Metabolic Acid-Base Disorders:

A Practical Approach

Robert Pettignano, MD
Medical Director
Children’s Healthcare of Atlanta at Hughes Spalding
 Acid-Base Disorders
Objectives

 Define
– pH
– acidosis/alkalosis
– mixed disturbances
– anion gap
 Describe pathophysiology of metabolic acidosis/alkalosis
 Review compensatory mechanisms
 Describe clinically relevant signs, symptoms, disturbances
associated with acidosis and abnormal anion gaps.

2
 Acid-Base Disorders
• pH
– Hydrogen ion (H+) activity
– represents the negative log of H+ concentration
– Normal 7.35-7.45 + 0.03

3
 Acid-Base Disorders
“A Few Definitions”
• Acidemia/alkalemia
– alterations in blood pH
• Acidosis/alkalosis
– process that shifts blood pH in a predictable direction

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 Acid-Base Disorders
“A Few Definitions”
• Respiratory
– PCO2 regulation problem
• Metabolic
– HCO3- (bicarb) regulation problem
• Compensation
– Secondary changes to minimize pH deviation

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 Acid-Base Disorders
“A Few Definitions”
• Simple disturbance
– 1o abnormality occurring from a single process
• Mixed disturbance
– Two or more abnormalities occurring simultaneously

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 Acid Base Analysis

• Normals:
– pH: 7.35 - 7.45
– pCO2: 35 - 45 mmHg
– HCO3: 22 - 26 mEq/L
– Base difference: -2 to +2

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 Acid Base Disorders
Metabolic Acidosis
• Acidemia
– in blood H+ concentration
– pH < 7.35
– initiated by bicarb
» metabolic
– Produced by
» addition nonvolatile acid
» loss of alkali

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 Acid-Base Disorders
Metabolic Acidosis
• The bodies response to acidosis
– buffering
» extracellular
» intracelluar
– respiratory compensation
– renal excretion of H+

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 Acid-Base Disorders
Anion “Gap”

• Actually no gap exists

• Anion gap (mEq/L) = Na+ - ( Cl- + HCO3-)
normal - 8-12 mEq/L

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 Acid-Base Disorders
Increased Gap Acidosis
• Anion gap > 12
• HCO3- 2o to buffering by H+
• unmeasured anions
• Cl- normal

what are the causes of this type of acidosis?

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 Acid-Base Disorders
Increased Gap Acidosis
• acid production • Toxic substance
– Lactic acidosis ingestion
– Ketoacidosis – Salycylate
» diabetic – methanol
» alcoholic – Ethylene glycol
» starvation
– Paraldehyde
– Uremia
• Massive rhabdomyolysis

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 Acid-Base Disorders
Normal Gap
• Anion Gap 8-12
• HCO3-
• CL-

what are the causes of this type of acidosis?

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 Acid-Base Disorders
Normal Gap
• Gut • Renal
– Diarrhea – RTA
– Bowel fistula – Carbonic anhydrase
– Ileal loop inhibitors

what are some clinical

manifestations of acidosis?
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 Acid-Base Disorders
Metabolic Acidosis
• Clinical Features:
– Hyperventilation
– Hypotension
– GI disturbances
– Hyperkalemia
– Hypercalcemia
– Osteopenia

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 Acid-Base Disorders
Metabolic Acidosis
• Treatment
– correct underlying disorder
– correct pH if < 7.2
– Total HCO3- replacement
HCO3- (needed) = Base deficit x wt x 0.06
– Replace 1/2 bicarb over 8-12 H

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 Acid-Base Disorders
Metabolic Alkalosis

• Alkalemia
– in blood HCO3- concentration
– pH > 7.44
– 1/5th HCO3 dissipated to CO2 gas
» HCO3- + H+ H2CO3 CO2 + H2O
– Produced by:
» too much exogenous base
» loss of H+

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 Acid-Base Disorders
Metabolic Alkalosis
• Persists only if
– excess HCO3- is no excreted
– production and loss of H+ are equal
• The bodies response
– pCO2
– retention H+

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 Acid-Base Disorders
Metabolic Alkalosis
• Two basic categories
– Chloride-sensitive (responsive)
– Chloride-insensitive (resistant)
• Differentiated by
– response to NaCl
– level of urinary Cl-
» urinary CL- < 10-15 mEq/L (responsive)
» urinary Cl- > 10-15 mEq/L (resistant)

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 Acid-Base Disorders
Chloride Responsive Alkalosis
• Diuretics
• Cystic Fibrosis
• GI losses
– NG suction
– emesis
– chloride wasting diarrhea
» congenital (children)
» villous adenoma
» laxatives

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 Acid-Base Disorders
Chloride Resistant
Alkalosis
• Excess mineralscorticoid
 Adrenal
a) Cushings
b) Conns Syndrome
c) licorice
 Exogenous steroid
 Bartters Syndrome

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 Acid-Base Disorders
Metabolic Alkalosis

• Treatment
– Correct underlying disorder
– Chloride responsive
a) replace volume with NaCl
b) correct hypokalemia
c) Ammonium chloride and HCl (extreme) cases
– Chloride resistant
a) treat underlying problem
b) replace K+ as needed

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 Acid-Base Disorders
Mixed
• Two or more simple disturbances occurring
simultaneously
• Diagnosis difficult
• Can use
– formulas for compensatory changes
– nomograms
– systems approach

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 Acid-Base Disorders
Mixed
• Systems approach
– History/symptoms
– Consider
» disease states
» medications
» past/present treatments
– Physical exam
– Lab data

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 Acid-Base Disorders
Metabolic Acidosis
Summary
 High anion gap
(normaochloremic) acids added

 Normal anion gap

(hyperchloremic) bicarbonate lost

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 Acid-Base Disorders
Primary Metabolic
Disorders Summary
 pH and pCO2 change in the same direction and
pH is abnormal
 For metabolic acidosis,
pCO2 = 1.5 (HCO3) + 8
For metabolic alkalosis,
pCO2 = 0.7 (HCO3) + 20

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 Acid-Base Disorders
Metabolic Acidosis
Summary

 Chloride-responsive (Cl- depletion, volume

depletion)
 Chloride-resistant (K+ depletion, volume
expansion)

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 Acid Base Analysis

• Basic Concepts:
– H+ ions regulated by
» pCO2
» HCO3
– Compensatory mechanisms keep pCO2/HCO3 ratio
constant.

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 Acid Base Analysis
• Is the disturbance respiratory or metabolic ??
– If pH and pCO2 change in the same direction and pH is
abnormal = metabolic
– If pH is normal and pCO2 is abnormal = mixed
– If pH and pCO2 change in opposite directions and pCO2
is abnormal = respiratory

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 Primary and Secondary
Acid-Base Changes
Primary Disorders Compensatory Response
pCO2 HCO3-
(Respiratory acidosis) (Metabolic alkalosis)
pCO2 HCO3-
(Respiratory alkalosis) (Metabolic acidosis)
HCO3- pCO2
(Metabolic acidosis) (Respiratory alkalosis)
HCO3- pCO2
(Metabolic alkalosis) (Respiratory acidosis)

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 Acid Base
Analysis
Rule #1:

IF: pH and pCO2 change in

the same direction
AND: the pH is abnormal
THEN: the primary disorder is
metabolic

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 Acid Base Analysis

Rule #2:
IF: pH is low (metabolic acidosis)
THEN: pCO2 should be 1.5 (HCO3) + 8 (+ 2)

IF: pH is high (metabolic alkalosis)

THEN: pCO2 should be 0.7 (HCO3) + 20
(+ 1.5)

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 Acid Base Analysis

Rule #3:
IF: the pH is normal
AND: the pCO2 is abnormal
THEN: a mixed metabolic-respiratory
disorder is present

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 Acid-Base Disorders
Case Presentation 1

Immediately after a cardiac arrest, a patient (70

kg) has a pH 7.25, pCO2 of 28, and [HCO3-] of
12 mEq/L

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 Acid-Base Disorders
Case Presentation 1
• pH < 7.37, so the problem is an acidosis
• [HCO3-] < 24 mEq/L and pCO2 < 40 so this is a
metabolic acidosis

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 Acid-Base Disorders
Case Presentation 1

• pCO2 = (1.5 x [HCO3-]) + 8 = (1.5 x 12) + 8 =

26
• Expected pCO2 of 26 mmHg is very similar to the
actual measured value of 28, so this is a simple
metabolic acidosis

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 Acid-Base Disorders
Case Presentation 2

A young man with a fever of 103.2oF and a fruity

odor on his breath has a blood gas with pH of
7.35, pCO2 of 17, and [HCO3-] of 9

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 Acid-Base Disorders
Case Presentation 2
• pH < 7.37 indicates an acidosis
• [HCO3-] < 24 and pCO2 < 40, thus a metabolic
acidosis is present

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 Acid-Base Disorders
Case Presentation 2

• The expected compensation in pCO 2 can be

calculated as follows
pCO2 = 1.5 x [HCO3-] + 8 = (1.5 x 9) + 8 = 21.5
• Expected pCO2 is 22 but the actual result is 17
mmHg, indicating a second process which is a
respiratory alkalosis

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 Acid-Base Disorders
Case Presentation 3

A 30 y.o. female 30 weeks pregnant presents

with nausea and vomiting; blood gas reveals a
pH 7.55, pCO2 of 25, and [HCO3-] of 22

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 Acid-Base Disorders
Case Presentation 3
• pH < 7.44 indicates alkalosis
• [HCO3-] < 24 and pCO2 < 40 thus a respiratory
alkalosis is present

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 Acid-Base Disorders
Case Presentation 3

• Expected compensation is calculated:


[HCO3-] = 5 x pCO2 /10 = 5 x 15/10 =

•
7.5
• The calculated [HCO3-] is then 24-7.5 or 16-17
mmol, but the actual bicarbonate level is 22,
indicating a relative metabolic alkalosis.

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 Acid-Base Disorders
Case Presentation 4
Miss Z, a 28 y.o. woman with a 15 year history of
diabetes mellitus, was brought to the hospital in a
coma.
– Afebrile, but breathing rapidly and deeply
– BP 120/70, pulse 90/min regular with orthostatic changes in
both
– No other neurologic findings
– Diabetic retinopathy only found in physical exam

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 Acid-Base Disorders
Case Presentation 4
• Glucose 500 mg/dL • BUN 20 mg/dL
• Serum ketones not done • Creatinine 1.3 mg/dL
• Na+ 133 mEq/L • Arterial blood pH 7.08
• K+ 4.0 mEq/L – PaCO2 14 mmHg
• Cl- 96 mEq/L – PaO2 98 mmHg

• HCO3- 4 mmol/L

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 Acid-Base Disorders
Case Presentation 4

• What are the clues in the history and physical

examination that lead to the diagnosis of the
underlying disorder?
• What is the etiology of the acid-base disturbance?
• How would you diagnose the acid-base
disturbance?
• What other conditions are associated with
ketoacidosis?
• What is the appropriate therapy?

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 Acid-Base Disorders
Case Presentation 5
Mr. S, a 45 y.o. man weighing 70 kg, had acute
gastrointestinal bleeding, following by hypotension
and confusion. He was noted to have labored
breathing

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 Acid-Base Disorders
Case Presentation 5
• Glucose 126 mg/dL • BUN 90 mg/dL
• Na+ 140 mEq/L • Creatinine 1.2 mg/dL
• K+ 4.2 mEq/L • Arterial blood pH 6.97
• Cl- 104 mEq/L – PaCO2 12 mmHg
• HCO3- 3 mmol/L – PaO2 96 mmHg

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 Acid-Base Disorders
Case Presentation 5

• Considering the clinical setting, what is the most

likely causes?
• What is the acid-base disturbance?
• What mechanism could be responsible for the acid-
base disturbance?
• What laboratory test would help you make the
diagnosis?
• What is the appropriate therapy ?

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 Acid-Base Disorders
Case Presentation 6
Mr. B, a 42 y.o. man alcoholic brought to the hospital
in a coma
• BP 130/80, respiratory rate 24/min
• Mild hepatosplenomegaly, no edema or jaundice
• No focal neurologic signs
• Fundoscopic exam was inadequate

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 Acid-Base Disorders
Case Presentation 6
• Glucose 90 mg/dL • BUN 30 mg/dL
• Na+ 140 mEq/L • Blood ketones trace
• K+ 5.5 mEq/L positive
• Cl- 105 mEq/L • Arterial blood pH 7.05
• HCO3- 6 mmol/L – PaCO2 16 mmHg
– PaO2 88 mmHg
• Serum osmolality 340
mOsm/kg

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 Acid-Base Disorders
Case Presentation 6

• What is the acid-base disturbance?

• What may cause this acid-base disturbance in
alcoholics?
• What additional physical or laboratory findings
would help with the differential diagnosis of the
acid-base disturbance?
• How does the serum osmolality help with the
diagnosis in this case?
• How would you treat this disturbance?

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 Acid-Base Disorders
Case Presentation 7
• Miss K, 78 y.o. woman, admitted with episodic
diarrhea and weight loss for 3 months. Physical
exam revealed only evidence of volume
depletion. During the first week in the hospital
the patient was observed to have 8 to 10 watery
bowel movements/day and lost 5 lbs. from her
admission weight despite medication to control
her diarrhea.

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 Acid-Base Disorders
Case Presentation 7

Admission After 1 week

BUN 18 mg/dL BUN 28 mg/dL Arterial blood:
Na+ 138 mEq/L Na+ 135 mEq/L pH 7.24
K+ 3.9 mEq/L K+ 3.0 mEq/L PaCO2 27 mmHg
Cl- 100 mEq/L Cl- 110 mEq/L PaO2 100 mmHg
HCO3- 27 mmol/L HCO3- 13 mmol/L

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 Acid-Base Disorders
Case Presentation 7

• What is the acid-base disturbance after 1 week?

• What is the cause of the acid-base disturbance?
• What other gastrointestinal disturbances can cause
an acidosis
• What is the cause of the fall in serum K +
concentration?
• Assuming no further diarrhea, what would be
appropriate treatment?

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 Acid-Base Disorders
Case Presentation 8
Mr. P, a 23 y.o. man with a history of calcium oxalate
stone, presented after passing another radio-
opaque stone. He denied any history of drug
ingestion or gastrointestinal disorder, but does
have a family history of stone disease. Physical
exam is normal.

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 Acid-Base Disorders
Case Presentation 8
• Glucose 90 mg/dL • BUN 15 mg/dL
• Na+ 140 mEq/L • Creatinine 1.0 mg/dL
• K+ 3.0 mEq/L • Calcium 9.2 mg/dL
• Cl- 115 mEq/L • Phosphorus 4.0 mg/dL
• HCO3- 15 mmol/L • Total protein 6.0 g/dL
• Arterial blood pH 7.35 (Albumin/globulin normal)

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 Acid-Base Disorders
Case Presentation 8

• What is the acid-base disturbance most likely to

be?
• Given the clinical setting, what is the most likely
diagnosis?
• What is the pathophysiologic basis for this
disorder?
• How would you treat this disorder?

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 Acid-Base Disorders
Case Presentation 9
A 55 y.o. man experienced repeated vomiting and
anorexia for four days. One week previously he
had medicated himself with ibuprofen because of
lower back aching. Although the vomiting had
subsided he sought medical attention because of
continuing anorexia and lightheadedness upon
arising. The past medical history was insignificant.

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 Acid-Base Disorders
Case Presentation 9

Physical Examination
Supine Standing
BP 100/70 mmHg 90/60 mmHg
Pulse rate 90 108
Resp rate 10
o
Temperature 98.8 F
Weight 68 kg

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 Acid-Base Disorders
Case Presentation 9

Serum Chemistry Panel

• Na+ 143 mEq/L • BUN 35 mg/dL
• K+ 3.0 mEq/L • Creatinine 1.7 mg/dL
• Cl- 85 mEq/L • Total protein 8.5 g/dL
• Total CO2 39 mMols/L • Albumin 5.5 gm/dL

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 Acid-Base Disorders
Case Presentation 9

• CBC • Urinalysis
– WBC 8,500/mm3 – Specific gravity: 1.018
– HgB 16 gm/dL – Protein - Trace
– PLT 292,000/mm3 – Sediment - No formed
elements
– pH: 6.0

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 Acid-Base Disorders
Case Presentation 9

• Based on the history, physical findings, and initial lab results,

how would you characterize the intravascular volume of this
patient?
• What are your thought about the acid-base balance status of
the patient?
• How would you explain the elevated anion gap of 19 mEq/L?
• How does vomiting actually result in metabolic alkalosis?

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 Acid-Base Disorders
Case Presentation 9
• If vomiting, which results in the net addition of 200 to 300
mEq of HCO3- to body fluids a day, induces metabolic
alkalosis, why does ingesting 500 mEq/day of NaHCO3 fail to
produce a significant metabolic alkalosis? Why is the renal
excretion of bicarbonate impaired after vomiting?
• How does a decrease in ECF volume impair the ability of the
kidneys to excrete bicarbonate?

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 Acid-Base Disorders
Case Presentation 9
• How does a total body chloride deficit impair renal
bicarbonate excretion?
• What role does hypokalemia play in maintaining
alkalosis?
• Why is the hypoventilation that accompanies
metabolic alkalosis a physiologic epiphenomenon of
the alkalosis and not a truly compensatory
mechanism?

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 Questions ?

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