ABG

APPROACH TO
INTERPRETATION OF ABG
• Know the primary disorder
• Compute for the range of compensation
• For metabolic acidosis  get anion gap
• For high anion gap  get change in anion gap
and compare with change in bicarbonate
 COMPENSATORY RESPONSE
Disorder pH Primary Disturbance Compensatory
Response

Dec HCO3
Metabolic Acidosis (loss of HCO3 or gain in Dec pCO2
(hyperventilation)
H+)

Inc pCO2 Inc HCO3

Respiratory Acidosis (hypoventilation) (HCO3 generation)

Inc HCO3
Metabolic Alkalosis (gain in HCO3 or loss of Inc pCO2
(hypoventilation)
H+)

Dec pCO2 Dec HCO3

Respiratory Alkalosis (hyperventilation) (HCO3 consumption)
 COMPENSATORY RESPONSES
DISORDER PRIMARY COMPENSATORY
RESPONSE
Metabolic ↓HCO3 1.2 mmHg decrease in PCO2 for every
Acidosis 1meq/L fall in HCO3
Metabolic ↑HCO3 0.7 mmHg elevation in PCO2 for every
Alkalosis 1meq/L rise in HCO3
Respiratory ↑PCO2 1meq/L increase in HCO3 for every
Acidosis 10mmHg rise in PCO2
Respiratory ↓PCO2 2meq/L reduction in HCO3 for every
Alkalosis 10mmHg fall in PCO2
 Case 1
• A 55 year-old female, a known diabetic for 10 years, came in at
the ER for a 3 day history of fever and productive cough with
anasarca, abdominal pain and vomiting
• Labs:
– RBS – 22 (396)
– BUN – 3.6
ABG:
– Crea- 323 mmol/L
pH – 7.135
– Ca – 1.88
pCO2 – 20.2
– Alb – 22
pO2 – 89
– Urine ketone +++
HCO3 – 12.4
– Na - 129 BE – -9.0
– K – 3.8 O2 sats – 98%
– Cl – 98
– Phos – 3.2
– USG – 1.030
 ABG:
Case 1 pH – 7.135
pCO2 – 20.2
pO2 – 89
HCO3 – 12.4
• Interpret ABG BE – -9.0
O2 sats – 98%
– Look at the pH Room air
• Acidotic
– What caused the pH
• Metabolic acidosis
– Compute for compensation
• Decrease in pCO2 = 1.2 x change in bicarbonate
– Expected pCO2:
• Expected pCO2 = 26
• Expected pCO2 is higher than actual pCO2 (20.2), therefore
there is concomitant respiratory alkalosis
 Case 1:
• Interpret ABG
– If metabolic, compute the anion gap
• Get the corrected Na:
– Corrected Na = (RBS – 100) x 0.016 + Na
– Corrected Na = 134
• Compute the anion gap:
– Anion gap = Na – HCO3 – Cl
– Anion gap = 23.6
– HAGMA
 Case 1:
• Interpret ABG
– Get delta-delta:
• Change in anion gap
– Change = AG - 12
– Change = 11.6
• Change in bicarbonate
– Change = 24 – bicarbonate
– Change = 11.6
• Change in AG = change in bicarbonate
– Therefore: pure HAGMA
• Otherwise:
– Change in AG > change in bicarbonate: HAGMA + metab alkalosis
– Change in AG < change in bicarbonate: HAGMA + NAGMA
 Case 1: ABG:
pH – 7.135
pCO2 – 20.2
• Interpret ABG pO2 – 89
HCO3 – 12.4
– Check for pO2 BE – -9.0
O2 sats – 98%
• Correlate with FiO2 Room air
– LPM to FiO2 at nasal cannula: 4 x LPM + 20
• Hypoxemia (pO2 at FiO2 21%)
– Mild: 80-90
– Moderate: 60-80
– Severe: < 60
 Case 1:
• Final ABG interpretation:
– High anion gap metabolic acidosis with
concomitant respiratory alkalosis, mild hypoxemia
 Case 1:
• Conditions that lead to metabolic acidosis:
– HAGMA
• DKA
• Alcoholic ketoacidosis
• Lactic acidosis
• Renal insufficiency
• Starvation
• Salicylate intoxication
• Methanol intoxication
• Ethylene glycol intoxication
– NAGMA
• Diarrhea
• Pancreatic fluid loss
• Ileostomy
• Carbonic anhydrase inhibitors
• RTA
• Arginine and lysine in parenteral nutrition
 Case 2:
• Case 2: A 55 year-old female, a known diabetic for 10 years came in at the ER for a 3-
day history of fever and productive cough with anasarca, abdominal pain and vomiting

• RBS – 22
• BUN – 13.2
• Crea – 323
ABG:
• Ca – 1.62
pH – 7.535
• Alb – 22 pCO2 – 45.22
• Urine ketone + pO2 – 89.00
• Na – 117 HCO3 – 30.40
• K – 2.8 BE – 6.0
• Cl – 98 O2 sats – 98%
• Phos – 6.2
• USG – 1.025
 Case 2:
ABG:
• Interpret ABG pH – 7.535
– Look at the pH pCO2 – 45.22
pO2 – 89.00
• Alkalotic HCO3 – 30.40
– What caused the pH BE – 6.0
O2 sats – 98%
• Metabolic alkalosis 10 lpm
– Compute for compensation
• increase in pCO2 = 0.7 x change in bicarbonate
– Expected pCO2:
• Expected pCO2 = 44.48
• Expected PCO2 is near actual pCO2. Therefore, patient has
compensated metabolic alkalosis
 Case 2: ABG:
pH – 7.535
pCO2 – 45.22
• Interpret ABG pO2 – 89.00
HCO3 – 30.40
– Check for pO2 BE – 6.0
O2 sats – 98%
• Correlate with FiO2 10 lpm
– LPM to FiO2 at nasal cannula: 4 x LPM + 20
• Hypoxemia (pO2 at FiO2 21%)
– At FiO2 21%, pO2 should be at least 90
– Target pO2 = 90 / 0.21 x FiO2
– Target pO2 - 257
– hypoxemia
 Case 2
• Final ABG interpretation:
– Compensated metabolic alkalosis, with hypoxemia
 Case 2:
• Conditions associated with metabolic alkalosis:
– Diuretic therapy
– Posthypercapnia
– Vomiting
– Nasogastric suction
– NaHCO3
– Refeeding alkalosis
– Primary aldosteronism
– Hyperreninism
– Liddle’s syndrome
– Licorice (exogenous mineralocorticoids)
 Case 3:
• A 50 year old male, with a 50 pack year smoking history presents at the ER for chronic cough,
weight loss, with a 3 day history of high-grade fever and dyspnea for which he took cotrimoxazole
800/160 mg TID. Early this morning, he was found unresponsive and was then brought to the ER.
On PE, there was note of tachypnea, poor air entry and ocassional wheezing all over

• RBS – 6.3
• BUN – 8.3
• Crea- 96 ABG:
• Ca – 1.92 pH – 7.135
• Alb – 22 pCO2 – 70.2
• USG – 1.035 pO2 – 49.00
• Na – 163 HCO3 – 24.20
• K – 7.8 BE – -2.0
• Cl – 98 O2 sats – 78%
• Phos – 4.6
• 12L ECG – ST, NA, NSSTWCs
 Case 3:
• Interpret ABG ABG:
pH – 7.135
– Look at the pH pCO2 – 70.2
• acidotic pO2 – 49.00
HCO3 – 24.20
– What caused the pH BE – -2.0
• Respiratory acidosis O2 sats – 78%
– Compute for compensation 5 LPM

• increase in HCO3 = 1/10 x change in pCO2 (acute)

• Increase in HCO3 = 3/10 x change in pCO2 (chronic)
– Expected HCO3: (acute)
• Expected HCO3 = 27
• Expected HCO3 is higher than actual HCO3 (24.20). Therefore, patient
has uncompensated respiratory acidosis
 Case 3: ABG:
pH – 7.135
pCO2 – 70.2
• Interpret ABG pO2 – 49.00
HCO3 – 24.20
– Check for pO2 BE – -2.0
O2 sats – 78%
• Correlate with FiO2 5 LPM
– LPM to FiO2 at nasal cannula: 4 x LPM + 20
• Hypoxemia (pO2 at FiO2 21%)
– Expected pO2 = 90/0.21 x FiO2
– Expected pO2 = 171
– hypoxemia
 Case 3
• Final ABG interpretation:
– Uncompensated respiratory acidosis with
hypoxemia
 Case 3
• Conditions associated respiratory acidosis:
– Airway obstruction
– Respiratory center depression
– Neuromuscular defects
– Restrictive defect
 Case 4:
• A 50 year old male, with a 50 pack-year smoking history presents at the ER for chronic cough,
weight loss, with 3 day history of low grade fever and dyspnea for which he took cotrimoxazole
800/160 mg TID. Early this morning, he was found unresponsive and was then brought to the
ER. On PE, there was note of tachypnea, poor air entry and occasional wheezing all over

• RBS – 6.3
• BUN – 14.3
ABG:
• Crea – 96
pH – 7.48
• Ca - 2.42 pCO2 – 30.2
• Alb – 22 pO2 – 49.00
• USG – 1.015 HCO3 – 25.50
• Na – 113 BE – -1.8
• K – 7.8 O2 sats – 78%
• Cl – 98
• Phos – 4.6
• 12L ECG – ST, NA, shortened Qt, peaked T waves
 Case 4: ABG:
pH – 7.48
• Interpret ABG pCO2 – 30.2
pO2 – 49.00
– Look at the pH HCO3 – 25.50
• alkalosis BE – -1.8
O2 sats – 78%
– What caused the pH 6 LPM
• Respiratory alkalosis
– Compute for compensation
• decrease in HCO3 = 2/10 x change in pCO2 (acute)
• decrease in HCO3 = 5/10 x change in pCO2 (chronic)
– Expected HCO3: (acute)
• Expected HCO3 = 22.04
• Expected HCO3 is lower than actual HCO3 (25.50). Therefore, patient
has concomitant metabolic alkalosis
 Case 4: ABG:
pH – 7.48
pCO2 – 30.2
• Interpret ABG pO2 – 49.00
HCO3 – 25.50
– Check for pO2 BE – -1.8
O2 sats – 78%
• Correlate with FiO2 6 LPM
– LPM to FiO2 at nasal cannula: 4 x LPM + 20
• Hypoxemia (pO2 at FiO2 21%)
– Target pO2 = 90/0.21 x FiO2
– Target pO2 = 189
– hypoxemia
 Case 4:
• Final ABG interpretation:
– Respiratory alkalosis with concomitant metabolic
alkalosis
 Case 4:
• Conditions associated with respiratory alkalosis:
– High altitude
– V/Q mismatch
– Severe anemia
– Infection
– trauma
– Hepatic failure
– Gram negative septicemia
– Interstitial lung disease
– Pneumonia
– Pulmonary embolism
– Pulmonary edema