ABG interpreter
Interpretation
Calculate the anion gap (if a metabolic acidosis exists):
Interpretation
Respiratory acidosis with metabolic acidosis
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Cardiac arrest, intoxication, multiorgan failure
Respiratory alkalosis with metabolic alkalosis
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Cirrhosis with diuretics, Pregnancy with vomiting, Overventilation of COPD
Respiratory acidosis with metabolic alkalosis
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COPD with diuretics, vomiting, NG suction, severe hypokalemia
Respiratory alkalosis with metabolic acidosis
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Sepsis, Salicylate toxicity, Renal failure with HF, pneumonia, Advanced liver disease
Metabolic acidosis with metabolic alkalosis
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Uremia or ketoacidosis with vomiting, NG suction, diuretic
Selected etiologies of respiratory alkalosis
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CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infection
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Hypoxia: lung disease, profound anemia, low FiO2
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Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia, pneumothorax, pulmonary emboli
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Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins
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Pregnancy, liver disease, sepsis, hyperthyroidism
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Incorrect mechanical ventilation setting
Selected etiologies of respiratory acidosis
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Airway obstruction
- upper
- lower: COPD, asthma, others
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CNS depression
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Sleep disorder breathing (OSA or OHS)
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Ventilatory restriction
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Increase CO2 production: shivering, rigor, seizures, malignant hyperthermia, hypermetabolism, increase intake of carbohydrates
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Incorrect mechanical ventilation setting
Selected causes of metabolic alkalosis
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Hypovolemia with Cl- depletion
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GI loss of H+: Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich food
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Renal loss H+: Loop and thiazide diuretics, post-hypercapnia (After institution of mechanical ventilation)
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Hypervolemia Cl-expansion
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Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic syndrome)
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hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids, hyperreninemia
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Severe hypokalemia, renal artery stenosis, bicarbonate administration
Selected etiologies of elevated anion gap metabolic acidosis
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Methanol intoxication
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Uremia
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DKA, alcoholic ketoacidosis, starvation ketoacidosis
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Paraldehyde toxicity
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Isoniazid
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Lactic acidosis :
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Type A: tissue ischemia
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Type B: Altered cellular metabolism, MALA (metformin-associated lactic acidosis)
-
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Ethanol or ethylene glycal intoxication (frequently associated with an osmolar gap)
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Salicylate intoxication
Selected etiologies of normal anion gap metabolic acidosis
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GI loss of HCO3
- Diarrhea, ileostomy, proximal colostomy, ureteral diversion
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Renal loss of HCO3
- proximal RTA
- carbonic anhydrase inhibitor (acetazolamide)
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Renal tubular disease
-
ATN
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Chronic renal disease
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Distal RTA
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Aldosterone inhibitor or absence
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NaCl infusion, TPN, NH4+ admistration
Internal consistency of the values using the Henderson-Hasselbach equation
(If there is a discrepancy between the pH and the [H+], the ABG may not be valid.)
[H+] = 24(PaCO2) =
[HCO3-]
PH
Approximate [H+] (nmol/L)
7.00 100
7.05 89
7.10 79
7.15 71
7.20 63
7.25 56
7.30 50
7.35 45
7.40 40
7.45 35
7.50 32
7.55 28
7.60 25
7.65 22
Test is valid
or
PCO2 < 30
HCO3 >30
Is there alkalemia or acidemia present?
Acidosis
pH < 7.35
or
PCO2 ≥45
HCO3 ≤ 15
Normal pH
7.35-7.45
and
PaCO2 35-45
HCO3 16-28
Alkalosis
pH > 7.45
or
PCO2 ≤35
HCO3 ≥28
Is the disturbance respiratory or metabolic?
Respiratory acidosis pH PaCO2
Respiratory alkalosis pH PaCO2
Metabolic acidosis pH PaCO2
Metabolic alkalosis pH PaCO2
Is there appropriate compensation for the primary disturbance?
Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8
Acute respiratory acidosis Increase in [HCO3-]= ∆ PaCO2/10
Chronic respiratory acidosis Increase in [HCO3-]= 3.5(∆ PaCO2/10)
Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-)
Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆ PaCO2/10)
Chronic respiratory alkalosis Decrease in [HCO3-] = 5(∆ PaCO2/10)
Calculate the anion gap (if a metabolic acidosis exists)
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A standard anion gap is approximately 12 meq/L AG= [Na+]-( [Cl-] + [HCO3-]
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In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the “normal” anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration.
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If the anion gap is elevated, calculate the osmolar gap in compatible clinical situations.
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Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure.
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Toxic ingestion is suspected.
-
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OSM gap = measured OSM – (2[Na+] + glucose/18 + BUN/2.8 +Ethanol/4.6)
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The OSM gap should be < 10.
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If there is an increased anion gap, evaluate the ratio of the change in the anion gap (∆AG) to the shift in bicarbonate concentration (∆[HCO3-]), expressed as ∆AG/∆[HCO3-]
This ratio should lie between 1.0 and 2.0 to indicate that uncomplicated anion gap metabolic acidosis is present.
If it falls outside this range, another metabolic disorder may be present:
if ∆AG/∆[HCO3-] < 1.0, a concurrent non-anion gap metabolic acidosis is likely
if ∆AG/∆[HCO3-] > 2.0, a concurrent metabolic alkalosis is likely to be present.