Module 3: Acid-Base Balance

Normal arterial pH range

7.35–7.45; small deviations profoundly affect enzymes, oxygen delivery, and organ function.

Buffer systems

Chemical buffers (bicarbonate, phosphate, proteins) that quickly resist pH changes.

Respiratory control of acid-base balance

Lungs regulate CO2 elimination; acts within minutes.

Renal control of acid-base balance

Kidneys regulate HCO3− retention/excretion and H+ excretion over hours to days.

Henderson–Hasselbalch equation

pH is determined by the ratio of bicarbonate to CO2 in the blood.

Primary controller of HCO3−

Kidneys regulate the bicarbonate concentration.

Primary controller of CO2

Lungs regulate carbon dioxide (CO2) elimination.

Arterial blood gas (ABG)

A test measuring pH, PaCO2, and HCO3− to assess acid-base status.

PaCO2

Partial pressure of CO2 in arterial blood; normal 35–45 mmHg; primary respiratory driver.

HCO3−

Bicarbonate; normal 22–26 mEq/L; primary metabolic driver.

pH

Measure of acidity; deviations define acidemia (

Acidemia

ABG pH below 7.35.

Alkalemia

ABG pH above 7.45.

Primary acid-base disorders

Disorders whose primary change drives the pH abnormality (respiratory or metabolic).

Compensation

The opposite system adjusts to move pH toward normal; can be respiratory or renal.

Uncompensated

Abnormal pH with a normal opposite parameter; no compensation yet.

Partially compensated

Abnormal pH with the opposite parameter also abnormal in the opposite direction.

Fully compensated

pH normal with abnormal opposite parameter; compensation complete.

Respiratory acidosis

pH

Metabolic acidosis

pH <7.35 due to HCO3− <22 mEq/L (loss of base or acid gain).

Respiratory alkalosis

pH >7.45 due to PaCO2 <35 mmHg (excess exhalation of CO2).

Metabolic alkalosis

pH >7.45 due to HCO3− >26 mEq/L (loss of acid or gain of base).

Acute respiratory acidosis

Abrupt onset with no time for renal compensation; pH falls quickly.

Chronic respiratory acidosis

Develops over days–weeks with renal compensation (↑HCO3−).

Acute respiratory alkalosis

Sudden hyperventilation with little time for metabolic compensation.

Chronic respiratory alkalosis

Prolonged hyperventilation with renal compensation (↑HCO3− loss).

Kussmaul respirations

Deep, rapid breathing often seen in metabolic acidosis as compensation.

ABG pattern: respiratory acidosis

Low pH with high PaCO2; HCO3− may be normal (acute) or elevated (chronic).

ABG pattern: metabolic acidosis

Low pH with low HCO3−; PaCO2 may be low if compensation is present.

ABG pattern: respiratory alkalosis

High pH with low PaCO2; HCO3− may be normal (acute) or low (chronic).

ABG pattern: metabolic alkalosis

High pH with high HCO3−; PaCO2 may be high if compensating.

Primary respiratory disorders management

Treat underlying cause (airway obstruction, ventilation support, CNS depression reversal).

Naloxone

Opioid reversal agent used to reverse respiratory depression.

Flumazenil

Benzodiazepine reversal agent; use with caution due to seizure risk.

Noninvasive ventilation

BiPAP; supports ventilation without intubation.

Trendelenburg position in respiratory distress

Not recommended; can worsen breathing and is generally avoided in acute respiratory failure.

Oxygen therapy target in CO2 retainers

Maintain SpO2 around 88–92% to avoid suppressing hypoxic drive.

Albuterol (SABA)

Bronchodilator used for acute bronchospasm and COPD/asthma; monitor for tremor and tachycardia.

Ipratropium

Anticholinergic bronchodilator; slower onset than SABA; dries mucous membranes.

Methylprednisolone

IV corticosteroid to reduce airway inflammation; monitor for hyperglycemia and infection.

Piperacillin–tazobactam

Broad-spectrum antibiotic used for pneumonia and sepsis-related infections.

Anion gap

Difference between measured cations and anions: Na+ + K+ − (Cl− + HCO3−); normal ≈ 8–12 mEq/L.

High anion gap etiologies

Conditions with added acids (e.g., DKA, lactic acidosis, toxins) causing an elevated gap.

MUDPILES

Mnemonic for common high anion gap causes: Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates.

Normal anion gap metabolic acidosis

Metabolic acidosis without an elevated anion gap; causes include bicarbonate loss or Renal tubular acidosis.

DKA management

Insulin and IV fluids to correct hyperglycemia and halt ketone production; monitor potassium.

Lactic acidosis

Metabolic acidosis from excess lactic acid production; seen in sepsis, shock, hypoperfusion.

Diarrhea effect on acid-base

Loss of bicarbonate causing metabolic acidosis.

Gastric acid loss effect on acid-base

Vomiting/NG suction causing metabolic alkalosis.

Chronic loop diuretics effect on acid-base

Can cause metabolic alkalosis via loss of H+ and K+.

Potassium in acid-base disorders

Potassium shifts (hypo/hyperkalemia) influence acid-base balance and cardiac risk.

Hypokalemia in metabolic alkalosis

Common electrolyte disturbance that accompanies metabolic alkalosis.

Sodium bicarbonate therapy in metabolic acidosis

IV bicarb reserved for severe acidosis (pH < 7.1) or specific poisonings.

Insulin in DKA

Insulin therapy halts ketogenesis and lowers glucose; requires potassium monitoring.

Dialysis in metabolic acidosis

Renal replacement therapy for severe CKD/AKI with acidosis when kidneys fail.

BiPAP indications

Noninvasive ventilation used in acute respiratory failure when appropriate.

Naloxone administration risks

May cause withdrawal or rebound symptoms; monitor after reversal.

Hyperventilation causes

Anxiety, pain, fever, hypoxemia, CNS stimulation, PE, high altitude.

Respiratory compensation for metabolic acidosis

Hyperventilation lowers PaCO2 to raise pH toward normal.

Renal compensation for respiratory acidosis

Kidneys retain HCO3− to raise pH toward normal.

Renal compensation for respiratory alkalosis

Kidneys excrete HCO3− to lower pH toward normal.

Respiratory compensation for metabolic alkalosis

Hypoventilation to retain CO2 and raise acidity toward normal.

Sodium bicarbonate risk in alkalosis

Can worsen alkalosis or cause volume and electrolyte disturbances.

Acid-base balance in COPD

Chronic CO2 retainers require cautious oxygen therapy to avoid CO2 narcosis.

Metabolic acidosis ABG hallmark

Low pH with low HCO3−; PaCO2 may be low if compensated.

Metabolic alkalosis ABG hallmark

High pH with high HCO3−; PaCO2 may be high if compensating.

Respiratory acidosis ABG hallmark

Low pH with high PaCO2; HCO3− may be normal or elevated in compensation.

Metabolic acidosis key interventions

Treat underlying cause (DKA, diarrhea, CKD) and monitor electrolytes.

Respiratory alkalosis key interventions

Treat underlying cause (anxiety, pain, hypoxemia) and manage breathing.

COPD patient oxygen target

Aim for SpO2 88–92% to avoid suppressing hypoxic drive while maintaining oxygenation.

ABG stepwise interpretation order

1) Determine acidemia/alkalemia by pH; 2) Identify primary driver (PaCO2 vs HCO3−); 3) Assess compensation (opposite parameter).

Acid–base disturbance vs compensation

Disturbance is primary process; compensation is the secondary adjustment to normalize pH.

Systemic targets in respiratory acidosis

Treat obstruction, ventilation support, and reverse CNS depression when present.

Systemic targets in respiratory alkalosis

Identify and treat triggers like anxiety, hypoxemia, fever; adjust ventilation if needed.

Compensation never overcorrects

pH will not swing past normal solely due to compensation.

Normal ABG reference range tooltip

pH 7.35–7.45; PaCO2 35–45 mmHg; HCO3− 22–26 mEq/L.