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normal panel
pH | pCO2 | pO2 | HCO3
7.35 - 7.45 | 35 - 45 | 80 - 100 | 22 - 26
respiratory acidosis
pH
PaCO2
pH < 7.35
PaCO2 > 45 mmHg
causes of respiratory acidosis (5)
central hypoventilation
sedatives, opioids, anesthetics, CNS injury
neuromuscular disorders
MG, Guillan-Barre Syndrome
pulmonary diseases
COPD, asthma, pneumonia, pulmonary edema
chest/pleural restriction
ventilatory hypoventilation
respiratory acidosis: clinical presentation (6)
altered mental status, confusion, seizures, coma
neurological damage and symptoms similar to stroke/CNS mass
cerebral vasodilation → increased intracranial pressure → HA, etc
blunted respiratory drive
can ↑ CO and pulmonary pressure in mild/mod (PaCO2 50 -55)
↓ contractility and CO in severe/prolonged (PaCO2 > 80)
respiratory acidosis: effects (3)
increased CO2 retention
compensation by HCO3 reabsorption
every 10 mmHg ↑ pCO2 above 40 mmHg, HCO3 ↑ ~1 mEq/L [acute]
every 10 mmHg ↑ pCO2 above 40 mmHg, HCO3 ↑ ~4 mEq/L [chronic]
increased K+ from extracellular shift
H+ shifts inward to compensate for increased acidity — Hyperkalemia
acute respiratory acidosis treatment
restore oxygenation and ventilation
might need mechanical ventilation
treat underlying cause
acute respiratory acidosis treatment: treat underlying cause
bronchospasm
sedation
infections
bicarbonate
bronchospasm → bronchodilators
sedation → naloxone/flumazenil (seizure risk)
infections → antibiotics
bicarbonate → avoid overcorrection of it (may suppress respiratory drive)
chronic respiratory acidosis treatment
treat underlying causes (of hypoventilation)
do not treat chronic compensation unless acute exacerbation occurs
titrate O2 to SpO2 88 - 92% (excess O2 worsens V/Q mismatch → ↑ PaCO2
respiratory alkalosis
pH
PaCO2
pH > 7.45
PaCO2 < 35 mmHg
respiratory alkalosis: causes (5)
central hyperventilation
anxiety, pain, fever, sepsis, pregnancy, stroke, trauma)
drug-induced
salicylates, progesterone, catecholamine, nicotine, theophyline)
hypoexemia or tissue hypoxia
mechanical ventilation too fast
liver failure or CNS disorders
respiratory alkalosis: clinical presentation
usually asymptomatic
lightheadedness, confusion, syncope, seizures
decreased cerebral blood flow
↑ catecholamine sensitivity → arrhythmias
n/v due to cerebral hypoxia/alkalemia
respiratory alkalosis: effects (3)
increased CO2 loss
compensation by increased HCO3 excretion
every 10 mmHg ↓, pCO2 below 40 mmHg, HCO3 ↓ ~ 2 mEq/L [acute]
every 10 mmHg ↓, pCO2 below 40 mmHg, HCO3 ↓ ~ 4 - 5 mEq/L [chronic]
decreased HCO3 (excretion) and K+ (inward shift)
H+ shifts outwards to compensate for lack of acid in circulation — Hypokalemia
acute respiratory alkalosis: treatment
pH > 7.5
focus on cause of hyperventilation
O2 tx for hypoxemia
rebreathing for anxiety/stress-induced hyperventilation
mechanical ventilation, sedation, paralysis (if severe) - arrhythmias/seizures
in ventilated pts, reduce set respiratory rate or tidal volume to correct iatrogenic alkalosis
chronic respiratory alkalosis: treatment
pH ≤ 7.5
treat underlying cause
mild, asymptomatic → tx unnecessary
mixed acid-base disorders: diagnostic approach
pH levels
primary cause (metabolic or respiratory)
determine expected compensation
compare expected to observed compensation
compensation NOT at expected level → likely a mixed disorder
if metabolic acidosis → calculate AG
mixed-acid base disorders occur —
when 2+ primary acid-base disturbances are present at the same time
mixed-acid base disorders: clues
pH or HCO3 or PaCO2 not in expected compensatory range
clinical hx suggests > 1 process
compensation equations

compensation should be — of expected calculation for metabolic disorders
within 2
if compensation of PaCO2 < expected, then respiratory alkalosis (not enough CO2
if compensation of PaCO2 > expected, then respiratory acidosis (too much CO2
mixed metabolic acidosis and respiratory acidosis
MOA
overall
clinical scenarios
management
MOA
concurrent accumulation of acid
Failure of compensation d/t limiting corrective responses
Respiratory acidosis prevents expected ↓ PaCO₂
Metabolic acidosis prevents renal buffering (↑ HCO₃⁻)
overall
decreased pH
clinical scenarios
Cardiorespiratory arrest
Chronic lung disease + shock/sepsis
Metabolic acidosis + respiratory failure
management
treat BOTH concurrently
→ oxygen delivery/ventilation
→ correct acidosis with alkali if SEVERE
mixed metabolic alkalosis and respiratory alkalosis
MOA
overall
clinical scenarios
management
MOA
Concurrent loss of acid and retention of base
Respiratory alkalosis prevents compensatory ↑ PaCO₂
Metabolic alkalosis prevents renal excretion of HCO₃⁻
overall
increased pH
clinical scenarios
ICU or post-op patients on mechanical ventilation, sepsis, pain, CNS injury, or medications
Vomiting, nasogastric suctioning, or massive blood transfusions
Cirrhosis or chronic respiratory acidosis patients over-ventilated or on diuretics
management
treat BOTH simultaneously
→ Adjust ventilator or correct cause of hyperventilation
→ Replace NaCl and KCl to correct metabolic alkalosis
mixed metabolic acidosis and respiratory alkalosis
MOA
overall
clinical scenarios
management
MOA
↓ HCO₃⁻ + excessive ↓CO₂
Respiratory alkalosis lowers PaCO₂
Metabolic acidosis decreases HCO₃⁻
overall
pH appears overall normal
clinical scenarios
Advanced liver disease or sepsis
Salicylate intoxication
Pulmonary–renal syndromes or hypoxemia
management
Identify and treat the underlying cause
Support oxygenation and ventilation as needed
Avoid overcorrection
mixed metabolic alkalosis and respiratory acidosis
MOA
overall
clinical scenarios
management
MOA
Concurrent HCO₃⁻ retention and CO₂ retention
Metabolic alkalosis ↑ HCO₃⁻, blunting respiratory drive
Respiratory acidosis ↑ PaCO₂, worsening alkalosis compensation
overall
pH may appear near normal
clinical scenarios
COPD or chronic respiratory acidosis on diuretics or salt restriction
Glucocorticoid therapy
Chronic heart failure with volume depletion
management
→ Discontinue diuretics if possible
→ Administer NaCl and KCl to enhance bicarbonate excretion
→ Use cautiously in heart failure to avoid fluid overload