Coronary Artery Disease

Because smoking is prevalent among patients presenting for thoracic surgery, these patients are also at risk for having cardiovascular disease, including coronary and peripheral vascular disease. In particular, patients with coronary disease need to be optimized medically before proceeding with surgery. These patients may have atherosclerosis and hypertension and may be taking β-blockers and statins, which should be continued through the perioperative period, including the day of surgery. Statin use has been shown to reduce perioperative cardiovascular risk in patients undergoing vascular surgery.

Patients with coronary disease may also be taking aspirin unless contraindicated. If a coronary stent has been placed, aspirin is generally required for lifetime use. Most coronary stents currently being placed are drug eluting and necessitate taking another antiplatelet drug such as clopidogrel, which also may need to be continued for 1 year. Typically, clopidogrel is stopped at least 5 days before surgery and preferably 7 days to allow for placement of neuraxial analgesia. Aspirin should be continued both preoperatively and postoperatively and especially needs to be continued if the stent has been recently placed. American College of Cardiology guidelines suggest that, if possible, surgery should be delayed for 1 year after a drug-eluting stent placement. This delay is not likely to be feasible in the presence of a possible lung cancer, which could spread during a prolonged delay. However, some studies have upheld the 6-week delay after bare-metal stents but suggested the risks after drug-eluting stents are minimal after 6 months ( Fig. 14.1 ). The risk of the stent thrombosing perioperatively would generally outweigh the additional risk of bleeding with continuing aspirin therapy. A recent large prospective study of slightly more than 10,000 patients did show that continuing aspirin perioperatively increased bleeding risk without impacting cardiovascular risk. However, that study excluded patients with drug-eluting stents placed within 1 year.

Risk of major 30-day postoperative cardiac events after elective noncardiac surgery in more than 2000 patients after coronary artery stents. The risks after bare-metal (BM) stents become minimal after 6 weeks and after 6 months for drug-eluting (DE) stents.

(Data from Wijeysundera ND, Wijeysundera HC, Wasowicz M, et al. Risk of elective major noncardiac surgery after coronary stent insertion. Circulation . 2012:126:1355.)

Intraoperatively, avoiding excessive myocardial oxygen demand, which could cause myocardial ischemia, is important. Elevated heart rate can be controlled with β-blockade. The short-acting β-blocker esmolol may be useful to acutely control the tachycardia and hypertension that may result from sympathetic stimulation during laryngoscopy, intraoperative stimulation, and emergence from general anesthesia. The placement of a double-lumen tube (DLT) may be more difficult than placement of a single-lumen tube (SLT), and prolonged laryngoscopy is more likely to cause sympathetic stimulation. Nitroglycerin can also be useful to treat hypertension in these situations and can be used together with esmolol, especially if the heart rate is high and hypertension persists. Nitroglycerin can provide both venodilation and dilation of coronary arteries.

In addition to demand-related ischemia, adequate supply of oxygen to the myocardium must be maintained. A relatively low hemoglobin oxygen saturation, which may occur during one-lung ventilation (OLV), may not be tolerated in patients at risk for myocardial ischemia. The lowered oxygen blood content could contribute to the development of myocardial ischemia, which could also lead to arrhythmias. If the oxygen saturation level does drop, it may be necessary to reinstitute two-lung ventilation or add continuous positive airway pressure (CPAP) in such situations. In surgeries via thoracoscopy, it may only be possible to use a limited amount of CPAP without impairing surgical conditions.

The presence of anemia can impact both myocardial supply and demand. A lowered hemoglobin level reduces the oxygen blood content. In addition, anemia may lead to a compensatory tachycardia, increasing myocardial oxygen demand. Anemia, especially in the presence of tachycardia, will not be well tolerated, and these patients should be transfused accordingly. Patients who are treated with β-blockers intraoperatively may not tolerate anemia well.

Recovering from a thoracotomy incision would be accompanied by more pain than from a thoracoscopy. The pain causes sympathetic stimulation and increases myocardial demand. Effective postoperative pain control is especially important in such patients, and an epidural or paravertebral catheter is recommended if possible. Advanced planning is needed in the case of a patient taking clopidogrel, such that it is discontinued 1 week in advance, as per the guidelines of the American Society of Regional Anesthesia. Otherwise, the surgery will either need to be postponed or performed without the benefit of an epidural or paravertebral catheter, which might increase the perioperative pulmonary risk in patients with severe lung disease.

Patients with smoking history and significant coronary disease may have experienced prior myocardial infarction and have resulting cardiomyopathy. Such patients may have an internal cardioverter-defibrillator, which will require a perioperative management strategy. A high inspired oxygen concentration is needed to help tolerate OLV without hypoxemia, limiting the ability to use nitrous oxide (N ₂ O ₂ ). Most commonly, potent inhaled agents are used, although the use of more than 1 minimum alveolar concentration (MAC) may interfere with hypoxic pulmonary vasoconstriction (HPV). Patients with a low left ventricular (LV) ejection fraction may not tolerate the myocardial depressant effects of higher doses of the potent inhaled agents. The concomitant intraoperative use of remifentanil can provide analgesia without vasodilation or myocardial depression and will facilitate a rapid emergence after surgery without prolonged respiratory depression. Its use may allow for a reduction in the amount of potent inhaled agent. Although higher amounts of the potent inhaled agents can inhibit HPV, the use of sevoflurane has been shown to reduce the level of inflammatory mediators during thoracic surgery compared with propofol and remifentanil. It may be necessary to infuse a vasopressor concomitantly with the anesthetic agents to maintain an adequate perfusion pressure. If the cardiomyopathy is severe, it may be prudent to place a central venous catheter to provide central access for the administration of medications such as norepinephrine or phenylephrine. Strategies to manage patients with coronary artery disease are summarized in Box 14.1 .

Box 14.1

Strategies for Perioperative Management for Patients With Coronary Artery Disease

• •
  

  Maintain preoperative aspirin if a coronary stent is present.

  
  
• •
  

  Maintain preoperative β-blocker.

  
  
• •
  

  Hold clopidogrel 7 days preoperatively if possible to allow for neuraxial analgesia.

  
  
• •
  

  Avoid hypoxemia during one-lung ventilation.

  
  
• •
  

  Avoid anemia.

  
  
• •
  

  Avoid tachycardia.

  
  
• •
  

  Maintain adequate perfusion pressure.

  
  
• •
  

  Use epidural or paravertebral postoperative analgesia.

Valvular Heart Disease

Patients with coexisting valvular disease also need special consideration when presenting for thoracic surgery. Patients with aortic stenosis, in particular, need maintenance of cardiac preload, systemic vascular resistance (SVR), and myocardial contractility. Such patients may not tolerate higher amounts of potent inhaled agents because of vasodilation and myocardial depression. Patients with aortic stenosis are likely to have compensatory concentric LV hypertrophy and diastolic dysfunction. Patients undergoing thoracic surgery are prone to atrial arrhythmias, especially if there is a thoracotomy incision. Patients with aortic stenosis and ventricular hypertrophy are likely to poorly tolerate such arrhythmias because of an increased dependence on the atrial contraction for ventricular filling. The sympathetic block and vasodilation associated with epidural analgesia may also not be well tolerated. A dilute concentration of local anesthesia should be used, such as 0.1% bupivacaine, and the epidural should be activated gradually. In addition to maintaining adequate hydration and avoiding excessive myocardial depression and vasodilation, it may be necessary to also infuse a vasoconstrictor during the general anesthetic. The addition of intravenous (IV) remifentanil may be a beneficial adjunct to provide analgesia without myocardial depression or vasodilation.

In the case of a subvalvular outflow tract obstruction, the intraoperative management would differ from that with valvular aortic stenosis. A subvalvular outflow tract obstruction may occur with hypertrophic cardiomyopathy. If there is a significant pressure gradient, it is important to avoid increases in myocardial contractility; β-blockade may be useful in this situation. It is particularly important to maintain adequate preload and afterload to avoid outflow tract obstruction and systolic anterior motion of the mitral valve with its associated mitral regurgitation. As with aortic stenosis and associated ventricular hypertrophy, atrial arrhythmias are poorly tolerated. Patients with regurgitant valvular disease are likely to better tolerate the use of inhaled potent agents because of the associated vasodilation that promotes forward flow with such disease present. It is important to also maintain adequate cardiac preload in these patients.

In the past, the placement of a pulmonary catheter would have been indicated in the presence of significant ventricular dysfunction or valvular disease for monitoring pulmonary artery pressures (PAPs) and measurement of cardiac outputs. Currently, the vast majority of thoracic operations are done without the use of this monitoring technique, which has not been shown to improve outcome. Pulmonary artery catheters (PACs) are also prone to being misused because of misinterpretation of data. The presence of severe pulmonary hypertension, however, is an indication for monitoring with a PAC to guide the administration of nitric oxide (NO) or other pulmonary vasodilators.

The use of the arterial tracing for evaluation of systolic pressure or pulse pressure variation is predictive of fluid responsiveness. A respiratory-related decrease of greater than 13% would suggest that the patient would be fluid responsive. A change of 9% to 13% has been shown to reflect an intermediate range of predictability, a gray zone in which the patient may be fluid responsive. If the systolic pressure or pulse pressure variation is less than 9%, it is unlikely that the patient would be fluid responsive. There has been some question about the usefulness of central venous pressure (CVP) to predict fluid responsiveness during anesthesia. However, in the open-chest context of thoracotomy, CVP may be more useful than the dynamic preload monitors to predict fluid responsiveness. A general goal of fluid management for thoracic surgery is to avoid excessive fluid administration and possible pulmonary edema that is more likely to occur after larger lung resections, particularly right pneumonectomy. An accurate prediction of fluid responsiveness might avoid the use of unnecessary IV fluid challenges.

Cardiomyopathies

During OLV for thoracotomy or thoracoscopy, there will be an obligate 20% to 30% shunt through the nonventilated lung. If the cardiac output also is decreased, the fall in mixed venous oxygen saturation will lead to a fall in arterial oxygen saturation. Thus patients with cardiomyopathies may tolerate OLV poorly. They need monitoring of venous saturation and inotropes to support cardiac output. This is particularly a concern in patients having video-assisted thoracoscopic (VATS) cardiac sympathectomy procedures for refractory ventricular arrhythmias. These procedures are being done with increasing frequency for ventricular tachyarrhythmias refractory to medical or ablative therapies and for long QT syndrome. The approach is by left or bilateral VATS. Intraoperative considerations include reprogramming of implanted electronic antitachycardia devices, percutaneous defibrillator pads, and provisions to optimize cardiac output and oxygenation during OLV. These patients recover slowly from episodes of desaturation during OLV, so it is best to avoid desaturation with prophylactic measures discussed later in the section on management of OLV.

Pulmonary Hypertension

Patients with pulmonary hypertension (mean pulmonary artery [PA] pressure >25 mm Hg by catheterization or systolic PAP >50 mm Hg on echocardiography) may present for a variety of noncardiac thoracic surgical procedures, including pulmonary resections for malignant or benign lesions, esophageal surgery, or vascular surgery. Compared with patients with normal pulmonary pressures, patients with pulmonary hypertension are at increased risk of respiratory complications and the need for prolonged intubation after noncardiac surgery. Much has been written about anesthesia for patients with pulmonary hypertension. The classification of pulmonary hypertension is discussed in Chapter 7 , and it includes primary and secondary causes of pulmonary hypertension, including pulmonary arterial hypertension, pulmonary venoocclusive disease, left heart disease, lung disease and chronic hypoxemia, pulmonary thromboembolic disease, and a variety of autoimmune, metabolic, and systemic disorders. Anesthesiologists often encounter two main types of pulmonary hypertension: pulmonary hypertension caused by left heart disease and pulmonary hypertension caused by lung disease ( Box 14.2 ). Most of the anesthesia literature has focused on patients with underlying cardiac disease. However, patients who present for noncardiac surgery are more likely to have pulmonary hypertension secondary to lung disease and the anesthetic management is very different for these two types of pulmonary hypertension. This section focuses on patients with pulmonary hypertension caused by lung disease. Much of what has been learned about anesthesia for patients with this type of pulmonary hypertension has come from clinical experience with pulmonary endarterectomies and lung transplantation.

Box 14.2

Modified Classification of Pulmonary Hypertension for Anesthesia

Left Heart Disease

• •
  

  Systolic dysfunction

  
  
• •
  

  Diastolic dysfunction

  
  
• •
  

  Mitral valvular disease: stenosis, regurgitation

  
  
• •
  

  Congenital cardiac disease

Lung Disease

• •
  

  Pulmonary vascular disease

  
  
• •
  

  Chronic lung diseases, hypoxemia, sleep apnea

  
  
• •
  

  Thromboembolic pulmonary hypertension

  
  
• •
  

  Miscellaneous: autoimmune, metabolic, and systemic disorders

Although estimates vary widely depending on disease severity and the method of measurement, the prevalence of pulmonary hypertension in severe chronic lung disease ranges from 40% to 50%. As PAP rises, evidence of cor pulmonale develops as increased strain causes the right ventricle to hypertrophy and become dysfunctional. In the United States, cor pulmonale accounts for 10% to 30% of all heart failure admissions, of which 84% are secondary to chronic obstructive pulmonary disease. The risk of right ventricular (RV) ischemia is also increased. The right ventricle is normally perfused throughout the cardiac cycle. However, the increased RV transmural and intracavitary pressures associated with pulmonary hypertension may restrict perfusion of the right coronary artery during systole, especially as PAPs approach systemic levels. Avoiding hypotension is key to managing these patients.

The impact of pulmonary hypertension on RV dysfunction has several anesthetic implications. The hemodynamic goals are similar to other conditions in which cardiac output is relatively fixed. Care should be taken to avoid physiologic states that will increase pulmonary vascular resistance (PVR) such as hypoxemia, hypercarbia, acidosis, and hypothermia. Conditions that impair RV filling, such as tachycardia and arrhythmias, are not well tolerated. Ideally, under anesthesia, RV contractility and SVR are maintained or increased, and PVR is decreased. This would ensure forward flow and minimize the risk of RV ischemia. In practice, these goals can be a challenge to achieve because anesthetics are commonly associated with a decrease in SVR (e.g., propofol and inhalational agents) and a variable effect on PVR.

Ketamine is a useful anesthetic agent in pulmonary hypertension caused by lung disease. Ketamine is well known for its sympathomimetic effects: ketamine increases cardiac contractility and SVR. However, its effect on PVR is controversial. Although concern is often raised over ketamine’s potential to worsen pulmonary hypertension, animal and human clinical studies have suggested that in some contexts it may decrease PVR. Anecdotally, at the authors’ (A.H., P.D.S.) institution, ketamine is commonly and safely used for anesthetic induction of patients with severe pulmonary hypertension. Inodilators such as dobutamine and milrinone may improve hemodynamics in patients with pulmonary hypertension secondary to left heart disease. However, they tend to cause tachycardia and decreased SVR, potentially leading to hemodynamic deterioration of patients with pulmonary hypertension caused by lung disease. To maintain a systemic blood pressure that is greater than the pulmonary artery pressure, vasopressors, such as phenylephrine or norepinephrine, are commonly used. Of the two, norepinephrine is preferable in pulmonary hypertension because it maintains cardiac index and decreases the ratio of PAP to systemic blood pressure (SBP). In contrast, phenylephrine causes the cardiac index to drop while the PAP:SBP ratio remains unchanged. Increasingly, vasopressin is also used to maintain systemic pressures. Vasopressin appears to significantly increase SBP without affecting PAP in patients with pulmonary hypertension ( Fig. 14.2 ). In patients with severe pulmonary hypertension, selective inhaled pulmonary vasodilators, including NO (10–40 ppm) or nebulized prostaglandins (prostacyclin 50 ng/kg per minute) ( Fig. 14.3 ), should be considered. A useful pharmacologic management strategy for the failing right ventricle in patients with pulmonary hypertension caused by lung disease is the combination of a potent IV vasoconstrictor and an inhaled pulmonary vasodilator ( Box 14.3 ). Patients requiring inhaled NO can be weaned with oral sildenafil postoperatively.

In vitro maximal vasoconstriction dose-response curves of human radial (left) and pulmonary (right) arteries to vasopressin and norepinephrine (NorEpi.). All vasoconstrictors studied (including phenylephrine and metaraminol) showed similar dose-response patterns in both types of arteries except vasopressin, which showed no constriction of pulmonary arteries.

(Data from Currigan DA, Hughes RJA, Wright CE, et al. Vasoconstrictor responses to vasopressor agents in human pulmonary and radial arteries. Anesthesiology . 2014;121:930–936.)

Prostacyclin can be delivered continuously into a standard anesthetic circuit and the dose titrated as needed. In the image, prostacyclin is delivered by nebulization to the ventilated lung via a double-lumen tube during thoracic surgery and one-lung ventilation in a patient with pulmonary hypertension.

Box 14.3

Management Principles for Pulmonary Hypertension Secondary to Lung Disease

• 1.
  

  Avoid hypotensive and vasodilating anesthetic agents whenever possible.

  
  
• 2.
  

  Ketamine does not exacerbate pulmonary hypertension.

  
  
• 3.
  

  Support mean systolic arterial pressure with vasopressors: norepinephrine, phenylephrine, vasopressin.

  
  
• 4.
  

  Use inhaled pulmonary vasodilators (nitric oxide, prostacyclin) in preference to IV vasodilators PRN.

  
  
• 5.
  

  Use thoracic epidural local anesthetics cautiously and with inotropes PRN.

  
  
• 6.
  

  Monitor cardiac output.

IV, Intravenous; PRN, as needed.

The extremes of tidal volumes (high and low) can cause compression of the extraalveolar or interalveolar blood vessels, both of which contribute to an increased PVR. As a result, a ventilation strategy that avoids atelectasis as well as lung hyperinflation should be used.

Echocardiography is useful for diagnosis and management of patients with pulmonary hypertension. However, it should be appreciated that transthoracic echocardiographic assessments of RV systolic pressure may be ±10 mm Hg compared with catheterization measurements in more than 40% of patients, with a tendency toward underestimation. Transesophageal echocardiography (TEE) is commonly recommended for intraoperative monitoring of RV function in patients with pulmonary hypertension. Although echocardiography is extremely useful to differentiate between a normally functioning right ventricle and a dilated hypokinetic right ventricle (and this correlates with outcome in cardiac surgery), for minute-to-minute continuous objective monitoring of RV function, TEE is not yet the ideal monitor. This is because the right ventricle is a very complex nongeometric structure in three dimensions. At present, continuous monitoring of minor changes in regional RV function with standard two-dimensional TEE is, at best, difficult. Advances in echocardiography technology, particularly three-dimensional TEE, may make continuous objective monitoring of RV function possible in the future.

At present, the basis of intraoperative monitoring for patients with pulmonary hypertension having noncardiac thoracic surgery remains the PAC. However, it must be understood that PA data alone can be misleading in these patients. Rising PAPs are almost always a bad sign. Falling PAPs may be a good sign indicating pulmonary vasodilation or may be a very bad sign indicating impending RV decompensation. Thus PAP data must be followed in concert with cardiac output, mixed venous saturation, and CVP data.

Although there have been multiple case reports of the successful use of lumbar epidural analgesia and anesthesia in obstetric patients with pulmonary hypertension, there are very few reports of the use of thoracic epidural analgesia in pulmonary hypertension. Patients with pulmonary hypertension caused by lung disease seem to be extremely dependent on tonic cardiac sympathetic innervation for normal hemodynamic stability. In patients undergoing thoracotomy for lung resection, the use of a thoracic epidural impaired baseline RV contractility, but did not affect the compensatory increase in RV contractility brought on by an acute increase in RV afterload. Because of the increased risk of postoperative respiratory complications in these patients, the use of postoperative thoracic epidural analgesia is often desirable. However, it must be appreciated that these patients will often require a low-dose infusion of inotropes or vasopressors during thoracic epidural local analgesia. This may necessitate continued central venous catheterization and intensive care unit admission. Paravertebral analgesia has been associated with better postthoracotomy hemodynamic stability versus thoracic epidural analgesia in patients with normal cardiac function, but this has not been studied specifically in pulmonary hypertensive patients.

The patient populations discussed above (coronary artery disease, cardiomyopathies, and pulmonary hypertension) are those who would be considered to be at high risk for thoracic surgery by open thoracotomy, carrying an increased risk for cardiac, pulmonary, and overall complications. Traditionally, these patients may not have been considered appropriate surgical candidates as a result. However, new evidence has demonstrated the safety of VATS techniques in high-risk patients, with reduced complication rates compared with high-risk patients undergoing open thoracotomy and comparable complication rates to non–high-risk patients undergoing VATS.

Double-Lumen Tubes

Disadvantages

Difficult Intubation

Double-lumen tubes are somewhat bulky and may be more difficult to insert and position compared to SLTs. It may be challenging to switch from a DLT to an SLT and vice versa if the patients require postoperative ventilatory support. The use of tube exchange catheters may trigger a cardiovascular response, which can be detrimental to patients with cardiac disease. Tracheal intubation causes a stress response, resulting in increased sympathetic activity that may result in hypertension, tachycardia, and arrhythmias. These changes in hemodynamics can be harmful to patients with hypertension and myocardial ischemia because of inadequate perfusion of the coronary arteries.

Airway Injuries

Previous studies have found a higher incidence of postoperative sore throat; hoarseness; and in some cases, pharyngeal or bronchial tree laceration ( Fig. 14.4 ) associated with DLT use. Use of an EBB is associated with decreased postoperative hoarseness and fewer days with a sore throat compared with a DLT. Moreover, the blocker technique was associated with a decreased incidence of vocal cord injuries. Any added injury to patients with cardiac disease, who are often on anticoagulant therapy for cardiac stents or arrhythmia, can add a significant increased risk of complications and prolong recovery.

Image taken through a fiberoptic bronchoscope of a laceration of the posterior membranous portion of the left mainstem bronchus just distal to the carina caused by a left-sided double-lumen tube.

Endobronchial Blockers for Lung Separation

Endobronchial blockers can be placed to achieve lung separation and may offer several advantages to patients with cardiac disease. The most significant advantage is the decrease in hemodynamic stress. Because the EBB is inserted through an SLT, it is less stimulating than the insertion and manipulation of a DLT. EBBs can be advantageous in patients with difficult airways or abnormal tracheobronchial trees. In addition, patients with tracheostomies or those who require a nasal intubation are often managed with EBBs. Finally, some patients arrive from the intensive care unit to the operating room (OR) with endotracheal tubes (ETTs) in place; insertion of an EBB would be the best option to avoid changing of the existing SLT.

Lung Separation in Thoracic Aortic Aneurysm Surgery

Because of the close anatomic relationship, a thoracic aortic aneurysm can potentially compress the airway at the level of the trachea or, more often, left mainstem bronchus (LMB). Patients who present with a descending thoracic aortic aneurysm and LMB compression who require lung isolation should be managed with a right-sided DLT ( Fig. 14.5 ). Placement of a left-sided DLT is both difficult and dangerous in these patients, presenting the risk of airway trauma and rupture of the aneurysm. A DLT in a descending thoracic aortic aneurysm repair improves surgical exposure and makes it easier to remove blood and secretions. The use of EBBs for thoracic aneurysm repair should be limited to situations in which intubation or endobronchial placement of a DLT is difficult.

Image taken through a fiberoptic bronchoscope of a posterior compression of the left mainstem bronchus caused by an aneurysm of the descending thoracic aorta.

Lung Separation for Esophageal Surgery

In the United States, 17,000 new patients are diagnosed each year with esophageal cancer, and 15,000 die from the disease. The most common type of esophageal cancer is squamous cell carcinoma, usually in sicker patients with history of heavy smoking and alcohol abuse, who may be physically debilitated, with chronic obstructive pulmonary disease (COPD) and poor lung function. Adenocarcinoma is usually found in patients with gastroesophageal reflux disease.

There are three techniques of surgical approach for esophageal resection: (1) Ivor Lewis esophagectomy: abdominal incision followed by open right thoracotomy with an anastomosis located in the upper chest; (2) transhiatal esophagectomy: the esophageal tumor is removed through an abdominal incision without thoracotomy in which the stomach is pulled posterior to the sternum to perform an anastomosis in the left neck; and (3) minimally invasive esophagectomy: both the abdominal and the thoracic procedures are performed through laparoscopy and thoracoscopy, respectively.

For procedures in which the surgeon has to perform dissections in the right hemithorax, OLV can be provided either by a DLT or by independent EBB. There are several reasons to prefer EBBs for these procedures. Aspiration is a major concern in these patients. Residual food may be present proximal to the obstruction or previous radiation therapy may compromise esophageal function. A rapid-sequence or awake intubation is recommended, and securing the airway with an SLT followed by placement of an EBB is the safest approach. These procedures can be lengthy and with significant amounts of fluid administration, which may cause airway edema. If the patient requires postoperative respiratory support, changing the DLT to an SLT carries the risk of losing control of the airway and should be performed with the help of tube exchange catheters and videolaryngoscopy. Regardless of which device is used, ultimately, the level of familiarity and comfort of the anesthesiologist and surgeon dictate the best management of the patient.

Hypoxemia

A major concern that influences anesthetic management for thoracic surgery is the occurrence of hypoxemia during OLV. There is no universally acceptable value for the safest lower limit of oxygen saturation during OLV. An arterial oxygen saturation of 90% (PaO ₂ ~60 mm Hg) is commonly seen as the lowest acceptable limit. However, the lowest acceptable saturation will be higher in patients with organs at risk of hypoxia because of limited regional blood flow (e.g., coronary or cerebrovascular disease) and in patients with limited oxygen transport (e.g., anemia or decreased cardiopulmonary reserve). It has been shown that during OLV, patients with COPD desaturate more quickly during isovolemic hemodilution than normal patients.

Previously, hypoxemia occurred frequently during OLV. Reports from 1950 to 1980 described an incidence of hypoxemia (arterial saturation <90%) of 20% to 25%. Current reports describe an incidence of less than 5%. This improvement is most likely due to several factors: improved lung isolation techniques such as routine FOB to prevent lobar obstruction from DLTs, improved anesthetic agents that cause less inhibition of HPV, and better understanding of the pathophysiology of OLV. The pathophysiology of OLV involves the body’s ability to redistribute pulmonary blood flow to the ventilated lung. The anesthesiologist’s goal during OLV is to maximize PVR in the nonventilated lung while minimizing PVR in the ventilated lung. Key to understanding this physiology is the appreciation that PVR is correlated with lung volume in a hyperbolic fashion. PVR is lowest at functional residual capacity (FRC) and increases as lung volume rises or falls above or below FRC. The anesthesiologist’s aim, to optimize pulmonary blood flow redistribution during OLV, is to maintain the ventilated lung as close as possible to its FRC while facilitating collapse of the nonventilated lung to increase its PVR.

Most thoracic surgery is performed in the lateral position. Patients having OLV in the lateral position have significantly better PaO ₂ levels than patients during OLV in the supine position because of gravitational enhancement of blood flow to the dependent, ventilated lung. This applies both to patients with normal lung function and to those with COPD.

Hypoxic Pulmonary Vasoconstriction

Hypoxic pulmonary vasoconstriction can decrease the blood flow to the nonventilated lung by as much as 50%. The stimulus for HPV is primarily the alveolar oxygen tension (PAO ₂ ), which stimulates precapillary vasoconstriction redistributing pulmonary blood flow away from hypoxemic lung regions via a pathway involving NO or cyclooxygenase synthesis inhibition. The mixed venous PO ₂ (P _v O ₂ ) is also a stimulus, although it is considerably weaker than PAO ₂ . HPV has a biphasic temporal response to alveolar hypoxia. The rapid-onset phase begins immediately and reaches a plateau by 20 to 30 minutes. The second (delayed) phase begins after 40 minutes and plateaus after several hours. The offset of HPV is also biphasic, and PVR may not return to baseline for several hours after a prolonged period of OLV. This may contribute to increased desaturation during the collapse of the second lung during bilateral thoracic procedures. HPV also has a preconditioning effect, and the response to a second hypoxic challenge will be greater than to the first challenge.

The surgical trauma to the lung can affect pulmonary blood flow redistribution. Surgery may oppose HPV by the release of vasoactive metabolites locally in the lung. Conversely, surgery can dramatically decrease blood flow to the nonventilated lung by deliberately or accidentally mechanically interfering with either the unilateral pulmonary arterial or venous blood flow. Ventilation increases blood flow through a hypoxic lung more than in a normoxic lung, which is generally not of clinical relevance but does complicate studies of HPV. HPV is decreased by vasodilators such as nitroglycerin and nitroprusside. In general, vasodilators can be expected to cause a deterioration in P _a O ₂ during OLV. Thoracic epidural sympathetic blockade probably has little or no direct effect on HPV, which is a localized chemical response in the lung. However, thoracic epidural anesthesia can have an indirect effect on oxygenation during OLV if it is allowed to cause hypotension and a fall in cardiac output.

Choice of Anesthetic

All the volatile anesthetics inhibit HPV in a dose-dependent fashion. The older volatile agents were potent inhibitors of HPV, which may have contributed to the high incidence of hypoxemia reported during OLV in the 1960s and 1970s; many of these studies used 2- to 3-MAC doses of halothane.

In doses of 1 MAC or less, the modern volatile anesthetics (isoflurane, sevoflurane, and desflurane) are weak and equipotent inhibitors of HPV. The inhibition of the HPV response by 1 MAC of a volatile agent such as isoflurane is approximately 20% of the total HPV response, and this could account for only a net 4% increase in total arteriovenous shunt during OLV, which is a difference too small to be detected in most clinical studies. In addition, volatile anesthetics cause less inhibition of HPV when delivered to the active site of vasoconstriction via the pulmonary arterial blood than via the alveolus. This pattern is similar to the HPV stimulus characteristics of oxygen. During established OLV, the volatile agent only reaches the hypoxic lung pulmonary capillaries via the mixed venous blood. No clinical benefit in oxygenation during OLV has been shown for total IV anesthesia above that seen with 1 MAC of the modern volatile anesthetics.

The use of nitrous oxide–oxygen (N ₂ O–O ₂ ) mixtures is associated with a higher incidence of postthoracotomy radiographic atelectasis (51%) in the dependent lung than when air–oxygen mixtures are used (24%). N ₂ O also tends to increase PAPs in patients who have pulmonary hypertension, and N ₂ O inhibits HPV. For these reasons, N ₂ O is usually avoided during thoracic anesthesia.

Cardiac Output

The effects of alterations of cardiac output during OLV are complex. Increasing cardiac output tends to cause increased PAPs and passive dilation of the pulmonary vascular bed, which in turn opposes HPV and has been shown to be associated with increased arteriovenous shunt (Qs/Qt) during OLV. However, in patients with a relatively fixed oxygen consumption, as is seen during stable anesthesia, the effect of an increase in cardiac output is to increase the mixed venous oxygen saturation (S _v O ₂ ). Thus increasing cardiac output during OLV tends to increase both shunt and S _v O ₂ , which have opposing effects on PaO ₂ . There is a ceiling effect to the amount that S _v O ₂ can be increased. Increasing the cardiac output to supranormal levels by administering inotropes such as dopamine tends to have an overall negative effect on PaO ₂ . Conversely, allowing the cardiac output to fall will lead to falls in both shunt and S _v O ₂ with a net effect of decreasing PaO ₂ . It is very important to maintain cardiac output in patients with limited cardiac reserve.

Ventilation Strategies During One-Lung Ventilation

The strategy used to manage the ventilated lung during OLV plays an important part in the distribution of pulmonary blood flow between the lungs. It has been the practice of many anesthesiologists to use the same large tidal volume (e.g., 10 mL/kg ideal body weight) during OLV as during two-lung ventilation. This strategy decreases hypoxemia, probably by recurrently recruiting atelectatic regions in the dependent lung, and may result in higher PaO ₂ values during OLV when compared with smaller tidal volumes. However, there is a trend to use smaller tidal volumes with positive end-expiratory pressure (PEEP) during OLV for several reasons. First, the incidence of hypoxemia during OLV is much lower than 20 to 30 years ago. Second, there is a risk of causing acute injury to the ventilated lung with prolonged use of large tidal volumes. And third, a ventilation pattern that allows cyclic atelectasis and recruitment of lung parenchyma seems to be injurious. The ventilation technique needs to be individualized depending on the patient’s underlying lung mechanics.

Respiratory Acid-Base Status

The efficacy of HPV in a hypoxic lung region is increased in the presence of respiratory acidosis and is inhibited by respiratory alkalosis. However, there is no net benefit to gas exchange during OLV from hypoventilation because the respiratory acidosis preferentially increases the pulmonary vascular tone of the well-oxygenated lung, and this opposes any clinically useful pulmonary blood flow redistribution. Overall, the effects of hyperventilation usually tend to decrease pulmonary vascular pressures.

Positive End-Expiratory Pressure

Resistance to blood flow through the lung is related to lung volume in a biphasic pattern and is lowest when the lung is at its FRC. Keeping the ventilated lung as close as possible to its normal FRC using modest amounts of PEEP favorably encourages pulmonary blood flow to this lung. Several intraoperative factors that are known to alter FRC tend to cause the FRC of the ventilated lung to fall below its normal level; these include lateral position, paralysis, and opening the nondependent hemithorax, which allows the weight of the mediastinum to compress the dependent lung. Attempts to measure FRC in human patients during OLV have been complicated by the presence of a persistent end-expiratory airflow in COPD patients. Many patients do not actually reach their end-expiratory equilibrium FRC lung volume as they try to exhale a relatively large tidal volume through one lumen of a DLT. These patients develop dynamic hyperinflation and an occult positive end-expiratory pressure (auto-PEEP).

Auto-PEEP

Auto-PEEP (also called intrinsic PEEP) is most prone to occur in patients with decreased lung elastic recoil such as older adults and those with emphysema. Auto-PEEP increases as the inspiratory/expiratory (I:E) ratio increases (i.e., as the time of expiration decreases). This auto-PEEP, which averages 4 to 6 cm H ₂ O in most series of lung cancer patients studied, opposes the previously mentioned factors, which tend to diminish dependent-lung FRC during OLV. The effects of applying external PEEP through the ventilator circuit to the lung in the presence of auto-PEEP are complex. Patients with a very low auto-PEEP (<2 cm H ₂ O) will experience a greater increase in total PEEP from a moderate (5 cm H ₂ O) external PEEP than those with a high level of auto PEEP (>10 cm H ₂ O). Whether the application of PEEP during OLV will improve a patient’s gas exchange depends on the individual’s lung mechanics. If the application of PEEP tends to shift the expiratory equilibration position on the compliance curve towards the lower inflection point (LIP) of the curve (i.e., toward the FRC), then external PEEP is of benefit ( Fig. 14.6 ). However, if the application of PEEP raises the equilibration point such that it is further from the LIP, then gas exchange deteriorates.

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