Pericardial Tamponade

Chapter 54

Pericardial Tamponade

Scott M. Lilly, Steven A. Malosky and Victor A. Ferrari

Pericardial tamponade occurs when fluid accumulation within the pericardial space raises intrapericardial pressure to a level that impairs diastolic filling of the heart. This impairment results in elevated venous pressures and tachycardia, mechanisms that can initially maintain cardiac output. As the effusion enlarges and intrapericardial pressure continues to rise, however, cardiac output and systolic blood pressure eventually fall, and shock and death can ensue if not treated promptly. In describing the syndrome of pericardial tamponade, it is difficult to improve on the seminal description provided by Richard Lower, a 17th-century Cornish physiologist. He wrote:

Just as the Heart labors when affected by disease within, so it does when oppressed from without by disease of its covering. So it happens that when that same covering of the Heart is filled with an effusion, and the walls are compressed with water on every side, so that they cannot dilate to receive the blood; then truly the pulse diminishes until at length it is suppressed by even more water, when syncope, and death itself follows.

Anatomy of the Pericardium

The heart and great vessels are surrounded by and tethered to the pericardium. The pericardium has two layers consisting of a serous membrane and a fibrous sac. The serous membrane lines the outside of the heart and proximal great vessels (visceral pericardium or epicardium) as well as the inside of the fibrous sac (parietal pericardium). The potential space between the visceral and parietal pericardium is the pericardial space. The pericardial sac is attached anteriorly to the sternum, posteriorly to the vertebral column, and inferiorly to the diaphragm. It is drained by an extensive lymphatic system by which interstitial fluid, pericardial fluid, and lymph are routed from the pericardial space to the venous system through lymphatic channels in the right pleural space and the thoracic duct.

The pericardial space normally contains between 20 and 60 mL of colorless fluid, containing 1.7 to 3.5 g/dL of protein and electrolytes in concentrations similar to serum. Pressure within the pericardial space is influenced by both intracardiac and intrapleural pressures, and it varies from –5 cm H₂O to +5 cm H₂O during a normal respiratory cycle.

Function of the Pericardium

The function of the pericardium remains a puzzle, and the congenital absence of the pericardium has no adverse effect on survival or exertional capacity. A number of roles have been suggested, including prevention of excessive dilatation of the heart, prevention of adhesions to surrounding chest structures, and maintenance of the heart in a stable geometric position within the chest. Although the pericardium does prevent distention of the heart under artificial fluid loading conditions in animals, the relevance of this to humans is questionable. An additional proposed role may be to maintain a stable diastolic coupling between the left and right ventricles over a range of hemodynamic states.

Causes of Pericardial Effusion

Fluid accumulation within the pericardial space is a prerequisite for the development of cardiac tamponade with rare exception, such as massive pleural effusions, tension pneumothorax, or pneumopericardium. Because the native pericardium is generally stiff and noncompliant, in the acute setting as little as 100 to 200 mL of fluid can cause tamponade. In the chronic setting, pericardial effusions may contain up to 2 L of fluid without tamponade, owing to slow distention of the fibrous sac. Fluid may accumulate within the pericardium as a result of infection or inflammation of the pericardium (serositis, pericarditis) or from neoplastic disorders. Iatrogenic causes include hemopericardium caused by central venous catheter perforation, a puncture of the right atrium or ventricle by a pacemaker wire, or a prior endomyocardial biopsy. Purulent pericarditis results from bacterial infection of the pericardium and is characterized by a syndrome of fever, chest pain, and a pattern often suggestive of pericarditis on the electrocardiogram. Blood or thrombus in the pericardium after trauma or thoracic surgery may also result in tamponade (Table 54.1).

TABLE 54.1

Differential Diagnosis of Pericardial Effusion

HIV, human immunodeficiency virus.

Diagnosis

Tamponade should be suspected in any patient with unexplained hypotension. A change in mental status or the onset of oliguria may be early signs of systemic hypoperfusion. An enlarged cardiac silhouette on chest radiograph or changes consistent with pericarditis on the electrocardiogram (ECG) may be early clues, which, although nonspecific, should prompt the clinician to exclude tamponade as a contributing etiology.

Symptoms

Tamponade is primarily a hemodynamic diagnosis, and symptoms may be subtle, particularly at the outset. Chest discomfort is a noteworthy complaint and may be referable to pericarditis—sharp in quality and prolonged in duration. In this setting, chest pain may be relieved by the patient changing position, classically by leaning forward and worsened by lying supine. With large chronic effusions, extracardiac mechanical compression of the esophagus or the recurrent laryngeal or phrenic nerves may result in dysphagia, hoarseness, cough, or singultus (hiccupping). Once tamponade has resulted in decreased cardiac output and hypotension, dyspnea is the most common symptom and manifestations of cerebral hypoperfusion (anxiety, confusion, somnolence) may also be appreciated.

Physical Examination

Early signs of increased intra-pericardial pressure include tachycardia without hypotension and a slightly increased respiratory rate (Table 54.2). Paradoxical pulse (pulsus paradoxus) develops later and refers to a decline in systolic blood pressure of more than 15 mm Hg on inspiration. In the setting of tamponade the heart has a “fixed volume,” such that inspiratory-driven increases in venous return to the right ventricle reduce left ventricular outflow via compression of the left ventricle between the septum and pericardial fluid. Though highly sensitive for cardiac tamponade, pulsus paradoxus is not a specific finding and occurs with other common intensive care unit (ICU) conditions such as advanced obstructive airway disease or positive pressure ventilation.

TABLE 54.2

Typical Progression of Effusion to Tamponade

RAP right atrial pressure; RVEDP, right ventricular end-diastolic pressure; PAEDP, pulmonary artery end-diastolic pressure; PAWP, pulmonary artery wedge pressure; LVEDP, left ventricular end-diastolic pressure; ↑, increased; ↑↑, marked increase; ↓, decreased; ↓↓, marked decrease; =, equal; <, less than. Note.: These represent typical values and progression for illustrative purposes but will be affected by age, acuity of fluid collection, and comorbid conditions.

Jugular venous distention is a nearly constant finding with cardiac tamponade, but it is also evident in other conditions frequently encountered in the ICU. Although subtle, identifying the contour of the jugular venous pulse should be attempted, as the attenuation (or absence) of the y descent is an early sign of impaired diastolic filling (Figure 54.1). The heart sounds may be muffled but are usually audible, and a pericardial friction rub may be heard or palpated.

Figure 54.1 A, Simultaneous right atrial (RA) pressure tracing, pericardial pressure tracing (arrows), and V2 lead electrocardiogram in a patient with tamponade. Note (1) increased RA pressure, (2) equalization of RA pressure with pericardial pressure (except for delayed “a” wave in pericardial pressure [arrows] compared to “a” wave in RA pressure), and (3) preserved “x” descent of the RA pressure tracing with attenuated “y” descent. B, Simultaneous aortic (AO) tracing (upper tracing) and pulmonary arterial (PA) pressure tracing (lower tracing) in the same patient prior to pericardiocentesis. Note (1) tachycardia, (2) inspiratory decrease in peak aortic pressure and coincident increase in peak pulmonary arterial pressure (arrow), and (3) discordant respirophasic changes in pulse pressure amplitude in aortic and pulmonary arterial (PA) pressures (arrows). C, Same patient after pericardiocentesis, without tachycardia, and concordant normal respirophasic changes in aortic (upper tracing) and pulmonary arterial (lower tracing) pressure waveforms.

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Jul 7, 2016 | Posted by admin in CRITICAL CARE | Comments Off

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