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Letters to Editor
Mind the gap!!: Reversal of The EtCO2 gradually came down up to 45 mm Hg. ABG
at this point showed pH: 7.252, PCO2: 53, PO2: 105.1,
arterial to end‑tidal CO2 gradient HCO3‑: 23, SO2: 99.6%. The patient was extubated after
reversal of neuromuscular blockade. Post‑operatively,
in thoracoscopic bronchogenic subcutaneous emphysema was present around the port
cyst excision sites and intercostal drain site.
The PaCO2 ‑ EtCO2 gradient is largely dependent on
Sir, the physiological dead space and the slope of the
alveolar plateau in phase 3 of the capnograph. An
End‑tidal CO2 (EtCO2) is used as a surrogate to assess increase in the dead space can result in an increase
adequacy of ventilation since it provides an estimate of in the gradient. Negative PaCO2 ‑ EtCO2 values were
the arterial CO2 (PaCO2). The PaCO2 is normally higher first observed during anaesthesia more than 50 years
than EtCO2 by 2‑5 mmHg. However, in conditions ago by Nunn and Hill. Reversal of the gradient can be
where there is ventilation‑perfusion mismatch, the seen normally in 50% of infants, pregnant, and obese
EtCO2 may not accurately reflect the PaCO2. Reversal of patients. Other causes are mechanical ventilation
the normally positive PaCO2‑EtCO2 gradient may occur with large tidal volumes and low frequency, increased
also termed as negative arterial to EtCO2 gradient. We cardiac output and CO2 production, low functional
encountered a similar situation in a 2 year old child residual capacity (FRC) and total lung compliance.[1]
weighing 10 kg posted for thoracoscopic excision of a Thoracoscopy involves CO2 insufflation in the thorax
left bronchogenic cyst. for better visualisation and access. If there is a
preexisting communication between the pleura and
The patient had a history of fever and cough on and the bronchial tree, there can be direct absorption of
off for 1 year. Computed tomography scan showed a CO2 and falsely high EtCO2 readings.[2] This can lead
31 mm × 28 mm × 38 mm fluid density lesion seen to negative PaCO2 ‑ EtCO2 gradient where PaCO2 may
in posterior mediastinum causing severe compression be only mildly elevated. There are reported cases
of the left main bronchus with resultant obstructive of negative arterial to end‑tidal gradient in cases of
emphysema. The air entry was diminished on the malignant hyperthermia (MH).[1,3] The PCO2 of most
left side. All other investigations were within normal alveolar gas is less than PaCO2, but in the terminal
limits. After premedication, anaesthesia was induced part of the expirate, the alveolar PCO2 may increase
with sevoflurane and injection Atracurium 0.6 mg/kg. rapidly towards mixed venous PCO2 and exceeds
Right endobronchial intubation was done with 4.5 mm PaCO2 in the presence of MH because a large amount
ID endotracheal tube (ETT). The absence of air entry on of CO2 is discharged into the lungs.[3] In our case,
the operative left side was confirmed by auscultation.
the reasons could be multiple, i.e., bronchopleural
The patient was given right lateral position and was
communication, and low FRC under anaesthesia. In
ventilated using pressure control mode achieving tidal
addition, the presence of subcutaneous emphysema
volume of 6 ml/kg. After CO2 insufflation in the thorax,
suggests extensive CO2 tracking and absorption
there was rise in the EtCO2 and the inspiratory pressure
contributing to the hypercarbia.[4] CO2 desufflation
requirement. EtCO2 reached up to 60 mmHg after
and resumption of two lung ventilation led to the
which we started manually ventilating the patient.
normalisation of EtCO2 without any deleterious effects.
However, EtCO2 continued to rise till 113–115 mm Hg.
Endotracheal suction was done to rule out the blockage In the event of severe intraoperative increase in the
of ETT. Air entry was present on the right side with EtCO2, we need to correlate the EtCO2 value with
no adventitious sounds. The oxygen saturation was PaCO2 value using an ABG. Rising EtCO2 may not
around 94%. An arterial blood gas (ABG) was sent always translate to rising PaCO2. Various causes of
which revealed pH: 7.298, PCO2: 45.6, PO2: 223, negative gradient should be ruled out.
HCO3‑: 21.8 and SO2: 96%. Thus, there was reversal
of PaCO2 ‑ EtCO2 gradient. Due to the rising EtCO2, Financial support and sponsorship
deroofing of the cyst was done instead of excision, Nil.
insufflation was stopped, and the patient was made
supine after closure of ports. The tube was withdrawn Conflicts of interest
into the trachea, and bilateral air entry was confirmed. There are no conflicts of interest.
Indian Journal of Anaesthesia | Volume 61 | Issue 2 | February 2017 181
Page no. 89
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Letters to Editor
Priyanka Pradeep Karnik, Ketan S Kulkarni, 4. Hudcova J, Schumann R. Arterial to end‑tidal CO2 laparoscopic
gradient reversal during pheochromocytoma resection. Can J
Nandini Malay Dave, Madhu Garasia Anaesth 2006;53:409‑12.
Department of Paediatric Anesthesiology, Seth G.S. Medical College,
KEM Hospital, Mumbai, Maharashtra, India This is an open access article distributed under the terms of the Creative
Commons Attribution‑NonCommercial‑ShareAlike 3.0 License, which allows
others to remix, tweak, and build upon the work non‑commercially, as long as the
Address for correspondence: author is credited and the new creations are licensed under the identical terms.
Dr. Priyanka Pradeep Karnik,
Department of Paediatric Anaesthesiology, Seth G.S. Medical Access this article online
College, KEM Hospital, Mumbai, Maharashtra, India. Quick response code
E‑mail: piyu_85007@yahoo.com Website:
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REFERENCES
1. Lin HT, Wang SC, Zuo Z, Tsou MY, Chan KH, Yuan HB. DOI:
Increased requirement for minute ventilation and negative 10.4103/0019-5049.199864
arterial to end‑tidal carbon dioxide gradient may indicate
malignant hyperthermia. J Chin Med Assoc 2014;77:209‑12.
2. Biles DT, Carroll GJ, Smith MV, Flynn RT. Elevated end‑tidal
How to cite this article: Karnik PP, Kulkarni KS, Dave NM,
carbon dioxide during thoracoscopy: An unusual cause.
Garasia M. Mind the gap!!: Reversal of arterial to end-tidal CO2
Anesthesiology 1994;80:953‑5.
gradient in thoracoscopic bronchogenic cyst excision. Indian J
3. Kwetny I, Finucane BT. Negative arterial to end‑tidal carbon
Anaesth 2017;61:181-2.
dioxide gradient: An additional sign of malignant hyperthermia
© 2017 Indian Journal of Anaesthesia | Published by Wolters Kluwer - Medknow
during desflurane anesthesia. Anesth Analg 2006;102:815‑7.
Anaesthetic and haemodynamic The patient was taken up for surgery within 4 h of
admission. Invasive blood pressure (BP) and central
management of Boerhaave’s venous pressure (CVP) monitoring were initiated, which
revealed a BP of 70/50 mm Hg and CVP of 4 mmHg.
syndrome Arterial blood gas (ABG) analysis revealed severe
hypoxia (PO2‑63 mmHg on FiO2 0.4) and severe metabolic
acidosis (pH 7.12) with elevated lactate (6.67 mmol/L)
Sir,
levels. The patient was receiving dopamine infusion
Boerhaave’s syndrome is a rare and lethal condition at 8 µ/kg/min. A combination of crystalloid (normal
involving complete transmural laceration of the saline 0.9% ‑ 0.5 L) and colloid resuscitation (Voluven™
oesophagus.[1] It can be difficult to diagnose because 6% ‑ 0.3 L) was performed, titrated to a CVP of 10 mmHg.
there are no classic symptoms, and the perforation Noradrenaline infusion was started at 0.05 µ/kg/min and
can masquerade many clinical conditions such as titrated to a target mean arterial pressure of 65 mmHg. He
acute myocardial infarction, tension pneumothorax[2] was administered intravenous piperacillin‑tazobactam,
or pneumoperitoneum. Literature reports a mortality metronidazole and voriconazole. After rapid sequence
of 100%, if untreated. We report this case to illustrate induction with etomidate 12 mg, midazolam 2 mg,
possible anaesthetic implications of this disease. fentanyl 150 µg and succinylcholine 100 mg, trachea was
intubated with a left‑sided (37 French) double‑lumen
A 52‑year‑old male, a known alcoholic presented to tube (DLT). Anaesthesia was maintained with
us with severe drowsiness, in a state of circulatory sevoflurane 1.5% and vecuronium. During one‑lung
shock, 15 h after the onset of projectile vomiting ventilation, we encountered difficulty in maintaining
and chest pain. On chest auscultation, left‑sided oxygen saturation (despite increasing FiO2 to 1.0 and
crepitations were present. Haemogram revealed positive end‑expiratory pressure to 8 cmH2O) and
haemoglobin of 9 g/dl and white blood cell count resumed two lung ventilation thrice. The serial ABGs,
of 11 × 109/L. Electrocardiogram was normal and central venous oxygen saturation (CvO2) and lactate
troponin T was negative. Chest X‑ray revealed levels were monitored [Table 1]. Thoracotomy revealed
left lung opacities, blunting of costophrenic angle a 3 cm longitudinal perforation in the distal oesophagus.
and pneumomediastinum [Figure 1]. Computed The perforation was sutured. A nasogastric tube was
tomography of chest confirmed oesophageal rupture, inserted, and the pleural cavity was lavaged with saline
as there was extravasation of contrast from the distal and the chest wall was closed in layers. A feeding
oesophagus into the mediastinum. jejunostomy was performed. Fluid management was
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