The thoracic surgery patient population can present significant challenges to clinical care. Patients often are older, current, or former smokers, and sicker than other surgical populations. It is not uncommon for these patients to present with underlying chronic lung disease, some form of arteriovascular disease, hypertension, diabetes, and baseline renal insufficiency. They have diminished physiologic reserve and more limited ability to recover from perioperative complications. In particular, they are prone to pulmonary complications, which are very poorly tolerated. As a result, they may require the services of an intensive care unit (ICU) and its highly trained, specialized staff more frequently than other patient populations. This chapter reviews critical care issues specific to thoracic surgery patients, general issues of management related to sepsis and acute respiratory distress syndrome (ARDS), and strategies for avoiding the common nosocomial complications of critical care.

Secretion Retention, Atelectasis, Pneumonia

Thoracic surgery patients are at increased risk of secretion retention and atelectasis. General anesthesia, particularly when accompanied by one lung ventilation (OLV), causes a marked decrease in functional residual capacity (FRC), which promotes atelectasis. Surgical manipulation of the lung can lead to retained blood and secretions, with partial or complete airway obstruction. Gas flow is further hindered by bronchospasm and decreased compliance of the operative lung. Splinting from postoperative pain, or conversely, respiratory depression from opiates or benzodiazepines further limit lung expansion. Patients with preexisting chronic obstructive pulmonary disease (COPD), asthma, bronchitis, or pneumonia will be at greatest risk. Similarly, patients with impaired cough reflexes, including those who have had airway resection with anastomosis (e.g., sleeve resection) would be expected to have greater difficulty clearing secretions. Secretion retention over time results in both hypoxemia and hypercarbia. It also predisposes the patient to pneumonia.

Preventing secretion retention and atelectasis requires a systematic, multidisciplinary approach. Time under general anesthesia should be limited to the minimum required to complete the procedure. Patients should be extubated immediately whenever possible. Fiberoptic bronchoscopy immediately before extubation facilitates the removal of blood and secretions from the proximal airways. Excellent analgesia combined with aggressive early ambulation will promote recruitment of lung volume and clearance of secretions. Chest physiotherapy further aids this process. Any patient with a preoperative pulmonary infection should undergo aggressive, culture-directed, antibiotic therapy during the immediate perioperative period.

Treatment of retained secretions and atelectasis includes aggressive chest physiotherapy and mobilization. Humidified oxygen, nebulized saline, and bronchodilators can help thin secretions and promote gas flow. Patients with copious, thick secretions may benefit from nebulized N-acetylcysteine or dornase (DNAse), with bronchodilator pretreatment to mitigate treatment-induced bronchospasm. Any patient having significant trouble clearing their secretions should be evaluated for the possibility of vocal cord dysfunction, which is a known complication of certain thoracic surgical procedures and results in a markedly impaired cough. A small subset of patients may require more aggressive interventions including repeated awake fiberoptic bronchoscopy, intermittent noninvasive ventilation, use of an Acapella® device or vibratory vest, assisted cough using an inexuflator device, or in the most severe cases, intubation and mechanical ventilation. Patients who require intubation primarily for secretion clearance should be evaluated for early tracheostomy.

Postpneumonectomy Pulmonary Edema

Approximately 2% to 9% of pneumonectomy patients will experience early onset idiopathic acute lung injury (ALI). It is characterized by the development of diffuse infiltrates followed by significant hypoxemia in the first 1 to 3 days postoperatively. In contrast to late onset ALI, no etiology is readily apparent. Pulmonary capillary wedge pressures are normal to low, and the alveolar fluid has high protein content. Studies using radiolabeled albumin have been consistent with a pulmonary capillary leak syndrome.¹ The relative rarity of this event has precluded the possibility of prospective analysis.

Retrospective analyses have identified multiple factors associated with the development of postpneumonectomy pulmonary edema (Table 6-1).² The exact etiology remains unknown. It has been postulated that ventilator-induced lung injury, oxygen toxicity, tissue injury with cytokine release, loss of lymphatic drainage, pulmonary hypertension, and shear injury to the capillary endothelium from increased blood flow through the remaining pulmonary artery all contribute to the development of capillary leak and the subsequent accrual of interstitial lung water. Once a capillary leak develops, movement of fluid from the pulmonary vasculature to the interstitium is governed by hydrostatic and colloid osmotic pressures, as described by Starling’s law. Few recommendations can be made regarding strategies to prevent postpneumonectomy pulmonary edema, but it would seem prudent to use lung-sparing ventilation with lower tidal volumes and plateau pressures and to limit intravascular fluid to the minimum needed to support end-organ perfusion. Likewise, hypercarbia, hypoxia, and pain should be avoided because of the propensity to increase pulmonary arterial pressures. Once established, postpneumonectomy pulmonary edema is treated the same as any other case of ALI or ARDS, with lung-sparing ventilation and good supportive care.

Atrial Arrhythmias

Atrial fibrillation and atrial flutter are common after thoracic surgery. The incidence can be as high as 44% following extrapleural pneumonectomy.³ A number of factors have been associated with the occurrence of atrial arrhythmias (Table 6-2). Etiologies may include elevated catecholamines, myocardial ischemia, pulmonary hypertension, atrial enlargement, hypoxemia, electrolyte imbalances, mechanical displacement of the heart, and vagal nerve irritation. Trials in the cardiac surgery population have shown that prophylaxis with beta blockers, calcium channel blockers, sotalol, amiodarone, statins, or corticosteroids may decrease the incidence of atrial fibrillation.^4,5

The few clinical trials performed in lung resection patients suggest that both calcium channel blockers and beta blockers, given prophylactically, decrease the incidence of atrial tachydysrhythmia by roughly 50%.⁶ Hemodynamically stable patients with atrial arrhythmias can be treated with beta blockers or calcium channel blockers to achieve rate control. The ability of calcium channel blockers to reduce pulmonary vascular resistance (PVR) and right ventricular pressures makes this drug class an appealing choice for primary treatment in lung resection patients.

Digoxin may be used as an additional agent to improve rate control but care must be taken to avoid toxicity, particularly in the setting of renal insufficiency. Amiodarone is a useful agent for those patients who maintain a high ventricular response rate despite maximum therapy with other agents or who become hypotensive with first line agents. However, amiodarone can cause primary acute lung toxicity in patients who have undergone thoracic resections, and, therefore should be reserved as a second line therapy.⁷

The risk of third-degree heart block must be carefully evaluated if more than one nodal blocking agent is to be used simultaneously. Unstable patients may require electrical cardioversion to restore sinus rhythm. Unfortunately, the factors that led to the atrial arrhythmia are usually still present after surgery, and recurrence of the arrhythmia is common after either electrical or initial chemical cardioversion. Of note, however, the majority of patients with new onset atrial arrhythmia after surgery will be back in sinus rhythm within 6 weeks. This makes rate control with anticoagulation, if not otherwise contraindicated, a practical approach in this patient population.

Bronchospasm and Chronic Obstructive Pulmonary Disease Exacerbation

COPD is a common comorbidity in the thoracic surgery patient population. Intubation and airway manipulation can exacerbate a patient’s COPD. The increased resistance to airflow increases the work of breathing and may result in frank respiratory distress. Associated “auto-peep” or dynamic hyperinflation, resulting from trapped alveolar gas, further increases the work of breathing, adversely affects gas exchange, and causes hemodynamic instability if venous return is impaired. Patients with COPD should be maintained on their home bronchodilator and inhaled steroid regimen throughout the perioperative period. The rare patient will require systemic steroids to treat an exacerbation of their COPD. Early extubation followed by aggressive mobilization is critical to avoiding the cycle of airway irritability, bronchospasm, dynamic hyperinflation, and respiratory distress.

Hypotension

Postoperative hypotension can be categorized as problems of pump function or venous return. Myocardial ischemia is a cause of acute ventricular dysfunction. Likewise, acute onset or worsening of pulmonary hypertension can lead to right ventricular failure (see Hyperglycemia). Venous return problems limiting effective diastolic filling of the heart are more common. Dehydration or acute hemorrhage leads to absolute hypovolemia. Tension pneumothorax, pericardial tamponade, pulmonary embolism, severe dynamic hyperinflation, mediastinal shift, and cardiac herniation will limit venous return despite normal intravascular volume. Finally, some patients may exhibit hypotension with a normal cardiac output and a low systemic vascular resistance. The increase in venous capacitance creates a state of relative hypovolemia. This low-tone state is typical of sepsis, but may also be seen with sympathectomies that are either pharmacologically induced from local anesthetics given via a thoracic epidural, or mechanically induced from trauma to the sympathetic chain during surgery. Central venous pressure (CVP) monitoring can be very helpful in distinguishing between the various causes of postoperative hypotension. If pulmonary hypertension and right heart failure is suspected, early placement of a pulmonary artery catheter (PAC) is advised.

Pulmonary Hypertension and Right Ventricular Failure

Acute onset of pulmonary hypertension with subsequent right ventricular failure is one of the most dreaded perioperative complications following thoracic surgery. Unless it is immediately recognized and successfully managed it can become rapidly fatal. Preexisting COPD, with its intrinsic loss of pulmonary microvasculature, limits the ability of the remaining lung to compensate for an abrupt increase in pulmonary blood flow following pulmonary resection and predisposes the patient to acute perioperative pulmonary hypertension. Preoperative evaluation, including echocardiography and cardiac catheterization can help to identify those patients with significant preoperative pulmonary hypertension. It should be understood, however, that these tests are done at rest, and sometimes under conscious sedation; therefore, may not accurately predict the pulmonary artery pressures that may occur postoperatively under the conditions of stress and hypermetabolism. Even a reassuring preoperative catheterization with a balloon occlusion trial does not completely rule out the possibility of postoperative right ventricular failure.

Patients with acute right ventricular failure will often present with hypotension and evidence of low cardiac output including oliguria, a high CVP and peripheral edema. Patients also may complain of dyspnea and lightheadedness, particularly with exertion. Unlike patients with biventricular failure, there generally is an absence of pulmonary edema, and left atrial pressures are low. Right ventricular dysfunction can occur in the setting of right ventricular pressure overload, volume overload, or impaired contractility. An electrocardiogram and echocardiogram will help exclude right ventricular ischemia or infarction, which if present, may require urgent therapy to treat an acute coronary syndrome. Likewise, the patient should be assessed for the likelihood of acute pulmonary embolism, as this can cause pulmonary hypertension and right ventricular failure and requires specific therapy.

Initial treatment of right ventricular failure is aimed at correcting reversible causes of pulmonary hypertension including hypoxia, hypercarbia, and acidosis. Pain and fever, because of their associated hypermetabolic state, can also cause pulmonary hypertension and should be rapidly treated. Volume management can be complex. Cardiac output is preload dependent; however, right-sided volume overload can adversely affect left ventricular output through septal shift and intraventricular dependence. The combination of echocardiography and PAC measurements can be helpful in identifying the optimum volume status for each patient. Right ventricular function and systemic blood pressure can be supported with the use of inotropes (dopamine, epinephrine, and norepinephrine) and inodilators (dobutamine, milrinone). A PAC is helpful for titrating therapy. If an inodilator results in an improved cardiac output but worsened systemic hypotension, low-dose vasopressin may be used to maintain systemic blood pressure without increasing pulmonary artery pressures. Unfortunately, the inotropes and inodilators are all arrhythmogenic and also increase myocardial oxygen consumption.