Pericardial Tamponade

Today’s morning report case involved a woman with a previous history of metastatic malignancy presenting with dyspnea.  She was found on imaging to have a substantial pleural effusion as well as a substantial pericardial effusion.  We spoke about a number of valuable learning topics:

·      Whenever you are confronted with someone with a pericardial effusion or even a patient with a condition that would predispose to effusions, you should consider pericardial tamponade as a diagnostic entity.  Without considering it, you won’t test for it or diagnose it!

·      Conditions that predispose to effusions are:

o   Pericarditis can produce serous or blood effusions, especially for anticoagulated patients

o   Infections such as tuberculosis

o   Malignancies like lung cancer, lymphoma, or any metastatic disease

o   Uremia producing uremic pericarditis and an effusion

o   Post-myocardial infarction pericarditis leading to an effusion

o   Conditions leading to arterial bleeding within the pericardial sac (dissections, iatrogenic injury, etc.)

·      It is important to note that the pericardium is a rigid structure that can become compliant with time.  Therefore, malignant effusions that have as much as 1.5L of fluid may not produce pericardial tamponade if they develop slowly.  By contrast, 30cc of arterial blood from a coronary artery dissection immediately into a rigid pericardium can rapidly produce tamponade.

·      There are several features to find on physical examination when we discuss pericardial tamponade:

o   From a vital sign perspective, patients are often hypotensive.  This has to do with impairment of atrial info to both sides of the heart owing to increased pericardial pressure.

o   It is valuable to perform a pulsus paradoxous in this and other conditions.  The pulsus paradoxus is inaptly named because it is actually an exaggeration of a normal phenomenon.  To measure it, take a blood pressure with auscultation – when deflating the cuff slowly, you will hear Korotkoff sounds only on expiration beginning at a certain pressure.  Note this pressure and continue – you will then hear the sounds throughout the respiratory cycle.  The difference between those two pressures is the pulsus paradoxus.  Many have suggested that this phenomenon occurs due to reduced pulmonary vascular resistance upon inspiration, increased venous inflow into the RA/RV, and then septal bowing into the LV impairing LV outflow.  While this makes sense, it is not seen echocardiographically even during tamponade.  Instead, the mechanism is thought to be related to the gradient of pressure in the pulmonary veins (mostly affected by the intrathoracic pressure) and the left atrium (mostly affected by pericardial pressure).  Normally, when you breathe in, your intrathoracic pressure becomes negative meaning that there is a slight impediment to flow from pulmonary veins to left atrium.  That impediment (and the pulsus paradoxus) becomes larger if the negative pressure in the thorax increases (e.g. during an asthma exacerbation, COPD exacerbation, or pulmonary embolism) or if there is an impediment to left atrial inflow (high intrapericardial pressure).  Pulsus paradoxus does not occur (at least to the same level) with constrictive pericarditis because the issue there is not pressure being transmitted onto the atrium, but rather rigid pericardium that resists stretching as soon as the heart fills.

o   Frequently overlooked but useful according to the JAMA rational clinical exam, is tachycardia.

o   When examining the patient’s neck, you will often notice distended neck veins, once again owing to obstruction of venous inflow.

o   The JVP waveform (easier to view on a central venous catheter than by eye) will usually show a blunted y-descent which can help distinguish tamponade from other pericardial problems.  The y-descent occurs when the tricuspid valve opens and passive filling of the ventricles begins – high pericardial pressures inhibit right atrial and right ventricular inflow.  The x-descent is still prominent in tamponade because there is a vacuum phenomenon that occurs during ventricular systole allowing blood to enter despite the high pericardial pressures.

o   One often hears muffled heart sounds, but this isn’t as common as you may think.

o   On ECG, the common findings are low voltages (usually if there is a lot of pericardial fluid) and electrical alternans meaning that the QRS axis changes from beat-to-beat.  You can think of the heart “swinging” in the pericardial sac.

·      To treat tamponade, which is a mechanical problem, usually a mechanical solution is required.  Pericardiocentesis can be performed percutaneously, but surgical options such as a pericardial window are also possible.  The medical management of tamponade in the interim usually involves provision of a lot of intravenous fluids.

·      Tamponade needs to be distinguished from two other syndromes – Constrictive Pericarditis and Restrictive Cardiomyopathy.

	Tamponade	Constrictive Pericarditis	Restrictive Cardiomyopathy
Vitals	+++ Pulsus paradoxus, hypotension	Smaller pulsus, hypotension	Hypotension
JVP	Elevated	Kussmaul sign (rise with inspiration)	Kussmaul sign
Apex Beat	Impalpable	Impalpable or retracting on systole	Palpable
Heart sounds	Muffled	Pericardial knock	S3 but no knock
Ventricular Interdependence (on angiography)	High	High	None (e.g. concordant respiratory changes on simultaneous RV/LV recording)

·      It’s worth noting that there are situations where the pulsus paradoxus is absent despite the patient having tamponade.  The main one is a large atrial septal defect, which allows equalization of the atrial pressures and obliterates the pulsus.

Further Reading:

Little, W. C., & Freeman, G. L. (2006). Pericardial disease. Circulation, 113(12), 1622-1632.

Roy, C. L., Minor, M. A., Brookhart, M. A., & Choudhry, N. K. (2007). Does this patient with a pericardial effusion have cardiac tamponade?. JAMA, 297(16), 1810-1818.