STEP wise explanation to read an ABG, diagnose simple as well as complex acid base disorders with relevance to history and laboratory findings.

1. - DR. AISHWARYA JOSHI
- MODERATOR: DR. CHANDAN DAS
- IMS and SUM HOSPITAL
- BHUBANESWAR

2.  Normal- pH- 7.35-7.40-7.45
 pCO2- 36-40-44 mm Hg
 HCO3- 22-24-26 mmol/L
 Buffering, in seconds- Extracellular- HCO3 & NH3, Intracellular- proteins &
PO4
 Lungs- change in arterial pCO2, in minutes
 Kidneys- change in HCO3 excretion, in hours/days

3. Acidosis: process that lowers the extracellular fluid pH
(reduction in HCO3 or elevation in pCO2)
 Metabolic acidosis: low pH and low HCO3
 Respiratory acidosis: low pH and high pCO2
Alkalosis: process that raises extracellular pH (elevation
in HCO3 or fall in pCO2)
 Metabolic alkalosis: high pH and high HCO3
 Respiratory alkalosis: high pH and low pCO2

4.  Simple- one defect with appropriate compensation
 Mixed- more than one defect

6.  Metabolic acidosis: respiratory compensation begins in the first hour.
Winter’s equation: pCO2 = 1.5 x (HCO3) + 8 + 2
 Metabolic alkalosis: rise of 0.6 mmHg pCO2 for 1 meq/L HCO3 elevation
 Respiratory acidosis:
 acute: HCO3 increases 1meq/L for every 10 mmHg rise of pCO2
 Chronic (renal compensation complete in 3-5 days): HCO3 increases
3.5meq/L for every10 mmHg rise of pCO2
 Respiratory alkalosis:
 acute: HCO3 increases 2 meq/L for every 10 mmHg fall of pCO2
 Chronic: HCO3 increases 4 meq/L for every 10 mmHg fall of pCO2

7. Hypoventilation
 CNS- depression, trauma, Pickwickian syndrome, polio, tetanus
 Nerve/muscle- GBS, myasthenia, myopathies, snake venom
 Lung- ARDS, aspiration, edema, pneumothorax, restrictive lung
disease, COPD , Acute airway obstruction—upper airway,
laryngospasm, bronchospasm
 Airway- asthma, broncho/laryngospasm
 Inadequate mechanical ventilation

8.  Hyperventilation
 CNS- head injury, CVA , hepatic encephalopathy
 Psychogenic
 Pain, fever, stress
 Lung- PE, pneumonia, asthma, edema
 High altitude
 Progesterone in pregnancy, cytokines in sepsis, toxins in CLD
 Iatrogenic

9. High anion gap- added acids
 Ketoacidosis- DM, alcoholic, starvation
 Lactic acidosis- shock, extreme exertion
 ARF/CRF
 Rhabdomyolysis
 Toxins- ethylene glycol, methanol, salicylates
Normal anion gap- hyperchloremic bicarbonate loss
 GI HCO3 loss: diarrhea, ureteral diversions
 Renal HCO3 loss: RTA, aldosterone inhibitors, carbonic anhydrase inhibitors
 Iatrogenic: normal saline

10. Chloride depletion- U Cl<10 mmol/L- saline responsive
 Vomiting
 Diuretics
K depletion- U Cl>20 mmol/L- saline resistant
 Hyperaldosteronism
 Cushing’s syndrome
 Bartter’s syndrome
Other
 Laxative abuse
 Severe hypoalbuminemia
 Refeeding alkalosis

11.  DO HISTORY AND PHYSICAL EXAMINATION CLUE AN ACID BASE
DISORDER?
 VERIFY WHETHER THE LAB VALUES ARE CONSISTENT.
 pH- LOW-NORMAL-HIGH?
 IS THE PRIMARY DISTURBANCE METABOLIC, RESPIRATORY OR BOTH. IF
BOTH, THEN PICK THE ONE WHICH SEEMS MORE SEVERE.
 IS THE DISTURBANCE ACUTE OR CHRONIC? HAVE COMPENSATORY
CHANGES OCCURED?
 IF METABOLIC ACIDOSIS, ESTIMATE THE ANION GAP.
 IS ANY SECONDARY OR TERTIARY DISTURBANCE PRESENT?

13. The patient has a low pH (acidemia)
• The PCO2 is high (respiratory acidosis) and the bicarbonate is at the upper end of
normal. The low pH and high PCO2 imply that the respiratory acidosis is the
primary process
• The anion gap is 10 and is, therefore, normal. The patient does not have an
elevated anion gap acidosis.
• There is no compensatory process. Although the measured bicarbonate is just
above normal.
• Summary: An acute, uncompensated respiratory acidosis leading to acidemia.

14. Case 2: A 60 year-old man is brought into clinic by his
family who are concerned that he is more somnolent than
normal. On further history, they report that he has been
having problems with morning headaches and does not feel
very refreshed when he wakes up. An arterial blood gas is
performed and reveals: pH 7.37, PCO2 57, PO2 70, HCO3 -
32.

15. Acid-base status:
• The patient has a low pH (acidemia)
• The PCO2 is high (respiratory acidosis) and the bicarbonate is high (metabolic
alkalosis). The low pH in combination with the high PCO2 tells us that the
respiratory acidosis is the primary process.
• The metabolic alkalosis is the compensatory process.
• Summary: A chronic respiratory acidosis with a compensatory metabolic alkalosis.

16.  A 65 year-old man is brought to the hospital with complaints of
severe nausea and weakness. He has had problems with peptic
ulcer disease in the past and has been having similar pain for the
past two weeks. Rather than see a physician about this, he opted
to deal with the problem on his own and, over the past week, has
been drinking significant quantities of milk and consuming large
quantities of antacids (calcium carbonate). On his initial
laboratory studies, he is found to have a calcium level of 11.5
mg/dL, a creatinine of 1.4 and bicarbonate of 35. The resident
working in the ER decides to draw a room air arterial blood gas,
which reveals: pH 7.45, PCO2 49, PO2 68, HCO3 - 34. On his
chemistry panel, the sodium is 139, chloride 95, HCO3 34.

17. Acid-base status:
• The patient has a high pH (alkalemia)
• The PCO2 is high (respiratory acidosis) and the bicarbonate is high (metabolic
alkalosis). The high pH and the high bicarbonate tell us that the metabolic alkalosis
is the primary process.
• The anion gap is 10. This is a normal value
• The respiratory acidosis is the compensatory process
• The delta gap is 10 – 12 = -2. The delta delta is -2 + 34 = 32. This value is above
26 and tells us that a metabolic alkalosis is present. This is the same process that
was identified in the second step above.
• Summary: A primary metabolic alkalosis with respiratory compensation.

18.  In patients with normal AG acidosis or AG attributable to
non metabolizable anion due to CKD should receive
NaHCO3 to increase it to a value of 22mmol/L.
Pure AG acidosis owing to accumulation of
metabolizable organic acid anion require iv NaHCO3 if
acidaemia is severe i.e. pH <7.1 as 50mEq in 300 ml sterile
water over 30-45 mins in initial 1-2h of therapy. The goal is to
increase HCO3 to 10-12 mmol/L and pH to ~7.2 but to clearly
not to increase these values to normal.

19. Primarily, treat the underlying cause.
Remove the factors that sustain inappropriate
increase in HCO3 reabsorbtion
1. ECFV contraction: NS, acetazolamide.
2. Potassium deficiency

20. Acute: Restoration of alveolar ventilation by NIV or
Intubation
Chronic: Improvement of lung function with sufficient Cl
and K to enhance HCO3 excretion

21.  Alleviation of underlying disorder
 Rebreathing from a paper bag during symptomatic attacks. Beta
blockers can ameliorate peripheral manifestations of
hyperadrenergic state.

22.  Mixed acid-base disturbances are combinations of two or more primary acid-base
disturbances.
 To identify mixed acid-base disorders, blood gas analysis is used to identify primary
acid-base disturbance and determine if an appropriate compensatory response has
developed. Inappropriate compensatory responses (inadequate or excessive) are
evidence of a mixed respiratory and metabolic disorder.
 In high anion gap metabolic acidosis, the change in the anion gap should
approximate the change in serum bicarbonate.

24. A 45 year-old woman with a history of inhalant abuse
presents to the emergency room complaining of dyspnea.
She has an SpO2 of 99% on room air and is obviously
tachypneic on exam with what appears to be Kussmaul’s
respirations. A room air arterial blood gas is performed and
reveals: pH 6.95, PCO2 is 9, PO2 is 128, HCO3 - 2. A
chemistry panel revealed sodium of 130, chloride 98, HCO3
= 2

25. The patient has a very low pH (acidemia)
• The patient has a low PCO2 (respiratory alkalosis) and a very low bicarbonate
(metabolic acidosis). The low pH in conjunction with the low bicarbonate tells us
that the metabolic acidosis is the primary process
• The anion gap is elevated at 30. This tells us that the patient has a primary
elevated anion gap metabolic acidosis.
• The respiratory alkalosis is the compensatory process, although in this case,
despite a huge compensatory increase in minute ventilation, the patient still has a
very low pH.
• The delta gap is 30-12 = 18 and the delta-delta is 18 + 2 = 20. Since the delta-
delta is below 22, we know that there is an additional non-gap metabolic acidosis as
well. • Summary: Combined elevated anion gap and non-gap metabolic acidoses
with compensatory respiratory alkalosis.

26. A 47 year-old man with a history of heavy alcohol use
presents with a two days history of severe abdominal pain,
nausea and vomiting. On exam, his blood pressure is 90/50
and he is markedly tender in his epigastrum. His initial
laboratory studies reveal a sodium of 132, chloride 92,
HCO3 - 16, creatinine 1.5, amylase 400 and lipase 250. A
room air arterial blood gas is drawn and reveals pH 7.28,
PCO2 34, PO2 88, HCO3 - 16.

27. The patient has a low pH (acidemia)
• The PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic
acidosis). The combination of the low pH and the low bicarbonate tells us that the
metabolic acidosis is the primary process
• The anion gap is elevated at 24. This tells us that the patient has a primary
elevated anion gap metabolic acidosis
• The respiratory alkalosis is the compensatory process
• The delta gap is 24-12 = 12. The delta delta is 12 + 17 = 29. Because the delta-
delta is greater than 26, we know that the patient has a concurrent metabolic
alkalosis.
• Summary: Primary elevated anion gap metabolic acidosis with respiratory
compensation and a concurrent metabolic alkalosis.

28. 24 yo white male s/p gunshot wound to the abdomen required
splenectomy and ileostomy. The pt is intubated, sedated and
paralyzed. He has an NG tube in place, is on multiple antibiotics and
has required post-op pressors.
PE: T 39o BP 100/60, P 113
Looks terrible!
Lots of tubes and drains

29. • pH: 7.61 high, alkalosis
• pCO2: 30 low, respiratory alkalosis
• HCO3: 29 high, metabolic alkalosis
• Anion Gap: 140 - ( 94 + 29) = 17
• Delta change HCO3: (17-12= 5)+29 (observed) = 34 (‘true’ value
without acidosis)
• Answer:
• metabolic alkalosis
• anion gap metabolic acidosis
• respiratory alkalosis

30. TREATMENT OF THE UNDERLYING
CAUSE IS THE MAINSTAY.
JUDGE THE SEVERITY OF THE PRIMARY
DISTURBANCE AND APPROACH
ACCORDINGLY WITH THE USE OF
RESPIRATORY AIDS OR HCO3.