Chapter 106: Pericardiocentesis

The pericardium is a protective double-lined sac that surrounds the heart. The function of the pericardium is to reduce the friction between the heart and surrounding mediastinal structures and also to provide a barrier against spread of infection and malignancies to the heart. Though most cardiac conditions affect the 4 chambers of the heart, its blood supply and/or the conduction system, the surrounding pericardium plays an important role in normal cardiac physiology and disease.

Under certain pathologic conditions, pericardial disease can lead to palpitations, hypotension, and acute cardiac decompensation.¹ Patients presenting with pericardial tamponade accompanied by impending hemodynamic collapse require emergency pericardiocentesis. (An excellent video presentation by Fitch et al in the N Engl J Med. should be viewed in conjunction with this review.)²

The normal pericardium is a double-layered membrane that encases the heart and the origin of the great cardiac vessels. The outer fibrous layer (the parietal pericardium) is attached to the surrounding mediastinal structures: the diaphragm, sternum, and costal cartilages; while the inner serous layer (the visceral pericardium) lies on the surface of the heart and is contiguous with the epicardium.³ The pericardial lining secretes 15 to 35 mL of serous pericardial fluid (an ultrafiltrate of plasma that contains proteins, electrolytes, and phospholipids) that lubricates the surfaces of the heart to minimize the friction for the contracting heart, and drains through the mediastinal and tracheobronchial lymph nodes.² Posteriorly, the pericardium stops at the base of the left atrium so that the posterior wall of the left atrium is not covered by the pericardial space.

With chronic pericardial fluid that accumulates gradually, pericardial compliance is able to increase to accommodate the slowly accumulating larger volumes. However, because the pericardium is a relatively stiff structure, intrapericardial pressure rises rapidly as intrapericardial volume becomes too large or the volume increases acutely, compressing the cardiac chambers, which could lead to pericardial tamponade.⁴

In suspected pericardial disease, transthoracic echocardiography (TTE) (including 2-dimensional (2D) TTE, M-mode echocardiography, pulse-wave Doppler, and inferior vena cava imaging, collectively 2D TTE) is the first-line imaging technique. 2D TTE can image the size, location, and relative pericardial volume and serve as a guide to therapeutic intervention (pericardiocentesis) (Figure 106–1).^4,5

Pericardial effusion is the accumulation of greater than 50 mL pericardial fluid within its 2 layers, which can be due to numerous etiologies. Levy found the most common causes of large pericardial effusions were idiopathic (33%), iatrogenic (16%), malignancy (13%), following acute myocardial infarction (MI) (9%), renal failure (uremia, dialysis) (6%), and collagen vascular disease (6%).⁶ Etiologies can vary with institution and referral populations. Pericarditis, a nonspecific inflammation of the pericardium, can be associated with inspiratory chest pain, worse lying than sitting, may be accompanied by a friction rub that may be lost if the effusion is large and may be associated with palpitations and atrial or ventricular arrhythmias.

Pericardial effusion is recognized by echocardiography as an echo-free space between the visceral and the parietal pericardial linings posteriorly in the parasternal long-axis and short-axis views (see Figure 106–1). With M-mode and 2D TTE, a semiquantitative estimate of the pericardial effusion volume can be made by the size and extent of the anterior and posterior echo-free space (if not loculated).⁷ A pericardial effusion limited posteriorly, less than 1 cm, is usually less than 250-mL volume (ie, small); greater than 1 cm effusion posteriorly is around 250 to 500 mL (small-moderate); a circumferential, posterior and anterior 1 cm echo-free space is approximately 500 mL (moderate); and if the circumferential echo-free space is greater than 1 cm there is more than 500 mL of effusion (large) (Figure 106–2). A large effusion accompanied by swinging of the heart, may indicate pericardial tamponade and more than 1 L of fluid. Estimation of the fluid volume is relative to cardiac size, which may depend on cardiac chamber enlargement and patient’s body surface area. The physiologic consequences of pericardial effusion depend on the effusion volume, rate of fluid accumulation, presence of ventricular hypertrophy, pulmonary hypertension, and the presence or absence of cardiac compression. With increase in effusion size, the fluid extends laterally and once it exceeds 250 to 300 mL, it can appear anteriorly while the patient is in the supine position (Figures 106–2, 106–3, 106–4, 106–5).

Pericardial effusions are usually transudates, seen on 2D TTE as a black nonechogenic (anechoic) space. However, infected or bloody fluid can appear as a hazy-gray rather than clear fluid and should suggest an abnormal exudative content. If not loculated, the pericardial effusion fluid around the heart is dynamic, and shifts with systole and diastole as the heart beats. This is to be distinguished by masses in the pericardial space or postoperative hematomas, which are usually relatively noncompressible. Loculated effusions may occur postoperatively in cardiothoracic surgery or due to exudates or inflammatory states following recurrent pericarditis that can occur with infections, viral pericarditis, recurrent rheumatic pericarditis, or in renal disease (Figure 106–6). Loculated effusions are usually localized, and not circumferential, but may have hemodynamic significance by compression of chambers or vena cava or pulmonary veins. Hematomas appear as immobile, flat or protruding, echodense thickening, usually anteriorly, and may be traumatic or postoperative (common following cardiac surgery where the pericardial space may be violated, uncommon following thoracic or abdominal surgery).

Pericardial fluid should be differentiated from the normal pericardial fat pad that is usually seen anterior to the heart lying within the pericardial sac and has speckled, hyperechoic areas because it is reticulated with echodense fibrous tissue and fatty tissue. The fat pad tissue does not significantly compress with cardiac contraction as free fluid does.

Pleural effusions, which can be easily confused with pericardial effusions, can be distinguished by certain key features. On the parasternal long-axis view, the pericardial reflection usually stops at the atrial-ventricular groove posteriorly, where the left ventricular posterior wall meets the posterior mitral annulus and there is usually no pericardial reflection behind the posterior left atrium; therefore, fluid behind the left atrium and aorta usually represents a pleural effusion (see Figure 106–1). Frequently, atelectatic lung tissue can be seen in the pleural space as well. If there is both a pericardial and pleural effusion, it can be easier to differentiate the 2 spaces. The descending aorta usually lies behind the left atrium and also demarcates the end of the pericardial reflection on the posterior surface of the heart. Fluid, therefore, behind the descending aorta would represent pleural effusion, not pericardial. If the probe is placed far laterally around the chest, the presence of a pleural effusion can be confirmed.

Pericardial effusion can be differentiated from ascites, which can be potentially confusing when imaging from the subxiphoid position. Ascites is usually closer to the liver, separated from heart by the fibrous band of pericardium. With significant ascites, the falciform ligament can be seen as a linear band extending from the liver to the pericardium traversing the black nonechoic ascites.

When fluid accumulates slowly, the parietal pericardium can stretch to accommodate large volumes of fluid. However, if the development and accumulation of the effusion is very rapid or the volume exceeds the capacity of the pericardial space to stretch to contain the volume, increases in intrapericardial pressure begins to impact intracardiac pressure, elevation and equalization of diastolic intracardiac and pericardial pressures, decrease cardiac output, and exaggerated inspiratory decrease in systolic pressure (> 10 mm called pulsus paradox)^4,5 (Figure 106–7).

Circumstances that can lead to pericardial tamponade include all those that cause pericardial effusions including uremic renal failure, hypothyroidism, coronary vessel perforation during percutaneous interventions in the catheterization laboratory, a bleed following cardiac surgery, rupture or dehiscence following valve surgery or aortic dissection, bleeding into the pericardium from a neoplasm, infection (viral, bacterial, fungal, tubercular), or a marked inflammatory response.¹ One study of 173 patients who underwent pericardiocentesis cited the etiologies as malignant (33%), acute or chronic pericarditis (26%), trauma (12%), uremia (6%), postpericardiotomy (5%), infection (5%), collagen vascular disease (3%), and radiation (2%).⁸

Tamponade following cardiac surgery may be due to bleeding from anticoagulants for prosthetic valves, delayed cessation of antiplatelet drugs, oozing from vascular or aortic anastomoses, or irritation from chest tubes. Loculated effusions may create regions of focal cardiac tamponade that may present with hypotension, but difficult to diagnose unless suspected, especially after cardiac surgery.

Clinically, patients with tamponade may have dyspnea, weakness, tachycardia, and hypotension. On anterior-posterior (AP) x-ray, a large cardiac silhouette, projecting a “water bottle-shaped” heart, in a patient with clear lung fields suggests the presence of a pericardial effusion with at least 250 mL of fluid. An electrocardiogram (ECG) may show signs of pericarditis with sinus tachycardia, and PR depression in leads 2, 3, and aVF. A valuable ECG sign indicative of potential cardiac tamponade is electrical alternans. Computed tomography (CT) and magnetic resonance imaging (MRI) scans may show incidental large effusions suggestive of tamponade.^5,9,10,11 If the patient is stable, hemodynamics in the catheterization laboratory will show equilibration of average diastolic pressure across the cardiac chambers produced by the extrinsic pericardial pressure and ventricular interdependence, an inspiratory increase on the right-sided pressures with a concomitant decrease on the left-sided filling pressures—pulsus paradoxus.

Echocardiography is the most expedient modality to diagnose pericardial effusion and confirm the presence of pericardial tamponade. Echocardiography demonstrates circumferential pericardial fluid and compressed cardiac chambers (Figures 106–8). Among echocardiographic signs, the most characteristic is the diastolic right atrial and right ventricular compression. Right atrial collapse may also be seen in patients with hypovolemia who do not have tamponade. With greater compression, the left atrium may also collapse, a more specific finding. The diastolic collapse of the right ventricle usually connotes large enough external pressure to impact stroke volume. Doppler of aortic or pulmonic systolic flow discloses marked respiratory variations: On inspiration, the right ventricle fills at the expense of the left ventricle, seen as increased peak filling pulsed-wave Doppler velocity; both the ventricular and atrial septa move sharply leftward, reversing on expiration when the left ventricle fills at the expense of the right ventricle (Figure 106–9). A greater than 25% change in peak Doppler flow velocity obtained from the left ventricular outflow track or through the aortic valve, obtained by pulsed Doppler in the apical 4-chamber/5-chamber view or of the pulmonic valve, may connote pericardial tamponade (Figure 106–10). Pulsus paradoxus may also be seen with pulmonary embolism, chronic asthma, chronic obstructive pulmonary disease (COPD) and croup, but may be absent in low cardiac output states. The absence of any cardiac chamber collapse has greater than 90% negative predictive value for cardiac tamponade.¹²

Importantly, pericardial tamponade is a clinical diagnosis based on the presence of tachycardia and hypotension, which can be supported by echo/Doppler findings. Therefore, clinical suspicion of the presence of tamponade or the imminent development of tamponade is extremely important in prevention of acute cardiac collapse. Under certain circumstances, especially with hypertrophy of the left and/or right ventricle and pulmonary hypertension, which may be seen in hypertensive patients with chronic renal failure, who are prone to recurrent pericardial effusion, there may not be the typical findings of tamponade, because the ventricular hypertrophy limits the impact of the external compression on ventricle interdependence.

Management of Acute Cardiac Tamponade

Patients presenting with hypotension and tachycardia in which pericardial pressure from the volume of pericardial effusion causes cardiac compression have cardiac tamponade and require emergency pericardiocentesis that should be performed with echo guidance. The European Society of Cardiology’s recent position statement on the triage of patients with potential cardiac tamponade proposed a stepwise scoring system to triage patients requiring pericardiocentesis.¹³ The paper incorporates etiology, clinical presentation, and imaging findings (with primary emphasis on echo findings) to determine whether urgent pericardiocentesis, surgical approach, or intervention can be delayed¹⁴ (Figure 106–11).

Pericardial drainage may be performed in the catheterization laboratory with hemodynamic measurement, with sterile technique in which both transthoracic echo and fluoroscopy can be utilized. However, sudden circulatory collapse may mandate the use of pericardiocentesis with imaging where the patient presents, in the emergency ward, ICU, or in the regular ward bed. Surgical drainage may be required if drainage cannot be achieved by percutaneous needle, in the presence of an active intrapericardial bleed, cardiac trauma or laceration, or complicating aortic dissection.

Medical treatment of acute cardiac tamponade can briefly temporize, but even volume infusion may increase intracardiac volume and pressures, thus increasing pericardial pressure and interventricular dependence, exacerbating the hypotension. Mechanical ventilation with positive airway pressure should be avoided in patients with tamponade, because this decreases venous return and may potentiate hypotension.

Pericardiocentesis is the most expedient method to resolve the impending circulatory collapse.¹⁵ The immediate treatment of cardiac tamponade is drainage of the pericardial fluid by either needle pericardiocentesis or surgical pericardial window.

Relative contraindications include suspected effusion due to aortic dissection, traumatic hemopericardium, or myocardial rupture in which the pericardiocentesis may exacerbate the underlying condition that may be temporarily in equilibrium. Anticoagulation or bleeding dyscrasias are relative contraindications, depending on the acuity of the situation and the severity of bleeding disorder.

Medical personnel should be gowned, gloved, and masked. Patients should be sterilely draped and have pulse oximetry, heart rate, and blood pressure continuous monitoring. Emergent intubation or sedation with short-acting hypnotics or anxiolytics may induce more pronounced decompensation.¹⁶

Materials needed which can be found in prepackaged commercial sets usually include a 21-gauge needle attached to a 5-mL syringe for subcutaneous lidocaine (1%) injection, a scalpel for small skin incision, a 7- to 9-cm 16- to 18-gauge spinal needle or a sheath over the needle catheter, a J-tipped flexible guidewire, a dilator to slip over the guidewire, a 3-way stopcock, a pigtail catheter or dedicated catheter for centesis procedures, several half-filled 10-mL saline syringes, and syringes (20 and 50 mL) for aspiration. An alligator ECG lead can be attached to the needle to monitor for current of injury as the needle is forwarded and hits the epicardium and generates ST elevation (“current of injury”) (Table 106–1).

Before draping and preparing the patient, ECHO imaging should confirm the presence of the effusion, whether the fluid is loculated, the presence of adhesions, the appropriate drainage window, and the approximate angle for needle insertion. Select a window in which the effusion can be clearly visualized, preferably all 4 cardiac chambers (Figure 106–12). The ECHO probe can either be placed in a long sterile plastic sheath with ultrasonic gel at the tip for the probe and used adjacent to the needle in the sterile field or ECHO imaging can also be done at the apex, remote from the needle insertion site at the subxiphoid window or image from the subxiphoid window if the apex window is deemed the safer approach. The echo probe can then be manipulated under the sterile drape, off the sterile field by an experienced echocardiographer physician or sonographer while the pericardiocentesis itself is performed by another experienced physician.

The subxiphoid approach, just underneath the left costal margin, is also the safest for pericardiocentesis performed without ECHO or fluoroscopic guidance, because it avoids the coronary arteries, internal mammary artery, and is extrapleural (Figure 106–12). The alternative apical approach for pericardiocentesis may be closer to the skin surface, but may carry a greater risk of cardiac and pulmonary complications unless the performer is experienced with this approach. Using sterile technique, the skin should be prepared with a chlorhexidine-based solution and sterilely drape the chest and abdomen with an open window for the procedure location. While monitoring hemodynamically, administer enough anxiolytics and topical pain medicine so the patient is relatively immobile during the procedure to avoid complications such as arrhythmias and cardiac laceration during needle insertion. After topical anesthesia with lidocaine, a small, superficial puncture is made for the spinal needle insertion site with a scalpel blade. The long spinal needle (a 16- to 18-gauge sheathed needle can be used so the metal core can be withdrawn and aspiration injections can be done through the sheath) is slowly advanced at a 30° to 45° angle with its hub depressed so that the point is pointing toward the left shoulder just under the xiphisternum, from the subcostal window. The needle is then advanced slowly, until the piercing of the fibrous pericardium is felt while continuously aspirating (Figure 106–13). Normal pericardial fluid is clear and straw-colored. Aspiration of bloody fluid may be pericardial, pleural, or intracardiac. Once fluid is aspirated back, the sterile clamp can be placed at the skin surface securing the needle and avoiding accidental advancement. By either echo guidance technique, though the tip of the pericardiocentesis needle itself may not be seen, the presence of the needle in the pericardial space is confirmed by “contrast” echo created by rapidly injecting either the aspirated fluid or sterile-agitated saline back into the space creates echogenic microbubbles within the pericardial space (Figure 106–14). The microbubbles are easily seen echo-flowing rapidly into the pericardial space, but move slowly in an exudate or bloody effusion. If the needle is not in the pericardial space, microbubbles may be seen injected into a cardiac chamber or may not be seen if injected into a pleural space. Visualizing the microbubbles in the right ventricle or another cardiac chamber requires removal of the needle and very careful monitoring for worsening tamponade if the cardiac puncture site doesn’t self-seal. Repeat the procedure until the needle position is confirmed by the microbubbles.

Once the needle is confirmed to be in appropriate position, a guidewire is then introduced through the needle and a dilator passed over the guidewire to manually drain with 20- or 50-mL syringes, with strict sterile control. Fluid drainage can be followed by ECHO to the point of minimal residual fluid. Because of the steep slope of the intrapericardial pressure-volume curve, aspirating a small volume (50 mL) may be enough to decompress the heart and recover blood pressure and slow the heart rate (Figure 106–7). The source and quality of fluid will determine if a drain should remain in place.

Bloody effusions from iatrogenic cardiac laceration or trauma may require surgical repair. For prolonged drainage, a guidewire passed through the sheath or needle will facilitate the introduction of a pigtail angiographic catheter. However, a drain may occlude, be an irritant, causing arrhythmias and is a potential source of infection. A follow-up TTE should be performed a few hours postpericardiocentesis to ascertain that no further accumulation has occurred.

Loculated effusions may present a problem because a single needle position may only remove fluid from one isolated pocket and those patients may require a pericardial window with lysis of adhesions in the pericardial space.

Pericardiocentesis is usually very safe using ECHO guidance with almost an immediate hemodynamic response of improved blood pressure and slowing of the heart rate.^15,17,18

Familiarity with the anatomic approaches and contiguous structures will ensure a better outcome.¹⁹ In a large series by the Mayo Clinic, ECHO-guided pericardiocentesis by experienced personnel was safe with a low incidence of minor complications (3.5%) or major complications (1.2%) such as requiring emergency surgery.²⁰ Cardiac laceration, atrial or ventricular arrhythmias, or vascular injury are very rare complications.

Pericardial effusions are common, but when they accumulate rapidly or generate enough pressure to impair intracardiac filling, pericardial tamponade can develop. Clinical suspicion, rapid recognition, and confirmation of tamponade by TTE followed by prompt echo-guided pericardiocentesis and drainage of the pericardial fluid can be lifesaving.