Submodule
Buffer Systems and Organ Control
The bicarbonate to carbon dioxide ratio links cellular acid production to pulmonary ventilation and renal acid handling.
- Henderson-Hasselbalch relationship
- Volatile and fixed acid
- Pulmonary carbon dioxide removal
- Renal bicarbonate and ammonium handling
Name the state precisely
Acidemia means arterial pH is below the reference range, while alkalemia means it is above. Acidosis and alkalosis describe physiologic processes that push pH in either direction. More than one process can coexist, so a nearly normal pH never excludes a serious mixed disorder.
Link the ratio to organ function
The lungs regulate PaCO₂ through alveolar ventilation within minutes. The kidneys reclaim filtered bicarbonate, generate new bicarbonate, and excrete net acid through titratable acids and ammonium over hours to days. Compensation limits a pH change but does not remove the underlying cause.
Keep oxygenation separate
PaO₂ and oxygen saturation address oxygenation, while PaCO₂ reflects ventilation. A venous blood gas can often support acid-base assessment when oxygenation is evaluated separately, but an arterial sample is required when precise arterial oxygenation or a large arterial-venous difference matters.
Quick check
Submodule
A Systematic Blood Gas Method
A fixed sequence prevents a striking value from distracting from the complete physiologic pattern.
- Clinical context and sampling
- pH direction
- Primary respiratory or metabolic process
- Oxygenation, electrolytes, and repeat trends
Start with validity and context
Confirm sample type, collection conditions, and whether the chemistry bicarbonate and blood gas bicarbonate are reasonably concordant. Identify immediate threats such as shock, hypoxemia, toxic exposure, severe hyperkalemia, altered mental status, or inability to sustain compensatory ventilation.
Determine the dominant direction
If pH is low, decide whether low bicarbonate or high PaCO₂ best explains the acidemia. If pH is high, decide whether high bicarbonate or low PaCO₂ best explains the alkalemia. When pH is near normal, its position relative to 7.40 and the expected compensation help reveal the dominant process.
Never stop after the first label
After identifying a primary process, calculate the expected compensatory response. Then calculate the anion gap when metabolic acidosis is present or suspected. A mismatch indicates an additional primary disorder, not unusually strong compensation.
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Submodule
Expected Compensation and Mixed Disorders
Compensation is predictable within a range. Values outside that range expose a second primary process.
- Winter's formula
- Metabolic alkalosis compensation
- Acute and chronic respiratory change
- Double and triple disorders
Use Winter's formula for metabolic acidosis
Expected PaCO₂ equals 1.5 times bicarbonate plus 8, with a range of plus or minus 2 mmHg. A measured PaCO₂ above the range indicates concurrent respiratory acidosis. A value below the range indicates concurrent respiratory alkalosis.
Estimate other compensations
In metabolic alkalosis, PaCO₂ generally rises about 0.7 mmHg for each 1 mmol/L rise in bicarbonate above 24, with a broad range of about plus or minus 5. In acute respiratory acidosis, bicarbonate rises about 1 mmol/L per 10 mmHg PaCO₂ increase; in chronic disease, about 3.5 to 4. In acute respiratory alkalosis, bicarbonate falls about 2 mmol/L per 10 mmHg PaCO₂ decrease; in chronic disease, about 4 to 5.
Respect time course and uncertainty
Renal compensation requires time, so an apparently chronic pattern is not plausible immediately after an acute event. These empirical rules are approximations. Integrate repeat measurements, baseline lung and kidney function, and treatments already given.
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Submodule
Anion Gap and Metabolic Acidosis
The anion gap detects unmeasured anions. Albumin correction and delta analysis keep a normal-looking value from hiding a complex disorder.
- Anion gap and albumin correction
- GOLD MARK causes
- Normal-gap metabolic acidosis
- Delta gap and urine studies
Calculate and correct
Without potassium, the anion gap equals sodium minus chloride plus bicarbonate. The local normal range depends on the assay. A common albumin correction adds about 2.5 mEq/L for each 1 g/dL that albumin is below 4 g/dL. The French expert panel recommends the albumin-corrected gap over the uncorrected value for distinguishing acid load from base loss.
Use current etiologic groups
GOLD MARK organizes common high-gap causes: glycols, oxoproline, L-lactate, D-lactate, methanol, aspirin, renal failure, and ketoacidosis. The mnemonic is a prompt, not a substitute for exposure history, measured lactate and ketones, kidney function, osmolar gap, and targeted toxicology.
Investigate normal-gap acidosis
Bicarbonate loss through diarrhea, renal tubular acidosis, urinary diversion, chloride-rich fluid, and impaired renal acid excretion can produce hyperchloremic acidosis. The urine anion gap and urine pH are selected tools when the cause is not obvious, not universal screening tests.
Use delta relationships cautiously
Comparing the rise in anion gap with the fall in bicarbonate can reveal an additional metabolic alkalosis or normal-gap acidosis. Baseline gap, albumin, timing, renal function, and prior fluid therapy can change the relationship, so report it as supporting evidence rather than a standalone diagnosis.
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Submodule
Metabolic Acidosis and Alkalosis Treatment
pH severity identifies risk, but therapy succeeds only when it reverses acid generation, base loss, chloride depletion, mineralocorticoid activity, or impaired excretion.
- Cause-directed metabolic acidosis care
- Nuanced bicarbonate use
- Chloride-responsive alkalosis
- Chloride-resistant alkalosis
Treat the acid source or base loss
Restore perfusion and source control in shock, administer insulin and fluids for diabetic ketoacidosis while managing potassium, stop toxic exposure, replace bicarbonate losses when clinically appropriate, and use kidney replacement therapy for selected severe or refractory states. Lactate is a severity marker that requires rapid diagnosis and repeated assessment of the response.
Use bicarbonate as a defined intervention
Bicarbonate is not a universal response to a low pH. In BICARICU-2, bicarbonate did not lower 90-day mortality in critically ill adults with pH at or below 7.20 and moderate to severe acute kidney injury, although kidney replacement therapy occurred less often. Cause, ventilation, sodium load, fluid balance, calcium, potassium, and the clinical objective all shape the decision.
Classify metabolic alkalosis by maintenance mechanism
Vomiting, nasogastric loss, and many diuretic states often produce chloride depletion and volume contraction. After the precipitant is addressed, chloride and potassium replacement can permit bicarbonate excretion. A low urine chloride supports a chloride-responsive pattern, but recent diuretic exposure can complicate interpretation.
Treat resistant alkalosis by cause
Mineralocorticoid excess, severe potassium depletion, and some renal disorders can sustain alkalosis despite chloride. Address the driver and potassium deficit. Acetazolamide can increase bicarbonate excretion in selected edematous patients, with monitoring for potassium loss and kidney effects. Acid infusion is a specialist rescue therapy, not routine care.
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Submodule
Respiratory Disorders and Integrated Cases
Respiratory acid-base disorders are ventilation disorders. Treatment protects gas exchange and reverses the trigger while the complete pattern is reassessed.
- Acute and chronic hypoventilation
- Hyperventilation and hypoxemia
- Ventilatory failure
- Medication and toxicologic causes
Treat respiratory acidosis by restoring ventilation
Opioids, sedatives, neuromuscular weakness, obstructive lung disease, airway disease, and ventilator problems can reduce alveolar ventilation. Support the airway, use targeted reversal when appropriate, treat bronchospasm or infection, and provide noninvasive or invasive ventilation when needed. Routine bicarbonate does not correct the ventilatory failure and can add carbon dioxide.
Treat respiratory alkalosis by finding the driver
Pain, anxiety, hypoxemia, sepsis, pregnancy, liver disease, salicylate toxicity, and inappropriate ventilator settings can cause hyperventilation. Exclude organic illness and correct the cause. Paper-bag rebreathing can worsen hypoxemia and is not recommended.
Recognize failing compensation
A patient with metabolic acidosis depends on increased ventilation to control pH. A PaCO₂ above Winter's range, falling mental status, fatigue, or reduced minute ventilation may signal impending respiratory failure. If intubation is required, the ventilator must initially support the high pre-intubation minute ventilation while definitive care proceeds.
Quick check
Module test
Check the connections.
Each attempt draws 10 questions from the complete 100 question bank.
Each attempt draws a fresh set and rearranges the answer choices.
References
Current clinical foundation.
Lecture material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.