CURS MEDICINA INTERNA

ANUL IV
Bolile pericardului
Definitions
• Pericardial sac: the stiff fibrous sac that contains the heart
and roots of the great vessels
• Inner layer called visceral: a membrane composed of a single
layer of mesothelial cells adherent to the epicardial surface
of the heart
• Outer layer called parietal, fibrous pericardium: about 2 mm
thick in normal humans and surrounds most of the heart; it
is largely acellular and contains both collagen and elastin
fibers.
• Pericardial space (cavity) lies between these layers
• Pericardial Sinuses
• Transverse sinus
• Oblique sinus
Pericardial Sinuses
Function of Pericardium
• May limit RV filling when LV is dilated, protecting LV against
overload & lungs from edema
• Distribute diastolic pressures evenly
• Barrier for heart when thoracic cavity inflamed
• Support structure
THE PASSIVE ROLE OF THE NORMAL
PERICARDIUM IN HEART DISEASE

• When the cardiac chambers dilate rapidly, the restraining effect of

the pericardium and its contribution to diastolic interaction can
become markedly augmented, resulting in a hemodynamic picture
resembling both cardiac tamponade and constrictive pericarditis.
• The most common example is acute RV myocardial infarction (MI) +
inferior LV MI. Here, the right heart dilates markedly and rapidly
such that total heart volume exceeds the pericardial reserve
volume. As a result of increased pericardial constraint and
augmented diastolic interaction, left- and right-sided filling
pressures equilibrate at elevated levels and a paradoxical pulse and
inspiratory increase in systemic venous pressure (Kussmaul sign)
may be observed.
• Other conditions where similar effects are seen include acute
pulmonary embolus and subacute mitral regurgitation.
Pressures
• Pressure in the pericardial sac is normally < pressure in the
heart

• Effusion can lead to greater pericardial pressure than

intracardiac pressure

• Rapid accumulation of pericardial fluid, even a small amount,

can cause the pericardial pressure > intracardiac pressure

• Slower collecting, large amounts of pericardial fluid may also

be > pressure than intracardiac, but may be tolerated longer
Pericardial Fluid
• Normally small amount (<30cc’s) of lymphatic
fluid that lies between the inner & outer layers
of the pericardium

• It usually looks echolucent

• Decreases friction during cardiac contraction

Pericardial Effusion
• Abnormal collection of fluid in the pericardial sac
• Trace, small, moderate, large; acute or chronic
• May be clear, infective or malignant effusion; may
contain fibrinous strands; trauma or cardiac surgery
complication may result in hemopericardium
• Usually first seen in posterior basal region of heart
• Then medially and laterally and around apex
• Very large effusions can lead to appearance of
swinging heart
• Can be circumferential or loculated (post-op,
trauma)
Pericardial Effusion

Sudden increase: up to 200 ml: OK

between 200 and 300 ml: can be
fatal

Slow increase: up to 2 liters: OK

Causes of Pericardial Disease
• Secondary to:
• Infection (bacterial, viral,
AIDS, fungal, TB)
• Systemic illnesses
(collagen diseases,
rheumatic fever, lupus)
• Trauma (hemo?)
• Post –op
• Neoplasm, metastasis
• Aortic dissection
• Post MI (Dressler’s
syndrome)
• Renal disease, uremia
• Radiation therapy
• Heart failure
• Metabolic disorders
• Idiopathic
• others
Symptoms
• Patient may not experience any symptoms with
minimal or mild effusion
• Depends on diagnosis
• Pericarditis
• Pericardial effusion
• Pericardial tamponade
• Constrictive pericarditis
Acute Pericarditis
• Incidence – Post mortem 1-6%, diagnosed in only 0.1% of
hospitalized patients. 5% of patients seen in emergency
rooms with CP and no MI.
• Sequelae – Cardiac tamponade
Recurrent pericarditis
Pericardial constriction
•
Etiology
Idiopathic
• Infectious : Viral (echovirus, coxsackievirus, adenovirus, cytomegalovirus, hepatitis B, infectious
mononucleosis, HIV/AIDs) Bacterial(Pneumococcus, Staphylococcus, Streptococcus,
mycoplasma, Lyme disease, Haemophilus influenzae, Neisseria meningitidis, and others)
Mycobacteria (Mycobacterium tuberculosis, Mycobacterium avium-intracellulare), Fungal
(histoplasmosis, coccidiomycosis), Protozoal
• Immune-inflammatory: Connective tissue disease(systemic lupus erythematosus, rheumatoid
arthritis, scleroderma, mixed), Arteritis (polyarteritis nodosa, temporal arteritis), Inflammatory
bowel disease, Early post–myocardial infarction, Late post–myocardial infarction (Dressler
syndrome), late postcardiotomy/thoracotomy, late posttrauma,
• Drug induced (e.g., procainamide, hydralazine, isoniazid, cyclosporine)
• Neoplastic disease Primary: mesothelioma, fibrosarcoma, lipoma, and so on / Secondary[*]:
breast and lung carcinoma, lymphomas, Kaposi sarcoma
• Radiation induced
• Early postcardiac surgery: Hemopericardium, Trauma, Post–myocardial infarction free wall
rupture
• Device and procedure related: percutaneous coronary procedures, implantable defibrillators,
pacemakers, post–arrhythmia ablation, post–atrial septal defect closure, post–valve
repair/replacement
• Dissecting aortic aneurysm / Aortic dissection
• Trauma Blunt and penetrating, post–cardiopulmonary resuscitation
• Congenital Cysts, congenital absence
• Miscellaneous Cholesterol (“gold paint” pericarditis)
• Chronic renal failure, dialysis related
• Chylopericardium
• Hypothyroidism and hyperthyroidism
Pathogenesis
1) Vasodilation:
 transudation of fluid
2) Increased vascular permeability
 leakage of protein
3) Leukocyte exudation
neutrophils and mononuclear cells

Pathology
depends on underlying cause and severity of inflammation
serous pericarditis
serofibrinous pericarditis
suppurative (purulent) pericarditis
hemorrhagic pericarditis
History
• Acute pericarditis almost always presents with chest pain.
• A few cases are diagnosed during evaluation of associated
symptoms such as dyspnea or fever or incidentally in conjunction
with noncardiac manifestations of systemic diseases such as
rheumatoid arthritis or systemic lupus erythematosus (SLE).
• The pain of pericarditis can be severe.
• It is variable in quality but often sharp and almost always pleuritic.
• It usually does not have the viselike, constricting, or oppressive
features of ischemic discomfort.
• Pericardial pain typically has a relatively rapid onset and sometimes
begins remarkably abruptly.
• It is most commonly substernal, but can also be centered in the left
anterior chest or epigastrium.
History
• Left arm radiation is not unusual.
• The most characteristic radiation is the trapezius ridge, which is
highly specific for pericarditis.
• Pericardial pain is almost always relieved by sitting forward and
worsened by lying down.
• Associated symptoms can include dyspnea, cough, and occasionally
hiccoughs.
• An antecedent history of fever and/or symptoms suggesting a viral
syndrome are common.
• Carefully review the past medical history for clues to specific
etiological diagnoses. A history of cancer or an autoimmune
disorder, high fevers with shaking chills, skin rash, or weight loss
should alert the physician to specific diseases that can cause
pericarditis.
Differential diagnosis of
chest pain
• Diagnoses most easily confused with pericarditis include
pneumonia or pneumonitis with pleurisy (which may coexist
with pericarditis), pulmonary embolus/infarction,
costochondritis, and gastroesophageal reflux disease.
• Acute pericarditis is usually relatively easily distinguished from
myocardial ischemia/infarction on clinical and other grounds,
but coronary angiography is occasionally required to resolve
this issue.
• Other considerations include aortic dissection, intraabdominal
processes, pneumothorax, and herpes zoster pain before skin
lesions appear.
• Acute pericarditis is occasionally the presenting manifestation
of a preceding, clinically silent MI.
Clinical Presentation
• Patients with uncomplicated acute pericarditis often appear
uncomfortable and anxious and may have low-grade fever and sinus
tachycardia.
• Physical Exam- 85% have audible friction rub during the course of
their disease (best heard at the left sternal border at end of
expiration with the patient leaning forward)
• The rub has three components- atrial systole, ventricular systole
and rapid ventricular filling during early diastole.
• Similar to the sound made when walking on crunchy snow.
• The rub is usually loudest at the lower left sternal border, often
extends to the cardiac apex, and is best heard with the patient
leaning forward.
• It is often dynamic, disappearing and returning over short periods
of time.
ECG
• Stages of pericarditis:
I- Diffuse ST elevation and PR segment depression
(seen in more than 80%) - in all leads except AVR
and often V1.
II- Normalization of the ST and PR
III- Widespread T- wave inversions
IV- Normalization of the T waves
• A reliable distinguishing feature is the ratio of
ST segment elevation (in millimeters) to T-wave
amplitude in lead V6; ratio > 0.24
Laboratory
• Hemogram : modest elevations of the wbc count, typically 11,000 to
13,000 ml with a mild lymphocytosis, are common in acute idiopathic
pericarditis; higher counts are an alert for the presence of other
etiologies, as is anemia.
• ESR should be no more than modestly elevated in acute idiopathic
pericarditis. Unusually high values may be a clue to etiologies such as
autoimmune diseases or tuberculosis.
• Cardiac Enzymes and Troponin Measurements
• Large numbers of patients without other evidence of myocarditis or MI
have elevated creatine kinase MB fraction and/or troponin I values. This
suggests a significant incidence of concomitant, otherwise silent
myocarditis. Pericarditis patients with elevated biomarkers of myocardial
injury almost always have ST segment elevation.
• Another concern in patients with elevated biomarkers is silent MI
presenting with subsequent pericarditis.
Chest Radiograph
• Usually normal in uncomplicated acute idiopathic pericarditis.
• Occasionally, small pulmonary infiltrates or pleural effusions are
present, presumably because of viral or possibly mycoplasma
infections.
• Other abnormalities suggest diagnoses other than idiopathic
pericarditis:
• bacterial pericarditis often occurs in conjunction with severe pneumonia,
• tuberculous pericarditis can occur with or without associated pulmonary
infiltrates
• mass lesions and enlarged lymph nodes suggestive of neoplastic disease
also have great significance.
• Pulmonary vascular congestion may signal coexistent, severe
myocarditis.
• Small to even moderate effusions may not cause an abnormal
cardiac silhouette; thus even modest enlargement is a cause for
concern that a significant effusion is present.
Echocardiography
• Normal in most patients with acute idiopathic pericarditis.
• The main reason for its performance is to exclude an
otherwise silent effusion.
• No modern data delineate the incidence of effusions in such
patients.
• Most do not have effusions, but small ones are fairly
common and not a cause for concern.
• Moderate or larger effusions are unusual and may signal a
diagnosis other than idiopathic pericarditis.
• Echocardiography is also useful in delineating whether
associated myocarditis is severe enough to alter ventricular
function, as well as in detection of MI.
Pericardial Effusion on 2D
• Echolucent space separating epicardium & pericardium
• Landmark
• Pericardial effusion is seen above DAO

• Can be difficult to differentiate from pleural effusion, which is

posterior to the DAO
Small Effusion

• Small- usually limited

to posterior region,
clear space seen in sys
& dias

• Separation of up to
1cm
Moderate Effusion
• Tend to extend laterally
to apex and anteriorly
around RV
• Echo-free space seen in
systole & diastole,
anteriorly & posteriorly
• Separation of ~ 1 - 2cm
at widest point
Large Effusion
• Large- more extension
all around, may see
swinging heart

• Separation of > 2 cm
Large Effusion
PERICARDIAL
EFFUSION AND
TAMPONADE
Etiology
• idiopathic pericarditis
• any infection,
• neoplasm (20% of large, symptomatic effusions without an obvious
cause based on routine diagnostic examination constitute the initial
presentation of a previously unrecognized cancer),
• autoimmune,
• inflammatory process (including postradiation and drug induced)
• after cardiac surgery (unusual for them to cause tamponade and they
almost always resolve within several weeks),
• severe circulatory congestion (small to moderate transudative effusions)
• blunt and penetrating trauma
• following post-MI rupture of the free wall of the left ventricle,
• complication of percutaneous cardiac procedures and device
implantation
• aortic dissection
Pathophysiology and Hemodynamics
• Cardiac tamponade is characterized by a continuum from an effusion
causing minimally detectable effects to full-blown circulatory collapse.
• Clinically, the most critical point occurs when an effusion reduces the
volume of the cardiac chambers such that cardiac output begins to decline.
• Determinants of the hemodynamic consequences of pericardial effusion
are the level of pressure in the pericardial sac and the ability of the heart
to compensate for elevated pressure.
• The pressure depends on the amount of fluid and the pericardial pressure-
volume relation.
• The compensatory response to a significant pericardial effusion includes
increased adrenergic stimulation and parasympathetic withdrawal, which
cause tachycardia and increased contractility. Patients who cannot mount a
normal adrenergic response (e.g., those receiving beta-adrenergic blocking
drugs) are more susceptible to the effects of a pericardial effusion.
• In the terminal stages of tamponade, a depressor reflex with paradoxical
bradycardia may supervene.
Pericardial Tamponade
Clinical Presentation
• History pertinent to a specific etiology may be elicited.
• Many patients with effusions also have pericardial pain. However,
effusions do not by themselves cause symptoms unless tamponade is
present.
• Patients with tamponade may complain of true dyspnea, the mechanism
of which is uncertain because no pulmonary congestion occurs
• Pericardial pain and/or a nonspecific sense of discomfort often dominate
the clinical picture.
• Patients with tamponade almost always are more comfortable sitting
forward.
• In pericardial effusion without tamponade, the cardiovascular
examination is normal except that if the effusion is large, the cardiac
impulse may be difficult or impossible to palpate and the heart sounds
muffled.
Clinical Presentation
• Tubular breath sounds may be heard in the left axilla or left
base because of bronchial compression.
• Beck's triad of hypotension, muffled heart sounds, and elevated
jugular venous pressure remains a useful clue to the presence
of severe tamponade.
• Ewart’s sign: in large PE’s an area of dullness to percussion
below left scapula
• Kussmaul’s sign: JVD that increases with inspiration
• jugular venous distention = elevated rt ht pressures
• Patients with tamponade are almost always uncomfortable,
with signs reflecting varying degrees of reduced cardiac output
and shock including tachypnea; diaphoresis; cool extremities;
peripheral cyanosis; depressed sensorium.
Clinical Presentation
• Hypotension is usually present, although in early
stages compensatory mechanisms maintain the blood
pressure.
• Tachycardia is the rule unless heart rate–lowering
drugs have been administered, conduction system
disease coexists, or a preterminal bradycardic reflex
has supervened.
• Tamponade can be confused with anything that causes
hypotension, shock, and elevated jugular venous
pressure including myocardial failure, right heart
failure caused by pulmonary embolus or other causes
of pulmonary hypertension, and RV MI.
Paradoxical pulse
• A paradoxical pulse is the rule, but it is important to
be alert to those situations in which it may not be
present.
• The paradoxical pulse is quantified by cuff
sphygmomanometry by noting the difference
between the pressure at which Korotkoff sounds
first appear and that at which they are present with
each heart beat.
• In severe tamponade, the inspiratory decrease in
arterial pressure is palpable and most obvious in
arteries that are distant from the heart.
Electrocardiogram
• The ECG abnormalities characteristic of pericardial
effusion and tamponade are reduced voltage and
electrical alternans
• Reduced voltage is nonspecific and can be caused by
several other conditions including emphysema,
infiltrative myocardial disease, and pneumothorax.
• Electrical alternans is specific but relatively insensitive
for large effusions.
• It is caused by anterior-posterior swinging of the heart
with each heartbeat.
• When pericarditis coexists, the usual ECG findings may
be present.
Note lead V1 alternating QRS amplitude
Chest Radiograph
• The cardiac silhouette remains normal until
pericardial effusions are at least moderate in size.
• With moderate and larger effusions, the
anteroposterior cardiac silhouette assumes a
rounded appearance
• Lateral views may reveal the pericardial fat pad
sign, a linear lucency between the chest wall and
the anterior surface of the heart representing
separation of parietal pericardial fat from
epicardium.
• The lungs characteristically appear oligemic.
Echocardiography
• Because of convenience and ease of application, M-mode and two-
dimensional Doppler echocardiography remain the standard noninvasive
diagnostic methods for detection of pericardial effusion and assessment
of tamponade.
• A pericardial effusion appears as a lucent separation between parietal
and visceral pericardium.
• Separation is present for the entire cardiac cycle.
• Small effusions are first evident over the posterobasal left ventricle.
• As the fluid increases, it spreads anteriorly, laterally, and behind the left
atrium, where its limit is demarcated by the visceral pericardial
reflection. Ultimately, the separation becomes circumferential.
• Ordinarily, tamponade does not occur without a circumferential effusion
and the diagnosis should be viewed with skepticism if this is not the case
• Computed tomography (CT) and magnetic resonance (MR) are more
precise than echocardiography for imaging the pericardium itself.
Pericardial Effusion
Separation between visceral
Severity and parietal pericardium /cm

Mild < 0.5

Moderate 0.5 to 2

Severe >2
Tamponade
RV collapse
M-mode Timing of Diastolic
Collapse in Tamponade
Doppler Findings w/
Tamponade
• Exaggerated (>25%) respiratory variations in peak
flow velocities of MV & TV
– TV flow increases with inspiration; decreases w/ expiration
– MV flow decreases w/ inspiration; increases w/ expiration
• Can be technically difficult in case of swinging heart

• PW Doppler of SVC & hepatic veins may also show

alterations in flow patterns
– SVC fwd flow reduced in diastole
– HV flow may show loss of fwd flow with expiration
 Doppler timing

Slower sweep speed helpful

Complications
• Reduced CO
• due to impaired ventricular filling
• HR increases to compensate for lower SV
• Hypotension

• Shock

• Death
Pericardial Vs. Pleural
Effusions
Pericardial fluid is anterior to the DAo.
Left pleural effusion can be confusing to distinguish from
pericardial effusion.
Hint: use probe to image around to the patient’s side to see
if you can better visualize a pleural effusion.
Pleural effusion is posterior to the DAo, LV & LA
Subcostal view is most helpful for effusions.
Co-existing Effusions

Pl. Effusion & Per. Effusion Pl. Effusion alone

Post-Op Effusions
• Be attentive to recent cardiac post-op patients
• May be loculated
• Hemorrhagic effusion present?
• Compressing hematoma?
• Observe chamber sizes & shape
• Investigate unexplained Doppler findings
Echo Findings
• A pericardial effusion (usually mod-lrg)
• RA systolic collapse (F. 256-257)
• RV diastolic collapse
• M-mode helpful for timing of RV collapse
• Dilated IVC with < 50% collapse with inspiration
• Swinging heart?
Important to note
• Tamponade physiology is a clinical & hemodynamic process
• Varying degrees & echo findings
• Utility of echo is in assessing for effusion
• lack of pericardial effusion can r/o tamponade, beware of missing
loculated effusion
• clinical findings must be weighed, echo findings alone do not
make this diagnosis
Pericardiocentesis
• Draining of pericardial fluid to relieve tamponade
• Needle or catheter placed with EKG or echo
guidance (with agitated saline or contrast), or
w/o guidance (blind)
• Can be done along with cath using fluoroscopy
guidance (uses contrast)
• Pericardial window can be surgically created to
drain effusion
Constrictive Pericarditis
• Thickening and stiffening of pericardium
• Layers thicken & adhere together eliminating the pericardial
space; or echo-dense fluid may be seen
• Eventually heart becomes stiff & restricts diastolic
filling….results in reduced CO
• Usually affect all 4 chambers
Constrictive Pericarditis
• Causes:
• Chronic pericarditis and fibrosis caused by
infection, neoplasm or uremia
• TB, viruses, or trauma
• Prior pericardiotomy; radiation therapy;
idiopathic
• Years following surgery
• Idiopathic
• Any restrictive cardiomyopathy present?
Pressure Changes
Clinical findings
• Pericardial knock may be heard
• rapid early diastolic filling followed by a prominent halt
of flow produces a “knock”
• Minimal pericardial effusion
• JVD; Kussmaul’s sign
• Symptoms of heart failure:
• Dyspnea, orthopnea, PND, fatigue, wt. gain, cough
• Hepatomegaly often w/ ascites or LE edema
• Often no murmurs heard
Clinical findings-cont.
• Sometimes hard to tell from myocardial process
• Low voltage EKG
• A-fib
• CXR may show cardiomegaly if effusion
• Diagnosis usually definitive by cardiac cath which
obtains diastolic pressures

• symptoms often non-specific or subtle

Echo Findings
• M-mode:
• May show thickened pericardium

• Flattened motion of the LVPW during diastole

• Railroad track sign - parallel epi/peri echoes
• Abnormal septal motion/septal bounce

• If calcific, any acoustic shadowing seen?

M-mode Findings
2D Findings
• 2D:
• Bright pericardial reflection, *beware of gain
• Pericardial effusion, if present

• Dilated, non-collapsing IVC & dilated hepatic veins

• Thickened pericardium (better evaluated from

CT/MRI)
Echo findings
Doppler Findings

• Increased MV E velocity, decreased deceleration time,

diminished A velocity (restrictive filling pattern with
respiratory variations)

• Exaggerated respiratory variations

• TV increases w/ inspiration; decreases w/ expiration
• MV decreases w/ inspiration; increases w/ expiration

• Evaluate during normal, quiet breathing

• Normal TDI E¹ and E/E¹ in patient with CHF symptoms

Diagnosing Constrictive Pericarditis V.
Restrictive CM
• Constrictive pericarditis
• Restrictive pattern w/
increased resp. variation
• Nml chamber sizes
• Thickened pericardium
• Abn. septal motion
• TDI E¹ nml
• MV Vp increased
• Restrictive cardiomyo.
• Restrictive pattern w/ nml
resp. variation
• Biatrial enlargement
• Nml pericardial thickness
• Nml septal motion
• TDI E¹ reduced
• MV Vp reduced
• Eval for infiltrative dz
Pericardial Tumor
• Mesothelioma can involve pericardium
• Primary tumors are rare

• Metastatic involvement occurs more often due

to CA of lung, breast, melanoma, lymphoma,
leukemia, others

• Benign pericardial cyst, clot, lipomas, or

teratoma may be found within the pericardium
• Cysts are echolucent, often near RA
Tumor cont’d

• Tumors by 2D echo generally echogenic w/o

distinct border located on pericardial surface

• Metastases usually accompanied by large

effusion; w/ or w/o tamponade
TEE
• Better in detecting pericardial thickness,
metastases or intrapericardial clot

• Comparable to CT and MRI for measuring

thickness of pericardium