Pericardium and Pericardial Space

The pericardium is a two-layered fibroelastic sac surrounding the heart.¹ The pericardium is avascular but well innervated, so inflammation induces severe pain. The visceral pericardium is a single-cell layer that adheres to the epicardium. The outer parietal pericardium consists mostly of collagen with some elastin. These two layers create the pericardial space, which normally contains 15 to 50 mL of serous fluid.² Pericardial fluid provides lubrication for cardiac contractility and acts as a “shock absorber” for deceleration forces.

The pericardium is a tense structure, but it also has some elasticity. These properties limit the amount of cardiac dilation that is possible during diastole and enhance mechanical interactions between the atria and ventricles during systole.³ This semi-elastic property can also tolerate an acute (i.e., over a period of hours to days) accumulation of pericardial fluid (80 to 120 mL) without significantly increasing intrapericardial pressure, which is the flat portion of the pressure-volume curve for pericardial pressure (Fig. 16-1).^4,5 Once a critical volume is reached, adding as little as 20 to 40 mL can double intrapericardial pressure (the steep portion of the pressure-volume curve [see Fig. 16-1]) and cause clinical decompensation (cardiac tamponade). Cardiac tamponade typically occurs with an intrapericardial pressure of 15 to 20 mm Hg.⁶

Slow and chronic accumulation of pericardial fluid (over a period of weeks to months) causes the pericardium to expand circumferentially, and it can accommodate several liters of fluid with minimal alteration in intrapericardial pressure. Patients with this condition may be asymptomatic despite large effusions. No specific pericardial volume predicts the hemodynamic consequences of an effusion. Such consequences depend on the acuity of accumulation of the fluid.

Pathophysiology of Pericardial Tamponade

To generate an effective stroke volume, the left ventricle (LV) must be filled, and this process relies primarily on adequate filling of the right ventricle (RV). Normal inspiration promotes RV filling. Negative intrathoracic pressure increases venous return to the right side of the heart. This reduces wall tension in the RV, which causes dilation and more filling of the chamber.

Elevated intrapericardial pressure (i.e., early tamponade) results in abnormal RV filling and then abnormal LV filling. In this situation, the free wall of the RV cannot expand against the pericardial fluid during inspiration. To accommodate the filling, the interventricular septum bows abnormally into the LV, which reduces its volume. LV filling, stroke volume, and ultimately cardiac output are reduced.⁷ This phenomenon is responsible for pulsus paradoxus (PP, described later in this chapter), which is sometimes observed with tamponade.⁸ LV filling is also reduced by the collapse of right-sided structures. After a critical volume is reached on the pressure-volume curve (see Fig. 16-1), the intrapericardial pressure is transmitted to the inferior vena cava (IVC) and right atrium. These thin-walled structures then become compressed and reduce filling of the RV.

The atria and pulmonary circulation are at much lower pressure than systemic arterial pressure and are also vulnerable to rising intrapericardial pressure (Fig. 16-2). Late in tamponade a “pressure plateau” occurs in which right atrial pressure, RV diastolic pressure, pulmonary artery diastolic pressure, and pulmonary capillary wedge pressure are virtually identical. This equalization of chamber pressure leads to a reduction in venous return and the echocardiographic hallmark of tamponade: diastolic collapse of the RV. At this point, hemodynamic collapse is imminent, with severe hypotension, bradycardia, and potentially pulseless electrical activity (PEA) developing. Unless intrapericardial pressure is decreased immediately, cardiac arrest will ensue.⁹

Compensatory Mechanisms and Pericardiocentesis

To maintain physiologic cardiac output, the sympathetic nervous system increases the heart rate, arterial vasoconstriction (to maintain mean arterial blood pressure), and venoconstriction (to maintain normal venous-atrial and atrioventricular filling gradients). Early in tamponade, these compensatory mechanisms are usually effective in maintaining adequate cardiac output.

Compensatory mechanisms also preserve normal cardiac contractility and myocardial perfusion.7,10,11 However, when pericardial pressure overwhelms the compensatory mechanisms, coronary perfusion pressure is reduced, which leads to myocardial ischemia. Experimental induction of severe tamponade demonstrated microscopic ischemic cardiac injury.¹² Lactic acidosis (resulting from reduced cardiac output and systemic hypoperfusion) may directly cause cardiac depression and thereby reduce cardiac contractility and, ultimately, cardiac output.⁹

Removal of pericardial fluid (i.e., pericardiocentesis) reverses the pathophysiologic processes just described by improving cardiac filling and output. Interestingly, the pressure-volume relationship of the pericardial space demonstrates hysteresis; that is, withdrawing a certain quantity of fluid reduces intrapericardial pressure more than addition of the same amount of fluid increases intrapericardial pressure. This effect, however, is not universal and may vary among patients and in various disease states (Fig. 16-3).²

Special Considerations in Patients with Pericardial Effusion and Tamponade

Under normal circumstances, positive pressure ventilation (e.g., mechanical ventilation) reduces venous return to the right side of the heart by increasing intrathoracic pressure. This could be detrimental for patients with tamponade because right-sided filling is already compromised and further reductions can lead to severe hemodynamic instability.¹³ Therefore, positive pressure ventilation should be avoided in patients with known or suspected tamponade unless it is absolutely necessary.

Low-pressure pericardial tamponade is defined as a hemodynamically significant effusion with lower than expected intrapericardial pressure.¹⁴ This category of tamponade occurs in certain hypovolemic patients with subacute or chronic effusions (e.g., associated with long-term diuretic use, dehydration, excessive dialysis).¹⁵ The diagnosis may be challenging because the classic symptoms and findings on physical examination (e.g., distended neck veins) may be absent.¹⁶ Fluid boluses may temporize the hemodynamic compromise while pericardial decompression is being arranged.

Acute Hemopericardium

Acute hemopericardium, or rapid accumulation of blood in the pericardial space, can have a traumatic or nontraumatic etiology. It is one of the most feared causes of tamponade because the semi-elastic pericardium cannot accommodate acute increases in pericardial fluid and clinical deterioration can be rapid. This diagnosis can be challenging to make because there may be little or no evidence during the initial evaluation (e.g., pericardial size might be normal on a chest radiograph).

Nonhemorrhagic Effusions

Nonhemorrhagic pericardial effusions usually accumulate slower than acute hemopericardium does (over a period of weeks to months). Chronic fluid accumulation allows the pericardium to stretch circumferentially and accommodate up to 2000 mL of fluid without any hemodynamic compromise.⁵² Effusions that grow slowly allow the circulatory system to adapt to the intrapericardial pressure, thereby further maintaining hemodynamic stability. Thus, asymptomatic patients with moderate to large effusions may not need emergency pericardiocentesis, in contrast to patients with acute hemopericardium.^53,54

Nonhemorrhagic effusions have several causes (see Box 16-1), and the exact one may not be obvious during the initial evaluation without diagnostic pericardiocentesis. Common causes of nonhemorrhagic effusions are discussed in the following sections.

Special Considerations in Pericardial Disease

Pericardial tamponade is classically described as being secondary to circumferential effusion, which causes a generalized increase in pericardial pressure and compression of multiple cardiac chambers. Loculated effusions (caused by a local hematoma or an infectious process) or pericardial adhesions (from previous inflammation) can compress one or two cardiac chambers and thus reduce both cardiac filling and cardiac output.69,70

Constrictive pericarditis occurs following chronic pericardial inflammation, infection, or mediastinal irradiation. These processes cause scarring, fibrosis, or calcification, and the pericardium eventually becomes a nonelastic and “constrictive” sac around the heart. Myocardial relaxation and cardiac filling are impaired, and diastolic dysfunction ensues. Without echocardiography, constrictive pericarditis can be difficult to distinguish from pericardial tamponade.¹

Effusive-constrictive pericarditis is defined by the presence of both pericardial effusion and pericardial constriction. It may be quite difficult to differentiate between effusive-constrictive pericarditis and pericardial tamponade in stable patients because both are associated with effusions.⁷¹ Fortunately, distinguishing between these diagnoses is less important in hemodynamically unstable patients because they are treated identically (i.e., with pericardiocentesis).⁷²

Pneumopericardium is an interesting, though rare cause of cardiac tamponade. It is most commonly associated with pneumothorax caused by barotrauma (e.g., mechanical ventilation).⁷³ It also occurs spontaneously during acute asthma exacerbations,⁷⁴ and it can follow blunt chest injury.^75,76 Although typically benign, tension pneumopericardium has been reported as a cause of life-threatening tamponade after blunt^77,78 and penetrating chest trauma.^79,80

History: Patient Profile and Symptoms

The historical features of pericardial effusions are nonspecific and the diagnosis may be overlooked initially. However, an astute clinician might be suspicious based on comorbid conditions (e.g., warfarin therapy or a history of myxedema) and the time course of the symptoms (e.g., free-wall rupture several days after MI, dyspnea in a patient with uremic pericarditis). Box 16-2 lists important details to be ascertained from the history when pericardial effusion is suspected.⁸⁴

Physical Examination

Physical examination of patients with pericardial effusion (e.g., displaced point of maximal impulse, muffled heart sounds) lacks sensitivity and specificity. If the history suggests pericardial effusion, the physical examination should focus on determining the underlying cause (e.g., stigmata of hypothyroidism) to guide definitive diagnostic testing (e.g., echocardiography). Ironically, many pericardial effusions are not diagnosed from the history or findings on physical examination but are found incidentally during the evaluation for other diseases.

In 1935, Beck characterized the physical manifestations of tamponade with two triads—one for chronic and one for acute tamponade.⁸⁵ Beck’s “chronic” triad consists of increased central venous pressure (CVP) (i.e., distended neck veins), ascites, and a small, quiet heart. “Beck’s triad” is a classic description of acute cardiac compression, which includes increased CVP, decreased arterial pressure, and muffled heart sounds. Almost 90% of patients have one or more of these “acute” signs,⁸⁶ but only about 33% demonstrate the complete triad.^9,87 The utility of this triad is further limited because all three signs are usually observed shortly before cardiac arrest.

It would be clinically desirable to identify patients in early tamponade, before hemodynamic collapse. Unfortunately, findings on physical examination in early tamponade are nonspecific and may be indistinguishable from those of other critical diseases (e.g., septic shock, right heart failure).⁵⁷ Patients initially seen in late tamponade also have nonspecific findings. They may be agitated, panic-stricken, confused, uncooperative, restless, cyanotic, diaphoretic, acutely dyspneic, or hemodynamically unstable. Such patients should undergo a brief and focused physical examination because the time between initial evaluation and full arrest may be brief.

Some of the findings on physical examination associated with tamponade are described below. A more comprehensive list is presented in Box 16-3.

Diagnostic Testing

Diagnostic testing should be initiated when pericardial effusion or tamponade is suspected. Definitive diagnosis requires imaging such as CT or, preferably, cardiac ultrasound (Fig. 16-5B). Bedside ultrasound is the fastest and most reliable diagnostic tool because it is noninvasive, does not emit radiation, and can be performed at the bedside without transporting unstable patients outside the ED.

As discussed previously, pericardial effusions are occasionally discovered incidentally during evaluation for other disorders. For example, the chest film and ECG of a patient being assessed for acute coronary syndrome (ACS) may suggest tamponade. If the clinical context supports pericardial effusion as the primary diagnosis rather than ACS, further workup for the effusion (e.g., an echocardiogram) should be ordered. If neither diagnosis is more likely than the other, dual workups may be necessary.

Treating Pericardial Effusions and Tamponade

Treatment of pericardial effusions in the ED depends on the degree of hemodynamic compromise. Patients with stable effusions should be treated supportively while the underlying cause (known or suspected) is addressed. For example, stable patients with pericardial effusions secondary to uremia may best be treated with dialysis, observation, and serial echocardiograms.¹²⁰ Even when the diagnosis is unknown there may be no need to perform emergency pericardiocentesis if the effusion is small to moderate.¹²¹ Deferring diagnostic pericardiocentesis to the inpatient setting may be preferred because the cardiac catheterization laboratory or operating room is a more sterile and controlled environment than the ED.⁵⁷

Patients with evidence of tamponade need urgent pericardiocentesis (discussed in the next section). Even those with early tamponade who are stable can decompensate quickly with little warning. Fluid boluses may improve hemodynamics temporarily, especially in patients with concomitant hypovolemia.⁸⁹ Administration of vasopressors and an inotrope is a temporizing measure and should be initiated while preparing for emergency pericardiocentesis. Finally, positive pressure ventilation (e.g., mechanical ventilation) should be avoided if possible because as discussed in the section on physiology, it can lead to hemodynamic collapse secondary to changes in intrathoracic pressure.

Diagnostic Pericardiocentesis

Use of pericardiocentesis to determine the cause of nonhemorrhagic effusions is common practice, even though opinions on its utility vary.52,122,123 Recovery of neoplastic cells, blood, bacteria, and viruses from pericardial fluid can be valuable in making the diagnosis. Measurement of pericardial fluid pH can also be helpful because inflammatory fluid is significantly more acidotic than noninflammatory fluid.¹²⁴ When a specific cause is suspected, additional diagnostic testing may be useful (e.g., adenosine deaminase in patients with tuberculosis and carcinoembryonic antigen in those with suspected malignancy).¹²⁵

The diagnostic accuracy of pericardiocentesis is variable, and certain diagnoses are unlikely to be made from pericardial fluid. In one large series, fluid samples were obtained in 90% of aspirations, but the specific cause was determined from only 24% of those specimens.¹²⁶ Another series demonstrated false-negative cytologic results in certain cases of lymphoma and mesothelioma.¹²⁶ In some HIV patients, effusions secondary to Kaposi’s sarcoma and cytomegalovirus infection have been diagnosed by pericardial biopsy following nondiagnostic fluid analysis.^127,128

The most helpful clinical predictors of diagnosis before pericardiocentesis are the size of the effusion (larger effusions and tamponade are more likely to yield a diagnosis) and signs of inflammation (e.g., fever, pericardial friction rub, ST-segment elevation).⁵⁸ Unfortunately, the only definitive methods of diagnosis are pericardial fluid aspiration and analysis and pericardial biopsy.

Subxiphoid pericardiotomy can also be used in stable patients with pericardial effusion. This technique collects both pericardial fluid and a pericardial biopsy specimen, and because a tissue sample is obtained, a definitive diagnosis is more likely.¹²⁹ This procedure can be performed safely in the operating suite without general anesthesia.¹³⁰ In a prospective series of 57 patients who underwent subxiphoid pericardiotomy, a definitive diagnosis was obtained in 36%, a probable diagnosis in 40%, a possible diagnosis in 16%, and no diagnosis in 7%. It is uncertain whether this technique is safer than ultrasound-guided pericardiocentesis, but published reports show low rates of complications in experienced hands.⁵⁸

Diagnostic pericardiocentesis has limited utility for hemopericardium secondary to traumatic causes. When used diagnostically after trauma to assess for the presence of pericardial bleeding, the procedure has a false-negative rate (i.e., no blood aspirated) of between 20% and 40%.95,131–133 The high false-negative rate is due to the fact that posttraumatic blood tends to clot within the pericardial space and therefore cannot be aspirated.¹⁹ Furthermore, pericardiocentesis should not delay emergency thoracotomy if cardiac tamponade is suspected.¹³⁴ If there is uncertainty about the presence of tamponade, the focused abdominal sonography in trauma (FAST) examination rapidly and noninvasively identifies pericardial fluid.^135–137

Therapeutic Pericardiocentesis

The ultrasonographic finding of a large pericardial effusion in a stable patient should lead to early cardiology or cardiothoracic surgery consultation for percutaneous drainage or placement of a pericardial window. Patients with a pericardial effusion who remain hypotensive despite fluid resuscitation require emergency therapeutic drainage. The decision to wait for consultants is best made by the emergency physician at the bedside and should be based on clinical judgment. For patients in extremis, pericardiocentesis should be performed immediately even if consultation is unavailable. The clinician who performs the procedure should be the one who is most experienced in both sonography and pericardial fluid aspiration.

Temporizing Measures

Cardiac tamponade is an emergency that requires urgent therapy. Therapy typically consists of either pericardial drainage by needle aspiration or placement of a pericardial window. These procedures cannot be readily performed in an ED, so temporizing methods are the mainstay of therapy unless the patient is unstable (e.g., in PEA arrest). The most common therapeutic procedures used as temporizing measures in the setting of tamponade are intravascular volume expansion and administration of vasopressors.5,14,146 Although most textbooks and protocols encourage the use of these temporizing methods, they are backed by only sparse scientific evidence.^147,148 Studies in animals have shown an increase in cardiac output and improvement in blood pressure with expansion of central blood volume; the validity of this in humans with cardiac tamponade is uncertain. Fluid resuscitation in a trauma patient with penetrating cardiac injury might cause deterioration. Animal experiments indicate that the response depends on whether fluid boluses produce recurrent bleeding from the cardiac wound.¹⁴⁹ Despite the lack of evidence, judicious volume expansion with or without an adjunctive vasopressor before definitive therapy may be the only option for patients with tamponade.

Norepinephrine, isoproterenol, dopamine, and dobutamine have all been evaluated as the vasopressor of choice in patients with cardiac tamponade. Norepinephrine and isoproterenol increased cardiac output in animal models of tamponade but failed to increase it in humans.150,151 Dopamine and dobutamine increased cardiac output and improved hemodynamics in the setting of tamponade.^33,148 Either of these agents may be helpful as a temporizing agent, but theoretically, dobutamine might be preferable because of its greater β-adrenergic activity.¹⁵¹

Preparation

Before preparing for pericardiocentesis, place all resuscitation equipment at the bedside in anticipation of clinical deterioration. Most patients undergoing pericardiocentesis in the ED have already experienced hemodynamic collapse and are lying supine. If the patient is able to cooperate, elevate the chest 30 to 45 degrees to bring the heart closer to the chest wall. Sedation of stuporous patients is typically forgone because of the risk for further hemodynamic collapse. If the patient is awake and undergoing the procedure without obvious hemodynamic compromise, short-acting medications (e.g., midazolam or fentanyl) are preferred.

Every effort should be made to ensure aseptic technique. Prepare the chest and upper part of the abdomen with a chlorhexidine-based solution. Drape the patient and ensure that all care providers involved in the procedure are wearing a sterile hat, mask, gown, and gloves. If the patient is awake, anesthetize the skin and the proposed route with 1% lidocaine (see Review Box 16-1). Because the pericardium is extremely sensitive, it should be anesthetized.¹⁵²

The approach to pericardiocentesis depends on the clinical status of the patient, the availability of ultrasound, and the distribution of pericardial fluid. Pericardial fluid is not always distributed circumferentially in the pericardial sac, so ultrasound can quickly identify the maximal effusion pocket and demarcate the appropriate site for needle placement. Pericardiocentesis with ultrasound guidance is currently the safest and most reliable method for the diagnosis and treatment of pericardial effusion and tamponade.¹⁵³ Studies of echocardiography-directed pericardiocentesis have found that the apical approach is the best site for puncture.^145,154,155 Cadaver studies have corroborated this finding and demonstrated greater safety with an apical approach. However, these studies also revealed that an apical approach is associated with a greater incidence of pneumothorax than a traditional subcostal approach is. Before the advent of ultrasound guidance, the subxiphoid approach (discussed later in this chapter) was the preferred method of pericardiocentesis. It is still used frequently during cardiac arrest and when ultrasound is not readily available.

ECG Monitoring

If ultrasound is not readily available to guide needle placement, electrocardiographic monitoring can serve as a useful adjunct. Electrocardiographic monitoring is used to prevent puncture of the ventricle. When using this method, an assistant is essential to ensure sterile technique, observe for dysrhythmias, and make sure that the electrocardiographic machine is functioning properly.

After all equipment is sterile, attach an alligator clip from one of the precordial leads (e.g., V₁) to the distal end of the spinal needle. Record a rhythm strip of this lead (the “exploring electrode”) continuously. Advance the needle through the skin while remembering that any contact with the epicardium will cause a current-of-injury pattern that can be seen on the ECG. Typically, this is represented as a wide-complex premature ventricular contraction with an elevated ST segment (Fig. 16-13). When a current-of-injury pattern is seen, the needle is probably touching the epicardium. Withdraw it several millimeters to prevent laceration of the myocardium or coronary vessels. After slight withdrawal, the needle should be within the pericardial space. Aspirate any fluid, but watch for any changes on the ECG. Electrocardiographic monitoring is not infallible: if the patient has an abnormal myocardium from conditions such as a previous MI or the formation of scar tissue, no current-of-injury pattern will be generated on the rhythm strip.

Ultrasound-Guided Pericardiocentesis

Pericardiocentesis has traditionally been performed blindly. This approach was associated with a low success rate and a high rate of complications, such as inadvertent puncture of the lung, ventricle, or epicardial vessels. Using ultrasound to both diagnose and guide pericardiocentesis has resulted in increased success rates, as well as a lower rate of complications. The techniques are described in the Ultrasound Box.

Subxiphoid/Subcostal Approach

As mentioned earlier, the traditional blind subxiphoid approach can still be used for pericardiocentesis in the ED (e.g., for patients in cardiac arrest and when ultrasound is not available). The technique is performed as follows: introduce the needle 1 cm inferior to the left xiphocostal angle at a 30-degree angle to the skin (Fig. 16-14). Because the heart is an anterior structure, angles greater than 45 degrees may lacerate the liver or stomach. Aim toward the left shoulder and advance the needle slowly while continuously maintaining negative pressure on the syringe to aspirate any fluid. Aspirate with an “in-and-out” vector only, not “side to side,” which may lacerate tissue. If no fluid is aspirated, withdraw the needle completely and redirect it in a deeper posterior trajectory. If no fluid is aspirated after redirecting the needle, withdraw the needle and redirect it, working from the patient’s left to right, until it is aimed at the right shoulder. Recommendations regarding needle trajectory vary widely, including toward the right shoulder, sternal notch, and left shoulder.^146,152

Apical Approach

The apical approach is sometimes used as an alternative to the subcostal approach to drain a pericardial effusion when ultrasound is available. Use ultrasound to identify the largest area of the apical effusion (Fig. 16-15A) or simply feel for the apex. If the apex cannot be palpated, it typically lies within the area of cardiac dullness, often between the fifth, sixth, or seventh intercostal space, between the midclavicular and midaxillary lines. Introduce the needle 1 cm lateral to and into the intercostal space below the apical heartbeat. Advance the needle over the cephalad border of the rib and aim it toward the right shoulder to avoid the neurovascular bundle located caudal to the rib space. This area is close to the lingula and the left pleural space, thus making pneumothorax a frequent complication. Theoretically, this technique is used because the coronary vessels are small at the apex; therefore, if a ventricle is entered, it is the thick-walled LV, which is more likely to seal off after ventricular injury. With echocardiographic guidance, the apical approach is used more commonly.¹⁵⁶

Parasternal Approach

The parasternal approach is an alternative approach to the previously described techniques. First, identity the largest area of the parasternal effusion on ultrasound if possible. If ultrasound is not available or if the effusion is not clearly identified on the ultrasound image, proceed by introducing the needle 1 cm lateral to the sternal border at the left fifth or sixth intercostal interspace. Advance the needle over the cephalad border of the rib to avoid the neurovascular bundle on the caudal aspect of the rib. Avoid going too far laterally from the sternal border because of potential injury to the internal mammary artery.¹⁵⁷ Occasionally, a right parasternal approach may be used when ultrasound predicts superior access to an effusion from this direction.

Tsang and coworkers¹⁵⁸ described this technique for ultrasound-guided pericardiocentesis in 1998. The ideal site for skin puncture is where the largest area of fluid accumulation is closest to the skin surface. On ultrasound, this is indicated by a large anechoic (black) area at the top of the screen, usually corresponding to the left anterior chest wall (rather than the subcostal region). This approach also avoids injury to the liver (common with the subcostal approach). Inadvertent puncture of the lung is also prevented with this approach because air in the lung will not conduct sound waves and will prevent visualization of the heart when located immediately beneath the probe. Avoid choosing a site that could puncture the internal mammary artery, which lies 3 to 5 cm from either parasternal border, or the neurovascular bundle, which is located at the inferior border of the rib. Mark the best site with a sterile pen.

Procedure and Technique

Confirm the trajectory and depth of the needle before puncturing the skin. Be aware that repositioning the patient alters the position of the heart and pericardial sac within the chest, so reassessment will be necessary. Prepare the skin antiseptically and place a sterile cover over the ultrasound probe. If time permits, anesthetize the selected area with 1% lidocaine, with the superior border of the adjacent rib being used as a landmark. Select an 18-gauge spinal needle. Ideally, the needle should have a sheath that allows it to be withdrawn after the pericardial space is entered. This helps avoid injury to the heart and other vital structures. Attach a saline-filled syringe to the needle, and gently aspirate while slowly advancing the needle. Keep the ultrasound probe on the chest wall, immediately adjacent to the aspiration site.

Once the pericardial space is entered, inject agitated saline to confirm needle placement, particularly if the pericardial fluid is grossly bloody or if there is any question about needle position (see Fig. 16-15B). Prepare a saline echocardiographic contrast medium by using two 5-mL syringes, one with saline and the other with air. Connect them via a three-way stopcock to the needle and catheter. Rapidly inject saline between the syringes and then inject it into the sheath. Monitor the entrance of the agitated saline into the pericardial space sonographically—it appears as a brightly echogenic stream. If the use of agitated saline proves to be inconclusive or suboptimal, use an echocardiographic contrast agent (e.g., Definity) as a safe and successful alternative.^159,160 Contrast agents contain gas microbubbles, which markedly enhance the fluid echo by introducing multiple liquid-gas interfaces. Inject this solution as a bolus. If the contrast material clears immediately after administration (as occurs with agitated saline) or persists temporarily within the cardiac chambers, an intracardiac location is suggested.

Fluid Aspiration and Evaluation

Removal of even a small amount of pericardial fluid (e.g., 30 to 50 mL) usually results in either return of spontaneous circulation or hemodynamic improvement. After any approach used for pericardiocentesis, place a temporary drain not only to ensure rapid access into the pericardial sac but also to allow more fluid to be removed quickly if hemodynamic collapse recurs. After needle placement is confirmed, a temporary drain can be placed by the Seldinger technique, described in Chapter 22.

Remove the syringe from the needle, advance a guidewire through the needle, and then remove the needle. Position a dilator (6- to 8-Fr Cordis) over the wire. If a dilator is not used, particularly with the subxiphoid approach, the pigtail catheter tip may get caught in the subcutaneous tissue and make placement of the catheter difficult. Remove the dilator and slide an introducer sheath dilator (6- to 8-Fr Cordis) over the wire. Remove the wire and the dilator while leaving the introducer sheath in place. Insert the pigtail angiocatheter through the introducer sheath, and aspirate fluid to confirm placement.154,158 After the catheter is advanced into place, it should be secured with a suture to ensure that it does not migrate after the procedure; an appropriate catheter dressing should be applied. The catheter should be attached to a three-way stopcock and connected to a water seal to drain by gravity. The pigtail catheter allows prolonged drainage and safe access into the pericardial sac without requiring the introduction of another needle.^161,162 If drainage of pericardial fluid becomes sluggish, flush the catheter with a heparinized saline solution to ensure patency of the lumen.¹⁵²

Aspiration of blood during pericardiocentesis raises the possibility of cardiac puncture. Blood retrieved from the ventricle usually clots faster than bloody fluid aspirated from the pericardium. In general, hemorrhagic pericardial effusions have local fibrinolytic activity, which prevents clot formation. If the bleeding is brisk enough, however, blood may still clot and does not necessarily point toward ventricular puncture. The hematocrit of pericardial fluid should always be lower than that of a sample from the systemic vascular system, except in patients with aortic dissection or acute myocardial rupture. These circumstances aside, a hematocrit value similar to that for systemic blood should raise concern for an intracardiac needle location. Several other simple laboratory tests can differentiate normal from abnormal pericardial fluid, but they require the availability of a centrifuge system and time. Under normal conditions, pericardial fluid is less than 50 mL in volume and clear to pale yellow in color with no red or white blood cells, inflammatory markers, bacteria, or cancer cells and with a glucose concentration similar to that of blood.

Immediately following the procedure, obtain a chest film to ensure the absence of pneumothorax and free air under the diaphragm. Place the patient on continuous cardiac monitoring for 24 hours and watch for signs of reaccumulating fluid or iatrogenic complications. Repeating the ultrasound examination in 24 hours is recommended. Diagnostic evaluation of nonhemorrhagic fluid is similar to that for pleural fluid (see Chapter 9).

Suture the pigtail catheter to the skin, but be careful to not occlude the catheter by tying it too tightly. Wrap the catheter in gauze at the skin and cover it with a sterile dressing. Attach the catheter to suction tubing and a drainage system.

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