Anesthesia for patients with pericardial disease and/or cardiac tamponade

INTRODUCTION — Patients with acute or chronic pericardial diseases (eg, constrictive pericarditis, acute pericardial effusion, cardiac tamponade) often require therapeutic surgical intervention or invasive diagnostic procedures that may be scheduled as elective, urgent, or emergency cases. These patients present unique perioperative challenges and specific considerations for the anesthesia care team. This topic addresses preanesthetic assessment and preparations, patient optimization, and intraoperative anesthetic management for interventions to treat pericardial pathology.

Medical and surgical aspects of pericardial diseases are discussed in other UpToDate topics including:

●(See "Cardiac tamponade".)

●(See "Pericardial effusion: Approach to diagnosis".)

●(See "Constrictive pericarditis: Diagnostic evaluation".)

●(See "Acute pericarditis: Treatment and prognosis".)

PREANESTHETIC ASSESSMENT AND MANAGEMENT

Assessing diagnostic tests — For elective or semi-urgent cases, the following diagnostic results are typically available:

●Electrocardiogram – Electrocardiographic findings in patients with cardiac tamponade, pericardial effusion, or constrictive pericarditis are described in separate topics. (See "Pericardial effusion: Approach to diagnosis", section on 'ECG findings' and "Differentiating constrictive pericarditis and restrictive cardiomyopathy", section on 'Electrocardiogram'.)

●Chest radiograph – The chest radiograph may reveal evidence of a pericardial effusion, particularly enlargement of the cardiac silhouette (cardiothoracic ratio >50 percent) and, in some cases, pulmonary edema.

●Echocardiography – Echocardiography is often employed to diagnose and localize pericardial effusion (eg, determining its size or recognizing loculated effusions or clot formations that border pericardial adhesions) since this modality is readily available and low cost [1-4]. Also, thoracic ultrasound may detect pleural effusions in patients with chronic pericardial effusion [5]. Furthermore, point-of-care echocardiography can determine the need for emergency lifesaving intervention in the setting of acute cardiac tamponade. (See 'Assessing hemodynamic impact' below and "Pericardial effusion: Approach to diagnosis", section on 'Echocardiography'.)

Preoperative echocardiography in patients with constrictive pericarditis may reveal that a pericardial effusion is also present (eg, in a patient with worsening symptoms in the preoperative period) (see "Constrictive pericarditis: Diagnostic evaluation", section on 'Echocardiography'), and aids in differentiating constrictive pericarditis from restrictive cardiomyopathy, as discussed separately. (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy", section on 'Noninvasive testing'.)

●Cardiac magnetic resonance – If echocardiography examination is inconclusive, computed tomography or cardiac magnetic resonance imaging may be employed to definitively diagnose constrictive pericarditis. (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy", section on 'Pericardial imaging' and "Differentiating constrictive pericarditis and restrictive cardiomyopathy", section on 'Cardiovascular magnetic resonance (CMR)'.)

Assessing hemodynamic impact — Patients with pericardial pathology (eg, constrictive pericarditis, acute pericardial effusion, cardiac tamponade) have reduced cardiac filling due to external forces. Hemodynamic effects are directly related to the total volume of the effusion and chronicity of its development. The pericardium can accommodate a large volume of fluid if accumulation occurs slowly, typically over weeks to months [6]. For example, if the rate of bleeding is slow or the pericardium periodically decompresses by emptying blood into the pleural space, a patient may initially appear stable. However, due to the poor compliance of the pericardium, the faster the accumulation of blood or fluid, the more severe the hemodynamic compromise (figure 1). Thus, acute accumulation of as little as 50 mL of fluid can cause tamponade physiology. Severe hypotension becomes evident once the volume trapped in the pericardial sac increases enough to compress the heart and compromise cardiac output [7].

●Hemodynamically unstable patients – For hemodynamically unstable patients with shock from cardiac tamponade, emergency pericardiocentesis and placement of a drainage catheter may provide temporary relief even before patient transport to the operating room. Procedural details are discussed separately. (See "Emergency pericardiocentesis" and "Pericardial effusion: Approach to management".)

However, such emergency procedures may be technically challenging because of the need to locate a potentially small amount of fluid causing tamponade physiology, and because clotted blood can be difficult to aspirate through a small-lumen catheter. Additional cardiac surgical treatment under general anesthesia is typically necessary. (See 'Induction of anesthesia' below.)

●Stable patients – Clinically stable patients may be reevaluated with sonography (eg, focused cardiac ultrasound with transthoracic echocardiography, or transesophageal echocardiography [TEE]) in the immediate preoperative period, either in the emergency department, intensive care unit, or after transport to the operating room [8]. (See "Emergency ultrasound in adults with abdominal and thoracic trauma", section on 'Pericardial and limited cardiac examination' and "Overview of perioperative uses of ultrasound", section on 'Echocardiography'.)

Also, preoperative volume status is assessed, including responses to any recent fluid boluses. In most cases, fluid administration to augment preload prior to induction of anesthesia is prudent to prevent hypovolemia [3].

Intravascular access and monitoring

●Cardiac tamponade – Large-bore IV access is obtained and an intra-arterial blood pressure (BP) catheter is inserted before induction of general anesthesia. After induction of general anesthesia, a TEE probe is typically inserted as intraoperative TEE examinations are useful to assess adequacy of the drainage procedure, as well as to evaluate ventricular and cardiac valve function after pericardial drainage [2].

●Pericardiectomy – In addition to the monitors noted above, large-bore central venous catheter access is ensured, typically after anesthetic induction, in any patient with the potential for sudden and significant hemorrhage. A pulmonary artery catheter may also be inserted if frequent episodes of hemodynamic instability due to cardiac manipulation and blood loss are anticipated. (See "Anesthesia for cardiac surgery: General principles", section on 'Intravascular cardiac monitors'.)

Preparations before induction of general anesthesia — Premedication is generally avoided, particularly if impending hemodynamic instability is likely. Before induction of general anesthesia, preparations include [1-3]:

●Ensuring immediate availability of resuscitation fluids, including typing and cross-matching red blood cells with access to rapid release of several red blood cell units, is prudent in cases where rapid transfusion may become necessary (eg, planned pericardiectomy, possibility of cardiac chamber injury). (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Pretransfusion testing'.)

●Preparing vasoactive agents for administration of boluses or via continuous infusion (table 1 and table 2).

●Positioning defibrillator/pacing pads (figure 2).

●Ensuring thorough communication among cardiac surgical team members regarding the planned procedure in a preoperative briefing. (See "Patient safety in the operating room", section on 'Timeouts and briefing in the operating room'.)

●For severely compromised patients, ensuring readiness for immediate intervention with surgeons gowned and gloved, and the patient prepped and draped before administration of anesthetic induction agents

TREATMENT OF PERICARDIAL EFFUSION AND/OR TAMPONADE

Assessing urgency — Causes of compressive cardiac syndrome include idiopathic, infectious, autoimmune and inflammatory, neoplastic, cardiac, traumatic, or metabolic processes (table 3).

Acute traumatic causes of cardiac tamponade include:

●Percutaneous coronary interventions (PCI) can lead to coronary artery perforation or myocardial injury, which can result in cardiac tamponade and death. While the incidence of coronary artery perforation after regular PCI is less than 1 percent, a higher incidence of 4 to 9 percent occurs when the indication for PCI is chronic total occlusion [9]. This is likely due to the greater complexity of these lesions and the selected interventional approach (eg, rotational atherectomy). (See "Specialized revascularization devices in the management of coronary heart disease", section on 'Rotational atherectomy'.)

●Tamponade after cardiac surgery may at times be rapid in onset, and mediastinal re-exploration following cardiac surgery likely is the most common "compressive," cardiac syndrome that most anesthesiologists will encounter, with an incidence estimated to be 0.1 to 0.6 percent [10-12]. Exacerbating factors include preoperative coagulopathy, need for systemic anticoagulation during the intervention, complex cardiac surgical procedures, or need for repeat sternotomy. In some cases, a more regional form of cardiac tamponade is observed. This occurs when one chamber of portion of the heart is compressed by a loculated effusion or clot. Focal compression of the right or left atrium or atrioventricular groove may produce hemodynamic findings typical of cardiac tamponade, or may more selectively affect right- or left-sided hemodynamic parameters.

●Penetrating wounds of the heart resulting in hemorrhagic shock or cardiac tamponade, depending upon whether blood can escape the pericardial space. The right ventricle (RV) is the most commonly injured chamber due to its anterior position within the chest cavity, and the left ventricle (LV) ventricle is the next most commonly injured chamber. Atrial injuries are less common and typically less severe. Notably, cardiac tamponade may also occur after blunt chest trauma. (See "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Cardiac injury'.)

With clinically significant pericardial effusion or tamponade, signs may include elevated jugular venous pressure, narrowed pulse pressure, pulsus paradoxus, and Kussmaul's sign [1,2,13]. Symptoms may include chest pain, dyspnea related to decreased cardiac output or concomitant pleural effusions, or syncope which indicates impending hemodynamic deterioration. Patients with severe tamponade physiology present with acute shock.

Urgent therapeutic relief may be necessary for hemodynamically unstable patients with significant pericardial effusions or tamponade physiology (algorithm 1) [1,2]. In cooperative patients, a pericardial drain can be placed under local anesthesia, or emergency needle pericardiocentesis can be performed prior to induction of general anesthesia (algorithm 2). (See 'Induction of anesthesia' below.)

Interventional approaches — One of several interventional approaches may be selected by the surgeon or proceduralist:

●Pericardiocentesis – Advantages of pericardiocentesis include minimally invasiveness, typically with the ability to employ local anesthesia. In some cases, hemodynamic stability may be achieved by performing pericardiocentesis before induction of general anesthesia for surgical exploration and more definitive pericardial drainage [2,14]. In other cases, pericardiocentesis may be necessary for diagnostic purposes when neoplastic or infectious causes of effusion are suspected.

●Pericardial window – Creation of a pericardial window may be necessary if pericardiocentesis cannot be performed (eg, a loculated or posterior effusion), if fluid drainage is inadequate, or when reaccumulation of fluid is anticipated. A pericardial window may be performed via an open thoracotomy, video-assisted thoracoscopic surgery approach, or via median sternotomy [2,14].

●Percutaneous balloon pericardiotomy – Percutaneous balloon pericardiotomy has been described as an approach that may reduce the rate of recurrent pericardial effusion for malignant pericardial effusions [15].

●Pericardial sclerosis – Use of pericardial sclerosing agents is another technique that has been used to treat pericardial effusions due to malignancy or post-infarction pericarditis, with the goal of reducing the incidence of recurrent effusions [16]. Intrapericardial fibrinolytic therapy has also been described [17,18].

Hemodynamic goals — Hemodynamic goals for cardiac tamponade can be summarized as "full, fast, and strong" [2,3,19]:

●Full – Full refers to intravascular volume. Intravenous (IV) fluids are administered to optimize preload before induction and until relief of the tamponade.

Any manipulation that may decrease venous return to the heart should be avoided (eg, positive pressure mechanical ventilation with large tidal volumes, high peak airway pressures).

●Fast – Fast refers to heart rate (HR). Bradycardia should be avoided because tachycardia is the most important compensatory mechanism for preserving cardiac output. Ideally, the patient is in sinus rhythm to facilitate ventricular filling with each atrial contraction, which is especially important in patients with acute diastolic dysfunction. Tachycardia is acceptable and often necessary in this setting; however, treatment for other arrythmias may be necessary

●Strong – Strong refers to myocardial contractility. In addition to avoiding drugs that impair contractility, administration of vasopressor and inotropic agents (eg, phenylephrine, norepinephrine, and vasopressin) to maintain hemodynamic stability may be necessary prior to induction of anesthesia and up until the time of relief of tamponade (table 1). High doses of anesthetic agents that may cause myocardial depression are avoided (eg, high doses of propofol or volatile inhalation anesthetics).

We employ an intra-arterial catheter for continuous blood pressure (BP) monitoring. Information derived from other cardiovascular monitors such as transesophageal echocardiography (TEE) or transthoracic echocardiography is useful. In addition, a large-bore central venous catheter is often inserted to ensure that adequate fluid resuscitation can be achieved, and to target a high normal central venous pressure. A pulmonary artery catheter may be useful, particularly if ongoing postoperative resuscitation is anticipated.

Induction of anesthesia — During induction of anesthesia in a patient with tamponade physiology, loss of sympathetic tone may result in hemodynamic collapse. This can occur due to the combination of decreased preload (due to decreased venous return to the heart), reduced systemic vascular resistance (due to systemic vasodilation), and direct myocardial depression (an adverse effect of many anesthetic agents). Initiation of positive pressure ventilation will exacerbate the decrease in preload by decreasing venous return to the heart.

Hemodynamically unstable patients — In patients with actual or impending hemodynamic instability, the need for vasoactive or inotropic therapy is likely during anesthetic induction regardless of the selected technique (table 1). Strategies to avoid hemodynamic collapse include:

Surgical management strategies — Management strategies for patients with pericardial effusion or cardiac tamponade depend on the urgency of the procedure and whether the patient is cooperative (algorithm 2) [1]. In some cases, pericardiocentesis or surgical needle subxiphoid decompression of the pericardium is performed with local anesthesia in a spontaneously breathing awake patient. Removal of only a small amount of fluid may dramatically improve hemodynamic stability because of the steep curve of the pressure-volume relationship of the pericardial contents (figure 1) [19]. After such partial relief of the tamponade, a safer induction of general anesthesia can be accomplished.

In other cases, the surgeon prepares for immediate access to the pericardium by being gowned and gloved, with the patient prepped and draped before asking the anesthesiologist to proceed with induction of general anesthesia. (See 'Preparations before induction of general anesthesia' above.)

Ventilation management strategies — Options include the following [1-3]:

●Allowing spontaneous ventilation with delay of endotracheal intubation until the pericardial sac is opened. If there are no contraindications (eg, aspiration risk, significant obesity, severe orthopnea, or an uncooperative patient), an inhalation induction technique is ideal. To minimize coughing and straining while maintaining spontaneous ventilation, we select sevoflurane. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Inhalation induction (sevoflurane, halothane, nitrous oxide)'.)

Another option for maintaining spontaneous ventilation is IV induction with ketamine, which has minimal respiratory depressant effects (see "General anesthesia: Intravenous induction agents", section on 'Ketamine'). While anesthetic induction with etomidate provides hemodynamic stability, patients typically cease to breathe spontaneously. With either induction technique, manipulation of the airway should be avoided unless a sufficiently deep level of anesthesia has been achieved.

●Inducing anesthesia with an IV agent (eg, ketamine), then using low tidal volumes with a relatively high respiratory rate to minimize mean airway pressure during controlled positive pressure ventilation (PPV). If such tidal volumes are well tolerated without exacerbating hemodynamic instability, then a neuromuscular blocking agent (NMBA) may be administered to facilitate endotracheal intubation. Then during PPV, avoid large tidal volumes and high inspiratory pressures that may decrease preload by decreasing venous return to the heart. A relatively fast respiratory rate may be used to provide adequate minute ventilation. In patients without significant pulmonary hypertension, mild hypercarbia is acceptable.

Selection of anesthetic agents — If IV induction is selected, we administer ketamine to induce general anesthesia and take advantage of its centrally mediated sympathetic nervous system stimulation, resulting in significant increases in HR, mean arterial pressure, and plasma epinephrine levels [2,20]. However, this stimulatory effect of ketamine depends upon the presence of adequate sympathetic and myocardial reserve; otherwise, hypotension may ensue due to direct myocardial depression [21]. Etomidate is an alternative if ketamine is not readily available. (See "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

If inhalation induction is selected, we use sevoflurane since this agent minimizes coughing and straining while maintaining spontaneous ventilation. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Inhalation induction (sevoflurane, halothane, nitrous oxide)'.)

Induction agents that induce vasodilation are avoided (eg, standard doses of IV propofol or large doses of volatile anesthetic agents) (see "Anesthesia for thoracic trauma in adults", section on 'General anesthesia'). Opioids are avoided or administered in low titrated doses during the induction sequence since vagally mediated bradycardia can lead to decreased cardiac output. (See "Perioperative uses of intravenous opioids in adults: General considerations", section on 'Prevention and management of adverse opioid effects'.)

Hemodynamically stable patients — Induction of anesthesia with an IV agent (ketamine or etomidate) followed by endotracheal intubation can be safely accomplished in patients who are hemodynamically stable without evidence of tamponade. However, the patient is typically positioned to allow for immediate surgical preparation and draping. Thus, the operation can proceed expeditiously if hemodynamic deterioration occurs during induction.

Endotracheal tube selection — Selection of an endotracheal tube (ETT) depends on the planned surgical technique.

●A subxiphoid approach typically does not require lung isolation and one lung ventilation (OLV).

●Thoracotomy and/or video-assisted thoracoscopic surgery approaches typically do require OLV (see "One lung ventilation: General principles"). If the patient is hemodynamically unstable, it may not be feasible to take any extra time to properly position a double-lumen endotracheal tube. In such cases, we typically position a single lumen ETT and subsequently place an endobronchial blocker to achieve lung isolation [22]. (See "Lung isolation techniques", section on 'Double-lumen endobronchial tubes' and "Lung isolation techniques", section on 'Bronchial blockers'.)

Notably, some patients may not tolerate OLV during an intrathoracic surgical approach to treat cardiac tamponade. Options include attempting to achieve hemodynamic stability with fluid boluses and inotropic/vasodilator agents, altering ventilation strategies (eg, returning to spontaneous ventilation and/or providing controlled PPV with very low tidal volume and a relatively high respiratory rate until the tamponade is relieved).

Maintenance of anesthesia

●Anesthetic agents – Maintenance of anesthesia is typically accomplished with combinations of a volatile inhalation anesthetic agents plus supplemental IV opioids, as well as ketamine or propofol. Nitrous oxide is avoided because it may expand a pneumothorax resulting from the surgical incision and dissection and might also result in hypoxemia. In patients managed with PPV, short- or intermediate-acting NMBAs may be used as necessary. (See 'Ventilation management strategies' above.)

●Vasoactive agents – Continuous IV infusions of vasopressor or inotropic agents may be necessary to maintain hemodynamic stability (table 1), but are typically discontinued after relief of cardiac tamponade. (See 'Hemodynamic considerations after tamponade relief' below.)

Hemodynamic considerations after tamponade relief — Once cardiac tamponade is relieved, hemodynamic conditions usually change dramatically. Sudden severe increases in BP and HR may occur due to more complete circulation of endogenously generated and exogenously administered catecholamines. As BP increases, bleeding from other vascular injuries may worsen. These phenomena should be anticipated and treated with a volatile inhalation agent, beta blocker, and/or vasodilator (table 2).

Some patients will have a paradoxical hemodynamic collapse after otherwise uneventful pericardial drainage [2,23]. Pericardial decompression syndrome with hemodynamic deterioration can occur immediately after relief of tamponade or up to 48 hours later. Although not completely understood, this phenomenon may be due to more rapid expansion of right-sided heart chambers impairing left-sided filling, a sudden increase in RV preload resulting in RV dilation and failure, or sudden vasodilatory collapse due to imbalance in the sympathetic-parasympathetic system [2,23,24]. Mortality rate has been reported at 29 percent [25]. Supportive care includes continuous infusions of inotropic and/or vasopressor agents to manage LV and/or RV failure guided by TEE and other invasive cardiovascular monitoring. Although there are no established means to prevent pericardial decompression syndrome, prolonged drainage with a pericardial drain in place after alleviation of tamponade may reduce its incidence [24].

Postoperative management

●Postoperative disposition – Many patients remain intubated and are transferred to the ICU to monitor the effusion or manage postoperative hemodynamic instability due to underlying disease processes or surgical and/or coagulopathic bleeding. Careful attention to intravascular filling status and the patient’s response to fluid boluses, as well as administration of inotropic and vasoactive infusions is monitored (table 1). Serial postoperative TEE examinations may be useful to assess ventricular volume and function, and whether pericardial fluid or blood has reaccumulated.

●Postoperative pain management – To provide postoperative analgesia, a longer acting opioid such as morphine or hydromorphone may be administered before emergence from anesthesia. Local anesthetic infiltration of the wound and/or intraoperative placement of regional nerve blocks (ie, intercostal nerve blocks) may be accomplished by the surgeon or anesthesiologist.

PERICARDIECTOMY

General considerations

Assessing severity — Various pericardial diseases may result in constrictive pericardial syndromes, although the majority are idiopathic or viral in origin (table 3) [2,26] (see "Constrictive pericarditis: Diagnostic evaluation"). Although relatively rare, constrictive pericarditis following previous cardiac surgery occurs in 0.2 to 0.4 percent of patients [27].

In contrast to patients with pericardial effusions, patients with constrictive pericarditis typically have nonspecific chronic symptoms such as fatigue, dyspnea, very limited exercise tolerance, anorexia, weight loss or cachexia, or symptoms of right heart failure [28]. Signs may include evidence of volume overload, with elevated jugular venous pressure, Kussmaul's sign, or evidence of right heart failure (eg, central venous pressure >15 mmHg) [29]. Patients with severe end stage disease may have cachexia, liver dysfunction and renal dysfunction [29,30]. However, patients with constrictive pericarditis do not present to the operating room for urgent pericardial stripping and pericardiectomy since these are elective procedures reserved for severe cases [28,31,32]. (See "Constrictive pericarditis: Diagnostic evaluation".)

Surgical options — The traditional surgical approach for pericardiectomy is via a median sternotomy; however, thoracotomy with the need for lung isolation and one-lung ventilation (OLV) may be selected for some cases. Complete pericardiectomy (phrenic nerve to phrenic nerve) including inferior ventricular walls and diaphragmatic pericardium is performed in all cases if technically feasible [27,33]. Anterior pericardiectomy portends a higher failure rate, and repeat pericardiectomy procedures have a higher mortality rate [27].

Pericardiectomy requires cardiac surgery with cardiopulmonary bypass (CPB) in 40 to 60 percent of cases [33]. Although some cases are performed without CPB, personnel and equipment to rapidly institute CPB remain on standby. Initiation, management, and the weaning process for CPB are discussed in separate topics:

●(See "Initiation of cardiopulmonary bypass".)

●(See "Management of cardiopulmonary bypass".)

●(See "Weaning from cardiopulmonary bypass".)

As noted above, preoperative communication with the surgeon is necessary to thoroughly understand the planned procedure. (See 'Preparations before induction of general anesthesia' above and "Patient safety in the operating room", section on 'Timeouts and briefing in the operating room'.)

Hemodynamic goals — The anesthetic approach to constrictive pericarditis requires careful management of cardiac and respiratory physiology. In general, hemodynamic goals for patients with constrictive pericarditis are similar to those for patients with pericardial effusion or tamponade [2] (see 'Hemodynamic goals' above):

●Full – Maintain filling pressures to avoid decreases in cardiac output.

●Fast – Maintain heart rate (HR) throughout the perioperative period. Since stroke volume is limited in patients with constrictive pericarditis, the main compensatory mechanism is increased HR.

●Strong – Although many patients have underlying normal systolic function, those with decreased systolic function (eg, when constrictive pericarditis and restrictive cardiomyopathy coexist) are more likely to require continuous intraoperative infusions of vasopressor/inotropic agents (table 1).

Administration of IV fluids and vasopressor/inotropic agents may be necessary to maintain hemodynamic stability (table 1).

Induction and maintenance of anesthesia

●Anesthetic and vasoactive agents – Although intravenous (IV) induction is typically selected and may be accomplished with a variety of agents, ketamine or etomidate are most commonly used. (See "General anesthesia: Intravenous induction agents".)

We avoid or minimize anesthetic agents and doses that (see 'Hemodynamic goals' above):

•Decrease preload due to decreased venous return to the heart

•Reduce systemic vascular resistance due to systemic vasodilation

•Cause direct myocardial depression (eg, high doses of propofol or volatile inhalation agents)

•Induce bradycardia (eg, high doses of opioids)

●Neuromuscular blocking agents – Inflammation and difficulty identifying the phrenic nerves may necessitate selection of a short-acting neuromuscular blocking agent (NMBA) during induction and maintenance to allow minimal neuromuscular blockade while the phrenic nerve is identified during the dissection phase by employing surgical nerve stimulation. (See "Clinical use of neuromuscular blocking agents in anesthesia".)

●Ventilation management strategies – Unlike patients with cardiac tamponade physiology where positive pressure ventilation adversely impacts cardiac filling (see 'Maintenance of anesthesia' above), intrathoracic and intracardiac pressures are dissociated in patients with constrictive pericarditis such that the respiratory cycle has little effect on overall hemodynamics [29]. Due to overall restriction in cardiac volume, left ventricular (LV) filling and right ventricular (RV) filling occur in alternate phases during the respiratory cycle, each at the expense of the other [29].

Postoperative management — As with other major cardiac surgical procedures, patients remain intubated after pericardiectomy, and are transferred to the intensive care unit. (See "Anesthesia for cardiac surgery: General principles", section on 'Transport and handoff in the intensive care unit'.)

Potential problems in the early postoperative period include [1,34,35]:

●Persistent bleeding.

●Hemodynamic instability.

●Persistent evidence of diastolic dysfunction, despite surgical removal of the parietal pericardium.

●New or worsening RV dysfunction, which is treated supportively (see "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Hemodynamic management'). Occasionally, extracorporeal membrane oxygenation or a temporary RV assist device is needed. (See "Short-term mechanical circulatory assist devices".)

●New or worsened tricuspid regurgitation (TR) as a result of acute RV overload and dilation. Significantly elevated pulmonary artery pressure (PAP) may be noted. In some cases, if TR is persistent after pericardiectomy, tricuspid valve annuloplasty is performed [2,36].

Although postoperative morbidity and mortality after pericardiectomy has decreased over several decades, 30-day mortality for radical pericardiectomy remains at approximately 5 percent [33,34,37,38].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately [39]. (See "Society guideline links: Pericardial disease".)

SUMMARY AND RECOMMENDATIONS

●Assessing hemodynamic impact and urgency – Urgent therapeutic relief may be necessary for hemodynamically unstable patients with pericardial effusion and cardiac tamponade physiology. In cooperative patients, the surgeon may use local anesthesia to place a pericardial drain or perform needle pericardiocentesis before induction of general anesthesia. (See 'Assessing hemodynamic impact' above and 'Assessing urgency' above.)

●Intravenous access and monitoring – Ensure that large-bore intravenous (IV) access and an intra-arterial blood pressure (BP) catheter is inserted before induction. After induction, a transesophageal echocardiography (TEE) probe is often inserted. (See 'Intravascular access and monitoring' above.)

●Preanesthetic preparations – Before induction of anesthesia (see 'Preparations before induction of general anesthesia' above):

•Prepare IV resuscitation fluids (including cross-matched blood when indicated)

•Prepare vasoactive agents (table 1 and table 2)

•Position defibrillator/pacing pads (figure 2)

•Communicate with cardiac surgical team members regarding the planned procedure

•For severely compromised patients, ensure readiness for immediate intervention with surgeons gowned and gloved, and patient prepped and draped before anesthetic induction

●Hemodynamic goals – Hemodynamic goals include (see 'Hemodynamic goals' above and 'Hemodynamic goals' above):

•Full – Optimize preload with administration of IV fluids before induction and until relief of the tamponade, and avoid manipulations that decrease venous return (eg, positive pressure mechanical ventilation with large tidal volumes, high peak airway pressures).

•Fast – Avoid bradycardia; tachycardia is the most important compensatory mechanism to preserve cardiac output.

•Strong – Administer vasopressor and inotropic agents (eg, phenylephrine, norepinephrine, and vasopressin (table 1)) as needed during induction and until relief of tamponade. Avoid high doses of anesthetic agents that may cause myocardial depression.

●Management of pericardial effusion and/or cardiac tamponade

•Induction of anesthesia – In hemodynamically unstable patients, strategies include (see 'Hemodynamically unstable patients' above):

-Surgical approaches – Pericardiocentesis or surgical needle subxiphoid decompression of the pericardium may be performed with local anesthesia in a spontaneously breathing awake patient. Removal of only a small amount of fluid can dramatically improve hemodynamic stability before anesthetic induction.

-Selection of anesthetic agents – For IV induction, we suggest ketamine (Grade 2C), because its sympathetic nervous system stimulation typically increases heart rate (HR), BP, and plasma epinephrine levels. For inhalation induction, we suggest sevoflurane (Grade 2C), since this agent minimizes coughing and straining while maintaining spontaneous ventilation. Avoid induction agents that induce vasodilation or bradycardia.

-Ventilation management strategies – Avoid positive pressure mechanical ventilation with large tidal volumes or high peak airway pressures. Options include allowing spontaneous ventilation with delay of endotracheal intubation until the pericardial sac is opened. If controlled ventilation is selected, use low tidal volumes with a relatively high respiratory rate to minimize mean airway pressure.

-Endotracheal tube selection – A subxiphoid approach typically does not require lung isolation and one lung ventilation (OLV). However, thoracotomy and/or video-assisted thoracoscopic approaches typically do require OLV.

•Maintenance of anesthesia – Combinations of a volatile inhalation anesthetic agents plus supplemental IV opioids and ketamine or propofol are usually employed to maintain anesthesia. Nitrous oxide is avoided. (See 'Maintenance of anesthesia' above.)

•Hemodynamic considerations after tamponade relief – Sudden severe increases in BP and HR may occur after tamponade relief due to restoration of cardiac filling and more complete circulation of endogenously generated and exogenously administered catecholamines, and must be treated with a volatile inhalation agent, beta blocker, and/or vasodilator (table 2). (See 'Hemodynamic considerations after tamponade relief' above.)

•Postoperative management – Many patients remain intubated and are transferred to the intensive care unit to manage persistent postoperative hemodynamic instability. Postoperative pain relief may include administration of a longer acting opioid (eg, morphine, hydromorphone), local anesthetic infiltration of the wound, and/or intraoperative placement of a regional nerve blocks (ie, intercostal nerve blocks). (See 'Postoperative management' above.)

●Management of pericardiectomy

•Surgical options – Approaches via a median sternotomy do not require OLV; however, thoracotomy with lung isolation may be selected for some cases. Cardiopulmonary bypass (CPB) is necessary in 40 to 60 percent of cases. (See 'Surgical options' above.)

•Induction and maintenance of anesthesia (see 'Induction and maintenance of anesthesia' above)

-Anesthetic agents – Although IV induction may be accomplished with a variety of agents, avoid agents and doses that decrease preload, or cause vasodilation, myocardial depression, or bradycardia.

-Neuromuscular blocking agents – A short-acting neuromuscular blocking agent (NMBA) may be selected to allow identification of the phrenic nerve via surgical nerve stimulation during dissection.

•Postoperative management – Similar to other major cardiac surgical procedures, patients remain intubated and are transferred to the intensive care unit. (See 'Postoperative management' above.)