US Probe: When Does an Effusion Become Pericardial Tamponade?

Author: Stephen Alerhand, MD (@SAlerhand; Ultrasound Fellow and Instructor of Emergency Medicine, Icahn School of Medicine at Mount Sinai) // Edited by: Brit Long, MD (@long_brit), Alex Koyfman, MD (@EMHighAK), and Manpreet Singh, MD (@MprizzleER)


Pericardial tamponade occurs when fluid within the pericardial sac impairs filling of the right-sided chambers, leading to a decrease in cardiac output and hemodynamic compromise. It is neither a clinical nor an echocardiographic diagnosis alone. Rather, the echocardiogram carries diagnostic value and should be performed when there is an elevated pre-test probability for tamponade based on the history and physical exam. It must be noted, however, that just like the echocardiogram, the clinical exam and vital signs lack specificity for pericardial tamponade [1, 2]. In some cases, the echocardiographic signs of tamponade may even be seen prior to clinical signs.

Here, we will illustrate the core echocardiographic findings of pericardial tamponade:

Pericardial Effusion

The pericardial cavity between the myocardium and pericardial sac normally contains < 50 mL of lubricating fluid. With only 15-35 mL, separation of these layers can be visualized with high sensitivity and accuracy by point-of-care ultrasound (POCUS) [3, 4] in both the medical and trauma settings [5, 6]. With sufficient volume, the heart may be seen swinging within the pericardial sac (Video 1), though the sensitivity is low [7]. This is manifested on the electrocardiogram (ECG) as electrical alternans.

Video 1 – Heart swinging within pericardial sac. Sometimes it will swing from superficial to deep, coming into and out of view.

A single cardiac view can misrepresent the volume of the effusion. It is therefore important to acquire multiple different views of the effusion for better characterization. Nevertheless, the size of the effusion can be estimated as follows [8, 9]:

Image 1 – Small pericardial effusion in parasternal long axis view (PSLAX)
Image 2 – Large pericardial effusion in subxiphoid view (SX)

That being said, the size of the effusion does not necessarily predict pericardial tamponade. More important in predicting tamponade are the rate of rise of the effusion and the pericardial compliance [12]. This in turn determines the filling pressures within the pericardial space in relation to those within the cardiac chambers during diastole. For instance, even 50 mL of fluid can lead to hemodynamic compromise if it has accumulated rapidly [13], as the pericardial space is acutely non-compliant. Conversely, larger volumes can be accommodated by the stretching of a more compliant pericardium over longer periods of time and may not cause hemodynamic compromise. However, once the pericardium’s compliance reaches a certain threshold, even a small increase in pericardial fluid can lead to tamponade. This concept is well-represented by a pressure-volume curve (Image 3 [14]).

Image 3 – Ivens, E.L., B.I. Munt, and R.R. Moss, Pericardial disease: what the general cardiologist needs to know.Heart, 2007. 93(8): p. 993-1000.

Among others, there are two false-positives that may be mistaken for a pericardial effusion:

  • Pleural effusion

    • Pericardial effusions lie anterior to the descending aorta, and pleural effusions lie posterior.
(Video 2 – From James Tsung [])
  • Pericardial fat pad

    • Distributed in anterior atrioventricular groove
    • Appears echoic as opposed to anechoic (often described as having a “stippled appearance”
    • Moves in concert with the myocardium during the cardiac cycle
(Video 3 – From James Tsung [])

A pericardial effusion can be visualized in any of the four main cardiac views. Previously shown were effusions in the PSLAX and subxiphoid SX views. Below are effusions in the parasternal short (PSAX) (Image 4) and apical 4-chamber (A4C) views (Image 5).

Image 4 – Effusion in the PSAX view
Image 5 – Effusion in the A4C view

Diastolic Right Ventricular Collapse

The right ventricle (RV) collapses when the intrapericardial pressure exceeds the intracardiac pressure. The intrapericardial pressure is proportional to the pericardial fluid volume and the stiffness of the pericardial sac as follows [15]:

The RV has a thinner, more compliant wall and lower pressure system than the left ventricle (LV). Its pressure is at its lowest in early diastole, so naturally, this is the point in the cardiac cycle at which an increase in intrapericardial pressure will cause the ventricle to bow inward. The severity of tamponade is correlated with the duration of the chamber’s collapse [16], that is, the period of diastole over which the intrapericardial pressure exceeds the RV filling pressure. The outflow region collapses first, followed by the basal segment once tamponade progresses.

If the RV filling pressures are elevated at baseline, however, it follows that diastolic collapse will less likely occur. This may be the case with: acute or chronic cor pulmonale, pulmonary hypertension, severe LV failure, or other etiologies of RV hypertrophy [11, 17-20]. Positive-pressure ventilation will exert this effect as well. In contrast, diastolic RV collapse may occur earlier if the filling pressure is lower at baseline, such as with hypovolemia [21].

Diastolic collapse of the RV carries a high specificity (75-90%), with a relatively lower sensitivity (48-60%) [22-25]. This is more specific but less sensitive than the next echocardiographic finding to be discussed: systolic right atrial (RA) collapse [26]. Altogether, the absence of any chamber collapse has a 90% negative predictive value for tamponade [27]. These values for sensitivity and specificity may be affected by changes in blood volume. For instance, collapse of the RV may occur even earlier if the RV pressures are lower at baseline.

Diastolic RV collapse can be visualized in all four cardiac views:

Parasternal long axis (PSLAX)

Video 4 – Diastolic RV collapse in the PSLAX view.

The axis of the heart is a little bit off-axis, as the aortic outflow tract is not well visualized. Nevertheless, as the mitral valve (MV) opens to indicate diastole, the RV outflow tract (RVOT) anterior wall can be seen collapsing downward. Some educators have likened this to a “little man jumping on a trampoline.”  For learning purposes, the second half of the clip has been played at slow speed.

Image 6 – M-mode of Video 3.

In a tachycardic patient, the precise timing of the MV opening and RVOT anterior wall movement can be difficult to ascertain. In such cases, M-mode can be used to acquire a still image. This will demonstrate whether the RVOT anterior wall is bowing downward at the same time as the E-wave of the MV opening. Here is a still image re-created using Ben Smith MD’s M.mode.ify program found at

Video 5 – No diastolic collapse in a chronic pericardial effusion

Parasternal short axis (PSAX)

Video 6 – Diastolic collapse in the PSAX view at the mitral valve level.

Once again, as the “fish-mouth” representing the MV valve opens, the RV free wall collapses downward.

Apical 4-chamber (A4C)

Video 7 – Diastolic RV collapse in the A4C view (from Matthew Riscinti and Benjamin Clearly, generously provided by our friends at The POCUS Atlas []).


Video 8 – No diastolic collapse in a chronic pericardial effusion

Subxiphoid (SX)

Video 9 – Diastolic RV collapse in the SX view.

The RV is seen to barely expand at all due to compression by the increased intrapericardial pressure.

Video 10 – No diastolic collapse in a chronic pericardial effusion (from Robert Jarman, generously provided by our friends at The POCUS Atlas []).

Systolic Right Atrial Collapse

The RA is at its lowest pressure during systole, or more precisely, in late diastole at the onset of atrial relaxation. During this period, it is most susceptible to collapse from increased intrapericardial pressure. Its pressure during systole is lower than that of the RV in diastole, so systolic RA collapse is therefore the earliest echocardiographic sign of tamponade [28].

The specificity of systolic RA collapse varies for tamponade (33-100%) [25, 29, 30]. It increases when duration of chamber collapse lasts > 1/3 of the cardiac cycle [23, 31, 32]. Otherwise, it may simply be mistaken for normal atrial systole [27, 32]. The sensitivity for tamponade is higher, ranging from 50% in early tamponade to 100% with its progression [25, 30].

Systolic RA collapse can be best visualized in the A4C view (Video 11). On their Ultrasound Podcast episode, Matt Dawson and Mike Mallin likened this to a “little man punching a trampoline” ( It can also be visualized in the SX view (Video 12).

Video 11 – Systolic RA collapse in the A4C view. Time the closing of the MV valve with the upward and inward motion of the RA free wall (from Matthew Riscinti and Benjamin Clearly, generously provided by our friends at The POCUS Atlas []).


Video 12 – Systolic RA collapse in the SX view (from Joshua Guttman)

Plethoric Inferior Vena Cava with Minimal Respiratory Variation.

A plethoric inferior vena cava (IVC) in tamponade is caused by the hindrance of systemic venous return into the RA, which cannot fully accommodate the incoming preload due to compression by increased intrapericardial pressure. This is a very sensitive sign for tamponade (95-97%) [25, 33, 34] and carries high negative predictive value [33]. It has much lower specificity (~40%) and can be caused by several other cardiac conditions including congestive heart failure (CHF) and tricuspid regurgitation, among others [25].

A plethoric IVC can be visualized in the subcostal plane (Video 13). The diameter should be measured about 2-3 cm from the IVC-RA junction, usually around the level of the hepatic vein draining into the IVC (Image 7).

Video 13 – Plethoric IVC with minimal respiratory variation
Image 7 – Site of IVC measurement, 2-3 cm from IVC-RA junction

Exaggerated Respiratory Cycle Changes in Mitral and Tricuspid In-flow Velocities as a Surrogate for Pulsus Paradoxus

Pulsus paradoxus is simply the exaggeration during tamponade of the normal respiratory variation in systolic blood pressure (SBP). It is therefore important to first understand the physiology that governs that variation. Normally during expiration, the positive intrathoracic pressure pushes air out of the lungs through the left side of the heart. In corresponding fashion, more blood is pushed through the left side of the heart, leading to a higher stroke volume manifested as a higher SBP. The two sides of the heart reside within the same enclosed pericardial sac and compete for space. As a result, the increase in left-sided blood flow causes bulging of the intraventricular septum, and the RV volume within the same pericardial space decreases. This relationship between the two ventricles is referred to as ventricular interdependence.

During inspiration, the negative intrathoracic pressure conversely pulls air into the lungs. With a drop in pulmonary vascular resistance, blood flow correspondingly flows down its pressure gradient from the IVC through the right side of the heart into the pulmonary vasculature where it pools. Once again, we see ventricular interdependence at play. Since the LV has a higher pressure than the RV, the RV only minimally bulges into the LV’s space, though still causing a drop in LV stroke volume manifested as a decrease in SBP of < 10 mmHg.

These effects are exaggerated during pericardial tamponade. The accumulated fluid within the pericardial sac occupies space otherwise available only to the ventricles. During inspiration, the RV will expand as mentioned earlier. Only now, the increased intrapericardial pressure has caused the RV and LV end-diastolic pressures to equalize. As a result, the intraventricular septum will indent more toward the LV and hinder its ability to accumulate blood volume, demonstrating an exaggerated ventricular interdependence. This manifests as an abnormally large decrease in SBP by 20 mmHg known as pulsus paradoxus.

Just as with the chamber collapses mentioned earlier, there are several baseline cardiac characteristics for which pulsus paradoxus is less likely to develop. The most common to consider include ventricular hypertrophy or dysfunction [17, 18, 35], severe pulmonary hypertension, increased circulating volume [36], and also positive-pressure ventilation [10, 37].

A surrogate for the increase in blood flow across the respective mitral and tricuspid cardiac valves is the respective in-flow velocities of this blood flow through the valves. These velocities and their changes during the respiratory cycle can be measured using Doppler echocardiography [38, 39] (Image). Studies have shown variance in these percentages of change that define pulsus paradoxus [27, 38-41]. This occurs due to imprecise and varying alignments, sample volumes, and patient positions during measurement. For our purposes, we will use the following: During inspiration, expect a 25% decrease in MV in-flow velocity, and a 40% increase in TV in-flow velocity. Of note, this may also occur with marked dyspnea, severe chronic obstructive pulmonary disease, and pulmonary embolism [42]. Variation up to 10% can occur without tamponade.

The MV and TV in-flow velocities are measured using pulse wave Doppler from the A4C view, with the gate placed at the tips of the valve leaflets. The flow velocities should be measured at the first heartbeat after the change in respiratory phase. In other words, sample the tallest E-wave peak and compare it to the lowest (Image 8).

Image 8 – Greater than 25% change with inspiration in the MV in-flow velocity as measured by pulse wave Doppler. This is a surrogate for decreased left heart filling that correlated with a drop in SBP > 10 mmHg.


Bedside echocardiography can help diagnose pericardial tamponade when there is already a degree of clinical suspicion. The core findings include: a pericardial effusion, diastolic RV collapse (high specificity), systolic RA collapse (earliest sign), plethoric IVC with minimal respiratory variation (highly sensitive), and exaggerated respiratory cycle changes in MV and TV in-flow velocities as a surrogate for pulsus paradoxus. For a future US Probe…Similar to making the diagnosis itself, the decision to perform a pericardiocentesis will depend on the echocardiographic findings together with the clinical condition of the patient, as well as the suspected etiology of the effusion.


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