Cardiovascular Adaptations and Complications

  • Alessia Pedoto
  • David Amar


Changes in right ventricular anatomy and function can occur at several stages of lung resection, starting after induction of general anesthesia and positioning, followed by one lung ventilation and surgical dissection. Compensatory mechanisms may not occur in patients with advanced COPD who are at risk of developing long-term complications. Several tests are available during the intraoperative period to evaluate right heart function and their merits are reviewed. Supraventricular arrhythmias are a common complication after thoracic surgery, depending on the side and the extent of the dissection. Atrial fibrillation is the most common postoperative rhythm disturbance after lung resection. Several pathophysiologic mechanisms as well as prophylactic and/or therapeutic maneuvers have been proposed. Older age and intrapericardial pneumonectomy are among the risk factors that strongly correlate with this condition. Acute coronary syndrome after thoracic surgery is rare but is associated with a high risk of death. Patients at risk are the ones with preoperative coronary artery disease and abnormal exercise testing. There are no clear recommendations on the role of preoperative cardiac catheterization and coronary revascularization. Cardiac failure can result from either right or left heart dysfunction, and can be transient or long standing. Symptoms may be subtle at rest and become evident during exertion. Cardiac herniation is a rare complication that may occur after intrapericardial pneumonectomy and is associated with a high mortality rate. Clinical and electrocardiographic signs are very nonspecific, and treatment is surgical. Mediastinal shift is the result of changes in the postpneumonectomy space. A high index of suspicion is needed for the diagnosis, which can present with severe hemodynamic compromise or respiratory symptoms. Postpneumonectomy syndrome may occur in the late postoperative period. It is characterized by an extreme mediastinal shift which causes dynamic compression of the distal airway and respiratory insufficiency. Treatment is surgical.


Coronary Artery Bypass Grafting Pulmonary Arterial Pressure Lung Resection Electrical Cardioversion Mediastinal Shift 
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Key Points

  • Changes in right ventricular anatomy and function can occur at several stages of lung resection, starting after induction of general anesthesia and positioning, followed by one lung ventilation and surgical dissection. Compensatory mechanisms may not occur in patients with advanced COPD who are at risk of developing long-term complications. Several tests are available during the intraoperative period to evaluate right heart function and their merits are reviewed.

  • Supraventricular arrhythmias are a common complication after thoracic surgery, depending on the side and the extent of the dissection. Atrial fibrillation is the most common postoperative rhythm disturbance after lung resection. Several pathophysiologic mechanisms as well as prophylactic and/or therapeutic maneuvers have been proposed. Older age and intrapericardial pneumonectomy are among the risk factors that strongly correlate with this condition.

  • Acute coronary syndrome after thoracic surgery is rare but is associated with a high risk of death. Patients at risk are the ones with preoperative coronary artery disease and abnormal exercise testing. There are no clear recommendations on the role of preoperative cardiac catheterization and coronary revascularization.

  • Cardiac failure can result from either right or left heart dysfunction, and can be transient or long standing. Symptoms may be subtle at rest and become evident during exertion. Cardiac herniation is a rare complication that may occur after intrapericardial pneumonectomy and is associated with a high mortality rate. Clinical and electrocardiographic signs are very nonspecific, and treatment is surgical.

  • Mediastinal shift is the result of changes in the postpneumonectomy space. A high index of suspicion is needed for the diagnosis, which can present with severe hemodynamic compromise or respiratory symptoms. Postpneumonectomy syndrome may occur in the late postoperative period. It is characterized by an extreme mediastinal shift which causes dynamic compression of the distal airway and respiratory insufficiency. Treatment is surgical.


Lung resection, especially if extensive, can cause acute and chronic changes in right cardiac anatomy and function. This can result from either transient or sustained pressure or volume overload [1], and can be worsened by preexisting abnormalities. Any pathology associated with pulmonary hypertension and chronic hypoxia (such as end stage COPD or connective tissue interstitial lung disease) can cause baseline right ventricular dysfunction (see Table 44.1) [2]. Multiple intraoperative factors, such as induction of general anesthesia, institution of one lung ventilation (OLV) and lateral decubitus, followed by manipulation of the pulmonary circulation or triggering of the inflammatory response, are all known contributors [3]. While cardiac adaptations occur with time after lung resection, cardiac complications, especially arrhythmias, are commonly seen in the immediate postoperative period before patient discharge.
Table 44.1.

Causes of right ventricular failure.

Pressure overload

Left heart failure (most common)

Pulmonary embolus (common)

Pulmonary hypertension

Right ventricular outflow tract obstruction

Peripheral pulmonary stenosis

Double chamber right ventricle

Systemic right ventricle

Volume overload

Tricuspid regurgitation

Pulmonary regurgitation

Atrial septal defect

Anomalous pulmonary venous return

Sinus of valsalva rupture in the right atrium

Coronary artery fistula in the right atrium or right ventricle

Carcinoid syndrome

Rheumatic valvulitis


Right ventricular myocardial ischemia

Intrinsic myocardial processes

Cardiomyopathy and heart failure

Arrhythmogenic right ventricular dysplasia


Inflow limitation

Tricuspid stenosis

Superior vena cava stenosis

Congenital defects

Ebstein’s anomaly

Tetralogy of Fallot

Transposition of the great vessels

Double outlet right ventricle with mitral atresia

Pericardial disease

Constrictive pericarditis

Adapted from Ref. [2]

Cardiac Adaptations

Cardiac adaptation can occur in the immediate intraoperative period, after induction of general anesthesia and positioning or in the postoperative phase.

Intraoperative Changes in Right Ventricular Function and Anatomy Related to One Lung Ventilation and Positioning

Pulmonary arterial pressures can increase after induction of general anesthesia, as a consequence of positive pressure ventilation, placement of the patient in the lateral decubitus, opening of the chest and initiation of OLV [4]. Mediastinal shift, gravity-related changes in pulmonary perfusion and hypoxic vasoconstriction can also contribute to higher pulmonary arterial pressure. In patients with normal pulmonary vascular compliance, an increase in right cardiac output can compensate for the higher afterload without significant changes in pulmonary arterial pressures. This may not occur in patients with advanced COPD, even in the presence of baseline right ventricular hypertrophy [3], theoretically making this population at higher risk for intra- and postoperative cardiac complications. Preexisting significant pulmonary hypertension can worsen during OLV or clamping of the pulmonary artery. Ligation of the main pulmonary artery during pneumonectomy (right more than left), or lung transplantation in patients with severe COPD can cause acute right heart overload and consequent dilation followed by ischemia or arrhythmias, either intra- or postoperatively [5, 6]. A temporary “clamp test” of the pulmonary artery can be done intraoperatively to evaluate the clinical and echocardiographic response of the right heart to acute shifting of blood to the remaining pulmonary circulation. However, this maneuver rarely changes the intraoperative management, since the results may be difficult to observe or interpret as soon as the clamp is applied. If there are any intraoperative concerns of potential hemodynamic instability or right heart dysfunction, trans-esophageal echocardiography (TEE) can be used by itself or combined with pulmonary arterial catheter data. While TEE is a valuable “real-time” tool to evaluate left ventricular function, its role in assessing right ventricular function is less clear. Despite the superficial location of the right heart, its irregular and asymmetric shape makes the motion and volume calculations much more difficult and less detailed than the left side [1]. In case of high suspicion for perioperative right heart dysfunction, such as in patients with a predicted postoperative FEV1 less than 40%, detailed preoperative testing becomes extremely important and is highly recommended [7].

Acute and Late Phase Changes in Right Ventricular Anatomy After Lung Resection

Intraoperative increases in resting pulmonary arterial pressure and pulmonary vascular resistance are usually proportional to the extent of the resection, and tend to normalize in the immediate postoperative period. However, right ventricular function slowly declines over time, suggesting adaptive or reactive processes that can lead to right ventricular hypertrophy [4]. The most of the changes in right ventricular ejection fraction are seen during exercise and depend on the level of exertion. Compensatory mechanisms are more efficient during moderate exercise, while at maximal exertion the right ventricular stroke volume becomes fixed at a certain value independently from the increase in the workload and the time from surgery [4]. The extent of the resection and the compensatory volume expansion of the remaining lung can cause changes in the mediastinal anatomy with a rotation of the heart in the chest cavity. Left ventricular function may be affected as well, with changes in filling and contraction. Furthermore, it seems that the degree and efficacy of cardiac compensation after lung resection are significantly better when surgery is performed on younger patients [4].

Lung surgery is currently the most common therapy for nonmetastatic resectable lung cancer, as part of a multimodality treatment with chemotherapy [8] and radiation [9]. Nowadays, surgical candidates are much older, due to the improvement in surgical and anesthesia techniques, and with more extensive comorbidities [10], which contribute to a higher risk of postoperative changes in cardiac function. Cardiac and pulmonary diseases are common factors that may significantly influence the postoperative course and increase mortality rates [10]. However, severe pulmonary hypertension (mean pulmonary arterial pressure >  45 mmHg) [11] is present only in 3.7% of this patient population, despite their long smoking history and the presence of variable degrees of COPD [12]. Ninety per cent of patients with FEV1 less than 50% have mean pulmonary arterial pressures of about 20 mmHg, and only 5% may have values greater than 35 mmHg [12].

Several studies have been done to evaluate postoperative right ventricular function (see Table 44.2 [3]). Most of them had a small sample size and extremely variable methodology, which makes the results difficult to compare. Some agreement exists for patients after pneumonectomy, where there is an increase in pulmonary arterial systolic pressure and right ventricular diastolic volume or systolic pressure on transthoracic echocardiography [3]. These changes occur in the second postoperative day (POD) and persist after 4 years [3], suggesting an evolution of the cardiovascular response over time [4]. The increase in diastolic volume as well as in pulmonary arterial systolic pressure and the mild tricuspid regurgitation which is observed on two-dimensional echocardiography are all attributed to an increase in both afterload and catecholamine tone after clamping of the pulmonary artery. Despite these changes, 30-day mortality rates seem to be unaffected, except for one study where changes in right ventricular function were associated with respiratory failure and poor FEV1. Most of the studies showed an increased incidence of tachyarrhythmias after pneumonectomy, which was transient in the majority of cases and not associated with either heart failure or long-term complications [3].
Table 44.2.

Summary of the literature analyzing right ventricular changes after lung surgery.


Time of the study

Type of surgery


Results lobectomy pneumonectomy



Venuta et al. [67]

4 years

Lobe (N  =  36)


No changes


FEV1  <  60%, h/o MI, angina, valvular ds, AF, cardiac surgery

Mild increase in PASP and RVDV not clinically significant to cause RVH

Pneumonectomy (N  =  15)

↑PASP moderate TVI

Foroulis et al. [68]

6 months

Lobe (N  =  17)




Postoperative BPF, empyema, respiratory failure, MI

Small study, higher PASP in pneumonectomy patients at 6 months (R  >  L cases), with higher incidence of postoperative AF and SVT requiring treatment, attributed to RV dilatation

Pneumonectomy (N  =  35)





Amar et al. [24]

1 month

Pneumonectomy (N  =  70)



No changes in R and L atrial diameter, EF, TR and RVSP

AF, lung resection, lesser operations, unresectable

Study to evaluate role of diltiazem and digoxin on AF. Echo done as part of their follow up

Amar [60]

1 week

Lobe (N  =  47)




Wedge, prior thoracic surgery, nonsinus rhythm

RVSP of 31, not affecting RV systolic function unless respiratory failure occurs

Pneumonectomy (N  =  39)


Kowalewski et al. [5]

2 days

Lobe (N  =  9)


No changes



Not very accurate and nonstandard right heart volumes calculations which can underestimate large volumes. RVEF usually underestimates the true value by echo due to RV geometry

Pneumonectomy (N  =  22)



Smulders et al. [69]

5 years

Pneumonectomy (N  =  15)



R side  =  cardiac lateral shift. ↓RVEDV, nl LV function


No signs of RVH at 5 years

L side  =  rotation, nl RVEDV, ↓LVEF

↑HR, ↓SV

Katz et al. [6]


Lung transplantation (N  =  32)


Immediate ↓PAP (systolic+mean), and ↓RV size posttransplantation, normalization of septal geometry in severe pulmonary HTN (↓RVED area)


CPB used in all cases of severe pulmonary HTN

All the studies listed are prospective in nature

N number of cases; TTE trans-thoracic echocardiography; RVDD right midventricular diastolic diameter; PASP pulmonary arterial systolic pressures; TVI tricuspid valve insufficiency; FEV 1 forced expiratory volume at one second; MI myocardial infarction; AF atrial fibrillation; RVDV right ventricular diastolic volume; RVH right ventricular hypertrophy; TR tricuspid regurgitation; BPF bronchopleural fistula; SVT supraventricular tachycardia; RV right ventricle; R right; L left; EF ejection fraction; RVSP right ventricular systolic pressure; RVEDV right ventricular end diastolic volume; RVEF right ventricular ejection fraction; MRI magnetic resonance imaging; LV left ventricle; SV stroke volume; TEE trans-esophageal echocardiography; PAP pulmonary arterial pressure; HR heart rate; HTN hypertension; CPB cardiopulmonary bypass

Cardiac Complications

Supraventricular Arrhythmias (Atrial Fibrillation, Atrial Flutter and Supraventricular Tachycardia)

Supraventricular tachyarrhythmias occur in approximately 18% of patients undergoing noncardiac thoracic surgery [13]. The most important risk factors are age of 60 years and older [14] and intrapericardial pneumonectomy [15]. Other markers associated with this complication seem to be an elevated white blood cell (WBC) count on POD one [16] and an elevated perioperative N-terminal-pro-B-type natriuretic peptide [17]. Atrial fibrillation (AF) is the most common rhythm disturbance, followed by supraventricular tachycardia (SVT), atrial flutter and premature ventricular contractions (PVCs). The diagnosis is usually made on the second POD (with a range of 1–7 days), with a good response to pharmacological cardioversion [14, 18, 19, 20].

Sustained ventricular tachyarrhythmias are quite rare after lung resection [13]. Nonsustained ventricular tachycardia (more than three consecutive beats) has an incidence of 15% and can occur in the first 96 hours after lung resection, especially in patients with preoperative left bundle branch block [21]. It is rarely associated with hemodynamic instability requiring treatment at any time. There is no association with age, other clinical factors or core temperature upon arrival to PACU. On multivariate analysis, an independent association seems to exist between nonsustained ventricular tachycardia and postoperative atrial fibrillation (POAF). Vagal withdrawal or irritation, and/or a surge in sympathetic activity are all proposed mechanisms. These findings differ from the cardiac surgical literature, where the presence of postoperative ventricular tachycardia often leads to poor outcome [13].

Suggested Risk Factors

POAF can be an isolated complication or associated with respiratory or infectious disease [14]. It is typically transient and reversible and seems to affect individuals with an electrophysiologic substrate for arrhythmias present before or as a result of surgery [22]. Despite the good prognosis, if persistent, POAF is associated with a 1.7% risk of developing cerebrovascular accidents [13]. Thromboembolic events are often responsible and can occur within 24–48 h from the onset of the sustained POAF. If sinus rhythm fails to be restored within this time frame, anticoagulation should be considered weighing the risk of postoperative bleeding [13]. The most recent American Heart Association (AHA) guidelines on management of AF unrelated to surgery provide similar recommendations for which antithrombotic medications one should employ in postoperative patients depending on the patient’s risk (i.e., presence of a prosthetic valve, etc., prior cerebrovascular accidents or no risk factors) [23].

Several mechanisms have been proposed to explain POAF, but no consistent factors other than age have been proven. Aging per se has been associated with loss of about 90% of normal sinus nodal fibers [24] and remodeling of the atrial myocardium, with changes in the sinoatrial and atrioventricular nodal conduction, as well as an increased sensitivity to catecholamine activity, especially after surgical trauma in the area [13]. Triggering of the inflammatory response with activation of the complement and several proinflammatory cytokines has also been suggested as a contributing factor for POAF in this age population [25]. This thought is supported by the finding of a doubling in WBCs count that has been observed in patients older than 60 years of age on POD 1, with a threefold increase in the odds of developing POAF [16]. Catecholamine-induced leukocytosis via α and β2-receptor activation is a known phenomenon which could in part explain this finding. The use of thoracic epidural analgesia as a modality to cause sympathectomy and prevent POAF has led to disappointing results [26], maybe due to the high individual variability of sympathetic blockade. Other suggested contributing factors include stretching or inflammation of the pulmonary veins, hilar manipulation and mediastinal shift [22]. Aggravating mechanisms are the use of positive inotropic agents, i.e., dopamine, as well as anemia, fever, hypoglycemia, postoperative ischemia and surgical complications [18, 27].

Presenting symptoms of rapid POAF include dyspnea, palpitations, dizziness, syncope, respiratory distress and hypotension. Pulmonary embolism or myocardial ischemia and electrolyte abnormality are most commonly included in the differential diagnosis [28]. According to the AHA guidelines, trans-thoracic echocardiography should be part of the workup for new onset POAF to rule out any structural disease, if such information is not already available [29]. Similarly, the AHA guidelines do not recommend “ruling out” pulmonary embolism, thyrotoxicosis or myocardial ischemia if there are no accompanying clinical signs or symptoms [29].

The presence of postoperative arrhythmias is indirectly associated with an increased rate of morbidity. However, in the presence of heart failure or prolonged hypotension, arrhythmias can be a direct cause of death [19]. Length of hospital stay and costs are increased in patients with arrhythmias, highlighting the importance of prevention when possible [14, 30]. In most of the cases, POAF resolves prior to hospital discharge and the great majority of these patients are completely cured at 6 weeks from surgery [25]. Patients are considered at risk for postoperative supraventricular arrhythmias if they have two or more of the risk factors listed in Table 44.3, and if so, they may be started on pharmacological prophylaxis either preoperatively or in the immediate postoperative period. Several regimens are available to prevent or treat atrial tachyarrhythmias.
Table 44.3.

Proposed risk factors for supraventricular tachyarrhythmias.

Age >60

Male gender

History of paroxysmal atrial fibrillation

Prolonged P wave duration

Preoperative HR >72 bpm

Elevated BNP level

Increased WBC count on POD 1

Intrapericardial procedure

HR heart rate; bpm beats per minute; BNP brain natriuretic peptide; WBC white blood cell count; POD postoperative day

Adapted from Refs. [13, 14, 19, 22]

Role of Medications Used for Treatment or Prevention

β-Blockers have become popular as preventive medications due to their cardioprotective effects. They are used as prophylactic agents with the rationale of counteracting the effects of the high sympathetic tone that occurs after surgery, which may enhance patient susceptibility to dysrhythmias. β-Blockers inhibit intracellular calcium influx via a second messenger and have a membrane stabilizing effect [31]. Their respiratory side effects become particularly important after lung resection since they may worsen pulmonary function in the postoperative period. Pulmonary edema has been described as a potential side effect [32], as well as hypotension and bradycardia. Moreover, in patients on chronic β-blockers, withdrawal may lead to rebound tachycardia and related complications [33]. The β-blocker length of stay study (BLOS) analyzed the effects of β-blockers after cardiac surgery used as prophylactic agents in patients both naïve and already taking β-blockers. The goal was to prevent POAF, and possibly decrease the length of stay in the hospital and ICU. Despite a small decrease in the incidence of POAF in the patients already on a β-blocker, an increased length of stay was observed in the very same group [34]. This was attributed to the development of adverse cardiac and pulmonary effects. Recently, the Perioperative Ischemic Evaluation (POISE) trial showed that aggressive β-blockade in patients at risk or with atherosclerotic disease can reduce postoperative myocardial infarction and even POAF but at the cost of an increase in mortality related to cerebrovascular events in patients who had hypotension and decreased cerebral perfusion [35]. These findings have been consistent with other trials using lower doses of β-blockers, which questioned the safety of this strategy [36].

Sotalol is a class III antiarrhythmic with significant activity as a nonselective β-blocker and a potassium channel blocker. Potassium current blockade prolongs both the action potential and the QT interval, predisposing to ventricular dysrhythmias such as Torsades de Pointes [33]. This can occur at both therapeutic and toxic dosages [31]. Because of its renal excretion, the use is contraindicated in patients with a creatinine clearance less than 46 mL/min. As with other β-blockers, sotalol is effective in decreasing POAF, but does not reduce hospital length of stay or postoperative morbidity. Bradycardia can be significant enough to stop its use [22]. According to the American College of Cardiology recommendations, sotalol may be harmful if used to pharmacologically cardiovert AF [29]. Unfortunately, most of the data on this medication come from the cardiac surgical population [28].

The calcium channel blockers verapamil and diltiazem are used both as prophylactic and therapeutic agents for the treatment of POAF. They decrease intracellular calcium entry by directly blocking the L-type calcium channel and slowing the sino-atrial automaticity and atrio-ventricular nodal conduction [31]. This class of drugs seems to reduce pulmonary vascular resistance and right ventricular pressure as well, making this an attractive option after major lung resection [32]. Hypotension is one of the major side effects, especially with verapamil, and one of the most common reasons to stop these medications. Calcium channel blockers cause a 40% decrease of postoperative myocardial infarction rates and a 45% reduction of ischemia when used in the cardiac surgical population [32]. Diltiazem is superior to digoxin when used to prevent POAF after intrapericardial or standard pneumonectomy [24]. However, both drugs have equal effect on postoperative ventricular ectopy, echocardiographic changes in right ventricular function and hospital length of stay. In the largest study to prevent POAF in thoracic surgical patients, diltiazem was safe and effective in reducing the rate of POAF of almost 50% [30].

Prophylactic digitalization to prevent POAF is not recommended any longer since there are no proven benefits and potential associated side effects [37]. Digoxin does not seem to restore normal sinus rhythm in patients with chronic AF, and as a single agent it does not adequately control the ventricular response unless given at very high doses [37], or when combined with β-blockers or calcium channel blockers [38]. Better results are seen when used in patients with chronic AF and heart failure with systolic dysfunction [37]. Digitalis toxicity and the difficulty of assessing proper plasma levels remain the main limiting factors for its use [19]. Moreover, calcium channel blockers have demonstrated to have better results in preventing POAF with fewer side effects [24]. Digoxin should be avoided in patients with renal insufficiency, electrolyte disturbances (hypokalemia, hypomagnesemia and hypercalcemia), acute coronary syndromes and thyroid disorders. The main mechanism of action is by enhancing vagal stimulation at the atrioventricular node, thus decreasing ventricular response during atrial arrhythmias [33]. There is also an inhibition of the sympathetic response which is unrelated to the increase in cardiac output, and a binding of the myocardial sodium–potassium ATP-ase channel, blocking its transport [38]. The increase in intracellular calcium promotes cardiac contractility.

Amiodarone is a multiple sodium–potassium–calcium channel blocker and a β-adrenergic inhibitor. It is often used to maintain sinus rhythm after electrical cardioversion in the general population. As a prophylactic agent, it works best when administered 1 week prior to cardiac surgery [39]; however, the precise mechanism of action is unknown [40]. The sodium–calcium–potassium channel blockade causes an increase in the duration of the action potential and the refractory period in the cardiac tissue. As a result, hypotension, bradycardia and QT prolongation can be significant, especially in patients with congestive heart failure and left ventricular dysfunction [27]. Other side effects seen with prolonged use include hypo or hyperthyroidism, hepatic and neurotoxicity, and prolongation of warfarin half-life [40]. However, pulmonary toxicity remains the main concern of amiodarone therapy after lung resection [32]. It can occur at lower dosages than the ones used in the general population, and can manifest as chronic interstitial pneumonitis, bronchiolitis obliterans, adult respiratory distress syndrome (ARDS) or a solitary lung mass [27]. In a very small prospective randomized study, Van Mieghem et al. [41] examined the role of amiodarone prophylaxis on POAF after lung resection, and compared it to verapamil. The interim analysis showed no difference between the two drugs. However, the study was stopped prematurely due to an increased incidence of ARDS in the amiodarone group (7.4% in the patients who had a right pneumonectomy vs. 1.6% for other types of lung resections), and a higher mortality rate. This occurred despite using standard intravenous regimens and having therapeutic plasma concentrations. Two mechanisms were proposed: an indirect one, by increasing inflammatory mediators, and a direct one, by causing direct damage to the cells and subsequent fibrosis. Independently from the etiology, they recommended to avoid amiodarone after lung resection. By surgically decreasing the amount of lung parenchyma available, standard doses of amiodarone can account for higher pulmonary concentrations of the drug which may reach toxic levels. These results were not confirmed by later studies, when amiodarone was used for a short time period [13]. A recent prospective randomized study on 130 patients undergoing to lung resection showed a decreased incidence of AF in the amiodarone group (13.8 vs. 32.3% in the control), with no difference in respiratory or cardiac complications [42]. The lack of double blinding and the selection bias represented by a high exclusion rate of cases of intraoperative AF are the main limitations for this study. Overall, the ­efficacy of amiodarone in preventing POAF does not seem to be ­different from diltiazem [13]. Its main indication still remains as a ­second tier drug for POAF refractory to rate control drugs or as a therapeutic agent for POAF coupled with preexcitation conduction abnormalities, such as Wolff–Parkinson–White syndrome [29].

Magnesium is indicated in the case of hypomagnesemia. The data on the use of magnesium are mainly from the cardiac surgical literature and are conflicting. One randomized controlled study done on 200 patients undergoing cardiopulmonary bypass surgery showed a decreased incidence of POAF when magnesium sulfate was administered for prophylaxis [43]. However, several other trials in similar surgical population have given conflicting results on the benefits of magnesium and POAF prophylaxis, with the only agreement to maintain magnesium levels within normal values [33]. Except in patients with acute renal failure, magnesium has a relatively safe profile.

Statins (3-hydroxy-3-methylglutaratyl coenzyme-A reductase inhibitors) have been shown to suppress electrical remodeling and prevent POAF in animal models [27]. They are powerful lipid lowering drugs highly effective in preventing coronary artery disease [23]. Studies conducted in hypercholesterolemic patients on statins undergoing coronary artery bypass grafting (CABG) showed a decrease in postoperative major cardiac events [44]. This effect was potentiated by simultaneously taking β-blockers [45]. The main benefits of statins seem to occur when these drugs are started in the preoperative period. When administered one week prior to on pump CABG, they decreased the incidence of POAF, as well as hospital length stay [22, 45]. After major lung resection, patients already on statins prior to surgery showed a threefold decrease in the probability of developing POAF [46]. One possible explanation seems to be related to their antiinflammatory or antioxidant mechanism, and observational studies conducted in patients undergoing major lung resection have observed an increase in C-reactive protein and interleukin 6 in the postoperative period [47].

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) have been suggested to reduce the incidence of POAF in patients with coexisting heart failure and systolic left ventricular dysfunction, but not in cases associated with systemic hypertension [48]. They may also play a role in maintaining sinus rhythm after electrical cardioversion. The data in the literature have focused mainly on the role of these drugs on the outcome in patients with chronic AF. The prophylactic use of ACEIs/ARBs to prevent POAF remains quite controversial, with both positive [22] and negative [49] findings. Inhibition of the renin–angiotensin–aldosterone system seems to attenuate left atrial dilatation, atrial fibrosis and to contribute in slowing conduction in animal studies, all factors that can trigger and maintain reentry circuits. These effects seem to be potentiated in patients with chronic heart failure when β-blockers are added [22].

Role of Postoperative Chemical and Electrical Cardioversion

Chemical and electrical cardioversion: Pharmacological cardioversion seems to be the most effective when started within 7 days from the onset of AF [29]. Drugs that can chemically cardiovert AF with variable success include flecainide, propafenone and ibutilide [13]. Ibutilide has been shown to have modest success in converting acute AF after cardiac surgery, and it may be associated with polymorphic ventricular tachycardia, especially in the presence of electrolyte abnormality [29]. Single oral doses of flecainide (300 mg) or propafenone (600 mg) seem to be safe, cardioverting, respectively, 91 and 76% of the cases within 8 hours from the onset of AF. In order to be eligible to receive these drugs, patients must be free from cardiac structural disease, such as left ventricular hypertrophy, mitral valve disease, coronary artery disease or heart failure [50]. The potential side effects for both drugs include ventricular tachycardia, heart failure and conversion to atrial flutter with rapid ventricular response [29].

Electrical cardioversion is used to treat AF in case of hemodynamic instability, with a success rate of 67–94% [27]. Biphasic waveforms are more successful than monophasic, using a current around 100–200 J and in a synchronized mode. Higher energy can be used for patients with high body mass index, prolonged AF or left atrial enlargement. Bradycardia (more common in patients on antiarrhythmics prior to cardioversion), ventricular tachyarrhythmias (in case of shock applied during repolarization), hypotension, pulmonary edema (probably due to myocardial stunning) and embolism are all potential complications. Electrolytes should be checked and normalized before cardioversion. In the case of digitalis toxicity and hypokalemia, cardioversion should be avoided due to the high incidence of ventricular fibrillation. In this setting, low currents and prophylactic lidocaine should be used. Since bradycardia can be profound up to the point of asystole, pacing capabilities should be also readily available [27].

Acute Coronary Syndrome

Myocardial ischemia may occur transiently after lung resection and be present as an electrocardiographic finding in 3.8% of patients, while infarction can occur in 0.2–0.9% of the cases [8, 51, 52]. The diagnosis of symptomatic perioperative myocardial infarct is associated with a 30–50% risk of death [23]. The incidence is increased in the presence of preoperative coronary artery disease and abnormal exercise testing. Patients are at the highest risk during the first three PODs, when a high degree of monitoring is suggested.

There are no definite recommendations for preoperative invasive testing or interventions. Most of the decision making should be based on the clinical presentation [53]. In patients at high risk (such as the ones with unstable angina, uncompensated chronic heart failure, arrhythmias and severe valvular disease) cardiac catheterization is highly recommended and followed by coronary artery revascularization, if necessary [28]. There are no prospective randomized studies on prophylactic CABG prior to elective surgery and whether this is superior to percutaneous revascularization (PCI). If patients require revascularization, elective surgery needs to be postponed, with the dilemma of how long to wait, especially in the case of cancer, where there is potential disease progression [54]. Cardiac stents, especially the drug eluting ones, represent a significant problem due to the prolonged need for anticoagulation. Stopping dual antiplatelet therapy (aspirin and clopidogrel) is associated with a quite high risk of stent thrombosis, while continuing it leads to an increased risk of intra- and postoperative bleeding and precludes the possibility of using regional anesthetic techniques [55]. The duration of the anticoagulation is usually based upon the type of stent: 4–6 weeks for bare metal stents and 12–24 months for drug eluting ones [23]. The risk of stent thrombosis is higher for drug eluting stents, especially if the stent is long, at a bifurcation, if the revascularization is incomplete, or the patient has history of diabetes or heart failure [56]. A nonrandomized observational prospective study done in noncardiac surgery patients who had cardiac stents placed within a year from surgery found a 44.7% rate of postoperative cardiac complications and a 4.7% mortality rate [57]. The dual antiplatelet therapy was stopped on average 3 days prior to surgery and substituted with intravenous unfractionated heparin or subcutaneous enoxaparin. Most of the complications occurred within the first 35 days from the stent placement and were cardiac in nature. Bleeding was not a significant variable. Despite the absence of randomization and the lack of information about the type of stent used, this study stresses several important points. Once the antiplatelet treatment is stopped, low molecular weight heparin should be used (heparin alone is insufficient); all non life saving procedures should be postponed at least for 6–12 weeks from the stent placement, and aspirin should be continued as long as possible prior to surgery [55, 57]. Prophylactic revascularization (CABG vs. PCI) does not seem to add further benefits over optimal medical treatment in patients with cardiac risk undergoing elective major vascular surgery [54]. Long-term survival as well as myocardial infarction, death and hospital length of stay seems to be unchanged. However, CABG is associated with less postoperative myocardial infarctions and decreased hospital length of stay when compared to PCI, probably because of better revascularization [58]. According to the American College of Cardiology, revascularization should be reserved for patients with unstable angina or advanced coronary artery disease [23]. In case the stents need to be placed before surgery, bare metal stents are preferred due to their lower risk of thrombosis. In both cases, elective surgery needs to be appropriately delayed to prevent graft or stent thrombosis.

Heart Failure and Cardiac Herniation

Heart failure can occur after major lung resection as a result of right or left sided dysfunction. Right heart failure can result from changes either in contractility or afterload. Unfortunately, most of the studies looking at changes in right ventricular function after lung resection were small, and found minor and transient differences when compared to the preoperative period. An increase in right ventricular end-diastolic volume has been observed as a reversible finding during the first two PODs [28], as well as a mild increase in pulmonary arterial pressures and pulmonary vascular resistance [59]. While postoperative changes in pulmonary arterial pressures, central venous pressures and pulmonary vascular resistance seem to be subtle at rest, they may become significant during exercise. Changes in right ventricular function are usually able to compensate for the former, but they may fail for the latter, leading to pulmonary hypertension [28]. When trans-thoracic echocardiography has been used to evaluate right ventricular function after pneumonectomy, it has shown only a mild increase in pulmonary arterial pressure which is not associated with ventricular dysfunction [60]. Other possible causes of right ventricular failure, although rare, include pulmonary embolism and cardiac herniation. Left side heart failure is usually a consequence of right heart dysfunction, either by decreasing left ventricular preload or shifting the interventricular septum [28]. Acute ischemia and valvular disease may also be contributing factors. Cardiac herniation, a rare complication after pneumonectomy, may be responsible for both right and left heart failure. It occurs more commonly after intrapericardial pneumonectomy, right more than left, and leads to a 50% mortality rate [28]. Herniation can be secondary to an incomplete surgical closure of the pericardium or the breakdown of a pericardial patch [61]. One main contributing factor includes an increase in intrathoracic pressure, such as with coughing. Changes in position, with the operative side being dependent, positive pressure ventilation, rapid lung reexpansion or suction on the chest tube are all other possible causes. Symptoms depend on the side of the herniation. Right-sided cases present with superior vena cava syndrome, due to kinking of the superior vena cava and decreased right ventricular filling, with subsequent hypotension, tachycardia and shock. Left-sided cases present with arrhythmias and ischemia, causing myocardial infarction, hypotension and ventricular fibrillation if left untreated [62]. This appears to be related to less cardiac rotation, with subsequent pericardial compression on the myocardium. Clinical presentation and electrocardiographic findings are fairly nonspecific in suggesting the diagnosis, stressing the role of chest radiography and a high index of suspicion. Treatment is surgical, with repositioning of the heart and placement of a patch. In order to minimize hemodynamic instability, the patient should be kept on the ­lateral decubitus with the operative side up [61].

Mediastinal Shift and Postpneumonectomy Syndrome

Mediastinal shift can occur intraoperatively or in the postoperative period as a result of changes in the postpneumonectomy space. At the end of surgery, once the chest is closed, some surgeons evacuate the air and fluid that fills the empty space aiming to bring the mediastinum back to midline. Excessive fluid drainage can lead to ipsilateral mediastinal shift and contralateral lung expansion, with decreased venous return and significant hypotension [63]. A high index of clinical suspicion, careful monitoring of the hemodynamics and communication with the surgical team are needed at this point of the operation to avoid hemodynamic collapse. When excessive fluid accumulates in this space, contralateral mediastinal shift occurs, leading to compression of the remaining lung and secondary respiratory insufficiency. This is seen more often in the postoperative period, and the use of intracavitary pressures monitoring can guide the drainage of the excess fluid if needed [63]. CT scan studies have shown obliteration of the postpneumonectomy space with fluid over time, elevation of the hemidiaphragm and expansion of the contralateral lung [64]. In the case of extreme mediastinal shift, dynamic compression of the distal airway can occur, leading to the so-called “postpneumonectomy syndrome” [65, 66]. This is a rare and late complication, which can occur at a median of 7 years from surgery. It is more common in females, children and with right-sided procedures (even though it has been described for left cases as well). It manifests with exertional respiratory insufficiency, stridor and recurrent infections. Respiratory symptoms are caused by dynamic compression of the distal trachea and mainstem bronchus and treatment involves the use of airway stents or thoracotomy and repositioning of the mediastinum via saline filled prosthesis (see also Chap. 41).


In the last few decades, a significant improvement in the surgical and anesthetic techniques has made pneumonectomy and major lung resection safer. The introduction of epidural analgesia, minimally invasive surgical techniques and the introduction of short acting anesthetics have all contributed to decrease the incidence of postoperative complications. Fast track strategies and careful selection of patients undergoing to lung resection procedures have also played an important role in postoperative and long-term outcome. Better utilization of step down and acute postoperative care units have decreased the rate of ICU admissions, saving costs. Since the average age of patients requiring lung resection is increasing, anesthesiologists and surgeons will be facing more complex cases, due to the presence of multiple comorbidities. Careful preoperative work up, customizing the type of surgery as well as planning for in hospital and post discharge rehabilitation options will prove to be essential for decreasing even further the possible complications and improving the overall care.

Clinical Case Discussion

A 65-year-old-man with squamous cell cancer of the right upper lobe underwent a right intrapericardial pneumonectomy. Surgery was 150 min and uneventful. Estimated blood loss was 700 cc, and 700 cc of ringer’s lactate was used during the case. Urinary output was 100 cc. The patient was extubated in the operating room at the end of the case. A thoracic epidural was used intraoperatively, and the patient was comfortable in PACU. As part of the postoperative blood work, troponin levels were checked and the first set was 1.66 (1.07 and 0.52 the second and the third one). ST segment elevations transiently occurred on POD 1 in correspondence to a fourth troponin of 1.55.

On POD 2, subcutaneous emphysema was noted on the right chest wall, neck and eye (see Fig. 44.1). While walking, he had an episode of desaturation and tachycardia. Chest X-ray is shown. Electrocardiogram showed rapid SVT, with hypotension (HR  =  128, BP  =  88/45). The patient was transferred to the ICU where he was intubated. He slowly became hemodynamically unstable, requiring multiple pressors.
Fig. 44.1.

Radiographic changes on postoperative days 2.

CXR on POD 2


What are common cardiac complications after lung resection?
  • Arrhythmias (atrial fibrillation, atrial flutter and SVT).

  • Ischemia and acute coronary syndrome.

  • Heart failure and cardiac herniation.

  • Mediastinal shift and postpneumonectomy syndrome.

  • Arrhythmias: Who is at risk (suggested pathophysiology, role of WBC and inflammatory response, BNP levels)? What we can do to prevent it (rate or rhythm control? Preoperative medications?)? How do we treat postoperatively (medications vs. cardioversion)? Risks/side effects of the treatment.

  • Acute coronary syndrome: What are known risk factors? Preoperative stenting vs. medical treatment for patients with a positive stress test. Is myocardial ischemia preventable (role of preoperative statins/beta blockers)? What is the treatment? How does it affect mortality?

  • Cardiomegaly/cardiac failure: Who is at risk (role of the extent of dissection, preoperative risk factors)? How does it affect mortality?

  • Mediastinal shift: Why does this happen (extent of dissection)? How common is cardiac herniation? Pathophysiology and diagnosis.


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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Alessia Pedoto
    • 1
  • David Amar
    • 1
  1. 1.Department of Anesthesiology and Critical Care MedicineMemorial Sloan-Kettering Cancer CenterNew YorkUSA

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