The pericardial space surrounds the heart like the pleural space surrounds the lungs. Normally, 10 to 50 mL of fluid fills the space and reduces friction between the heart and surrounding mediastinal structures. The pericardial sack that contains this space also provides a barrier to infection and malignancy and helps distribute transmural pressure evenly amongst different cardiac chambers. If a pericardial effusion (excess pericardial fluid) tensions the pericardial sack, it increases the chamber pressures relative to the great veins. This relative pressure change prevents chamber filling. If venous pressures cannot equally rise, then cardiac output drops. This compromised hemodynamic state is known as cardiac tamponade.
The following conditions can cause pericardial effusions via hemorrhage, obstructed lymphatic flow, high RA pressure, or local inflammation. Always consider TB pericarditis in settings where tuberculosis is still endemic.
Pericardial effusions can be described as small, moderate, or large based on their general thickness. However, it is crucial to understand that excess pericardial wall tension, not effusion size, exerts the hemodynamic effects that cause cardiac tamponade. Some small pericardial effusions that form quickly or inside a stiff pericardial sac can cause high pericardial wall tension and cardiac tamponade despite their small size. On the other hand, some large effusions have no hemodynamic significance because they develop slowly, and the pericardium has permanently stretched out to relieve tension. In addition, some apparently benign effusions may become hemodynamically significant and lead to shock if there is a rapid drop in compensating venous pressure, such as from bleeding, hemodialysis, or when vasodilators are given. Increasing thoracic pressure by starting positive pressure ventilation can further impair cardiac filling and worsen the hemodynamic effects of a pericardial effusion.
Therefore, while we may describe an effusion as small, moderate, or large – it is more important to look for clues that the cardiac chambers are not filling adequately despite sufficient venous return.
Pericardial disease can be easy to overlook and often presents with non-specific exam findings and complaints such as chest pain or shortness of breath. Ultrasound can help us determine if a pericardial effusion is present with high accuracy1–3. However, PoCUS yields only subtle clues about whether chambers are filling adequately. Therefore, diagnosing cardiac tamponade involves PoCUS or other imaging findings of pericardial fluid plus clinical indicators of poor chamber filling, such as tachycardia, hypotension, and peripheral vasoconstriction that improve when venous return increases, such as with changes in positioning or fluid administration. Pericardial tamponade often presents with the following non-specific physical exam findings that can improve with treatments that increase venous return.
Shock is a late finding and can quickly progress to cardiac arrest, often with pulseless electrical activity.4 Tamponade-induced tachycardia and hypotension that improves with fluids may be confused with sepsis. Likewise, pericardial effusion-induced distended neck veins and cardiomegaly may be confused with heart failure. However, PoCUS can quickly identify a pericardial effusion and lead the clinician to consider pericardial tamponade. Conversely, the absence of a pericardial effusion on ultrasound virtually rules out pericardial tamponade. The main exception to this high negative predictive valve is patients who recently underwent cardiothoracic surgery and may have a small loculated effusion and require an empiric return to the operating room.
The pericardium appears on all views as a thin hyperechoic border, usually more prominent posteriorly, deep to the heart. Typically, the pericardial space is too small to see with ultrasound. However, as pericardial fluid accumulates, it appears as an anechoic zone or ‘stripe’ surrounding the heart.
Short-axis views can reveal how fluid surrounds the heart and help identify small or localized effusions. Use caution to avoid confusing pleural fluid and pericardial fluid. In the PLAX view, pleural effusions usually track posterior to the descending thoracic aorta, and pericardial effusions track anterior to the descending thoracic aorta. As a rule, obtain at least two views and fan through the entire heart before ruling in or out the presence of a pericardial effusion. To best assess for clues of tamponade, first capture video clips, then review them carefully frame by frame.
When pericardial fluid impairs RV filling, it often causes RV diastolic collapse, which is apparent on the PLAX and A4C views as abnormal inward motion of the RV free wall during diastole (when the tricuspid valve is open). However, this finding may be absent or missed if the RV free wall is not well visualized or if it is not compliant, such as might occur with chronic pulmonary hypertension. Finding RV diastolic collapse is relatively specific for tamponade but should be combined with other findings and clinical indicators of poor cardiac filling before making a diagnosis.
When pressure via pericardial fluid impairs RA filling, it often causes pronounced RA systolic collapse, which is apparent on the SC4C and A4C views as abnormal inward motion of the RA free wall during systole (when the tricuspid valve is closed). This finding is less often absent in tamponade (more sensitive) than RV diastolic collapse. However, it is only specific if the collapse occurs for >1/3 of systole. Determining this can be difficult without a careful frame-by-frame analysis. Again, do not use this clue alone to rule in cardiac tamponade.
When pericardial fluid confines the space available for chambers to expand, it makes them compete for space and exaggerates ventricular interdependence, where filling one chamber affects the filling of the other. This appears as abnormal interventricular septal motion. As inspiratory effort decreases intrathoracic pressure, it enhances RV filling, which briefly shifts the interventricular septum to the left and impairs LV filling, causing an intermittent drop in stroke volume and systolic blood pressure during inspiration. Pulses paradoxus is an exaggerated variation in blood pressure with breathing and indicates increased interventricular independence. Abnormal septal motion can also occur with constrictive pericarditis, hyperinflation, isolated RV overload, or with a left bundle branch block where the RV contracts before the LV.5
When pericardial fluid impairs cardiac filling, fluid accumulates in the large veins, and increased venous pressure helps sustain cardiac filling. Therefore, a distended IVC with less than 50% collapse during inspiratory effort is a sensitive finding for tamponade. To have tamponade and IVC collapse >50% would require significant RV and RA collapse, as discussed above. Therefore, cardiac tamponade can be ruled out if IVC collapses >50% and there is no obvious abnormal right heart collapse.
To rule in cardiac tamponade, ensure that PoCUS findings are consistent with other clinical findings that suggest the body is compensating to maintain perfusion despite impaired cardiac filling. These include peripheral vasoconstriction with cool extremities, lower blood pressure, and tachycardia unchanged or improved with IV fluids or elevating the legs.
To avoid hemodynamic collapse, patients with pericardial tamponade require the ability to maintain compensatory systems and prompt interventions to promote right heart filling.
Pericardiocentesis can be lifesaving, especially when the patient is hypotensive despite non-invasive measures to promote cardiac filling. When possible, involve the appropriate specialist who can perform this procedure and install a definitive drain in a controlled setting such as the ICU or operating room. Acute traumatic or post-operative hemopericardium often requires surgical intervention. In this case, pericardiocentesis should not delay surgery. Increasing systolic blood pressure with pericardial drainage may paradoxically worsen a cardiac rupture or aortic dissection. In these cases, removing a small volume may avoid cardiac arrest as a bridge to definitive surgical treatment. A generalist can quickly use a needle and catheter to remove pericardial fluid if the appropriate specialist is unavailable. This procedure is especially useful for generalists who work in low-resource settings where tuberculous pericarditis is relatively common.
To perform a quick, relatively safe pericardiocentesis, use ultrasound to determine the best location and trajectory for needle insertion. Scan and compare both the sub-xiphoid and apical approaches. Look for the site where the distance to pericardial fluid is minimized, and no lung tissue or vascular structures overly the heart. It is not necessary to visualize the needle as it is inserted. Instead, simply determine the safest location and angle of insertion beforehand.
A longer 7-9cm 18g needle and catheter are preferable if available. If using a standard 4.5cm 18g intravenous catheter, the sub-xiphoid approach is often unsuccessful, as the needle will stretch the tissue and not be long enough to puncture through. The pericardial space is usually more superficial when approached from the cardiac apex. After determining the best apical site and trajectory with ultrasound, prep the area and, in a sterile fashion, pass the needle between ribs just above the lower of the two, as if doing a thoracentesis. The apex of the heart also has a thicker wall and smaller coronary vessels. With a sub-xiphoid or parasternal approach, there is theoretically a higher chance of puncturing a thinner chamber wall or large epicardial coronary vessel. Ultrasound guidance reduces the risk of puncturing the lung when using an apical approach.
If available, keep the patient on continuous oxygen saturation and ECG monitoring during and after the procedure. Use an injection anesthetic beforehand for comfort, but avoid sedatives that can precipitate cardiovascular collapse. Be aware that LV or RV failure can develop when the tamponade is released if the heart cannot cope with the significant increase in cardiac filling that follows. This is known as pericardial decompression syndrome, and it may occur more often in patients with chronic effusions and underlying cardiac dysfunction.6,7 To prevent this, consider slowly draining the effusion and avoid giving multiple boluses before the procedure if you anticipate underlying cardiac dysfunction. Be prepared to sit the patient up, provide supplemental oxygen and diuretics, or even give inotropes/vasopressors or assist with ventilation.
Ultrasound guidance can minimize the risk of hitting the lung or heart and causing arrhythmias, cardiac lacerations, or pneumothorax. Ultrasound can also identify large vessels or vascular structures overlying the pericardium. Avoid the intercostal neurovascular bundle by passing the needle just above the lower rib as you would for a thoracentesis. To avoid infection, use a strict sterile technique and only leave the catheter in place if necessary.
In a series at the Mayo Clinic going back to 1979, when ultrasound was first introduced, of 1127 consecutive ultrasound-directed pericardiocentesis procedures performed by various clinicians, only 1.2% suffered complications requiring any intervention. More than 70% of these patients had had an invasive procedure or malignancy-related pericardial effusion. After careful use of ultrasound to identify the best approach location, only 21% of patients received pericardiocentesis from the sub-xiphoid approach. Five patients had chamber lacerations requiring surgical repair. One patient died (<0.1%) who had severe pulmonary hypertension, and the needle punctured the RV. Five patients developed a pneumothorax requiring a chest tube. One patient had an intercostal artery hemorrhage requiring surgery for hemostasis. One patient developed ventricular tachycardia. One patient developed bacteremia that was attributed to the pericardial catheter placement.8 A larger review suggests that patients whose pericardial effusion is associated with pulmonary hypertension, especially pulmonary artery hypertension, are at higher risk of post-procedure shock and death.7 Therefore, be aware of this risk and carefully consider whether a pericardiocentesis is necessary if the patient’s right ventricle is dilated.
Pericardial fluid can tension the pericardial sac and exert pressure on the cardiac chambers, which impairs cardiac filling. This is known as cardiac tamponade. It is not effusion size but the relationship between venous pressure and pericardial pressure that determines the hemodynamic significance of a pericardial effusion. Thus, cardiac tamponade is more common with rapid pericardial fluid accumulation, poor pericardial compliance, low venous pressure, and relatively higher intra-thoracic pressure. PoCUS can rule out the possibility of cardiac tamponade, but to rule in the diagnosis requires a combination of sonographic and traditional physical exam findings such as tachycardia, hypotension, and peripheral vasoconstriction. Basic measures are available to stabilize and prevent the progression of cardiac tamponade, but definitive treatment may require decompression with a surgical pericardial window or pericardiocentesis. Be aware that LV or RV failure can rapidly develop when the tamponade is released, and the heart cannot cope with the significant increase in cardiac filling, so be prepared with supplemental oxygen, diuretics, and potential ventilatory support.