Adult Chest Surgery

Chapter 5. Anesthesia Management

Anesthetic management of the thoracic surgical patient may improve operative conditions, efficiency, and outcome. Overlap exists in the territories of responsibility between thoracic surgeons and anesthesiologists, highlighting the importance of communication and mutual understanding. This chapter provides a brief overview of the general conduct of anesthesia for pulmonary resections, followed by a discussion of selected concepts in thoracic anesthesia of utility to thoracic surgeons.


Barring extremes of pathophysiology (e.g., end-stage chronic obstructive pulmonary disease), lesion-related hazards (e.g., compression of vital structures), or important coexisting disease states, the conduct of anesthesia for pulmonary resection is largely dictated by the surgical approach. For thoracotomy, the most common strategy consists of general anesthesia with paralysis, an arterial catheter (and possibly a central venous catheter), double-lumen tube (DLT), thoracic epidural, and immediate postoperative extubation.

Before induction, antibiotics, sedatives, and nebulized bronchodilator treatments are administered as indicated, and the epidural is positioned and tested. After induction, diagnostic bronchoscopy may be performed via a large (8.0–8.5 mm) endotracheal tube or laryngeal mask airway (LMA). Findings that may affect the lung isolation plan should be noted by the anesthesia team at this time. Lung isolation by DLT or bronchial blocker (BB) then is imposed, with confirmation of position by pediatric fiberoptic bronchoscopy. After lateral decubitus positioning, repeat bronchoscopy is recommended. Ventilator parameters must be adjusted with initiation of one-lung ventilation (OLV) to ensure adequate gas exchange and to prevent barotrauma. Surgical entrance of the pleural space permits direct evaluation of the quality of lung isolation. Suctioning of secretions may aid atelectasis. Blood products should be available and checked before hilar dissection. Cross-clamp of the pulmonary artery typically does not cause changes in central venous pressure (CVP) or hemodynamics in patients with adequate cardiopulmonary reserve, and oxygenation should improve (see below). On cross-clamping of the bronchus, unchanged ventilatory compliance should be confirmed. If available, bronchoscopic visualization of the stump is useful before stapling. A "leak test" is commonly used by providing 20–30 cm H2O of positive pressure ventilation to the submerged stump. Recruitment of any remaining lung is accomplished with incremental 5-second periods of 20–40 cm H2O of positive pressure ("recruitment maneuvers"). After closure and supine repositioning, a final bronchoscopy via a large tube or LMA may necessitate a tube exchange. Rapid emergence and extubation depend on the strategic use of short-acting anesthetic agents; limited narcotic use; full reversal of muscle relaxation; control of secretions, bronchospasm, and pain (thoracic epidural); and return of airway reflexes, sensorium, and adequate respiratory efforts. Respiratory mechanics are greatly aided by raising the head of the bed more than 30 degrees at emergence (see Chap. 8).

Variations on the foregoing and procedure- or lesion-specific issues are presented as "bullet points" at the conclusion of this chapter.


The anesthesiologist should be equally invested in assessments of cardiopulmonary reserve and coexisting disease states, as discussed in Chapter 4. Beyond that, the broad goal of the preoperative anesthetic evaluation is to identify issues with an aim toward reducing perioperative risk through preemption or preparation. The history, physical examination, and review of radiographic information should be targeted to anticipate problems with induction, airway management, lung isolation, vascular access, and pain management. Acute processes (e.g., respiratory infections) or the need to optimize treatment of existing conditions occasionally may justify postponement, but the semielective nature of thoracic oncologic surgery often mandates a higher risk tolerance.

Induction risk is increased in patients with threatened major airways, tamponade physiology, difficult airway anatomy, and traumatic or emergency scenarios. Paraneoplastic or associated syndromes (e.g., carcinoid syndrome, myasthenia gravis, Eaton-Lambert syndrome) have specific management implications (see below). Factors predictive of desaturation during OLV may be identified in advance (Table 5-1).

Table 5-1. Factors Associated with Desaturation during OLV

·   High percent perfusion or ventilation to operative lung

·   Low baseline PaO2

·   Right-sided surgery

·   Normal or restrictive pattern by spirometry

·   Supine surgical position



Patient medication regimens, in general, should not be disrupted, with the exception of insulin, oral hypoglycemic agents, and anticoagulants. Guidelines for how long anticoagulants should be held before placing an epidural have been published in a consensus statement by the American Society of Regional Anesthesia(Table 5-2). Patients with ischemic cardiac disease may benefit from thoracic epidural analgesia (TEA) and invasive hemodynamic monitoring despite a minimally invasive surgical approach. In such patients, perioperative beta-adrenergic blockade should not be withheld for fear of bronchospasm. Avoiding inhalational anesthetics and narcotics by use of total intravenous anesthetic (TIVA) techniques, together with TEA, may enable early extubation despite severe obstructive lung disease.

Table 5-2. Recommended Duration to Hold Anticoagulants before Epidural



Aspirin/nonsteroidal anti-inflammatory drug/COX-2


Unfractionated heparin (5000 units subcutaneous)


Unfractionated heparin (intravenous, therapeutic)

4 h

Low-molecular-weight heparin


  High dose

24 h

  Low dose

12 h


3 days

Selective ADP inhibitors


  Clopidogrel (Plavix)

7 days

  Ticlopidine (Ticlid)

14 days

Glycoprotein IIb/IIIa inhibitors


  Tirofiban (Aggrastat)

2 h

  Eptifibatide (Integrelin)

4 h

  Abciximab (Reopro)

36 h


Adapted from reference 1.


Invasive arterial blood pressure monitoring is indicated for most thoracotomies and many lesser procedures in which there is unstable or severe cardiac disease or the opportunity for catastrophic bleeding. Central venous blood pressure monitoring is significantly distorted by alterations in intrathoracic pressure during thoracic surgery, but such catheters are useful when venous access is problematic or for postoperative volume management. Central lines are best placed on the operative side because a pneumothorax in the nonoperative chest would be problematic during OLV.

Pulse oximetry is a standard, invaluable monitor but possesses limitations that deserve to be understood. Pulse oximetry does not measure oxygen saturation directly. Red (660 nm) and near-infrared (940 nm) light is emitted from diodes and attenuated by the tissue and blood through which it passes. The pulsatile portion of the signal is presumed to be arterial blood. The SpO2 value is derived from the ratio of pulse-added absorbances at 940 nm (oxygenated hemoglobin) and 660 nm (reduced hemoglobin). Motion, ambient light, and venous pulsations can introduce artifact. Other species of hemoglobin will introduce error. Carboxyhemoglobin falsely elevates SpO2. High methemoglobin levels lead to an SpO2 of 85% regardless of PaO2. SpO2 readings below 85% should not be considered precise.

Monitoring for myocardial ischemia is compromised during left-sided thoracic surgery by the inability to place electrocardiogram leads in physiologic positions. Even in right-sided surgery, the position of the heart relative to the chest is altered, reducing electrocardiographic sensitivity. Transesophageal echocardiography may prove useful as a monitor of ischemia as well as right-sided heart function in response to pulmonary artery cross-clamping but does not necessarily predict subsequent right-sided heart failure. Transesophageal echocardiography also may help to guide surgical decisions in the evacuation of loculated pericardial effusions or the assessment of pulmonary venous anastomoses after lung transplantation. Pulmonary artery catheters are used infrequently in thoracic surgery because of the potential pitfalls in interpretation,the risk of entrapment in resection staple lines, and the limited need for left-sided filling pressures or cardiac output determinations. Right-sided heart pressures (CVP) are generally of greater value.

Capnography has become a standard monitor and reliably confirms alveolar ventilation and cardiac output. The capnogram shape roughly correlates with the degree of obstructive disease (Fig. 5-1). The gradient between end-tidal CO2 and PaCO2 is affected by the amount of dead space, which can be significant and variable in thoracic surgical patients. Acute changes in capnogram waveforms may signal bronchospasm, tube malposition, circuit disconnection, ventilator valve malfunction, or exhausted CO2 absorbant. Acute pulmonary embolism results in a sudden decrease in end-tidal CO2 (increased dead space). High end-tidal CO2 levels also can be the earliest sign of malignant hyperthermia. Effective chest compressions during cardiac arrest are reflected by the return of a capnogram.

Figure 5-1.


Capnograms depicting exhaled CO2 in a patient with normal (A) and severely obstructive pulmonary function (B).


In the lateral decubitus position, the head and neck should be supported in line with the spine, with attention to protecting the eyes and dependent ear. Lateral neck flexion may cause traction injury of the suprascapular nerve and postoperative shoulder pain. An axillary roll placed caudad to the axilla relieves pressure on the dependent humeral head and axillary nerves and vessels. Excessive abduction of the nondependent arm (>90 degrees to the torso) may cause brachial plexus injury or contribute to shoulder pain. Ulnar nerves at the elbow and the dependent peroneal nerve are vulnerable and should be padded.


Induction implies loss of consciousness. Inhalation of volatile anesthetics (e.g., sevoflurane or desflurane) can achieve induction with maintenance of spontaneous ventilation. Intravenous inductions (e.g., propofol, thiopental, or etomidate) usually produce apnea. Propofol is used most commonly for its favorable antiemetic and kinetic profile. As a continuous infusion, propofol (with or without narcotic) is a TIVA or a useful sedative in lower doses. Etomidate is a cardiostable induction agent but is associated with greater nausea and may inhibit adrenal function. Ketamine has sympathomimetic and analgesic activity but may cause tachycardia, increased pulmonary artery pressure, and disturbing hallucinations. Ketamine is most useful for inducting patients with hypovolemia, tamponade, or bronchospasm or as an adjunct.

Physiology of Induction

It is critically important to understand the negative effects of induction on venous return and the caliber of airways. Induction in the supine position causes a 20% reduction in functional residual capacity (FRC), amounting to roughly 500 mL. This reduction in FRC occurs irrespective of the agents used (excepting ketamine), the imposition of paralysis, or the preservation of spontaneous ventilation, and it persists for some hours after emergence. Airway calibers and resistance to airflow may be affected correspondingly. Patients with variable obstruction of major airways (e.g., anterior mediastinal mass effect) may convert to life-threatening complete obstruction on induction.

Induction impairs venous return by removal of the thoracic pump effect, imposition of positive-pressure ventilation, and vasodilation from induction agents. Increased intrathoracic pressure from positive end-expiratory pressure (PEEP; from the ventilator or auto-PEEP) will further reduce the gradient for venous return. Dynamic hyperinflation of lungs from auto-PEEP may exert pressure on the heart (with a closed chest), further impairing diastolic filling. Induction thus may unmask tamponade-like effects from large pleural or pericardial effusions or anterior mediastinal masses. Great vessels may be held open by traction during spontaneous ventilation but partially collapse under the weight of a large tumor on induction. The common mechanistic denominator, venous return to the heart, must be considered and defended at the time of induction.

Strategies for High-Risk Inductions


Collapse of threatened major conducting airways may occur as a result of the decrease in FRC, as well as loss of the traction effect of inspiration that accompanies induction. Such "dynamic obstruction" may result from intraluminal masses, tracheomalacia, or large anterior mediastinal masses. Predicting which patients will lose patency with induction remains a judgment based primarily on symptoms and radiographic studies. Generally, patients who are asymptomatic at full expiration while supine will tolerate an intravenous induction. Coughing or dyspnea with this maneuver or tracheal lumens of less than 50% of normal by computed tomographic (CT) scan are treated more conservatively at my institution. Upright and supine flow-volume loops will sensitively illustrate dynamic obstruction but are of limited predictive value for induction. Intermediate concern may prompt a spontaneous-breathing (inhalation) induction, or an awake, topically anesthetized fiberoptic examination before induction. If the latter reveals non-reassuring anatomy, the stenotic region should be stented with an endotracheal tube before induction. Rigid bronchoscopy, patient repositioning, and jet ventilation are potential rescue maneuvers that should be immediately available. Short-acting agents for induction and muscle relaxation should be used initially in the event that resumption of spontaneous ventilation is required. Distal tracheal/carinal obstruction should prompt a more conservative approach because of the greater difficulty of emergently stenting such lesions with a tube or rigid bronchoscope. It is possible to place a DLT into a bronchus as a stent under local anesthesia. Placement of an LMA with topical anesthesia to the pharynx offers a convenient approach for awake fiberoptic examination of the entire trachea (Fig. 5-2). Local anesthetic delivered through the working port of the bronchoscope then can anesthetize the vocal cords and trachea. Rapid absorption by mucosal surfaces makes it important to be cognizant of the recommended thresholds for local anesthetic toxicity.

Figure 5-2.


Bronchoscopic view of the vocal cords via a laryngeal mask airway (LMA).


Patients at risk include those with large pleural or pericardial effusions, hypovolemia, severe obstructive lung disease, or large masses compressing the heart or great veins. Preemptive vasoconstrictors, intravascular volume expansion, use of cardiostable induction agents, patient positioning, avoidance of an epidural test dose, and use of graded inspiratory volumes and long expiratory times will preserve venous return in most inductions. When clinical and/or radiographic/echocardiographic evidence suggests higher risk, induction with maintenance of spontaneous ventilation is a more conservative approach. Preinduction drainage of pericardial or pleural fluid under local anesthesia should be considered in symptomatic (dyspneic) patients. Lower extremity large-bore intravenous access is essential for patients with superior vena cava syndrome. Tension pneumothorax should be considered in patients with bullous emphysema and recalcitrant hypotension after induction. Intraarterial blood pressure monitoring before induction is indicated for all high-risk patients, as is a plan for resuscitation should cardiovascular collapse occur.


Induction risk is also increased for patients with unfavorable airway anatomy, significant symptoms of gastroesophageal reflux, bronchospasm, or unstable coronary or severe valvular heart disease. Not uncommonly, competing priorities mandate compromise of one or the other concern. While aspiration risk argues for a rapid-sequence intravenous induction, this avenue may be contraindicated by difficult airway anatomy. Patients with unfavorable upper airway anatomy predictive of a difficult intubation (e.g., morbid obesity or micrognathia) should have an airway established under local anesthesia (e.g., LMA or awake fiberoptic intubation) before induction unless it is documented or apparent that the patient can be ventilated by mask. Use of short-acting agents (e.g., propofol or succinylcholine) is prudent whenever the airway is in question.


Failure to fully expire the preceding tidal volume at inspiration results in air trapping or auto-PEEP (Fig. 5-3). Auto-PEEP may lead to hemodynamic instability (including cardiac arrest) and barotrauma from dynamic hyperinflation. During OLV, excessive auto-PEEP in the dependent lung impairs gas exchange by diverting pulmonary blood flow to the nondependent lung. The incidence and severity of auto-PEEP roughly correlate with the severity of obstructive disease (Fig. 5-4) and is further exacerbated by the higher airflow resistance of DLTs and by inappropriate ventilator settings.

Figure 5-3.


Schematic depiction of the development of dynamic pulmonary hyperinflation (auto-PEEP) and its resolution with a period of apnea. (From Myles PS, Ryder IG, WeeksAM, et al: J Cardiothorac Vasc Anesth 11:100, 1997, with permission.)


Figure 5-4.


Relationship between the degree of airflow obstruction (FEV1/FVC) and dynamic pulmonary hyperinflation (auto-PEEP). (From Ducros L, Moutafis M, Castelain MH, et al: J Cardiothorac Vasc Anesth 13:35, 1999, with permission.)


Options for lung isolation remain threefold: DLTs, BBs, and endobronchial intubation.

Double-Lumen Tubes

The default choice for lung isolation in most cases is a left DLT for its ease of insertion, comfortable margin for error, and capacity to deflate either lung depending on which lumen is clamped. Auscultation may be used to confirm position, but direct visualization by fiberoptic bronchoscopy is increasingly a standard of care (Fig. 5-5). Up to 30% of patients with DLTs positioned by auscultation require repositioning when subsequently examined by fiberoptic bronchoscopy.If the left DLT passes into the right main stem bronchus instead of the left, the fiberoptic bronchoscope may be used as a stylette via the bronchial lumen to guide the tube into the left bronchus after withdrawal to the trachea. Reconfirmation of DLT position should be performed after turning the patient to the lateral decubitus position.

Figure 5-5.


A. Optimally positioned left-sided DLT. B. Bronchoscopic view via tracheal lumen of carina, DLT, and bronchial cuff (blue) correctly positioned.


Right-sided DLTs have a fenestration in the bronchial lumen for the right upper lobe that must be aligned by fiberoptic bronchoscopy (Fig. 5-6). Common indications include any surgery in which pathology exists or any surgery intended in the left main stem bronchus (e.g., left pneumonectomy, sleeve resection, bronchopleural fistula repair, or left single-lung transplant). The likelihood of displacement is greater for a right-sided DLT than for a left-sided DLT. Because of this, some practitioners prefer to use a left-sided DLT (or a BB) for left pneumonectomy and to withdraw the apparatus before division of the bronchus. Right-sided DLTs cannot accommodate an anomalously short right main stem bronchus.

Figure 5-6.


A. Optimally positioned right-sided DLT. B. Bronchoscopic view via bronchial lumen with right upper lobe aligned with the fenestration.

Current DLTs have D-shaped lumens with favorable airflow resistance characteristics. They are disposable and made of polyvinylchloride with low-pressure, high-volume cuffs. They are stiffer and larger than single-lumen tubes and have the potential to traumatize vocal cords and the distal airway. Compared with BBs, the large lumens of DLTs offer a route for air egress and active suctioning to accelerate collapse of the operative lung.

Bronchial Blockers

BB options now range from simple balloon-tipped Fogarty vascular embolectomy catheters to blocker systems (e.g., Univent (Fuji Systems Corporation, Tokyo, Japan), Arndt (Cook Critical Care, Bloomington, IN USA), and Cohen (Cook Critical Care, Bloomington, IN USA)) (Fig. 5-7). Blockers are generally easier to place than DLTs in patients with anatomically difficult airways, and they obviate the need for multiple tube changes. Blockers may also be used to achieve lung isolation via nasotracheal intubations or tracheostomy tubes, to isolate hemoptysis, or to tamponade mucosal bleeding from a bronchial lesion. Modern blocker systems have central lumens that permit air to egress and insufflation of oxygen (CPAP). They can even be positioned to selectively deflate individual lobes in patients who would not tolerate complete lung collapse. BBs are more useful for left-sided procedures. When positioned in the short right main stem bronchus, they are easily displaced with repositioning or surgical manipulation of the lung. A sudden inability to ventilate when using a BB likely signifies a blocker that has popped out into the trachea. The appropriate reflex is to announce the situation and deflate the blocker balloon to establish ventilation if time does not permit bronchoscopic examination.

Figure 5-7.


A. Arndt wire-guided BB (Cook) passed through a single-lumen tube into the left main stem bronchus. B. Bronchoscopic view of the same BB.

Endobronchial Intubation

Endobronchial intubation may be achieved with traditional single-lumen tubes advanced into main stem bronchi or with specifically designed endobronchial tubes with more favorable (short and distal) cuff designs and a fenestration for the right upper lobe. Indications for endobronchial intubation in adults include carinal resections or patients with prior pneumonectomy and bronchopleural fistula. In emergent massive hemoptysis from the left lung, blind advancement of an endobronchial tube into the right main stem bronchus can be lifesaving. Endobronchial intubation is also useful for pediatric patients in whom currently available DLT sizes fail to fit.

Special Lung Isolation Situations

Tracheal deviation or a splayed carina may make intubation of the left main stem bronchus difficult. A right-sided DLT or BB, if appropriate, likely would be easier than a left-sided DLT for such situations. Saber-sheath tracheas may occlude the tracheal lumen of a DLT. An anomalous short right main stem bronchus predicts a poor fit for a right-sided DLT. A left-sided DLT, BB, or endobronchial tube (depending on the planned surgery) should be considered in its stead. An efficient option for lung isolation for patients with difficult intubation status is to perform a fiberoptic intubation with a single-lumen tube together with a BB or, alternatively, to change to a DLT over an airway-exchange catheter. Wire-guided BB systems enable placement of a BB into individual lobes.


Efficient gas exchange depends on tight matching of pulmonary ventilation (/ mismatch is the residual blood flow through the operative, nondependent lung, which constitutes pure shunt. Although individual variations can be substantial, blood flow to that lung is reduced on average from 45% to 55% of cardiac output to approximately 20% principally by gravity and hypoxic pulmonary vasoconstriction (HPV). Additional shunt is invariably present in the dependent lung as well owing to the circumferential restrictive forces imposed by the weight of the mediastinum, the dependent hemidiaphragm, and the anteroposterior stabilizers. / mismatch also may exist to varying degrees within the ventilated dependent lung from parenchymal disease such as chronic obstructive pulmonary disease, secretions, bronchospasm, and so forth. Maneuvers to minimize nondependent and dependent lung shunt and dependent lung / mismatch are the basis for optimizing oxygenation during OLV.


HPV is critical both to reduce nondependent lung blood flow and to fine-tune / matching in the dependent lung. The mechanism of HPV remains unknown but appears to be mediated by voltage-sensitive potassium channels in response to (primarily) alveolar hypoxia and (secondarily) low mixed venous oxygen saturation. HPV is a rapid local response unique to the pulmonary vasculature and does not depend on intact vascular endothelium or autonomic innervation. Most vasodilators inhibit HPV, including nitrates (e.g., nitroglycerin and nitroprusside) nitric oxide, isoproterenol, terbutaline, adenosine, dobutamine, and to a lesser extent, calcium channel antagonists. Inhaled anesthetic agents (e.g., isoflurane, sevoflurane, desflurane, and halothane) all inhibit HPV in a dose-dependent fashion. Within clinically relevant concentrations (<1 minimum alveolar concentration), however, their effect is of minimal significance. Hypercapnia/acidosis enhances and hypocapnia/alkalosis inhibits HPV. The net effect of any variable on oxygenation during OLV depends on the combined effects on HPV (direct and indirect), cardiac output, and mixed venous oxygen tension and cannot be predicted.


Optimal single-lung ventilatory settings are controversial and often require a compromise between optimal recruitment of the dependent lung (large tidal volumes) and risk of barotrauma. This balance is most delicate in patients with severe obstructive disease who are prone to auto-PEEP. Such patients may benefit from a protective ventilatory strategy (5–7 mL/kg tidal volumes) and transient permissive hypercapnia. There is no firm evidence at this time, however, that "traditional" ventilatory strategies (10 mL/kg) are injurious or that protective ventilatory strategies improve outcome.


The incidence of hypoxemia during OLV has dropped from more than 20% in the 1970s to less than 1%owing to improved DLT designs, increased use of the fiberoptic bronchoscope, and improved understanding of the physiology of OLV. Treatment options for hypoxemia during OLV are listed in Table 5-3. Which maneuver to employ first depends on the clinical scenario. In rapid, severe desaturation, reinflation should be the first move, coordinated with the surgeon. If time permits, passage of a bronchoscope to confirm tube/blocker position and to rule out obstruction, secretions, blood, kinks, and so forth is prudent.

Table 5-3. Treatment Options for Hypoxemia during OLV

FIO2 = 1

Bronchoscopy to rule out

  Tube malposition


  Other sources of obstruction

PEEP to the dependent lung

CPAP to the nondependent lung

Reinflate nondependent lung

Cross-clamp nondependent pulmonary artery (if surgically appropriate)


CPAP and Optimal PEEP during OLV

Continuous positive airway pressure (CPAP; 5–10 cm H2O) delivered to the nondependent lung generally will improve oxygenation but may partially reinflate the lung and interfere with the conduct of surgery. PEEP delivered to the dependent lung may improve oxygenation through recruitment of atelectatic lung units. Each patient has an optimal PEEP level beyond which oxygenation will deteriorate as a consequence of increased nondependent lung shunt. Extreme air trapping may result in hemodynamic instability and barotrauma. The degree of auto-PEEP is not measurable by standard operating room ventilators but can be detected by briefly disconnecting the circuit and observing for end-expiratory airflow. Patients likely to benefit from dependent lung PEEP are patients predisposed to dependent lung atelectasis (e.g., those with restrictive disease, obesity, and young patients with a normal FEV1). In contrast, patients with severe obstructive disease likely will have unavoidable levels of auto-PEEP equal to or in excess of their optimal PEEP. Low levels of extrinsic (ventilator imposed) PEEP will not increase total PEEP in patients with significant auto-PEEP. A useful strategy therefore is to begin with less than 5 cm H2O of extrinsic PEEP and to increase PEEP incrementally with SpO2 as a guide in patients who are hypoxemic during OLV.

Other Strategies to Improve Oxygenation during OLV

When surgical cross-clamping of the pulmonary artery is imminent, marginal saturations can be tolerated with the knowledge that cross-clamping invariably will improve oxygenation by eliminating nondependent lung shunt. Minor improvements in oxygenation occasionally can be achieved by eliminating drugs that inhibit HPV or by delivering nebulized bronchodilators to the dependent lung. Because inhalational anesthetics inhibit HPV and most intravenous agents do not, TIVA has been proposed to improve oxygenation during OLV. Clinical studies are currently inconclusive on this matter, which is complicated by secondary effects on oxygenation through changes in cardiac output and mixed venous oxygen saturation.Similarly, inhaled nitric oxide, which might be expected to reduce nondependent lung shunt and improve dependent lung blood flow, has proved to be ineffective in improving one-lung oxygenation in a number of human studies.5


The priority for early extubation of pulmonary resection patients influences most anesthesiologists to select relatively short-acting agents. For induction, propofol is widely favored for its low incidence of nausea as well as its kinetics. Vecuronium is a convenient muscle relaxant because of its neutral hemodynamic effects as well as its intermediate duration. Of the currently used potent inhalational agents, sevoflurane and desflurane are both rapidly eliminated as a consequence of their low solubility. Desflurane has more airway irritant effects than sevoflurane, but this is not a clinically significant issue when adequate anesthetic depth is present. Both are eliminated more rapidly than isoflurane. Nitrous oxide is often avoided because of the potential to expand in closed spaces (e.g., blebs, pneumothoraces, and endotracheal tube cuffs) and because its use requires a reduction in FIO2. Unless contraindicated (e.g., history of bleomycin therapy), a high FIO2 is often necessary to achieve a safe margin of oxygenation during OLV. Narcotics are useful in limited doses as a supplement to anesthetic depth and to blunt airway reflexes. Excessive narcotic effect blunts respiratory drive, clouds the sensorium, induces nausea and constipation, and delays extubation. Therefore, narcotics generally are used judiciously before intubation and sparingly thereafter. The ultra-short-acting narcotic remifentanil is particularly useful to blunt airway reflexes before tube exchanges at the terminus of the case without delaying extubation. TIVA (usually propofol ± remifentanil) may be advantageous for maintenance in patients with severe obstructive disease, in whom elimination of inhaled agents can be delayed significantly or for patients undergoing rigid bronchoscopy.


A midthoracic epidural catheter is justified for most thoracotomies, whether full posterolateral or limited muscle-sparing, and is best placed before induction. An awake patient will respond dramatically and early to any needle contact with nerve roots or spinal cord. Epidural needle-induced nerve damage has been reported with thoracic epidurals performed in anesthetized patients. After aspiration, an initial test dose (e.g., 3 mL of 2% lidocaine with epinephrine 1:200,000) should be administered with monitors in place to serve three vital functions. Failure to aspirate clear fluid and absence of dense motor block or exaggerated hypotensive response suggest that the catheter position is not erroneously subarachnoid. Failure to aspirate blood and absence of an epinephrine-induced spike in heart rate suggest that the catheter is not erroneously positioned within a blood vessel. Third, the development of a midthoracic band of analgesia within 10–15 minutes strongly suggests an appropriately positioned epidural catheter.

After induction, if significant blood loss or hypotension is probable, it is wise to delay the imposition of a dense thoracic epidural (sympathetic) block. Patients with unstable coronary disease may benefit from early initiation of the block, with care to preserve coronary perfusion (diastolic) pressure. In all other situations, the timing of initiation and intraoperative management of the TEA is largely dictated by the blood pressure. However it is managed, a dense blockade at the terminus of surgery is imperative to achieve extubation after thoracotomy. Claims of a "preemptive analgesic" advantage from early initiation of TEA have not been established.


Barring unusual blood loss, a target positive fluid balance in the first 24 hours of less than 20 mL/kg with less than 2 L of intraoperative crystalloid has been recommended for pulmonary resection surgery.This relatively restrictive practice, particularly intended for pneumonectomy patients, stems from the finding that postpneumonectomy pulmonary edema (PPPE; incidence = 2–4%) has a high mortality and has been associated with higher fluid balances.While the etiology of such PPPE is unknown, it is characterized by low pulmonary wedge pressures and high protein edema fluid. Thus increased pulmonary capillary permeability is presumed, and any intravascular fluid over and above what is essential to hemodynamic stability will redistribute to pulmonary interstitium proportionately. Contributing factors include reduced lymphatic drainage and right-sided surgery (because lymphatic compromise is greater after right pneumonectomy).

Postulated causes of PPPE, besides fluid overload, include oxygen toxicity, lung hyperinflation, or ventilator-induced lung injury. The latter possibility has influenced many anesthesiologists to limit OLV tidal volumes to 6–7 mL/kg rather than to the traditional 10 mL/kg. Prolonged elevated airway pressures during OLV for thoracic surgery have been identified as risk factors for PPPE.Postoperative management of chest drainage also may influence the degree of hyperinflation of the residual lung. Whether prevention of lung hyperinflation will eliminate PPPE remains to be tested. While fluid restriction alone fails to eliminate PPPE,it is sensible to limit the magnitude of pulmonary capillary transudates should endothelial injury occur. The essential caveat is that intravascular volume should not be reduced to the point where the thoracic epidural is not tolerated or to the peril of end-organ perfusion.


Jet ventilation (JV) systems deliver pulses of oxygen from a high-pressure source (20–50 lb/in2) via a narrow-orifice attachment or catheter placed either within the airway or attached to a rigid bronchoscope. Upper or lower airway surgery may be performed by JV without the interference or fire hazard of an endotracheal tube. The manually triggered Sanders JV system (Fig. 5-8) is the simplest example. By Bernoulli's principle, ambient air is entrained at the mouth of the jet, increasing the tidal volume and decreasing the FIO2 by an unpredictable amount. Because it is an open system, inhalational anesthetics cannot be used, and end-tidal CO2 cannot be monitored. There is risk of aspiration and barotrauma, but in experienced hands, JV is safe and effective. Most commonly, JV is used for surgery (including laser surgery) of major conducting airways.

Figure 5-8.


Sanders jet ventilator.

High-frequency ventilation is an umbrella term for any of a variety of delivery systems that use small (e.g., 2 mL) tidal volumes at frequencies of 60–2400 breaths/min. High-frequency ventilation may be delivered through a standard endotracheal tube or through a small-diameter jet orifice (high-frequency JV). Mechanisms of gas exchange in high-frequency ventilation include mass movement, Taylor dispersion (i.e., enhanced diffusion), coaxial gas flow, and pendelluft movement. Purported advantages include lower mean airway pressures and a motionless operative field. Advantageous applications to patients with large bronchopleural fistulas or tracheobronchial disruptions have been advocated but poorly supported by data. As with JV, the ability to use small-diameter catheters improves surgical conditions and exposure.

High-frequency oscillatory ventilation improves gas exchange by its push-pull effect but results in a shimmering operative field, which may disrupt surgery. Low-flow apneic ventilation (essentially turning the ventilator off and applying CPAP with 100% O2) can sustain adequate oxygen saturations in many patients for 5–10 minutes when there is a surgical need for a motionless field. Acidosis and CO2 accumulation (which rises by 6 mm Hg in the first minute and then by 3 mm Hg/min thereafter) limit the duration of apneic oxygenation.


Sources of pain after thoracotomy include soft tissue, ribs, intercostal nerves, pleura, diaphragm, and pulmonary parenchyma. Afferents mediating this pain include intercostal nerves (4–8) and the vagal and phrenic nerves. No single modality ablates all sources of thoracotomy pain.

Ipsilateral shoulder pain is reported by 80% of thoracotomy patients who have functional epidurals. It is likely that the epidural unmasks shoulder pain by covering the dominant incisional pain. Shoulder pain is multifactorial. Postulated causes include referred pain (from the diaphragm, pericardium, pleura or bronchus), and pain from ligamentous injuries to the shoulder due to positioning or surgical mobilization of the scapula. Phrenic blockade reduces the incidences of shoulder pain by more than 50%,and shoulder blocks have variable efficacy. Systemic nonsteroidal anti-inflammatory drugs are the most consistently effective but carry risk of renal, gastrointestinal, or bleeding complications.

Chronic postthoracotomy pain syndrome (persistent pain along incision site for more than 2 months after thoracotomy, unrelated to recurrence or infection) is reported in over 50% of patients. The pain is neurolytic in nature and presumed to result from trauma to intercostal nerves. Entrapment by sutures, direct trauma, and crush injuries from retractors or instruments (including thoracoscopes) are among the postulated mechanisms. The severity is variable, with fewer than 10% of patients seeking treatment for postthoracotomy pain syndrome.

Thoracic Epidural Analgesia

TEA represents the current standard for acute postthoracotomy pain control. Small-bore multiport catheters inserted via 17-gauge needles into the midthoracic epidural space provide an avenue for intermittent bolus, continuous infusion, or patient-controlled delivery of analgesics. Most use a dilute solution of local anesthetic (e.g., bupivacaine, ropivacaine, or levobupivacaine) and opioid. The combination produces synergism of effect and permits reduced dosages. Fentanyl, meperidine, and hydromorphone are popular opioid choices because they possess intermediate lipophilicity. Highly lipophilic opioids (e.g., sufentanil) are absorbed quickly and produce greater systemic symptoms (i.e., sedation). Morphine is hydrophilic and thus spreads more broadly within the epidural space with risk of higher levels, pruritus, and delayed respiratory depression. The very dilute dose of bupivacaine, enabled by the synergistic effect of the opioid, has the advantage of producing very little motor blockade of respiratory muscles.

The most common side effect from TEA is hypotension from local anesthetic blockade of presynaptic sympathetic nerves. Sympatholysis results in dilation of venous capacitance vessels, venous pooling (especially in the splanchnic bed), and possibly reduced cardiac contractility. Treatment consists of intravascular volume expansion, vasopressors, and inotropes. Other complications of TEA are listed in Table 5-4.

Table 5-4. Complications of Thoracic Epidural Analgesia

·   Postdural puncture headache

·   Inadvertent subarachnoid (spinal) block

·   Local anesthetic toxicity—seizures, heart block, cardiac arrest

·   Epidural infection

·   Nerve injury

·   Epidural hematoma

·   Nerve injury from needle on compression by epidural hematoma or abscess

·   Horner syndrome

·   Hypotension

·   Urinary retention

·   Sedation

·   Respiratory depression

·   Pruritus

·   Failure to work



Evolving neurologic deficits in a patient who had a TEA should prompt urgent magnetic resonance imaging to rule out an epidural hematoma or abscess with spinal cord compression. Local anesthetic toxicity generally produces jitteriness progressing to seizures. Bupivacaine toxicity may manifest first with blockade of cardiac conduction. Treatment requires supportive care until the local anesthetic effects wear off. In extreme bupivacaine toxicity, this may require cardiopulmonary bypass. Central nervous system toxicity may not be evident during general anesthesia, highlighting the importance of a test dose preceding induction. Aspiration from the catheter before each injection serves to rule out migration of the catheter into blood vessels.

Contraindications to TEA include coagulopathy, infection at the insertion site, local anesthetic allergy (extremely rare), and patient refusal. Relative contraindications include sepsis, preexisting neurologic deficit, and tumor involvement at the site.

Perioperative outcome is improved by epidural analgesia. Meta-analyses indicate that epidural analgesia is associated with reduced pulmonary (infection, atelectasis)10 and cardiac (myocardial infarction)11 complications. Even when compared with equianalgesic systemic narcotic regimens, TEA confers superior "dynamic" analgesia while coughing. The cardiosympatholytic effect protects against myocardial ischemia and reduces postoperative supraventricular arrhythmias. The cardioprotective effects of TEA depend on how it is managed. Significant hypotension may counteract its beneficial anti-ischemic effects. Chronic postthoracotomy pain is reduced in patients with aggressive management of acute postoperative pain with TEA, lending support for a potential preemptive effect.

Pain Management Other Than Tea

Intravenous patient-controlled analgesia with opioids is used most commonly for video-assisted thoracic surgery (VATS) or sternotomy incisions, which, barring significant cardiopulmonary disease, do not warrant TEA. If TEA is used for sternotomy incisions, parenteral narcotics or parasternal blocks are often required to supplement the most cephalad portion. As mentioned previously, dynamic analgesia with patient-controlled analgesia is inferior to TEA. The need for adjuncts, including intercostal or paravertebral blocks, nonsteroidal anti-inflammatory drugs, or ketamine, is not uncommon. Paravertebral blocks rival TEA and only impose a unilateral sympathectomy but have a higher technical failure rate and last only 12–18 hours. Intercostal blocks are simple and familiar to surgeons. Rapid vascular uptake of local anesthetics after intercostal blockade limits duration to 4–8 hours and raises the risk of toxicity. To include the lateral cutaneous branch, intercostal blocks must be applied posterior to the posterior axillary line. A rule-of-thumb safe limit for intercostal blocks using bupivacaine with epinephrine is 2.5 mg/kg.

Cryotherapy to exposed intercostal nerves before chest closure produces a blockade lasting up to 6 months. Concern that it might cause chronic neuralgia has prevented its widespread acceptance.

Interpleural catheters delivering local anesthetics tend to be unreliable because the agents distribute within the chest by gravity and are lost to chest drainage. Transcutaneous electrical nerve stimulation, acupuncture, and hypnotherapy are used only occasionally as adjuncts in thoracic anesthesia. Lumbar intrathecal morphine (0.2–0.3 mg) provides 24 hours of good analgesia for patients in whom TEA is contraindicated. The high incidence of pruritus and concern over delayed respiratory depression from ascension within the spinal canal have limited its popularity.


Cervical Mediastinoscopy

·   Intravenous access adequate for potential bleeding

·   Right-hand pulse oximeter (or arterial line, if indicated) to detect innominate artery compression

·   Limit nitrous oxide usage (pneumothorax potential)

VATS Pulmonary Resection

·   TEA and arterial line if poor cardiopulmonary reserve or high probability to convert to open resection.

·   Consider TEA when large utility port is anticipated (e.g., VATS lobectomy).

·   Early lung isolation and active suctioning of operative lung secretions to promote atelectasis in operative lung.

·   Avoid operative lung CPAP if possible.

·   Leak test after resection (sustained positive pressure of 20–30 cm H2O with chest filled with saline).

·   Recruitment maneuvers (up to 40 cm H2O sustained positive pressure) to maximally reexpand remaining lung.

·   If converted to thoracotomy without TEA, employ intercostal blocks and moderate-dose opioids for emergence, followed by awake TEA versus paravertebral blocks.


·   Ensure absence of anesthesia "hardware" in operative bronchus and pulmonary artery.

·   Assess stability at time of pulmonary artery test-clamp (CVP should not change).

·   Assess for compliance changes with bronchial cross-clamp before staples are fired.

·   Leak test as above.

·   Conservative fluid management because of risk of PPPE.

·   Be prepared for cardiac herniation when returning patient to supine position (especially right pneumonectomy).

·   Mediastinal shift may be cause of moderate instability at end of case.

·   Assiduous care to avoid disruption of bronchial stump when exchanging tubes.

Extrapleural Pneumonectomy

·   Large intravenous access, arterial line, TEA, CVP on operative side, nasogastric tube.

·   Four units of bank blood in operating room.

·   Avoid sympathetic (epidural) block until hemostasis is achieved.

·   Prevent exacerbation of blood loss by hypertension during dissection phase.

·   Be prepared for intermittent hypotension from surgeon-induced impairment of venous return. Temporize with vasopressors, and communicate with surgeons.

·   PEEP to dependent lung frequently advantageous (restrictive physiology).

·   Leak test after specimen is removed, as per pneumonectomy.

·   Benign transient ST-segment elevation on electrocardiogram is frequently seen during "wash phase" (? temperature effect).

·   Terminus of case as per pneumonectomy; higher risk of cardiac herniation (especially with right EPP).


·   TEA, arterial line, large intravenous access, and CVP (sparing left neck), nasogastric tube.

·   Liberalize intravenous fluids to account for deficit and substantial insensible losses.

·   Avoid dense sympathetic block until final anastomosis.

·   Avoid large doses of alpha-adrenergic agonists because they may affect conduit tone (length).

·   Have glucagon (1 mg) available if requested for smooth muscle relaxation (conduit length).

·   Assiduous care to avoid esophageal intubation at time of endotracheal tube exchange (consider tube exchange catheter).

·   Consider postoperative ventilation if there is significant airway edema.

Anterior Mediastinal Mass

·   See "Strategies for High-Risk Inductions".

·   Lower extremity intravenous access if superior vena caval compression.

·   Assess risk of tamponade by echocardiogram.

·   Consider awake, topically anesthetized fiberoptic assessment of airway in symptomatic patients.

·   Rigid bronchoscopy option must be available as a backup.

·   Maintain spontaneous ventilation until airway is ensured.

·   Assess risk of airway obstruction based on symptoms and CT scan.

·   Arterial line for symptomatic patients.


·   Low FIO2 during electrocautery with open trachea (fire hazard)

Rigid Bronchoscopy/Core-Out

·   Initial bronchoscopy awake or spontaneously breathing if airway is tenuous (as above).

·   Ventilate by jet or sideport of rigid scope.

·   Total intravenous anesthesia.

·   Arterial line to assess PaCO2 (if using jet).

·   Consider Heliox if severely stenotic.

Laser Core-Out

·   Lowest possible FIO2; avoid N2O (supports combustion).

·   Wavelength-specific eye protection for patient and personnel.

·   Fuel sources away from laser path.

·   Saline-filled syringe within reach.

·   LMA or rigid bronchoscope for distal airway lesions.

·   If intubation is required, use "laser safe" tube (with saline in cuff).

·   Consider Heliox if severely stenotic.

·   Induction considerations as per threatened major airways.

Photodynamic Therapy

·   Blue goggle eyewear protection for patient and personnel.

·   Limit patient's skin exposure to overhead/intense light.

·   Rotate pulse oximeter probe to new site every hour.

·   General anesthesia is not imperative but is often expedient and allows for motionless target.

Lung Volume-Reduction Surgery

·   Similar anesthesia whether VATS or sternotomy.

·   Arterial line, TEA, ± CVP.

·   Support induction with vasopressors/fluid bolus.

·   Dynamic hyperinflation is unavoidable.

·   Delicate balance between adequate ventilation and barotrauma.

·   Err on side of permissive hypercapnia rather than barotrauma to dependent lung during OLV.

·   Minimal or no intravenous narcotics or sedatives (except remifentanil).

·   Total intravenous anesthesia.

·   Arterial blood gases to establish ETCO2–PaCO2 gradient.

Tracheal Resection/Reconstruction

·   Be prepared to ventilate distal, divided trachea via jet (with catheter) or sterile tube over the field.

·   Alternative technique is use of long, thin endotracheal tube placed orally, advanced beyond lesion, with surgeon working around it.

·   A third technique is to jet via an orally placed catheter with tip situated near lesion.

·   Induction considerations as per threatened major airways.

·   Smooth emergence may be facilitated by use of remifentanil for final bronchoscopy.

·   Prevent head extension after anastomosis.

Bronchopleural Fistula

·   If small air leak, single-lumen tube for initial bronchoscopy.

·   If large, consider awake bronchoscopy, followed by lung (fistula) isolation, before positive-pressure ventilation.

·   Ensure patent chest drain before positive-pressure ventilation.

·   Attention to prevent further disruption of stump by endotracheal tube.

·   If large, consider alternative modes of ventilation (spontaneous, JV, high-frequency JV) and TIVA.

·   Protect against cross-contamination with position and lung isolation.

Carcinoid Syndrome

·   Arterial line for prompt detection of carcinoid crisis.

·   Octreotide (somatostatin analog) pretreatment, infusion, or immediate availability.

·   Avoid sympathomimetic drugs.

·   Thoracic epidural to blunt sympathetic response to thoracotomy.

·   Potential significant bleeding or mediator release from tumor manipulation.

·   Evaluate for carcinoid heart disease or associated endocrinopathies. 

o    Hyperglycemia

o    Cushing's syndrome

o    Increased antidiuretic hormone (ADH) and melanocyte-stimulating hormone (MSH).

Myasthenia Gravis

·   Associated with thymoma.

·   Skeletal muscle weakness owing to autoimmune destruction of acetylcholine receptors at neuromuscular junction.

·   Increased sensitivity to non-depolarizing muscle relaxants.

·   Resistance to succinylcholine.

·   Increased sensitivity to narcotics.

·   Symptomatic improvement with preoperative plasmapheresis.

·   Maintain preoperative anticholinesterase treatment.

·   Eliminate nondepolarizing muscle relaxant use if possible.

·   Succinylcholine is usually okay, but duration may be prolonged by plasmapheresis and anticholinesterase usage.

·   Monitor for myasthenic versus cholinergic crisis.

·   Close observation for postoperative respiratory failure.

·   Low threshold for postoperative ventilatory support.

Myasthenic (Eaton-Lambert) Syndrome

·   Associated with small cell carcinoma of the lung.

·   Proximal limb skeletal muscle weakness.

·   Improved strength with activity (posttetanic facilitation) in contrast to myasthenia gravis.

·   Autoimmune-mediated reduction in quanta of acetylcholine released from motor neurons.

·   Increased sensitivity to both non-depolarizing and depolarizing muscle relaxants.

·   Poor response to anticholinesterase drugs.

·   Avoid all muscle relaxants if possible.


1. Horlocker TT, Wedel DJ, Benzon H, et al: Regional anesthesia in the anticoagulated patient: Defining the risks (Second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med28:172–97, 2003. [PubMed: 12772135]

2. Benumof J: Anesthesia for Thoracic Surgery. Second edition: Philadelphia, Saunders, 1995:266–268.

3. Klein U, Karzai W, Bloos F, et al: Role of fiberoptic bronchoscopy in conjunction with the use of double-lumen tubes for thoracic anesthesia: A prospective study. Anesthesiology 88:346–50, 1998. [PubMed: 9477054]

4. Slinger P: Management of one-lung anesthesia: Review course lectures. Anesth Analg 100:89, 2005. 

5. Ramsay JG, Murphy M. Postoperative respiratory failure and treatment. Chapter 18 in Kaplan J, Slinger P (eds), Thoracic Anesthesia. Third edition: Philadelphia, Churchill Livingstone, 2003:397–422.

6. Zeldin RA, Normandin D, Landtwing D, Peters RM: Postpneumonectomy pulmonary edema. J Thorac Cardiovasc Surg 87:359–65, 1984. [PubMed: 6700243]

7. Licker M, de Perrot M, Spiliopoulos A, et al: Risk factors for acute lung injury after thoracic surgery for lung cancer. Anesth Analg 97:1558–65, 2003. [PubMed: 14633519]

8. Turnage WS, Lunn JJ: Postpneumonectomy pulmonary edema: A retrospective analysis of associated variables. Chest 103:1646–50, 1993. [PubMed: 8404079]

9. Scawn ND, Pennefather SH, Soorae A, et al: Ipsilateral shoulder pain after thoracotomy with epidural analgesia: The influence of phrenic nerve infiltration with lidocaine. Anesth Analg 93:260–4, 2001. [PubMed: 11473840]

10. Ballantyne JC, Carr DB, deFerranti S, et al: The comparative effects of postoperative analgesic therapies on pulmonary outcome: Cumulative meta-analyses of randomized, controlled trials. Anesth Analg 86:598–612, 1998. [PubMed: 9495424]

11. Beattie WS, Badner NH, Choi P: Epidural analgesia reduces postoperative myocardial infarction: A meta-analysis. Anesth Analg 93:853–8, 2001. [PubMed: 11574345]

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