Situation: A 28-year-old man weighing 64 kg undergoes elective open repair of an inguinal hernia under general anesthesia. Succinylcholine was given for intubation, and anesthesia is maintained with sevoflurane. Forty minutes after induction, the anesthesia provider diagnoses malignant hyperthermia and stops the sevoflurane. An arterial blood gas (ABG) is drawn, reporting the partial pressure of arterial carbon dioxide (PaCO2) and bicarbonate (HCO3−). Normal ranges: pH 7.35–7.45, PaCO2 35–45 mmHg, HCO3− 22–26 mEq/L. pH: 7.08 PaCO2: 66 mmHg HCO3−: 19 mEq/L Which conclusion should guide the team's next actions?

A high PaCO2 with a low HCO3− means respiratory and metabolic acidosis are present together. In malignant hyperthermia, hypermetabolic muscle produces excess carbon dioxide and lactic acid, so the crisis is still active: dantrolene is continued and repeated until signs resolve, along with hyperventilation and treatment of acidosis and hyperkalemia.

ABG interpretation The arterial blood gas shows a pH of 7.08, which is a severe acidemia. The PaCO2 of 66 mmHg is markedly elevated above the normal range of 35–45 mmHg, indicating a respiratory acidosis. At the same time, the HCO3− of 19 mEq/L is below the normal range of 22–26 mEq/L, which points to a coexisting metabolic acidosis. This combination of a high PaCO2 and a low bicarbonate is the key finding: the patient has a mixed respiratory and metabolic acidosis, not a simple respiratory acidosis with renal compensation.

Why this pattern fits malignant hyperthermia In malignant hyperthermia, the skeletal muscle enters a hypermetabolic state because calcium release from the sarcoplasmic reticulum becomes abnormally accelerated after exposure to triggering agents such as volatile anesthetics or succinylcholine ^[1]. The muscle cells burn through adenosine triphosphate at an extreme rate, which generates two major acid loads. First, excessive carbon dioxide is produced through aerobic metabolism and must be cleared by the lungs. When production overwhelms ventilation, the PaCO2 climbs, producing a respiratory acidosis. Second, when oxygen delivery cannot keep pace with the enormous metabolic demand, anaerobic metabolism takes over and lactic acid accumulates, producing a metabolic acidosis. Therefore, an elevated PaCO2 together with a falling bicarbonate in the setting of suspected malignant hyperthermia means the crisis is still active and both acid sources are present.

Why the other options are incorrect Option 1 is wrong because sevoflurane does not directly cause acidosis; it triggers the hypermetabolic response in susceptible individuals, and simply turning it off does not immediately stop the ongoing muscle breakdown and acid production. Option 2 is wrong because a low bicarbonate in this acute setting is not renal compensation. Renal compensation for respiratory acidosis takes hours to days and would produce an elevated bicarbonate, not a low one. A low bicarbonate here reflects metabolic acid accumulation, primarily lactic acid. Option 4 is wrong because ventilation alone cannot correct the metabolic component. Even aggressive hyperventilation will lower the PaCO2, but it will not remove the lactic acid or stop the underlying hypermetabolic process.

Clinical implications for the team The mixed acidosis confirms that the malignant hyperthermia episode is not yet controlled. The team should continue administering dantrolene, which inhibits calcium release from the sarcoplasmic reticulum and directly interrupts the hypermetabolic cycle ^[1]. Dosing is repeated until signs resolve, including normalization of PaCO2, correction of acidosis, and stabilization of temperature and heart rate. Hyperventilation with 100% oxygen is used to blow off carbon dioxide, but it is an adjunct, not the primary treatment. The metabolic acidosis may require sodium bicarbonate in severe cases, and hyperkalemia from muscle breakdown must be anticipated and treated because it can cause life-threatening arrhythmias ^[1]. Key point! A falling bicarbonate during an acute MH crisis is not compensation; it is evidence of ongoing lactic acidosis and indicates that dantrolene must be continued or repeated.

Connecting the ABG to the underlying mechanism The JSA guideline emphasizes that unexplained hypercarbia is one of the earliest signs of malignant hyperthermia ^[1]. In this patient, the PaCO2 of 66 mmHg is well above the threshold of 55 mmHg mentioned in the guideline for end-tidal carbon dioxide, and it occurred despite ongoing mechanical ventilation. This reflects the enormous carbon dioxide production from hypermetabolic muscle. The low bicarbonate of 19 mEq/L adds the metabolic component, which is consistent with lactic acid generation as the muscle shifts to anaerobic metabolism. Case reports have also described hypercapnia and mixed acidosis as prominent or even isolated early signs of malignant hyperthermia, reinforcing that ABG changes can signal the crisis before a dramatic temperature rise occurs . Watch out! Do not wait for a high temperature to diagnose malignant hyperthermia; hypercarbia and mixed acidosis may appear first, and early dantrolene administration is critical for survival .

ABG component	Finding	Interpretation in MH
pH	7.08	Severe acidemia from combined respiratory and metabolic acidosis
PaCO2	66 mmHg	Excess CO2 production from hypermetabolic muscle exceeds ventilatory clearance
HCO3−	19 mEq/L	Low bicarbonate reflects lactic acid buffering, not renal compensation

The ABG pattern therefore points to a single conclusion: the malignant hyperthermia crisis is still active, and the team must continue dantrolene while simultaneously supporting ventilation, correcting acidosis, and monitoring for hyperkalemia.