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Dr. S.

Mathanalagan
MBBS (SL) MD (SL)
Anaesthesiologist & Intensivist
22/12/2008

Outline
1.

Brief review of the acid-base physiology

2.

Overview of systematic approach to diagnosing


acid-base disorders from the ABG

3.

Cases

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ACID BASE PHYSIOLOGY


pH = -log [H+]
H
Thus pH of

H+
H+
H+
+

H+

7.0 = 10-7M H+ or 100nM H+

pH of 8.0 = 10-8M H+ or 10nM H+


Normal blood pH is 7.4 = 10-7.4M or 40 nM H+
pH extremes of 6.8 and 7.8 will lead to death

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Acid: chemical species that can donate a proton (H+)


Base: chemical species that can accept (gain) a proton
conjugate
base

acid

H+

HA

HA H+ AHA H+ A-

acid

conjugate
acid

HA + H2O

H3O+ + A-

base
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H+

A-

conjugate
base
4

Equilibrium Constant for an Acid-Base Reaction


[H+] [A-]
= Ka
[HA]
[H+] = Ka [HA]
[A-]

[HA]
log [H+] =log Ka + log
[A-]
[A-]
pH = pKa + log
[HA]

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-AEMIA: describes a condition of the blood

For describing blood pH problems we say:


Acidaemia: pH < 7.35

Alkalaemia: pH >7.45
Normal blood pH range is 7.35-7.45
pH limits of 6.8 or 7.8 are incompatible with life
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-OSIS: Describes a process


Acidosis: Process producing acidaemia (pH<7.35)
Either an excessive amount of acid or a decrease in
alkaline substances is the cause
Alkalosis: Process producing alkalaemia (pH>7.45)
Either too many alkaline substances or not enough acid
substances.

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Sources of daily acid load


CELL
METABOLISM

DIET
Proteins,
acidic or alkali foods

Volatile H+
CO2

Toxins
drugs

H+

Non-volatile
abnormal
metabolic acids
(lactic,
acetoacetic,
hydroxybutyric,
formic, glycolic)

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EXTERNAL
FLUID

BLOOD IN
CAPILLARIES

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Traditional approach
Based on bicarbonate/CO2 relationship, thereby

respiratory & renal systems.


Body pH is maintained by
Chemical buffers
Respiratory compensation
Renal compensation

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Chemical buffers
Weak acid & its conjugate base.
Efficiency of buffer depends on
Concentration of the buffer concentration of the

buffer components (limited effectiveness when one


component is > 8 times the other)
pK of the buffer in relation to pH of the working
environment
open/closed system

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Buffering systems
H+ (aq) HCO3- (aq)

CELLS

H2CO3 (aq)

Metabolism
H+

H2O + CO2 (g)

CO2
Proteins

O2
Hb

Phosphate

External
Fluid

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Blood
in
Capillaries
12

Intra and extracellular buffering


% contribution

Intracellular

RBC

Other cells

Proteins

60%
30%
10%

50%
2%
48%

Plasma

Interstitial fluid

23%
75%
2%

9%
90%
1%

CO2-HCO3
Org Phosphates

Extracellular
Proteins
CO2-HCO3
Inorg Phosphates
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The Carbonic acid-Bicarbonate buffer in the blood

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Closed

Open system concept


CO2=11.2
HCO3- = 14
pH = 6.20

+ 10 H+
CO2 = 1.2

+ 10 CO2 lost

HCO3- = 24
pH = 7.40

CO2 = 1.2

CO2 = 0.9

HCO3- = 14

HCO3- = 14

pH = 7.17

pH = 7.29

Open
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Compensated
16

Lung and kidney help enhance the homeostatic


function of the buffers.

CO2

pH ~~

[Kidney]
[Lung]

HCO3- + H+

HCO322/12/2008

H+ : Phosphoric
acid, NH4+

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Renal Regulation

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Time course of distribution, buffering, respiratory


compensation and renal excretion of an acid load
H+ Load
100

Distribution
and extracellular
buffering

Cell
buffering
Respiratory
compensation

Renal H+
secretion

50

0
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12
Hours

24

72
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Primary Acid-Base Disorders


As dictated by the Henderson-Hasselbalch equation,
disturbances in either the respiratory component (pCO2) or
metabolic component (HCO3-) can lead to alterations in pH.

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Metabolic Acidosis
(Too little HCO3-)

Metabolic Alkalosis
(Too much HCO3-)

Respiratory Acidosis
(Too much CO2)

Respiratory Alkalosis
(Too little CO2)

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Causes of acid-base imbalances


Metabolic acidosis
Diabetic ketoacidosis
Diarrhea
Renal failure
Shock
Salicylate overdose
Sepsis

Metabolic alkalosis

Loss of gastric secretions


Overuse of antacids
Potassium-wasting diuretics

Respiratory acidosis

Respiratory alkalosis

Hypoventilation, possibly related to:


Drug overdose
Chest trauma
Airway obstruction
COPD
Pulmonary edema
Neuromuscular disease

Hyperventilation, possibly related to:


Anxiety
Hypoxia
High altitude
Excessive ventilator assistance
Pregnancy
Fever
Initial stage of pulmonary embolus

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Gastrointestinal losses can create acid-base disturbances


Vomiting:
Loss of H+
leading to
alkalosis
Highly acidic, pH = 1.0

Secretes HCO3Diarrhea:
Loss of HCO3leading to
acidosis

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pH varies from
4.0 to 8.0

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Compensation
When a primary acid-base disorder exists, the body
attempts to return the pH to normal via the other half of
acid base metabolism.

Primary metabolic disorder Respiratory compensation


Primary respiratory disorder Metabolic compensation

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Primary Disorder

Compensatory Mechanism

Metabolic acidosis

Increased ventilation

Metabolic alkalosis

Decreased ventilation

Respiratory acidosis

Increased renal reabsorption of HCO3in the proximal tubule


Increased renal excretion of H+ in the
distal tubule

Respiratory alkalosis

Decreased renal reabsorption of HCO3in the proximal tubule


Decreased renal excretion of H+ in the
distal tubule

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Cardiovascular effects acidosis


Reduced cardiac output, reduced arterial blood

pressure

Reduced hepatic and renal blood flow

Centralization of blood volume


Reentrant arrhythmias & a reduction in the threshold

for ventricular fibrillation

A sympathetic discharge is triggered, but acidaemia

attenuates the effects of catecholamines

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Metabolic effects of acidosis


Reduced uptake of glucose by tissues (insulin resistance)
Inhibits anaerobic glycolysis by depressing 6-

phosphofructokinase activity.

Uptake of lactate by the liver is reduced .

From the consumer of lactate, liver becomes a producer.


Hyperkalemia

Increased protein breakdown and development of a

catabolic state

Impaired brain metabolism, resulting in progressive

obtundation and coma.

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Clinical effects of acidosis


Cardiac contractility is depressed

Peripheral arterial vasodilatation & Central

venoconstriction: Central & pulmonary compliance


reduced minimum volume overload can cause
pulmonary edema
Hyperventilation (TV) Kussumal respiration
Depression of CNS: lethargy, headache, stupor and
coma
Glucose intolerance

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Stewarts approach
Principles
Electrochemical neutrality
In aqueous solutions in any compartment the sum of all the
positive ions must equal the sum of all the negatively charged
ions
Conservation of mass
Amount of a substance remains constant unless it is added,
removed, regenerated or destroyed; the total concentration is
the sum of the concentration of dissociated and
undissociated forms
Law of mass action
Dictates the dissociation equilibria of incompletely
dissociated substances
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[H+] in any aqueous solution depends upon water

dissociation
Influenced only by independent variables pCO2
[proportional], total weak acid concentration (ATOT)
[proportional], strong ion difference (SID) [inversely
proportional]
Dependent variables [H+], [OH-], [HA], [A-], [HCO3-],
[CO32-]
pCO2 controlled by ventilation
ATOT = proteins + phosphates
SID is the amount by which strong cations exceed strong
anions (unmeasured ions)
SID + [H+] + [OH-] = 0 (law of electrical neutrality)
SID > 0 implies presence of unmeasured anions i.e.
alkalosis; SID < 0 indicates the presence of unmeasured
cations i.e. acidosis

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K +5

K +5

Serum

Ca ++ 5

Simplification

SID
HCO3- 25
Prot 16
PO4- 1

Mg ++ 2

SID
Lactate
SO4 - 1

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Na+

Cl-

Na+

Cl-

140

105

140

105

30

SID plasma = (Na+ + K+ + Ca2+ + Mg2+) (Cl- + lactate/SO42-);

but, the simplification is (Na+ + K+) (Cl-)


SID cells = (K+ + Mg2+); anions are very low and Na+ ~ ClApparent SID in plasma (SIDa) = (Na+ + K+ + Ca2+ + Mg2+)
(Cl- + lactate); disease states consider organic strong ions
as well normal 40-48meq/l
Effective SID (SIDe) = HCO3- + albumin + phosphate no
assumption about which strong ions constitute the SID in
plasma
Strong ion gap (SIG) = SIDa SIDe indicates the
presence of other unmeasured strong anions e.g. sulphate,
ketoacids, pyruvate, acetate, gluconate
SIG is normally zero value; like anion gap in traditional
approach but not affected by albumin/lactate

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Explanations
Hyperchloraemia develops due to the relatively high [Cl-] of

saline compared to the normal plasma; this reduces SID


and increases water dissociation to H+ (acidosis).
Prolonged vomiting with loss of gastric HCl reduces the
plasma Cl relative to Na; therefore SID increases & alkalosis
results.
Administration of NaHCO3 increases Na+ load & thereby
SID; dissociation of plasma water falls in order to maintain
electro neutrality & free H+ reduced; HCO3 act as buffer but
cannot influence pH as is a dependent variable.
Hyperalbuminaemia (e.g. ECF fluid loss in cholera) will
cause acidosis by decreasing SIG; reverse happens with
hypoalbuminaemia (critically ill).
Hyperphosphataemia (CRF) causes acidosis by reducing
SIG.

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ARTERIAL BLOOD GAS (ABG)

pH, pCO2, pO2 Measured directly


HCO3-, O2 saturation (usually) Calculated from pH, pCO2, and pO2
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Practical Approach
Stage 1: Identify the primary acid base disorder
1. Check the pH

If the pH < 7.35, acidaemia (and at least 1 acidosis) is present.


If the pH > 7.45, alkalaemia (and at least 1 alkalosis) is present.

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2. Check the PaCO2


If the pH and PaCO2 are both abnormal, compare
the directional change.
If both change in the same direction the primary acid
base disorder is metabolic.
If both change in the opposite direction the primary
acid base disorder is respiratory.
pH < 7.35 and PaCO2 < 40 metabolic acidosis
pH < 7.35 and PaCO2 > 40 respiratory acidosis
pH > 7.45 and PaCO2 < 40 respiratory alkalosis
pH > 7.45 and PaCO2 > 40 metabolic acidosis
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If either the pH or PaCO2 is normal, there is mixed

metabolic and respiratory acid base disorder (one is an


acidosis and the other is an alkalosis).
If the pH is normal, the direction of change in PaCO2
identifies the respiratory disorder.
If the PaCO2 is normal, the direction of change in pH
identifies the metabolic disorder.

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Concept of Base Excess


BE is the amount of acid (H+) or base (HCO3-) that must

be added to return blood pH to 7.40 and PaCO2 to 40


mmHg at full O2 saturation & 37C.
(Deviation of patients HCO3- from 24 mmol/ L
after pH is corrected to 7.4)

It is usually derived from a monogram.


A negative value indicates metabolic acidosis and a

positive value indicates metabolic alkalosis.


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Standard bicarbonate
HCO3- concentration in plasma of blood which has

been equilibrated at a PaCO2 of 40 mm Hg & with


O2 in order to fully saturate Hb.
Std HCO3- reduced in metabolic acidosis, and
increased in metabolic alkalosis
Actual HCO3- : measured under clinical condition
Act HCO3- > Std HCO3- indicates Respiratory
acidosis
Act HCO3- < Std HCO3- indicates Respiratory
alkalosis
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Stage 2: Evaluate compensatory responses

3. Choose the appropriate compensation formula


Most prominent
disorder

Compensation formula

Metabolic acidosis

pCO2 1.5 [HCO3-] + 8 ( 2)

Metabolic alkalosis

pCO2 0.7 [HCO3-] + 21 ( 2)

Respiratory acidosis

For every 10 in pCO2, pH decreases by:


0.08 (in acute respiratory acidoses)
0.03 (in chronic respiratory acidoses)

Respiratory alkalosis

For every 10 in pCO2, pH increases by:


0.08 (in acute respiratory alkaloses)
0.03 (in chronic respiratory alkaloses)

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4. Determine if the degree compensation is


appropriate
Alternative formula for respiratory disorders
1 for 10 rule for acute hypercapnia
Expected HCO3- = 24 + 0.1 (PaCO2 40)

Uncompensated
2 for 10 rule for acute hypocapnia
Expected HCO3- = 24 0.2 (40 PaCO2)
4 for 10 rule for chronic hypercapnia
Expected HCO3- = 24 + 0.4 (PaCO2 40)
Compensated
5 for 10 rule for chronic hypocapnia
Expected HCO3- = 24 0.5 (40 PaCO2)

(If it isnt, a second acid-base disorder is likely present)


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In primary metabolic disorder, if the measured and

expected PaCO2 are equivalent, the condition is fully


compensated.
If measured PaCO2 > expected PaCO2, there is
superimposed respiratory acidosis.
If measured PaCO2 < expected PaCO2, there is
superimposed respiratory alkalosis.

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In primary respiratory disorder, use the measured and

expected pH to evaluate acute or chronic, partially or


fully compensated.
For respiratory acidosis, if measured pH < expected
pH, there is superimposed metabolic acidosis; if
measured pH > expected pH, there is superimposed
metabolic alkalosis.
For respiratory alkalosis, if measured pH > expected
pH, there is superimposed metabolic alkalosis; if
measured pH < expected pH, there is superimposed
metabolic acidosis.

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Stage 3: Use the Gaps to evaluate the metabolic acidosis

5. Calculate the anion gap


Anion gap = [Na+] ( [Cl-] + [HCO3-] )

If the anion gap is elevated, an elevated gap metabolic acidosis is


likely present.

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6. If an elevated gap acidosis is present, calculate the


delta-delta (Gap Gap) ratio, to determine if a
second metabolic disorder is present
Gap Gap ratio = AG Excess
HCO3- deficit
DeltaDelta = Measured anion gap Normal anion gap(12)
Normal [HCO3-](24) Measured [HCO3-]
Gap Gap ratio < 1 indicates the coexistence of a normal AG
metabolic acidosis.
Gap Gap ratio < 1 indicates the coexistence of a normal AG
metabolic alkalosis.
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7. If a metabolic acidosis is present, check the urine


pH
Urine pH > 6.0 in the setting of an acidosis Suggests RTA

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8. Generate a differential diagnosis

If multiple disorders are present, they may be:


All related to the same process
All independent of one another

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Overview of Biochemical Homeostasis

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Summary of the Approach to ABGs


Check the pH
2. Check the PaCO2
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
1.

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Case 1
A 26 year old man with unknown past medical history is
brought in to the ER by ambulance, after friends found
him unresponsive in his apartment. He had last been
seen at a party four hours prior.
ABG:

pH
PCO2
HCO3P O2

7.25
60
26
55

Lab: Na+
K+
ClHCO3-

137
4.5
100
25

Acute, uncompensated respiratory acidosis


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ACID-BASE Parameters

Acid
pH

Normal

Alkaline

HCO3-

PaCO2

If the pH and PaCO2 fall in the same column - other than

normal, of course - the problem is respiratory.


If the pH and HCO3- fall in the same column, the problem is
metabolic.
Expected pH = 7.4 0.08 x 20/10 = 7.24 ~ measured pH

Thus, the diagnosis is acute, uncompensated respiratory

acidosis.

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Case 2
A 67 year old man with diabetes and early diabetic
nephropathy (without overt renal failure) presents for a
routine clinic visit. He is currently asymptomatic.
Because of some abnormalities on his routine blood
chemistries, you elect to send him for an ABG.

ABG:

pH
PCO2
HCO3P O2

7.35
34
18
92

Lab: Na+
K+
ClHCO3Cr

135
5.1
110
16
1.4

Urine pH: 5.0


Combined metabolic acidosis and respiratory alkalosis
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ACID-BASE Parameters

Acid
pH

Normal

Alkaline
PaCO2

HCO3-

Expected PaCO2 = (1.5 x 18) + 8 = 35


Thus, the diagnosis is combined metabolic acidosis and

respiratory alkalosis.
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Case 3
A 68 year old woman with metastatic colon cancer
presents to the ER with 1 hour of chest pain and
shortness of breath. She has no known previous cardiac
or pulmonary problems.

ABG:

pH
PCO2
HCO3P O2

7.49
28
21
52

Lab: Na+
K+
ClHCO3-

133
3.9
102
22

Acute, uncompensated respiratory alkalosis


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ACID-BASE Parameters

Acid
HCO3-

Normal

Alkaline
pH
PaCO2

Expected pH = 7.4 + 0.08 x 12/10 = 7.49


Thus, the diagnosis is acute, uncompensated respiratory

alkalosis.
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Case 4
A 6 year old girl with severe gastroenteritis is admitted
to the hospital for fluid rehydration, and is noted to have
a high [HCO3-] on hospital day #2. An ABG is ordered:
ABG:

pH
PCO2
HCO3P O2

7.47
46
32
96

Lab: Na+
K+
ClHCO3-

130
3.2
86
33

Urine pH: 5.8


Primary metabolic alkalosis with a superimposed
respiratory acidosis
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ACID-BASE Parameters

Acid
PaCO2

Normal

Alkaline
pH
HCO3-

Expected PaCO2 = (0.7 x 32) + 21 = 43.4 2


Thus, the diagnosis is primary metabolic alkalosis with a

superimposed respiratory acidosis.


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Case 5
A 75 year old man with morbid obesity is sent to the ER by
his skilled nursing facility after he developed a fever of 103
and rigors 2 hours ago. In the ER he is lucid and states that
he feels terrible, but offers no localizing symptoms. His ER
vitals include a heart rate of 115, and a blood pressure of
84/46.

ABG:

pH
PCO2
HCO3PO2

7.12
50
13
52

Lab: Na+
K+
ClHCO3-

138
4.2
99
15

Urine pH: 5.0


Acute uncompensated respiratory acidosis and
superimposed metabolic acidosis
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ACID-BASE Parameters

Acid

Normal

Alkaline

pH
PaCO2
HCO3-

Expected pH = 7.4 0.08 = 7.32


Thus, the diagnosis is acute uncompensated respiratory

acidosis and superimposed metabolic acidosis.


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Case 6
A 25 year old man with type I diabetes presents to the ER
with 24 hours of severe nausea, vomiting, and
abdominal pain.
ABG: pH
PCO2
HCO3P O2

7.15
30
10
88

Lab: Na+
K+
ClHCO3Cr

138
5.6
88
11
1.1

Urine pH: 5.0


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Primary metabolic acidosis with


superimposed respiratory acidosis

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ACID-BASE Parameters

Acid
pH

Normal

Alkaline
PaCO2

HCO3-

Expected PaCO2 = (1.5 x 10) + 8 = 23


Thus, the diagnosis is primary metabolic acidosis with

superimposed respiratory acidosis.


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Case 7
A 62 year old woman with severe COPD comes to the ER
complaining of increased cough and shortness of breath
for the past 12 hours. There are no baseline ABGs to
compare to, however, her HCO3- measured during a
routine clinic visit 3 months ago was 34 meq/L.

ABG:

pH
PCO2
HCO3P O2

Urine pH
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7.21
85
33
47

Lab: Na+ 135


K+
4.0
Cl90
HCO3- 34

5.5
Acute on chronic respiratory acidosis

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ACID-BASE Parameters

Acid
pH

Normal

Alkaline
HCO3-

PaCO2

Expected pH = 7.4 (0.03 x 45/10) = 7.265


Thus, the diagnosis is acute on chronic respiratory acidosis.

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Case 8
A 36 year old man with a history of alcoholism is
brought to the ER after being found on the floor of his
apartment unresponsive, soiled with vomit, and with an
empty pill bottle nearby.

ABG:

pH
PCO2
HCO3P O2

Urine pH

7.03
75
19
48

Lab: Na+
134
K+
5.2
Cl90
HCO3- 20

5.0

Mixed respiratory and metabolic acidosis


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ACID-BASE Parameters

Acid

Normal

Alkaline

pH
PaCO2
HCO3-

Expected pH = 7.4 0.08 x 35/10 = 7.12


Thus, the diagnosis is mixed respiratory and metabolic

acidosis.
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THANK YOU
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