Volume 31, Issue 2 pp. 121-128

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Cardiopulmonary effects of thoracoscopy in anesthetized normal dogs

Simon T Kudnig BVSc, MVS, MS, MACVSc,

Simon T Kudnig BVSc, MVS, MS, MACVSc

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Eric Monnet DVM, PhD, Diplomate ACVS, Diplomate ECVS,

Eric Monnet DVM, PhD, Diplomate ACVS, Diplomate ECVS

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Miriam Riquelme DVM,

Miriam Riquelme DVM

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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James S Gaynor DVM, MS, Diplomate ACVA,

James S Gaynor DVM, MS, Diplomate ACVA

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Denise Corliss CVT,

Denise Corliss CVT

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Mowafak D Salman BVMS, PhD,

Mowafak D Salman BVMS, PhD

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Simon T Kudnig BVSc, MVS, MS, MACVSc,

Simon T Kudnig BVSc, MVS, MS, MACVSc

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Eric Monnet DVM, PhD, Diplomate ACVS, Diplomate ECVS,

Eric Monnet DVM, PhD, Diplomate ACVS, Diplomate ECVS

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Miriam Riquelme DVM,

Miriam Riquelme DVM

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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James S Gaynor DVM, MS, Diplomate ACVA,

James S Gaynor DVM, MS, Diplomate ACVA

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Denise Corliss CVT,

Denise Corliss CVT

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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Mowafak D Salman BVMS, PhD,

Mowafak D Salman BVMS, PhD

Department of Clinical Sciences, Colorado State University, Fort Collins, CO, USA

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First published: 29 March 2004

https://doi.org/10.1111/j.1467-2987.2004.00162.x

Citations: 10

Eric Monnet, Department of Clinical Sciences, Colorado State University, 300 W. Drake Road, Fort Collins, CO 80523, USA. E-mail: [email protected]

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Abstract

Objective To evaluate the effect of an open-chest condition on oxygen delivery in anesthetized dogs.

Study design Prospective, controlled experimental study.

Animals Eight clinically normal adult Walker Hound dogs weighing 25.6–29.2 kg.

Methods Eight anesthetized dogs underwent an open-chest operation after the insertion of thoracoscopy cannulae in the lateral chest walls . A Swan Ganz catheter was used to both measure hemodynamic parameters and obtain mixed venous blood samples for blood gas analysis. A dorsal pedal catheter was placed to both measure arterial blood pressure and obtain blood samples for blood gas analysis. Oxygen delivery index and oxygen extraction ratio were calculated. A randomized block anova for repeated measures was used to evaluate the effect of the treatment on hemodynamic and pulmonary parameters.

Results Creation of an open chest did not significantly affect oxygen delivery index (DO₂I; p = 0.545). It induced a significant decrease in arterial oxygen partial pressure (PaO₂; p = 0.018) and arterial oxygen content (CaO₂; p = 0.025). It induced a significant increase in shunt fraction (p = 0.023), physiologic dead space (p = 0.015), and alveolar-arterial oxygen difference (p = 0.019). Arterial partial pressure of carbon dioxide (PaCO₂; p = 0.766) and arterial hemoglobin oxygen saturation (SaO₂; p = 0.178) were not significantly affected. Diastolic (DPAP; p = 0.050) and mean (MPAP; p = 0.033) pulmonary arterial pressures were significantly increased by opening the chest. Other hemodynamic parameters were not significantly affected.

Conclusions Opening the thoracic cavity is not detrimental to hemodynamic function and oxygen delivery in normal dogs, although impaired gas exchange does occur.

Clinical relevance Close monitoring of patients is recommended during open-chest thoracoscopy as adverse effects on gas exchange can contribute to hypoxemia.

Introduction

Patients undergoing thoracic surgery are at risk for hypoxemia and hemoglobin (Hb) desaturation. The combined effect of anesthetic agents (Rehder & Sessler 1973; Hedenstierna et al. 1985), muscle paralysis and mechanical ventilation (Froese & Bryan 1974), lateral recumbency (Craig et al. 1962; Rehder et al. 1972; Werner et al. 1984), and atelectasis from opening the chest (Yoshida & Takaori 1991; de Gray et al. 1997) can result in increased shunt fraction ( Q̇_s/Q̇_t), ventilation–perfusion ( V̇/Q̇) mismatch, and arterial hypoxemia (Yoshida & Takaori 1991; de Gray et al. 1997). The relationship between inspired oxygen (PiO₂) and Hb saturation (SaO₂) is represented by a curvilinear curve (Roe & Jones 1993; Sapsford & Jones 1995; de Gray et al. 1997). An increased Q̇_s/Q̇_t causes the curve to shift downward, while a decreasing V̇/Q̇ ratio shifts the curve to the right (Roe & Jones 1993; Sapsford & Jones 1995; de Gray et al. 1997). Thus, after opening the chest, higher levels of PiO₂ are required to maintain the same SaO₂. Under these circumstances, it may be difficult to maintain a normal SaO₂ even with a fraction of inspired oxygen (FiO₂) of 1.

Thoracoscopy is replacing thoracotomy in many operative procedures to improve the visibility of thoracic structures (Lewis et al. 1992; Garcia et al. 1998; Faunt et al. 1998b; Jackson et al. 1999; Walsh et al. 1999; Isakow et al. 2000; Dupre et al. 2001; MacPhail et al. 2001; Radlinsky et al. 2002) and to decrease the morbidity associated with thoracotomy (Hazelrigg et al. 1991; Landreneau et al. 1993; Radlinsky et al. 2002). The cardiopulmonary effects of bilateral hemithorax ventilation with sustained pneumothorax have been studied in dogs (Faunt et al. 1998a). Insufflation of CO₂ beyond an intrathoracic pressure of 3 mm Hg produces significant detrimental effects on cardiac output (CO) in dogs (Daly et al. 2002; Polis et al. 2002). One-lung ventilation in anesthetized dogs with a closed chest has no effect on CO, but does cause an increased shunt fraction ( Q̇_s/Q̇_t) and a reduction in arterial partial pressure of oxygen (PaO₂; Cantwell et al. 2000). The cardiopulmonary effects of an open-chest during thoracoscopy in dogs, however, have not been evaluated and are an important consideration for thoracoscopic procedures with or without one-lung ventilation. The purpose of this study was to evaluate the net effect of an open-chest after thoracoscopic cannula placement on oxygen delivery index (DO₂I) to tissues. Our hypothesis was that open-chest thoracoscopy would not have any detrimental effect on DO₂I to peripheral tissue in anesthetized dogs.

Materials and methods

Experimental design

This study was approved by the Animal Care and Use Committee at Colorado State University. Eight healthy, intact, purpose-bred Walker Hound dogs of mixed gender weighing between 25.6 and 29.2 kg were studied. All dogs were clinically normal based on physical examination and the results of a complete blood count and serum biochemical analysis. Each dog served as its own control. Cardiopulmonary variables were recorded during closed-chest two-lung ventilation (closed chest) and open-chest two-lung ventilation (open chest). Data were collected 15 minutes after the onset of each experimental condition to allow equilibration of cardiopulmonary parameters. At the completion of the experiment, the dogs were entered in another phase of the study with the induction of one-lung ventilation. A continuous infusion of fentanyl (Fentanyl citrate injection, USP, Abbott Laboratories, North Chicago, IL, USA; 2–4 µg kg⁻¹ hour⁻¹ IV) was administered, and a transdermal fentanyl patch (Duragesic, Fentanyl transdermal system, Janssen Pharmaceutica Products, L.P., Titusville, NJ, USA; 7.5 mg) was simultaneously placed to alleviate pain during recovery from anesthesia. The dogs were recovered in a critical care unit under standard care as for client-owned animals and were adopted at the end of the study.

Anesthesia

A cephalic vein was catheterized with an 18-SWG over-the-needle catheter (Insyte, Becton Dickinson Infusion Therapy Systems Inc., Sandy, UT, USA), and a 10 mL kg⁻¹ fluid bolus of lactated Ringer's solution (Lactated Ringer's Injection, USP, Abbott Laboratories, North Chicago, IL, USA) was administered intravenously. Anesthesia was induced with propofol (PropoFlo, Abbott Laboratories, North Chicago, IL, USA; 3.0 mg kg⁻¹ IV), followed by diazepam (Diazepam Injection, USP, Elkins-Sinn Inc., Cherry Hill, NJ, USA; 0.3 mg kg⁻¹ IV). After endotracheal intubation, anesthesia was maintained with isoflurane (IsoFlo, Abbott Laboratories, North Chicago, IL, USA) in oxygen at an end-tidal concentration of 1.85–1.95% (approximately 1.5 × minimum alveolar concentration), delivered through a precision out-of-circuit vaporizer (Isoflurane precision vaporizer, Vetland, Louisville, KY, USA) from a semiclosed circle re-breathing circuit. An agent analyzer (Ohmeda 5330 Agent Monitor, Ohmeda, Louisville, CO, USA) was used to measure the end-tidal isoflurane concentration. A side-stream capnograph (Sidestream End Tidal CO₂ Sensor Model 20021, Medical Data Electronics, Arleta, CA, USA) was connected to the endotracheal tube to measure end-tidal carbon dioxide (Pe′CO₂). Lactated Ringer's solution and dextran 70 (6% Gentran 70 and 0.9% sodium chloride injection; Baxter Healthcare Corporation, Deerfield, IL, USA) were each administered at 5 mL kg⁻¹ hour⁻¹ during anesthesia. An esophageal temperature probe (Reusable temperature probe, Yellow Springs Instrument Co. Inc., Yellow Springs, OH, USA) was advanced to the level of the heart base to measure core body temperature. The patient was paralyzed with atracurium (Atracurium Besylate Injection, Faulding Pharmaceutical Co., Elizabeth, NJ, USA; 0.2 mg kg⁻¹ IV initial bolus and 0.1 mg kg⁻¹ IV as needed). Muscle relaxation was assessed using a nerve stimulator (Mini Stim Model MS-1, Life-Tech. Inc., Houston, TX, USA) over the peroneal nerve, observing a response to a ‘train of four’ electrical impulse. Mechanical ventilation was performed using a volume-limited ventilator (Narkomed DA, 2 L volume-limited ventilator, North American Drager, Telford, PA, USA) to achieve a Pe′CO₂ of 35–45 mm Hg (4.7–6.0 kPa) throughout the experiment. Respiratory rate (7–16 breaths minute⁻¹) and tidal volume (14–15 mL kg⁻¹) were kept constant during the experiment. A Wright's respirometer (Wright's respirometer type PM) was used to measure expiratory tidal volume. A warm water blanket was used to maintain body temperature.

Catheterization

A 20-SWG over-the-needle catheter (Insyte, Becton Dickinson Infusion Therapy Systems Inc., Sandy, UT, USA) was placed in the dorsal pedal artery and connected to a fluid-filled transducer (CDXpress, Argon, Maxxim Medical, Athens, TX, USA). The pressure transducer was zeroed to the level of the right atrium. Systolic (SAP), diastolic (DAP) and mean (MAP) arterial blood pressures were recorded continuously on a pressure monitor (Lifescope 6, Nihon/Kohden, Tokyo, Japan). Continuous ECG and pulse oximetry (Datex-Ohmeda Earclip pulse oximetry sensor, Ohmeda, Louisville CO, USA) were also recorded on the monitor.

The dogs were positioned in right lateral recumbency. An 8-F introducer (The Arrow Percutaneous Sheath Introducer System, Arrow International Inc., Reading, PA, USA) was placed into the left jugular vein with the Seldinger technique. A 110-cm-long 7.5-F Swan Ganz catheter with the proximal injectate port 30 cm from the catheter tip (Opticath catheter, Abbott Critical Care Systems, Abbott Laboratories, North Chicago, IL, USA) was placed through the jugular vein introducer, to the level of the pulmonary artery. Verification of the catheter position was made by observing the characteristic pressure waveforms on a pressure monitor (Marquet, Series 7000 Monitor, Marquette Electronics Inc., Milwaukee, WI, USA). The distal port of the Swan Ganz catheter was connected to a fluid-filled pressure transducer. The pressure transducer was zeroed to the level of the right atrium. Systolic (SPAP), diastolic (DPAP) and mean (MPAP) pulmonary arterial pressures were recorded continuously on the pressure monitor.

Creation of an open-chest

The left hemithorax was clipped and surgically prepared. An open-chest condition was achieved during a left-sided lateral thoracoscopic approach with 12 mm cannulae (Thoracic Trocar Sleeve, Ethicon Endo-Surgery Inc., Johnson & Johnson Healthcare Systems, Fort Worth, TX, USA) placed at the fourth, sixth, and tenth intercostal spaces. The cannulae were open to the atmosphere so that air moved into the chest as soon as they were placed and was free to move in and out through the cannulae during intermittent positive pressure ventilation (IPPV).

Data collection

Blood samples were collected from the dorsal pedal artery catheter, and a blood gas analyzer (IRMA Blood Analysis System Series 2000, Diametrics Medical Inc., St. Paul., MN, USA) was used to measure arterial parameters reported in Table 1. Hemodynamic data reported in Table 2 were collected with the catheter in the dorsal pedal artery and the Swan Ganz catheter in the pulmonary artery. The Swan Ganz catheter was used to collect venous blood samples, and the blood gas analyzer was used to measure mixed venous parameters reported in Table 1. CO was measured by a thermodilution technique by injecting 10 mL of iced saline through a closed injection system (CO-Set Closed Injectable Delivery System, Baxter Healthcare Corporation, Edwards Critical-Care Division, Santa Ana, CA, USA) into the right atrium. A cardiac output computer (Explorer Oximetry Computer, Baxter Healthcare Corporation, Edwards Critical-Care Division, Santa Ana, CA, USA) was used to calculate CO. The mean of three consecutive CO measurements was used for each data point. The Hb content was measured using a spectrophotometric hematology system (ADVIA 120 Hematology system, Bayer Corporation, Norwood, MA, USA).

Table 1. The effect of opening the chest on pulmonary parameters in anesthetized normal dogs

Variable	Closed chest	Open chest	p-value	Power
PaO₂ (mm Hg)	447 ± 51	361 ± 98	0.018	N/A
PaO₂ (kPa)	60 ± 7	48 ± 13	0.018	N/A
PaCO₂ (mm Hg)	41 ± 3	41 ± 3	0.766	0.776
PaCO₂ (kPa)	5 ± 0.4	6 ± 0.4	0.766	0.776
PvO₂ (mm Hg)	69 ± 22	67 ± 12	0.514	0.532
PvO₂ (kPa)	9 ± 3	9 ± 2	0.514	0.532
pHa	7.337 ± 0.034	7.333 ± 0.025	0.744	0.755
HCO₃⁻a	22 ± 0.9	22 ± 0.8	0.898	0.903
ABEa	−4.4 ± 1	−4.5 ± 0.8	0.926	0.929
SaO₂ (%)	98.84 ± 0.05	99.68 ± 0.32	0.178	0.195
SvO₂ (%)	89.06 ± 5.3	89.35 ± 3.9	0.7780	0.7875
Pe′CO₂ (mm Hg)	36 ± 2	34 ± 2	0.049	N/A
Pe′CO₂ (kPa)	4.8 ± 0.3	4.5 ± 0.3	0.049	N/A

Data are expressed as mean ±standard deviation.
A p-value <0.05 was considered the minimum level of significance.
PaO₂: arterial partial pressure of oxygen; PaCO₂: arterial partial pressure of carbon dioxide; PvO₂: mixed venous partial pressure of oxygen; pHa: arterial pH; HCO₃⁻a: arterial bicarbonate concentration; ABEa: arterial acid base excess; SaO₂: arterial oxygen saturation; SvO₂: mixed venous oxygen saturation; Pe′CO₂: End-tidal carbon dioxide; N/A: not applicable.

Table 2. The effect of opening the chest on hemodynamic parameters in anesthetized normal dogs

Variable	Closed chest	Open chest	p-value	Power
SAP (mm Hg)	106 ± 11	111 ± 13	0.296	0.316
DAP (mm Hg)	58 ± 5	62 ± 9	0.236	0.255
MAP (mm Hg)	73 ± 7	79 ± 8	0.127	0.141
RAP (mm Hg)	7 ± 1.6	8 ± 1.9	0.088	0.099
PAOP (mm Hg)	8 ± 3	8 ± 2	0.815	0.823
SPAP (mm Hg)	24 ± 4	25 ± 4	0.080	0.090
DPAP (mm Hg)	11 ± 3	14 ± 3	0.050	N/A
MPAP (mm Hg)	16 ± 3	18 ± 4	0.033	N/A
HR (beats minute⁻¹)	107 ± 19	116 ± 12	0.031	N/A
Core body temperature (°C)	36.6 ± 1	36.6 ± 1	0.080	0.090

Data are expressed as mean ±standard deviation.
A p-value <0.05 was considered the minimum level of significance.
SAP: systolic arterial pressure; DAP: diastolic arterial pressure; MAP: mean arterial pressure; RAP: right atrial pressure; PAOP: pulmonary arterial occlusion pressure; SPAP: systolic pulmonary arterial pressure; DPAP: diastolic pulmonary arterial pressure; MPAP: mean pulmonary arterial pressure; HR: heart rate; N/A: not applicable.

Calculations

From the cardiopulmonary measurements, cardiac index (CI), alveolar oxygen tension (P_AO₂), arterial oxygen content (CaO₂), mixed venous oxygen content (CvO₂), pulmonary capillary blood oxygen content (Cc′O₂), systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI), oxygen extraction ratio (O₂ ER), DO₂I, Q̇_s/Q̇_t, physiologic dead space (V_D/V_T), and the alveolar-arterial oxygen difference (P_A-aO₂) were calculated according to the following formulas:

1
CI = CO/body surface area (L minute⁻¹ m⁻²)
2
P_AO₂ = [FiO₂ × (P_B − P_H2_O)]– 1.2 PaCO₂ (mm Hg)
3
CaO₂ = (1.36 × Hb × SaO₂) + 0.003 × PaO₂ (mL dL⁻¹)
4
CvO₂ = (1.36 × Hb × SvO₂) + 0.003 × PvO₂ (mL dL⁻¹)
5
Cc′O₂ = (1.36 × Hb × 100/100) + 0.003 × P_AO₂ (mL dL⁻¹)
6
SVRI =[(MAP − RAP)/CI] × 80 (dynes seconds cm⁻⁵ m⁻²)
7
PVRI =[(MPAP − PAOP)/CI] × 80 (dynes seconds cm⁻⁵ m⁻²)
8
O₂ ER = (CaO₂ − CvO₂)/CaO₂ (%)
9
DO₂I = CaO₂ × CI × 10 (mL minute⁻¹ m⁻²)
10
Q̇ _s/Q̇_t = (Cc′O₂– CaO₂/Cc′O₂–CvO₂) × 100 (%)
11
V_D/V_T = (PaCO₂ − e′CO₂)/PaCO₂ (%)
12
P_A-aO₂ = P_AO₂ − PaO₂ (mm Hg)

where FiO₂ = the fractional concentration of inspired oxygen, P_B = barometric pressure, and P_H2_O = vapor pressure of water (46.93 mm Hg at 36.6 °C).

Statistical analysis

A randomized block anova for repeated measures was used to evaluate the effect of treatment (closed chest and open chest) on hemodynamic and pulmonary parameters (expressed as mean ± standard deviation). A p-value <0.05 was considered the minimum level of significance. When the p-value from the anova was significant, individual comparisons were made between treatment groups (closed chest and open chest) using Fisher's least significant difference test. Power calculations were performed using a statistical software package (Solo Power Analysis 1.0, BMDP Statistical Software, Los Angeles, CA, USA).

Results

Hemodynamic and pulmonary data are presented in Tables 1–3. Creation of an open chest induced a significant decrease in PaO₂ (p = 0.018) and CaO₂ (p = 0.025) because of a significant increase in Q̇_s/Q̇_t (p = 0.023). Creation of an open chest induced a significant increase in V_D/V_T (p = 0.015) and P_A-aO₂ (p = 0.019) and a significant decrease in Pe′CO₂ (p = 0.049). Arterial partial pressures of CO₂ (p = 0.766; power = 0.776) and SaO₂ (p = 0.178; power = 0.195) were not significantly affected. Opening the chest did have an effect on hemodynamic parameters with a significant increase in HR (p = 0.031), DPAP (p = 0.050), and MPAP (p = 0.033). Oxygen delivery index was not significantly affected by placement of cannulae for thoracoscopy (p = 0.545; power = 0.562).

Table 3. The effect of opening the chest on calculated cardiopulmonary parameters in anesthetized normal dogs

Variable	Closed chest	Open chest	p-value	Power
CI (L minute⁻¹ m⁻²)	5 ± 2	6 ± 2	0.426	0.445
CaO₂ (mL dL⁻¹)	23.07 ± 2	22.77 ± 2	0.025	N/A
SVRI (dynes seconds cm⁻⁵ m⁻²)	1066 ± 250	1064 ± 276	0.981	0.982
PVRI (dynes seconds cm⁻⁵ m⁻²)	136 ± 36	150 ± 53	0.495	0.513
O₂ ER (%)	15 ± 5	14 ± 4	0.169	0.186
DO₂I (mL minute⁻¹ m⁻²)	1229 ± 478	1292 ± 390	0.545	0.562
Q̇ _s/Q̇_t (%)	9 ± 5	17 ± 9	0.023	N/A
V_D/V_T (%)	11 ± 7	18 ± 4	0.015	N/A
P_A-aO₂ (mm Hg)	97 ± 54	182 ± 97	0.019	N/A

Data are expressed as mean ±standard deviation.
A p-value <0.05 was considered the minimum level of significance.
CI: cardiac index; CaO₂: arterial oxygen content; SVRI: systemic vascular resistance index; PVRI: pulmonary vascular resistance index; O₂ ER: oxygen extraction ratio; DO₂I: oxygen delivery index; Q̇_s/Q̇_t: shunt fraction; V_D/V_T: physiologic dead space; P_A-aO₂: alveolar-arterial oxygen difference; N/A: not applicable.

Discussion

Oxygen delivery was not significantly affected by the creation of an open chest with the placement of thoracoscopy cannulae. Opening the thoracic cavity had no significant effect on CI, and the reduction in CaO₂ was not sufficient to impair DO₂I. Although the reduction in CaO₂ was statistically significant, the degree of change was not biologically significant. Placement of the thoracoscopy cannulae had no significant effect on SaO₂; however, a 19% reduction in PaO₂ did occur.

Placement of the thoracoscopy cannulae resulted an increase in Q̇_s/Q̇_t, resulting in an increase in P_A-aO₂ and a reduction in both PaO₂ and CaO₂. Increased Q̇_s/Q̇_t after opening the thoracic cavity results from atelectasis of the alveoli and a reduction in the functional residual capacity (FRC) of the lungs (Craig et al. 1962; Sabanathan et al. 1990; de Gray et al. 1997). Alveolar atelectasis occurs because of compression of the dependent lung by the heart, the mediastinum, and the abdominal organs (Nunn 1961; Froese & Bryan 1974; Hedenstierna et al. 1985; Yoshida & Takaori 1991; Cohen 1997). This results in an increase in the amount of each tidal volume being delivered to the poorly perfused, non-dependent lung lobe, resulting in an alteration of the V̇/Q̇ ratio (Nunn 1961; Werner et al. 1984; Yoshida & Takaori 1991; de Gray et al. 1997; Dunn 2000). Administration of atracurium results in a greater displacement of the non-dependent diaphragm because the motion of the diaphragm is no longer determined by active contraction (Cohen 1997). Upon opening the chest, the upper lung is no longer restricted by the inward displacement of the diaphragm, resulting in a further increase in the ventilation of the poorly perfused non-dependent lung lobes (Cohen 1997).

Placement of thoracoscopy cannulae reduced PaO₂ by 19% but did not result in a significant reduction of SaO₂. Intercostal thoracotomy is usually associated with a significant reduction in PaO₂ and SaO₂, with a 29–39% reduction in PaO₂ being documented in other studies (Yoshida & Takaori 1991; Rustomjee et al. 1994). In clinical cases, we commonly see about a 40% decrease in PaO₂ during thoracotomy in dogs. In contrast to thoracoscopy, intercostal thoracotomy allows the upper lung to over-inflate as the thoracic wall does not limit its expansion (Cohen 1997). Over-inflation results in a very high ventilation–perfusion ratio in the non-dependent lung (Cohen 1997). The inflation of the dependent lung, on the other hand, is reduced, resulting in atelectasis and low V̇/Q̇. Because the thoracic wall is intact, thoracoscopy prevents an over-inflation of the non-dependent lung. A higher proportion of ventilation, therefore, will occur in the dependent lung, resulting in a smaller Q̇_s/Q̇_t and a lower reduction in PaO₂, SaO₂, and CaO₂. Nevertheless, changes to gas exchange and intrapulmonary gas distribution do occur with thoracoscopy, as evidenced by the increase in Q̇_s/Q̇_t from 9% to 17% after opening the chest in this study.

Physiologic dead space significantly increased in this study without a variation in PaCO₂. During intercostal thoracotomy, V_D/V_T increases often with an increase in PaCO₂, because the ventilation of poorly perfused alveoli in the more compliant non-dependent lungs is increased (Nunn 1961). Each lung moves to a lower lung volume in the pressure–volume curve that has a different effect on the compliance of the dependent and non-dependent lungs (Cohen 1997; Benumof & Alfery 2000; Dunn 2000). The non-dependent lung moves from a flat, non-compliant portion of the pressure–volume curve to a steep, more compliant part (Benumof & Alfery 2000). Conversely, the dependent lung moves from the steep, compliant part of the curve to a lower, flat, and less compliant part, resulting in a loss of FRC (Benumof & Alfery 2000; Dunn 2000). The distribution of ventilation, therefore, is altered with most of the tidal volume being delivered to the less-perfused non-dependent lung (Nunn 1961; Hatch 1966; Rehder et al. 1972). This augmentation of ventilation in the non-dependent lung is ‘wasted’ because these alveoli are inefficient at eliminating CO₂ (Nunn 1961; West 2000b). Therefore, during intercostal thoracotomy, the Pe′CO₂ can be unchanged despite an increase in PaCO₂, resulting in an increase in V_D/V_T (Nunn 1961; Wagner et al. 1998). Because the thoracic wall is intact with thoracoscopy, the change in compliance and the alteration of intrapulmonary gas distribution would be expected to be less than those occurring during thoracotomy. This is supported by the lack of effect of thoracoscopy in this study on PaCO₂. The small decrease in Pe′CO₂ from opening the chest with thoracoscopy cannulae resulted from an increase in V_D/V_Tand an increase in wasted ventilation. As evidenced by the unchanged PaCO₂, the degree of wasted ventilation would be expected to be less with thoracoscopy than with thoracotomy.

In this study, the only hemodynamic parameters significantly affected by opening the thoracic cavity were HR, MPAP, and DPAP. Yoshida & Takaori (1991) demonstrated significant increases in MPAP and PVRI after opening the chest in dogs undergoing thoracotomy. Pulmonary vascular resistance is a function of CO, MPAP, and PCWP (Borst et al. 1956; Roos et al. 1961; West & Dollery 1965; West 2000a). Pulmonary vascular resistance may be less affected during thoracoscopy than it is during thoracotomy, as the intrapulmonary gas distribution is less affected. Over-inflation of the non-dependent lung during thoracotomy can over-stretch the alveoli, resulting in a compression of the alveolar capillaries, while atelectasis of the dependent lung reduces the capillary diameters because of collapse of the alveoli (Borst et al. 1956; Roos et al. 1961; West & Dollery 1965; West 2000a). Use of colored microspheres would enable us to further understand the alteration in distribution of blood flow at the level of capillaries that occurs after opening the thoracic cavity. Werner et al. (1984) documented a significant increase in CI after opening the chest in human patients undergoing thoracotomy. This finding, however, may have been related to surgical stimulus as there was a concurrent significant increase in HR. We also found an increase in HR after placement of thoracoscopy cannulae, which is most likely because of surgical stimulus. Our observed change in HR, however, while being statistically significant was not biologically significant and did not affect CO.

To facilitate IPPV in these patients, atracurium was administered as needed to maintain muscle paralysis. An appropriate plane of anesthesia was maintained with the administration of isoflurane at an end-tidal concentration of 1.85–95% (approximately 1.5 × minimum alveolar concentration). At the completion of the experiment, analgesia was maintained with an IV fentanyl infusion and a transdermal fentanyl patch.

One limitation to our study is that the power of our statistics is limited. A power of 80% gives confidence in the rejection of the null hypothesis (Campbell & Machin 1999). The number of dogs evaluated in this study did limit our confidence in the non-significant comparisons between treatment groups. Thus, our conclusion that opening the chest with thoracoscopy does not have any detrimental effect on CI and DO₂I must be made with some reservation. While increasing the number of dogs in this study would have improved the power values, it is unlikely that a detrimental effect on cardiac index and oxygen delivery would have been identified. The second limitation to this study was that the dogs evaluated were healthy dogs, free of any cardiopulmonary disease. As a result, the detrimental effect of opening the chest on SaO₂ was not as dramatic as that expected in diseased patients where Hb desaturation can occur during thoracic surgery. Finally, we did not have a group of dogs undergoing thoracotomy to enable a comparison between the cardiopulmonary effects of open-chest thoracoscopy versus intercostal thoracotomy. While this study suggests that thoracoscopy has less detrimental cardiopulmonary effects than thoracotomy, this would need to be proven in a controlled study.

Conclusions

Open chest thoracostomy is not detrimental to hemodynamic function and oxygen delivery in normal dogs, although significant increases in HR, MPAP, DPAP, Q̇_s/Q̇_t, V_D/V_T, and P_A-aO₂ do occur. The increase in Q̇_s/Q̇_t and associated V̇/Q̇ mismatching result in a reduction in PaO₂ and CaO₂. The detrimental effects of thoracoscopy on gas exchange and pulmonary gas distribution appear to be less than those of intercostal thoracotomy; however, a controlled study would be required to substantiate this. Nevertheless, the adverse effects on gas exchange with an open-chest thoracoscopy will potentiate those observed when one-lung ventilation is used in more advanced thoracoscopic procedures.

Acknowledgement

This study was supported by the Surgeon-In-Training Research Grant awarded by the American College of Veterinary Surgeons.

References

Benumof JL, Alfery DD (2000) Anesthesia for thoracic surgery. In: Anesthesia (5th edn). RD Miller (ed.). Churchil Livingstone, Philadelphia, PA, USA, pp. 1665–1752.
Google Scholar
Borst HG, McGregor M, Whittenberger JL et al. (1956) Influence of pulmonary arterial and left atrial pressures on pulmonary vascular resistance. Circ Res 4, 393–399.
10.1161/01.RES.4.4.393
CAS PubMed Web of Science® Google Scholar
Campbell MJ, Machin D (1999) The randomized controlled trial. In: Medical Statistics. A Commonsense Approach (3rd edn). MJ Campbell, D Machin (eds). John Wiley and Sons Ltd., Chichester, England, pp. 115–126.
Google Scholar
Cantwell SL, Duke T, Walsh PJ et al. (2000) One-lung versus two-lung ventilation in the closed-chest anesthetized dog: a comparison of cardiopulmonary parameters. Vet Surg 29, 365–373.
10.1053/jvet.2000.7545
CAS PubMed Web of Science® Google Scholar
Cohen E (1997) Physiology of the lateral position and one-lung ventilation. Chest Surg Clin N Am 7, 753–771.
CAS PubMed Web of Science® Google Scholar
Craig JOC, Bromley LL, Williams R (1962) Thoracotomy and contralateral lung. A study of the changes occurring in the dependent and contralateral lung during and after thoracotomy in lateral decubitus. Thorax 17, 9–15.
10.1136/thx.17.1.9
CAS PubMed Google Scholar
Daly CM, Swalec-Tobias K, Tobias AH et al. (2002) Cardiopulmonary effects of intrathoracic insufflation in dogs. J Am Anim Hosp Assoc 38, 515–520.
10.5326/0380515
PubMed Web of Science® Google Scholar
Dunn PF (2000) Physiology of the lateral decubitus position and one-lung ventilation. Int Anesthesiol Clin 38, 25–53.
10.1097/00004311-200001000-00004
CAS PubMed Web of Science® Google Scholar
Dupre GP, Corlouer JP, Bouvy B (2001) Thoracoscopic pericardectomy performed without pulmonary exclusion in 9 dogs. Vet Surg 30, 21–27.
10.1053/jvet.2001.20344
CAS PubMed Web of Science® Google Scholar
Faunt KK, Cohn LA, Jones BD et al. (1998a) Cardiopulmonary effects of bilateral hemithorax ventilation and diagnostic thoracoscopy in dogs. Am J Vet Res 59, 1494–1498.
10.2460/ajvr.1998.59.11.1494
CAS PubMed Web of Science® Google Scholar
Faunt KK, Jones BD, Turk JR et al. (1998b) Evaluation of biopsy specimens obtained during thoracoscopy from lungs of clinically normal dogs. Am J Vet Res 59, 1499–1502.
10.2460/ajvr.1998.59.11.1499
CAS PubMed Web of Science® Google Scholar
Froese AB, Bryan AC (1974) Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology 41, 242–255.
10.1097/00000542-197409000-00006
CAS PubMed Web of Science® Google Scholar
Garcia F, Prandi D, Pena T et al. (1998) Examination of the thoracic cavity and lung lobectomy by means of thoracoscopy in dogs. Can Vet J 39, 285–291.
CAS PubMed Web of Science® Google Scholar
De Gray L, Rush EM, Jones JG (1997) A noninvasive method for evaluating the effect of thoracotomy on shunt and ventilation perfusion inequality. Anaesthesia 52, 630–635.
10.1111/j.1365-2044.1997.153-az0159.x
CAS PubMed Web of Science® Google Scholar
Hatch D (1966) Ventilation and arterial oxygenation during thoracic surgery. Thorax 21, 310–314.
10.1136/thx.21.4.310
CAS PubMed Web of Science® Google Scholar
Hazelrigg SR, Landreneau RJ, Boley TM et al. (1991) The effect of muscle-sparing versus standard posterolateral thoracotomy on pulmonary function, muscle strength, and postoperative pain. J Thorac Cardiovasc Surg 101, 394–400.
PubMed Web of Science® Google Scholar
Hedenstierna G, Strandberg A, Brismar B et al. (1985) Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation. Anesthesiology 62, 247–254.
10.1097/00000542-198503000-00007
CAS PubMed Web of Science® Google Scholar
Isakow K, Fowler D, Walsh P (2000) Video-assisted thoracoscopic division of the ligamentum arteriosum in two dogs with persistent right aortic arch. J Am Vet Med Assoc 217, 1333–1336.
10.2460/javma.2000.217.1333
CAS PubMed Web of Science® Google Scholar
Jackson J, Richter KP, Launer DP (1999) Thoracoscopic partial pericardectomy in 13 dogs. J Vet Intern Med 13, 529–533.
10.1111/j.1939-1676.1999.tb02205.x
CAS PubMed Web of Science® Google Scholar
Landreneau RJ, Hazelrigg SR, Mack MJ et al. (1993) Postoperative pain-related morbidity: video assisted thoracic surgery versus thoracotomy. Ann Thorac Surg 56, 1285–1289.
10.1016/0003-4975(93)90667-7
CAS PubMed Web of Science® Google Scholar
Lewis RJ, Caccavale RJ, Sisler GE et al. (1992) One hundred consecutive patients undergoing video-assisted thoracic operations. Ann Thorac Surg 54, 421–426.
10.1016/0003-4975(92)90431-3
CAS PubMed Web of Science® Google Scholar
MacPhail CM, Monnet E, Twedt DC (2001) Thoracoscopic correction of persistent right aortic arch in a dog. J Am Anim Hosp Assoc 37, 577–581.
10.5326/15473317-37-6-577
CAS PubMed Web of Science® Google Scholar
Nunn JF (1961) The distribution of inspired gas during thoracic surgery. Ann R Coll Surg Engl 28, 223–237.
CAS PubMed Google Scholar
Polis I, Gasthuys F, Gielen I et al. (2002) The effects of intrathoracic pressure during continuous two-lung ventilation for thoracoscopy on the cardiorespiratory parameters in sevoflurane anaesthetized dogs. J Vet Med A Physiol Pathol Clin Med 49, 113–120.
10.1046/j.1439-0442.2002.00404.x
CAS PubMed Web of Science® Google Scholar
Radlinsky MG, Mason DE, Biller DS et al. (2002) Thoracoscopic visualization and ligation of the thoracic duct in dogs. Vet Surg 31, 138–146.
10.1053/jvet.2002.31062
PubMed Web of Science® Google Scholar
Rehder K, Sessler AD (1973) Function of each lung in spontaneously breathing man anesthetized with thiopental-meperidine. Anesthesiology 38, 320–327.
10.1097/00000542-197304000-00004
CAS PubMed Web of Science® Google Scholar
Rehder K, Hatch DJ, Sessler AD et al. (1972) The function of each lung of anesthetized and paralyzed man during mechanical ventilation. Anesthesiology 37, 16–26.
10.1097/00000542-197207000-00004
PubMed Web of Science® Google Scholar
Roe PG, Jones JG (1993) Analysis of factors which affect the relationship between inspired oxygen partial pressure and arterial oxygen saturation. Br J Anaesth 71, 488–494.
10.1093/bja/71.4.488
PubMed Web of Science® Google Scholar
Roos A, Thomas LJ, Nagel EL et al. (1961) Pulmonary vascular resistance as determined by lung inflation and vascular pressures. J Appl Physiol 16, 77–84.
10.1152/jappl.1961.16.1.77
CAS PubMed Web of Science® Google Scholar
Rustomjee T, Wagner A, Orton EC (1994) Effect of 5 cm of water positive end-expiratory pressure on arterial oxygen tension in dogs during and after thoracotomy. Vet Surg 23, 307–310.
10.1111/j.1532-950X.1994.tb00489.x
CAS PubMed Web of Science® Google Scholar
Sabanathan S, Eng J, Mearns AJ (1990) Alterations in respiratory mechanics following thoracotomy. J R Coll Surg Edinb 35, 144–150.
CAS PubMed Google Scholar
Sapsford DJ, Jones JG (1995) The PiO₂ vs. SpO₂ diagram: a non-invasive measurement of pulmonary oxygen exchange. Eur J Anaesthesiol 12, 375–386.
CAS PubMed Web of Science® Google Scholar
Wagner AE, Gaynor JS, Dunlop CI et al. (1998) Monitoring adequacy of ventilation by capnometry during thoracotomy in dogs. J Am Vet Med Assoc 212, 377–379.
10.2460/javma.1998.212.03.377
CAS PubMed Web of Science® Google Scholar
Walsh PJ, Remedios AM, Ferguson JF et al. (1999) Thoracoscopic versus open partial pericardectomy in dogs: comparison of postoperative pain and morbidity. Vet Surg 28, 472–479.
10.1111/j.1532-950X.1999.00472.x
CAS PubMed Web of Science® Google Scholar
Werner O, Malmkvist G, Beckman A et al. (1984) Gas exchange and haemodynamics during thoracotomy. Br J Anaesth 56, 1343–1349.
10.1093/bja/56.12.1343
PubMed Web of Science® Google Scholar
West JB (2000a) Blood flow and metabolism – how the pulmonary circulation removes gas from the lung and alters some metabolites. In: Respiratory Physiology – the Essentials (6th edn). Lippincott Williams & Wilkins, Philadelphia, PA, USA, pp. 29–44.
Google Scholar
West JB (2000b) Ventilation-perfusion relationships – how matching of gas and blood flow determines gas exchange. In: Respiratory Physiology – the Essentials (6th edn). Lippincott Williams & Wilkins, Philadelphia, PA, USA, pp. 45–61.
Web of Science® Google Scholar
West JB, Dollery CT (1965) Distribution of blood flow and the pressure-flow relations of the whole lung. J Appl Physiol 20, 175–183.
10.1152/jappl.1965.20.2.175
Web of Science® Google Scholar
Yoshida H, Takaori M (1991) Pulmonary gas exchange and ventilation–perfusion relationships during hypocapnia and thoracotomy in anaesthetized dogs. Can J Anaesth 38, 527–532.
10.1007/BF03007594
PubMed Web of Science® Google Scholar

Received 20 February 2003; accepted 18 June 2003.

Citing Literature

Volume31, Issue2

April 2004

Pages 121-128

Cardiopulmonary effects of thoracoscopy in anesthetized normal dogs

Abstract

Introduction

Materials and methods

Experimental design

Anesthesia

Catheterization

Creation of an open-chest

Data collection

Calculations

Statistical analysis

Results

Discussion

Conclusions

Acknowledgement

References

Citing Literature

References

Information

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Cardiopulmonary effects of thoracoscopy in anesthetized normal dogs

Abstract

Introduction

Materials and methods

Experimental design

Anesthesia

Catheterization

Creation of an open-chest

Data collection

Calculations

Statistical analysis

Results

Discussion

Conclusions

Acknowledgement

References

Citing Literature

References

Related

Information