# Acid Base 4. Acid Base Disorders

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```					Acid Base 4. Acid Base Disorders
Steve Wood, Ph.D., swood@umhs-sk-physiology.org

Learning Objectives

Interpret acid base status using data for arterial PCO2,
pH, and [HCO3-].

Use the Henderson-Hasselbalch equation and
Davenport diagram to explain acid base balance and
compensation for altered pH.

Describe the four primary disturbances of acid-base
balance and the mechanisms and time course for
compensation for each.

Calculate “base excess” and “anion gap” and use the
results to characterize acid base disorders.

Describe possible causes of the four primary
disturbances of acid-base balance.

I. Acid base is part of arterial blood gas analysis:
•   Arterial blood gases provide info three important conditions of your patient:
ventilation, oxygenation, and acid base status.
•   Example: asthma patient has blood drawn for ABGs. Results
measured pH = 7.3                   (7.35 – 7.45)
PaO2 = 80 mm Hg (75 – 100)
SaO2 = 95 %           (94 – 100)
PaCO2 = 52 mm Hg (36-42)

calculated HCO3- = 25 mEq/L       (22 – 26)
•   What do these values tell you about:
Ventilation?
Oxygenation?
acid base status?

Acid Base Regulation                                                    5/19/2012   Page 1
II. Clinical Tool: Graph of Henderson-Hasselbalch Equation
pH = pK’ + log [HCO3-]
PCO2 x 

A. Construction of the Davenport Diagram
Step 1. Titrate a bicarbonate solution with fixed acid or base at constant values
of PCO2 and calculate [HCO3-] at a given pH from the rearranged HH equation
50
-     (pH – pK                                                                                   60
[HCO3 ] = 10        ) x PCO2 x α               45
-     (7.4-6.1)
For pH 7.4, HCO3 =10               x 40 x      40

40
.03 = 23.9                                     35

HCO3-
-     (7.2-6.1)             30
For pH 7.2, HCO3 =10               x 40 x                                           20
25
0.03 = 15.1                                    20
For pH 7.6 HCO3- =10(7.6-6.1) x 40 x           15

0.03 = 37.9                                    10

These values are plotted on a HCO3-             5

vs. pH diagram. This is then                    0
7  7.1  7.2  7.3   7.4 7.5   7.6  7.7                                     7.8
repeated for PCO2 = 20 mmHg and                                      pH
PCO2 = 60 mmHg.
Step 2. Starting at pH 7.4 and PCO2 = 40 change PCO2 to 60, 80, and 20 mm Hg
PCO2 80  60
and measure pH and calculate [HCO3-] at each
PCO2.
HCO3-, mEq/L

40
35
20
If there were no buffer in blood, pH
25                                    Buffer line
slope  [Hb]           would change with almost no change
15
in [HCO3-] since the change in [H+] is
Second step   – starting at pH 7.4 and PCO2 = 40
change CO2 and measure pH and HCO3-
0
7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8
pH                                                 CO2 + H2O= H2CO3 = H+ + HCO3-
-
measured in nanomoles and [HCO3 ] is                           1.2mM                    0.000,040mM 24 mM
measured in millimoles; e.g., doubling                 (40 mm Hg x 0.03)                      pH 7.4
of [H+] from 40 to 80 nmoles/L would                              Double PCO2 with no buffer present
increase HCO3- by only 0.000040 mEq.                           2.4 mM                  0.000,080mM 24.000,040mM
However, because of hemoglobin                          (80 mm Hg x 0.03)
buffering [H+] there is a high flux of                                                     pH = 7.1

CO2 and HCO3- increases by much more.

Acid Base Regulation                                                                                               5/19/2012          Page 1
50
PCO2 80         60
45

40

35                                           40
30                                                      20
HCO3-

25

20

15

10

5

0
7    7.1   7.2     7.3     7.4   7.5   7.6   7.7        7.8
pH

B. Effect of buffers
CO2 + H2O = H2CO3 =         H+ +    HCO3-
Because a buffer is Present, pH                                               50
H + buf Hbuf                                        +   -=

changes less for a given change                  PCO2 80    60                45
Buffer line
slope  [Hb]
in PCO2. This is beneficial when                                 40
40

35
PCO2is changing away from                                              20     30

HCO3-
normal. However, when PCO2 is                                                 25

5 g/dL (anemia)
20
changing to compensate for a                                                  15
15 g/dL (nl)
metabolic disturbance, the pH                                                 10

5
will change less for a given                                        20 g/dL (polycythemia)
0

change in PCO2; i.e., the                                                          7   7.1   7.2   7.3   7.4
pH
7.5    7.6    7.7     7.8

compensatory change in PCO2
will have to be greater to get the pH back to normal. This is because the pH
changes along a buffer curve with the same slope as the normal buffer curve for
hemoglobin buffer.

C. Base Excess.
Since HCO3- changes with PCO2 how do you determine the metabolic
component of a given change in pH? Any point that is not on the normal buffer
line has a base excess. The number will be either positive (renal increase of
bicarbonate) or negative (renal excretion of bicarbonate). Points 1 and 3 are
located on the normal buffer line so the base excess is zero. Any point on the
normal buffer line has a base                 Base Excess shows the extent
excess of zero (no renal                of renal compensation. BE = actual measured
plasma [HCO3-] and the [HCO3-] value on the buffer line.
compensation). Any point on          50
PCO2 80
the PCO2 = 40 line is metabolic      45                          60
BE
[HCO3-] mEq/L

and there is no respiratory          40
1 27-27=0
35                 2              40
compensation. Base excess is         30
20 2 33-27=+5
used to describe the extent of       25
1
renal compensation for               20                                           3 20-20=0
3
respiratory disturbances. Base       15
4 15-20=-5
5             4
excess is also used to describe      10
5 15-24=-9
5
the extent of a metabolic             0
disturbance. The effect of              7 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8
respiratory compensation                                     pH

Acid Base Regulation                                                                                                                           5/19/2012      Page 1
during a metabolic disturbance will actually increase the base excess.

D. Clinical Tool
A bedside tool which does not require a calculator or graph is a useful
approximation; i.e., a change in pH of 0.1 unit due entirely to metabolic change
would equal a bicarbonate change of 6 meq/L. A change of 0.1 pH due entirely
to a respiratory disturbance would equal a PCO2 change of 12 mm Hg.

Δ6 HCO3-  0.1 pH
Δ12 PCO2  0.1 pH

For example, if arterial blood gases show a pH of 7.3 and a PCO2 of 52, then the
disturbance is uncompensated respiratory acidosis; i.e., the change of PCO2 of 12
mm Hg completely accounts for the change in pH of 0.1 unit. If the PCO 2 change
is 12 and the pH change is less than 0.1 it indicates that renal compensation has
occurred. This tool is not accurate if pH change is more than 0.15units.

Calculating exact values: Remember that values for pH, PCO2, and HCO3- MUST
obey the Henderson-Hasselbalch equation. If you know 2 of the 3 values, you
can calculate the exact value of the third value. For example, if you had values of
HCO3- = 30 and PCO2 = 10 mm Hg, the exact value of pH would be pH = 6.1 + log
30/(10 x 0.03) = 6.1 + log 30/.3 = 6.1 + log 100 = 6.1 + 2 = 8.1. For a HCO3- of 12
and a PCO2 of 40, the pH would be 6.1 + log 12/(40 x 0.03) = 6.1 + log 10 = 7.1.

III. Acid Base Disorders
A. Metabolic acidosis
1) Summary. This is acidosis due to a primary metabolic abnormality. It's
convenient to classify metabolic acidosis as either:
 normal anion gap            ABG: pH = 7.20; PaO2 = 90                          -
pH 
[HCO3 ]
acidosis                         PCO2 = 40; HCO3- = 12
P CO
 high anion gap
2
35

acidosis                     30
Metabolic
HCO3-

25
2) Causes                               20
acidosis
Metabolic acidosis is a
15                            How will compensation
clinical disturbance                                                  occur????
characterized by an increase            10   PCO2 = 40
Is compensation complete?
in total body acid. Metabolic
acidosis can result from                     7.1         7.4               7.7
pH
several general causes:                                       ABG: pH = 7.32; PaO2 = 95
PCO2 = 30; HCO3- = 9

Acid Base Regulation                                                             5/19/2012           Page 1
(1) failure of the kidneys to excrete metabolic acids normally formed in the
body,
(2) formation of excess quantities of metabolic acids in the body,
(3) addition of metabolic acids to the body by ingestion or infusion of acids,
(4) loss of base from the body fluids, which has the same effect as adding
an acid to the body fluids.

3) Anion gap (AG). The law of electrical neutrality requires that plasma does
not have a net charge. Because all
cations, measured and                   Anion Gap
Law of Electochemical Neutrality:
unmeasured, must equal all              Total anions = total cations there is no anion gap
anions, measured and                    But not all ions are normally measured
unmeasured. MC + UC = MA + UA.          Anion Gap = measured cations – measured anions
Therefore, MC – MA = UA – UC =          = (Na+ + K+) – (Cl- + HCO3-)
AG. In some labs, only Na+ is           The normal anion gap is:
(Na+ + K+) – (Cl- + HCO3-)
measured for the cations. The AG
(140 + 5) - (105 + 25)
is normally 8-18 mEq/L, with an          145 – 130 = 15
average value of 12. It is due          Albumin is normally the major unmeasured anion.
primarily to unmeasured protein
anions, esp. albumin. The anion       AG is useful to determine kind of acidosis: Extra
unmeasured anions such as acetoacetate and lactate
gap allows for the differentiation    increase the "gap". Mineral acids, e.g., HCl have
of 2 groups of metabolic acidosis.    little or no effect on “gap”
Metabolic acidosis with a high AG
is associated with the addition of
endogenously- or exogenously-generated acids. Metabolic acidosis with a
normal AG is associated with the loss of HCO3 or the failure to excrete H+
from the body.

High AG examples (normal chloride; low bicarbonate)

   Lactic acidosis -
   Ketoacidosis - Beta-hydroxybutyrate, acetoacetate
   Renal failure -
   Salicylate, methanol, ethylene glycol
   Massive rhabdomyolysis (release of H+ and organic anions from
damaged muscle)

Normal AG examples (high chloride; low bicarbonate)

 Diarrhea
 Renal tubular acidosis
 HCl ingestion
 Carbonic anhydrase inhibitors

Acid Base Regulation                                                         5/19/2012   Page 1
4) Signs and Symptoms. The best recognized sign of metabolic acidosis is
Kussmaul respirations, a form of hyperventilation that serves to increase minute
ventilatory volume. This is slow, deep breathing resulting in hyperventilation.

5) Uncompensated metabolic acidosis is not expected. The only
cases where you might see uncompensated metabolic acidosis would be:

       Patient on a ventilator
       Patient with CNS depression (barbiturate overdose)
       Patient with damage of loss of normal glossopharyngeal nerve function
(no carotid body input to brain)

B. Metabolic alkalosis
1) Summary

This disorder is commonly iatrogenic, related to administration of base (e.g.
bicarbonate, milk-alkali syndrome), diuretics (e.g. furosemide), hypokalaemia or
hypovolaemia. Loss of acid from the stomach by ongoing vomiting is a common
cause.

2) Causes

Metabolic alkalosis is an acid-base disturbance caused by an elevation in plasma
bicarbonate (HCO3) concentration. Causes of metabolic alkalosis include the
following:

    Loss of hydrogen ions: loss                    ABG: pH = 7.5; PaO2 = 90
of H+ results in increased        35
PCO2 = 40; HCO3- = 30

HCO3-. Hydrogen ions may          30

be lost through the kidneys                                         Metabolic
HCO3-

25

or the GI tract; e.g.,            20
alkalosis
vomiting. Shift of               15                              How will compensation
occur????
hydrogen ions into the           10
PCO = 40 2

Is compensation complete?
intracellular space: This
mainly develops with                   7.1          7.4               7.7
pH
hypokalemia. As the
extracellular potassium concentration decreases, potassium ions move
out of the cells. To maintain neutrality, hydrogen ions move into the
intracellular space.
that exceed the capacity of the kidneys to excrete this excess
bicarbonate may cause metabolic alkalosis.

Acid Base Regulation                                                                   5/19/2012     Page 1
3) Compensation. mechanisms include buffering and Hypoventilation:
metabolic alkalosis causes inhibition of the respiratory center, resulting in
hypoventilation and increased PCO2 levels. Hypoventilation may actually occur
to an extent sufficient to cause hypoxemia.

4) Signs and Symptoms. Severe alkalosis causes diffuse systemic arteriolar
constriction with reduction in tissue perfusion including cerebral and coronary
blood flow.

C. Respiratory acidosis
1) Summary
By definition, a high PCO2 indicates hypoventilation and causes respiratory
acidosis. This is usually due to lung disease (e.g., COPD), respiratory failure or
depression of brain
respiratory centers. In              ABG = PO2 = 73; pH 7.2; PCO2 = 64; HCO3- = 26

chronic hypercapnia the                        PCO2 = 64 mm Hg
PCO2 = 40 mm Hg
35
kidneys compensate by
stimulating H+ secretion            30

25
HCO3-

acidosis
bicarbonate.                        20
Possible causes?
15                  How will compensation occur?
2. Causes                                                          ABG = PO2=73;
10
pH 7.3; PCO2=64;
HCO3- =34
Typical causes of                                7.1      7.4                 7.7
hypoventilation include:                                  pH

     Central Nervous System Depression (Sedatives, CNS disease, Obesity
Hypoventilation syndrome)
     Pleural Disease (Pneumothorax)
     Lung Disease (COPD, pneumonia)
     Musculoskelatal disorders (Kyphoscoliosis, Guillain-Barre, Myasthenia
Gravis, Polio)

3. Signs and Symptoms.

     Cyanosis if accompanying hypoxemia is present, and the finding of
clubbing may indicate the presence of a chronic respiratory disease.
     Mental status may be depressed in severe elevations of PaCO2.

Acid Base Regulation                                                                 5/19/2012         Page 1
D. Respiratory alkalosis

1) Summary

There is a long list of causes of this disorder. Ventilatory stimulation by hypoxia
is one possible cause. If hypoxia is not present, think of central causes related to
pain or anxiety (panic attack). Other possibilities are aspirin (salicylate) toxicity,
improper ventilator settings, and pregnancy.

2) Causes
ABG: PO2=110; pH=7.6; PCO2=16; HCO3-=19

Typical causes of respiratory alkalosis                                            PCO2 = 40 mm Hg

35
involve hypoxic and other stimulations                 30
PCO2 = 16 mm Hg

of the respiratory center of the medulla:              25
HCO3-

20                                       Respiratory
    Hypoxia – e.g., high altitude, lung           15
alkalosis

diseases producing hypoxemia                                                       Possible causes?
Compensation?
10

    Anxiety
    Fever                                               7.1            7.4                      7.7

pH
    Salicylate intoxication
    Cerebral disease (e.g. tumor, encephalitis)
    Hepatic cirrhosis (inc. progesterone)
    Pregnancy (inc. progesterone)
    Excessive mechanical ventilation

Signs and Symptoms.

Tetany may occur due to calcium
binding by negatively charged amino
acid residues on protein
At plasma calcium ion concentrations
about 50 percent below normal, the
peripheral nerves become so excitable
that spontaneous sustained
contractions of muscles occur (tetany).

Acid Base Regulation                                                                      5/19/2012                Page 1
E. Mixed acid base disorders
It is common in intensive care units to have mixed acid base disorders; e.g.,
diabetics with metabolic acidosis and pulmonary problems leading to respiratory
acidosis. Even triple disorders are sometimes present; e.g., an alcoholic with
ketoacidosis who begins vomiting (metabolic alkalosis) and developes respiratory
alkalosis due to hyperventilation from liver dysfunction and alcohol withdrawl.
http://www.accessmedicine.com/content.aspx?aID=56001

IV. Summary of Diagnosis of Acid Base Disorders

Arterial blood sample

<7.38              > 7.42
pH?

acidosis                               alkalosis
HCO3-                                         HCO3-
PCO2 > 40 mm Hg                         PCO2 < 40 mm Hg
<24 mEq/L                                     >24 mEq/L

metabolic             respiratory           metabolic         respiratory

Respiratory                 Renal                Respiratory        Renal
compensation                compensation         compensation       compensation

PCO2< 40 mm Hg            BE > 0 mEq/L         PCO2 > 40 mm Hg      BE < 0 mEq/L

IV. Summary of Lecture
Acid Base Regulation                                                      5/19/2012     Page 1
•    Metabolic acidosis - pH from HCO3- : diarrhea; renal disease; make it or take
it acidosis. Anion gap may be high or normal
•    Metabolic alkalosis - ↑pH from ↑HCO3- : vomiting; bicarb. Infusion; diuretics;
hypokalemia
•    Respiratory acidosis - pH from ↑PCO2 : CNS depression; lung disease;
nerve/muscle disease
•    Respiratory alkalosis - ↑pH from  PCO2 : hypoxia; CNS; aspirin; ventilator;
pregnancy
•    pH of 0.1 = PCO2 = 12 mmHg OR HCO3- = 6 mEq/L. If not, = compensation

Practice Problems:

(case studies are available at
http://www.anaesthesiamcq.com/AcidBaseBook/ab9_6.php#cases

PCO2 (mm Hg)
Plasma [HCO3-] (mEq/L)

120           80 60                 40        30 20
9
3
40                                                                 15
8
10
30           5
1
8                                               4
20
2             6             7
10
6.8   7.0           7.2           7.4           7.6         7.8    8.0

Point Acid Base Status
pH
1
2
3
4
5
6
7
8
9
10

1. An emphysema patient who was well compensated (normal pH) for
chronic CO2 retention was admitted to the emergency room after

Acid Base Regulation                                                                                                      5/19/2012   Page 1
suddenly developing severe shortness of breath on exertion. Arterial
blood gas analysis showed the following values:
PaO2 = 50 mmHg; PaCO2 = 80 mmHg;
pH = 7.3; HCO3 = 40 mEq/L. The patient’s acid base status is best described as:

A. chronic metabolic alkalosis with respiratory compensation
B. chronic respiratory acidosis with renal compensation
C. chronic metabolic acidosis with respiratory compensation
D. acute respiratory alkalosis with renal tubular acidosis

2. COPD patient in respiratory failure. ABG report:
PaO2 = 35 mm Hg; PaCO2 = 64 mm Hg; pH = 7.2
Hb = 10 g/dL
HCO3- = 26 mEq/L

Acid base status is most accurately described as:
A. Uncompensated metabolic acidosis
B. Uncompensated respiratory acidosis
C. Compensated respiratory acidosis
D. Compensated metabolic acidosis

3. Cholera patient with vomiting and diarrhea. ABG shows:

PaO2 = 88 mm Hg; PaCO2 = 28 mm Hg; pH = 7.25; HCO3- = 12 mEq/L

The patient’s acid base status on room air is:
A.   Compensated respiratory acidosis
B.   Uncompensated respiratory acidosis
C.   Uncompensated metabolic acidosis
D.   Compensated metabolic acidosis

4. 6-year-old boy found unconscious with half empty container of ethylene glycol
(antifreeze) nearby. ABG and blood chemistry results:
PaO2 = 67 mm Hg; PaCO2 = 38 mm Hg; pH = 7.2; HCO3- = 12 mEq/L
Na+ = 135 mEq/L; K+ = 8 mEq/L; Cl- = 101 mEq/L

Acid Base Regulation                                                    5/19/2012   Page 1
Patient’s anion gap is:
A. +22 mEq/L
B. +32 mEq/L
C. +19 mEq/L
D. +30 mEq/L

5. A 65-year-old male was admitted to the ER after becoming increasingly confused and
complaining that he “could not breathe”. Physical exam revealed a barrel-chested,
obese patient with peripheral and central cyanosis. The patient’s wife stated that he
was a heavy smoker and drinker and that he had chronic obstructive pulmonary
disease (COPD). Arterial blood gas data and blood chemistry showed the following
(normal range in parentheses):
PaO2 =        40 mm Hg       (75 - 100 mm Hg)
PaCO2 =       90 mm Hg       (36 - 42 mm Hg)
pH =          7.30           (7.35 – 7.45)
total CO2 =   50 mEq/L       (28 – 32 mEq/L)
[Hb] =        20 g/dL        (13 – 16 g/dL)
+
Na =          150 mEq/L      (134 – 144 mEq/L)

The most accurate diagnosis of this patient is:
A) acute (uncompensated) respiratory acidosis with anemia, arterial hypoxemia
and positive base excess.
B) chronic (renal compensation) respiratory acidosis with polycythemia,
hyperventilation and negative base excess.
C) chronic (renal compensation) respiratory acidosis with polycythemia,
hypoventilation and positive base excess.
D) chronic metabolic alkalosis (respiratory compensation) from
hyperaldosteronism with negative base excess and polycythemia from
hypoxemia

Acid Base Regulation                                                    5/19/2012   Page 1
6. A patient with an acid base disturbance has been under observation for 7 days in
the ICU and his clinical progress has been “mapped” on the above Davenport
diagram. His chart showing all of the blood gas and pH data had coffee spilled on it
and the only datum still legible is his base excess, which is + 10 mEq/L. Which point
on the Davenport diagram represents this patient?

A) 8
B) 5
C) 4
D) 6

Topic: definition & calculation of base excess
LO: Calculate “base excess” and “anion gap” and use the results to characterize
acid base disorders.

Acid Base Regulation                                                     5/19/2012   Page 1

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