Hilary P. Grocott
G. Burkhard Mackensen
1. Patients presenting for pericardial drainage procedures require a thorough, but often urgent, preoperative evaluation in order to understand the etiology of the effusion and any associated hemodynamic instability, such as tamponade.
2. Echocardiography plays a central role in the diagnosis of effusion and pericardial tamponade and can guide drainage.
3. Thoracoscopic procedures and subxiphoid approaches are the most common techniques for definitive drainage of pericardial effusion. However, ultrasound-guided needle pericardiocentesis can be used for emergent drainage in the unstable patient.
4. The anesthetic technique needs to be tailored to the individual patient characteristics, but can be accomplished successfully with inhalational, as well as intravenous induction techniques. The hemodynamic goals of augmented preload with maintenance of afterload, contractility, and heart rate should be targets.
The patient is a 37-year-old woman with stage 4 breast cancer who presents with increasing shortness of breath, reduced exercise tolerance and intermittent chest discomfort. She has also complained of worsening headaches for the past few weeks. She has a history of receiving Adriamycin chemotherapy, interrupted for reasons unclear to her, and was healthy before her cancer diagnosis 3 years ago. She has been unable to lie flat for 24 hours and has poor venous access. She has steroid induced diabetes. Medications include lansoprazole, iron and lorazepam at night.
Vital signs: BP 90/40, HR 110, room air SaO2 89%.
Laboratory examination is notable for: hemoglobin 8.2, WBC 5.8, platelets 164, BUN 40, creatinine 1.4, glucose 145.
Chest wall echocardiogram revealed a large pericardial effusion.
She is listed for a pericardial window procedure via thoracoscopy.
Pericardial window procedures allow the drainage of fluid from the pericardial space and are performed with relative frequency by the cardiothoracic surgical team. In order to provide optimal anesthetic management for such patients, a thorough understanding of the associated pathophysiology and the various etiologies of pericardial effusion is essential.
Pericardial tamponade can occur in numerous acute conditions such as penetrating chest trauma, or present in the decompensated state of various subacute processes such as malignant tumors (Table 16–1). Although pericardial effusions can occur in isolation, they often occur in combination with other clinical conditions such as pleural effusions. This can confuse the clinical picture considerably, as symptoms of dyspnea and orthopnea can be secondary to the pleural effusion and/or other pulmonary involvement. Frequently the therapeutic intervention for pericardial effusion involves concomitant pleural drainage.
Table 16–1. Etiology of Pericardial Effusion/Pericarditis
The clinical presentation and perioperative management strategy of these patients depend upon the rapidity of fluid accumulation. The variable hemo-dynamic consequences of excessive pericardial fluid accumulation bring special anesthetic considerations that need to be understood in order to adequately care for these patients.3
The post-cardiac surgical patient represents a unique group presenting for pericardial drainage. The clinical presentation of tamponade in this patient population must frequently be differentiated from cardiogenic shock, either from global left ventricular failure, or from isolated right ventricular failure. In addition, these patients rarely present with the classic signs and symptoms of cardiac tamponade due to the prior pericardial disruption from the preceding cardiac surgical procedure, as well as the likelihood that the fluid in these postoperative patients is hemorrhagic, often with loculated thrombus. The anesthesiologist needs to be familiar with the incidence and common locations of these effusions, in addition to the echocardiographic features of cardiac tamponade in this patient population.4-6
PATHOPHYSIOLOGY OF CARDIAC TAMPONADE
The clinical presentation of pericardial effusion is generally dependent upon both the speed of accumulation and the total volume of the pericardial fluid.7 Spodick, in a recent extensive review, outlined the relationship between the pericardial stretch induced by the accumulating fluid and the subsequent development of increasing intrapericardial pressure.8 Figure 16–1 demonstrates the intrapericardial pressure curves in slowly developing effusions versus those that develop more rapidly. These pressure curves represent the impact that an accumulating effusion can exert on diastolic function. In general, cardiac filling is dependent upon the difference between the intracardiac and the intrapericardial pressure; this difference is conventionally defined as the myocardial transmural pressure. As intrapericardial pressure increases, there is a compression of all the cardiac chambers. As the chambers become smaller, the cardiac inflow becomes limited, and with this, there is a corresponding reduction in diastolic compliance. Eventually, there is an equalization of pericardial and cardiac chamber pressures and the myocardial transmural pressure becomes zero (with cessation of both cardiac filling and forward blood flow). The progression to this equalization is dependent upon the relative stretch of the pericardium and the rate of fluid accumulation. This equalization is a dynamic process, fluctuating due to various extracardiac factors such as the influence of pressure changes arising during ventilation.
Figure 16–1. Pericardial pressure–volume (or strain–stress) curves are shown in which volume increases slowly or rapidly over time. In the left-hand panel, rapidly increasing pericardial fluid first reaches the limit of the pericardial reserve volume (the initial flat segment) and then quickly exceeds the limit of parietal pericardial stretch, causing a steep rise in pressure, which becomes even steeper as smaller increments in fluid cause a disproportionate increase in the pericardial pressure. In the right-hand panel, a slower rate of pericardial filling takes longer to exceed the limit of pericardial stretch, because there is more time for the pericardium to stretch and for compensatory mechanisms to become activated. (Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690, with permission. © 2003 Massachusetts Medical Society. All rights reserved.)
Ventilation (both spontaneous as well as positive pressure) can have significant consequences on myocardial filling and consequent hemodynamic effects. Respiratory variation in cardiac filling normally occurs due to the influence exerted through the transmission of negative intrathoracic pressure on transmural pressure during spontaneous ventilation.9,10 During inspiration, transmural pressure and right heart filling transiently increase, at the expense of a shift in the interventricular septum toward the left ventricle. With normal compliance, the pericardial space usually accommodates most of this shift. This accommodation is incomplete, however, and it is normal for a slight fall in systolic pressure to occur during inspiration. Because the right ventricular diastolic volume increases with inspiration, this is transmitted to the left heart after several cardiac cycles, and manifests as an increase in blood pressure following expiration. These two factors combine to produce the minor, yet normal respiratory variation in systolic blood pressure.
The changes in stroke volume (SV) seen during inspiration that manifest as respiratory variation with continuous blood pressure monitoring have also been suggested to be secondary to pleural pressure-induced changes in the capacitance of the pulmonary venous bed. Katz et al concluded that there is a pooling of blood in the pulmonary veins due to the negative pressures occurring during inspiration.11Although this may be a contributing factor under normal conditions, others attribute the respiratory-induced changes in stroke volume to the competition of the right heart for the relatively fixed total diastolic volume with the resultant reduction in inspiratory left ventricular filling.6,7,9,12
With the development of tamponade, however, and its associated reduction in cardiac chamber compliance, the left heart cannot expand into the constricted pericardial space, resulting in a reduction in forward flow. This results in pulsus paradoxus, manifested as a significant reduction in systolic pressure during inspiration. Pulsus paradoxus, defined as an inspiratory systolic arterial pressure reduction more than or equal to 10 mm Hg during spontaneous ventilation, is a hallmark of significant tamponade.13 The increase and decrease in the arterial pulse volume can often be palpated, but is usually demonstrated by either an invasive arterial pressure monitor or other pulse-contour monitoring device. Concomitant with pulsus paradoxus is either a steady (and often increased) central venous pressure during inspiration.
Although pulsus paradoxus is usually present in the most serious forms of tamponade, it can be notably absent in some (Table 16–2). As a result, when present it is a useful guide to identifying a potentially high-risk patient, but its disparate sensitivity and specificity presents some limitations. Notable absence of pulsus paradoxus, despite significant hemodynamic compromise, can be seen in cases of loculated effusion causing only localized chamber compression (ie, regional pericardial tamponade) that similarly limits filling, independent of respiratory variation. It can also be seen in severe right ventricular hypertrophy (RVH) with pulmonary hypertension, severe preexisting arterial hypertension, atrial septal defects (ASD) and severe aortic insufficiency (AI). Furthermore, the specificity of pulsus paradoxus outside the setting of discreet clinical suspicion has been questioned, as it has also been reported to be present in severe chronic obstructive pulmonary disease (COPD), exacerbations of asthma, obesity, congestive heart failure (CHF) and significant hypovolemia.3 The differential diagnosis of pulsus paradoxus is outlined in Table 16–3.
Table 16–2. Conditions Where Pulsus Paradoxus May Not Manifest
Table 16–3. Differential Diagnosis of Pulsus Paradoxus
DIAGNOSIS OF PERICARDIAL EFFUSION AND TAMPONADE
The clinical signs and symptoms of pericardial tamponade have been well described. However, the general nonspecificity of the clinical presentation leads to the reliance on other diagnostic modalities. The electrocardiogram (EEG) usually demonstrates tachycardia and may show small voltages, with changes in size due to swinging of the heart within the pericardium (electrical alternans). Auscultation of the heart may reveal muffled heart sounds as well as possible pericardial friction rubs. The finding of a pericardial rub, classically described as being triphasic corresponding to atrial systole, ventricular systole and rapid filling during early diastole, needs to be distinguished from that of a pleural rub, which varies with respiration.6
Elevated central venous pressure (CVP) and distension of the jugular veins are frequently seen with tamponade. Although the CVP waveform often demonstrates elevated pressures, it should not be relied upon for diagnosis; as a result, in the acute management of these patients, any delay in therapy should not be undertaken in order to secure central venous access. Though not always reliable, the CVP waveform can be used to differentiate tamponade from constrictive pericarditis: the “square-root” appearance of the waveform is seen in constrictive pericarditis but not with tamponade. The chest x-ray may demonstrate an enlarged cardiac silhouette; the presence of cardiomegaly indicates an effusion of at least 250 mL.6 Other radiographic studies (such as computerized tomography [CT] and magnetic resonance imaging [MRI]) may also demonstrate pericardial fluid accumulation.
Echocardiography plays a central role in the diagnosis of pericardial effusion.14-16 Ultrasound evaluation of the heart and surrounding structures adds critical information regarding the intracardiac blood flow velocities, as well as the volume and composition of the pericardial fluid. For example, differentiating circumferential fluid from loculated effusions is particularly important in the post-cardiac surgery patient, as the pericardial space and mediastinum may contain an abundance of loculated thrombus. Normally, there is less than 5 to 10 mL of fluid in the pericardial space, with larger collections being pathologic and easily detected by echocardiography.17 The amount of pericardial fluid present may be estimated by echocardiography by measuring the distance between the parietal and visceral pericardium (the interpericardial distance). Mild, moderate and large effusions correspond to interpericardial distances of 0.5 cm, 0.5 to 2.0 cm and greater than 2.0 cm respectively.17 Figure 16–2demonstrates a circumferential collection of fluid in the pericardial space with Figure 16–3 demonstrating a smaller apical effusion. Localized collections, frequently loculated and thrombotic in nature, can also result in similar hemodynamic sequelae (Figure 16–4). Discriminating between a simple effusion and tamponade depends upon accurate interpretation of both 2-D echocardiographic and Doppler assessments of blood flow.
Figure 16–2. A transgastric short-axis transesophageal echocardiographic (TEE) image of a moderately large pericardial effusion. Note the circumferential fluid between the epicardium and the pericardium (arrows). RV = right ventricle; LV = left ventricle.
Figure 16–3. A transesophageal echocardiographic (TEE) 4-chamber view of small effusion near the apex of the heart (arrows). RV = right ventricle; LV = left ventricle. (With kind permission from Springer Science+Business Media: Grocott et al27.)
Figure 16–4. A transgastric short-axis transesophageal echocardiographic (TEE) image of a large effusion in a patient 2 weeks following cardiac surgery. Note the fibrinous loculations (arrows) between the pericardial and epicardial surfaces.
In addition to direct chamber compression, increases in pericardial pressure can result in collapse of chamber walls during the cardiac cycle. As the right atrium generally has the lowest pressure of the cardiac chambers, it is usually the first to collapse. This is represented by invagination of the right atrial wall during ventricular systole, which represents the period where atrial pressures are lowest.18 A similar atrial systolic collapse of the left atrium or collapse of the right ventricle during diastole (most notable at the apex) can also occur. In addition to the 2D images which may show variable amounts and distribution of the effusion, Doppler assessments of transmitral flow show characteristic patterns in both the spontaneously breathing and positive pressure ventilation patient.12,19-21
Quantitative assessment of the transvalvular (ie, tricuspid and mitral) Doppler flow characteristics and its variation with respirations is central to the echocardiographic diagnosis of pericardial tamponade (Figure 16–5).9 In normal patients, early diastolic filling velocity (E wave) across the tricuspid and pulmonary valves usually increases slightly with inspiration. Correspondingly, early diastolic inflow velocities across the mitral and aortic valves decrease slightly. In patients with tamponade, early filling (E wave) velocities across the tricuspid (and pulmonary) valve increase sharply (up to 80%) while the mitral and aortic velocities decrease. The reduction in transmitral early filling velocity ranges from 25% to 35%.14,22 The changes in transvalvular flows, and the physiologic reasons behind them, are akin to the blood pressure changes defined by pulsus paradoxus. That is, with spontaneous inspiration, the trans-tricuspid flow increases consequent with the increased venous return due to the negative intrathoracic pressure. The corresponding decreases in stroke volume (accentuated with tamponade) are due to the leftward shift of the interventricular septum, as well as due to the pooling of blood in the pulmonary venous bed.
Figure 16–5. A Doppler tracing obtained using transesophageal echocardiography (TEE) of the transmitral flow in spontaneously breathing patients with pericardial tamponade. Note the reduction in velocities that occur during inspiration, highlighting the echocardiographic correlate of pulsus paradoxus. (With kind permission from Springer Science+Business Media: Grocott et al27.)
Numerous approaches have been described to diagnose and treat pericardial effusions. These include needle pericardiocentesis, percutaneous catheter drainage and balloon pericardiotomy, pericardioperitoneal shunt, subxiphoid pericardial window, and pericardial window through either anterolateral thoracotomy or thoracoscopy.23 Needle pericardiocentesis, best performed with ultrasound guidance, can be used to obtain fluid for diagnostic purposes, and depending on the etiology, definitive drainage. The optimal drainage procedure for non-constrictive effusions is not clear, and varies according to operator preference and familiarity. Choice of drainage procedures is partly dependent on the etiology of the effusion as well as the clinical condition of the patient. Constrictive pericarditis is best treated with pericardiectomy through a sternotomy in order to allow a more thorough removal of a large portion of the diseased pericardium.
The most common surgical approaches involve either subxiphoid access to the pericardial space or a direct intrathoracic technique via either thoracotomy or video-assisted thoracoscopy (VATS). Compared with the subxiphoid window, the advantage of the thoracotomy or a VATS approach is that it allows the fashioning of a pleuropericardial window for continued drainage from the pericardial space into the adjoining pleural space.24,25 Whereas this may not always address the primary reason for the fluid collection itself, it does prevent the development of an ongoing pericardial effusion and decreases the risk of recurrent tamponade. Any subsequent pleural accumulation, if significant, can be managed via subsequent tube thoracostomy.
The acuity of presentation, the patient’s signs and symptoms, as well as the planned surgical approach are all important considerations when determining the anesthetic management strategy for the patient with pericardial effusion. Most importantly, the perioperative management of the patient with pericardial effusion/tamponade requires a multidisciplinary approach that is based on clear communication amongst the entire operative team.
The preoperative assessment, intraoperative management and immediate postoperative period all require careful consideration. Preoperative assessment of the patient should begin with a focused history and physical examination in order to elicit the etiology of the pericardial effusion (and any concomitant conditions) as well as the severity of the hemodynamic compromise. Although ideally a thorough and complete preoperative evaluation should be undertaken, the time required to do this must be balanced by the overall condition of the patient. Frequently, there is limited time for an extensive evaluation as the urgency of the situation often dictates rapid intervention. An evaluation for the presence of tamponade should be foremost as the preoperative evaluation proceeds. Key symptoms to identify and explore include tachypnea, dyspnea, orthopnea, lightheadedness, and chest pain/pressure. Physical examination should include an evaluation of vital signs and an assessment of any respiratory compromise, including the presence of decreased oxygen saturation and adequacy of air entry on chest auscultation. Tachycardia, hypotension, pulsus paradoxus, and jugular venous distension should be identified, with cardiac auscultation focusing on the presence of any pericardial rubs or muffling of the heart sounds. A brief anesthetic history, list of current medications and any allergies should also be noted.
The extent of preoperative investigations is dependent on the stability of the patient and the urgency of surgery. Laboratory investigations should focus on hematologic (hemoglobin and platelet count), coagulation (INR, aPTT), and biochemical analysis (particularly electrolytes and creatinine level to assess renal function). If conditions allow, a chest x-ray, CT scan or MRI can all be useful, however, an echocardiogram can be essential in confirming the correct diagnosis of pericardial effusion and tamponade.
Pre-induction invasive arterial blood pressure monitoring is essential. Although useful, central venous access is clearly optional and its establishment should not delay urgent pericardial decompression in severely compromised patients. Preparation for induction should include the availability of adequate fluids for resuscitation as well as ready access to vasopressors (such as phenylephrine or norepinephrine boluses and infusions) and inotropic agents (particularly epinephrine).
Several anesthetic approaches can be utilized for patients presenting for a drainage procedure.3,26,27 Figure 16–6 summarizes the various anesthetic management strategies that can be considered. The patient that presents with significant symptoms and signs of compromise (such as dyspnea in the recumbent position, or overt pulsus paradoxus) needs to be managed with extreme caution. If hemodynamic collapse is imminent, a percutaneous approach to relieve the immediate compromise is warranted, followed by subsequent definitive treatment. On the other hand, the asymptomatic patient who demonstrates no hemodynamic consequence can be managed more conventionally and with considerably more preparation and time. However, a vast number of patients lay between these two clinical extremes.
Figure 16–6. Management strategies for patients with varying severity of pericardial effusion/tamponade. *Conditions that might preclude inhalational induction include significant aspiration risk, severe orthopnea, or an uncooperative patient. (With kind permission from Springer Science+Business Media: Grocott et al27.)
Local anesthesia, with supplemental sedation (for example with ketamine, which allows the maintenance spontaneous ventilation), may be used for needle pericardiocentesis or subxiphoid windows procedures. Otherwise, general anesthesia is required, usually with concomitant endotracheal intubation. For patients requiring general anesthesia, attention should be paid to maintaining—and usually augmenting—preload, along with the maintenance of afterload, contractility, and heart rate (optimally in sinus rhythm).
Considerable attention needs to be directed to airway and ventilatory management. Positive pressure ventilation should be avoided when possible, and if and when it is required, it should be instituted cautiously with only the minimal inspiratory pressure required to provide adequate minute ventilation. The combination of positive pressure ventilation, which decreases venous return, as well as the vasodilation and direct myocardial depression caused by the anesthetic agents can result in life-threatening hypotension. When conditions allow, an inhalational induction technique is ideal and should aim to minimize coughing and straining while maintaining spontaneous ventilation; the use of sevoflurane therefore offers many advantages. Premedication with any agents that can depress respiration should be avoided, as these can prolong induction by reducing minute ventilation. Care should be taken to ensure a deep level of anesthesia before any manipulation of the airway is attempted. Invariably, hypotension from vasodilation occurs and can be treated with a continuous vasopressor infusion as the inhalational induction continues.
Intravenous (IV) induction of anesthesia can be safely accomplished in patients with pericardial effusion who are hemodynamically stable without evidence of tamponade. However, consideration should be given to positioning the patient to allow for surgical preparation and draping, so that the operation can proceed expeditiously once the patient is anesthetized and the airway secured if the hemodynamics deteriorate during induction. This preparation for immediate surgical intervention can also be prudent during inhalational induction, with careful attention not to provide any noxious stimuli to the patient during induction that may lead to coughing and/or apnea.
Once the airway is instrumented, the choice of endotracheal tube is partly dependent upon the surgical technique utilized. Subxiphoid approaches can be accomplished without the need for lung isolation and one-lung ventilation (OLV). However, OLV is usually required for some thoracotomy and VATS approaches. This can be achieved with a double lumen tube, or with a single-lumen endotracheal tube in conjunction with an endobronchial blocker.28 One of the limitations of thoracoscopy is the difficulty in tolerating OLV encountered occasionally. In this population, the subxiphoid approach may be a better operative choice.
Maintenance of anesthesia can be accomplished with various combinations of inhalational agents, intravenous opioids, propofol, and benzodiazepines. The possibility of a breach of the pleural space, as well as the possibility of preoperative hypoxemia, should preclude the use of nitrous oxide. Muscle relaxants may be utilized if necessary, but ideally only when the patient has been demonstrated able to tolerate positive pressure ventilation. Continuous intravenous infusions of vasopressor or inotropic agents may be required to maintain hemodynamic stability, but should be considered temporizing measures that have their own adverse consequences due to excessive vasoconstriction that may limit overall cardiac output.
Long acting opioids (ie, morphine or hydromorphone) can be given prior to emergence of anesthesia for postoperative analgesia. In addition, consideration should be given to either local anesthetic infiltration of the wound or the performance of regional nerve blocks (ie, intercostal blocks) by the surgeon or anesthesiologist. The decision to extubate at the conclusion of the procedure should depend on the patient’s cardiovascular and respiratory status. Similarly, the need for intensive postoperative monitoring is dependent upon the overall status of the patient. Patients may require a period of continuous monitoring in a post anesthesia care unit (PACU) or an intensive care unit (ICU) setting.
In summary, patients presenting for pericardial drainage procedures require a thorough, but often urgent, preoperative evaluation in order to understand the etiology of the effusion and any associated hemodynamic instability, such as tamponade.
Thoracoscopic procedures and subxiphoid approaches are the most common techniques for definitive drainage of pericardial effusion. However, ultrasound-guided needle pericardiocentesis can be used for emergent drainage in the unstable patient.
The anesthetic technique needs to be tailored to the individual patient characteristics, but can be accomplished successfully with inhalational, as well as intravenous induction techniques. The hemodynamic goals of augmented preload with maintenance of afterload, contractility, and heart rate should be targets.
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