Acid and Anion

“The First Concern”
“the first concern in any life

threatening illness
is to maintain
an adequate supply of oxygen
to sustain oxidative metabolism”
[Marino 2nd ed.]

The Oxygenation Profile
• ABG Overview
• Allows evaluation of arterial oxygen
– Sa02
– Pa02
• Allows evaluation of alveolar (pulmonary)
oxygen
– A-a gradient
– P/F ratio
• Allows evaluation of serum-cellular environment
– pH
PaO2-FiO2 ratio
• Normal PaO2/FiO2 is 300-500
• <250 indicates a clinically significant gas
exchange derangement
ABG Overview
• Facilitates determination of ventilation
– PaC02
• Facilitates evaluation of tissue metabolism
and/or renal function
– Base calculation
– Bicarbonate calculation (may use total serum C02)
– Lactic acid from arterial gas
• Facilitates evaluation of primary and secondary
problems as well as compensatory efficiency
Chemistry Profile Overview
• Facilitates evaluation of tissue metabolism or
renal failure
– Total serum C02 (direct measure of reserve serum
buffer and is used to calculate bicarbonate)
– Serum blood glucose
– Serum ketones
– Lactic acid : chemistry special laboratory
• Facilitates evaluation of problem and

compensation
Potassium
• Potassium : weather vein : The serum K
can be used as a poor man’s pH meter in
the absence of pH measure.
• This can help to differentiate between
acidosis vs. compensated alkalosis for
example in the setting of a low HCO3.
• This effect is stronger for inorganic
acidoses.
Acid-base Terminology
• Acidemia: blood pH < 7.35
– Acidosis: a primary physiologic process that,
occurring alone, tends to cause acidemia.
Examples: metabolic acidosis from
decreased perfusion (lactic acidosis);
respiratory acidosis from hypoventilation. If
the patient also has an alkalosis at the same
time, the resulting blood pH may be low,
normal, or high.
• Alkalemia: blood pH > 7.45
– Alkalosis: a primary physiologic process that,
occurring alone, tends to cause alkalemia.
Examples: metabolic alkalosis from
excessive diuretic therapy; respiratory
alkalosis from acute hyperventilation. If the
patient also has an acidosis at the same time,
the resulting blood pH may be high, normal,
or low.
• Primary acid-base disorder: One of the
four acid-base disturbances that is
manifested by an initial change in HCO3-
or PaCO2.
• Compensation: The change in HCO3- or
PaCO2 that results from the primary event.
Compensatory changes are not classified
by the terms used for the four primary
acid-base disturbances.
Acid-Base Disturbances
• Are common in critical patients
• May be complex or mixed
• Are often confusing
• Requires accurate analysis to facilitate
appropriate treatment
Focus on Metabolic Acidosis

5 Step Approach
• Acidemic or Alkalemic : Check pH
• Is the overriding disturbance respiratory or
metabolic?
– If respiratory, is it acute or chronic?
– If metabolic acidosis is present, is there an wide AG.
• If metabolic acidosis disturbance is present is the
respiratory system compensating adequately?
WINTER’S FORMULA.
• Are other metabolic disturbances present in a
patient with a anion gap metabolic acidosis?
– This is the famous delta delta approach which aims at
calculating the bicarbonate level before the generation of
the anion gap acidosis.
– Measured bicarbonate + (AG – 12)
The Profile
Components of the ABG and Chemistry Panel

that are indicators in acid-base balance/imbalance.
pH | pCO2 | pO2 | O2 Sat| (H+)HC03| Base| Total CO2
Direct measure of acid

Inversely reflects acid (estimates one of the
major buffers)
The Profile
Cells: Producer Kidney: Regulator
• Produces acid during • Major volume and
metabolism: acid transported electrolyte regulator
as carbonic acid
• Tissue acids increase in insulin • Acid regulator
deficiency states • Base regulator
• Tissue acids increase in tissue
hypoxia states
Lung: Acid regulator
Cells: Regulate pH
• Acidosis: acid (H+) uptake in • Rate and depth of
exchange for potassium breaths depends on the
release provides buffer effect carbonic acid and
and promotes intracellular therefore the pH
hypokalemia
• Alkalosis: acid (H+) release in
exchange for potassium
uptake provides buffer effect
and promotes intracellular
hyperkalemia
The Profile
• Direct Effects from Acid : Presence or
Absence
• pH: directly reflects acid
– When acid goes up, pH goes down
– Acids are formed as end products of protein,
carbohydrate, and fat metabolism.
– To maintain the body’s normal pH (7.35-7.45),
the H2C03 must be controlled:
• H+ must be neutralized (buffer and cells) or
excreted (requires renal function)
• C02 must be regulated via ventilation
15
Respiratory = PCO2
pCO2 is directly measured (not

calculated), and is a reliable indicator of
respiratory acid-base disturbances. The
correlation between pCO2 and respiratory
pH is direct, consistent, and linear.
And there’s an equivalent

measurement for metabolic…
… and it’s NOT bicarb…
In pure metabolic disorders, bicarb is a
useful measurement, but if you’ll remember
the equilibrium formula:
H20 + CO2 ↔ H2CO3 ↔ H+ + HCO3-
…you’ll notice that HCO3 can be affected by
respiratory (CO2) or metabolic (H+) components,
and therefore isn’t a specific marker for either.
In fact, the relationship between metabolic acidosis
and bicarbonate is neither consistent nor linear.
• Direct Effects from Acid Presence or
Absence
• CO2 = Acid
– CO2 =  pH
– CO2 = pH
• HCO3 - = Base (opposite of H+: acid)
–  HCO3 - (think H+ {acid}) = pH
–  HCO3 - (think H+ {acid}) = pH
The Profile
CO22 + H22O H22CO33 H++ + HCO33--
1. When carbonic acid goes up, pH goes down.

2. Attempts to compensate are made via the shift of
carbonic acid to the unaffected side.
• Requiring increased clearance via ventilation
(RR x Tidal volume) when the problem is
either metabolic (tissue production) or renal
(acid clearance, buffer production).
• Requiring increased renal clearance
(increased carbonic acid presented to the
kidney, separation of H+ from HC03 ) excreting
acid and retaining buffer.
CO22 + H22O H22CO33 H++ + HCO33--
1. H2C03 is carbonic acid:

when it increases pH goes down
when it decreases pH goes up
2. C02 is a pre-form of H2C03:
The partnership of C02 +H20 yields carbonic acid
3. H+ is a pre-form of H2C03:
The partnership of H+ and HC03 yields carbonic acid
4. H+ is a byproduct of tissue metabolism and is increased when:
1.) metabolic disorders at the tissue level donate more H+
(hypoxia, failure of lactate-pyruvate conversion, ketosis)
2.)there is failure to clear acid (renal failure) and produce
HC03 from H2C03
Modified Henderson and
Hasselbalch Equation
• H+ = 24 x PCO2/HCO3
• Equation emphasizes that the [H] depends
on a ratio and not absolute concentrations.
CO22 + H22O H22CO33 H++ + HCO33--

COMPENSATION
COMPENSATION
Increase
Increase RR
RR pH PROBLEM
PROBLEM
Increase
Increase Tidal
Tidal Ketosis
Ketosis
Volume
Volume Lactic
Lactic acidosis
acidosis
If the problem is metabolic ( ketosis or lactic acidosis both increasing H+

production), compensation occurs via increasing the minute ventilation (RR x
TV) and blowing off C02: Rapid compensatory mechanism: should occur
immediately
CO22 + H22O H22CO33 H++ + HCO33--
pH COMPENSATION
COMPENSATION
PROBLEM
PROBLEM
Renal
Renal excretion
excretion of
of H+
H+
Pulmonary
Pulmonary failure
failure
Retaining
Retaining HC0
HC033 --
Slow
Slow compensation
compensation
If the problem is ventilation failure ( C02 retention) , slow compensation requiring

renal regulation occurs: H2C03 is separated in the renal tubules into H+ and HC03 -
CO22 + H22O H22CO33 H++ + HCO33--

pH
In severe sepsis, it is common to see metabolic failure first ( H+ up)

with respiratory compensation (C02 down). Eventually respiratory
failure can follow. When both systems fail, the original and then the
compensatory system, the carbonic acid , H2C03, will increase with no
where to dissociate (cannot be shifted to its compensatory side). pH
will drop sharply.
Acid-Base Perfect Values (Acceptable

range)
• pH= 7.40 (7.35 - 7.45)
– H2CO3 affects the ph (H2CO3↑, pH↓)
• PCO2 = 40 (35 – 45)
• HCO3 - = 24 (22 - 26) opposite of H+
• Interpretation of the arterial blood gas
• Determine
– 1) The problem is named by the direction of
the pH in respect to perfect : acidosis or
alkalosis
• When not perfect, the pH goes (from perfect) in the
acid or alkaline direction
• Is the pH up (alkaline) or down (acid)?
• Determine
• Is the pH inside or outside the range of
normal?
– Inside range
» May just be normal variation : PCO2. HCO3
- are within range of normal
» May be a problem , but compensation has
occurred. Find the culprit which is the cause
of the pH changed
– Outside range
» NEVER normal, always a primary problem
» NOT compensated, that is why the pH is out of range
» FREQUENTLY reflects two primary problems
• Determine
• Step 2) The problem is named by the causative culprit
which affects the pH
• Is the pH up (alkaline) or down (acid)?
• If the pH is down that reflects acid
• If the problem is respiratory, PCO2 has to be up
• If the problem is metabolic ( either production or
regulation) , the HCO3 - has to be down,
Remember, HCO3 – moves inversely to H+ and
what you really want to know about is the
absence or presence of acid
• Determine
• Step 3) if the pH is down and outside
range
– NEVER normal
– NAME the problem
• PCO2 direct measure of acid, if the cause is PCO2 it goes in
the opposite direction of the pH
• HCO3 – calculation of buffer (H+ assumed) think
H+ and if the cause, H+ it goes in the opposite
direction of the pH
• Step 4) if the pH is down, but inside range
– may be a normal variation ( all three
measures within range)
– It is abnormal:
• If one of the two measures (PCO2 ,HCO3 – ,(H+
assumed) is abnormal ( out of range ):
– Determine if the culprit is what caused the pH shift:
– If yes, THERE HAS to be compensation from
the other system, otherwise pH CANNOT be
normal range
measures CO2 pH Bicarb (H+)
perfect 40 7.40 24 (H+)

range 35-45 7.35-7.45 22-26
note 21 7.52 15 ( H+↑)

note 65 7.22 23( H+↑)
note 65 7.355 36
Measures CO2 pH HCO3 (H+ )
perfect 40 7.40 24 (perfect)
range 35-45 7.35- 22-26 ( H+↑ - H+↓ )
7.45
sample 44 7.36 24 ( H+ perfect)
CO2 44, pH 7.36, HCO3 24

• www.barbaramclean.com
Case #1:
• 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 #1:
• pH=7.37, PaCO2=22, and HCO3=12
Is compensation appropriate?
• HCO3 is decreased by 12
mmoles/l
• PaCO2 should decrease by 1 to
1.5 times the fall in HCO3; expect
PaCO2 to decrease by 12-18 mm
Hg or be between 22-28 mm Hg
• 24 – (12)= 12
• Pac02 1 to 1.5 times (bicarb)
• Step 1: Name the problem:
– pH shift towards acid or alkaline (from perfect)
• Step 2: Name the problem:
– pH inside or outside range
• Step 3: Name the cause
– Causative factor must be what affects the pH
• Step 4: Is there compensation
– pH within range but not perfect
Example 1:
pH = 7.26 : pH is a symptom of the primary
problem: In this case acidosis!
• pH is on the acid side and outside the
range of normal.
•This is an acute problem (acute means the
pH is out of range).
• Find the cause, using C02 and HC03 (H+)
CO2 = 60 mmHg
↑ CO2 =  pH
Example
pH = 7.26
CO2 = 60 mmHg= acid
↑ CO2 =  pH
1. Acute: pH out of range
2. Acidosis: pH down
3. Respiratory: C02 is up and out of range ( more acid: failure
to ventilate)
Name the initial problem: acute respiratory acidosis
Example 1
• HCO3 = Base (opposite of H+ acid)
–  HCO3 (think H+ {acid}) = pH
–  HCO3 (think H+ {acid}) = pH
Example
pH = 7.26
CO2 = 60 mmHg= acid
HCO3 = 28 ( up and slightly out of range, therefore H+ is slightly down:
headed towards compensation)
1. Acute: pH out of range (if pH out of range, there is NOT compensation,
never normal)
2. Acidosis: pH down
3. Respiratory: C02 is up and out of range ( more acid: failure to ventilate)
Name the initial problem: acute respiratory acidosis ( acute means uncompensated)
Assessing Compensation Example; Five hours later
• HCO3 = Base (opposite of H+ acid)
–  HCO3 (think H+ {acid}) = pH
–  HCO3 (think H+ {acid}) = pH
Example
pH = 7. 351
CO2 = 60 mmHg= acid
HCO3 = 35 ( up and out of range, therefore H+ is down)
Do you still have a problem?
YES! acidosis (pH down but inside range) caused by ventilation failure (
C02 up and outside range)
BUT if there is a problem (C02) and pH is in range there has to be
compensation, and that only occurs from the non problem side !
RENAL: shifted the increase in carbonic acid (↑C02 + H20 → ↑ H2C03
which is then presented to the functional kidney which separates the
↑ H2C03 into HC03 and H+
The Oxygeanation Profile

range 35-45 7.35-7.45 22-26 ( H+↑ - H+↓ )
21 7.36 12 ( H+↑↑↑ )
CO2 21, pH 7.36, HCO3 12 ( H+↑↑↑ )
Answer: Respiratory rate is 26. Patient is blowing off C02 and which
removes C02. If the patient was hyperventilating and that was
the problem, the pH would be up and alkalotic. When evaluating
further, the low HC03 indicates a significant increase in H+
(metabolic acid). HC03 ↓↓ (H+ ↑↑) , pH ↓ but in range: Only way
that happens is compensation!
Answer:. Compensated metabolic acidosis. Compensated!!
Increased metabolic acid causing increased carbonic acid is
compensated with an increase in ventilation( C02↓ and RR↑)
Buffering Systems
• A buffer is a chemical that can bind
excessive H+ or OH– without a significant
change in pH
• A buffering pair consists of a weak acid
and its conjugate base
• The most important plasma buffering
systems are the carbonic acid–
bicarbonate system and hemoglobin
44
Carbonic Acid–Bicarbonate Pair
• Operates in both the lung and the kidney
• The greater the partial pressure of carbon
dioxide, the more carbonic acid is formed
– At a pH of 7.4, the ratio of bicarbonate to carbonic
acid is 20:1
– Bicarbonate and carbonic acid can increase or
decrease, but the ratio must be maintained
45
• If the amount of bicarbonate decreases,
the pH decreases, causing a state of
acidosis
• The pH can be returned to normal if the
amount of carbonic acid also decreases
– This type of pH adjustment is referred to as
compensation
• The respiratory system compensates by
increasing or decreasing ventilation
• The renal system compensates by producing
acidic or alkaline urine
46
47
Other Buffering Systems
• Protein buffering
– Proteins have negative charges, so they can
serve as buffers for H+
• Renal buffering
– Secretion of H+ in the urine and reabsorption
of HCO3–
• Cellular ion exchange
– Exchange of K+ for H+ in acidosis and
alkalosis
48
Buffering Systems
49
Metabolic Alkalosis
• Respiratory compensation raises PCO2 by 0.7
mmHg for every 1 meq/L rise in HCO3
• Causes include vomiting, intake of alkali,
diuretics, or very commonly, NG suction without
the use of proton-pump inhibitors or H2 blockers
Respiratory Acidosis
• Compensation occurs in 2 steps
– 1. Cell buffering that acts within minutes to hours
– 2. Renal compensation that is not complete for 3-5
days
• IN ACUTE: Bicarb rises 1 meq/L for every
10 mmHg elevation in PCO2
– or for every 1 up of PCO2, pH should fall .0075
• IN CHRONIC: Bicarb rises 3.5 for every

10
– or for every 1 up of PCO2, pH should fall .0025
– due to tighter control of pH by increased renal excretion of acid
as ammonium
Respiratory Alkalosis
• ACUTE: Plasma bicarb falls by 2 for every
10 fall in PCO2
• CHRONIC: Bicarb falls by 4 for every 10
fall in PCO2
Anion Gap
If Metabolic acidosis is present, is anion gap
wide (> 20)?
• Calculate the anion gap (AG). If the anion gap is ≥ 20,
there is a primary metabolic acidosis regardless of pH
or serum bicarbonate concentration. The acidosis is due
to increased H+
• Gap is generally wide only with ↑ metabolic ACID
production ( Lactic Acid/ Ketoacid)
Principle: The body does not generate a wide anion gap

as a compensatory mechanism for a primary disorder.
With a wide AG, metabolic acidosis is ALWAYS the
primary disorder!
Anion Gap
Anion gap is “a concept used to estimate electrolyte (anions & cation)
levels in the serum and {measures or estimates the , sic} conditions
that influence them” (Taber’s Cyclopedic Medical Dictionary, 2005).
Normal Anion Gap = (Na+) - (Cl- + HCO3-) = 12 (+/- 2)
• Positive charged ions and negative charged ions are relatively equal
in normal physiology. In vivo physiology all equal!
• The measured ions (lab analysis) are represented by Na+, Cl- and
HC03- (or total serum C02), the external measured gap of 12 (+/- 2)
is considered acceptable
Na+ (Cl - + HCO3 -)

Anion Gap
Anion Gap = (Na+) - (Cl- + HCO3-)
• When there is an increase in unmeasured ions, there will be a gap
between the + and – measures
• A gap of > 20 implies a metabolic increase in acid production.
• Lactic Acid and Ketoacid donate H+ .
• H+ binds to HC03 and/or Cl changing the charge
• HC03 and/or Cl ↓
• The gap between + and – gets wide
(Cl - + HCO3 -)↓↓ : light on the negatives
(Lactic acid or ketones donated H+)↑↑ heavy on the positives
Na+ constant
7.22 12
• 1. 145 - (12 + 122)= 11
• 2. 138- (12+ 104)= 22
• 149-( 12+90)= 47
Anion Gap
• Used to confirm type of metabolic acidosis with ABG
• Used to diagnose metabolic acidosis without ABG
• Affected by:
– albumin (for each 1 gm decrease in albumin , add three
points to gap)
– hyperchloremia (usually from fluid resuscitation)
• High Cl- causes decrease in available HC03-
• High Cl- binds to H+ → HCl
• Cannot compensate because is not a compound that can be blown
off
• Metabolic acidosis with normal gap: non-gap acidosis
– most commonly occurs in hyperchloremia
Anion Gap
range 35-45 7.35- 22-26 ( H+↑ - H+↓ )
7.45
10 7.31 5 (H+↑↑↑)
.
Answer: HC03 is down and outside of range which means
H+ is up and outside of range: Acidosis. This is
metabolic acidosis. Although there is an attempt to
compensate, the ventilatory drive is at its limits.
CO2 10, pH 7.31, HCO3 5, Na 135, Cl 90

Anion gap: Na – (Cl – HCO3) = 135 (90+5) = 135-95 = 40
Anion Gap
CO2 10, pH 7.31, HCO3 5, Na 135, Cl 90
Anion gap: Na – (Cl – HCO3) = 135 (90+5) = 135-95 = 40
The wide anion gap supports the presence of increased

metabolic acids!
First question: What is the glucose and diabetic history?
Second question: Does the patient have lactic acidosis?
Third question: If neither, does history support acid
ingestion?
Anion Gap
• Helps to identify the type of metabolic
acidosis
– Non-anion gap acidosis
• chloride
– Anion gap acidosis suggests
• DKA
• Lactic acidosis
Watch Out In…….
• Decrease in unmeasured anions
– Hypoalbuminemia
• Increase in unmeasured cations
– Hypercalcemia
– Hypermagnesemia
– Hyperkalemia
– Multiple myeloma
– Lithium toxicity
ABG analysis
• Respiratory compensation ( metabolic acidosis)
results in 1.2 mm Hg fall in PCO2 for every 1
meq/L fall in bicarb
• pCO2 = 1.5 (HCO3) + 12
• Winters formula
– Calculates expected PaCO2 for metabolic acidosis
– PaCO2 = 1.5 x HCO3 + 12
• Determine anion gap (AG) – AG = NA – (HCO3+
CL)
– AG metabolic acidosis
– Non AG acidosis – determined by delta gap
Calculating Gap
• Calculate the excess anion gap (total anion gap –
normal anion gap) and add this value to the measured
bicarbonate concentration:
– if the sum is > than normal bicarbonate (> 30) there is an
underlying metabolic alkalosis
– if the sum is less than normal bicarbonate (< 23) there is an
underlying nonanion gap metabolic acidosis
1. Excess AG = Total AG – Normal AG (12)
2. Excess AG + measured HCO3 = > 30 or < 23?
• Principle: 1 mmol of unmeasured acid titrates 1 mmol

of bicarbonate (  anion gap =  [ HCO3])
Why is this true?
• For each 1 mmol acid titrated by the
carbonic acid buffer system, 1 mmol of
HCO3 is lost via conversion to CO2 and
H2O and 1 mmol of the sodium salt of the
unmeasured acid is formed.
1 mmol  in HCO3 = 1mmol in AG
• Therefore, the sum of the new (excess)
anion gap and the remaining (measured)
bicarbonate values should equal the
normal bicarbonate concentration
ABG analysis
• Delta gap
– Delta HCO3 = HCO3 (electrolytes) + change in AG
• Delta gap < 24 = non AG acidosis
• Delta gap > 24 = metabolic alkalosis
Is there more than one problem?
• Now evaluate the metabolic component of
acid/base regulation remembering that the
metabolic side is affected by
– Production of H+ (ketosis, lactic acidosis)
– Excess ingested acids (i.e., salicylate )
– Excretion of acid (renal)
– Regulation of bicarbonate (renal, Chloride)
Principle: There may be two sides to the

problem. At the very least, you expect
compensation to occur.
Mixed Acid-base Disorders are
Common
• In chronically ill respiratory patients, mixed
disorders are probably more common than
single disorders
• In renal failure (and other conditions)
• Always be on the lookout for mixed acid-
base disorders. They can be missed!
Tips to Diagnosing Mixed
Acid-base Disorders
• TIP 1. Do not interpret any blood gas data for acid-base
diagnosis without closely examining the serum
electrolytes: Na+, K+, Cl-, and CO2.
– A serum CO2 out of the normal range always represents some
type of acid-base disorder (barring lab or transcription error).
– High-serum CO2 indicates metabolic alkalosis &/or bicarbonate
retention as compensation for respiratory acidosis.
– Low-serum CO2 indicates metabolic acidosis &/or bicarbonate
excretion as compensation for respiratory alkalosis.
– Note that serum CO2 may be normal in the presence of two or
more acid-base disorders.
Tips to Diagnosing Mixed Acid-
base
• TIP 2.Disorders (cont.)
Single acid-base disorders do not lead to
normal blood pH. Although pH can end up in the
normal range (7.35 - 7.45) with a single mild
acid-base disorder, a truly normal pH with
distinctly abnormal HCO3- and PaCO2
invariably suggests two or more primary
disorders.
– Example: pH 7.40, PaCO2 20 mm Hg, HCO3- 12
mEq/L in a patient with sepsis. Normal pH results
from two co-existing and unstable acid-base disorders
- acute respiratory alkalosis and metabolic acidosis.
Tips to Diagnosing Mixed Acid-
base
• TIP 3.Disorders (cont)
Simplified rules predict the pH and
HCO3- for a given change in PaCO2. If the pH
or HCO3- is higher or lower than expected for
the change in PaCO2, the patient probably has a
metabolic acid-base disorder as well.
Predicted changes in HCO3- for a directional
change in PaCO2 can help uncover mixed
acid-base disorders.
• A normal or slightly low HCO3- in the presence of hypercapnia
suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO2
50 mm Hg, HCO3- 22 mEq/L. Based on the rule for increase in
HCO3- with hypercapnia, it should be at least 25 mEq/L in this
example; that it is only 22 mEq/L suggests a concomitant metabolic
acidosis.
• b) A normal or slightly elevated HCO3- in the presence of

hypocapnia suggests a concomitant metabolic alkalosis, e.g., pH
7.56, PaCO2 30 mm Hg, HCO3- 26 mEq/L. Based on the rule for
decrease in HCO3- with hypocapnia, it should be at least 23 mEq/L
in this example; that it is 26 mEq/L suggests a concomitant
metabolic alkalosis.
Tips to Diagnosing Mixed Acid-base
Disorders (cont.)
• TIP 4. In maximally-compensated metabolic
acidosis, the numerical value of PaCO2 should
be the same (or close to) as the last two digits of
arterial pH. This observation reflects the formula
for expected respiratory compensation in
metabolic acidosis:
– Expected PaCO2 = [1.5 x serum CO2] + (8 ± 2)
• In contrast, compensation for metabolic alkalosis
(by increase in PaCO2) is highly variable, and in
some cases there may be no or minimal
compensation.
Case #2:
• 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/“malingering” over
two months. A recent “complete physical”
demonstrated decreased DTRs
symmetrically, without other abnormal
findings. Exam shows shallow, tachypneic
respiratory effort.
Case #2
• What baseline information is required?
• PaCO2=40 mm Hg, HCO3=7, pH=6.88
• Are the data internally consistent?
+ PaCO 2
[ H ] = 24 × −
HCO 3
Case #2:
• [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?
• PaCO2 WNL, ergo, “Metabolic Acidosis”
• Metabolic Acidosis
– PaCO2should fall by 1 to 1.5 mm Hg x the fall
in plasma [HCO3]
• HCO3 decreased by 17, so we expect
PaCO2 to be decreased by 17-26
• PaCO2 WNL; since PaCO2 inappropriately
high, there is a combined metabolic
acidosis and respiratory acidosis
Case #3
• 33 y/o with DKA presents with the
following:
– Na = 128, Cl = 90, HCO3 = 4, Glucose = 800
– 7.0/14/90/4/95%
Case # 3
• PaCO2=14 mm Hg, HCO3=4, pH= 7.0
+
PaCO 2
[ H ] = 24 × −
HCO 3
Case # 4
• Triple disorder
– AG acidosis
– Respiratory acidosis
– Non AG acidosis
• History would suggest AG acidosis is
secondary to hypotension with lactic acid
build up and the patient is not able to
compensate with his COPD therefore
there is no respiratory compensation and
the non AG acidosis is secondary to
diarrhea with associated HCO3 loss.
Case # 4
• 40 y/o with pneumonia and low BP on
dopamine. She has been having N/V over
the last three days
• Na = 130, Cl = 90, HCO3 = 10
• ABG = 7.26/15/65/10/90%
• PH = acidemia
• AG = 130 – (90 + 10) = 30
• PC02 = 1.5(10) + 8 = 23
• Delta HC03 = 10 + (30 –12) = 28
Case #4
• Answer
– AG acidosis
– Respiratory alkalosis
– Metabolic alkalosis
– Patient has sepsis causing AG acidosis
and respiratory alkalosis. Previous N/V
caused baseline metabolic alkalosis
Case #5
• 65 y/o with respiratory failure and COPD
– ABG on vent. 7.60/40/60/30/90%, HCO3 = 30
– Baseline ABG 7.35/60/55/30/88%, HCO3 = 30
– Questions:
• What is wrong with this situation ?
• What will happen if it is not changed ?
• How do we fix it ?
Case #5
• Vent. ABG = 7.25/35/80/10/95%, HCO3

=10
– Questions:
• What is the acid/base status of the patient ?
• What equation would you use to determine the
changes that need to be made to the ventilator ?
• What should we do with the ventilator ?
ABG analysis
• Pitfalls
– Trying to interpret the acid base status without
using the prior formulas
– Using the HCO3 on the ABG which is
calculated (must use the HCO3 from lytes)
– Not drawing the lytes and ABG at the same
time
– Failing to make sure the ABG correlates with
patents clinical situation
Case # 6
• An ill-appearing alcoholic male presents
with nausea and vomiting.
– ABG - 7.4 / 41 / 85 / 22
– Na- 137 / K- 3.8 / Cl- 90 / HCO3- 22
Case # 6
• Anion Gap = 137 - (90 + 22) = 25
 anion gap metabolic acidosis
• Winters Formula = 1.5(22) + 8  2 = 39  2
 compensated
• Delta Gap = 25 - 10 = 15
• 15 + 22 = 37
 metabolic alkalosis
Case # 7
• 22 year old female presents for attempted
overdose. She has taken an unknown
amount of Midol containing aspirin,
cinnamedrine, and caffeine. On exam she
is experiencing respiratory distress.
Case # 7
• ABG - 7.47 / 19 / 123 / 14
• Na- 145 / K- 3.6 / Cl- 109 / HCO3- 17
• ASA level - 38.2 mg/dL
Case # 7
• Anion Gap = 145 - (109 + 17) = 19
• Winters Formula = 1.5 (17) + 8  2
= 34  2
 uncompensated
• Delta Gap = 19 - 10 = 9
9 + 17 = 26
 no metabolic alkalosis
Case #8
• 47 year old male experienced crush injury
at construction site.
• ABG - 7.3 / 32 / 96 / 15
• Na- 135 / K-5 / Cl- 98 / HCO3- 15 / BUN-
38 / Cr- 1.7
• CK- 42, 346
Case #8
• Anion Gap = 135 - (98 + 15) = 22
• Winters Formula = 1.5 (15) + 8  2= 30  2
 compensated
• Delta Gap = 22 - 10 = 12
• 12 + 15 = 27
 mild metabolic alkalosis
Strong Ions
H+ + K+ + Na+ = Cl- + HCO3- + OH-

You need electroneutrality, or you would
glow.
If your blood was saline, Na+ would have to equal Cl-.
If you added potassium bicarbonate…
And then added a bunch of other ions…
Which ones of these matter, and which are clutter?
Strong Ions
Mg++ Ca++ K+ Na+ Cl- Others (lactate, etc)

These are the “Strong Ions,” so-called because they
do not readily combine with other ions or lose their
charge. Conversely, H+ and HCO3- readily combine,
and are called “weak ions.”
The difference between the strong cations and

strong anions is called the Strong Ion Difference (SID),
and indicates the net ionic charge of the weak anions;
so it indicates the relative strength of H+ and HCO3-.
Strong Ion Difference
Remember, SID = strong cations – strong
anions. It indirectly measures weak ions
(HCO3 and A-).
SID = HCO3- + A-
[Just for the record, HCO3 + A- was called “Buffer Base” as far
back as the 1950’s – SID was “invented” by Stewart in 1980.]
You can get HCO3 by Henderson-Hasselbach if you
know pCO2 and pH (this is the calculated ABG value).
You can get A- if you know ATOT and pH.
Base Excess
• Definition: The amount of a strong acid
(like HCl) needed to bring blood to 7.40.
• Assumes 100% oxygenation, 37oC, and
pCO2 of 40.
Normal = 0
Used to calculate the metabolic component of

an acid-base disturbance.
Base Excess calculations
Calculated the same way, in practice, as

SID: Buffer Base = HCO3- + A-
HCO3 calculated by pH & pCO2 (blood gas machine)
A- calculated using pH & hemoglobin (whole blood)
OR A- calculated using albumin & phos (plasma)
BE = Buffer Base – “expected buffer base”
(expected if pH = 7.4 and pCO2 = 40)
Membranes & Ions – you guys
should feel right at home!
There are flavors of Base Excess: Base
ExcessErythrocyte; Base ExcessPlasma; Base
ExcessECF (entire extracellular fluid); Base
ExcessWhole Blood – how do we decide what
to use?
The Gibbs-Donnan equilibrium describes the
behavior whenever a membrane separates
impermeable ATOT buffer (Hgb) while allowing
passage of other ions (Cl-, HCO3-).
Standard Base Excess
aka “Base Excess of ECF.” ECF includes
plasma, red cells, and the surrounding
interstitial fluid. It’s where the action takes
place in the body regarding acid-base
movement.
Blood-gas machines calculate SBE as:
SBE = 0.9287 * (HCO3- - 24.4 + (14.83 * (pH – 7.4)
And guess what – it turns out that ATOT, while

fascinating, doesn’t really matter clinically. A nice
advantage for SBE.
And SBE makes a pretty
nomogram.
Compare & Contrast:
And the math is easier.
How do you figure out if compensation is normal?
In metabolic acidosis, If ΔpCO2 = SBE, then it’s normal.
In metabolic alkalosis, If ΔpCO2 = SBE * 0.6, then it’s

normal.
And the math is easier.
In acute respiratory disorders, if SBE = 0 (+/- 5), then it’s

normal.
In chronic respiratory disorders, if ΔpCO2 ( 0.4) = SBE,

then it’s normal.
ABG analysis
• Delta gap
– Delta HCO3 = HCO3 (electrolytes) + change in AG
• Delta gap < 24 = non AG acidosis
• Delta gap > 24 = metabolic alkalosis
– Note: The key to ABG interpretation is

following the above steps in order.
Simple Acid-Base Disorders:
• The compensatory variable always
changes in the SAME DIRECTION as the
primarily deranged variable
• Compensation is always more

pronounced in CHRONIC
RESPIRATORY disorders than in acute
respiratory disorders
8 Sequential Rules:
• Rule #4:
– must know if compensation is
appropriate
– compensation never overshoots
• Must have known “rules of thumb” to

interpret appropriateness of compensation
Rules of Compensation:
– PaCO2 should fall by 1 to 1.5 mm Hg x the
fall in plasma [HCO3]
• Metabolic Alkalosis
– PaCO2 should rise by .25 to 1 mm Hg x the
rise in plasma [HCO3]
• Acute Respiratory Acidosis
– Plasma [HCO3] should rise by ~1mmole/l for
each 10 mm Hg increment in PaCO2
• Chronic Respiratory Acidosis

– Plasma [HCO3] should rise by ~4mmoles/l for
• Acute Respiratory Alkalosis
– Plasma [HCO3] should fall by ~1-3 mmole/l for
each 10 mm Hg decrement in PaCO2, usually
not to less than 18 mmoles/l
• Chronic Respiratory Alkalosis
Case #1:
• 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 #1:
• Steps 1&2: must know pH, PaCO2, HCO3
• pH=7.37, PaCO2=22, and HCO3=12
• Step 3: are the available data consistent?
 H   24 
 PaCO
HCO 
2
3
Case #1:
• [H+]=44, equates to pH~7.36; data are
thus consistent
• What is the primary disorder?
• “_________Acidosis”
• Which variable (PaCO2, HCO3) is
deranged in a direction consistent with
acidosis?
• Primary disorder is “Metabolic Acidosis”
• HCO3 is decreased by 12 mmoles/l
• PaCO2 should decrease by 1 to 1.5 times
the fall in HCO3; expect PaCO2 to
decrease by 12-18 mm Hg or be between
22-28 mm Hg
• Since PaCO2 is 22 mm Hg, compensation
is appropriate, and the data are consistent
with a simple metabolic acidosis with
respiratory compensation
8 Sequential Rules:
• Rule #5:
– 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
• Rule #6:
– When compensatory responses do not lie
within the accepted range, by definition a
combined disorder exists.
Case #2:
• 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/“malingering” over
two months. A recent “complete physical”
demonstrated decreased DTRs
symmetrically, without other abnormal
findings. Exam shows shallow, tachypneic
respiratory effort.
Case #2: Steps 1, 2, and 3
• PaCO2=40 mm Hg, HCO3=7, pH=6.88
 H   24 
 PaCO
HCO 
2
3
Case #2:
• [H ]~140, which equates to a pH~6.85, so
+
data are internally consistent

• “___________ Acidosis”
• Which variable is deranged in a direction
which is consistent with acidosis?
• PaCO2 WNL, ergo, “Metabolic Acidosis”
– PaCO2 should fall by 1 to 1.5 mm Hg x the
fall in plasma [HCO3]
• HCO3 decreased by 17, so we expect
PaCO2 to be decreased by 17-26
• PaCO2 WNL; since PaCO2 inappropriately
high, there is a combined metabolic
acidosis and respiratory acidosis
Case #3:
• 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 #3:
• 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
• Orthostatic hypotension-?lactic acidosis
• SCD-decreased O2 delivery-?lactic
acidosis
• Cirrhosis-decreased lactate metabolism
Case #3:
• What baseline information is available?
• pH=7.55, PaCO2=66
• ‘lytes: Na+=166, K+=3.0, Cl-=90, HCO3=56
 H   24  HCO
 PaCO

2
3
Case #3:
• [H+]~28, equates to pH~7.55; consistent
• What is the primary abnormality?
• “_________ Alkalosis”
• PaCO2ed, HCO3 ed, therefore…….
• “Metabolic Alkalosis” presumed due to
emesis
• Is compensation appropriate?
Case #3:
• Metabolic Alkalosis
– PaCO2 should rise by .25 to 1 mm Hg x the
rise in plasma [HCO3]
• HCO3 ed by 32; PaCO2 should  by 8-32
• PaCO2 ed by 26, so compensation
appears appropriate
• What about multiple risk factors for lactic
acidosis?
Case #3:
• Could there be a concealed lactic
acidosis?
• What is the anion gap?
• Na+- (Cl- + HCO3), normally 12-14
• Anion gap here is 166 - (90 + 56) = 20
• ed anion gap implies metabolic acidosis
• Combined metabolic alkalosis &
metabolic acidosis therefore present
8 Sequential Rules:
• Rule #7: Always calculate the anion gap
• Often it is the only sign of an occult
metabolic acidosis
– acidotic patients partially treated with HCO3
– acidotic patients with emesis
• May be the only sign of metabolic acidosis
“concealed” by concomitant acid-base
disorders
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; the
assumption that the sum of all available cations=
the sum of all available anions. Restated as:
• Na+ + Unmeasured Cations (UC) = Cl- + HCO3 +

Unmeasure Anions (UA); conventionally
restated:
• Na+-(Cl-+HCO3)=UA-UC=Anion Gap=12 to 14
Anion Gap:
• Na+-(Cl-+HCO3)=UA-UC
• Serum albumin contributes ~1/2 of the total
anion equivalency of the “UA” pool. Assuming
normal electrolytes, a 1gm/dl decline in serum
albumin decreases the anion gap factitiously by
3 mEq/L. Therefore an anion gap of 12 mEq/L is
corrected to 17-18 mEq/L when the serum
albumin is half of normal; this is an important
correction factor in settings of chronic illness or
malnourished patients
Occult metabolic acidosis post-Rx:
Normal Ketoacidosis Post-RX

Na + 140 140 148
Cl- 105 105 98
HCO 3 25 10 25
ketones 0 15 15
AG 10 25 25
pH 7.40 7.30 7.40
PaCO 2 40 31 40
Case #4:
• 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. An ABG and electrolytes have
been accidentally drawn by the nurse.
Case #4:
• Available data: pH=7.53, PaCO2=12;
Na+=140, K+=3.0, Cl-=106, HCO3=10
H  
 24 
PaCO 2

HCO 3
Case #4:
• [H+]~29, so pH~7.51; data consistent
• “__________ Alkalosis”
alkalosis?
• ed PaCO2, ed HCO3; so “Respiratory
Alkalosis”
Case #4:
• Acute respiratory alkalosis
• PaCO2 ed by ~30 mm Hg; HCO3 should
fall by 3-9 mmole/l; HCO3  is too great, so
superimposed metabolic acidosis
Case #4:
• 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 #5:
• A 5 year old with Bartter’s Syndrome is
brought to clinic, where she collapses.
She has recently been febrile, but history
is otherwise unremarkable. An ABG and
serum electrolytes are obtained: pH=6.9,
PaCO2=81; Na+=142, K+=2.8, Cl-=87,
HCO3=16
Case #5:
• Are the data consistent?
  
H  24 
PaCO 2
HCO 
• [H ]=122, pH~6.9; data are
+
consistent
3
Case #5:
• “_________ Acidosis”
acidosis?
• Both; pick most abnormal value--
• “Respiratory Acidosis”
Case #5:
• Acute Respiratory Acidosis
– Plasma [HCO3] should rise by ~1mmole/l for
• Since HCO3 is inappropriately depressed,
compensation is not appropriate, and
there is a concomitant metabolic
acidosis as well
• AG=39, confirms metabolic acidosis
Case #5:
• 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 #5:
• Anion gap is 39, or 25-27 greater than
normal
• Typically, increases in anion gap correlate
with decreases in HCO3
• Assuming a 1:1 relationship, as anion
gap increases by 25, HCO3 should fall by
25
• Starting HCO3 must have been 16 + 25 =
41
Case #5:
• Therefore, starting HCO3 was ~41 mmol/l,
consistent with expected chronic metabolic
alkalosis. This metabolic alkalosis was
“concealed” by the supervening profound
metabolic and respiratory acidoses
associated with her arrest event.
• Final diagnosis: Metabolic alkalosis,
metabolic acidosis, & respiratory
acidosis
8 Sequential Rules; Rule #8
• Rule #8: 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.
Case #6:
• A 3 year old toddler is brought to the ER at
3 am after being found unarousable on his
bedroom floor, with urinary incontinence.
EMS monitoring at the scene revealed
sinus bradycardia. One amp of D50W and
5 mg of naloxone were given IV without
response. Vital signs are stable;
respiratory effort is regular, but tachypneic.
He is acyanotic.
Case #6:
• 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, HCO3=5, BUN=6
creatinine=1.7, glucose=804, PO4=12.3,
Ca++=9.8, NH4=160, serum osms=517
• pH=6.80, PaCO2=33, PaO2=298
Case #6:
• ________ Acidosis
• No; PaCO2 level is inappropriately high
• Are other disorders present?
• Respiratory acidosis (due to evolving
coma)
Case #6:
• 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, and fills the
specimen bag you placed on ER arrival.
Case #6:
• 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 urinalysis
– Serum ethylene glycol level
How Many Primary
Abnormalities Can Exist in One
• Three primary abnormalities is the max
Patient?
because a person cannot simultaneously
hyper and hypoventilate
• One patient can have both a metabolic
acidosis and a metabolic alkalosis –
usually one chronic and one acute
POINT!!!!! Rapid respiratory rate is
assumed to be compensatory for
metabolic acidosis until proven
otherwise
POINT!!!! Wide Anion Gap
• Used to confirm type of metabolic acidosis with ABG
• Used to diagnose metabolic acidosis without ABG
• Affected by:
– albumin (for each 1 gm decrease in albumin , add three
points to gap)
– hyperchloremia (usually from fluid resuscitation)
• High Cl- causes decrease in available HC03-
• High Cl- binds to H+ → HCl
• Cannot compensate because is not a compound that can be blown
off
• Metabolic acidosis with normal gap: non-gap acidosis
– most commonly occurs in hyperchloremia
So what about lactate?
Lactate
• Is serum Lactate a good marker of

adequacy of perfusion?
Lactate Levels
• Lactic acid is a product of carbohydrate
metabolism.
– Normal to produce 15 to 20 mmol/kg per day
– Normal plasma level is 0.5 to 1.5 meq/L
• Hyperlactatemia is considered to be present if the
level exceeds 4 to 5 meq/L
– Lactic acid is rapidly buffered by extracellular
bicarbonate resulting in lactate.
– Liver and kidneys convert lactate back to
pyruvate which is then converted to CO2 &
H2O or glucose
Lactate
• ↑Lactate production results from cellular
metabolism of pyruvate into lactate under
anaerobic condition
• blood lactate level in type A lactic acidosis
is related to the total oxygen debt and the
magnitude of tissue hypoperfusion
Lactate
• type A lactic acidosis, resulting from an
imbalance between tissue oxygen supply
and demand
• Elevated blood lactate levels associated
with metabolic acidosis are common
among critically ill patients with systemic
hypoperfusion, tissue hypoxia and
metabolic dysfunction
Targeting Lactate
• use as index of hypoperfusion in sepsis
complicated by several factors
– elevation may reflect reduced elimination, not
increased production
– epinephrine surge stimulates Na, K-ATPase
and promotes glycolysis
– pyruvate dehydrogenase enzyme dysfunction
in sepsis
– some organs produce more lactate than others
• elevation may depend upon the particular organ
compromised from sepsis
Targeting: Blood Lactate
• no study has targeted correction of lactate per se
• high lactate levels in critically ill patients associated
with increased mortality (Bakker et al. Chest 1991)
• utility of a single high initial lactate debated
– poor sensitivity and specificity
• lactate clearance better predictor of mortality
Bakker et al. (Am J Surg 1996)
– lac-time: time in which blood lactate > 2 mmol/l
– survivors had decreased lac-time
– lac-time also directed correlated with number of organ
failures
Nguyen et al. Crit Care Med 2004

• serial lactate levels may improve the prognostic value
and help guide therapy
Physiologic Effects of Acidosis
• Reduced cardiac contractility
• Pulmonary vasoconstriction
• Reduced systemic vascular tone
• Impaired response to catecholamines
• Compensatory hyperventilation
• Hypotension +Hyperventilation=
• THINK ACIDOSIS!!!
DKA defined
A life threatening complication of diabetes
(usually Type I) which requires a prompt,
organized, and rational approach to
treatment to minimize morbidity and
mortality
Lab criteria for DKA
All three criteria of the following criteria are
required to make the diagnosis of DKA:
hyperglycemia (BG > 250 mg/dl)

low bicarbonate (< 15 meq/l)
low pH (< 7.3) with ketonemia
Ketones and acidosis
Acidosis can be due to keto-acids (DKA) but
can be due to many other causes (both
gap and non-gap)
Patients who have not eaten in > 12 hours

may have low level “starvation” ketones
Anion Gap and Ketones
DKA - waste products of non-glucose
dependent pathway produce ketones
(betahydroxybutyrate and acetoacetate)
that are acids (H+/anion) build up in the
blood stream (increase in anion gap)
Lactic Acidosis
Why do we need oxygen?
• For oxidative phosphorylation
What is oxidative phosphorylation?
• ADP + Pi = ATP (requires energy)
• The formation of ATP
What does the oxygen do?
Lactic Acidosis
• Glycolysis:GlucosePyruvateAcetyl CoA
• Kreb’s:Acetyl CoANADH & FADH
• Electron transport chain (ETC)

– NADH & FADHATP
Lactic Acidosis
• The bulk of ATP is generated in the electron

transport chain (ETC) in the mitochondrion
• The energy for creating the high-energy
phosphate bond is generated at several
points in the ETC. So are hydrogen ions
Metabolic Acidosis
High -
(primary fall in serum bicarbonate)
Oxygen allows for ATP formation in

an electrically-neutral biologically safe manner
Metabolic Acidosis
(primary fall in serum bicarbonate)
Lactic Acidosis
• Type A:failure of oxidative
phosphorylation ( ) PyruvateLactate
• Type B: lactate production

overwhelms lactate metabolism
Lactic Acidosis
Type Aof(more
• Failure ETC: severe)
• Decreased Oxygen delivery
– Shock of any type
– Severe hypoxemia
– Severe Anemia
– Inhibitors (CO, CN)
Lactic Acidosis
Type B production
• Lactate (less severe)
overwhelms lactate
metabolism (not anaerobic)
• Malignancies (after chemotherapy)
• Hepatic failure
• Drugs (biguanides, AZT, INH)
Acid/Base
• Metabolic alkalosis
– Removal of gastric secretions
– Factitious Diarrhea (laxatives)
– Mineral corticoid excess
– Diuretics
– Posthypercapnic alkalosis
– Milk alkali syndrome
Metabolic Alkalosis
Chloride responsive
• Volume Contraction:
– NG suction
– Vomitting
– Diuretics
• Post Hypercapnia
• Hypokalemia
• Hypomagnesemia
• Carbenicillin, Penicillin
Metabolic Alkalosis
Chloride Unresponsive
• Adrenal Disorders
– Glucocorticoid Excess
– Mineralcorticoid Excess
• Exogenous Steroids
• Alkali Ingestion
• Licorice
• Bartter’s Syndrome
Metabolic Alkalosis
Signs and
• Muscle Symptoms
cramps
• Weakness
• Hypoxia
• Arrhythmias
Lactate Levels
• The other acid: Lactate Levels
• Lactic acid is a product of carbohydrate metabolism.
– It is normal to produce 15 to 20 mmol/kg of lactic acid per day.
– The normal plasma level is 0.5 to 1.5 meq/L
• Hyperlactatemia is considered to be present if the level exceeds 4 to
5 meq/L.
• Lactic acidosis is considered to be present if the elevated lactate
level is in conjunction with a gap >20 in the absence of elevated
glucose /ketosis.
– Lactic acid is rapidly buffered by extracellular bicarbonate
resulting in lactate.
– The liver and kidneys convert lactate back to pyruvate which is
then converted to CO2 & H2O or glucose.
•
Lactate Levels
• Is serum Lactate a good marker of adequacy of
perfusion?
– Increased lactate production results from cellular
metabolism of pyruvate into lactate under anaerobic
conditions.
– When lactate elevated there are two questions to
ask?
• What is the history and the evidence for acidosis?
– If tissues hypoxic, Serum bicarbonate cannot neutralize all the
lactic acid to lactate, acidosis occurs (Type A lactic acidosis)
• Is there a metabolic pathway or clearance problem?
– Typically not acidotic ( Type B lactic acidosis )
Lactate Levels
perfusion?
– Type A lactic acidosis primarily results from an imbalance between
tissue oxygen demand, delivery and use.
– The blood lactate level in type A lactic acidosis is related to the total
oxygen debt and the magnitude of tissue hypoperfusion.
• Elevated blood lactate levels associated with metabolic
acidosis are common among critically ill patients with
systemic hypoperfusion, tissue hypoxia and metabolic
dysfunction.
• Blood lactate levels also increase with clearance
failure , i.e., kidney or liver dysfunction
Lactate Levels
• No study has targeted correction of lactate per se.
• High lactate levels in critically ill patients have been associated with increased mortality 1 .
• Utility of a single high initial lactate have been debated
• Lactate clearance is a better predictor of mortality 2,3 .
– Lac-time: time it takes to clear 10% of lactate
– Time to clear < 24 hours , improves survival in Severe sepsis
– Lac-time also directly correlated with number of organ failures
• One lactate (lactic acid ) level is not as predictive or

evaluative as a series over 24 hours ( i.e., Q6H)
1. Bakker, J., Coffernils, M., Leon, M., Vincent, J.L. (1991). Blood lactate levels are superior to oxygen-derived variables
in predicting outcomes in human patient shock. Chest, 99, 956-962.
2. Bakker, J., Gris, P., Coffernils, M., Kahn R.J., Vincent, J.L. (1996). Serial blood lactate levels can predict the
development of multiple organ failure following septic shock. Am J Surg, 171(2), 221-226.
3. Nguyen, H.B., Rivers, E.P., Knoblich, B.P., et al. (2004). Early lactate clearance is associated with improved outcome
in severe sepsis and septic shock. Crit Care Med, 32(8), 1637-1642.
Lactic Acid Table
Targeting Blood Lactate
• Conclusion3: Serial
lactate levels may
improve the
prognostic value and
help guide therapy
3. Nguyen, H.B., Rivers, E.P., Knoblich, B.P., et al. (2004). Early lactate clearance is associated with improved
outcome in severe sepsis and septic shock. Crit Care Med, 32(8), 1637-1642.
Lactate Levels
CO2 21, pH 7.31, HCO3 11, Na 141, Cl 96
• Problem? Acute metabolic acidosis (situational
respiratory acidosis)
• Anion gap: 141 – (96 +11) = 34
• Lactic Acid Level: 8.9
• HR 148
• RR 27 Compensatory in order to ↑
oxygen delivery and ↓
carbonic acid
Summary
Physiologic effects of acidosis

Hypotension + Hyperventilation = THINK ACIDOSIS!!!
Understanding Tissue Oxygen
Components of Oxygen Delivery
• 1. Cardiac Output = Heart rate x stroke volume
• 2. Total hemoglobin (02 carrying capacity)
• 3. Saturation of hemoglobin
• First line compensatory mechanism ( patient)
• Increase the heart rate and stroke volume to increase
delivery when cells are hypermetabolic and/or when
oxygen is not functionally dissociating from its’
transporter, hemoglobin.
Lactate Levels
• The other acid: Lactate Levels
• Lactic acid is a product of carbohydrate metabolism.
– It is normal to produce 15 to 20 mmol/kg of lactic acid per day.
– The normal plasma level is 0.5 to 1.5 meq/L
• Hyperlactatemia is considered to be present if the level exceeds 4 to
5 meq/L.
• Lactic acidosis is considered to be present if the elevated lactate
level is in conjunction with a gap >20 in the absence of elevated
glucose /ketosis.
– Lactic acid is rapidly buffered by extracellular bicarbonate
resulting in lactate.
– The liver and kidneys convert lactate back to pyruvate which is
then converted to CO2 & H2O or glucose.
•
Lactate Levels
perfusion?
– Increased lactate production results from cellular
metabolism of pyruvate into lactate under anaerobic
conditions.
– When lactate elevated there are two questions to
ask?
• What is the history and the evidence for acidosis?
– If tissues hypoxic, Serum bicarbonate cannot neutralize all the
lactic acid to lactate, acidosis occurs (Type A lactic acidosis)
• Is there a metabolic pathway or clearance problem?
– Typically not acidotic ( Type B lactic acidosis )
Lactate Levels
perfusion?
– Type A lactic acidosis primarily results from an imbalance between
tissue oxygen demand, delivery and use.
– The blood lactate level in type A lactic acidosis is related to the total
oxygen debt and the magnitude of tissue hypoperfusion.
• Elevated blood lactate levels associated with metabolic
acidosis are common among critically ill patients with
systemic hypoperfusion, tissue hypoxia and metabolic
dysfunction.
• Blood lactate levels also increase with clearance
failure , i.e., kidney or liver dysfunction
Lactate Levels
• No study has targeted correction of lactate per se.
• High lactate levels in critically ill patients have been associated with increased mortality 1 .
• Utility of a single high initial lactate have been debated
• Lactate clearance is a better predictor of mortality 2,3 .
– Lac-time: time it takes to clear 10% of lactate
– Time to clear < 24 hours , improves survival in Severe sepsis
– Lac-time also directly correlated with number of organ failures
• One lactate (lactic acid ) level is not as predictive or

evaluative as a series over 24 hours ( i.e., Q6H)
1. Bakker, J., Coffernils, M., Leon, M., Vincent, J.L. (1991). Blood lactate levels are superior to oxygen-derived variables
in predicting outcomes in human patient shock. Chest, 99, 956-962.
2. Bakker, J., Gris, P., Coffernils, M., Kahn R.J., Vincent, J.L. (1996). Serial blood lactate levels can predict the
development of multiple organ failure following septic shock. Am J Surg, 171(2), 221-226.
3. Nguyen, H.B., Rivers, E.P., Knoblich, B.P., et al. (2004). Early lactate clearance is associated with improved outcome
in severe sepsis and septic shock. Crit Care Med, 32(8), 1637-1642.
Lactate Levels
Targeting Blood Lactate
Conclusion : Serial3
lactate levels may

improve the
prognostic value and
help guide therapy
3. Nguyen, H.B., Rivers, E.P., Knoblich, B.P., et al. (2004). Early lactate clearance is associated with improved
outcome in severe sepsis and septic shock. Crit Care Med, 32(8), 1637-1642.
Lactate Levels
CO2 21, pH 7.31, HCO3 11, Na 141, Cl 96
• Problem? Acute metabolic acidosis (situational
respiratory acidosis)
• Anion gap: 141 – (96 +11) = 34
• HR 148
• RR 27 Compensatory to ↑ oxygen
delivery and ↓ carbonic
acid
Summary
Physiologic effects of acidosis

Hypotension + Hyperventilation = THINK ACIDOSIS!!!
Understanding Scv02
Tissue Oxygenation
• The single MOST important issue is tissue
oxygenation.
• All physiologic components are designed to
maintain balanced tissue oxygen consumption
(demand).
• What are the components of Oxygen
Consumption?
– Oxygen delivery
– Metabolic demand at the cellular level
– Blood flow through the capillary
– Ability to dissociate oxygen from hemoglobin
Tissue Oxygenation
• There are two mechanisms designed to meet
oxygen consumption (demand)
– Increase oxygen delivery
– Increase the release (dissociation) of oxygen from
hemoglobin
• In the best of critical situations, both delivery and
dissociation increase to maintain cells
• failure of one mechanism will be supported by
compensation by the other
• In normal situations, short, intermittent increases in
oxygen consumption are supported with rapid temporary
compensation: increased oxygen delivery and a more
rapid dissociation of oxygen
Oxyhemoglobin
OXYGEN
Dissociation
Delivery
OXYGEN
Demand &
Consumption
Components of Oxygen Delivery
• 1. Cardiac Output = Heart rate x stroke volume
• 2. Total hemoglobin (02 carrying capacity)
• 3. Saturation of hemoglobin
• First line compensatory mechanism ( patient)
• Increase the heart rate and stroke volume to increase
delivery when cells are hypermetabolic and/or when
oxygen is not functionally dissociating from its’
transporter, hemoglobin.
• What is the purpose of saturating hemoglobin?
– Hemoglobin is the transporter of oxygen
• Each heme molecule binds 1.34 mLs of oxygen
– When oxygen is bound it is not usable
• Measure of bound oxygen in the arterial blood is the Sa02
(indirectly reflected by pulse oximetry Sp02)
– Only oxygen dissolved in blood can be used
• Measure of dissolved oxygen in the arterial blood is the Pa02
– The rate of oxygen use at the cell determines the
Pa02 which in turn affects the dissociation
Arterial
measures
reflect the
amount of
oxygen
available but
do not reflect
the cell use
• The amount of oxygen required by the cells
changes every second
– When demand/consumption increases, hemoglobin
releases oxygen more rapidly
• Shift to the right: release
– When demand/consumption decreases, hemoglobin
decreases release or latches on to oxygen
• Shift to the left: latched on
• Second compensatory mechanism: hemoglobin
more aggressively releases oxygen to dissolve
in the blood (partial pressure) to be used by the
cells
• Oxygen dissociation as a compensatory
response
• Shifts in the bound oxygen mean that there is a
change in the way oxygen is
– Taken up by the hemoglobin molecule at the alveolar
level (Sa02)
• Depends on the partial pressure of alveolar gas (PA02)
– Released related to the partial pressure of capillary
oxygen (Pa02, Pcap02)
• Capillary oxygen depends on the tissue oxygen (Pti02)
• Tissue oxygen goes down when cells are hypermetabolic
and/or the delivery is inadequate
Understanding Tissue
What affects oxygen dissociation?
Oxygen
• Hemoglobin has a steady and predictable affinity for
oxygen in a normal environment
• In acidosis ( signal that demand/consumption ↑), hemoglobin
releases oxygen more rapidly
• In alkalosis (signal that demand/consumption ↓), hemoglobin
decreases the release of oxygen
• Capillary integrity
• Amount and integrity of hemoglobin
• Enzymes required to release oxygen from hemoglobin (shifting)
• Shifting
• Determined by the partial pressure of dissolved oxygen in the
space (gas or fluid) surrounding the hemoglobin
Oxygenation
• Pulmonary Arteries = 40 mm Hg, 70%
saturated
• Blood goes through pulmonary capillaries:
oxygenates
• Pulmonary Veins =100 mm Hg, 100%
saturated
• Systemic Arteries = 95 mm Hg, 99%
saturated
• Blood goes through systemic capillaries:
releases oxygen, variable de-saturated
• Central Veins = 40 mm Hg, 70% saturated,
But …………
• Sa02 is pre-cell reservoir: 95-100%
• Sv02 is post cell left over: 60-80%
• Scv02 is global (upper extremities) post
cell left over: 65-85%
Measuring Oxygen Dissociation
• True Oxygen dissociation can only be measured in the
venous compartment
• Small veins represent only the tissues distal to them
• Large veins ( central or pulmonary artery) reflect a large
surface area
– Central vein : SVC : Scv02: saturation of central
venous oxygen (less the IVC and the coronary sinus)
– IVC, SVC & Coronary Sinus: Sv02: mixed in the RA
and the RV then measured in the pulmonary artery
(carrying total venous outflow including coronary
sinus)
Measuring saturation in the central or mixed
venous circulation
• Dissociation of oxygen from hemoglobin is a life saving
compensatory mechanism when tissue demand increases beyond
the oxygen delivery compensatory capabilities
• Sv02 ( mixed venous requiring a pulmonary artery catheter): normal
is 60-80 % saturation of hemoglobin (reserve in case of emergency:
never meant for standard use).
– When venous saturation decreases < 60%, this measure
indicates that the cells are using a greater amount of the
reserve.
– Cannot continue in this emergency state
– Therapy: increase delivery, decrease demand
Measuring saturation in the central venous
circulation (cont)1,2,3,4
• A triple lumen catheter with an oximetry tip can be inserted into the
SVC in order to give an indirect (surrogate) measure of Sv02
• Scv02 normal is 65-85 %, may have up to a 15% difference from the
Sv02.
– Less invasive
– Within 5-15% of Sv02
– Provides reliable endpoint tissue measure for resuscitation
1. Dueck, M.H., Klimek, M., Appenrodt, S., Weigand, C., Boerner, U. (2005). Trends but Not Individual Values of Central Venous
Oxygen Saturation Agree with Mixed Venous Oxygen Saturation during Varying Hemodynamic Conditions. Anesthesiology,
103(2), 249–257.
2. Reinhart, K., Kuhn, H., Hartog, C., Bredle, D.L.. (2004). Continuous central venous and pulmonary artery oxygen saturation
monitoring in the critically ill. Intensive Care Med, 30(8), 1572-1578.
3. Rivers, E., Nguyen, B., Havstad, S., et al. (2001). Early goal-directed therapy in the treatment of severe sepsis and septic
shock. N Engl J Med, 345, 1368-1377.
4. Tahvanainen, J., Meretoja, O., Nikki, P. (1982). Can central venous blood replace mixed venous blood samples? Crit Care
Med, 10(11), 758–761.
Tissue Oxygnation Measures
• mixed venous oxygen saturation (SvO2) →
balance between systemic oxygen delivery and
consumption during treatment of critically ill
patients
• central venous oxygen saturation (ScvO2) →
reflects degree of oxygen extraction from brain
and upper part of body → beneficial effects on
patient outcome by continuous
measurement----------Rivers et al. Early goal-directed therapy in the
treatment of severe sepsis and septic shock. NEJM 2001; 345:1368–1377 .
Oxygenation Patterns with Normal Function
Alveoli
Sv022 :0.6 – 0.8
RV LA
RA LV
Cell
Scv022 :0.65- 0.85
Sa022 :0.95 – 1.0
Venous Oxygenation Patterns
Dissociation
must be
measured in Sv02
Scv02
the venous
compartment
Pv02
Compensation in attempts to sustain Tissue Oxygen
PROBLEM
Oxygen delivery inadequate
OXYGEN for oxygen demand
Primary failure
release
COMPENSATION:
Shift to the right OXYGEN
Release oxygen to save Delivery
the cells
OXYGEN
MEASURE:
Scv02 ↓↓↓↓
Demand &
Always Compensatory Consumption
Always an EMERGENCY
Compensation Oxygenation
! ase
!!! ! e le t
ht f r ge
ig o n
t o r rate d ca
ift d n
Sh ease d it a
r
Inc s nee ate,asing
Sv022 Ce!
l l
i n
e
a by r
d
qu ele
it ivery sate
Scv022
l n
Deompe
c
Low
Pv022
PROBLEM
Scv02 normal to ↑↑↑↑ in the face of
suspicion (HR↑, RR↑ persistent
acidosis (LA))
MUST BE considered as failure to release
oxygen (in the presence of ↑↑LA) OXYGEN
Delivery
OXYGEN COMPENSATION:
release Cardiac output increases
Despite increase, tissue
OXYGEN hypoperfusion persists (↑↑LA)
Demand &
Consumption
Sv02
Normal to
High Cells do not
With need it!
Persistent OR
Lactic Cells need it
Acidosis but cannot
get it!
Pv02
Mixed Venous Gas
• ScvO2 is usually more than SvO2 by about
2–3% but two change in parallel
• In septic shock ScvO2 often exceeds SvO2
by about 8%
– correlation between these two parameters
may worsen
• ScvO2 should not be used alone in
assessment of cardiocirculatory system
Time Matters in
the Treatment of Sepsis
The Biggest Issue is Oxygen
• Scv02= 74%
– Serum C02 = 12
– AG = 25
– HR 148
• Everything OK?
• What is the problem (if any)
• Scv02= 84%
– Serum C02 = 24
– AG = 10
– HR 80
• Everything OK?
• Scv02= 54%
– Serum C02 = 19
– AG = 17
– HR 110
• Everything OK?
Compensation in attempts to sustain Tissue
Oxygen
CO2 21, pH 7.31, HCO3 11, Na 141, Cl 96
• Problem? Acute metabolic acidosis
• Anion gap: 141 – (96 +11) = 34
• Scv02= 74%
• HR 148
• RR 27
• Everything OK? What is the problem (if
any)
Compensation in attempts to sustain
Tissue Oxygen
Despite apparent compensation (assuming Cardiac output
↑ and ↑ RR) the patient continues in acute metabolic and
lactic acidosis with a wide anion gap. The Scv02 of 74%
indicates that the patient has oxygen in the reserve, and
in the face of untoward cellular demand (indicated by the
lactic acid and metabolic acidosis), he is unable to use it!
Treatment
• Consider adequacy of intra vascular volume, red cells,
inotropes
• After assuring arterial volume, consider reduction of
vasopressors (if any) and in the face of severe sepsis,
consider rhAPC.
Compensation in attempts to
sustain Tissue Oxygen
CO2 31, pH 7.34, HCO3 17, Na 134, Cl 100
• Problem? Acute metabolic acidosis
• Anion gap: 134– (100 +17) = 17
• Scv02= 51%
• HR 126
• RR 24
• Everything OK?
Compensation in attempts to
sustain Tissue Oxygen
Delivery of oxygen is not compensating for cellular
demand. The patient is maintaining function (barely)
secondary compensation: shifting oxygen off of
hemoglobin at the capillary level. While he is maintaining
himself at this moment the possibility that he may
decompensate is very real.
Treatment
• Evaluate cardiac efficiency
• Increase sedation and analgesia to decrease demand
• Consider adequacy of intra vascular volume, red cells,
inotropes .
Tissue Oxygen
Therapeutic Maintenance of Oxygenation in
Sepsis
• Increase Da02 : O2 delivery
– Volume
– Inotropes
– PRBC
• Decrease V02 :O2 consumption
– Sedation
– Analgesia
– Normothermia
• Improve O2 appropriate use
– Improve delivery
• Volume
• Inotropes
• PRBC
– Improve capillary flow
• Decrease vasopressors
• Consider rhAPC
– Decrease demand
Practical Approach
1. Check the pH
any variation from perfect
If the pH < 7.35, acidemia (and at least 1 acidosis) is present.
If the pH > 7.45, alkalemia (and at least 1 alkalosis) is present.

Practical Approach
2. Check the pCO2
Any variation from perfect
pH < 7.35 and pCO2 < 40  metabolic acidosis
pH < 7.35 and pCO2 > 40  respiratory acidosis
pH > 7.45 and pCO2 < 40  respiratory alkalosis

pH > 7.45 and pCO2 > 40  metabolic acidosis
Practical Approach
3. Choose the appropriate compensation formula
Most prominent Compensation formula

disorder
Metabolic acidosis pCO2 ≈ 1.5 [HCO3-] + 8
Metabolic alkalosis pCO2 ≈ 0.9 [HCO3-] + 16
Respiratory acidosis For every 10 Δ in pCO2, pH decreases by:
0.08 (in acute resp. acidoses)
0.03 (in chronic resp. acidoses)
Respiratory alkalosis For every 10 Δ in pCO2, pH increases by:
0.08 (in acute resp. alkaloses)
0.03 (in chronic resp. alkaloses)
Practical Approach
4. Determine if the degree compensation is
appropriate
(If it isn’t, a second acid-base disorder is likely present)

Practical Approach
5. Calculate the anion gap
Anion gap = [Na+] – ( [Cl-] + [HCO3-] )
If the anion gap is elevated, an elevated gap metabolic

acidosis is likely present.
Practical Approach
6. If an elevated gap acidosis is present, calculate
the delta-delta ratio, to determine if a second
metabolic disorder is present.
Delta–Delta = Measured anion gap – Normal anion gap

Normal [HCO3-] – Measured [HCO3-]
Practical Approach
7. If a metabolic acidosis is present, check the urine
pH.
Urine pH > 6.0 in the setting of an acidosis  Suggests RTA

Practical Approach
8. Generate a differential diagnosis
If multiple disorders are present, they may be:
All related to the same process

All independent of one another
Summary of the Approach to ABGs
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

Acid and Anion

Transféré par

Informations du document

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

Acid and Anion

Transféré par

Droits d'auteur :

Formats disponibles

“The First Concern”

“the first concern in any life

[Marino 2nd ed.]

• Facilitates evaluation of problem and

Focus on Metabolic Acidosis

Components of the ABG and Chemistry Panel

pH | pCO2 | pO2 | O2 Sat| (H+)HC03| Base| Total CO2

Direct measure of acid

pCO2 is directly measured (not

And there’s an equivalent

1. When carbonic acid goes up, pH goes down.

1. H2C03 is carbonic acid:

CO22 + H22O H22CO33 H++ + HCO33--

If the problem is metabolic ( ketosis or lactic acidosis both increasing H+

CO22 + H22O H22CO33 H++ + HCO33--

If the problem is ventilation failure ( C02 retention) , slow compensation requiring

CO22 + H22O H22CO33 H++ + HCO33--

In severe sepsis, it is common to see metabolic failure first ( H+ up)

Acid-Base Perfect Values (Acceptable

perfect 40 7.40 24 (H+)

note 21 7.52 15 ( H+↑)

CO2 44, pH 7.36, HCO3 24

perfect 40 7.40 24 (perfect)

CO2 21, pH 7.36, HCO3 12 ( H+↑↑↑ )

• IN CHRONIC: Bicarb rises 3.5 for every

Principle: The body does not generate a wide anion gap

Na+ (Cl - + HCO3 -)

(Lactic acid or ketones donated H+)↑↑ heavy on the positives

CO2 10, pH 7.31, HCO3 5, Na 135, Cl 90

The wide anion gap supports the presence of increased

• Principle: 1 mmol of unmeasured acid titrates 1 mmol

Principle: There may be two sides to the

• b) A normal or slightly elevated HCO3- in the presence of

• Vent. ABG = 7.25/35/80/10/95%, HCO3

H+ + K+ + Na+ = Cl- + HCO3- + OH-

Mg++ Ca++ K+ Na+ Cl- Others (lactate, etc)

The difference between the strong cations and

Used to calculate the metabolic component of

Calculated the same way, in practice, as

And guess what – it turns out that ATOT, while

In metabolic acidosis, If ΔpCO2 = SBE, then it’s normal.

In metabolic alkalosis, If ΔpCO2 = SBE * 0.6, then it’s

In acute respiratory disorders, if SBE = 0 (+/- 5), then it’s

In chronic respiratory disorders, if ΔpCO2 ( 0.4) = SBE,

– Note: The key to ABG interpretation is

• Compensation is always more

• Must have known “rules of thumb” to

• Chronic Respiratory Acidosis

data are internally consistent

• What acid-base disorders might be

• Na+ + Unmeasured Cations (UC) = Cl- + HCO3 +

Normal Ketoacidosis Post-RX

• Coexistant metabolic acidosis and

• Is serum Lactate a good marker of

Nguyen et al. Crit Care Med 2004

hyperglycemia (BG > 250 mg/dl)

Patients who have not eaten in > 12 hours

• Kreb’s:Acetyl CoANADH & FADH

• Electron transport chain (ETC)

• The bulk of ATP is generated in the electron

Oxygen allows for ATP formation in

• Type B: lactate production

• One lactate (lactic acid ) level is not as predictive or

Physiologic effects of acidosis