The document provides information on interpreting arterial blood gases (ABGs). It discusses: - How the lungs and kidneys work to maintain acid-base balance by regulating carbon dioxide and bicarbonate levels. - Key terms like pH, acidosis, alkalosis and how changes in pCO2 and HCO3 impact acid-base status. - The process for drawing an ABG sample and analyzing the results, including calculating values like oxygen saturation and alveolar-arterial gradient. - How to assess for primary acid-base disorders by looking at pH, pCO2 and HCO3 levels and whether compensation is appropriate. - Formulas like Winter's equation and those for calculating

1. Arterial Blood Gas
Interpretation
DR. GIRISH JAIN
PG 2ND YEAR
RESPIRATORY MEDICINE DEPARTMENT
MHATMA GANDHI MEDICAL COLLEGE,JAIPUR

2. BASICS
 The body produces acids daily
 15,000 mmol CO2
 50-100 mEq Nonvolatile acids
 The primary source is from metabolism of sulfur containing
amino acids (cystine, methionine) and resultant formation
of sulfuric acid.
 Other sources are non metabolized organic acids,
phosphoric acid, lactic acid, citric acid.
 The lungs and kidneys attempt to maintain balance

4. Respiratory Regulation
• 10-12 mol/day CO2 is
accumulated and is
transported to lungs as Hb-
generated HCO3 and Hb-bound
carbamino compounds where
it is freely excreted.
H2 O + CO2 ↔H2 CO3 ↔H+ +
HCO3
-
• Accumulation/loss of Co2
changes pH within minutes

5.  Balance affected by neurorespiratory control of
ventilation.
 During Acidosis, chemoreceptors sense ↓pH and
trigger ventilation decreasing pCO2.
 Response to alkalosis is biphasic. Initial
hyperventilation to remove excess pCO2 followed
by suppression to increase pCO2 to return pH to
normal

6. Renal Regulation
 Kidneys are the ultimate defense against the
addition of non-volatile acid/alkali
 Kidneys play a role in the maintenance of this HCO3¯
by:
– Conservation of filtered HCO3 ¯
– Regeneration of HCO3 ¯
 Kidneys balance nonvolatile acid generation
during metabolism by excreting acid.

7. • Renal Excretion of
acid – combining
hydrogen ions with
either urinary
buffers to form
titrable acid. eg:
Phosphate, urate,
ammonia

8. Basic terminology
• pH – signifies free hydrogen ion concentration. pH is inversely related to
H+ ion concentration.
• Acid – a substance that can donate H+ ion, i.e. lowers pH.
• Base –a substance that can accept H+ ion, i.e. raises pH.
• Anion – an ion with negative charge.
• Cation – an ion with positive charge.
• Acidemia – blood pH< 7.35 with increased H+ concentration.
• Alkalemia – blood pH>7.45 with decreased H+ concentration.
• Acidosis – Abnormal process or disease which reduces pH due to increase
in acid or decrease in alkali.
• Alkalosis – Abnormal process or disease which increases pH due to
decrease in acid or increase in alkali.

9. ABG – Procedure and Precautions
• Where to place -- the options
– Radial
– Femoral
– Brachial
– Dorsalis Pedis
– Axillary
• When to order an arterial line --
– Need for continuous BP monitoring
– Need for multiple ABGs

11.  Ideally - Pre-heparinised ABG syringes
- Syringe should be FLUSHED with 0.5ml
of 1:1000 Heparin solution and emptied.
DO NOT LEAVE EXCESSIVE HEPARIN IN THE
SYRINGE
HEPARIN DILUTIONAL HCO3
EFFECT PCO2
 Only small 0.5ml Heparin for flushing and discard it.

12.  Ensure No Air Bubbles. Syringe must be sealed immediately
after withdrawing sample.
– Contact with AIR BUBBLES
Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
Air Bubble + Blood = PO2 PCO2
 ABG Syringe must be transported at the earliest to the
laboratory for EARLY analysis via COLD CHAIN

13.  Patients Body Temperature affects the values of
PCO2 and HCO3.
ABG Analyser is controlled for Normal Body
temperatures
Any change in body temp at the time of sampling
leads to alteration in values detected by the
electrodes
 Cell count in PO2
 ABG Sample should always be sent with relevant
information regarding O2, FiO2 status and Temp .

14. Venous Sample
 Only the person who has drawn the sample can tell if
he has drawn a pulsating blood’ OR blood under
high pressure
 PaO2 < 40
 Partly mixed sample- Difficult to recognize
ARTERIAL VENOUS
pH 7.38-7.42 7.36-7.39
PaO2 80-100 38-42
PaCO2 36-44 44-48
HCO3 22-26 20-24
SaO2 95-100 75
CENTRAL VENOUS
7.37-7.40
50-54
45-49
22-26
78

15. Complications of arterial puncture-
• Arterial trauma.
• Arterial-spasm.
• Nerve damage.
• Bleeding with hematoma formation.
• Thrombus formation.
• Infection.

16. Contraindications-
• Cellullitis or infection over radial artery.
• Absence of palpable radial artery pulse.
• Negative Allen test.
• Coagulation defects.

18. Normal Values
ANALYTE Normal Value Units
pH 7.35 - 7.45
PCO2 35 - 45 mm Hg
PO2 72 – 104 mm Hg`
[HCO3] 22 – 30 meq/L
SaO2 95-100 %
Anion Gap 12 + 4 meq/L
∆HCO3 +2 to -2 meq/L

19. ASSESSMENT OF OXYGENATION
• How much oxygen is in the blood?
PaO2 vs. SaO2 vs. CaO2
• Alveolar-arterial O2 grdient

20. Alveolar Gas Equation
• PAO2 = PIO2 - 1.2 (PaCO2)
• PAO2 is the average alveolar PO2, and PIO2 is the partial
pressure of inspired oxygen in the trachea
PIO2 = FIO2 (PB – 47 mm Hg)
• FIO2 is fraction of inspired oxygen and PB is the
barometric pressure. 47 mm Hg is the water vapor
pressure at normal body temperature.

21. Alveolar-Arterial Gradient P(A-a)O2
• P(A-a)O2 is the alveolar-arterial difference in partial pressure of
oxygen.
• PAO2 is always calculated based on FIO2, PaCO2, and barometric
pressure.
• PaO2 is always measured on an arterial blood sample in a “blood
gas machine.”
• Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air
(it increases with age).
• A higher than normal P(A-a)O2 means lungs are not transferring
oxygen properly from alveoli into the pulmonary capillaries. Except
for right to left cardiac shunts.

22. • PaO2 ….is the pressure exerted by dissolved
oxygen, not a quantity of oxygen
• To quantify oxygen calculate CaO2

23. How much oxygen is in the blood?
PaO2 vs. SaO2 vs. CaO2
OXYGEN PRESSURE: PaO2
• Since PaO2 reflects only free oxygen molecules dissolved in plasma and
not those bound to Hb, PaO2 cannot tell us “how much” oxygen is in the
blood;
OXYGEN SATURATION: SaO2
• The percentage of all the available heme binding sites saturated with
oxygen is the Hb oxygen saturation (in arterial blood, the SaO2).
OXYGEN CONTENT: CaO2
• Only CaO2 (units ml O2/dl) tells us how much oxygen is in the blood; this is
because CaO2 is the only value that incorporates the Hb content. Oxygen
content can be measured directly or calculated by the oxygen content
equation:
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
Oxygen delivery = Cardiac output x CaO2

24. Assessment of ACID BASE Balance
• Definitions and Terminology
ACIDOSIS – presence of a process which tends to
 pH by gain of H + or loss of HCO3
-
ALKALOSIS – presence of a process which tends
to  pH by loss of H+ or gain of HCO3
-
If these changes, change pH, suffix ‘emia’ is added
 ACIDEMIA – reduction in arterial pH (pH<7.35)
 ALKALEMIA – increase in arterial pH (pH>7.45)

25. Simple Acid Base Disorder/ Primary Acid Base
disorder – a single primary process of acidosis or
alkalosis due to an initial change in PCO2 and HCO3.
Compensation - Normal response of the respiratory
system or kidneys to change in pH induced by a
primary acid-base disorder
 The Compensatory responses to a primary Acid Base
disturbance are never enough to correct the change in
pH , they only act to reduce the severity.
Mixed Acid Base Disorder – Presence of more than
one acid base disorder simultaneously .

26. Characteristics of Primary ACID
BASE Disorders
PRIMARY
DISORDER
PRIMARY RESPONSES COMPENSATORY
RESPONSESH+ ion pH Primary
Conc. Defect
Metabolic
Acidosis H+ pH HCO3
PCO2
Alveolar
Hyperventilation
Metabolic
Alkalosis H+ pH HCO3
PCO2
Alveolar
Hypoventilation
Respiratory
Acidosis H+ pH PCO2 HCO3
Respiratory
Alkalosis H+ pH PCO2 HCO3

27. Compensation
Metabolic Disorders – Compensation in these disorders leads to
a change in PCO2
METABOLIC ACIDOSIS:- for every 1 mmol fall in HCO3,
PCO2 fall with 1.20 mm of HG
Expect PCO2 = (1.5 x [HCO3]) + 8 + 2
(Winter’s equation)
METABOLIC ALKALOSIS:- for every 1 mmol increase in
HCO3, PCO2 increase with 0.7 mm of HG
Expect PCO2 = (0.7 x [HCO3]) + 21 + 1.5

28. In Respiratory Disorders
PCO2 Kidney HCO3 Reabsorption
Compensation begins to appear in 6 – 12 hrs and is fully
developed only after a few days.
1.ACUTE
Before the onset of compensation
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.2 meq/l
2.CHRONIC (>24 hrs)
After compensation is fully developed
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.4meq/l

29. Steps 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?

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

31. EXAMPLE ONE
 ABG 7.23/17/235
 BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr
5.1
• Answer PH = 7.23 , HCO3 7
• Acidemia

32. 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

33. EXAMPLE
 ABG 7.23/17/235
 BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
• PH is low , CO2 is Low
• PH and PCO2 are going in same directions then its most likely
primary metabolic will check to see if there is a mixed disoder.

34. Step 3-4: Is there appropriate compensation? Is
it chronic 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
– Chronic: for every 10 increase in pCO2 -> HCO3
increases by 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
Chronic: for every 10 decrease in pCO2 -> HCO3
decreases by 4 and there is a increase of 0.03 in PH

35. Step 3-4: Is there appropriate compensation? Is it
acute or chronic ?
 Metabolic Acidosis
Winter’s formula: pCO2 = 1.5[HCO3] + 8 ± 2
If serum pCO2 > expected pCO2 -> additional
respiratory acidosis
 Metabolic Alkalosis
 Expect PCO2 = (0.7 x [HCO3]) + 21 + 1.5
For every 10 increase in HCO3 -> pCO2 increases
by 7.5 mm of hg

36. EXAMPLE
 ABG 7.23/17/235
 BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5.
• Winter’s formula : 17= 1.5 (7) +8 = 18.5
• So correct compensation so there is only one
disorder Primary metabolic

37. Step 5: 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

38. EXAMPLE
• Calculate Anion gap
 ABG 7.23/17/235
 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

39. Step 6: Calculate the different
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

40. EXAMPLE : Delta Gap
 ABG 7.23/17/235
 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

41. Metobolic acidosis: Anion gap
acidosis

42. Nongap metabolic acidosis
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
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: nonrenal problem (most commonly GI)

43. RESPIRATORY ALKALOSIS

44. Causes of Respiratory Alkalosis
CENTRAL RESPIRATORY STIMULATION
(Direct Stimulation of Resp Center):
Structural Causes Non Structural Causes
• Head trauma Pain
• Brain tumor Anxiety
• CVA Fever
• Voluntary
PERIPHERAL RESPIRATORY STIMULATION
(Hypoxemia  Reflex Stimulation of Resp Center via
Peripheral Chemoreceptors)
• Pul V/Q imbalance
• Pul Diffusion Defects Hypotension
• Pul Shunts High Altitude

45. • INTRATHORACIC STRUCTURAL CAUSES:
1. Reduced movement of chest wall & diaphragm
2. Reduced compliance of lungs
3. Irritative lesions of conducting airways
• MIXED/UNKNOWN MECHANISMS:
1. Drugs – Salicylates Nicotine
Progesterone Thyroid hormone
Catecholamines
Xanthines (Aminophylline & related
compounds)
2. Cirrhosis
3. Gram –ve Sepsis
4. Pregnancy
5. Heat exposure
6. Mechanical Ventilation

46. Manifestations of Resp Alkalosis
• NEUROMUSCULAR: Related to cerebral Artery
vasoconstriction & 
Cerebral Blood flow.
1. Lightheadedness
2. Confusion
3. Decreased intellectual function
4. Syncope
5. Seizures
6. Paraesthesias (circumoral, extremities)
7. Muscle twitching, cramps, tetany
8. Hyperreflexia
9. Strokes in pts with sickle cell disease

47. • CARDIOVASCULAR: Related to coronary
vasoconstriction
1. Tachycardia
2. Angina
3. ECG changes (ST depression)
4. Ventricular arrythmias
• GASTROINTESTINAL: Nausea & Vomitting (cerebral
hypoxia)
• BIOCHEMICAL ABNORMALITIES:
 CO2 PO4
3-
Cl-  Ca2+

49. Homeostatic Response to Resp Alkalosis
 In acute resp alkalosis, imm response to fall in CO2 (&
H2CO3)  release of H+ by blood and tissue buffers 
react with HCO3-  fall in HCO3- (usually not less
than 18) and fall in pH
 Cellular uptake of HCO3- in exchange for Cl-
 Steady state in 15 min - persists for 6 hrs
 After 6 hrs kidneys increase excretion of HCO3-
(usually not less than 12-14)
 Steady state reached in 11/2 to 3 days.

50. Treatment of Respiratory Alkalosis
 Resp alkalosis by itself not a cause of resp failure
unless work of increased breathing not sustained by
resp muscles.
 Rx underlying cause
 Usually extent of alkalemia produced not dangerous.
 Admn of O2 if hypoxaemia
 If pH>7.55 pt may be sedated/anesthetised/
paralysed and/or put on MV.

51. RESPIRATORY ACIDOSIS

52. Causes of Acute Respiratory Acidosis
• EXCRETORY COMPONENT PROBLEMS:
1. Perfusion:
Massive Pulmonary thrombo embolism
Cardiac Arrest
2. Ventilation:
Severe pul edema
Severe pneumonia
ARDS
Airway obstruction
3. Restriction of lung/thorax:
Flail chest
Pneumothorax
Hemothorax

53. 4. Muscular defects:
Severe hypokalemia
Myasthenic crisis
5. Failure of Mechanical Ventilator
CONTROL COMPONENT PROBLEMS:
1. CNS:
Drugs (Anesthetics, Sedatives)
Trauma
Stroke
2. Spinal Cord & Peripheral Nerves:
Cervical Cord injury
Neurotoxins (Botulism, Tetanus, OPC)
Drugs causing Sk. m.paralysis (SCh, Curare,
Pancuronium & allied drugs, aminoglycosides)

54. Causes of Chronic Respiratory Acidosis
• EXCRETORY COMPONENT PROBLEMS:
1. Ventilation:
COPD
Advanced ILD
• Restriction of thorax/chest wall:
Kyphoscoliosis, Arthritis
Fibrothorax
Hydrothorax
Muscular dystrophy
Polymyositis

55. Causes of Chronic Respiratory Acidosis
• CONTROL COMPONENT PROBLEMS:
1. CNS: Obesity Hypoventilation Syndrome
Tumours
Brainstem infarcts
Myxedema
Ch sedative abuse
Bulbar Poliomyelitis
2. Spinal Cord & Peripheral Nerves:
Poliomyelitis
Multiple Sclerosis
ALS
Diaphragmatic paralysis

56. Manifestations of Resp Acidosis
• NEUROMUSCULAR: Related to cerebral A
vasodilatation &  Cerebral BF
1. Anxiety
2. Asterixis
3. Lethargy, Stupor, Coma
4. Delirium
5. Seizures
6. Headache
7. Papilledema
8. Focal Paresis
9. Tremors, myoclonus

57. Manifestations of Resp Acidosis
• CARDIOVASCULAR: Related to coronary
vasodilation
1. Tachycardia
2. Ventricular arrythmias (related to hypoxemia
and not hypercapnia per se)
• BIOCHEMICAL ABNORMALITIES:
 CO2
 Cl-
 PO4
3-

59. Homeostatic Response
to Respiratory Acidosis
 Imm response to rise in CO2 (& H2CO3)  blood
and tissue buffers take up H+ ions, H2CO3
dissociates and HCO3- increases with rise in pH.
 Steady state reached in 10 min & lasts for 8
hours.
 PCO2 of CSF changes rapidly to match PaCO2.
 Hypercapnia that persists > few hours induces an
increase in CSF HCO3- that reaches max by 24 hr
and partly restores the CSF pH.
 After 8 hrs, kidneys generate HCO3-
 Steady state reached in 3-5 d

60. Treatment of Respiratory Acidosis
 Correct underlying disorder if possible
 Alkali (HCO3) therapy rarely in acute and
never in chronic resp acidosis  only if
acidemia directly inhibiting cardiac functions
 Problems with alkali therapy:
1)Decreased alv ventilation by decrease in pH
mediated ventilatory drive
2)Enhanced carbon dioxide production from
bicarbonate decomposition

61. METABOLIC ACIDOSIS

62. Metabolic Acidosis
• pH, HCO3
• 12-24 hours for complete activation of
respiratory compensation
• PCO2 by 1.2mmHg for every 1 mEq/L HCO3
• The degree of compensation is assessed via
the Winter’s Formula
PCO2 = 1.5(HCO3) +8  2

63. Causes
• Metabolic Anion Gap
Acidosis
– M - Methanol
– U - Uremia
– D - DKA
– P - Paraldehyde
– L - Lactic Acidosis
– E - Ehylene Glycol
– S - Salicylate
Non Gap Metabolic
Acidosis
Hyperalimentation
Acetazolamide
RTA (Calculate urine
anion gap)
Diarrhea
Pancreatic Fistula

65. Treatment of Metabolic Acidosis
• When to treat?
•Severe acidemia  Effect on Cardiac function most
imp factor for pt survival but rarely lethal in absence of
cardiac dysfunction.
•Contractile force of LV  as pH  from 7.4 to 7.2
•However when pH < 7.2, profound reduction in cardiac
function occurs and LV pressure falls by 15-30%
•Most recommendations favour use of base when pH <
7.15-7.2 or HCO3 < 8-10 meq/L.

66. How to treat?
Rx Undelying Cause
HCO3- Therapy
• Aim to bring up pH to 7.2 & HCO3- 
10 meq/L
• Qty of HCO3 admn calculated:
0.5 x LBW (kg) x HCO3 Deficity
(meq/L)
However later studies contradicted above
observations and showed little or no
benefit from rapid and complete/over
correction of acidemia with HCO3.

67. Adverse Effects of HCO3- Therapy
  CO2 production from HCO3 decomposition 
Hypercarbia (V>A) esp when pul ventilation
impaired
 Myocardial Hypercarbia  Myocardial acidosis
Impaired myocardial contractility &  C.O.
  Coronary Artery perfusion pressure 
Myocardial Ischemia.
 Hypernatremia & Hyperosmolarity  Vol
expansion  Fluid overload
 Intracellular (paradoxical) acidosis esp in liver &
CNS ( CSF CO2)

68. METABOLIC ALKALOSIS

69. Metabolic Alkalosis
 Met alkalosis common (upto 50% of all disorders)
• pH, HCO3
• PCO2 by 0.7 for every 1mEq/L  in HCO3
 Severe met alkalosis assoc with significant mortality
1)Arterial Blood pH of 7.55  Mortality rate of 45%
2)Arterial Blood pH of 7.65  Mortality rate of 80%
 Metabolic alkalosis has been classified by the
response to therapy or underlying pathophysiology

70. Pathophysiological Classification of Causes of
Metabolic Alkalosis
1) H+ loss:
GIT Chloride Losing Diarrhoeal Diseases
Removal of Gastric Secretions
(Vomitting, NG suction)
Renal Diuretics (Loop/Thiazide)
Mineralocorticoid excess
Hypercalcemia
High dose i/v penicillin

71. 2) HCO3- Retention:
Massive Blood Transfusion
Ingestion (Milk-Alkali Syndrome)
Admn of large amounts of HCO3-
3) H+ movement into cells
Hypokalemia

72. Clinical features
Adrogue et al, NEJM 1998; 338(2): 107-111

73. Treatment of Metabolic Alkalosis
 Rx underlying cause resp for volume /Cl- depletion
 While replacing Cl- deficit, selection of
accompanying cation (Na/K/H) dependent
on:Assessment of ECF vol status
 Presence & degree of associated K depletion,
 Pts with vol depletion usually require replacement of
both NaCl & KCl.

74. Dialysis
• In presence of renal failure or severe fluid overload
state in CHF, dialysis +/- UF may be reqd to exchange
HCO3 for Cl & correct metabolic alkalosis.
Adjunct Therapy
• PPI can be admn to  gastric acid production in cases
of Cl-depletion met alkalosis resulting from loss of
gastric H+/Cl- (e.g. pernicious vomiting, req for
continual removal of gastric secretions.