Biochemical basis of Acid

Base Balance
 Q.How acid base balance is maintained in
normal human being?
• Normal body pH=7.4 equivalent to 40 nmole H
con. Per liter. This level is very important for
normal biological activity. this level of pH should
be maintained for proper functioning of the body.
on an average, the pH range may fluctuate from
7.35-7.45.
• During normal metabolic activity, body produces
both acid and bases but the acid production is
greater than the base production.
• So body is a net acid producer.in a normal
adult two types of metabolic acid are
produced.
• 1.Volatile acid- 15 mole/day in the form of
co2
• 2. Non volatile acid-70 mEq/day in the
form of H2so4, HCl,
• These metabolic acid has a major
consequences in alter the normal body
pH.
• Volatile acids are excreted through lung
via pulmonary route.non volatile acids are
excreted through kidney via urine.
• Before their excreation respiratory system
takes some time and kidney system also
takes certain time.
 Excreation of volatile acid:

• Co2 produced in cellular level due to

metabolic activity diffused into blood.in
blood co2 is transported in three form.
• A.in dissolved state=7%
• B. in the form of HCO3-&H+ (H2Co3)=70%
• In combination of Hb=23%
• From blood CO2 is diffused into alveoli of
lungs and their into the atmosphere.
Transport of carbon dioxide in the blood
 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
 pH Review

• pH = - log [H+]
• H+ is really a proton
• Range is from 0 - 14
• If [H+] is high, the solution is acidic; pH < 7
• If [H+] is low, the solution is basic or
alkaline ; pH > 7

8
9
10
• Acids are H+ donors.
• Bases are H+ acceptors, or give up OH- in
solution.
• Acids and bases can be:
– Strong – dissociate completely in
solution
• HCl, NaOH
– Weak – dissociate only partially in
solution
• Lactic acid, carbonic acid

11
 The Body and pH

• Homeostasis of pH is tightly controlled

• Extracellular fluid = 7.4
• Blood = 7.35 – 7.45
• < 6.8 or > 8.0 death occurs
• Acidosis (acidemia) below 7.35
• Alkalosis (alkalemia) above 7.45

12
13
 Small changes in pH can produce
major disturbances
• Most enzymes function only with narrow
pH ranges
• Acid-base balance can also affect
electrolytes (Na+, K+, Cl-)
• Can also affect hormones

14
 The body produces more acids than
bases
• Acids take in with foods
• Acids produced by metabolism of lipids
and proteins
• Cellular metabolism produces CO2.
• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-

15
 Control of Acids

1. Buffer systems
Take up H+ or release H+ as conditions
change
Buffer pairs – weak acid and a base
Exchange a strong acid or base for a
weak one
Results in a much smaller pH change

16
 Bicarbonate buffer

• Sodium Bicarbonate (NaHCO3) and

carbonic acid (H2CO3)
• Maintain a 20:1 ratio : HCO3- : H2CO3

HCl + NaHCO3 ↔ H2CO3 + NaCl

NaOH + H2CO3 ↔ NaHCO3 + H2O

17
 Phosphate buffer

• Major intracellular buffer

• H+ + HPO42- ↔ H2PO4-

• OH- + H2PO4- ↔ H2O + H2PO42-

18
 Protein Buffers

• Includes hemoglobin.
• Carboxyl group gives up H+
• Amino Group accepts H+

19
 2. Respiratory mechanisms

• Exhalation of carbon dioxide

• Powerful, but only works with volatile
acids
• Doesn’t affect fixed acids like lactic acid
• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-
• Body pH can be adjusted by changing rate
and depth of breathing

20
 3. Kidney excretion

• Can eliminate large amounts of acid

• Can also excrete base
• Can conserve and produce bicarb ions
• Most effective regulator of pH
• If kidneys fail, pH balance fails

21
 Rates of correction

• Buffers function almost instantaneously

• Respiratory mechanisms take several
minutes to hours
• Renal mechanisms may take several
hours to days

22
23
24
 Acid-Base Imbalances

• pH< 7.35 acidosis

• pH > 7.45 alkalosis
• The body response to acid-base
imbalance is called compensation
• May be complete if brought back within
normal limits
• Partial compensation if range is still
outside norms.

25
 Compensation

• If underlying problem is metabolic,

hyperventilation or hypoventilation can
help : respiratory compensation.
• If problem is respiratory, renal
mechanisms can bring about metabolic
compensation.

26
 Acidosis
• Principal effect of acidosis is depression of the
CNS through ↓ in synaptic transmission.
• Generalized weakness
• Deranged CNS function the greatest threat
• Severe acidosis causes
– Disorientation
– coma
– death

27
 Alkalosis
• Alkalosis causes over excitability of the central
and peripheral nervous systems.
• Numbness
• It can cause :
– Nervousness
– muscle spasms or tetany
– Convulsions
– Loss of consciousness
– Death

28
29
 Respiratory Acidosis

• Carbonic acid excess caused by blood

levels of CO2 above 45 mm Hg.
• Hypercapnia – high levels of pCO2 in
blood
• Chronic conditions:
– Depression of respiratory center in brain that
controls breathing rate – drugs or head
trauma
– Paralysis of respiratory or chest muscles
– Asthma,Pneumonia,Emphysema
30
 Respiratory Acidosis

• Acute conditons:
– Adult Respiratory Distress Syndrome
– Pulmonary edema
– Pneumothorax

31
 Compensation for Respiratory
Acidosis
• Kidneys eliminate hydrogen ion and retain
bicarbonate ion.
• Mechanism:↓pH→↑H+→H ion+ HCO3- →
H2CO3 → CO2 + H20 →pH backs towards
normal.

32
 Signs and Symptoms of Respiratory
Acidosis
• Breathlessness
• Restlessness
• Lethargy and disorientation
• Tremors, convulsions, coma
• Respiratory rate rapid, then gradually
depressed
• Skin warm and flushed due to vasodilation
caused by excess CO2

33
 Treatment of Respiratory Acidosis

• Restore ventilation
• IV lactate solution
• Treat underlying dysfunction or disease

34
35
 Respiratory Alkalosis

• Carbonic acid deficit

• pCO2 less than 35 mm Hg (hypocapnea)
• Most common acid-base imbalance
• Primary cause is hyperventilation
• Hysteria
• Hyperapnoea at high altitude.
• Meningitis,enchephalitis.
• Hepatic failure
36
 Respiratory Alkalosis
• Conditions that stimulate respiratory
center:
– Oxygen deficiency at high altitudes
– Pulmonary disease and Congestive heart
failure – caused by hypoxia
– Acute anxiety
– Fever, anemia
– Early salicylate intoxication
– Cirrhosis
– Gram-negative sepsis
37
 Compensation of Respiratory
Alkalosis
• By renal system
• Kidneys conserve hydrogen ion
• Excrete bicarbonate ion.

38
Treatment of Respiratory Alkalosis

• Treat underlying cause

• Breathe into a paper bag
• IV Chloride containing solution – Cl- ions
replace lost bicarbonate ions

39
40
 Metabolic Acidosis

• Decreased pH due to HCO3- deficit is called

metabolic acidosis.
• Bicarbonate deficit - blood concentrations of

bicarb drop below 22mEq/L

• Causes:
– Loss of bicarbonate through diarrhea or renal
dysfunction
– DM, Accumulation of acids (lactic acid or
ketones)
– Failure of kidneys to excrete H+ 41
• Ingestion of acid
• Formation of excessive quantities of
metabolic acid in the body.
• Loss of excessive alkali from the body.
• Intravenous administration of metabolic
acid.
• Poisoning by acidic eg. Acetyl salicylates
(aspirin) and methyl alcohol.
 Symptoms of Metabolic Acidosis

• Headache, lethargy
• Nausea, vomiting, diarrhea
• Coma
• Death

43
 Compensation for Metabolic
Acidosis
• By respiratory system
• Increased ventilation
• Renal excretion of hydrogen ions if
possible
• K+ exchanges with excess H+ in ECF
• ( H+ into cells, K+ out ofcells)
• Mechanism: ↓pH→↑respiration→ ↓ pCO2 to
HCO - →pH backs towards
match the lowered 3
normal.
44
Treatment of Metabolic Acidosis

• IV lactate solution

45
46
 Metabolic Alkalosis

• Bicarbonate excess - concentration in

blood is greater than 26 mEq/L
• Causes:
– Excess vomiting = loss of stomach acid
– Excessive use of alkaline drugs
– Certain diuretics
– Endocrine disorders
– Heavy ingestion of antacids
– Severe dehydration

47
 Compensation for Metabolic
Alkalosis
• Alkalosis most commonly occurs with
renal dysfunction, so can’t count on
kidneys
• Respiratory compensation difficult –
hypoventilation limited by hypoxia

48
 Symptoms of Metabolic Alkalosis

• Respiration slow and shallow

• Hyperactive reflexes ; tetany
• Often related to depletion of electrolytes
• Atrial tachycardia
• Dysrhythmias

49
 Treatment of Metabolic Alkalosis

• Electrolytes to replace those lost

• IV chloride containing solution
• Treat underlying disorder

50
51
Diagnosis of Acid-Base Imbalances

1. Note whether the pH is low (acidosis) or

high (alkalosis)
2. Decide which value, pCO2 or HCO3- , is
outside the normal range and could be
the cause of the problem. If the cause is
a change in pCO2, the problem is
respiratory. If the cause is HCO3- the
problem is metabolic.

52
 Acid-Base Biochemistry
Physiology
• 2 different processes
• Bicarbonate regeneration (incorrectly
reabsorption)
• Hydrogen ion excretion
 Acid-Base Biochemistry

Importance of Renal Bicarbonate Regeneration

• Bicarbonate is freely filtered through the glomerulus so
plasma and glomerular filtrate have the same
bicarbonate concentration
• At normal GFR approx 4300 mmol of bicarbonate would
be filtered in 24 hr
• Without re-generation of bicarbonate the buffering
capacity of the body would be depleted causing acidotic
state
• In health virtually all the filtered bicarbonate is recovered
 Acid-Base Biochemistry

• Renal Bicarbonate Regeneration involves the

enzyme carbonate dehydratase (carbonic
anhydrase)
• Luminal side of the renal tubular cells
impermeable to bicarbonate ions
• Carbonate dehydratase catalyses the formation of
CO2 and H2O from carbonic acid (H2CO3) in the
renal tubular lumen
• CO2 diffuses across the luminal membrane into
the tubular cells
 Acid-Base Biochemistry

• within the renal tubular cells carbonate dehydratase

catalyses the formation of carbonic acid (H2CO3) from CO2
and H2O
• Carbonic acid then dissociates into H+ and HCO3-
• The bicarbonate ions pass into the extracellular fluid and
the hydrogen ions are secreted back into the lumen in
exchange for sodium ions which pass into the extracellular
fluid
• Exchange of sodium and hydrogen ions an active process
involving Na+/K+/H+ ATP pump
• K+ important in electrolyte disturbances of acid-base
 Acid-Base Biochemistry

• Regeneration of bicarbonate does not involve net excretion

of hydrogen ions
• Hydrogen ion excretion requires the same reactions
occurring in the renal tubular cells but also requires a
suitable buffer in urine
• Principal buffer system in urine is phosphate
• 80% of phosphate in glomerular filtrate is in the form of the
divalent anion HPO42-
• This combines with hydrogen ions
• HPO42- + H+ ↔ H2PO4-
 Acid-Base Biochemistry

• Hydrogen ion excretion capacity

• The minimum urine pH that Can be
generated is 4.6 ( 25µmol/L)
• Normal urine output is 1.5L
• Without the phosphate buffer system the
free excretion of Hydrogen ions is less than
1/1000 of the acid produced by normal
metabolism
 Acid-Base Biochemistry

• The phosphate buffer system increases

hydrogen ion excretion capacity to 30-40
mmol/24 hours
• In times of chronic overproduction of acid
another urine buffer system
• Ammonia
 Acid-Base Biochemistry

• Ammonia produced by deamination of

glutamine in renal tubular cells
• Catalysed by glutaminase which is induced
by chronic acidosis
• Allows increased ammonia production and
hence increased hydrogen ion excretion via
ammonium ions
• NH3 + H+ ↔NH4+
 Acid-Base Biochemistry

• At normal intracellular pH most ammonia is present as

ammonium ions which can’t diffuse out of the cell
• Diffusion of ammonia out of the cell disturbs the equilibrium
between ammonia and ammonium ions causing more
ammonia to be formed
• Hydrogen ions formed at the same time!
• These are used up by the deamination of glutamine to
glutamate during gluconeogenesis
 Acid-Base Biochemistry

• Carbon dioxide transport

• Carbon dioxide produced by aerobic respiration
diffuses out of cells and into the ECF
• A small amount combines with water to form
carbonic acid decreasing the pH of ECF
• In red blood cells metabolism is anaerobic and
very little CO2 is produced hence it diffuses into
red cells down a concentration gradient to form
carbonic acid (carbonate dehydratase) buffered by
haemoglobin .
 Acid-Base Biochemistry

• Haemoglobin has greatest buffering capacity when

it is dexoygenated hence the buffering capacity
increases as oxygen is lost to the tissues
• Net effect is that carbon dioxide is converted to
bicarbonate in red cells
• Bicarbonate diffuses out of red cells down
concentration gradient and chloride ions diffuse in
to maintain electrochemical neutrality (chloride
shift)
 •Acid-Base Biochemistry

• In the lungs this process is reversed

• Haemoglobin is oxygenated reducing its
buffering capacity and generating hydrogen
ions
• These combine with bicarbonate to form
CO2 which diffuses into the alveoli
• Bicarbonate diffuses into the cells from the
plasma
72
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
 Treatment of Metabolic
Alkalosis
• Electrolytes to replace those lost
• IV chloride containing solution
• Treat underlying disorder

74
Diagnosis of Acid-Base Imbalances

1. Note whether the pH is low (acidosis) or

high (alkalosis)
2. Decide which value, pCO2 or HCO3- , is
outside the normal range and could be
the cause of the problem. If the cause is
a change in pCO2, the problem is
respiratory. If the cause is HCO3- the
problem is metabolic.

75
 Delta ratio
𝛥 ratio = 𝛥Anion gap/𝛥[HCO3-] = (AG – 12)/(24 - [HCO3-])

Delta ratio Assessment

<0.4 Hyperchloraemic normal anion gap acidosis

Combined high AG and normal AG acidosis
0.4 – 0.8 Note that the ratio is often <1 in acidosis associated
with renal failure
Uncomplicated high-AG acidosis
Lactic acidosis: average value 1.6
1-2
DKA more likely to have a ratio closer to 1 due to urine
ketone loss (if patient not dehydrated)
Pre-existing increased [HCO3-]:
>2 concurrent metabolic alkalosis
pre-existing compensated respiratory acidosis
 Compensation
Primary pH HCO -
PCO2 Compensation
3
Disturbance
Respiratory acidosis <7.35 Compensatory Primary Acute: 1-2 mEq/L increase in
increase increase 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 Primary Acute: 1-2 mEq/L decreasein
decrease decrease HCO3- for every 10 mm Hg
decrease in PCO2
Chronic: 4-5 mEq/L decreasein
HCO3- for every 10 mm Hg
decrease in PCO2
Metabolic acidosis <7.35 Primary Compensatory 1.2 mm Hg decrease in PCO2 for
decrease decrease every 1 mEq/L decrease in HCO 3-
Metabolic alkalosis >7.45 Primary Compensatory 0.6-0.75 mm Hg increase in PCO2
increase increase for every 1 mEq/L increase in HCO 3-
, 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 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
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
0-year-old man with a history of diabetes is brought to
emergency department with a 3-day history of feeling ill.
is non-adherent with his insulin. Urine ketones are 2+
d glucose is 4+.
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 CO2, total 10 mEq/L
Glucose 343 mg/dL Urea 49 mg/dL
Creatinine 1 mg/dL
tory suggests d NC iabetic ketoacidosis.
tabolic acidosis with appropriate respiratory
mpensation.
 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/dL
AG = 136-101-8=27 mEq/L Creatinine 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 Cl- 113 mEq/L
HCO3- 16 mEq/L Urea 74 mgl/dL
Creatinine 3.4 mmol/L
History is limited.
Metabolic acidosis with respiratory compensation.
 Description
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 mg/dL
Creatinine 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
 Calculate the anion gap
 AG = Na – Cl – HCO3 (normal 12 ± 2)
 AG corrected = AG + 2.5[4 – albumin]
 If there is an anion Gap then calculate the Delta/delta
gap (step 6). Only need to calculate delta gap (excess
anion gap) when there is an anion gap to determine
additional hidden metabolic disorders (nongap metabolic
acidosis or metabolic alkalosis)
 If there is no anion gap then start analyzing for non-anion
acidosis
 Malk high Urine Cl-
An 83-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/L
History is limited.
Metabolic alkalosis with respiratory compensation.
The cause is unknown, most likely excess adrenocortical
activity, current diuretic therapy, or idiopathic.
 EXAMPLE
• Calculate Anion gap
 ABG 7.23/17/235 on 50% VM
 BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin
4.

 AG = Na – Cl – HCO3 (normal 12 ± 2)
123 – 97 – 7 = 19

• No need to correct for albumin as it is 4

 EXAMPLE : Delta Gap
 ABG 7.23/17/235 on 50% VM
 BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin
4.

• Delta gap = (actual AG – 12) + HCO3

• (19-12) +7 = 14
• Delta gap < 18 -> additional non-gap
metabolic acidosis
• So Metabolic acidosis anion and non anion
gap
 Description
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/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 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/L
History and physical examination suggests bulimia.
Metabolic alkalosis with respiratory compensation.
The cause is most likely bulimia.
 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/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
 What is the primary disorder?

What disorder is present? pH pCO2 or HCO3

Respiratory Acidosis pH low pCO2 high

Metabolic Acidosis pH low HCO3 low
Respiratory Alkalosis pH high pCO2 low
Metabolic Alkalosis pH high HCO3 high
 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)