| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
From the Departments of *Anesthesia and Intensive Care, and Pediatric Surgery, Cairo University, Cairo, Egypt.
Address correspondence and reprint requests to Ahmed M. Mukhtar, 2 Zaafran St. from Ahmed Kamel St. behind Giza Governate Alharam, Cairo, Egypt. Address e-mail to Ahmed3m2003{at}yahoo.com.
Abstract
BACKGROUND: Although the cardiovascular effect of CO2 insufflation has not been reported in pediatric thoracoscopy, several clinical trials have demonstrated significant hemodynamic deterioration in adults. We investigated the concept of therapeutic hypercapnia for counteracting the hemodynamic effect of induced capnothorax.
METHODS: Twelve pediatric patients who underwent video-assisted thoracoscopic patent ductus arteriosus closure were enrolled in the study. Cardiorespiratory variables were determined during baseline T1 and after CO2 insufflation at pressures of 2 mm Hg T2, 4 mm Hg T3, 6 mm Hg T4, 8 mm Hg T5, and 10 mm Hg T6.
RESULTS: CO2 insufflation was not associated with any adverse hemodynamic effects. Cardiac output and central venous oxygen saturation increased progressively throughout the study protocol. Relative to baseline peak velocity, systolic flow time corrected for heart rate, heart rate, and central venous pressure increased significantly during insufflation, but systolic and diastolic blood pressure remained unchanged. Arterial CO2 increased from 40.7 ± 3 at T1 to 61 ± 1.6 at T6 mm Hg. Arterial oxygen tension increased from 170.9 ± 3.3 at T1 to 182 ± 2 at T6; arterial PH decreased from 7.31 ± 1.2 at T1 to 7.14 ± 4.6 at T6.
CONCLUSION: Hypercapnia targeting CO2 50–70 mm Hg was associated with increased cardiac output, central venous O2, and arterial O2 tension in patients undergoing video-assisted thoracoscopic patent ductus arteriosus closure using one-lung ventilation without any deleterious cardiopulmonary effects.
During the last decade, enthusiasm has grown for minimally invasive thoracic surgical approaches, resulting in an increase in the use of video-assisted thoracoscopy (VATS).1,2 This approach offers the advantages of a smaller incision, less postoperative pain, and a faster postoperative recovery compared with thoracotomy.3 Recent advances in surgical techniques, coupled with the introduction of high-resolution microchip cameras and smaller endoscopic instruments, have facilitated the application of VATS in pediatric patients.
CO2 insufflation is often used to achieve adequate exposure of intrathoracic structures and to facilitate the surgical procedure. Several authors have advocated insufflation of CO2 to expedite collapse of the lung for visualizing the intrathoracic structures.4–7 The clinical impact of positive-pressure pleural insufflation during VATS procedures remains controversial. Several investigators have found no significant sequelae with its use,8,9 whereas others have reported major problems.10,11
One of the sequelae of CO2 insufflation is the development of hypercapnia, which has traditionally been avoided in an attempt to keep hemodynamic variables normal. Recent evidence of the role of excessive tidal stretch (volutrauma) has prompted clinicians to avoid the use of high-tidal volume (VT) and to accept the resulting permissive hypercapnia. Therapeutic hypercapnia has evolved from the idea that, rather than being tolerated, elevated CO2 might be helpful.12
Little is known about the cardiovascular changes associated with artificial capnothorax during VATS procedures in pediatric patients. We therefore prospectively examined the alterations in hemodynamics, and the esophageal Doppler monitor (EDM) during thoracoscopic patent ductus arteriosus (PDA) clipping. We describe the hemodynamic effects of hypercapnia resulting from increased intrapleural pressure in pediatric patients.
METHODS
After obtaining institutional local ethical committee approval and informed, parental written consent, 12 patients scheduled to undergo PDA closure using VATS were studied. Patients with a PDA diameter equal to or more than 10 mm, significant pulmonary hypertension (defined as pulmonary artery systolic pressure more than 40 mm Hg), calcification in the duct, or transcatheter occlusion devices within the ductal lumen were excluded. In addition, patients with associated congenital cardiac defects were also excluded.
Five-lead electrocardiogram, noninvasive arterial blood pressure, pulse oximeter, capnography, and body temperature were routinely monitored. Anesthesia was induced with propofol 1–2 mg/kg and fentanyl-2 µg/kg. Atracurium 0.5 mg/kg was administered to facilitate endotracheal intubation. One-lung ventilation (OLV) was achieved with an appropriately sized single-lumen tube inserted in the right endobronchial position. The position of endotracheal tube was confirmed with a fiberoptic bronchoscope. A double-lumen central venous catheter and a 20-gauge catheter were inserted in the right radial artery for continuous monitoring of arterial blood pressure and sampling of blood for blood gas determination.
Anesthesia was maintained with end-tidal isoflurane 1%–1.5% in oxygen 100%. Mechanical ventilation was provided by Primus (Dräger, Germany) (initial VT, 7–8 mL/kg; respiratory rate, 16 breaths/min). The ventilatory frequency was adjusted during CO2 insufflation by means of repeated arterial blood gas analyses to maintain arterial partial pressure of carbon dioxide (Paco2) between 50 and 70 mm Hg and pH more than 7.1.
An esophageal Doppler probe (Cardio Q) was inserted orally and positioned to obtain the best arterial Doppler wave. The CardioQ (Deltex Medical, Chichester, UK) EDM measures the velocity of blood flow in the descending thoracic aorta. Integrating the velocity–time curve gives the distance traveled by the blood after cardiac systole, and multiplying this by the cross-sectional area (estimated by a nomogram) derives stroke volume and cardiac output (CO).13
Surgical Technique
Patients were placed in the right lateral decubitus position. Two thoracostomies were made for the introduction of 5-mm trocars (L-shaped elettrocautery and camera). The pleural cavity was insufflated with CO2 to facilitate exposure. The aortopulmonary window was dissected out to identify the PDA, recurrent laryngeal nerve, and subclavian artery. The pathologic ligaments were divided using 5 or 10 mm clips, and residual fibrous bands were taken down. Once the PDA was dissected, an appropriate sized vascular clip (LIGACLIP extra ligating clip TITANIUM, Ethicon, Cincinnati, OH; ENDOPATM, Ethicon, Sommerville, USA) was advanced and placed around the duct parallel to the aorta. After ductal closure, the left lung was inflated, the thoracostomies were closed. No chest tube drains were inserted. All patients were tracheally extubated in the operating room and then transferred to the intensive care unit.
Study Protocol
After insertion of a Verress needle, CO2 was insufflated in 2 mm Hg increments every 5 min at a flow of 1 L/min until it reach 10 mm Hg. Hemodynamic and respiratory variables were obtained at 6 time points: T1, baseline, immediately after insertion of the EDM and the patient then placed in the lateral decubitus position, T2, 5 min after CO2 insufflation at constant pressure levels of 2 mm Hg, T3, 4 mm Hg, T4, 6 mm Hg, T5, 8 mm Hg and T6, 10 mm Hg.
Measurements
Heart rate (HR), systolic and diastolic arterial blood pressure, EDM-derived variables [CO, peak velocity (PV), systolic flow time corrected for HR (FTc)], central venous pressure, central venous oxygen saturation (ScvO2), arterial oxygen tension (Pao2), Paco2, pH, and peak inspiratory pressure were recorded at the same aforementioned 6 time points. All the measurements were done before closure of the PDA.
Statistical Analysis
Data are presented as mean (sd). Data were analyzed using one-way ANOVA, if statistical significance was reached Tukey post hoc test was used to identify level of significance. A P value <0.05 was considered statistically significant. The software SPSS V10.0 for windows (SPSS, Inc., Chicago, IL) was used for statistical analysis.
RESULTS
Twelve pediatric patients, eight males and four females, were enrolled in and completed the study. Their mean (sd) age was 13 (1.2) yr and mean (sd) weight was 31 (3.8) kg. The mean (sd) operative time was 81 (22) min and the mean (sd) duration of CO2 insufflation was 79.7 (18) min.
CO did not differ significantly between T1 and T2. CO increased significantly starting from T3, reached its peak at T4, and then plateaued at T5 and T6 (Fig. 1). SCVCO2 increased progressively with higher levels of CO2 insufflating pressure starting from T3 and maintained throughout the procedure (Fig. 2).
|
|
Changes in FTc and PV were parallel and increased significantly starting from T3 and peaked at T5 (Fig. 3).
|
There was a significant increase in HR, whereas systolic and diastolic arterial blood pressure remained within the normal range at baseline and during CO2 insufflation. Central venous pressure significantly increased with CO2 insufflation (Table 1).
|
The stepwise increase in Paco2 led to a decrease in arterial pH. This was accompanied with a significant increase in Pao2 (Table 1).
VT was kept constant during CO2 insufflation at 7 mL/kg. Peak inspiratory pressure increased from 20.5 ± 1.0 at T1 to 24.5 ± at T6 P < 0.05. Respiratory rate had to be adjusted to maintain Paco2 between 50 and 70 mm Hg.
DISCUSSION
The present study demonstrated that mild degrees of permissive hypercapnia were not only tolerable but also had a potential protective effect against induced pneumothorax during VATS in a pediatric population undergoing PDA closure. Few studies have investigated the hemodynamic consequence of CO2 insufflation, and all of these reports were done in adult thoracoscopy.14,15 To the best of our knowledge, there has been no report concerning the cardiovascular effects of increased intrapleural pressure in the pediatric population during VATS.
CO measured by EDM increased progressively with CO2 insufflation compared with baseline values. This may correspond to development of hypercapnia with respiratory acidosis. Contrary to our finding, Jones et al.16 demonstrated significant hemodynamic deteroriation in an animal model during CO2 insufflation pressures of 5 mm Hg or more. More recently, Brock et al.15 stated that CO2 insufflation was associated with a clear deterioration in circulatory function. In contrast to our study design, Brock et al. maintained normocapnia throughout the procedure. Another difference is that we used an escalated stepwise increase of intrapleural pressure.
In line with our results, Millar et al.17 described the anesthetic management of a patient with severe respiratory failure in whom OLV had to be avoided in a VATS pleurectomy. CO2 insufflation was performed with a maximum pressure of 8 mm Hg, but no adverse hemodynamic events occurred.
Measurement of ScvO2 seems to be an attractive alternative to monitoring of mixed venous O2 saturation (SvO2).18 In the present study, we used ScvO2 as a surrogate to Svo2 as an index of tissue oxygenation. ScvO2 was increased progressively throughout the procedure. Under general anesthesia the global O2 demand can be considered in a relatively constant state and variability in O2 delivery arises only from O2 supply imbalance. Thus, the ScvO2 changes observed in our study during CO2 insufflation were probably due to increased CO.
The measurement of descending aortic blood flow via an esophageal ultrasound probe offers an alternative method of monitoring circulatory status, the measured variables include PV and FTc. PV (cm/s) is an index of left ventricular contractility whereas FTc reflects ventricular preload. Concurrent changes in PV and FTc reflect changes in afterload.13
In the present study, measurement from an EDM indicated a state of progressive decrease in the afterload (high PV, high FTc), which might have been a result of hypercapnia and respiratory acidosis. Baseline HR was fairly constant but increased with capnothorax. On the other hand, systolic and diastolic blood pressures were not changed throughout the study protocol. Hypercapnia causes a variety of effects on cardiovascular function, mediating alteration in preload, afterload, contractility, and CO. The direct effect of hypercapnic acidosis on the heart and vascular smooth muscle is to reduce contractility. However, these direct effects are opposed by a neurohumeral effect, thus resulting in an increase in sympathomimetic output. This leads to an increase in HR, systemic vasodilatation, and decrease in left ventricular afterload, which results in an increase in CO.19
Respiratory variables remained relatively unaffected by CO2 insufflation at various intrathoracic pressures; however, Pao2 increased progressively. The underlying mechanisms of improved Pao2 during hypercapnia are complex, but they reflect, in part, the effect of hypercapnic acidosis on accentuation of hypoxic pulmonary vasoconstriction.20 Specific hazards with the technique of endobronchial intubation are associated with OLV.21 A marked decrease in arterial oxygenation is the consequence of a nonventilated and collapsed lung. In our study, the increased intrapulmonary shunt with an increased Pao2 suggests that the atelectasis associated with increased intrapulmonary shunt was countered by an increase in CO and mixed venous oxygen content.22
During OLV, VT is frequently maintained at the same level as during two-lung ventilation without positive end-expiratory pressure, targeting normalization of CO2.23,24 This maintenance corresponds to a high-volume ventilation with potentially deleterious effects, even for a period of <90 min.25,26
Normalizating of CO2 at the expense of inducing undue lung stretch may not be appropriate. In mechanically ventilated intensive care unit patients reduced VT with an associated increased CO2 (permissive hypercapnia) has become an accepted practice.27,28 Recently, Michelet et al.29 demonstrated that the protective ventilatory strategy based on the reduction of VT is beneficial during OLV.
CO2 insufflation is crucial in small infants, especially when one-lung separation is difficult. However, we cannot judge with confidence whether our findings can be extrapolated to this group of patients.
In conclusion, mild hypercapnia and respiratory acidosis may minimize the deleterious effects of CO2 insufflation in pediatric patients undergoing VATS closure of PDA.
Footnotes
Accepted for publication September 11, 2007.
REFERENCES
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
P < 0.05 compared with T4.
