AcidBase

ACID
1
LUNGS

Balance

ALKALIES
20
KIDNEYS

Step wise Approach

Step 1 Is there a Acid-Base
Disorder?
Look at PaCO2 and HCO3 If both are
Normal, No Acid-base disorder

Step 2 Is it Acidosis or Alkalosis?

First look at the pH,Normal 7.35
7.45
pH < 7.35 suggests Acidosis
pH > 7.45 suggests Alkalosis

Step 3 Primary Disorder?

Look for pH, HCO3 and PaCO2
Low pH < 7.35 with
Low HCO3 Metabolic Acidosis
High PaCO2 Respiratory Acidosis

High pH > 7.45 with

High HCO3 Metabolic Alkalosis
Low PaCO2 Respiratory Alkalosis

Primary Acid-Base Disorders

Metabolic Acidosis Fall in HCO3

Metabolic Alkalosis Rise in HCO3
Respiratory Acidosis Rise in PaCO2
Respiratory Alkalosis Fall in PaCO2

When you see MetabolicThink of HCO3

When you see RespiratoryThink of
Paco2

pH 7.4, HCO3 24mEq/L, PaCO2 40mm Hg

Primary Acid-Base Disorders

Basic

pH

H+

Primary

Secondary

Meta. Acidosis

LOW

HIGH

HCO3 LOW

PaCO2 DECREASED

Meta. Alkalosis

HIGH

LOW

HCO3 HIGH

PaCO2 INCREASED

Resp. Acidosis

LOW

HIGH

PaCO2 HIGH HCO3 INCREASED

Resp. Alkalosis

HIGH

LOW

PaCO2 LOW

HCO3 DECREASED

Step 4 Expected Compensation

The Expected compensation can be
calculated from the chart.
Determine whether the actual value
matches with the expected
compensation.
If matching, it confirms the primary
disorder.

Expected Compensation
Disorder

Expected Compensation

Metabolic Acidosis
- Fall in HCO3

PaCO2 = (1.5 X HCO3) + 8

PaCO2 = HCO3 + 15

Metabolic Alkalosis
- Rise in HCO3

Rise in PaCO2
= 0.75 X Rise in HCO3

Respiratory Acidosis
-Acute Rise in HCO3
-6-24 Hr Fall in pH
-Chronic Rise in HCO3
-> 24 Hrs, Fall in pH

Rise in PaCO2
= 0.1 X Rise in PaCO2
= 0.01 X Rise in PaCO2
= 0.4 X Rise in PaCO2
= 0.003 X Rise in PaCO2

Respiratory Alkalosis
-Acute Fall in HCO3
-Acute Rise in pH
-Chronic Fall in HCO3
-Chronic Rise in pH

Fall in PaCO2
= 0.2 X Fall in PaCO2
= 0.01 X Fall in PaCO2
= 0.4 X Fall in PaCO2
= 0.002 X Fall in PaCO2

Step 5 Rule of Same Direction

Check the direction of changes
In Simple acid base disorders,
HCO3 and PaCO2 changes in the
same direction.
If HCO3 and PaCO2 changes are in
the opposite direction, it suggests a
mixed disorder. The values may be
more or less than the expected
values.

Compensation
Same
Direction
Rule

Bodys response to neutralize the

effect of initial insult on pH
homeostasis
Metabolic acidosis with low pH
stimulates respiratory centers to
cause hyperventilation. It washes
out co2 and decrease paCO2. This
is same directional compensation.

Step 6 Check the Anion Gap

Anion Gap is the Foot Print of metabolic
acidosis, even when the pH, HCO3 and
PaCO2 values are normal.
AG = Na (Cl + HCO3) = 12 (Normal)
AG Rise matches with the fall in HCO3
If AG exceeds the fall in HCO3, it
suggests co-existing metabolic alkalosis.
If AG is lesser than the fall in HCO3, it
suggests non-AG metabolic acidosis.

Acid Base Balance

PH is maintained by Intra and Extra

cellular chemical buffers and
respiratory & renal compensations.
PaCO2 is regulated by respiratory
system and CNS. Under excretion
of CO2 causes hypercapnoea and
over excretion causes
hypocapnoea.
HCO3 is regulated by Renal system.

Kidney regulates HCO3

Reabsorption of HCO3

80-90% by Distal Tubules

Rest by Proximal Tubules

Forming Titrable acids

Excreting NH4 in Urine
Kidney filters 4000mmol HCO3/day

Hasselbachs (H-H) Equation

pH = 6.1 + log HCO3
PaCO2 X 0.0301
H = 24 X PaCO2 = 40 mEq/lit
HCo3
Cl + HCO3 + Unmeasured Anions
= Na + Unmeasured Cations

Equations:-

Anion Gap = Na Cl HCo3

Delta Anion Gap = AG 10
24 HCO3
Osmolar Gap = 10-0 mosm/lit

= Measured Calculated Osmolarity

Calculated Osmolarity = 275-290

= 2 Na + Glu/18 + BUN/2.8
Urinary Anion Gap = Na + K Cl
= 20 0 mEq

Alveolar PaO2 = 110

Inspired Oxygen = 21%
Inspired O2 X 5 = 100 (Arterial PaO2)
PiO2 = (760 45 ) X 0.21 = 150
O2 Content of Blood =

(Hb X O2) + Dissolved O2

Alveolo-Arterial Gradient = 150mmHg

 Oxygenation Failure
Ventilation Perfusion
Abnormality

Ventilation Failure
Alv-Art gradient
maintained normal
PiO2 150
PCO2 80 (High)
A-aO2 150-80

Oxygen Dissociation Curve

Hb
Saturation

98% O2 is bound to Hb
Hb X 1.34 X SaO2
2% carried in plasma
PaO2 drives it to blood

paO2 mmHg

Respiratory Acidosis:
Acute
For every 10 mm rise in
PCO2;
pH drop of 0.08
1mmol rise of HCO3

C/F: Anxiety, Dyspnoea,

Confusion, Psychosis,
hallucinations.
Rx: Intubation, Assisted
Ventilation, Rx Cause
Avoid Rapid Correction
Use O2 Cautiously

Alveolar Hypoventilation

Chronic
For every 10 mm rise in
PCO2;
pH drop of 0.03
4 mmol/l drop in HCO3

C/F: Sleep Disturbances,

Memmory loss, papilledema,
personality change, tremors,
asterixis, headache
Rx: Lower PaCO2 slowly,
Supplement Cl & K, Improve
Lung function

D/D : Central Causes, Respiratory causes, Obesity,

Neuromuscular causes, Ventilator related

Respiratory Acidosis

Respiratory Alkalosis

Alveolar Hypoventilation Strong Ventilatory Stimulus

High pCO2 increase Kidneys excrete

H ions, decrease pH
bicarb, thus blood
Compensation by
levels of bicarb
kidneys is a slow
decrease.
process:
Kidneys Stop
excreting bicarbs,
thus increased
bicarbs in blood.

Respiratory Alkalosis

Strong Ventilatory Stimulus

Acute
For every 10mm drop
of PaCO2,

Chronic
For every 10mm drop
of PaCO2,

2mmol fall of HCO3

4mmol fall of HCO3

Dizziness, Confusion,
Critically Ill pts on
Seizures, hypotension,
mechanical ventilation,
arrhythmia, Low Ca.
poor prognosis.
Hypoventilation Syndrome, CNS Disease or injury,
Slicyltes, theophylline, pregnancy, Hyperthyroidism
Pulmonary embolism,
Rx Cause, Beta blockers, Ventilator settings

Anion Gap

Unmeasured = Proteins, Sulfates, Phosphates, Organic anions

= Ca, Mg, K

Decreased due to:

High unmeasured cations
Abnormal cations, Lithium
Cationic Ig in Plasma cell
dyscrasias
Acidosis : Low albumin
Hyperviscosity
Hyperlipidemia
Low Albumin Nephrotic S.

Increased due to:

High Unmeasured anions
Low Unmeasured cations
High anionic albumin,
High concentration,
alkalosis

High Anion Gap with Normal Albumin

Non-chloride acids with

Inorganic : phosphates, sulphates

Organic : Ketoacids, Urates, Lactate
Exogenous : Salicylates, Toxins
Un-identified anions

High Osmolar Gap

Alcohol, Ethanol, Methanol, Ethelene
Glycol, Mannitol, Sorbitol, Acetone,
Paraldehyde

Metabolic acidosis
C/F: Kussumaul Breathing, Hypotension, Headache,
Lethargy, Glucose intolerance
For every 1mmol fall in HCO3, 1.25 fall in PaCO2
High Anion Gap
Lactic Acidosis
Keto-acidosis
Diabetic, Alcohol
Starvation

Toxins
Salicylates, Methanol

Renal Failure
Ac / Chr

Alkali therapy only

when pH < 7.2

Normal Anion Gap

GI Loss of HCO3
Diarrhoea, GI Loops

Renal Tubular Acidosis

K High/ Low

Drug Induced K High

Diuretics, ACEI
Diabetic Nephropathy
NSAID, Septran

Alkali Therapy Oral/ IV

Effects of Low pH in M. Acidosis

Hyperventilation to decrease CO2,

High tidal volume,
Peripheral arterial vasodilatation,
Central Venoconstriction
Low vascular compliance,
Predispose to pulmonary edema,
Headache, lethargy, depression,
coma

Metabolic Acidosis : Low HCO3

Compensatory decrease in PaCo2
= (1.5 X HCO3) + 8 (+/- 2) Winters formula
= 1.25 mmHg per mmol HCO3 reduction
= HCO3 + 15

Last 2 digits of PH = pCO2

pH

HCO3

PaCO2

Base Ex

Uncompensated Low

Low

Low

Partial Compen. Low

Low

Low

Low

Compensated

Low

Low

Low

Lactic Acidosis
Type A
Poor Tissue
Perfusion
Shock
Circulatory failure
Severe Anaemia
CO & Cyanide
Poisoning

Type B

Aerobic Disorders
Malignancies
Diabetes
Renal Failure
Hepatic Failure
Seizures, AIDS
Cholera, Malaria
Phenformin, INH
AZT Analodues

Rx: Correction of cause, Avoid Vasoconstrictors,

NaHCO3 if acute severe acidemia < 7.1

Metabolic Alkalosis
H C O 3 G a in d u e to v o lu m e c o n c e n t r a t io n & L o w G F R
L o s s o f N o n - v o la t ile a c id s e . g . H C l
F o r e v e r y 1 m m o l r is e in H C O 3 ; 0 . 6 m m H g r is e in P a C O 2
D u e t o a lv e o la r h y p o v e n t ila t io n ( L o w C l, K , P O 4 )
C o n f u s io n , S e iz u r e s , P a r a s t h e s ia s , C r a m p s , T e t a n y , A r r h y t h m ia s
A s s e s s E C F V o lu m e , P la s m a K , U r in e C l,
M e a s u r e B P in U p r ig h t & r e c u m b e n t p o s it io n s
E C F V C o n t r a c t io n + L o w K

E C F V E x p a n s io n + H ig h B P

V o m it in g s / A s p ir a te

T h ia z id e s , L o o p D iu r e t ic s
L o w M g , B a r te r 's S y n d r o m e

IV N a C l / R L

I V I s o t o n ic S a lin e

C o r r e c t io n o f S t im u lu s , N a C l, K C l,
A c e t a z o la m id e , O r a l N H 4 C l, H e m o d ia ly s is

Maximum Compensation

Metabolic Acidosis : PCO2 drops to 10

Metabolic Alkalosis : PCO2 Max to 60
Respiratory Acidosis : Bicarb Max 35
Respiratory Alkalosis : Bicarb to 15

Mixed Disorders
Compare fall in HCO3 with Anion Gap,
If there is > 5 mEq discrepancy, it is a
mixed acid-base disturbance.
Anion Gap > HCO3 Fall = Metabolic
acidosis with HCO3 fall / Loss
Anion Gap < HCO3 Fall = Co-existing
Metabolic alkalosis is present.

A c id o s is
Low H C O 3

H ig h P C O 2

M e t a b o lic A c id o s is

R e s p ir a t o r y A c id o s is

> 1 2 A n io n G a p
K e t o s is

< 1 2 A n io n G a p
N o K e t o s is

U r in e S u g a r H ig h

U r in e S u g a r N o r m a l

H ig h C r e a t in in e

DKA

A lc o h o l / S t a r v a t io n

CRF

D r u g s , F lu id L o s s , R e n a l L o s s , R T A
L o w C r e a t in in e

> 2 .5 L a c ta te

< 2 .5 L a c ta te

L a c t ic A c id o s is

A b n . G u t F lo r a

ACIDOSIS
PH

NORMAL

ALKALOSIS

CAUSE

<7.35

7.4

>7.45

PCO2

>45

40

<35

RESPIRATORY

HCO3

<22

24

>26

METABOLIC

<95%

95-100%

HYPOXEMIA RESPIRATORY

<80

80-100

HYPOXEMIA RESPIRATORY

O2 SAT
PO2
BASE
EXCESS

-2 TO +2

ANY

Interpreting ABGs
1. Look at the pH - is the primary problem acidosis
(low) or alkalosis (high)
2. Check the CO2 (respiratory indicator)- is it less
than 35 (alkalosis) or more than 45 (acidosis)
3. Check the HCO3 (metabolic indicator)- is it less
than 22 (acidosis) or more than 26 (alkalosis)
4. Which is primary disorder (Resp. or Metabolic)?
If the pH is low (acidosis), then look to see if CO2 or HCO3 is
acidosis (which ever is acidosis will be primary).
If the pH is high (alkalosis), then look to see if CO2 or HCO3 is
alkalosis (which ever is alkalosis is the primary)..

Compensation
The Respiratory and Renal systems compensate for
each other in an attempt to return the pH to normal
ABGs show that compensation is present when the
pH returns to normal or near normal
If the non primary system is in the normal range
(CO2 35 to 45) (HCO3 22-26), then that system is
not compensating for the primary.
For example:
In respiratory acidosis (pH<7.35, CO2>45), if the
HCO3 is >26, then the kidneys are compensating
by retaining bicarbonate.
If HCO3 is normal, then not compensating.

SID : pCO2 : A TOT

SID : Strong Ion Difference
Net charge balance of all completely or
near completely dissociated ions.
(Na + K + Mg + Ca) (Cl + Lactate)
Normal SID is 40-42 mEq/Lit

A TOT : Total weak acid concentration :

It include proteins and phosphate.

Physiology
Total Body water is 60% of Weight
2/3rd of it is Intracellular fluid
1/3rd of it is Extracellular fluid
3/4th of ECF is interstitial fluid
1/4th of ECF is plasma or intravascular fluid

Fluid

Total

ICF

ECF

Interstitial

Plasma

% Body Wt

60%

40%

20%

15%

5%

For 70Kg

42

28

14

10.5

3.5

Electrolytes in Body Fluids

Electrolytes mEq/L

ECF

ICF

Sodium

142

10

Potassium

4.3

150

Chloride

104

Bicarbonate

24

Calcium

0.01

Magnesium

40

Phosphate / Sulphate

150

ECF

ICF

Cation

Sodium

Potassium, Magnesium

Anion

Chloride, Bicarbonate

Phosphate, Sulphate, Proteins

Electrolyte Disturbance
Sodium Balance determines the volume status
Water balance determines the tonicity,
(Na+ Concentration)
Volume Overload = Increased Total body Na+
(Regardless of its Concentration)
Euvolemia = Normal Total body concentration
Volume depletion = Decreased Total body Na
Hyponatermia = Relative water excess
Volume Replacement with N. saline

Hypernatremia = Relative water deficit

Volume Replacement with NS or RL, then change to
0.45% NaCl

Na < 130
Normovolemic

Hypervolemic

Hypovolemic

Renal Failure
Liver Failure
CHF

U osm > S osm

U osm > 300
Na > 20mEq/l

Urine Na < 20

U osm < S osm

Vomits, Diarrhoea
Burns, Poor Intake

Low Anion Gap

Yes

SIADH

No

Osmolar Gap
Yes

HYPOPROTEINEMIA

Urine Na > 20
Renal Loss
Diuretics, RTA,
Addisons, Na
losing Nephritis
Osmotic diuresis

No

WATER INTOXICATION

SICK CELL SYND

Hyponatremia
Plasma Osmolality Low

Yes

Maximum Volume of
Maximally Diluted Urine < 100 mOsm/Kg

Primary Polydipsia

No

ECF Volume
Decreased

Increased
Normal
Heart Failure, Cirrhosis,
Nephrotic Syndrome,
Renal Insufficiency

Urinary Na
SIADH, Hypothyroidism,
Adrenal Insufficiency

> 20 mmol/l

< 10 mmol/l
Extra-renal Na Loss

Salt Loosing Nephropathy, Hypoaldosteronism,

Diuretics, Vomitings

Hyponatremia
Asymptomatic patients with Na> 120 :
SIADH : Isotonic Saline for slow correction
<0.5mEq/l/hr, <10mEq/l first day &
<18mEq/l over first 2 days.
Acute symptomatic cases with cerebral
edema : Correction slowly 1.5 2 mEq/l/hr
for first 3-4 hrs to avoid osmotic pontine
demyelinosis.
Na < 110 : Hypertonic Saline initially
With CCF Edema : Colloids & Pressure
resuscitation : Poor Prognosis

Hypernatremia
Due to Excess NaCl given : Treat with Free
Water 200ml orally 4-6 hrly.
Impaired Thirst in bed ridden patients,
altered mental status
In hypertonic dehydration, correct volume
status first, then tonicity.
Correct plasma sodium at the rate
0.5mEq/l/hr or 12mEq/p/l/day
Water Deficit =
0.5 X {(Na/140) 1} for men
0.4 X {(Na/140) 1} for women

H Y P O K A L E M IA
S e r u m K < 3 .2 m E q /lit
H y p e r te n s iv e

N o n h y p e r te n s iv e

P r im a r y / S e c o n d a r y
H y p e r a ld o s te r o n is m

U r in a r y K

H ig h > 2 0 m E q /l

L o w < 2 0 m E q /l

S erum H C O 3

Low er G I Loss

Low & Low pH

L o w & H ig h p H

H ig h

A c e ta z o la m id e
K e to a c id o s is , R T A

A c u te
H y p e r v e n tila tio n

U r in a r y C l
< 2 0 m E q /lit
No

Yes

D iu r e tic s , N a H C O 3 ,
G e n ta m y c in , B a r tte r 's

U p p e r G IT C a u s e

Hypokalemia
Only a small fraction of K is Extra-cellular, so
Serum K levels do not express the total body K
In critical cases, it is better to keep the K
levels > 4mEq/lit
IV Replacement
No more than 20mEq/hr should be given
Peripheral lines :
10mEq in 100ml in 1Hr & 20mEq in 200ml over 2Hrs

Central lines
20mEq in 50ml in 1 Hr % 40mEq in 100ml over 2 Hrs

Hyperkalemia
Renal failure, Potassium replaced in patients
on ACEI or K sparing diuretics
Calcium levels & pH change K toxicity
K >6.5 : Symptoms- Weakness, parasthesia,
ileus, paralysis, cardiac arrest
Treat to avoid cardiotoxicity, shift K
intracellular, reduce total body K

10% Calcium Gluconate 10-20ml in 2-5 min

Sodabicarb 50ml IV in 2-5min (Redistribution)
2-3gm Glucose/ unit Insulin (Redistribution)
Kayexalate 15-60gm po / rectally (Elimination)

Hypophosphatemia
Phosphorus is an essential component of
phospholipids, nucleic acids and plays a role in
energy metabolism.
1% P is Extracellular, rest is intracellular & in
bones, Normal Levels 2.2-4.4mg/dl, 55%
ionised and active, symptoms below 2mg/dl
Causes : Alcohol abuse and withdrawal, feeding
after starvation, Respiratory alkalosis,
Malabsorption, Oral phosphorus binders,
Hyperalimentation, severe burns, Rx of DKA
Phosphate infusion 6mg/kg/hr over 6 hrs, then
oral phosphates ( 1gm Neutra-phos/day)

Hypomagnesemia
Mg : 99% Intracellular cation, useful in Na-K
ATPase pump, membrane stabilization, nerve
conduction, calcium channel function.
Causes : Alcoholism & withdrawal, Emesis,
Diarrhoea, RT suction, Parenteral nutrition,
Diabetes, refeeding, Drugs Diuretics,
aminoglycosides, cyclosporins
C/F : Hypo-kalemic, calcemia, lethargy,
confusion, seizures, prolonged PR, QT, Atrial
& ventricular arrhythmias.
Rx 2mg MgSO4 over 10mins IV, 0.5gm/hr
drip for 6 hrs.

Hypocalcemia
Low Ca in 70-90% ICU cases, low ionized
Ca in 15-50% cases with sepsis. Treat only
if below 0.8mmol/l
Intracellular overload of calcium causes
cellular dysfunction.
Rhabdomyolysis, hyperphosphatemia can
cause hypocalcemia
Calcium supplimentation may cause soft
tissue calcification.

Hypercalcemia
Causes of Hypercalcemia

Malignancy lung, breast, myeloma, lymphoma

Primary hyperparathyroidism
Immobilization, Sarcoid, Tuberculosis,
Drugs : Thiazides, Lithium, Theophylline
Hypervitaminosis A & D, Hyperthyroidism,
Milk Alkali syndrome

Treatment
Normal Saline : 200-400ml/hr for dehydration
Furosemide 10-40mg IV q4-6Hr
Prednisone : 40-100 mg/day

Sodabicarbonate Effects
Hypertonicity
Hyperosmolarity :
7.5% Sodabicarb is equal to 6% Saline, increase
osmolarity to 1700 mOsm/lit (Normal is 290 mOsm)
giving excessive stress on cells, thus we must give it 6
times diluted in water for injection or 5% Dextrose

Intracellular acidosis causes hypercapnoea to

exhale CO2. ( 1ml Sodabicarb = 22ml CO2)
Hypo ionised calcium
Decrease oxygen delivery
Hypokalemia

ABG analysis & Acid-Base

Disorders

Outline
1.
2.
3.
4.

Discuss simple steps in analyzing ABGs

Calculate the anion gap
Calculate the delta gap
Differentials for specific acid-base disorders

Steps for ABG analysis

1.
2.
3.
4.
5.
6.
7.

What is the pH? Acidemic or Alkalemic?

What is the primary disorder present?
Is there appropriate compensation?
Is the compensation acute or chronic?
Is there an anion gap?
If there is a AG, what is the delta gap?
What is the differential for the clinical processes?

Normal Values

Variable

Primary
Disorder

Normal Range

Primary
Disorder

pH

Acidemia

<- 7.35 - 7.45

->

Alkalemia

pCO2

Respiratory
alkalosis

<- 35-45 ->

Respiratory
Acidosis

Bicarbonate

Metabolic
acidosis

<- 22-26 ->

Metabolic
alkalosis

Step 1:
Look at the pH: is the blood acidemic or
alkalemic?

Step 2: 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

Step 3: Is there appropriate compensation?

Respiratory Acidosis
Acute: for every 10 increase in pCO2 -> HCO3 increases by 1
Also know for every acute increase of 10 in pCO2 there is a
decrease of 0.08 in pH MEMORIZE
Chronic: for every 10 increase in pCO2 -> HCO3 increases by 4
Also know for every chronic increase of 10 in pCO2 there is a
decrease of 0.03 in pH

Respiratory Alkalosis
Acute: for every 10 decrease in pCO2 -> HCO3 decreases by 2
Chronic: for every 10 decrease in pCO2 -> HCO3 decreases by 5

Step 3: Is there appropriate compensation?

Metabolic Acidosis
Winters 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

Step 4: Calculate the anion gap

AG = Na Cl HCO3 (normal 12 2)
AG corrected = AG + 2.5[4 albumin]
If AG > 20, a metabolic acidosis is always present
Differential for Anion Gap Metabolic Acidosis - MUDPILERS
Methanol
Uremia
Diabetic ketoacidosis, starvation ketoacidosis, EtOH ketoacidosis
Paraldehyde
INH, iron toxicity
Lactic acidosis
Ethylene glycol
Rhabdomyolysis
Salicylates

Step 5: Calculate the delta gap

Only need to calculate delta gap (excess anion
gap) when there is an anion gap present to
determine additional hidden metabolic disorders
(nongap metabolic acidosis or metabolic
alkalosis)
Delta gap = AG 12 + HCO3 (normal 23-30)
If delta gap > 30 -> additional metabolic
alkalosis
If delta gap < 23 -> additional nongap
metabolic acidosis
If delta gap 23 30 -> no additional metabolic
disorders

Nongap metabolic acidosis

For nongap metabolic acidosis, calculate the urine anion
gap
UAG = UNA + UK UCL
If UAG>0: renal problem
If UAG<0: nonrenal problem (most commonly GI)
In working kidneys: HCl + NH3 NH4CL, urine chloride
increases, UAG <0.
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, Addisons
Miscellaneous post-hypocapnia, toulene, sevelamer, cholestyramine
ingestion

Metabolic 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<10

Saline-resistant UCL >10

Vomiting

If hypertensive: Cushings, Conns, RAS,

renal failure with alkali administartion

NG suction

If not hypertensive: severe hypokalemia,

hypomagnesemia, Bartters, Gittelmans,
licorice ingestion

Over-diuresis

Exogenous corticosteroid administration

Post-hypercapnia

Respiratory 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

Respiratory 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

Examples
65yo M with CKD presenting with nausea,
diarrhea and acute respiratory distress.
ABG 7.23/17/235 on 50% VM
BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr
5.1
60yo M with COPD on steroids presenting with
worsening SOB, hypoxia, and hypotension
ABG 7.38/54/45 on RA
BMP Na 134/ Cl 77/ HCO3 33

Examples
28yo F who is 28 weeks pregnant, diabetic,
previous alcoholic who recently stopped insulin
and started binge drinking
ABG 7.60/21/104
BMP Na 136/ Cl 80/ HCO3 19
17yo F with a history of depression is brought
in altered to the ED by her mother, who
reports finding multiple empty medication
bottles around her.
ABG 7.50/20/95
BMP Na 140/ Cl 103/ HCO3 15

More examples
55yo M with chronic alcoholism is admitted after
a drinking binge with fever, hypoxia and a RLL
infiltrate.
ABG 7.50/20/80
BMP Na 145/Cl 100/HCO3 15
A 45yo F with Type 1 Diabetes is admitted with
a gastroenteritis, hyperglycemia and confusion.
ABG 7.10/50/102
BMP Na 145/Cl 100 / HCO3 15

More examples
80yo M with ESRD on HD misses two sessions
of dialysis and is brought in to the ED by his
family with complaints of confusion and
vomiting.
ABG 7.40/40/85
BMP Na 145/ Cl 100/ HCO3 25

Steps for ABG analysis

1.
2.
3.
4.
5.
6.
7.

What is the pH? Acidemic or Alkalemic?

What is the primary disorder present?
Is there appropriate compensation?
Is the compensation acute or chronic?
Is there an anion gap?
If there is a AG, what is the delta gap?
What is the differential for the clinical
processes?