Acid-Base

ABG/VBG Analyzer

Interprets acid-base status, compensation, mixed disorders, anion gap, delta ratio, oxygenation, and suggested next steps.

Sample Type ABG VBG

pH

pCO₂ mmHg

HCO₃ mEq/L

Na mEq/L

Cl mEq/L

Albumin g/dL

K mEq/L

Lactate mmol/L

Glucose mg/dL

BUN mg/dL

Creatinine mg/dL

PaO₂ mmHg

FiO₂

Clinical Context None selected COPD / hypercapnia DKA / hyperglycemia ESRD / renal failure Shock / sepsis Possible salicylate/toxin Diarrhea / GI bicarb loss Vomiting / NG suction / diuretics

Analyze Reset

Interpretation

Primary Read

Calculated Values

Mixed Disorder Check

Likely Causes to Consider

Suggested Next Steps

Initial Acid-Base Approach

Metabolic or respiratory?

• Metabolic = abnormal bicarb or anion gap
• Respiratory = abnormal pCO2

Check anion gap (AG = Na - Cl - HCO3)

• Normal AG: 4-12
• High AG → AGMA workup
• Normal AG + low bicarb → NAGMA
• High bicarb → metabolic alkalosis

If AG elevated, calculate delta-delta

• ΔAG = AG - 10
• ΔHCO3 = 24 - HCO3
  • ΔAG ≈ ΔHCO3 → pure AGMA
  • ΔAG > ΔHCO3 → AGMA + metabolic alkalosis
  • ΔAG < ΔHCO3 → AGMA + NAGMA

Ask:

• Is compensation appropriate?
• Is there another mixed disorder?

Compensation Cheat Sheet

Anion Gap Metabolic Acidosis (AGMA)

Common causes

• Lactic acidosis
• DKA/alcoholic/starvation ketoacidosis
• Renal failure/uremia
• Toxic alcohols
• Salicylates
• Acetaminophen toxicity
• Metformin
• Linezolid
• Propylene glycol
• Cyanide/CO poisoning

Lactic acidosis

• Inadequate oxygen delivery
  • Shock
  • Ischemia
  • Seizure
  • Severe anemia
• Adequate oxygen delivery
  • Liver failure
  • Malignancy
  • Thiamine deficiency
  • Beta agonists/epinephrine
  • Severe DKA

Workup

• CBC
• CMP/Ca/Mg/Phos
• Lactate
• Beta-hydroxybutyrate
• LFTs
• Toxicology if indicated
• Medication review
• Calculate delta-delta

Exam

• Shock
• Poor perfusion
• Cold extremities
• Abdominal ischemia
• Altered mentation

Treatment

• Treat underlying cause
• IV thiamine 200mg q12h if unclear etiology/alcohol use/malnutrition
• Dialysis for severe renal failure or intoxications
• Bicarb mainly helpful in uremic acidosis

Dialysis indications

• pH <7.15 despite treatment
• Methanol
• Ethylene glycol
• Severe salicylate toxicity
• Severe metformin acidosis

Pearls

• Mild lactic acidosis can occur with normal AG
• Chronic CKD patients may have elevated baseline AG
• Beta-hydroxybutyrate better than urine ketones

Normal Anion Gap Metabolic Acidosis (NAGMA)

Causes

• Diarrhea
• Pancreatic/biliary losses
• Normal saline
• Resolving DKA
• Renal insufficiency
• RTA
• TPN

Potassium clues

High/normal K

• Type IV RTA
• CKD
• NS infusion

Low K

• GI losses
• Type I/II RTA

Workup

• CMP/Ca/Mg/Phos
• UA
• Urine electrolytes
• Urine pH
• Urine osmolar gap

Urine osmolar gap
= Urine osm - 2(Na + K) - glucose/18 - urea/28

Interpretation

• 150 → adequate ammonium excretion
• <150 → impaired ammonium excretion

Type IV RTA

Causes

• Diabetes
• ACEI/ARB
• NSAIDs
• Adrenal insufficiency
• Heparin
• Obstructive uropathy
• K-sparing diuretics

Volume-based treatment

Hypovolemic

• Give sodium bicarbonate

Euvolemic

• Add bicarbonate
• Remove chloride

Hypervolemic

• Diurese chloride

RTA's

RTA Predictor

Rule-based estimate of RTA type from common lab patterns

Serum bicarb / HCO3

Serum potassium

Urine pH

Urine osmolar gap Select <150 mOsm >150 mOsm Unknown

Glucosuria without hyperglycemia Select Yes No Unknown

Other proximal tubule findings Select Low phos, uric acid, Mg, or generalized Fanconi pattern No Unknown

Medication pattern Select Amphotericin, lithium, ifosfamide, foscarnet Acetazolamide, topiramate, tenofovir, valproate, aminoglycoside ACE-I, ARB, spironolactone, TMP, heparin, tacrolimus, NSAID None/unknown

Clinical pattern Select Stones, nephrocalcinosis, autoimmune disease Multiple myeloma, Fanconi syndrome, proximal tubule dysfunction Diabetes, CKD, adrenal insufficiency, hypoaldosteronism None/unknown

Predict RTA Type Reset

Use only after confirming non-anion gap metabolic acidosis. This does not replace clinical judgment.

Renal Tubular Acidosis Comparison

	RTA-1 Generalized distal	RTA-2 Proximal	RTA-4 Aldosterone resistance or deficiency
Lab findings
Typical severity of acidosis	Bicarb ~10–20 mM	Bicarb ~12–20 mM	Mild, bicarb >17 mM
Potassium	↓↓	↓	↑ often primary manifestation
Other electrolytes		In generalized proximal tubule dysfunction: ↓ Ca, ↓ Mg, ↓ Phos, ↓ uric acid
Glucosuria	-	+	-
Urine pH	>5.3	Variable	Usually <5.5
Urine osmolar gap	<150 mOsm	>150 mOsm	<150 mOsm
Causes
Medications	Amphotericin NSAIDs Lithium Ifosfamide Foscarnet	Carbonic anhydrase inhibitors Acetazolamide Topiramate Mafenide acetate Aminoglycosides Tenofovir, antiretrovirals Valproic acid Chemotherapeutics	Trimethoprim, pentamidine Amiloride, triamterene Spironolactone, eplerenone ACE-I, ARB, renin inhibitors NSAIDs, beta-blockers Cyclosporine, tacrolimus Heparin
Genetic disorders	Wilson disease Sickle cell anemia Ehlers-Danlos Marfan syndrome	Wilson disease	Sickle cell anemia
Metabolic disorders	Hypercalciuria Hyperthyroidism Hyperparathyroidism Vitamin D intoxication	Hypocalcemia Hyperparathyroidism Vitamin D deficiency	Adrenal insufficiency
Other	SLE, RA, Sjogren syndrome, thyroiditis Primary biliary cirrhosis Cryoglobulinemia HIV-associated nephropathy Obstructive nephropathy Renal transplant rejection Amyloidosis Toluene abuse	Multiple myeloma, monoclonal gammopathy SLE, Sjogren syndrome Renal transplant rejection Amyloidosis Nephrotic syndrome Lead, cadmium, mercury poisoning Paroxysmal nocturnal hemoglobinuria	Diabetic nephropathy Hypertensive nephropathy Multiple myeloma, monoclonal gammopathy SLE, glomerulonephritis Renal transplant rejection Amyloidosis Obstructive nephropathy Sickle cell disease

Metabolic Alkalosis

Common causes

Saline responsive

• Vomiting
• NG suction
• Contraction alkalosis
• Chloride wasting

Saline unresponsive

• Hyperaldosteronism
• HypoK/hypoMg
• Excess alkali
• Ongoing diuretics

Compensatory

• Chronic hypercapnia
• COPD
• OHS

Workup

• History/volume status
• Urine chloride
• Urine potassium
• ABG/VBG

Urine chloride interpretation

• <10-30 → saline responsive
• 10-30 → saline unresponsive

If persistent/refractory
Check renin/aldosterone

Interpretation

• ↓ renin, ↑ aldosterone → primary hyperaldo
• ↑ renin, ↑ aldosterone → secondary hyperaldo
• ↓ renin, ↓ aldosterone → apparent mineralocorticoid excess

When NOT to treat

• Chronic compensatory alkalosis from chronic hypercapnia

Treatment

• Replete K aggressively
• Replete Mg
• NS if hypovolemic
• Acetazolamide if hypervolemic
• Hold/reduce loop diuretics
• PPI if vomiting/NG suction
• Dialysis rarely needed
• IV HCl only as last resort

Respiratory Acidosis

Diagnosis

• pCO2 >45
• Determine acute vs chronic by bicarb level

Symptoms

• Somnolence
• Delirium
• Headache
• Asterixis
• CO2 narcosis

Causes

Won’t breathe

• Opioids
• Benzos
• Alcohol
• Brainstem pathology
• Hypothyroidism

Can’t breathe

• Neuromuscular disease
• Cervical cord injury
• MG/GBS/ALS
• Obesity hypoventilation
• Pleural effusion
• COPD/asthma
• Airway obstruction

Breathing ineffective

• Pneumonia
• ARDS
• PE

Workup

• Exam
• RR/mental status
• Neuro exam
• Lung exam
• CMP/CBC/TSH/CK
• CXR/CT/MRI as indicated

Treatment

• Treat underlying cause
• Naloxone for opioids
• NIV for neuromuscular weakness
• COPD/asthma-specific therapy
• Permissive hypercapnia often acceptable on vent

Pearls

• Chronic hypercapnia usually well tolerated
• Avoid rapid normalization in chronic retainers

Respiratory Alkalosis

Diagnosis

• pCO2 <35

Symptoms

• Anxiety
• Paresthesias
• Cramps
• Delirium
• Arrhythmias

Causes

Pulmonary

• PE
• Pneumonia
• Asthma
• Pneumothorax

CNS

• Pain
• Anxiety
• Stroke
• Meningitis

Medications

• Salicylates
• Caffeine
• Nicotine
• Beta agonists
• Progesterone

Other

• Pregnancy
• Thyrotoxicosis
• Cirrhosis
• Early sepsis

Workup

• Salicylate level
• TSH
• LFTs
• Beta-HCG
• PE evaluation
• Sepsis workup

Treatment

• Treat underlying cause
• Adequate pain control/sedation
• Reduce RR or TV if ventilated

References

1. Adrogué, H. J., & Madias, N. E. (1998). Management of life-threatening acid-base disorders: First of two parts. The New England Journal of Medicine, 338(1), 26–34. https://doi.org/10.1056/NEJM199801013380106
2. Adrogué, H. J., & Madias, N. E. (1998). Management of life-threatening acid-base disorders: Second of two parts. The New England Journal of Medicine, 338(2), 107–111. https://doi.org/10.1056/NEJM199801083380207
3. Berend, K., de Vries, A. P. J., & Gans, R. O. B. (2014). Physiological approach to assessment of acid-base disturbances. The New England Journal of Medicine, 371(15), 1434–1445. https://doi.org/10.1056/NEJMra1003327
4. Kraut, J. A., & Madias, N. E. (2010). Metabolic acidosis: Pathophysiology, diagnosis and management. Nature Reviews Nephrology, 6(5), 274–285. https://doi.org/10.1038/nrneph.2010.33
5. Kraut, J. A., & Madias, N. E. (2012). Treatment of acute metabolic acidosis: A pathophysiologic approach. Nature Reviews Nephrology, 8(10), 589–601. https://doi.org/10.1038/nrneph.2012.186
6. Kraut, J. A., & Kurtz, I. (2015). Treatment of acute non-anion gap metabolic acidosis. Clinical Kidney Journal, 8(1), 93–99. https://doi.org/10.1093/ckj/sfu126
7. Palmer, B. F., Kelepouris, E., & Clegg, D. J. (2021). Renal tubular acidosis and management strategies: A narrative review. Advances in Therapy, 38(2), 949–968. https://doi.org/10.1007/s12325-020-01587-5
8. Palmer, B. F., & Clegg, D. J. (2023). Respiratory acidosis and respiratory alkalosis: Core Curriculum 2023. American Journal of Kidney Diseases, 82(3), 347–359. https://doi.org/10.1053/j.ajkd.2023.02.004