Pericardial Window Procedures

Hilary P. Grocott
Harleena Gulati
G. Burkhard Mackensen

Key Points

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.

Case Vignette

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.¹¹ Although 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