SIUSOM Biochemical basis of acidosis and alkalosis e valuating acid base disorders Outline Approach h istory physical examination d ifferentials clinical and laboratory studies ID: 209552
Download Presentation The PPT/PDF document "Eric Niederhoffer, Ph.D." is the property of its rightful owner. Permission is granted to download and print the materials on this web site for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.
Slide1
Eric Niederhoffer, Ph.D.SIU-SOM
Biochemical basis of acidosis and alkalosis:
e
valuating
acid base
disordersSlide2
Outline
Approach
h
istory
physical
examination
d
ifferentials
clinical
and laboratory
studies
compensation
Respiratory
a
cidosis
a
lkalosis
Metabolic
acidosis
alkalosis
Special cases
pregnancy
childrenSlide3
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 problemSlide4
Reference ranges and points Parameter
Reference range
Reference point
pH
7.35-7.45 7.40
P
CO
2
33-44 mm Hg 40 mm Hg
P
O
2
75-105 mm Hg
HCO
3
-
22-28
mEq
/L 24mEq/L
Anion gap 8-16
mEq
/L 12
mEq
/L
Osmolar
gap <10
mOsm
/L Slide5
Delta ratio
Delta
ratio
Assessment
<0.4
Hyperchloraemic
normal anion gap acidosis
0.4 β 0.8
Combined high AG and normal AG acidosisNote that the ratio is often <1 in acidosis associated with renal failure1 - 2 Uncomplicated high-AG acidosisLactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss (if patient not dehydrated) >2 Pre-existing increased [HCO3-]:concurrent metabolic alkalosispre-existing compensated respiratory acidosis
π₯ ratio = π₯Anion gap/π₯[HCO
3
-
] = (AG β 12)/(24 - [HCO
3
-
]
)Slide6
Compensation
Primary Disturbance
pH
HCO
3
-
P
CO
2
CompensationRespiratory acidosis<7.35Compensatory increasePrimary increaseAcute: 1-2 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2Chronic: 3-4 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2Respiratory alkalosis>7.45Compensatory decreasePrimary decreaseAcute: 1-2 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2
Chronic: 4-5
mEq
/L decrease in HCO
3
-
for every 10 mm Hg decrease in P
CO
2
Metabolic acidosis
<7.35
Primary decrease
Compensatory decrease
1.2
mm Hg decrease in P
CO
2
for every
1
mEq
/L decrease in HCO
3
-
Metabolic
alkalosis
>7.45
Primary increase
Compensatory
increase
0.6-0.75 mm Hg increase in P
CO
2
for every 1
mEq
/L increase in
HCO
3
-
, P
CO
2
should not rise above 55 mm Hg in compensationSlide7
Respiratory acidosis
P
CO
2
greater than expected
Acute or chronic
Causes
excess CO
2
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 CO
2
(
hypercatabolic
disorders)Slide8
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
P
O
2
61 mm Hg
P
CO2 58 mm Hg HCO3- 26 mEq/LHistory suggests hypoventilation, supported by increased PCO2 and lower than anticipated PO2.Respiratory acidosis (acute) due to no renal compensation.Slide9
Description
pH 7.18
P
O
2
61 mm Hg
P
CO
2
58 mm Hg HCO3- 26 mEq/L1-2 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/Ladd to 24 mEq/L (reference point) = 26-28 mEq/LSlide10
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
P
O
2
62 mm Hg PCO2 52 mm Hg HCO3- 29 mEq/LHistory suggests hypoventilation, supported by increased PCO2.Respiratory acidosis (chronic) with renal compensation.Slide11
Description
pH 7.39
P
O
2
62
mm Hg
P
CO2 52 mm Hg HCO3- 29 mEq/L3-4 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/Ladd to 24 mEq/L (reference point) = 28-29 mEq/LSlide12
Respiratory alkalosis
P
CO
2
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)Slide13
Ralk acute
A 17-year-old woman is brought to the physician with a 3-hour history of
epigastric
pain and nausea. She admits taking a large dose of aspirin. Her respirations are full and rapid.
pH 7.57
P
O
2
104 mm Hg PCO2 25 mm Hg HCO3- 23 mEq/LHistory suggests hyperventilation, supported by decreased PCO2.Respiratory alkalosis (acute) due to no renal compensation.Slide14
Description
pH 7.57
P
O
2
104 mm Hg
P
CO
2
25 mm Hg HCO3- 23 mEq/L1-2 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/Lsubtract from 24 mEq/L (reference point) = 21-22 mEq/LSlide15
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/LHistory suggests hyperventilation, supported by decreased PCO2.Respiratory alkalosis (chronic) with renal compensation.Slide16
Description
pH
7.44
P
O
2
69 mm Hg
P
CO
2 24 mm Hg HCO3- 16 mEq/L4-5 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/Lsubtract from 24 mEq/L (reference point) = 16-18 mEq/LSlide17
Metabolic acidosis
Plasma HCO
3
-
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)Slide18
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
P
O2 110 mm Hg K+ 4.8 mEq/L PCO2 19 mm Hg Cl- 101 mEq/L HCO3- 8 mEq/L CO2, total 10 mEq/L Glucose 343 mg/dL Urea 49 mg/dL Creatinine 1 mg/dLHistory suggests diabetic ketoacidosis.Metabolic acidosis with appropriate respiratory compensation.Slide19
Description
pH
7.26
Na
+
136
mEq
/
L PO2 110 mm Hg K+ 4.8 mEq/L PCO2 19 mm Hg Cl- 101 mEq/L HCO3- 8 mEq/L Glucose 343 mg/dL Urea 49 mg/dLAG = 136-101-8=27 mEq/L Creatinine 1 mg/dL1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3-.HCO3- decrease = 24-8 = 16 mEq/L PCO
2
decrease predicted = 1.2 x 16 = 19 mm Hg.
subtract from 40 mm Hg (reference point) = 21 mm HgSlide20
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 Cl- 113 mEq/L HCO3- 16 mEq/L Urea 74 mgl/dL Creatinine 3.4 mmol/LHistory is limited.Metabolic acidosis with respiratory compensation.Slide21
Description
pH 7.31 Na
+
134
mEq
/L
P
O
2
-- mm Hg K+ 2.9 mEq/L PCO2 31 mm Hg Cl- 113 mEq/L HCO3- 16 mEq/L Urea 74 mg/dL Creatinine 3.4 mg/dLAG = 134-113-16=5 mEq/L1.2 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 HgSlide22
Metabolic alkalosis
Plasma HCO
3
-
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)oraddition of base to ECF (milk-alkali syndrome)
Cl
-
depletion (loss of acid gastric juice)
K
+
depletion (primary/secondary
hyperaldosteronism
)
Other disorders (
l
axative abuse,
s
evere
hypoalbuminaemia
)Slide23
Urinary Chloride
Spot urine
Cl
-
less than 10
mEq
/L
o
ften
associated with volume depletionrespond to saline infusioncommon causes - previous thiazide diuretic therapy, vomiting (90% of cases)Spot urine Cl- greater than 20 mEq/Lo
ften
associated with volume expansion and
hypokalemia
r
esistant
to therapy with saline
infusion
causes:
e
xcess
aldosterone, severe K
+
deficiency, current diuretic therapy, Bartter
syndromeSlide24
Malk high Urine Cl-
An
8
3-year-old woman is brought to the physician with a 1-week 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 Cl- 86 mEq/L HCO3- 52 mEq/L Urine Cl- 74 mEq/LHistory is limited.Metabolic alkalosis with respiratory compensation.The cause is unknown, most likely excess adrenocortical activity, current diuretic therapy, or idiopathic.Slide25
Description
pH 7.58 Na
+
145
mEq
/L
P
O
2
60 mm Hg K+ 1.9 mEq/L PCO2 56 mm Hg Cl- 86 mEq/L HCO3- 52 mEq/L Urine Cl- 74 mEq/L0.6-0.75 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 HgSlide26
Malk low Urine Cl-
An 24-year-old woman is brought to the physician with a 3-month 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 Cl- 90 mEq/L HCO3- 39 mEq/L Urine Cl- 5 mEq/LHistory and physical examination suggests bulimia.Metabolic alkalosis with respiratory compensation.The cause is most likely bulimia.Slide27
Description
pH
7.52
Na
+
137
mEq
/L
PO2 78 mm Hg K+ 2.6 mEq/L PCO2 49 mm Hg Cl- 90 mEq/L HCO3- 39 mEq/L Urine Cl- 5 mEq/L0.6-0.75 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 HgSlide28
Special Cases
Pregnancy
β hyperventilation (respiratory alkalosis), hyperemesis (metabolic alkalosis or acidosis), maternal ketosis (metabolic acidosis)
Children
β
low bicarbonate reserve (N=12-16
mEq
/L), low acid excretion reserve, inborn errors in metabolism, diabetes, and poisoning (all metabolic acidosis)Slide29
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?