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CARDIOVASCULAR ANESTHESIA

Cardiopulmonary Dysfunction During Minimally Invasive Thoraco-Lumboendoscopic Spine Surgery

B. Vollmar, MD^*, A. Olinger, MD, U. Hildebrandt, MD, and M. D. Menger, MD^*

*Institute for Clinical & Experimental Surgery and Departments of Trauma Surgery and General Surgery, University of Saarland, Homburg/Saar, Germany

Address correspondence and reprint requests to Brigitte Vollmar, MD, The Center of Blood Research, Harvard Medical School, 200 Longwood Ave., Boston, MA 02115. Address e-mail to vollmar @cbr.med.harvard.edu.

	Abstract

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The endoscopic retroperitoneal approach to thoraco-lumbar anterior spine fusion is associated with CO₂ insufflation into the thoracic space. We studied the cardiopulmonary effects of this CO₂ thoraco-retroperitoneal insufflation compared with the conventional open surgical procedure using thoraco-phreno-lumbotomy in 12 pigs under balanced anesthesia, paralysis, and mechanical ventilation. During open surgery of the thoraco-lumbar spine, animals exhibited unchanged systemic and pulmonary hemodynamics, as well as ventilation and oxygenation variables. Animals retroperitoneally insufflated with CO₂ (12 mm Hg) exhibited a significant increase of PaCO₂ and a moderate decrease of PaO₂, SaO₂, and pH, with insignificant changes of central venous filling pressures and systemic hemodynamics. Endoscopic phrenotomy with thoracic CO₂ insufflation instantaneously and drastically affected hemodynamic status and pulmonary gas exchange with marked hypoxia, hypercapnia, systemic hypotension, tachycardia, and pulmonary hypertension within minutes. An increase of minute ventilation, inspiratory oxygen fraction, and positive end-expiratory pressure promptly reversed these cardiopulmonary effects. CO₂ evacuation allowed the animals to completely recover and regain almost baseline cardiopulmonary status, except for a reduced arterial blood pressure. Appropriate monitoring and immediate CO₂ desufflation may be beneficial in cases of therapy-resistent hemodynamic, oxygenation, and ventilation difficulties.

Implications: For endoscopic thoraco-lumbar spine fusion, CO₂ thoraco-retroperitoneum–induced cardiopulmonary dysfunction must be of concern, especially in patients with cardiopulmonary compromise. Appropriate monitoring and immediate CO₂ desufflation may be beneficial in cases of therapy-resistant hemodynamic, oxygenation, and ventilation difficulties.

	Introduction

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Recent advances in laparoscopic instrumentation and techniques have led to a remarkable development of minimally invasive surgical procedures involving virtually every organ. In lumbar spine surgery, an endoscopic transperitoneal and retroperitoneal approach has been described for common procedures, such as discectomies, fusions, and corpectomies (1,2). Because the advantages of these minimally invasive procedures—namely, minor surgical trauma, reduced postoperative pain and hospitalization, smaller incisions, shorter recovery, and hastened return to normal activity—are evident, we were encouraged to pursue an endoscopic retroperitoneal approach for thoraco-lumbar spinal procedures.

During the performance of endoscopic anterior thoraco-lumbar spine fusion, the retroperitoneum and, after phrenotomy, the thoracic space is insufflated with CO₂. This may similarily be the case if solely retroperitoneoscopic interventions, such as adrenalectomy, are complicated by accidental injury to the diaphragm. The influence of a CO₂ thoracoretroperitoneum on lung compression, CO₂ absorption, and cardiac function, however, is not yet known. Thus, we undertook the present study to analyze this new endoscopic procedure in terms of its hemodynamic and pulmonary effects because reports from laboratory and clinical studies have raised concerns about the effects of CO₂ insufflation on cardiopulmonary functions (3–6).

	Methods

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The experiments were approved by the German legislation on protection of animals and adhered to the guidelines for the handling of animals set by the National Institute of Health.

Twelve pigs of the Suabian Hall strain of either sex weighing 19–22 kg were sedated with azaperone (10 mg/kg body weight [BW] IM; Janssen, Neuss, Germany) and methomidate hydrochloride (10 mg/kg BW IM; Janssen), followed by the IV injection of etomidate (1 mg/kg BW; Janssen) for the induction of anesthesia. The trachea was intubated (7.5 mm inner diameter) and the animals were mechanically ventilated with an oxygen/nitrous oxide mixture (1:2 vol/vol). The inspired oxygen fraction (FIO₂ 0.21–0.30) was adjusted to maintain arterial PaO₂ >110 mm Hg at baseline. At a respiratory rate of 12 breaths/min, tidal volume (180–200 mL) was adjusted to maintain ETCO₂ at 35–45 mm Hg at baseline. Monitoring of peak inspiratory pressure revealed values <25 mm Hg, and positive end-expiratory pressure (PEEP) was kept at 2 mm Hg to prevent atelectasis. For surgical instrumentation, the animals were placed in a supine position on an external heating pad to maintain the body at a constant temperature. Balanced anesthesia was achieved throughout the experiment by the IV infusion of piritramide (10 mg · kg^-1 · h^-1; Janssen) and dihydrobenzperidole (0.01 mg · kg^-1 · h^-1; Janssen), as well as by isoflurane in the inspired gas (1 vol%–2 vol%; Abboth, Wiesbaden, Germany). Throughout the experimental procedure, the animals were paralyzed by an IV infusion of pancuronium bromide (0.03 mg · kg^-1 · h^-1; CuramedPharma, Karlsruhe, Germany), and they received an isotonic saline solution (10 mL · kg^-1 · h^-1). As shown previously, this anesthetic regimen provides sufficient anesthetic depth and hemodynamic stability even under conditions of major surgical stress (7,8).

A flow-directed 5F thermistor-equipped catheter (SP5105; Viggo-Spectramed, Duesseldorf, Germany) was inserted through the left external jugular vein under continuous pressure monitoring into the pulmonary artery for determination of pulmonary hemodynamics, sampling of mixed venous blood, and measurement of temperature, central venous pressure, and cardiac output. A fine 17-gauge polyethylene catheter (Vygon, Écouen, France) was placed in the internal jugular vein for infusion of volume and administration of anesthetic drugs. In the left carotid artery, a 7F side-arm introducer sheath (AD Krauth, Hamburg, Germany) was used for determination of systemic arterial blood pressure and sampling of blood.

Arterial and mixed venous blood gases were measured using a Chiron gas analyzer (Chiron Diagnostics, St-Leon-Rot, Germany). Cardiac output was measured by the thermodilution technique and is reported as the mean values of triplicate injections of 3 mL of ice-cold saline solution. Heart rate and all pressures were measured with the pigs in right lateral position and the transducers zeroed to the midchest position using membrane pressure transducers (DTX/Plus®; Ohmeda, Erlangen, Germany). The amplified pressure signals, as well as the limb-leaded electrocardiogram, were continuously displayed and recorded.

After insertion of the catheters, all animals were positioned in right lateral recumbency. In the endoscopic group, retroperitoneal access was achieved after placement of three trocars and insufflation of CO₂ at 12 mm Hg by an automatic insufflator, which guaranteed the maintenance of a pressure level of 12 mm Hg by appropriate adjustment of the gas flow. The diaphragm was then incised for exposure of the thoracic spine bodies at CO₂ insufflation at a pressure of 12 mm Hg. After final exposure of the thoraco-lumbar spine bodies (T14–16 and L1–2), bisegmental instrumentation (anterior fusion) with a tricortical bone block and a dynamic compression plate (DCP; Synthes, Davos, Switzerland) was performed to simulate adequate treatment of anterior interbody fusion for spine fracture. The operative procedure was completed by wound closure.

In each pig undergoing the open surgical approach, a thoraco-phreno-lumbotomy was performed to allow complete exposure of the distal thoracic (T14–16) and proximal lumbar (L1–2) spine. Instrumentation of the spine bodies was similar to that in the endoscopic group, i.e., bisegmental anterior interbody spine fusion. The operative procedure was again completed by layer-to-layer wound closure.

Hemodynamic measurements were taken at 30 -min intervals throughout the operative procedure up to a total observation period of 4 h, after which the animals were killed by using a bolus infusion of potassium chloride. Sampling of blood for blood gas analysis was performed at 30-min intervals during the operation and at 60-min intervals after the end of the operation. After phrenotomy, which was performed approximately 50 min after start of the operation, additional monitoring of both hemodynamics and blood gases was performed within the 60- to 90-min period after start of the operation. The protocol included a total of five phases: baseline conditions, CO₂ retroperitoneum, CO₂ thoraco-retroperitoneum, CO₂ thoraco-retroperitoneum with ventilatory adjustment, and release of CO₂ thoraco-retroperitoneum.

The hemodynamic and respiratory variables assessed were mean arterial blood pressure (MAP), systolic arterial blood pressure (SAP), cardiac output (CO), heart rate (HR), stroke volume (SV), right (RVSW) and left ventricular stroke work (LVSW), rate pressure product (RPP), central venous pressure (CVP), mean pulmonary artery pressure (MPAP), diastolic pulmonary artery pressure (DPAP), pulmonary capillary wedge pressure (PCWP), systemic (SVR) and pulmonary vascular resistance (PVR), peak respiratory pressure (PRP), tidal volume, ventilatory frequency, and ETCO₂, as well as arterial and mixed venous blood gases PO₂, PCO₂, pH, SO₂. Moreover, CO₂ insufflation pressure and, thus, retroperitoneal and intrathoracic pressure (after phrenotomy) was continuously monitored and kept at a constant level of 12 mm Hg.

SV was calculated as ([CO/HR] · 1000)mL; SVR as ([MAP-CVP] · [79.9/CO])dyne · s · cm^-5; PVR as ([MPAP-PCWP] · [79.9/CO])dyne · s · cm^-5; RVSW as ([SV · (MPAP-CVP)] · 0.0136)g; LVSW as ([SV · (MAP-PCWP)] · 0.0136)g; and RPP as (HR · SAP)mm Hg/min.

Ventilation settings were not adjusted unless a PaCO₂ 65 mm Hg or a PaO₂ 60 mm Hg was observed by using blood gas tension monitoring, at which time ventilator settings were adjusted by increasing ventilatory frequency up to 16–20 breaths/min, minute volume to 4–5 L/min, FIO₂ to 100%, and PEEP to 5 mm Hg.

Data are reported as means ± SEM. An analysis of variance for repeated measures, followed by a post hoc comparison test (Dunnett) was performed to test the effects of time and retro- and thoraco-retroperitoneum on cardiopulmonary and blood gas variables, including correction of the error according to the Bonferroni probabilities for repeated measurements. A P value of <0.05 was considered significant.

	Results

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Animals subjected to the open surgical procedure did not exhibit any significant changes of hemodynamic and ventilatory variables compared with baseline during the operative manipulation or up to 4 h after the operation (Tables 1 and 2). The anesthetic regimen and the ventilatory settings were kept constant throughout the whole observation period, i.e., no ventilatory adjustment was necessary in the control animals. The duration of the operative procedure ranged between 48 and 127 min.

Retroperitoneal insufflation of CO₂ only influenced the PaCO₂, with a significant increase from 41.8 ± 2.1 mm Hg at baseline to 51.9 ± 2.2 mm Hg, causing mild acidemia at 30 min of the 12- mm Hg CO₂ retroperitoneum with a slight increase of ETCO₂ (Fig. 1). No significant changes in PaO₂ and SaO₂ were observed although there was a tendency toward decreasing values (Fig. 1). The hemodynamic effects of the retroperitoneal CO₂ insufflation were also of moderate magnitude. SV remained unchanged due to a moderate increase of HR (105%) and CO (113%). Systemic arterial pressure and central filling pressures (CVP, MPAP) were insignificantly increased by 6% and 13%, respectively (Figs. 2 and 3).

View larger version (36K): [in this window] [in a new window]   Figure 1. Arterial blood gas parameters in ventilated pigs (n = 6) subjected to endoscopic thoraco-retroperitoneal anterior spine fusion. I = baseline (before operation), II = CO2 retroperitoneum, III = CO2 thoraco-retroperitoneum, IV = CO2 thoraco-retroperitoneum with ventilatory adjustment (fraction of inspired oxygen 100%, ventilatory rate 16–20 breaths/min, minute volume 4–5 L/min, positive end-expiratory pressure 5 mm Hg), V = CO2 evacuation. Values are means ± SEM. Analysis of variance for repeated measures, Dunnett's test with Bonferroni correction: *P < 0.05 versus values at time 0. PRP = peak respiratory pressure.

View larger version (36K): [in this window] [in a new window]   Figure 2. Systemic hemodynamic parameters in ventilated pigs subjected to endoscopic thoraco-retroperitoneal anterior spine fusion (n = 6). MAP = mean arterial blood pressure, SAP = systolic arterial blood pressure, HR = heart rate, SV = stroke volume, CO = cardiac output, SVR = systemic vascular resistance, RPP = rate pressure product, LVSW = left ventricular stroke work. I = baseline (before operation), II = CO2 retroperitoneum, III = CO2 thoraco-retroperitoneum, IV = CO2 thoraco-retroperitoneum with ventilatory adjustment (fraction of inspired oxygen 100%, ventilatory rate 16–20 breaths/min, minute volume 4–5 L/min, positive end-expiratory pressure 5 mm Hg), V = CO2 evacuation. Values are means ± SEM. Analysis of variance for repeated measures, Dunnett's test with Bonferroni correction: *P < 0.05 versus values at time 0.

View larger version (38K): [in this window] [in a new window]   Figure 3. Central venous and pulmonary hemodynamics in ventilated pigs subjected to endoscopic thoraco-retroperitoneal anterior spine fusion (n = 6). MPAP = mean pulmonary arterial blood pressure, DPAP = diastolic pulmonary arterial blood pressure, PCWP = pulmonary capillary wedge pressure, PVR = pulmonary vascular resistance, CVP = central venous blood pressure, RVSW = right ventricular stroke work. I = baseline (before operation), II = CO2 retroperitoneum, III = CO2 thoraco-retroperitoneum, IV = CO2 thoraco-retroperitoneum with ventilatory adjustment (fraction of inspired oxygen 100%, ventilatory rate 16–20 breaths/min, minute volume 4–5 L/min, positive end-expiratory pressure 5 mm Hg), V = CO2 evacuation. Values are means ± SEM. Analysis of variance for repeated measures, Dunnett's test with Bonferroni correction: *P < 0.05 versus values at time 0.

Ventilatory adjustment—increasing FIO₂, minute volume, and PEEP to 1.0, 4–5 L/min, and 5 mm Hg, respectively—corrected most of the hemodynamic and pulmonary alterations (Figs. 1–3), except the PRP, which continued to increase to 40.5 ± 2.0 mm Hg. At 120 min, the time point before CO₂ evacuation, the acid-base balance was restored, with a PaCO₂ of 45.7 ± 4.9 mm Hg and a pH of 7.44 ± 0.01 (Fig. 1). CVP, MPAP, PCWP, and PVR decreased, but did not reach baseline values, at 120 min (Fig. 3). HR regained baseline values, but MAP and SV were not completely normalized with the ventilatory adjustments, and LVSW still significantly differed compared with baseline values (Fig. 2). During the following 120 min after final desufflation of the thoraco-retroperitoneum, reduced MAP persisted, whereas all other hemodynamic and pulmonary variables no longer significantly differed from baseline values (Figs. 2 and 3). Beside CO₂ evacuation, nitrous oxide was again applied, PEEP was reduced to 2 mm Hg, and the respiratory rate and the tidal volume were reduced to 12 breaths/min and 180–200 ml, respectively. Thus, the control animals and the animals subjected to the endoscopic procedure differed in terms of ventilatory settings only during CO₂ thoraco-retroperitoneum.

	Discussion

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The thoraco-retroperitoneal approach for thoraco-lumbar spine fusion evaluated in this study includes CO₂ exposure of both the retroperitoneal and thoracic space. Whereas the initial restriction of CO₂ insufflation into the retroperitoneal space caused only moderate CO₂ absorption-linked blood acidosis without affecting hemodynamic and pulmonary function, both mechanical effects—insufflation pressure-induced decrease in pulmonary distensibility and diffusion-linked pharmacodynamic properties of CO₂—caused major hemodynamic and pulmonary dysfunction on diaphragmatic incision and thoracic CO₂ exposure.

As observed endoscopically, the increase of intrathoracic pressure mechanically restricted inspiratory lung distension, mimicking the situation of a tension pneumothorax. The concomitant large increase in PRP can be explained only by a decreased pulmonary distensibility, because constant tidal volumes were delivered by the ventilator. A comparable but far smaller effect has been observed on peritoneal insufflation-induced increase of intraabdominal pressure and volume, both of which may cause restriction and displacement of diaphragmatic excursion with compression of basal lung segments (9). As a result, peak airway pressure increases, whereas pulmonary compliance and vital capacity decrease (6,9). Consequently, CO₂ thoraco-retroperitoneum–induced pulmonary compression is manifested as a decrease in functional residual capacity with resultant alveolar collapse, i.e., perfused but not ventilated alveoli. The clinical picture of a tension pneumothorax can be mimicked by the CO₂ insufflation during thoracoscopy, when the lung fails to deflate adequately (10); however, thoracoscopy is normally performed without gas and under one-lung ventilation (11,12). This compression-induced ventilation/perfusion mismatch may partially account for the present observation of acute and pronounced systemic hypoxemia. This is supported by experiments in pigs demonstrating that, with induced progressive tension pneumothorax, oxygen saturation decreased immediately and continued to decline throughout the experiment to levels <50% of baseline (13). Hypoxia, in turn, causes bronchoconstriction and potentiates bronchomotor responsiveness (14), thus aggravating gas maldistribution and ventilatory imbalance. In parallel to the steep decline of PaO₂, PaCO₂ increased at phrenotomy and thoracic CO₂ insufflation. Beside hypoxia, it is conceivable that, in the present study, CO₂-induced central chemoreceptor stimulation evoked the observed increase of lung and airway resistance, as similarly described after CO₂ inhalation in sheep (15). Moreover, hypoxic pulmonary vasoconstriction, which normally counteracts the superfluous perfusion of nonventilated alveoli (16), is hampered by hypercapnia (17), thereby augmenting the CO₂ thoraco-retroperitoneum–induced pulmonary dysfunction. Considering Fick's law of diffusion, the increase of CO₂ is most probably due to the rapid increase in area for diffusion of CO₂ via direct gas exposure of the visceral and parietal pleurae (18). As with CO₂ absorption from intraperitoneal insufflation (18) intrathoracic CO₂ absorption might be limited, to some extent, because superficial pulmonary vasculature collapses when intrathoracic pressure increases above pulmonary capillary hydrostatic pressure, thereby diverting blood flow away from the pulmonary surface. However, the vascular collapse of remaining, still ventilated alveoli causes an increase of dead space ventilation with subsequent hypoxia and hypercapnia.

Moderate to severe hypercapnia, along with marked hypoxia, leads to sustained alterations in cardiac function. The observation of significantly increased central venous filling pressures but unchanged CO reflects a compensatory mechanism, as increasing HR offsets the effect of decreased left ventricular SV. Tachycardia might be not only a baroreceptor-mediated reflex response triggered by hypoxia-induced systemic hypotension, but also a reflex caused by hypercapnia-associated indirect stimulation of the autonomic nervous system with release of catecholamines (19). Considering the significant reduction of SV during thoracic CO₂ insufflation, a myocardial-depressant direct effect of hypercapnia-associated acidemia (20) seems to dominate over the theoretical catecholamine-associated increase of myocardial contractility (20). The concomitant decrease of SVR may underlie the predominance of direct myocardial effects of CO₂. CO₂ would, however, normally increase coronary blood flow (21), but coronary perfusion pressure must be suspected to decrease because systemic hypotension occurred together with pulmonary hypertension. This view is supported by experiments in newborn piglets, which demonstrate that the combination of hypoxia/hypercapnia with a tension pneumothorax blunted the increase of myocardial perfusion normally observed with hypoxia/hypercapnia alone (22). Thus, with respect to tachycardia-induced increase of cardiac oxygen demand and the concomitant shortage of coronary filling time (19), there will be an unfavorable balance between myocardial oxygen demand and supply.

Secondary to hypoxia and hypercapnia (13), the marked depression of systemic hemodynamics might additionally result from an equalization of the thoracic insufflation pressure and the central venous filling pressures. Partial collapse of large intrathoracic veins, as well as pressure on the pulmonary arteries with increased right ventricular afterload, may have resulted in increased central venous pressure with reduced venous return to the right heart (23,24). Increased right ventricular afterload coincided with the calculation of increased RVSW in the present study. A lung compression-associated increase in pulmonary arterial pressure and vascular resistance also leads to a decrease in pulmonary venous return to the left atrium, contributing to the compromised stroke volume (23,24). The differences in hemodynamic variables before and after ventilatory adjustment were achieved not only by reversal of hypoxia and hypercapnia, but also by expansion of the lungs and an increase in airway pressure. This, in turn, indicates that the observed hemodynamic and cardiopulmonary aberrations seem to be the net result of combined mechanical, vascular, and pharmacodynamic effects on thoracic CO₂ insufflation. The present study cannot elucidate the operative mechanisms with respect to ventilation, oxygenation, and hemodynamic dysfunction, which must be evaluated in further experiments, allowing differentiation between right- and left-sided causes, as well as between metabolically induced reduction of myocardial contractility versus reduced preload from vascular collapse as the cause for hemodynamic compromise. However, we show that the cardiovascular consequences during the combined CO₂ thoraco-retroperitoneum are significant and clinically important.

In summary, thoraco-lumboendoscopic spine surgery is associated with marked hemo- and cardiodynamic and pulmonary deteriorations on thoracic CO₂ insufflation. Rapid respiratory decompensation, i.e., hypoxemia from impaired gas exchange, with net alveolar hypoventilation and transpulmonary CO₂ absorption precede, and imply, a potential metabolic basis for the hemodynamic compromise. Preload reduction due to a mechanical effect with mediastinal shift, kinking, and obstruction or collapse of thoracic vessels might be an additional cause of hemodynamic compromise. Rutherford et al. (25) studied the hemodynamic responses to pneumothoraces in goats and found that vascular causes seem to play a secondary role for the hemodynamic effects compared with ventilation/oxygenation insufficiency. Although we showed that the adverse effects of CO₂ thoraco-retroperitoneum on pulmonary and cardiovascular function could largely be corrected intraoperatively by adjusting mechanical ventilation, this study underlines the need for sufficient hemodynamic monitoring, particularly in patients with inadequate cardiac reserves due to cardiovascular disease, and for prompt CO₂ evacuation in cases of therapy-resistant cardiopulmonary complications.

	Acknowledgments

 
This study was supported by the Association for Laparoscopic Spine Surgery, Homburg.

We thank Prof. Mertzlufft for the fruitful discussion.

	Footnotes

 
BV is supported by a Heisenberg Stipendium of the Deutsche Forschungsgemeinschaft (Vo 450/6-1).

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Vollmar, B. Articles by Menger, M. D. Search for Related Content PubMed PubMed Citation Articles by Vollmar, B. Articles by Menger, M. D.