Anesth Analg 2006;102:815-817
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000196515.06945.fb
ANESTHETIC PHARMACOLOGY
Negative Arterial to End-Tidal Carbon Dioxide Gradient: An Additional Sign of Malignant Hyperthermia During Desflurane Anesthesia
Igor Kwetny, MD, DEAA, and
Brendan T. Finucane, MB, BCh, FRCPC
Department of Anesthesiology and Pain Medicine, University of Alberta, Edmonton, Canada
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Abstract
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Widespread use of desflurane anesthesia has changed the clinical presentation of malignant hyperthermia (MH). Delayed onset of MH symptoms has been reported previously. A negative gradient between arterial to end-tidal CO2 ([a-ET]Pco2) was observed during anesthesia in pregnant patients and infants and has been associated with increased CO2 production, increased cardiac output, reduced functional residual capacity, and low lung compliance. The same conditions exist in cases of MH crisis. We describe an unusual case of MH in which a negative value of (a-ET) Pco2 gradient has been used as diagnostic and monitoring tool.
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Introduction
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Widespread use of desflurane anesthesia has changed the clinical presentation of malignant hyperthermia (MH). Delayed onset of MH symptoms has been previously reported (1–3). We present a unique case in which negative arterial to end-tidal CO2 gradient ([a-ET] Pco2) was used as a diagnostic and monitoring tool during MH crisis.
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Case Report
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A 43-yr-old man, weighing 105 kg, ASA physical status I, was scheduled for excision of an acoustic neuroma via the translabyrinthal approach. The patient had no previous exposure to general anesthetics. There was no known family history of MH or myopathies. He had no known allergies and was not taking any medications. Anesthesia was induced with fentanyl (2 µg/kg), propofol (2 mg/kg), 5 mg of rocuronium (defasciculating dose), and succinylcholine (100 mg), and anesthesia was maintained with 1 minimum alveolar anesthetic concentration of desflurane. After an uneventful endotracheal intubation, controlled ventilation was initiated with an air/oxygen mixture (fraction of inspired oxygen = 0.4) with the minute ventilation set at 8 L/min. In addition to standard monitoring, an arterial catheter (radial artery), a Foley catheter, and rectal temperature probe were inserted. A forced air warmer blanket (Bair Hugger, Arizant Healthcare, Eden Prairie, MN) was used to maintain normothermia.
Repeated boluses of morphine (7.5 mg) were administrated up to a total dose 0.3 mg/kg. Labetalol 10 mg was given 45 min after the anesthetic induction to maintain the systolic blood pressure <100 mm Hg. Dexamethasone 12 mg and mannitol 0.25 mg/kg were administrated 60 min and 120 min after the induction, respectively, at the surgeon's request.
Two and one-half hours after the induction, an arterial blood gas (ABG) revealed an increase in the concentration of lactic acid (5 mmol/L) and a negative (a-ET) Pco2 gradient (–0.7 mm Hg) (Table 1). There were no other signs of a hypermetabolic state at this time. The capnograph was recalibrated, and another ABG sample was drawn 200 min after the anesthetic induction, which revealed a further increase in lactic acid to 5.4 mmol/L. The (a-A) gradient for CO2 remained negative, and a mild metabolic acidosis was noted (Table 1). It was also noted that his heart rate had increased to 90 bpm, and his rectal temperature had increased from 36.6°C to 37.3°C within a 30-min period. A hypermetabolic state was suspected, and after the temperature had increased to 37.5°C, the warming blanket was turned off, and the tidal volume and minute ventilation were increased to 12 mL/kg and 17 L/min, respectively. A gradual increase in airway pressure was also noted at this time. The anesthesia tubing and valves were checked, and there was no rebreathing or airway obstruction. Approximately 300 min after the anesthetic induction, the patient's hemodynamics began to deteriorate. His heart rate increased to 120 bpm, systolic blood pressure decreased to 70 mm Hg, and body temperature continued to increase at rate of 0.1°C every 5 min up to maximum 39.9°C. Subsequent ABGs revealed a mixed metabolic and respiratory acidosis, and the lactic acid level increased to 7.4 mmol/L, and the negative (a-A) gradient for CO2 become more significant (Table 1). There was no other obvious reason for the hypermetabolic state, and MH was diagnosed by exclusion. The desflurane was turned off, and anesthesia was maintained with propofol 160 µg · kg–1 · min–1 by infusion. Dantrolene was administrated (2.4 mg/kg), and the patient rapidly improved. Cold saline IV and bicarbonate 0.5 mEq/kg were also administrated. Thirty minutes after the dantrolene administration, the ABG analysis showed a rapid improvement in the metabolic acidosis, a decrease in ETco2, and lactic acidosis, and the negative (a-ET) gradient for CO2 returned to the initial value (Table 1).
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Table 1. Intraoperative Laboratory Variables at Different Time Points: Potassium (K), pH, End-Tidal CO2 (ETco2), Paco2, (a-ET)CO2 Gradient, Lactate, and Temperature
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Upon completion of the surgery, the patient was tracheally extubated and transferred to the intensive care unit, where close monitoring continued for 36 h. There were no further signs of MH, and no additional dantrolene was given. The patient experienced muscle pains in the legs and back for 3 days after the surgery. Laboratory studies taken after surgery showed a hyperkalemia (6.4 mmol/L), and the creatine phosphokinase level was 1613 U/L. The patient's postoperative course was uneventful. The patient and family were informed and they were advised to wear a Medic Alert bracelet. The patient refused a muscle biopsy test.
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Discussion
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There are several interesting aspects in this case. First, this case supports previously published clinical observations that desflurane causes a slower clinical onset of MH than halothane (1–3). Kunst et al. (2) found that desflurane induced only a small calcium release in comparison to that observed with sevoflurane in vitro. Administration of succinylcholine was associated with a more rapid onset of MH with desflurane anesthesia and was more likely to produce masseter muscle rigidity (1). It is unlikely that succinylcholine was a major trigger in this case because of the absence of muscle rigidity and mild muscle breakdown.
Second, MH crises are usually associated with a profound lactic acidosis, which occurs as a part of metabolic stimulation (4). In our case, large levels of lactic acid were observed in arterial blood at an early subclinical stage of MH, before metabolic acidosis occurred. This abnormality allowed us to be suspicious of MH during an otherwise uneventful period of anesthesia. Measurement of lactic acid in arterial blood could be recommended as an early diagnostic and monitoring tool in patients suspected of MH.
Finally, this is the first published report describing a negative (a-ET) Pco2 gradient during an episode of MH. Negative (a-ET) Pco2 values were observed during anesthesia more than 40 years ago (5). A negative gradient was found in 12% of normal subjects during anesthesia and mechanical ventilation with large tidal volumes and low frequencies (6). This phenomenon was described during anesthesia in 50% of pregnant patients and 50% of infants (7–9). Several mechanisms have been postulated to explain the observed (a-ET) Pco2 differences during anesthesia. This includes an increased cardiac output and CO2 production, low total lung compliance, and reduced functional residual capacity. Patients who have experienced an MH episode have many of the features described above. During expiration, the alveolar Pco2 may increase toward that of mixed venous Pco2 more rapidly in the presence of MH because a larger amount of CO2 is discharged into the lung, which becomes smaller as expiration continues. The Pco2 of most alveolar gas is less than that in arterial blood. In the terminal part of the expirate, alveolar Pco2 increases rapidly and may exceed Paco2. This effect makes the Phase III slope of the capnogram steeper and increases the likelihood of sampling end-tidal Pco2 more than arterial Paco2 (10).
The probable reason for the negative baseline gradient in this case was obesity (body mass index, 30.7). During the MH episode, the negative gradient increased up to maximum of –12 mm Hg. The rapid decrease to baseline value after dantrolene infusion supports the assumption that dynamic changes of (a-ET) Pco2 difference could be useful as a diagnostic and monitoring tool in cases of suspected MH. The patient refused to have a muscle biopsy test; therefore, we have graded the patient's clinical findings according to a clinical grading scale (11) and found the likelihood of MH as "almost certain" (51 points).
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Footnotes
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Accepted for publication October 19, 2005.
Corresponding author: Dr Igor Kwetny, Department of Anesthesiology and Pain Medicine, University of Alberta, Clinical Sciences Building, Room 8-120, Edmonton, Alberta T6G 2G3, (780) 407-8861, Fax: (780) 487-7754: ikwetny{at}hotmail.com
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References
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- Allen GC, Brubaker CL. Human malignant hyperthermia associated with desflurane anesthesia. Anesth Analg 1998;86:1328–31.[Web of Science][Medline]
- Kunst G, Stucke AG, Graf BM, et al. Desflurane induces only minor Ca++ release from the sarcoplasmatic reticulum of mammalian skeletal muscle. Anesthesiology 2000;93:832–6.[Web of Science][Medline]
- Hoenemann CW, Halene-Holtgraeve TB, Booke M, et al. Delayed onset of malignant hyperthermia in desflurane anesthesia. Anesth Analg 2003;96:165–7.[Abstract/Free Full Text]
- Hopkins PM. Malignant hyperthermia: advances in clinical management and diagnosis. Br J Anaesth 2000;85:118–28.[Free Full Text]
- Nunn JF, Hill DW. Respiratory dead space and arterial to end-tidal CO2 tension difference in anaesthetized man. J Appl Physiol 1960;15:383–9.[Abstract/Free Full Text]
- Fletcher R, Jonson B. Deadspace and the single breath test for carbon dioxide during anaesthesia and artificial ventilation. Br J Anaesth 1984;56:109–19.[Abstract/Free Full Text]
- Shankar KB, Moseley H, Kumar Y. Negative arterial to end-tidal gradients. Can J Anaesth 1991;38:260–1.[Web of Science][Medline]
- Shankar KB, Moseley H, Kumar Y, Vemula V. Arterial to end-tidal carbon dioxide tension difference during caesarean section anaesthesia. Anaesthesia 1986;41:698–702.[Web of Science][Medline]
- Rich GF, Sconzo JM. Continuous end-tidal CO2 difference sampling within proximal endotracheal tube estimates arterial CO2 tension in infants. Can J Anaesth 1991;38:201–3.[Web of Science][Medline]
- Bhavani-Shankar K, Moseley H, Kumar AY, Delph Y. Capnometry and anaesthesia. Can J Anaesth 1992;39:617–32.[Web of Science][Medline]
- Larach MG, Localio AR, Allen GC, et al. A clinical grading scale to predict malignant hyperthermia susceptibility. Anesthesiology 1994;80:771–9.[Web of Science][Medline]
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Abstract
Introduction
