Effusion

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Pericardial Effusion - Tamponade

Anatomy of the Pericardium

The pericardium is a complex, fibrous structure that outlines and encloses the heart. This structure is anchored at the base to the great vessels and inferiorly to the diaphragm. It is composed of three main elements: the visceral layer, the parietal layer, and the pericardial fluid. The heart muscle's outer layer, the epicardium (which is also the visceral pericardium), is separated from the parietal pericardium by the pericardial sac, which contains the fluid. The pericardial tissue is highly echogenic. In terms of fluid, the pericardial space normally contains a few millilitres (ml) of serous fluid. Under normal conditions, the intrapericardial pressure is slightly negative, typically around -3 mmHg.

The pericardium serves several vital functions, including protecting the heart within the chest cavity, preserving myocyte function under stress, distributing hydrostatic forces over the heart, limiting acute distention of the heart chambers, and excluding extracardiac or intrathoracic disease from extending into the heart. The parietal pericardial layer is also key to ventricular interdependence, a phenomenon where this layer limits the heart's overall volume, meaning that the filling of one ventricle affects the filling of the other. Anatomically, the interatrial septum is bounded posteriorly by a fold of the pericardium in the pyramidal space, which forms the oblique sinus.

Pericardial Effusions and Cardiac Tamponade

A pericardial effusion is defined by the existence of an echo-free space between the epicardium and the parietal pericardium, indicating fluid accumulation. This accumulation results from diseases or external/iatrogenic trauma. When the effusion is large, fluid accumulates anteriorly between the right heart border and the chest wall, as well as posteriorly behind the left ventricle (LV). In patients with a large effusion, the whole heart may exhibit a characteristic pendular motion within the pericardial sac. Fibrinous material may sometimes be demonstrated within the effusion. Most effusions seen in pediatric patients are post-surgical and tend to resolve spontaneously. In neonates, effusions can be caused by hydrops fetalis, central venous catheter complications, or post-pericardiotomy syndrome. It is essential to differentiate a pericardial effusion from a pleural effusion, as both may cause an echo-free space behind the LV posterior wall. A pleural effusion differs from a pericardial effusion in that the pericardial echo will be in front of the echo-free space rather than behind it.

Cardiac tamponade is a critical state resulting from the increase in fluid volume and resulting intrapericardial pressure, which compresses the cardiac chambers and restricts filling, leading to a decrease in cardiac output. The speed of fluid accumulation is crucial, as a rapid accumulation can produce tamponade at much smaller volumes compared to a slow, chronic accumulation. Clinically, tamponade is often suspected due to findings such as low blood pressure, tachycardia, muffled heart sounds, low cardiac output symptoms, jugular venous distention and pulsus paradoxus. Pulsus paradoxus is characterized by a decline in systolic pressure greater than 10 mmHg during inspiration. The high pericardial pressure exerts its primary hemodynamic effect by impeding right heart filling. This elevated pressure causes the chamber wall to collapse in mid-diastole when the intrapericardial pressure exceeds the intracavity pressure. 

Echocardiographic signs of tamponade include an abnormal posterior motion or collapse of the right ventricular free wall in early diastole. Compression or marked concavity/inversion of the right atrial free wall is also a useful marker, particularly if prolonged during the cardiac cycle. In the context of tamponade, the physiological phenomenon of ventricular interdependence is emphasized: right ventricular filling is maintained at the expense of restricted left ventricular filling during inspiration, resulting in a greater reduction in systemic output. The urgency for drainage depends on the clinical picture, but in acute cardiac tamponade, immediate decompression via surgical drainage or pericardiocentesis is indicated and is potentially lifesaving

Pulsus paradoxus refers to an exaggerated inspiratory drop in systemic systolic blood pressure. Although the term was originally coined by Kussmaul to describe the apparent paradox of a weakening peripheral pulse despite preserved precordial activity, the physiologic direction of change is not truly paradoxical, as systolic pressure normally falls slightly during inspiration. Despite its name, pulsus paradoxus remains the most valuable bedside sign of cardiac tamponade, with a sensitivity of approximately 85% and specificity of around 76%. It may, however, be absent in certain conditions such as profound hypotension, pericardial adhesions, marked ventricular hypertrophy, atrial septal defect, severe aortic regurgitation, or other unusual hemodynamic states. The mechanism reflects increased ventricular interdependence within a constricted pericardial space. In normal physiology, inspiration augments venous return to the right heart, and the right ventricle expands outward with minimal compromise to the left heart. In tamponade, the pericardial sac becomes noncompliant due to acute fluid accumulation or marked chamber distension, so intracardiac diastolic pressures equilibrate and the heart has no room to accommodate changes in volume. During inspiration, the increase in right ventricular filling can only occur at the expense of the left ventricle, with septal shift limiting left ventricular diastolic volume, reducing stroke volume, and producing an exaggerated fall in systolic blood pressure with inspiration. Reference Here. Conditions that will mask pulsus paradoxus: Large ASDs; Aortic regurgitation; Right ventricular hypertrophy; Hypotension; Pericardial adhesions.

• RA systolic collapse 

  • Intrapericardial pressure > RA pressure 

  • Brief right atrial collapse can occur in the absence of tamponade physiology!! 

  • Inversion for >1/3 of systole has a high sensitivity and specificity for tamponade (94% sensitive 100% specific) 

  • In reality, RA collapse is hard to use as a parameter in neonates

• Reciprocal changes in RV and LV volumes 

  • Inspiration: Increase in RV volume, Decrease in LV volume, Septal shift to the LV

  • Expiration: Decrease in RV volume, Increase in LV volume, Normalization of septal motion

  • Correlation with pulsus paradoxus

  • The total pericardial volume (heart chambers + pericardial fluid) is fixed. When intrathoracic pressure becomes more negative during inspiration, enhanced RV filling limits LV filling. This pattern reverses during expiration

• Reciprocal changes in RV and LV filling 

  • The mitral and tricuspid valve inflows, and the Aortic and pulmonary outflow, and hepatic vein flow show large swings in amplitude. Exaggerated respiratory variation in the transvalvular flow is an important indicator of significant hemodynamic effusion. Normally, there is no more than ~10% variation in the amplitude of inflow and outflow signal. In tamponade, it can exceed 30%. 

  • Increased tricuspid valve inflow variability on spectral PW-Doppler (normal <40%); TV: Enhanced right ventricular diastolic filling with inspiration and a reversal of this pattern during expiration. >40% variation (E wave increases by more than 40% compared with expiration - some uses 50%) is not normal.

  • Increased mitral inflow variability on spectral PW-Doppler (normal <25%). MV: Enhanced left ventricular diastolic filling with expiration and a reversal of this pattern during inspiration >30% variation (E wave decreases by more than 30% compared with expiration) is not normal. Some use 10% as a cut-off for abnormal. 

• Inferior vena cava plethora

  • Dilated inferior vena cava 

  • In adults, >20mm in diameter 

  • Not very specific since plethora also seen in RV failure, pericardial constriction, and mech. ventilation!

Echocardiography examples

Pericardial effusion. Measurement should be taken in diastole. Tamponade is a diastolic problem, with restrictive filling. Here, the effusion seems circumferential. Not surprisingly, in a newborns that is lying on his back, the effusion collects posteriorly along the posterior wall of the LV. The fluid can be seen in parasternal short and long axis view in this particular case.

Evaluation of restricted filling - PW of RV and LV inflow. 

• • Increased tricuspid valve inflow variability on spectral PW-Doppler (normal <40%)

  • Increased mitral inflow variability on spectral PW-Doppler (normal <25%)

A good practice is to compress sweep time in order to observe variation in inflow Doppler velocities. This may be altered in individuals that are not spontaneously breathing.

Ref: https://pedecho.org/library/chd/pericardial-tamponade

Measurements should be done at the end of diastole. Here, as outlined by the ECG tracing, just before the P-wave.

Ultrasound signs of Tamponade

Right atrial collapse during ventricular contraction / systole. 

Swinging Heart (M-mode echocardiography): The heart appears to swing back and forth within the pericardial sac during systole and diastole due to the restricted movement caused by the pericardial effusion.

Respiratory flow variation across the atrio-ventricular valves (mitral or tricuspid). Doppler Surrogate of Pulsus Paradoxus.

Right ventricular collapse during ventricular relaxation (diastole) - tamponade is a diastolic and filling condition. This could be appreciated by M-Mode.

Inferior vena cava distended with minimal respiratory variability

More Information Here and Here.

Long axis subcostal / subxyphyoid view outlining circumferential pericardial effusion with collapse of the right atrium.

Subcostal/subxyphoid short axis view outlining circumferential effusion. The IVC is seen distended and without variation in caliber. This outlines some degree of tamponade physiology.

Apical view outlining the RV and RA collabse. RA collabse during systole and RV collapse during diastole. Large effusion not obliterating during diastole.

Parasternal views (long and short axis). One may appreciate the RV collapse during diastole, as well as the circumferential pericardial fluid. 

Emergency Pericardiocentesis Procedure

If doing echo-guidance - can use the subcostal or parasternal views. Regardless if echo-guidance or not, one should confirm diminished effusion (and improved flow mechanics) at the end of the case.

Multi-Disciplinary Pediatric Point of care Ultrasound Bootcamp Simulation Scenario 

The crashing neonate

Case shared by Dr Brahim Bensouda from Hôpital Maisonneuve Rosemont 

A newborn presented initially with significant retractions without bradycardia. Dr Bensouda, TnECHO specialist and Neonatologist member of the TnECHO Quebec Collaborative, had done the workshop on pericardiocentesis and had trained through simulation on how to perform this technique at the bedside. A TnECHO was obtained and the images are shared below.

The views above are in the subcostal area showing a large pericardial effusion. There is altered filling and contractility. The heart is moving in the pericardial pocket during contraction. The liquid is anechoic (black appearance). 

Milky pink fluid aspirated by emergency pericardiocentesis. After puncture, it is important to remove the needle from the catheter to avoid puncture of the muscle wall upon re-expansion while draining the pericardial fluid. The fluid should be sent for cytology / cell count (especially for lymphocytes), culture, total protein, LDH albumin level, triglycerides and biochemistry (electrolytes and glucose) - to evaluate if presence of total parenteral nutrition (TPN) fluid and intravenous lipid fluid. In this case, upon fluid drainage, one can see that the heart function is back to normal with adequate filling. A catheter is seen in the right atrium, which has been withdrawn.  The fluid analysis was compatible with extravasated TPN/Lipids. 

Pericardial Fluid Tests to Send

These are only considerations and should be tailored to the case scenario:

• Cell count + differential. High lymphocytes if chyle (typically the triglycerides will not be increased if the patient is NPO)

• Protein and Albumin

• LDH

• Glucose

• Infectious: 

  • Gram stain + bacterial culture

  • If consideration for viral: Viral PCR (especially enterovirus, CMV, HSV, adenovirus)

  • AFB stain + mycobacterial culture (if risk factors, for example for tuberculosis)

  • Fungal culture (if immunocompromised or post-surgical) 

• Cytology (if concern for malignancy, rare in neonates)

• pH (optional; mainly pleural fluids but can help differentiate infection)

• Triglycerides (if concern for chylopericardium)

• Cholesterol (helps differentiate chyle vs pseudochyle)

• Amylase (very rarely indicated; if concern for fistula/post-operative)

• Serum (paired)

  • Serum protein + LDH (Light’s criteria-style assessment)

  • Serum triglycerides

  • Serum inflammatory markers (CRP, procalcitonin)

  • Blood cultures (if concern for sepsis)

• If postoperative / ECMO / catheter-related

  • Consider pericardial drain tip culture

  • Heparin-PF4 antibody (if ECMO and thrombosis concerns)

Bilateral pleural effusions in the subxyphoid view.

Example of a right sided pleural effusion (before drainage)

After drainage:

Variations in inflow velocity explained

The variations in inflow velocity observed in cardiac tamponade, especially more pronounced on the right ventricle (RV) side compared to the left ventricle (LV) side, can be explained by the following mechanisms:

1. Intrathoracic Pressure Changes:

   • During respiration, intrathoracic pressure changes influence the venous return to the heart. In cardiac tamponade, the pericardial pressure is elevated and restricts the heart's ability to expand. However, the RV, being more compliant and under lower pressure compared to the LV, is more susceptible to these pressure changes.

   • During inspiration, the negative intrathoracic pressure increases venous return to the right side of the heart (RV). However, because the heart is constrained by the tamponade, this increased venous return cannot be accommodated, leading to an increase in RV inflow velocity. During expiration, the opposite occurs, reducing venous return and RV inflow velocity.

2. Ventricular Interdependence:

   • In cardiac tamponade, the constrictive pressure affects all chambers of the heart equally, but due to the fixed pericardial volume, any increase in volume of one chamber must be accompanied by a decrease in volume of another chamber. This interdependence is more noticeable in the RV because it is more affected by changes in intrathoracic pressure.

   • When the RV fills more during inspiration, it can lead to a transient reduction in LV filling (due to the shifting of the interventricular septum toward the LV). This mechanism results in less variation in LV inflow velocities because the LV operates at higher pressures and is less influenced by the intrathoracic pressure changes compared to the RV.

3. Pericardial Constraint:

   • The pericardial fluid in tamponade creates an equal pressure environment around the heart, but the thin-walled RV is more affected by this external pressure compared to the thicker-walled LV. Thus, changes in intrathoracic pressure during the respiratory cycle have a more significant impact on the RV filling dynamics.

4. Pressure-Volume Relationship:

   • The RV operates at lower pressures compared to the LV and is more compliant. This means the RV can accommodate changes in volume more readily than the LV, but within the constrained environment of tamponade, these changes manifest as variations in inflow velocity. The LV, being stiffer and working under higher pressures, exhibits less variation in inflow velocity under the same conditions.

Clinical findings in Tamponade

Symptoms:

1. Poor Feeding: Newborns may refuse to eat or have difficulty sucking.

2. Irritability or Lethargy: They may appear more irritable or unusually sleepy.

3. Tachypnea: Fast breathing due to decreased cardiac output and poor oxygenation.

4.  Pallor or Cyanosis: Pale or bluish skin indicating poor perfusion and oxygenation.

5. Decreased Urine Output: Oliguria due to reduced renal perfusion.

Physical Examination Findings:

1. Beck's Triad:

   • Hypotension

   • Hepatomegaly or Distended Neck Veins (Difficult to observe in newborns, but may be suggested by bulging fontanelles).

   • Muffled Heart Sounds: On auscultation, heart sounds may be faint due to the insulating effect of pericardial fluid.

2. Tachycardia: Rapid heart rate as a compensatory mechanism.

3. Pulsus Paradoxus: May be difficult to assess in newborns but can be inferred from significant respiratory variations in blood pressure.

4. Hepatomegaly: Enlarged liver due to venous congestion, palpable under the right costal margin.

5. Poor Peripheral Perfusion, Cold extremities, prolonged capillary refill time.

Diagnostic Test Findings:

1. Electrocardiogram (ECG): Low voltage QRS complexes and electrical alternans might still be seen, though obtaining a good quality ECG can be challenging.

2. Chest X-ray: Enlarged cardiac silhouette. A central line positioned in the heart may be the etiology of the tamponade/effusion (as such, one have to stop the fluid from running as one of the first step of management).a

3. Echocardiography (Echo): 

   1. Pericardial Effusion: Presence of fluid around the heart is easily visualized (usually anechoic around the heart and the subcostal view being the best approach).

   2. Diastolic Collapse: Collapse of the right atrium and ventricle due to increased pericardial pressure.