Hemodynamic pathophysiology

The primary hemodynamic pathophysiologic process in the development of tamponade is increased pericardial pressure that impairs diastolic filling [1–6]. Normal pericardial pressure is zero; any increase can have hemodynamic consequences. One way of looking at tamponade is that the effusion competes with the cardiac chambers to occupy the limited volume within and surrounded by the pericardium. Another way to think of tamponade is as a rubber band around the cardiac chambers, exerting a constrictive force and preventing adequate expansion. Resultant elevations in intracardiac diastolic pressures impair systemic and pulmonary venous return, leading to venous congestion and reduced cardiac output (Figure 19.2). As pericardial pressures increase, a variety of compensatory mechanisms are elicited, including sympathetic nervous system activation, which leads to tachycardia, increased ejection fraction, peripheral vasoconstriction, and sodium and fluid retention.

The pericardium is a relatively noncompliant structure and thus the relationship between pericardial pressure and volume is nonlinear. Pericardial pressure rises exponentially as pericardial fluid volume increases after a certain threshold is reached. Factors that influence the development of hemodynamic compromise in the setting of a pericardial effusion include the rate at which the fluid accumulates, the amount of pericardial fluid, the compliance of the pericardium, the size of the pericardial space, and ventricular compliance. The pericardium expands only minimally in the acute setting, but can greatly increase in size over prolonged periods of time. Thus, patients with a slowly developing effusion may be asymptomatic even with a large‐volume effusion. In contrast, if the rate of accumulation is rapid, even a small volume of effusion may trigger hemodynamic compromise (e.g., in the setting of cardiac trauma). The inherent compliance of the pericardium also plays a role in determining the hemodynamic significance of an effusion. Several disease processes may render the pericardium more stiff or noncompliant, allowing for a smaller effusion to cause cardiac tamponade. Left and right ventricular hypertrophy renders the heart most resistant to elevated pericardial pressures.

The hemodynamic effects of increased pericardial pressure occur on a spectrum and cardiac tamponade can be divided into three phases [5,7]. As the pericardial fluid accumulates, the pericardial pressure rises. Increasing pericardial pressure leads to increasing right atrial (RA) pressure. At this point, clinical signs of tamponade may be absent as the right heart, including right ventricular (RV) stroke volume, but not the left heart is compromised (phase 1). As pericardial fluid continues to accumulate and pericardial pressure rises, pulmonary capillary wedge pressure (PCWP) begins to rise and external compression of both left and right ventricles is present (phase 2). End‐diastolic pressures (EDP) throughout the cardiac chambers are elevated and within 5 mm Hg of each other, including RA, RVEDP, pulmonary artery, PCWP, and LVEDP. At this stage, classic signs and symptoms of cardiac tamponade are usually seen. In this phase, compensatory tachycardia maintains cardiac output in the presence of diminished stroke volume. Eventually, if pericardial pressures continue to rise and approximate RA and RV diastolic pressures, cardiac output falls, and cardiac tamponade progresses to shock with impaired tissue perfusion (phase 3).

Hemodynamic findings

See Table 19.1.

1. Elevated pericardial pressure (Figure 19.2).
   
2. Elevated and near equalization of end‐diastolic pressures (RA, RVEDP, pulmonary artery, PCWP, and LVEDP). Since cardiac filling pressure is intracardiac minus pericardial pressure, intracardiac pressures must increase as pericardial pressure increases to maintain a pressure gradient between the atria and ventricles (remember that blood flow through the heart is determined by pressure gradients).
   
3. Elevated RA pressures with a prominent X descent and blunted Y descent. In the setting of a hemodynamically significant pericardial effusion, diastolic filling is impaired and affected by pericardial pressure. A unique feature of cardiac tamponade is the continuous compression of the heart throughout the cardiac cycle. This limits the fall in ventricular pressure during early diastole and thus causes a decrease in the normal atrium to ventricular pressure gradient in early diastole. This, in turn, restricts the amount of early diastolic filling of the ventricles and blunts the Y descent seen in the atrial pressure tracings (Figure 19.3).
   

   In patients with tamponade, a relatively larger amount of atrial filling occurs following ventricular contraction, since as blood is ejected to the great vessels during ventricular systole, ventricular volume transiently falls, enabling atrial expansion and filling. RA pressure drops immediately following ventricular contraction as atrial volume increases; this large swing in RA pressure gradient in the setting of cardiac tamponade elicits an exaggerated RA X descent. The X descent may be exaggerated during inspiration since a decrease in pericardial pressure leads to augmentation of blood flow to the RV during inspiration (Figure 19.2). Conversely, the Y descent corresponds to passive ventricular filling and is blunted.

   
   

   Following removal of pericardial fluid with a resulting reduction in pericardial pressure, the Y descent in the RA tracing will become more apparent (Figure 19.4).

   
   
4. RV pressure tracing lacks the “dip and plateau” of constrictive pericarditis. Unlike constrictive pericarditis, cardiac tamponade is not characterized by rapid ventricular filling in early diastole, nor does RV pressure fall below pericardial pressure in early diastole. Therefore, there is no “dip and plateau” configuration in the RV tracing. RV hypertrophy is one exception to the rule. Because of the thickness of the RV free wall, early passive diastolic filling may still occur, and therein the Y descent is preserved.
   
5. Pulsus paradoxus, an exaggerated decrease in arterial systolic pressure during inspiration. It is because of compromised LV diastolic filling during inspiration. This is due to a chain of events: (a) pericardial and RA pressures decrease due to negative intrathoracic pressure; (b) this results in augmented systemic venous return to right‐sided chambers and a marked increase in RV volume; (c) this results in an increase in RV filling during inspiration that, in the setting of cardiac tamponade, compromises LV filling. Note that it is normal to have a drop in systolic blood pressure with inspiration and that pulsus paradoxus is defined by the magnitude of the decrease (an “exaggerated” drop). Pulsus paradoxus is variously defined as a drop of >12 mm Hg, a drop of ≥10 mm Hg, or a drop of ≥9% during normal inspiration (Figure 19.5). Note that pulsus paradoxus may not be present in patients with tamponade and
   
   
   
   • acute aortic regurgitation (i.e., acute aortic dissection)
     
   • elevated LVEDP
     
   • atrial septal defect
     
   • pulmonary hypertension
     
   • right ventricular hypertrophy
   
   
6. Respiratory variation in atrial pressures. Negative thoracic pressure is transmitted to the fluid‐filled pericardial space, unlike the situation in constrictive pericarditis, and influences atrial pressures.
   
7. Inspiratory traction. Described by Boltwood et al., this is the diastolic equalization of PCWP and RA pressures, predominantly during inspiration [8]. It is due to inspiratory traction of the taut pericardium by the diaphragm.
   
8. Stroke volume is decreased. Cardiac output will fall in absence of tachycardia.

Elevated diastolic pressures and equalization of end‐diastolic pressures

X descent is preserved, but Y descent is small or absent on RA pressure tracing

Pericardial pressure is elevated

RV pressure does not fall in early diastole (i.e., there is no dip and plateau configuration)

Pulsus paradoxus

Several clinical scenarios can mask the clinical diagnosis of tamponade. In the setting of hypovolemia and suspected tamponade, the typical hemodynamic findings may be masked. Low‐pressure effusions equilibrate only with right‐sided diastolic pressures and at first only during inspiration. A fluid bolus may elicit classic findings. Severe left ventricular dysfunction may also mask tamponade. In this setting, LV diastolic pressures are higher than RV diastolic pressures and the diagnosis of cardiac tamponade should be dependent on demonstrating elevated pericardial pressures equal to RA pressures. Regional cardiac tamponade can occur when some, but not all, cardiac chambers are compressed by loculated effusions. Typical hemodynamic abnormalities maybe found only in the compressed chambers or zones. In some cases, loculation may also produce classic tamponade, presumably by “stretching” the pericardium.

Tremendous efforts are expended in determining whether a patient is “in tamponade” and, thus, qualifies for emergent therapy. It is important to note that increased pericardial pressure is a clinical spectrum rather than an all‐or‐none phenomenon. The important questions are “What is the approximate pericardial pressure?” and “What effect is the pericardial fluid having on cardiac output, arterial blood pressure, and intracardiac pressures?” The determination of the need for pericardiocentesis must weigh the risk of the procedure versus these questions and other important considerations, including the rate of accumulation and the potential diagnostic value of obtaining pericardial fluid. The European Society of Cardiology Working Group on Myocardial and Pericardial Diseases has proposed a stepwise scoring system to be used in patients with suspect tamponade. A score ≥6 warrants immediate pericardiocentesis in the absence of contraindications [9].

Physical exam findings

The physical examination can provide clues to cardiac tamponade. Sinus tachycardia and hypotension with narrow pulse pressure are hallmarks. The clinician must remain aware that blood pressure may remain normal or even elevated until cardiovascular collapse is imminent.

Pulsus paradoxus, as already described, is an “exaggerated” drop in systolic blood pressure during normal inspiration (not forced inspiration). This is a common finding in moderate to severe tamponade. To measure pulsus paradoxus, the sphygmomanometer should be inflated to suprasystolic pressure, deflating until Korotkoff sounds are initially heard in expiration only. Then, the cuff should be deflated until Korotkoff sounds are heard throughout the respiratory cycle. The difference of these two pressures is the “paradox” (normal pulsus paradox is <10–12 mm Hg). This finding is neither specific nor sensitive and may be seen in other conditions, including constrictive pericarditis, severe obstructive pulmonary disease, restrictive cardiomyopathy, pulmonary embolus, obesity, and right ventricular infarction (Figure 19.6).

Jugular venous distension is usually present with a preserved X descent. In tamponade, venous waves in the neck are not outward pulsations, but rather X descents are apparent as a collapse from a high standing pressure level. The Y descent is typically not seen.

Kussmaul’s sign, which was originally described as an increase in the jugular venous pressure with inspiration but is now commonly used to describe the lack of a decrease in JVP with inspiration, is not classically seen in tamponade without a component of constrictive disease (i.e., effusive–constrictive disease) [10].

Beck’s Triad, described in 1935, is a cluster of findings in cardiac tamponade characterized by hypotension, muffled heart sounds, and jugular venous distension.

Pericardial friction rub may be heard in the setting of pericarditis.

Hemodynamics of cardiac tamponade as measured with echocardiography

The echocardiogram is a useful tool in the diagnosis of cardiac tamponade; however, it is important to note that cardiac tamponade is a clinical diagnosis. The echocardiogram is a relatively quick, noninvasive test, which may aid the clinician in delineating the size, morphology, hemodynamic impact, and location of the effusion. Important findings on echocardiography include the following:

• The presence of an effusion is the only sensitive sign in tamponade. The absolute size of the effusion is not as useful in predicting tamponade, with the caveat that larger effusions confer greater risk of tamponade.
  
• RV diastolic collapse occurring in early diastole is believed to occur only with higher pericardial pressures. However, the lack of RV diastolic collapse does not indicate a nonhemodynamically significant effusion.
  
• RA collapse occurring in late diastole or early systole is a relatively early sign of increased pericardial pressure.
  
• Small chamber sizes.
  
• Inferior vena cava plethora with attenuated respiratory variation.
  
• Significant changes in inflow across both mitral and tricuspid valves during inspiration. Doppler transmitral flow velocity paradoxus, a reciprocal respiratory variation in transvalvular right‐ and left‐sided flow velocities, has been thought to be a sensitive sign of tamponade. Normally there is no substantial variation in early diastolic filling velocities throughout the respiratory cycle. With cardiac tamponade, there are exaggerated increases in right‐sided flow velocities and exaggerated decreases in left‐sided flow velocities during inspiration (Figure 19.7). A substantial decrease in Doppler transmitral flow velocity with inspiration (>25%) may serve as an indicator of flow velocity paradoxus and tamponade physiology.
  
• Abnormal septal motion. On inspiration the ventricular septum moves toward the left heart, whereas the septum moves toward the right heart on expiration. The filling of the different ventricles is dependent on the position in the respiratory cycle; an echocardiographic demonstration of pulsus paradoxus.