Transcript Compensation

Biochemical basis of acidosis and alkalosis:
evaluating acid base disorders
Eric Niederhoffer, Ph.D.
SIU-SOM
Outline
• Approach
history
physical examination
differentials
clinical and laboratory studies
compensation
• Respiratory
acidosis
alkalosis
• Metabolic
acidosis
alkalosis
• Special cases
pregnancy
children
Approach
• History - subjective information concerning events,
environment, trauma, medications, poisons, toxins
• Physical examination - objective information
assessing organ system status and function
• Differentials - potential reasons for presentation
• Clinical and laboratory studies - degree of changes
from normal
• Compensation - assessment of response to initial
problem
Reference ranges and points
Parameter
Reference range Reference point
pH
7.35-7.45
7.40
PCO2
33-44 mm Hg
40 mm Hg
PO2
75-105 mm Hg
HCO3-
22-28 mEq/L
24mEq/L
Anion gap
8-16 mEq/L
12 mEq/L
Osmolar gap
<10 mOsm/L
Delta ratio
𝛥 ratio = 𝛥Anion gap/𝛥[HCO3-] = (AG – 12)/(24 - [HCO3-])
Delta ratio
Assessment
<0.4
Hyperchloraemic normal anion gap acidosis
0.4 – 0.8
1-2
>2
Combined high AG and normal AG acidosis
Note that the ratio is often <1 in acidosis associated
with renal failure
Uncomplicated high-AG acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due to urine
ketone loss (if patient not dehydrated)
Pre-existing increased [HCO3-]:
concurrent metabolic alkalosis
pre-existing compensated respiratory acidosis
Compensation
Primary
Disturbance
pH
HCO3-
PCO2
Compensation
Respiratory acidosis
<7.35
Compensatory
increase
Primary
increase
Acute: 1-2 mEq/L increase in
HCO3- for every 10 mm Hg increase
in PCO2
Chronic: 3-4 mEq/L increase in
HCO3- for every 10 mm Hg increase
in PCO2
Respiratory alkalosis
>7.45
Compensatory
decrease
Primary
decrease
Acute: 1-2 mEq/L decrease in
HCO3- for every 10 mm Hg
decrease in PCO2
Chronic: 4-5 mEq/L decrease in
HCO3- for every 10 mm Hg
decrease in PCO2
Metabolic acidosis
<7.35
Primary
decrease
Compensatory
decrease
1.2 mm Hg decrease in PCO2 for
every 1 mEq/L decrease in HCO3-
Metabolic alkalosis
>7.45
Primary
increase
Compensatory
increase
0.6-0.75 mm Hg increase in PCO2
for every 1 mEq/L increase in HCO3, PCO2 should not rise above 55 mm
Hg in compensation
Respiratory acidosis
PCO2 greater than expected
Acute or chronic
Causes
 excess CO2 in inspired air
(rebreathing of CO2-containing expired air, addition of
CO2 to inspired air, insufflation of CO2 into body
cavity)
 decreased alveolar ventilation
(central respiratory depression & other CNS
problems, nerve or muscle disorders, lung or chest
wall defects, airway disorders, external factors)
 increased production of CO2
(hypercatabolic disorders)
Racid acute
A 65-year-old man with a history of emphysema comes to
the physician with a 3-hour history of shortness of breath.
pH
7.18
PO2
61 mm Hg
PCO2
58 mm Hg
HCO3-
26 mEq/L
History suggests hypoventilation, supported by increased
PCO2 and lower than anticipated PO2.
Respiratory acidosis (acute) due to no renal compensation.
Description
pH
7.18
PO2
61 mm Hg
PCO2
58 mm Hg
HCO3-
26 mEq/L
1-2 mEq/L increase in HCO3- for every 10 mm Hg increase
in PCO2.
PCO2 increase = 58-40 = 18 mm Hg.
HCO3- increase predicted = (1-2) x (18/10) = 2-4 mEq/L
add to 24 mEq/L (reference point) = 26-28 mEq/L
Racid chronic
A 56-year-old woman with COPD is brought to the physician
with a 3-hour history of severe epigastric pain.
pH
7.39
PO2
62 mm Hg
PCO2
52 mm Hg
HCO3-
29 mEq/L
History suggests hypoventilation, supported by increased
PCO2.
Respiratory acidosis (chronic) with renal compensation.
Description
pH
7.39
PO2
62 mm Hg
PCO2
52 mm Hg
HCO3-
29 mEq/L
3-4 mEq/L increase in HCO3- for every 10 mm Hg increase
in PCO2.
PCO2 increase = 52-40 = 12 mm Hg.
HCO3- increase predicted = (3-4) x (12/10) = 4-5 mEq/L
add to 24 mEq/L (reference point) = 28-29 mEq/L
Respiratory alkalosis
PCO2 less than expected
Acute or chronic
Causes
 increased alveolar ventilation
(central causes, direct action via respiratory center;
hypoxaemia, act via peripheral chemoreceptors;
pulmonary causes, act via intrapulmonary receptors;
iatrogenic, act directly on ventilation)
Ralk acute
A 17-year-old woman is brought to the physician with a 3hour history of epigastric pain and nausea. She admits
taking a large dose of aspirin. Her respirations are full and
rapid.
pH
7.57
PO2
104 mm Hg
PCO2
25 mm Hg
HCO3-
23 mEq/L
History suggests hyperventilation, supported by decreased
PCO2.
Respiratory alkalosis (acute) due to no renal compensation.
Description
pH
7.57
PO2
104 mm Hg
PCO2
25 mm Hg
HCO3-
23 mEq/L
1-2 mEq/L decrease in HCO3- for every 10 mm Hg decrease
in PCO2.
PCO2 decrease = 40-25 = 15 mm Hg.
HCO3- decrease predicted = (1-2) x (15/10) = 2-3 mEq/L
subtract from 24 mEq/L (reference point) = 21-22 mEq/L
Ralk chronic
A 81-year-old woman with a history of anxiety is brought to
the physician with a 2-hour history of shortness of breath.
She has been living at 9,000 ft elevation for the past 1
month. Her respirations are full at 20/min.
pH
7.44
PO2
69 mm Hg
PCO2
24 mm Hg
HCO3-
16 mEq/L
History suggests hyperventilation, supported by decreased
PCO2.
Respiratory alkalosis (chronic) with renal compensation.
Description
pH
7.44
PO2
69 mm Hg
PCO2
24 mm Hg
HCO3-
16 mEq/L
4-5 mEq/L decrease in HCO3- for every 10 mm Hg decrease
in PCO2.
PCO2 decrease = 40-24 = 16 mm Hg.
HCO3- decrease predicted = (4-5) x (16/10) = 6-8 mEq/L
subtract from 24 mEq/L (reference point) = 16-18 mEq/L
Metabolic acidosis
Plasma HCO3- less than expected
Gain of strong acid or loss of base
Alternatively, high anion gap or normal anion gap metabolic acidosis
Causes
 high anion-gap acidosis (normochloremic)
(ketoacidosis, lactic acidosis, renal failure, toxins)
 normal anion-gap acidosis (hyperchloremic)
(renal, gastrointestinal tract, other)
Macid high AG
A 20-year-old man with a history of diabetes is brought to
the emergency department with a 3-day history of feeling ill.
He is non-adherent with his insulin. Urine ketones are 2+
and glucose is 4+.
pH
7.26
Na+
136 mEq/L
PO2
110 mm Hg
K+
4.8 mEq/L
PCO2
19 mm Hg
Cl101 mEq/L
HCO38 mEq/L
CO2, total 10 mEq/L
Glucose
343 mg/dL
Urea
49 mg/dL
Creatinine 1 mg/dL
History suggests diabetic ketoacidosis.
Metabolic acidosis with appropriate respiratory
compensation.
Description
pH
PO2
PCO2
HCO3-
7.26
110 mm Hg
19 mm Hg
8 mEq/L
AG = 136-101-8=27 mEq/L
Na+
K+
ClGlucose
Urea
Creatinine
136 mEq/L
4.8 mEq/L
101 mEq/L
343 mg/dL
49 mg/dL
1 mg/dL
1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in
HCO3-.
HCO3- decrease = 24-8 = 16 mEq/L
PCO2 decrease predicted = 1.2 x 16 = 19 mm Hg.
subtract from 40 mm Hg (reference point) = 21 mm Hg
Macid normal AG
A 43-year-old man comes to the physician with a 3-day
history of diarrhea. He has decreased skin turgor.
pH
7.31
Na+
134 mEq/L
PO2
-- mm Hg
K+
2.9 mEq/L
PCO2
31 mm Hg
Cl113 mEq/L
HCO316 mEq/L
Urea
74 mgl/dL
Creatinine 3.4 mmol/L
History is limited.
Metabolic acidosis with respiratory compensation.
Description
pH
PO2
PCO2
HCO3-
7.31
-- mm Hg
31 mm Hg
16 mEq/L
Na+
K+
ClUrea
Creatinine
134 mEq/L
2.9 mEq/L
113 mEq/L
74 mg/dL
3.4 mg/dL
AG = 134-113-16=5 mEq/L
1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in
HCO3-.
HCO3- decrease = 24-16 = 8 mEq/L
PCO2 decrease predicted = 1.2 x 8 = 10 mm Hg.
subtract from 40 mm Hg (reference point) = 30 mm Hg
Metabolic alkalosis
Plasma HCO3- greater than expected
Loss of strong acid or gain of base
Causes (2 ways to organize)
 loss of H+ from ECF via kidneys (diuretics) or gut (vomiting)
 gain of alkali in ECF from exogenous source (IV NaHCO3
infusion) or endogenous source (metabolism of ketoanions)
or
 addition of base to ECF (milk-alkali syndrome)
 Cl- depletion (loss of acid gastric juice)
 K+ depletion (primary/secondary hyperaldosteronism)
 Other disorders (laxative abuse, severe hypoalbuminaemia)
Urinary Chloride
Spot urine Cl- less than 10 mEq/L
 often associated with volume depletion
 respond to saline infusion
 common causes - previous thiazide diuretic therapy, vomiting
(90% of cases)
Spot urine Cl- greater than 20 mEq/L
 often associated with volume expansion and hypokalemia
 resistant to therapy with saline infusion
 causes: excess aldosterone, severe K+ deficiency, current
diuretic therapy, Bartter syndrome
Malk high Urine ClAn 83-year-old woman is brought to the physician with a 1week history of weakness and poor appetite.
pH
7.58
Na+
145 mEq/L
PO2
60 mm Hg
K+
1.9 mEq/L
PCO2
56 mm Hg
Cl86 mEq/L
HCO352 mEq/L
Urine Cl74 mEq/L
History is limited.
Metabolic alkalosis with respiratory compensation.
The cause is unknown, most likely excess adrenocortical
activity, current diuretic therapy, or idiopathic.
Description
pH
PO2
PCO2
HCO3-
7.58
60 mm Hg
56 mm Hg
52 mEq/L
Na+
K+
ClUrine Cl-
145 mEq/L
1.9 mEq/L
86 mEq/L
74 mEq/L
0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L
increase in HCO3-.
HCO3- increase = 52-24 = 28 mEq/L
PCO2 increase predicted = 0.6-0.75 x 28 = 17-21 mm Hg.
add to 40 mm Hg (reference point) = 57-61 mm Hg
Malk low Urine ClAn 24-year-old woman is brought to the physician with a 3month history of weakness and fatigue. Blood pressure is
90/60 mm Hg.
pH
7.52
Na+
137 mEq/L
PO2
78 mm Hg
K+
2.6 mEq/L
PCO2
49 mm Hg
Cl90 mEq/L
HCO339 mEq/L
Urine Cl5 mEq/L
History and physical examination suggests bulimia.
Metabolic alkalosis with respiratory compensation.
The cause is most likely bulimia.
Description
pH
PO2
PCO2
HCO3-
7.52
78 mm Hg
49 mm Hg
39 mEq/L
Na+
K+
ClUrine Cl-
137 mEq/L
2.6 mEq/L
90 mEq/L
5 mEq/L
0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L
increase in HCO3-.
HCO3- increase = 39-24 = 15 mEq/L
PCO2 increase predicted = 0.6-0.75 x 15 = 9-12 mm Hg.
add to 40 mm Hg (reference point) = 49-52 mm Hg
Special Cases
• Pregnancy – hyperventilation (respiratory alkalosis),
hyperemesis (metabolic alkalosis or acidosis), maternal
ketosis (metabolic acidosis)
• Children – low bicarbonate reserve (N=12-16 mEq/L),
low acid excretion reserve, inborn errors in metabolism,
diabetes, and poisoning (all metabolic acidosis)
Review Questions
• What is an effective approach to acid base problems?
• What are the normal ranges and reference points?
• What are the anion and osmolar gap?
• What is compensation?
• What are the characteristics of respiratory acidosis and
alkalosis?
• What are the characteristics of metabolic acidosis and
alkalosis?
• What is the utility of spot urine Cl-?
• What kinds of acid base conditions present during pregnancy
and infancy?