Metabolic Acidosis
From confirming the acid-base disorder to the anion-gap differential.
An educational representation of clinical reasoning, not a diagnostic algorithm or personalized medical advice — always apply clinical judgment and institutional protocols.
Caution
Escalate — Red Flags & Critical Warnings
- pH < 7.15 or hemodynamic instability accompanying the acidosis — this is an emergency requiring urgent source control, not bicarbonate correction alone.
- An anion gap acidosis with a markedly elevated osmolar gap — consider toxic alcohol ingestion and involve toxicology/nephrology early for possible dialysis.
Related Bedside Clinical Problems (26)
Bedside PresentationsTriaging rising PaCO2: distinguishing acute uncompensated acidemia from chronic compensation, identifying central vs pump vs dead-space failure, and titrating noninvasive ventilation.
Rapid bedside hemodynamic categorization: confirming MAP < 65 mmHg, assessing peripheral perfusion, POCUS cardiac/IVC profiling, and differentiating hypovolemic, distributive, cardiogenic, and obstructive etiologies.
Advanced multimodal hemodynamic rescue: second-line vasopressors (vasopressin, angiotensin II), inotropic augmentation, stress-dose steroids, metabolic correction, and mechanical circulatory support evaluation.
Linked Deep-Dive Topics (7)
Reference KnowledgeDifferential diagnosis (GOLD MARK vs HARDCARP), toxic alcohol osmolar gaps, Urine Anion Gap, and current sodium bicarbonate evidence including BICAR-ICU and BICARICU-2.
Stepwise 6-step interpretation algorithm, compensation formulas, albumin-corrected anion gap, delta ratio, and Stewart physicochemical (SID) principles.
Pathophysiology, SGLT2i euglycemic DKA, balanced fluid resuscitation, potassium-before-insulin safety rules, dextrose addition kinetics, and subcutaneous transition.
Resuscitate first, identify toxidromes and ECG/acid-base threats, use toxin-specific antidotes, and escalate early to poison-center, extracorporeal, or ECLS support when physiology demands it.
Principles of convection vs diffusion, filtration fraction, delivered effluent dosing (20–25 mL/kg/h), Regional Citrate Anticoagulation, and citrate toxicity.
Cellular dysoxia, DO2/VO2 physiology, the 4 shock phenotypes, dynamic fluid responsiveness (PLR/PPV) vs fluid tolerance (VExUS), and vasoactive pharmacology.
Sepsis-AKI microcirculatory decoupling, KDIGO staging, Furosemide Stress Test (FST), urine microscopy, and the AEIOU dialysis threshold framework.
Evidence status
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