one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance

1. ABG analysis & Acid-BaseABG analysis & Acid-Base
DisordersDisorders
2016

2. OutlineOutline
1. Discuss simple steps in analyzing ABGs
2. Calculate the anion gap
3. Calculate the delta gap
4. Differentials for specific acid-base disorders

3. Steps for ABG analysisSteps for ABG analysis
1. What is the pH? Acidemia or Alkalemia?
2. What is the primary disorder present?
3. Is there appropriate compensation?
4. Is the compensation acute or chronic?
5. Is there an anion gap?
6. If there is a AG check the delta gap?
7. What is the differential for the clinical processes?

4. Normal ValuesNormal Values
Variable Normal Range
pH 7.35 - 7.45
pCO2 35-45
Bicarbonate 22-26
Anion gap 10-14
Albumin 4

6. Step 1:Step 1:
 Look at the pH: is the blood acidemic or alkalemic?
 EXAMPLE :
 65y/M with CKD presenting with nausea, diarrhea
and acute respiratory distress
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
 ACIDMEIA OR ALKALEMIA ????

7. EXAMPLE ONEEXAMPLE ONE
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr
5.1
• Answer PH = 7.23 , HCO3= 7
• Acidemia

8. Step 2: What is theStep 2: What is the
primary disorder?primary disorder?

9. EXAMPLEEXAMPLE
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
• PH is low HCO3 is Low
• PH and HCO3 are going in same directions then its
most likely primary metabolic will check to see if
there is a mixed disorder.

10. Step 3-4: Is there appropriateStep 3-4: Is there appropriate
compensation? Is it chroniccompensation? Is it chronic
or acute?or acute?
Respiratory Acidosis
 Acute: for every 10 increase in pCO2 -> HCO3 increases by 1 and
there is a decrease of 0.08 in pH MEMORIZE
 Chronic: for every 10 increase in pCO2 -> HCO3 increases by 3.5/ 4
and there is a decrease of 0.03 in pH
Respiratory Alkalosis
 Acute: for every 10 decrease in pCO2 -> HCO3 decreases by 2 and
there is a increase of 0.08 in PH MEMORIZE
 Chronic: for every 10 decrease in pCO2 -> HCO3 decreases by 5
and there is a increase of 0.03 in PH

12. Step 3-4: Is there appropriateStep 3-4: Is there appropriate
compensation? Is it acute orcompensation? Is it acute or
chronic ?chronic ?
 Metabolic Acidosis
 Winter’s formula: pCO2 = 1.5[HCO3] + 8 ± 2 MEMORIZE
 If serum pCO2 > expected pCO2 -> additional respiratory
acidosis
 Metabolic Alkalosis
 For every 10 increase in HCO3 -> pCO2 increases by 6

13. EXAMPLEEXAMPLE
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
• Winter’s formula : 17= 1.5 (7) +8 = 18.5
• So correct compensation so there is only
one disorder Primary metabolic

14. Step 5: Calculate the anionStep 5: Calculate the anion
gapgap
 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

17. Anion Gap
When acid is added to the body, the [H+] increases and the [HCO3-]
decreases. In addition, the concentration of the anion, which is associated
with the acid, increases. This change in the anion concentration provides a
convenient way to analyze and help determine the cause of a metabolic
acidosis by calculating what is termed the anion gap.
The anion gap is estimated by subtracting the sum of Cl- and HCO3-
concentrations from the plasma Na concentration.
Na + Unmeasured cations = Cl- + HCO3- + Unmeasured anions
Anion gap = [Na] – ([Cl-] + [HCO3-])
The anion gap is defined as the quantity of anions not balanced by
cations.
This is usually equal to 12 ± 4 meq/L and is usually due to the
negatively charged plasma proteins as the charges of the other
unmeasured cations and anions tend to balance out.

18. If the anion of the acid added to plasma is Cl- , the anion gap will be
normal (i.e., the decrease in [HCO3-] is matched by an increase in [Cl-]
HCl + NaHCO3 → NaCl + H2CO3 → CO2 + H2O
In this setting, there is a meq. for meq. replacement of extracellular HCO3- by
Cl- ; thus, there is no change in the anion gap, since the sum of Cl- +
[HCO3-] remains constant.
This disorder is called a hyperchloremic acidosis, because of the
associated increase in the Cl- concentration.
GI or renal loss of HCO3- produces the same effect as adding HCl as the
kidney in its effort to preserve the ECV will retain NaCl leading to a net
exchange of lost HCO3- for Cl-.
In contrast, if the anion of the acid is not Cl- (e.g. lactate, β-
hydroxybutyrate), the anion gap will increase (i.e. the decrease in [HCO3-]
is not matched by an increase in the [Cl-] but rather by an increase in the
[unmeasured anion]:
HA + NaHCO3 → NaA + H2CO3 → CO2 + H2O, where A- is the
unmeasured anion.

19. EXAMPLEEXAMPLE
• Calculate Anion gap
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
 Albumin 4.
 AG = Na – Cl – HCO3 (normal 12 ± 2)
123 – 97 – 7 = 19
• No need to correct for albumin as it is 4

20. Step 6: Calculate theStep 6: Calculate the
different needed formulasdifferent needed formulas
Delta gap = (actual AG – 12) + HCO3
 Adjusted HCO3 should be 24 (+_ 6) {18-30}
 If delta gap > 30 -> additional metabolic alkalosis
 If delta gap < 18 -> additional non-gap metabolic
acidosis
 If delta gap 18 – 30 -> no additional metabolic
disorders

21. EXAMPLE : Delta GapEXAMPLE : Delta Gap
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
 Albumin 4.
• Delta gap = (actual AG – 12) + HCO3
• (19-12) +7 = 14
• Delta gap < 18 -> additional non-gap
metabolic acidosis
• So this pt has both anion gap and non
anion gap Metabolic acidosis

22. Metobolic acidosis: AnionMetobolic acidosis: Anion
gap acidosisgap acidosis

23. EXAMPLE: WHY ANIONEXAMPLE: WHY ANION
GAP?GAP?
 65yr M with CKD presenting with nausea, diarrhea
and acute respiratory distress
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
• anion gap portion its due to BUN of 119- UREMIA
• But would still check lactic acid

25. If all the acid dissociated in the ECF and all the buffering was by bicarbonate, then
the increase in the AG should be equal to the decrease in bicarbonate so the
ratio between these two changes (which we call the delta ratio) should be equal to
one.
more than 50% of excess acid is buffered intracellularly and by bone, not by
HCO3- .
In contrast, most of the excess anions remain in the ECF, because anions
cannot easily cross the lipid bilayer of the cell membrane. As a result, the
elevation in the anion gap usually exceeds the fall in the plasma [HCO3- ].
In lactic acidosis, for example, the ∆/∆ ratio averages 1.6:1.
On the other hand, although the same principle applies to ketoacidosis, the
ratio is usually close to 1:1 in this disorder because the loss of ketoacids
anions (ketones) lowers the anion gap and tends to balance the effect of
intracellular buffering. Anion loss in the urine is much less prominent in
lactic acidosis because the associated state of marked tissue hypoperfusion
usually results in little or no urine output.

26. Delta ratio

27. A low or negative anion gap is observed when hyperchloremia is
caused by high levels of cations,as seen in lithium toxicity , monoclonal IgG
gammopathy or disorders characterized by high levels of calcium or
magnesium.
A negative anion gap is caused by Pseudohyperchoremia in
bromide or intoxication .
A high anion gap with normal lactate levels in patient with
alcoholism may be an important clue for the diagnosis of alcoholic ketoacidosis.
Diagnosis is missed often as Ketostix reacts only with acetoacetate and not
with beta-hydroxybutyrate seen in alcoholic ketoacidosis.

28. Nongap metabolicNongap metabolic
acidosisacidosis
Causes of nongap metabolic acidosis - DURHAM
Diarrhea, ileostomy, colostomy, enteric fistulas
Ureteral diversions or pancreatic fistulas
RTA type I or IV, early renal failure
Hyperailmentation, hydrochloric acid administration
Acetazolamide, Addison’s disease
Miscellaneous – post-hypocapnia, toulene, sevelamer, cholestyramine ingestion
For non-gap metabolic acidosis, calculate the urine anion gap
UAG = UNA + UK – UCL
If UAG>0: renal problem
If UAG<0: non renal problem (most commonly GI)

29. Concept of Urinary anion gapConcept of Urinary anion gap
• Normal anion gap acidosis occurs when decrease in bicarbonate
concentration with an increase in chloride ions to retain electro
neutrality leading to hyperchloremic metabolic acidosis.
• Causes: GI loss,ureteric diversion ,defective urinary acidification
,impaired acid excretion in early renal failure ,infusion of large
volume of saline
• Rise in chloride causes more renal ammonium chloride
generation(more ammonia excretion by kidneys ) hence urinary
ammonium is used to differentiate between renal and extrarenal
causes of NAGMA .
• As Urinary ammonium is seldom measured Urinary anion gap is used
as surrogate marker of excretion of urinary ammonium.
• Normal Urinary anion gap : -25 to - 50
neGUTive UAG s/o loss of bicarbonates via GUT

30. EXAMPLE : NONEXAMPLE : NON
ANION GAP ACIDOSISANION GAP ACIDOSIS
 65yr M with CKD presenting with nausea, diarrhea
and acute respiratory distress
 ABG : pH 7.23/pCO2 17/ po2 235
 Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.1
• Most likely due to the diarrhea.

31. Urinary anion gap is unreliable when Polyuria is present,urinary pH exceeds
6.5 and urinary ammonium is excreted with other anion other than chloride ( eg
keto acids,acetylsalicylic acid,D-lactic acid,large quantities of penicillin .
Urinary osmolar gap is used in such situations
UOG = Urine osmolarity - 2 (NA+) + 2 (K+) + BUN/2.8 + Glucose /18
UOG < 40 : impairment of urinary ammonium excretion

32. Metabolic alkalosisMetabolic alkalosis
 Calculate the urinary chloride to differentiate saline responsive
vs saline resistant
 Must be off diuretics in order to interpret urine chloride
Saline responsive
UCL< 25 mmol/lt
Saline-resistant
UCL >40 mmol/lt
Vomiting If hypertensive: Cushings, Conn’s, RAS, renal
failure with alkali administartion
NG suction If not hypertensive: severe hypokalemia,
hypomagnesemia, Bartter’s, Gittelman’s,
licorice ingestion
Over-diuresis Exogenous corticosteroid administration
Post-hypercapnia Severe hypercalcemia

33. Chloride resistant metabolic alkalosis is also differentiated on the basis of
Urinary potassium levels :
A)If urinary potassium levels is < 20 mmol/day
s/o laxative abuse
B)If urinary Potassium levels is > 30 mmol/day
Based on Blood pressure status
1.Low or normal BP:
Barter syndrome: high urinary calcium
Gitelman syndrome: low urinary calcium
2.High BP
Conns syndrome
Pseudohyperaldosteroinemia
Often associated with hypokalemia

34. Respiratory AlkalosisRespiratory Alkalosis
Causes of Respiratory Alkalosis
Anxiety, pain, fever
Hypoxia, CHF
Lung disease with or without hypoxia – pulmonary embolus, reactive
airway, pneumonia
CNS diseases
Drug use – salicylates, catecholamines, progesterone
Pregnancy
Sepsis, hypotension
Hepatic encephalopathy, liver failure
Mechanical ventilation
Hypothyroidism
High altitude

35. Respiratory AcidosisRespiratory Acidosis
Causes of respiratory acidosis
CNS depression – sedatives, narcotics, CVA
Neuromuscular disorders – acute or chronic
Acute airway obstruction – foreign body, tumor, reactive airway
Severe pneumonia, pulmonary edema, pleural effusion
Chest cavity problems – hemothorax, pneumothorax, flail chest
Chronic lung disease – obstructive or restrictive
Central hypoventilation, OSA

36. Respiratory disorders(with or without intrinsicRespiratory disorders(with or without intrinsic
lung defect) are differentiated on the basis oflung defect) are differentiated on the basis of
aleveolar-arterial O2 differencealeveolar-arterial O2 difference
A-a oxygen tension difference in mmHg
=150-Pao2-1.25 x PaCo2
Respiratory alkalosis:
A-a difference <10 mmHg (<20 mmHg in elderly) :
Hyperventilation without lung patholgy
eg,fever,pregnancy
A-a difference > 10 mmhg (>20 mmHg in elderly) :
Hyperventilation with lung patholgy
eg,pneumonia,pulmonary embolism

37. Steps for ABG analysisSteps for ABG analysis
1. What is the pH? Acidemic or Alkalemic?
2. What is the primary disorder present?
3. Is there appropriate compensation?
4. Is the compensation acute or chronic?
5. Is there an anion gap?
6. If there is a AG, what is the delta gap?
7. What is the differential for the clinical processes?

42. Case 1
•An 8 month old female baby was admitted
•one day history of lethargy.,vomited several times ,appeared "intoxicated".
•obtunded , easily arousable and muscle tone was normal.
•Resp rate was 60/min. Pupils were normal. There was no evidence of
dehydration. Abdomen was soft and nontender. BP was 112/62. Peripheral
perfusion was clinically assessed as normal. Heart and chest examination was
normal. Plantar response was normal.
•Investigations: Na+ 135, K+ 4.2, Cl- 116, HCO3- 5.7, glucose 5.9 (All in mmol/l).
Urinalysis: pH 5.0, negative for glucose and ketones.
•Calcium oxalate crystals were seen on urine microscopy.
Arterial Blood Gases:
pH 7.19
pCO2 16 mmHg
pO2 110 mmHg
HCO3 6.2 mmol/l

43. Initial clinical assessment
Intoxicated ? as ethylene glycol or methanol
numerous calcium oxalate supports diagnostic of ethylene glycol
other possibilities: any inherited metabolic disorder which could result in a lactic
acidosis, renal tubular acidosis or an organic acidosis due to an inborn error of
metabolism , infantile pyloric stenosis
Acid-base diagnosis
1.pH The severe acidaemia indicates a severe acidosis is present
2.Pattern: The pattern of a low bicarbonate & low pCO2 indicates that this is a
metabolic acidosis
3.Clues: The anion gap is normal (ie 135-116-5.7 = 13.3mmol/l) and the
chloride is raised. Delta ratio = (Increase in AG / decrease in HCO3) = (13.3-12)/
(24-6) = 0.07 This means a normal anion gap metabolic acidosis
4.Compensation: The expected pCO2 is (1.5 x 6.2 + 8) = 17.3mmHg. The
actual pCO2 is close so respiratory compensation is maximal. It takes 12 to 24
hours for compensation to reach this maximal level & the history indicates
sufficient time has passed
5.Formulation: A normal anion gap (or hyperchloraemic) metabolic acidosis
with maximal respiratory compensation. There is no evidence of a respiratory
disorder, and the low delta ratio <0.4) indicates a 'pure' NAGMA.

44. 6.Confirmation: . A normal anion gap metabolic acidosis may be due to a GIT
cause (e.g. diarrhoea), a renal cause (e.g. renal tubular acidosis), or infusion of
certain solutions (e.g. ammonium chloride, excessive normal saline infusion).
There is no history or examination findings supporting a GIT cause.
The urine pH is 5 which is appropriately low and so does not support a diagnosis of
type 1 (or distal) renal tubular acidosis.
The absence of hypokalaemia & the severity of the acidosis are also against the
diagnosis of a type 2 renal tubular acidosis.
There is no history of drug (eg acetazolamide) or toxin ingestion. There is no
ketoacidosis. There have been no intravenous infusions.
The cause of the acidosis is not clear
Osmolar gap result is useful in metabolic acidosis if the cause is not obvious;
an elevated value indicates the presence of an excessive amount of a low
molecular solute (such as occurs in some ingestions (methanol, ethanol, ethylene
glycol)).
Chromatography of serum (searching for organic acids) detected a large
glycolic acid peak. This strongly points to ethylene glycol ingestion as the
diagnosis.
The distinctive calcium oxalate dihydrate crystals (distinctive folded envelope
appearance) were found in the urine and this further supports the diagnosis.

45. Case 2
•A 19 year old pregnant
•Insulin dependent diabetic patient
•polyuria and thirst. poor compliance with medical therapy.
•afebrile. Chest was clear. Circulation was adequate. Perioral herpes was
present.
•Urinalysis: 2+ ketones, 4+ glucose.
•Biochemistry on admission: Na+ 136, K+ 4.8, Cl- 101, bicarbonate 10,
glucose 19.0, urea 8.1 and creatinine 0.09 (all biochem results in mmol/l).
Arterial blood gases were collected on arrival.
Arterial Blood Gases:
pH 7.26
pCO2 16 mmHg
pO2 128 mmHg
HCO3 7.1 mmol/l

46. The diagnosis is obvious on history: the patient has a severe diabetic
ketoacidosis. With such an obvious diagnosis, why bother with the
systematic approach?
The systematic approach has several advantages:-
•The first step incorporates all this clinical expectation (i.e. in "the initial
clinical assessment" stage) so there is nothing lost. The obvious
diagnosis becomes the hypothesis which is tested in the rest of the
analysis.
detect the presence of other concurrent acid-base disorders that are
not obvious
other acid-base disaorders present, such as:
•a co-existent lactic acidosis (related to poor tissue perfusion)
•a hyperchloraemic metabolic acidosis (due replacement of keto-
anions lost in the urine with chloride by the kidney and as a result of
saline resuscitation fluids)
•a respiratory acid-base disorder is possible if (for example) pulmonary
infection is the cause, or if there is a decreased level of consciousness

47. Case 3
A 60 year old woman was admitted with lobar pneumonia. She was on a
thiazide diuretic for 9 months following a previous admission with congestive
cardiac failure. The admission arterial blood results were:
Arterial Blood Gases
pH 7.64
pCO2 32 mmHg
pO2 75 mmHg
HCO3 33 mmol/l
K+ 2.1 mmol/l
Initial clinical assessment
•severe hypokalaemia
The clinical history suggests the following as possibilities:
• respiratory acidosis related to respiratory failure
• respiratory alkalosis due to the dyspnea from decreased pulmonary
compliance due to the pneumonia
• metabolic alkalosis and hypokalaemia related to the diuretic
therapy

48. The acid-base diagnosis
1.pH: A net alkalaemia is present indicating an alkalosis
2.Pattern: The pCO2 is reduced despite an increase in HCO3.
When the pCO2 and the [HCO3] move in different directions from their
standard reference values, then at least two acid-base disorders are
present.
A low pCO2 occurs with respiratory alkalosis and a high bicarbonate occurs with
a metabolic alkalosis. This indicates that a mixed alkalosis is present
3. Clues: Hypokalaemia is common with a metabolic alkalosis. Other than
[K+], no electrolyte results are given.
A chronic respiratory alkalosis with a pCO2 of 32 mmHg would predict a [HCO3]
of about 20 mmol/l (by Rule 4) at maximal compensation. The actual value is
much higher than this so a metabolic alkalosis must also be present.
A metabolic alkalosis with [HCO3] of 33 mmol/l would predict a pCO2 of about
43 mmHg (by Rule 6). The pCO2 is lower so a respiratory alkalkosis is also
present
4. Compensation: The evidence is of a mixed disorder: metabolic alkalosis
and respiratory alkalosis.
.
5.Formulation: Mixed acid-base disorder with metabolic alkalosis and
respiratory alkalosis
6. Confirmation: No confirmatory tests

49. Diagnosis: A mixed alkalosis: A metabolic alkalosis due to to the thiazide diuretic
therapy and a respiratory alkalosis due to lobar pneumonia.
The metabolic alkalosis is probably chronic as the patient has been on these drugs
for some time. The hypokalaemia is assumed to be related to this.
A respiratory alkalosis is present. This is probably secondary to the dyspnoea from
decreased pulmonary compliance due to the pneumonia.
If the plasma [K+] were to drop further, there is a risk of generalised muscle
weakness. This can result in respiratory muscle failure and development of a
respiratory acidosis.
Overall: The situation here is consistent with a lady with a pre-existing chronic
metabolic alkalosis (related to thiazide therapy) who develops pneumonia which
results in hyperventilation (acute respiratory alkalosis) is response to the decreased
pulmonary compliance.

50. Case 4
•A 70 year old man
•severe congestive cardiac failure.
•unwell for about a week
•vomiting for the previous 5 days.
•no medication.
•He was hyperventilating and was very distressed.
•Biochemistry results: Na+ 127, K+ 5.2, Cl- 79, HCO3- 20, urea 50.5, creatinine
1.8 & glucose 130 mg/dl Anion gap 33
•Arterial Blood Gases :pH 7.58 ,pCO2 21 mmHg ,pO2 154 mmHg
HCO3 19 mmol/l
Initial Clinical Assessment
The history suggests the following possibilities:
• Respiratory alkalosis in response to the dyspnoea associate with the
congestive heart failure
• A lactic acidosis is possible if cardiac output is low and tissue
perfusion is poor
• Vomiting suggests metabolic alkalosis
The renal failure could be associated with a high anion gap acidosis

51. Acid-base Diagnosis
1. pH: pH is greater than 7.44 so an alkalaemia is present. The cause is an
alkalosis
2. Pattern: pCO2 & bicarbonate are both low suggesting either a metabolic
acidosis or a respiratory alkalosis. As we already know an alkalosis is present
then the primary disorder is a respiratory alkalosis.
3.Clues: The anion gap is noted to be very high (33 mmols/l) so there must be a
high-anion gap metabolic acidosis present as well. To briefly explore the 4
causes of a HAGMA:
o Ketoacidosis: The normal glucose makes ketoacidosis unlikely.
Urinalysis for ketones and glucose should be carried out.
o Renal failure: The creatinine is high enough to indicate a GFR low
enough (<20 mls/min) to cause hyperkalaemia (due impaired potassium excretion)
and metabolic acidosis (due to renal retention of acid anions)
o Toxic acidosis: There is no evidence presented of toxic ingestions and
no suggestive history (eg neurological symptoms)
o Lactic acidosis: No lactate results are reported so this cannot be
excluded.
4. Compensation: Asessing the compensation for a respiratory alkalosis
(using rule 4 - "the 5 for 10" rule): The expected HCO3 is (24 - 10) = 14. The actual
HCO3 is higher (19) which indicates the presence of a metabolic alkalosis.
5. Formulation: Triple acid-base disorder (respiratory alkalosis, high anion
gap metabolic acidosis & a metabolic alkalosis).

52. Confirmation: A lactate level should be checked to exclude a lactic acidosis. A
urine test for ketones and glucose should be done and should be routine
Clinical Diagnosis
Congestive cardiac failure with:
•respiratory distress causing respiratory alkalosis
•renal failure possibly of pre-renal cause causing a high anion gap metabolic
acidosis, and
•vomiting (causing a metabolic alkalosis) resulting in a complicated acid-base
picture.
Interestingly, all of these possibilities were suggested by the history.
A co-existing lactic acidosis is not excluded.

53. Evidence of a mixed disorder
A quick perusal of this set of results immediately indicates a significant mixed
acid-base disorders. The high anion gap indicates a severe metabolic
acidosis is present, but despite this the pH indicates alkalaemia so an even
larger alkalosis must be present to have caused this result. Additionally, the
severe hypochloraemia is also a powerful alerting signal to the presence of
an underlying metabolic alkalosis.
The diagnosis so far is: a high anion gap metabolic acidosis is present. These are
4 categories of causes for this condition:
• Renal failure
• Ketoacidosis
• Lactic acidosis
• Certain toxin overdoses

54. Conclusion is that there is no evidence of ketoacidosis.
Toxin ingestions (eg methanol, ethylene glycol, salicylates, paraldehyde) which
cause acidosis are excluded on the history so far. Any history of alcoholism
or if the patient appears intoxicated should prompt re-consideration of this
diagnosis.
The renal failure present in this case is sufficient to cause a metabolic
acidosis.
Impaired muscle tissue perfusion (due to the heart failure and the fluid loss
from the vomiting) will cause a lactic acidosis and this should be considered
here. A lactate level will quickly assess this possibility.
Prerenal acute renal failure can cause a metabolic acidosis by two
mechanisms: tissue hypoperfusion (lactic acidosis) and retention of acid anions
(acidosis of acute renal failure).
The diagnosis so far: High anion gap metabolic acidosis due to acute
prerenal renal failure and probably a coexistent lactic acidosis.

55. Metabolic alkalosis
The [HCO3] is inappropriately high for the rise in the anion gap.
The delta ratio is high (3.2) so lets consider the two possibilities that are consistent
by this and consider how they may be distinguished:
First possibility for a high delta ratio: A coexisting metabolic alkalosis is
present. Assessment: The history is consistent with this as severe vomiting is
present and this is an important cause of metabolic alkalosis.
Second possibility: The patient has a pre-existing chronic respiratory acidosis
with renal retention of bicarbonate. For example, if the patient had a chronic
hypercapnia with pCO2 of 60 mmHg, renal compensation would raise the [HCO3] to
32 mmols/l (based on the ‘4 for 10 rule’).
A bicarbonate level of 19 could represent a fall from 32 mmols/l: a decrement of 13
mmols/l (in this hypothetical example). If this hypothesis is correct, then there may
be no metabolic alkalosis.

56. What evidence can be found of a recent or long-standing chronic respiratory
acidosis? In this case, there is no history of chronic respiratory disease. CO2
retention requires severe lung disease. Current pCO2 is low so the patient is
obviously able to hyperventilate enough to drop his pCO2 despite the presence of
congestive heart failure!
Conclusion then is that a metabolic alkalosis is present.
The majority of causes of metabolic alkalosis are due to diuretic use or loss of
acidic gastric juice (vomiting or NG suction). A history of five days of vomiting
is the cause here. Diuretic use has been excluded on history.
The rise in the anion gap is normally larger than the fall in bicarbonate because at
least half of the buffering for metabolic acid-base disorders occurs
intracellularly (minimising the decrement in plasma [HCO3]) but the acid anions
remain extracellularly and contribute as excess unmeasured anions to the anion gap.
Diagnosis so far is:
• Metabolic alkalosis (due to persistent vomiting) as the major disorder (net
alkalaemia)
• Metabolic acidosis (due to renal failure and maybe lactic acidosis)

57. A final problem: low bicarbonate despite net alkalaemia
There is still a problem in the analysis of this case so far because although there is a
significant net alkalaemia (indicating the metabolic alkalosis is more severe then
the metabolic acidosis), the [HCO3] is reduced rather then elevated!
Consequently, a third primary acid-base disorder must be present and adding to
the net alkalaemia - that is, there must be a respiratory alkalosis. To approach this
using the compensation rules:
Is the respiratory compensation appropriate?
As the [HCO3] is less then 24 mmol/l, rule 5 for a metabolic acidosis (rather than rule
6) is best to assess this. The predicted pCO2 is about 36 mmHg. As the actual
pCO2 is much lower than this, the third primary acid-base disorder is a
respiratory alkalosis. This is secondary to the heart failure and the
hyperventilation stimulated by the dyspnoea. Any condition which decreases lung
compliance will cause dyspnoea. If the pulmonary oedema was more severe then a
respiratory acidosis would be a likely outcome.
Final Assessment
This patient has a triple acid-base disorder:
• Acute metabolic acidosis probably due to renal failure (?prerenal
failure) and possibly to lactic acidosis (hypoperfusion due heart failure and
hypovolaemia)
• Metabolic alkalosis due to severe vomiting
• Respiratory alkalosis due to dyspnoea from congestive heart failure.