Pericardial Effusion

Signs and symptoms

Chest Pain, pressure, discomfort

Light headedness, syncope
Palpitations
cough
dyspnea
Hoarseness
Anxiety and confusion
Hiccoughs

Diagnosis -> Physical Exam Findings

Classic Triad of Beck of Pericardial Tamponade

-Hypotension, muffled heart sounds, jugular venous distension

Pluses Paradoxus
Pericardial friction rub
Tachycardia
Hepatojugular reflux
Tachypnea
Decreased breath sounds
Ewart sign -> Dullness to percussion beneath the angle of left scapula
Hepatosplenomegaly
Weakened peripheral pulses, edema, and cyanosis

Lab Tests

Electrolyte levels
CBC with diff count
Cardiac biomarkers -> Troponin T, CK-MB, LDH (Elevated)
ESR, CRP
TSH
Blood Cultures
RF Levels
Immunoglobulin complex tests
ANA tests
Complement Levels
Pericardial fluid analysis

Early in the course of acute pericarditis, the ECG typically displays diffuse
ST elevation in association with PR depression; the ST elevation is usually
present in all leads except for aVR, although in postmyocardial infarction
pericarditis, the changes may be more localised.
 Management

Most acute idiopathic or viral pericarditis occurrences are self-limited

and respond to treatment with an NSAID. Prednisone may be
administered for severe inflammatory pericardial effusions or when
NSAID treatment has failed.

Autoimmune pericardial effusions may respond to treatment with anti-

inflammatory medications. In general, selection of an agent depends
on the severity of the patient's symptoms and the tolerability and
adverse-effect profiles of the medications.

Pharmacotherapy for pericardial effusion includes use of the following

agents, depending on the etiology:

NSAIDs (eg, indomethacin, ibuprofen, naproxen, diclofenac, ketoprofen,

aspirin)
Corticosteroids (eg, prednisone, methylprednisolone, prednisolone)
Anti-inflammatory agents (eg, colchicine)
Antibiotics (eg, vancomycin, ceftriaxone, ciprofloxacin, isoniazid,
rifampin, pyrazinamide, ethambutol)
Antineoplastic therapy (eg, systemic chemotherapy, radiation)
Sclerosing agents (eg, tetracycline, doxycycline, cisplatin, 5-
fluorouracil)
Hemodynamic support for pericardial effusion includes the following:

Hemodynamic monitoring with a balloon flotation pulmonary artery

catheter
IV fluid resuscitation
Surgical treatments for pericardial effusion include the following:

Pericardiostomy
Pericardotomy
Thoracotomy
Sternotomy
Pericardiocentesis
PhysiologyThe pericardial space normally contains 15-50 mL of fluid,
which serves as lubrication for the visceral and parietal layers of the
pericardium. This fluid is thought to originate from the visceral
pericardium and is essentially an ultrafiltrate of plasma. Total protein
levels are generally low; however, the concentration of albumin is
increased in pericardial fluid owing to its low molecular weight.The
pericardium and pericardial fluid provide important contributions to
cardiac function, including the following:
The parietal pericardium contributes to resting diastolic pressure, and
 is responsible for most of this pressure in the right atrium and ventricle
Through their ability to evenly distribute force across the heart, the
pericardial structures assist in ensuring uniform contraction of the
myocardium
The normal pericardium can stretch to accommodate a small amount
of fluid without a significant change in intrapericardial pressure,
although once this pericardial reserve volume is surpassed, the
pressure-volume curve becomes steep. With slow increases in volume,
however, pericardial compliance can increase to lessen the increase in
intrapericardial pressure.PathophysiologyClinical manifestations of
pericardial effusion are highly dependent on the rate of accumulation
of fluid in the pericardial sac. Rapid accumulation of pericardial fluid
may cause elevated intrapericardial pressures with as little as 80 mL of
fluid, while slowly progressing effusions can grow to 2 L without
symptoms.Understanding the properties of the pericardium can help to
predict changes within the heart under physiologic stress.By
distributing forces across the heart, the pericardium plays a significant
role in the physiologic concept of ventricular interdependence,
whereby changes in pressure, volume, and function in one ventricle
influence the function of the other.The pericardium plays a pivotal role
in cardiac changes during inspiration. Normally, as the right atrium and
ventricle fill during inspiration, the pericardium limits the ability of the
left-sided chambers to dilate. This contributes to the bowing of the
atrial and ventricular septums to the left, which reduces left ventricular
(LV) filling volumes and leads to a drop in cardiac output. As
intrapericardial pressures rise, as occurs in the development of a
pericardial effusion, this effect becomes pronounced, which can lead to
a clinically significant fall in stroke volume and eventually progress to
the development of pericardial tamponade.The pericardium plays a
beneficial role during hypervolemic states by limiting acute cardiac
cavitary dilatation.EtiologyThe cause of abnormal fluid production
depends on the underlying etiology, but it is usually secondary to
injury or insult to the pericardium (ie, pericarditis). Transudative fluids
result from obstruction of fluid drainage, which occurs through
lymphatic channels. Exudative fluids occur secondary to inflammatory,
infectious, malignant, or autoimmune processes within the
pericardium.In up to 60% of cases, pericardial effusion is related to a
known or suspected underlying process. Therefore, the diagnostic
approach should give strong consideration to coexisting medical
conditions.PrognosisMost patients with acute pericarditis recover
without sequelae. Predictors of a worse outcome include the following:

Fever greater than 38C

Symptoms developing over several weeks in association with
immunosuppressed state
 Traumatic pericarditis
Pericarditis in a patient receiving oral anticoagulants
A large pericardial effusion (>20 mm echo-free space or evidence of
tamponade)
Failure to respond to nonsteroidal anti-inflammatory drugs (NSAIDs)
Pericardial tamponadePericardial tamponade, which is heralded by the
equalization of diastolic filling pressures, can lead to severe
hemodynamic compromise and death. It is treated with expansion of
intravascular volume (small amounts of crystalloids or colloids may
lead to improvement, especially in hypovolemic patients) and urgent
pericardial drainage. Positive-pressure ventilation should be avoided, if
possible, as this decreases venous return and cardiac output.
Vasopressor agents are of little clinical benefit.