72. Case Report: Effusive Constrictive Pericarditis – University Hospitals Case Western

CardioNerds (Amit Goyal & Karan Desai) join University Hospitals Cleveland Medical Center cardiology fellows (Tarek Chami, Jamal Hajjari, and Haytham Mously) for some amazing pizza and coffee in Cleveland, Ohio! They discuss an important case of effusive constrictive pericarditis. Dr. Brian Hoit provides the E-CPR and assistant program director Dr. Claire Sullivan provides a message for applicants. We are grateful to chief fellow Scott Janus for his leadership in planning this episode! Episode notes were developed by Johns Hopkins internal medicine resident Colin Blumenthal with mentorship from University of Maryland cardiology fellow Karan Desai. Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her mid-70s presented to clinic with subacute onset shortness of breath. Her past medical history includes metastatic breast cancer s/p mastectomy, chemo/radiation, and hormonal therapy. Exam notable for tachycardia without hypoxia, muffled heart sounds, JVD with Kussmaul's sign, and 1+ LE edema. The patient was sent to the ED for evaluation of possible pericardial effusion. CTA chest in ED did not demonstrate a PE, but did show bilateral pleural effusions, and a moderate pericardial effusion with evidence of metastatic disease extending into the mediastinum. TTE obtained showing normal LVEF, moderate pericardial effusion with thickened pericardium, and significant respirophasic tricuspid and mitral inflow variations. Pulsus paradoxus was manually checked and found to be 16 mmHg. Due to concern for cardiac tamponade, she was taken to the cath lab for a RHC and pericardiocentesis. RHC prior to pericardiocentesis showed elevated left and ride sided filling pressures, blunted y decent in the RA, and equalization of diastolic pressures. Pericardiocentesis yielded 200 cc of bloody fluid with improvement, but continued elevation, in her L and R sided pressures. Blunted y decent did give way to a now rapid y descent concerning for constrictive pericarditis. She then underwent a cardiac MRI showing respirophasic septal motion suggestive of interventricular dependence and >1 cm thick pericardium with LGE c/w inflammation. Unfortunately, cytology of pericardial fluid was c/w a malignant effusion and despite treatment with a few months of anti-inflammatory therapy her symptoms did not improve. She then underwent a pericardial stripping with subsequent resolution of her symptoms. As her symptoms and hemodynamics were related to both the effusion and constriction, she was ultimately diagnosed with effusive constrictive pericarditis. Case Media ABCDEFGHIJKLMNOClick to Enlarge A. ECGB. CXRC-F. TTE (inflow velocities (mitral and tricuspid), IVC sniff test G-L: Right heart catheterization tracings M-N: Post pericardiocentesis TTE: Tissue Doppler O: Cardiac MRI CT Scan TEE - 1 TTE - 2 TTE - 3 TTE -4 CMR -1 CMR - 2 Episode Schematics & Teaching Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case What is cardiac tamponade, what causes it, and how does it lead to hypotension? The pericardial cavity typically holds 50 cc of fluid, which acts as a lubricant for the beating heart. Accumulation of additional fluid in this space can increase intrapericardial pressure and cause compression of the cardiac chambers. Rapid accumulation of small amounts of fluid can lead to tamponade as the pericardium will not have time to expand. In instances of a slow accumulation, large volumes might accumulate before tamponade occurs as the pericardium will expand to accommodate the fluid. Many conditions can cause tamponade. The most common are malignancy (>50% of all cases), infection (viral most common, though TB is common in developing countries), trauma/post procedural (e.g. cardiac surgery, pacemaker placement), uremia, rheumatologic (e.g. SLE, RA), drug induced (e.g. hydralazine, procainamide), and radiation-induced. Note the epidemiology is different from causes of pericarditis without tamponade. Increasing pericardial pressure leads to a compensatory increase in diastolic pressure in all chambers until they become similar to the pericardial pressure. This happens more rapidly in the right side of the heart due to lower diastolic pressures in these chambers. The elevated intracardiac diastolic pressures reduces the driving pressure for filling (Flow = pressure gradient / resistance and so ↓∆P = ↓Flow ); this reduces diastolic filling (preload) and a causes a compensatory increase in contractility and heart rate to maintain stroke volume and cardiac output (CO = HR x SV so as SV decreases, the HR increases). As diastolic filling continues to decrease the transmural distending pressure of the RA and RV will also decrease and eventually lead to diastolic collapse. As reviewed in previous posts (Mayo and Tennessee), as ventricular interdependence worsens, left ventricular cardiac output can be further compromised and contribute to hypotension. Enjoy Episodes #58 and #59 discussing constrictive pericarditis. Tamponade can be a difficult clinical diagnosis. How is it diagnosed, what are some of the basic clinical markers of cardiac tamponade, and which are most useful in diagnosis? Though definitive diagnosis requires pericardiocentesis with hemodynamic and clinical improvement, there are many features that are useful for identifying tamponade. Unfortunately, no one clinical or echocardiographic feature is diagnostic of tamponade and a clinical diagnosis relies on the assimilation of multiple abnormalities. Beck's triad of hypotension, jugular venous distension, and muffled heart sounds Originally described in 1935 by Dr. Claude Beck, it focuses on these signs of tamponade, which were derived from surgical patients and are more characteristic of acute tamponade from trauma or cardiac/aortic rupture. Though ~90% of patients in trauma series have at least one of these findings, only about ~30% have all three. Muffled heart sounds and hypotension are both poorly sensitive findings, making the sensitivity of the overall triad poor. Tachycardia Though not specific, tachycardia is a very sensitive marker of cardiac tamponade as in some series it is present in 81-100% of patients with a pooled sensitivity of around 80%. Elevated JVP Elevated JVP is one of the key findings in tamponade and is present in almost all cases. Increased early diastolic pressure limits filling during this period, blunting the y descent. Studies show sensitivity ranges from 53-88% with a pooled average of 75%. Kussmaul's sign Kussmaul's sign is the failure of the JVP to fall during inspiration. This is rarely seen in cardiac tamponade; it is much more common in constrictive pericarditis, where it can be seen in up to 50% of cases. EKG findings of low voltage or electrical alternans As fluid builds around the heart it can insulate the heart's electrical activity from the EKG leads leading to low voltage on the EKG. Additionally, as the heart oscillates within the distended pericardial sack, the QRS amplitude can oscillate, which is called electrical alternans. As low voltage can be seen in a variety of conditions it is poorly specific, but sensitivity is around 70%. Electrical alternans on the other hand is rarely seen in tamponade, but if present it has a PPV > 95%. Enlarged cardiac silhouette on CXR The cardiac silhouette on a CXR does not appear enlarged until a pericardial effusion is around 200 mL. Given that many conditions also cause an enlarged silhouette it has both poor sensitivity and specificity. What is a pulsus paradoxus and what is the pathophysiology? How do you measure it and how clinically useful is it in the diagnosis of tamponade? What conditions might cause it to be absent in tamponade? In a normal heart, inspiration decreases intrathoracic pressure, thus increasing right-sided filling. As the RV stretches to accommodate the volume, the interventricular septum bulges towards the left causing reduced left-sided filling and therefore a drop in blood pressure (this is ventricular interdependence). During expiration the opposite happens and the blood pressure increases. This process is exaggerated in cardiac tamponade as both ventricles are completing for a limited amount of space, which leads to a larger than normal drop in blood pressure during inspiration. This exaggerated drop is called pulsus paradoxus (though pulsus exaggeratus may be a better name!). Pulsus paradoxus can be measured with a blood pressure cuff while a patient is breathing normally.