patient’s IV falls out.
•He then has a seizure, is incontinent of urine.

Case #11:
•What is the calculated serum osmolality,
and does an osmolal gap exist?
•2(Na) + BUN/2.8 + Glucose/18
•Calculated=355, Measured=517
•What is the most likely diagnosis?
•How can this be confirmed definitively?
•Review of urinanalysis
•Serum ethylene glycol level

Case #11:
Anion gap metabolic
acidosis
Osmolal gap
Methanol, ethylene glycol
ethyl alcohol, isopropyl alcohol

You CAN have a respiratory problem and
a metabolic problem (and even a secondary
metabolic problem on top of that)
look at delta gap
Anion gap delta versus Bicarb delta

Normally in AG Met Acidosis
the number of anions above 14 should
equal the number of bicarb below 24
(Calculated anion gap - 14) versus (24 -
measured HCO3)

If Bicarb delta is less than the Anion
gap delta
Metabolic alkalosis as well

If Bicarb delta is more than the
Anion gap delta
Non AG metabolic acidosis as well

Most common AG met acidosis:
ketoacidosis, lactic acidosis, ASA
(IF ruled out investigate toxic alcohols)
ASA not only results in AG met
acidosis but also Resp alkalosis

A low glucose does not rule
out ketoacidosis
Look out for starvation, dehydration,
alcohol

Consider cyanide and carbon
monoxide in inhalation and burn
victims
Don’t be fooled by normal Osat and
PaO2 - Carbon monoxide needs
Carboxyhemoglobin

Isoniazid antidote is vit b6...think
about it in refractory seizures (esp
high risk TB populations)
Reduced arterial-venous oxygen sat
difference (<10%) suggests cyanide
toxicity
Cyanide antidote is induced
methemaglobinemia

Ethylene glycol or methanol antidote
is etoh or Fomepizole
Ethylene glycol in urine will
fluoresce using a Wood’s lamp
Calcium oxalate crystals in urine are
sign of possible ethylene glycol
ingestion

Most common loss of bicarb
by GI {Diarrhea}
or kidneys
{ Tubular acidosis or renal failure }

Metabolic Alkalosis - Saline
Responsive
Either loss of H+ or contraction (volume contraction
around constant HCO3)
Urine Cl <10
Gastric suction
Vomiting
Diuretics
Give Saline, gets better

Metabolic Alkalosis - Non Saline
Responsive
Retention of HCO3 associated with
mineralcorticoid excess
Urine Cl >20
Hyper aldosteronism
Exogenous steroids
Adenocarcinomoa
Bartter’s syndrome
Cushing’s syndrome

RAGMA
{Raised anion gap metabolic acidosis }
look for lactate, calculate Delta ratio,
Stewart Equation
When to calculate what ?

NAGMA
{Normal anion gap metabolic acidosis }
Calculate Urinary anion gap
Stewart Equation
Osmolar gap
When to calculate what ?

Osmolar Gap
The osmolality is measured in lab
Calculated osmolarity
(2 x [Na+]) + [glucose]/18 + [urea]/2.8
Osmolality {from lab.} – Osmolarity {calculated}
An osmolar gap > 10 mOsm/l is often stated to
be abnormal

Osmolar Gap
Significance
Indirect evidence for the presence of an
abnormal solute which is present in significant
amounts.
Ethanol, methanol & ethylene glycol -> will
cause an elevated osmolar gap.

Urinary Anion Gap {UAG}
[Na+]+ [K+] - [Cl-]

Clinical Use
Differentiate between GIT and renal
causes of a hyperchloraemic metabolic
acidosis

The decreased PaO
2
causes us to increase our
minute ventilation resulting in a lower PaCO
2.

In order that pH remain within normal limits,
the kidneys excrete HCO
3
-
to compensate for
the low PaCO
2
So ABG values are slightly different than
textbook sea level values
Blood Gas values { High altitudes }

The pH may be very low, i.e. < 7.00
Since both a metabolic acidemia
(anaerobic metabolism, lactic acidemia)
And a respiratory acidemia (inadequate
ventilation) will be causing the pH to fall.
In a code situation

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Remember that COPD patients may
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2
in the 88% range.
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