Severe intraoperative hypercarbia undetected by continuous end-tidal CO2 monitoring in a chronic smoker undergoing one-lung ventilation

Shagun Bhatia Shah; Binod Kumar Naithani; Vani Bhageria; Ajay Kumar Bhargava

doi:10.4103/0973-0311.183580

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CASE REPORT

Year : 2016 \| Volume : 17 \| Issue : 1 \| Page : 21-24

Severe intraoperative hypercarbia undetected by continuous end-tidal CO₂ monitoring in a chronic smoker undergoing one-lung ventilation

Shagun Bhatia Shah, Binod Kumar Naithani, Vani Bhageria, Ajay Kumar Bhargava
Rajiv Gandhi Cancer Institute and Research Centre, New Delhi, India

Date of Submission	15-Nov-2015
Date of Acceptance	21-Mar-2016
Date of Web Publication	17-Jun-2016

Correspondence Address:
Shagun Bhatia Shah
H. No. 174-175, Ground Floor, Pocket-17, Sector-24, Rohini, New Delhi - 110 085
India

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/0973-0311.183580

Abstract

One-lung ventilation is known to alter the physiology and result in a discrepancy between end-tidal CO₂ (ETCO₂) and arterial blood CO₂partial pressure despite protective mechanisms like hypoxic pulmonary vasoconstriction. Shunts in an emphysematous patient, lateral positioning and capnothorax may aggravate the discrepancy. We present here an incredible discrepancy of 40 mmHg which led us to question the very utility of ETCO₂monitoring in this subset of patients and consider alternative techniques.

Keywords: Capnothorax, end tidal-arterial blood CO₂gradient, lateral position, one-lung ventilation

How to cite this article:
Shah SB, Naithani BK, Bhageria V, Bhargava AK. Severe intraoperative hypercarbia undetected by continuous end-tidal CO₂ monitoring in a chronic smoker undergoing one-lung ventilation. Indian Anaesth Forum 2016;17:21-4

How to cite this URL:
Shah SB, Naithani BK, Bhageria V, Bhargava AK. Severe intraoperative hypercarbia undetected by continuous end-tidal CO₂ monitoring in a chronic smoker undergoing one-lung ventilation. Indian Anaesth Forum [serial online] 2016 [cited 2023 Jun 1];17:21-4. Available from: http://www.theiaforum.org/text.asp?2016/17/1/21/183580

Introduction

In addition to one-lung ventilation (OLV), capnothorax (for facilitating surgical exposure) places video-assisted thoracoscopic surgery (VATS) patients at a higher risk of hypercarbia than those undergoing open surgery. Increased partial pressure CO₂ (PaCO₂) from systemic absorption of the insufflated CO₂, combined with decrease in tidal volume and minute ventilation during OLV makes precise and uninterrupted monitoring of PaCO₂ vital during minimal access surgery. As per various studies undertaken, so far, the end-tidal (ET)-PaCO₂ difference during two-lung ventilation (TLV) in healthy patients with normal ventilation-perfusion matching, is between 2 mmHg and 5 mmHg and during OLV the difference increases to 5–8 mmHg.^[1],[2] A difference as large as 40 mmHg, as in our patient, has not been reported till date.

Case Report

Ours was a 69-year-old, 61 kg, 169 cm tall male reformed smoker with a smoking history of 50 pack years. He was scheduled for VATS left lower lobectomy and mediastinal lymph node dissection for bronchogenic carcinoma (5 cm × 4 cm adherent to parietal pleura). Intravenous hydrocortisone 100 mg, dexamethasone 8 mg, deriphylline and salbutamol puffs were given to optimize the patient. His arterial oxygen saturation as displayed on the pulse oximeter was 100% on room air and his preoperative arterial blood gas (ABG) immediately after arterial line placement (Ph-7.34; PCO₂ 49.1 mmHg; PO₂ 99 mmHg; Na ⁺ - 139 meq/l; K - 4.5 meq/l Ca - 1.24 meq/l Cl - 106 mg% HCO₃-25.5 meq/l; Lactate - 1.5 mg%) was borderline normal. A thoracic epidural catheter (T-11-12 interspace), left radial artery cannula, and central venous pressure (CVP) line were aseptically placed. After induction of anesthesia (with fentanyl 100 μg, propofol 70 mg and atracurium 50 mg) a left sided Robertshaw double lumen tube (DLT) 39F (Mallencrodt) was introduced into the left main bronchus and fixed at 29 cm after capnographic confirmation of tracheal intubation and fibreoptic bronchoscopic confirmation of lung isolation. The first ETCO₂ recorded by us immediately after intubation was 35 mmHg. The capnographic waveform was normal in shape. The right lung was ventilated via the tracheal lumen of the DLT while the bronchial lumen was clamped and continuous positive airway pressure of 5 mmHg applied to the left lung. An ETCO₂ of 32 mmHg was obtained by adjusting the ventilator parameters. The patient was placed in right lateral position and port placed at midaxillary line in 8^th intercostal space (ICS). The invasive systolic blood pressure was 85–90 mmHg, heart rate 88–98/min, CVP 8–9 mmHg and hourly urine output was 25–35 m throughout surgery. 10 ml of 0.125% epidural bupivacaine was given titrated to Invasive Blood Pressure. Anesthesia was maintained with a BIS-guided propofol (60–80 mg/h) infusion, 100% oxygen and PNS guided atracurium infusion during OLV. The tidal volume delivered was 400–450 ml (7–8 ml/kg body weight) during TLV and 300–350 ml (5–6 ml/kg) during OLV. Respiratory rate was 10–12/min during TLV and 13–14/min during OLV adjusted to maintain a P-ETCO₂ between 32 mmHg and 35 mmHg. The FiO₂ was 100% during OLV and the inspiratory: Expiratory ratio of 1:2 was maintained. An ABG sample taken an hour after onset of OLV showed a PaCO₂ of 70.9 mmHg while the ETCO₂ at this point was 30 mmHg (PH - 7.2; PO₂-333 mmHg; Na - 134 meq/l; potassium - 4.5 meq/l; calcium - 1.2 mmol/l; chloride - 108, bicarbonate - 27.2 and lactate 1.2 mmol/l). Causes of intraoperative hypercarbia, including hypoventilation, soda lime depletion and malignant hyperpyrexia were excluded. Proper DLT positioning was reconfirmed fibrotic bronchoscopically. The ABG analyzer unit was calibrated in the morning (4 h earlier) but since the discrepency between ETCO₂ and PaCO₂ was abnormally large, initially we suspected a calibration problem. Therefore, we took a repeat sample and divided it into two heparinized syringes. Both samples were simultaneously analysed by two different machines. First sample by the same machine (RadioMeter ABL800 BASIC) after re-calibration and the second sample by another ABG analyzer placed in the medical Intensive Care Unit. The results were still the same. The large gradient between the ETCO₂ and PaCO₂ persisted. A repeat sample taken after increasing tidal volume and respiratory rate and replacing the D-fend and ETCO₂ sampling line showed a PaCO₂ of 65 mmHg (pH - 7.264) at a corresponding ETCO₂ of 28 mmHg. The surgery lasted 6 h with duration of OLV being 5 h. Blood loss was 400 ml and 1 unit blood, and 700 ml of plasmalyte (physiological crystalloid) was transfused. A 32F ICD was placed via port incision in 8^th ICS. Toward the end of surgery, on TLV with air oxygen mixture of (60:40), the DLT was replaced with a single lumen tube (the PaCO₂ at this point was 60 mmHg while the corresponding ETCO₂ was 28 mmHg). The patient electively ventilated for 6 h before extubation over a bougie. The ETCO₂ was 27 mmHg while the PaCO₂ was 51 mmHg, according to an ABG sample taken 2 min before extubation.

Discussion

Normal, healthy lungs display a good match of alveolar ventilation and pulmonary capillary perfusion resulting in an ETCO₂ that closely correlates with the PaCO₂ (the gradient being 2–5 mmHg with ETCO₂ being the lower of the two).^[3] A difference exceeding 2–5 mmHg indicates that CO₂ removal by ventilation is not keeping pace with CO₂ production by metabolism or capnothorax/capnoperitoneum. Increased dead space ventilation (lung are ventilated, but not perfused) occurs in pulmonary embolism or decreased cardiac output. Shunted perfusion (lung are perfused but not ventilated) as in alveolar collapse, bronchial intubation, OLV,^[4] increased bronchoalveolar secretions causing mucus plugging/atelectasis cause ventilation perfusion mismatch. Whitesell et al. demonstrated that patients with underlying lung disease had a significantly greater ETCO₂ to PaCO₂ gradient when compared with patients with normal baseline pulmonary function (3.3 ± 0.6 mmHg vs. 0.8 ± 0.3 mmHg).^[5] Age, increased apparatus deadspace, lateral positioning and sampling errors can also widen the PaCO₂ gradient. With patients undergoing renal surgery, Pansard et al. reported that the ETCO₂ to PaCO₂ difference was 4.8 ± 3.9 mmHg 10 min after induction and increased to 7.9 ± 3.5 mmHg, 5 min after placement of the patients into the lateral decubitus “kidney rest” position.^[6]

The capnography unit used by us during the case is an integral part of the Drager Primus Worksatation's multiparameter monitor Infinity C700 (side stream type). The baseline or the inspiratory phase of our patient's capnogram was at 0 mmHg indicating that there was no rebreathing. The expiratory plateau showed a gentle upward slope which was barely discernable and the alpha angle was mildly obtuse 95°. This ruled out obstruction due to endotracheal tube (ETT) kinking, secretions or bronchospasm. The capnographic waveform was normal in shape. The degree of airway obstruction was not as much as that expected in a chronic obstructive pulmonary disease patient as our patient had been adequately optimized with bronchodilators and steroids preoperatively. Intra operative in-line duolin (salbutamol sulphate 2.5 mg + ipratropium bromide 500 mcg in 2.5 ml saline) nebulization was also given before OLV commenced. The tidal volume delivered was 300–350 ml (5–6 ml/kg) during OLV to avoid volutrauma and barotrauma to the single lung being ventilated.

Hypercarbia induces catecholamine release resulting in tachycardia, increased cardiac contractility and reduction in diastolic filling. This may derange myocardial oxygen supply to demand ratio with greater risk of myocardial ischemia. An anesthetized patient may develop tachycardia, arrhythmias,^[7] excessive sweating, hypertension and peripheral vasodilatation which may result in excessive intraoperative blood loss. Berner reported hemodynamic changes, pupillary dilatation, hyperkalemia and severe respiratory acidosis.^[8] Neural and respiratory effects of hypercarbia are masked by anesthesia and mechanical ventilation while the cardiovascular consequences are erroneously attributed to lighter planes/inadequate anesthesia. During OLV, our patient had a heart rate of 88–98 beats per minute despite opioids (240 μg fentanyl and 7.5 mg morphine) and adequate intravenous fluid balance (monitored by CVP and urine output) and occasional extrasystoles started appearing. The BIS values were between 40 and 45 even though the propofol infusion rate was just 60–80 mg/h and sevoflurane was turned off during OLV. We attribute this to hypercarbia. Blood pressure did not rise owing to an already low baseline normal and also due to the effect of epidural 0.125% bupivacaine. Hypercarbia results in delayed emergence from anesthesia. Differential diagnosis of delayed emergence can be classified into one of three causes firstly, drug effects (residual anesthetics; excess opioids; incomplete reversal; hepatic/renal failure); second, metabolic disorders (hypercarbia, hypoxemia, acidosis, hypo/hyperglycemia, hyponatremia, hypo/hyperthermia); and third, neurologic disorders (seizures, raised intracranial pressure, cerebral hemorrhage, preexisting obtundation etc). Since our patient displayed no other cause of delayed emergence except hypercarbia, we attributed the delayed recovery to hypercarbia by principle of exclusion.

During OLV, the bronchus of the lung to be operated is occluded by a bronchial blocker or isolated by a DLT, with oxygenation and ventilation supported by the nonoperative lung. Even with effective hypoxic pulmonary vasoconstriction, OLV causes an increase in the shunt fraction and perfusion of the nonventilated lung. Ip Yam et al.^[4] measured the arterial to ET-PCO₂ difference (PaCO₂-PETCO₂) in 22 patients undergoing lung resection in the lateral thoracotomy position during TLV and OLV. They subtracted the initial PaCO₂-PETCO₂ from successive values measured at 10-min intervals and found that PaCO₂-PETCO₂ values during TLV (1.3 ± 0.6 kPa) and OLV (1.2 ± 0.7 kPa) were similar in the same patient (1 kPa = 7.5 mmHg). The mean of 133 pairs of measurements with OLV was 1.1 kPa and even after correction, mean (PaCO₂-PETCO₂) varied in the range −0.7–0.8 kPa; individual extreme values were from −1.3–1.7 kPa. Interpatient variation was found to be greater than intrapatient for both net and corrected differences. Calculating a corrected difference nevertheless reduced interpatient variation from a mean square value of 2.44–0.61.

This wide variation in (PaCO₂-PETCO₂) suggests that the accuracy ETCO₂ as a surrogate for PaCO₂, although improved by the use of a corrected difference, is questionable during OLV. The arithmetic sum of normal gradient (2–5 mmHg), contributions by lateral positioning (3 mmHg), capnothorax (variable), underlying lung disease (3 mmHg) and OLV (8–10 mmHg) amounts to approximately 20 mmHg and not 40 mmHg which we witnessed. It appears that all these factors have a synergistic and not just additive effect which leads us to recommend another measure such as transcutaneous CO₂(TCCO₂) to monitor PaCO₂ especially in chronic smokers during OLV in VATS. The transcutaneous monitor measures the CO₂ that is produced by local tissue metabolism and the CO₂ released from the blood as it flows through the capillaries near the skin surface. The latter is in direct equilibrium with the capillary CO₂ which is in equilibrium with the arterial CO₂. Unlike ETCO₂, which typically underestimates actual CO₂, the transcutaneous method characteristically overestimates actual CO₂ by 5.2–6.4 mmHg due to the increased CO₂ production from local metabolism induced by heating to 42°C (working temperature).^{[9],[10],[11],[12]} The currently available TCCO₂ devices have an internal correction/calibration factor to correct for the heat-induced changes in CO₂ production. A commercial TCCO₂ measuring device (Sentec AG, Therwil, Switzerland) based on a Stow-Severinghaus-type CO₂ sensor is combined with a pulse oximeter clipped to the patient's earlobe.^[11] Oxygen saturation values are available immediately while TCCO₂ values are available after a 2–3 min calibration time. The present generation of transcutaneous CO₂ units has a lot of inherent problems. Their design needs to be improved upon for them to become popular in clinical practice.

Tobias ^[1] found the PaCO₂-PETCO₂ difference to be 3.9 ± 1.6 mmHg and the PaCO₂-TCCO₂ difference to be 2.5 ± 0.8 mmHg during TLV. During OLV, the former increased to 5.8 ± 2.3 mmHg, whereas the TC to PaCO₂ difference was still 2.7 ± 1.4 mmHg. During OLV, the PaCO₂-PETCO₂ difference was ≤5 mmHg in 6 of 15 patients whereas the PaCO₂-TCCO₂ difference was ≤5 mmHg in 14 of 15 patients. They concluded that during OLV, TCCO₂ monitoring mirrors PaCO₂ more accurately than ETCO₂. In another study, during TLV, TC-CO₂-PaCO₂ gradient was 3.0 ± 1.8 mmHg and the ET-PaCO₂ gradient was 6.2 ± 4.7 mmHg. During OLV, the difference between the TCCO₂ and PaCO₂ was 3.5 ± 1.7 mmHg and the ETCO₂ to PaCO₂ difference was 9.6 ± 3.6 mmHg. Nevertheless, ETCO2 retains its position as a standard of care in the OT as continuous waveform capnography serves other important functions such as confirmation of ETT position and ventilator disconnect alarm. An occasional large ventilatory breath (intermittent sighs/squeeze breaths) given during normal mechanical ventilation not only prevents atelectasis (especially in lung-protective mechanical ventilation with low tidal volume) but also enables more accurate sampling of alveolar gases and hence better quantification of PaCO₂. In patients where the lungs have inherent problems, initial establishment of PaCO₂-ETCO₂ by a baseline ABG sample taken immediately after intubation is crucial. Frequent determinations of this difference is also essential

Conclusion

The effects of OLV, lateral position, capnothorax and underlying lung disease on ETCO₂-PaCO₂ gradient are synergistic and not just additive. Severe hypercarbia warranting elective postoperative ventilation may go undetected, until too late, if ETCO₂ is the sole guide to arterial CO₂ levels. Once the baseline PaCO₂ gradient is determined by ABG, monitoring ETCO₂ may reduce the need for subsequent frequent ABG analysis allowing for safe, continuous monitoring with alarm limits adjusted for early warning for intervention before the patient is compromised. A sudden change in ETCO₂ merits PaCO₂ measurement via an ABG. An increase in the gradient from the baseline along with other clinical symptoms can indicate deterioration in the patient's condition.^[13] TCCO₂ monitoring despite inherent problems, may prove invaluable if available. Intermittent squeeze breaths/sighs are recommended to enable more accurate sampling of alveolar gases and hence better quantification of PaCO₂.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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