Daryoosh Derakhshan, PGY IV

Pericardial
Pericardium
Fibrous (outer) and Serosal (inner) components
Fibrous sac:
Composed of collagen fibers with interspersed short elastic fibrils
Continuous with the adventitia of the great vessels superiorly and attached to the central tendon of the diaphragm inferiorly.
Attached anteriorly to the sternum by sternopericardial ligaments.
Anterioinferior contact with costal cartilages of the left 4th to 6th ribs.
Lateral surfaces in contact with parietal pleura.
Posterior relation to major bronchi, esophagus, and descending thoracic aorta.
Phrenic nerves and pericardiophrenic vessels contained between the fibrous pericardium and the
mediastinal pleura
Serosal layer
Single layer of mesothelium that forms a parietal and visceral layer enclosing the pericardial cavity
Parietal layer + fibrous sac = parietal pericardium
Visceral layer AKA the epicardium
Epicardial adipose tissue exists between the visceral pericardium and the myocardium
Epicardial fat contains the coronary arteries, veins, lymphatics and nerve tissue.
LV contains little epicardial fat resulting in poor visualization or pericardium in this region
Parietal pericardium is between 0.8 to 1 mm thick
TTE unreliable for measuring pericardial thickness, however TEE has been shown to be reproducible.
Pericardial cavity normally contains less than 50ml of serous fluid.
Pericardial sinuses and
recesses
Transverse Sinus
A passage that separates the arteries located anteriorly from the atrial and veins posteriorly
Lies behind the ascending aorta and main pulmonary artery, above the roof of the LA
Extends upward along the right side of the ascending aorta, forming the Superior aortic recess
(between aorta and SVC)
Space between the ascending aorta and the RA is called the Inferior aortic recess.
It extends laterally, inferior to L and R pulmonary arteries, forming the L and right pulmonic
recesses.
Postcaval recess is an extension of the pericardial cavity which lies behind and on the right lateral
aspect of SVC.
Oblique Sinus
A cul-de-sac located behind the LA, delineated by the pulmonary veins and the IVC, leaning against
the carina.
Functions of the pericardium
Acute Pericarditis
Diagnosis of acute pericarditis is based on (2 or more)
(1) Atypical chest pain
(2) Pericardial rub
(3) Typical ECG changes
(4) New or worsening pericardial effusion
Other findings
Elevated CRP or ESR
Fever
Elevated WBC
Elevated Troponins
TTE can be helpful in differentiating acute pericarditis from myocardial
ischemia/injury by excluding wall motion abnormalities (5% of pts with pericarditis
demonstrate segmental wall motion abnormalities)
TTE to evaluate for pericardial effusion or tamponade physiology
CT: Transudative effusion (< 10 HFU), Exudative effusion ( 20-60 HFU),
Hemorrhagic (> 60 HFU)
Pericardial effusion
Pericardial Effusion
Fluid > 50cc is abnormal
50-100cc mild <10mm
100-500cc moderate 10-20mm
>500cc large 20-25mm
> 25mm very large
Measured in diastole
Transudative, Exudative, Hemopericardium, or pyopericardium
Aorta in parasternal long axis used as a point to differential between pericardial
and pleural effusions
Preferential accumulation of fluid posterolateral to the LV, along the inferolateral
wall of RV, and in the superior pericardial recess.
Cardiac Tamponade
A life-threatening condition caused by fluid accumulation in the pericardial sac that compresses the
cardiac chambers and inhibit normal filling
Characterized by elevation and equalization of cardiac diastolic and pericardial pressures, reduced
cardiac output, and an exaggerated inspiratory decrease in systolic BP > 10 mmHg (Pulsus
Paradoxus)
Types: (1) Acute/subacute/chronic (2) regional (3) Low-pressure
Low pressure tamponade:
secondary to overdiuresis, hemodialysis, hemorrhage, poor oral intake or vomiting
Cardiac filling is severely impaired, however the equalized pericardial and end-diastolic intracardiac pressures are normal at
< 10 mmHg.
Regional tamponde
Most often seen after cardiac surgery, pericardiotomy, or myocardial infarction.(early or late)
Mild tamponade (PEff pressure < 10 mmHg) general asymptomatic, moderate to severe tampoade
(PEff pressure > 15 mmHg) develop symptoms (tachycardia, dyspnea)
Hypotension is a late sign of tamponade, since heightened sympathetic tone maintains BP as CO is
decreasing
Compensatory mechanisms: (1) Tachycardia; (2)Increased systemic venous pressure; (3) Arterial
vasoconstriction
Cardiac filling occurs mostly during ventricular systole in tamponade (due to lower intrapericardial
pressures)
Ventricular Interdependence
Bulging of interventricular septum into the left ventricle during inspiration
secondary to increased CV return to the right heart decreased LV diastolic
filling decreased SV and CO (Pulsus Paradoxus)
Bulging of the IVS into the RV during expiration decreased RV diastolic filling
This phenomenon is responsible for the opposite respiratory variation seen in
mitral and tricuspid inflow.

Pulsus Paradoxus may be absent if coexisting: (1) Aortic insufficiency

(2) Atrial Septal Defect (3) Elevated LVEDP
Respiratory variation of valvular flow
Normally, respiratory change in peak E-wave mitral flow velocity is < 5%, with
minimal change in IVRT.
In tamponade this change is exaggerated
Greatest change in Mitral and Tricuspid inflow velocities (E-wave) are seen in the
first beat in inspiration and expiration (opposite effects)
During inspiration flow across TV increases (increased E-wave velocities) but flow across mitral
valve decreases (decreased E-wave velocities)
During expiration the opposite occurs
Respiratory variation of > 25% in Mitral inflow E-wave and > 60% in Tricuspid
inflow E-wave indicates tamponade physiology
Impaired inflow pattern
Chamber collapse
Chamber collapse occurs when intrapericardial pressures are above intracardiac pressures
This occurs when right atrial and right ventricular pressures are lowest, during their
relaxation phase
RA collapse occurs at early systole (near the peak of R-wave on ECG)
RV collapse occurs at early diastole (after the end of T-wave) Sens of 60-90%, Spec of 85-100%
RA collapse > 1/3 the R-R interval if involves > 30% of RA wall is nearly 100% sensitive
and specific for tamponade
In tamponade, RV collapse begins in early diastole and generally occurs with moderate
elevation in pericardial pressures, when CO has decreased by 20%.
RV collapse persists further into diastole, the more severe the tamponade is
RV free wall thinnest @ RVOT
Best seen in parasternal SAX
Specificity and sensitivity of right heart collapse improves as severity of tamponade
increases
RA collapse might have higher predictive value than RV collapse
Absence of chamber collapse has a > 90% NPV for cardiac tamponade.
EF slope
DT
Cardiac Tamponade
IVC Plethora
IVC dilation of > 2.1 cm with < 50% collapse with inspiration
Highly sensitive for tamponade, however not specific
Present in > 90% of cases
Absent in low-pressure
tamponade
Cardiac Tamponade
Hepatic Vein flow
Dilation of hepatic vein seen in tamponade
During inspiration, both systolic and diastolic peak velocities
increase (normal)
In the presence of a PEff inhibiting cardiac filling, flow velocities
decrease (from 50 to 20-40 cm/sec) and systolic venous flow
predominates since intrapericardial pressures decrease
significantly during ventricular ejection
Diastolic forward flow disappears completely with marked
tamponade
On the first beat of expiration, diastolic flow velocity decreases below all
other diastolic beats or reversal of flow is seen (Biphasic or a complete
reversal of the D-wave)
This corresponds to the time that tricuspid peak E-wave flow velocity is
Hepatic Vein Flow
Pulmonary vein flow
Constrictive Pericarditis
Thickened, scarred, inelastic, and often calcified non-
compliant pericardium limits diastolic filling of ventricles
Mostly a chronic condition
Etiologies US: CV surgery, Idiopathic, Viral
World-wide: Tuberculosis

Physical findings: Increased JVP with rapid Y descent,

Kussmauls sign, peripheral edema, hepatomegaly,
pericardial knock, ascites.
Constrictive Pericarditis
Unlike tamponade, early diastolic filling is more rapid than
normal (high peak E-wave flow velocity with short DT (<
160), Restrictive inflow pattern)
Restraining effects of the pericardium do not occur until mid-
diastole, after which little ventricular filling seen even at trial
contraction (small A-wave)
Rigid pericardium prevents the normal inspiratory
decrease in intrathoracic pressure to be transmitted to
cardiac chambers
Constrictive Pericarditis
Tissue Doppler
Mitral annular e velocity is normal or increased (8 cm/s) in
cases without associated myocardial involvement. This is due to
the exaggerated longitudinal motion of the heart which
compensates for the limited radial motion because of the rigid
pericardium. The longitudinal motion increases more as the
constriction worsens with higher filling pressures. Thus, in
constrictive pericarditis, E/e ratio is inversely proportional to the
pulmonary capillary wedge pressure. (annulus paradoxus)
In CP, tethering of the lateral mitral annulus to the thickened
pericardium causes the lateral annular e to be usually lower than
the e from the medial annulus.(annulus reversus)
 Tissue Doppler Velocity

Peak E of 8 cm/s.
-Sensitivity 89 %.
-Specificity 100%.
Am J Cardiol 2001;87:86-94.
 Constrictive Pericarditis
M-Mode Findings:
-Thickened Pericardium > 3mm
-On TEE measure on transgastric view,
anterior to RV in mid to late diastole
-Diastolic Flattening of LV Posterior Wall
-Abrupt posterior septal motion in early
diastole with inspiration (septal shutter
and bounce)
-Premature opening of Pulmonic Valve.
-Propagation velocity of early diastolic
transmitral flow on color M-mode is normal
or increased (>100 cm/sec)
Constrictive Pericarditis
 Constrictive Pericarditis

Mitral Inspiratory E < Expiratory ( 25%).

Tricuspid Inspiratory E > Expiratory ( 40%).
DT usually shortened ( 160 msec).
 Baseline pulsed-wave recording of mitral inflow with patient
in left lateral decubitus position.

Oh J K et al. Circulation 1997;95:796-799

 Constrictive Pericarditis

With Expiration:
Decreased diastolic forward flow.
Increase in diastolic flow reversal.
Constrictive Pericarditis

Smaller diastolic flow reversal in the SVC during

Color M-Mode Propagation Velocity

Slope 100 cm/s

Sensitivity 74%.
Specificity 91%.
Am J Cardiol 2001;87:86-94.
Constrictive Pericarditis
Doppler Diagnosis
Increased diastolic flow reversal velocity in
hepatic vein with expiration.

Mitral septal annulus velocity > 8 cm/sec.

25% respiratory variation in mitral E velocity

in 50%.

Color M-mode propagation velocity 100 cm/s.

TEE Study

Pericardial thickness of 3 mm:

-Sensitivity 95%.
-Specificity 86%.
JACC 1997;29:1317-23.
 Constrictive Pericarditis (Mayo Clinic)

Circ 2003;108:1852-57.
Obstructive Airway Disease

-Highest mitral E velocity occurs at end of

expiration.
-Increase in SVC flow with inspiration >
35%
& decrease with expiration.
Effusive Constrictive
Pericarditis
The hallmark of this condition is elevated RA pressure,
elevated RV and LV end-diastolic pressures with associated
dip and plateau ventricular waveforms, and respiratory
interventricular dependence occurring after
pericardiocentesis
Etiologies: Idiopathic (most common), radiation- and
malignancy-related.
Epicarditis: involvement of both the visceral and parietal
pericardium.
Pericardial tumors
Benign
Teratoma (MC), Lipoma, Fibroma, Hemangioma, Lymphangioma
Can be found in both parietal pericardium and epicardium
Primary Malignant
Malignant mesothelioma is the MC malignant primary tumor of the pericardium,
followed by Angiosarcoma
Invasion into the myocardium is possible
Most are nonresectable at the time of diagnosis.
Secondary Malignant
Local invasion or metastasis from Lymphoma, Melanoma, Lung and breast carcinoma
Diagnostic yield of pericardial fluid cytology is high in secondary malignancies from
solid tumor metastasis, but can be quite low in cases of hematologic malignancies
Melanoma frequently invades the myocardium
CMR and CT for tissue characterization and assessment for invasion might be
necessary in suspicious pericardial tumors
Pericardial Cyst and
Diverticuli
Pericardial Cyst
Most are congenital, however they can be infectious (hydatid
cysts)
Congenital pericardial cysts are fluid-filled, unilocular sacs lined
by mesothelial cell
No communication with the pericardial space.
They are rarely of clinical significance, unless they are large
enough to cause compression symptoms
Monitor with CMR or CT every 1-2 years
Indications for resection/drainage: (1) Symptoms; (2) Large size;
(3) Potential for rupture or (4) Malignancy.
Pericardial Cyst

Most common in the right cardiophrenic angle

Pericardial Cyst
Pericardial Diverticula
Very rare
They can be congenital or acquired malformations
Out-pouchings or herniations through a defect in the
parietal pericardium and occur most often at the
costophrenic angles
Unlike cysts, diverticula can change in size (often
decreasing), even within a short period of time.
Differentiation of the diverticulum from a cyst is based on
the presence of a communication with the pericardial
space
Change in contour and size related to body position or
respiration.
Congenital Absence of the Pericardium
Five types:
Complete absence of the entire pericardium
Complete absence (Left or right sided)
Partial absence (Left or right sided)
Most common type is the complete absence of the left pericardium
More common in males (3:1)
30% also have ASD, Bicuspid AV, PDA or Bronchogenic cysts.
Patients with complete absence of the entire pericardium are
general asymptomatic and do no require any interventions
Patients with partial left-sided defects present with greatest risk
Compression, herniation, or strangulation of cardiac chambers (most
common with LAA), great arteries and coronary arteries
Congenital Absence of the Pericardium
This condition is suspected on echo when:
Unusual imaging windows
The appearance of an enlarged RV
Reduced compliance with an absent left-sided pericardium
Normal-sized RV can appear enlarged due to the levoposition of the heart
tangential image through RV
Excessive cardiac motion
Abnormal interventricular septal motion
Parasternal LAX apex is pointed posteriorly
M-Mode shows paradoxical septal motion in systole and diastole
and excessive posterior wall anterior motion, absence of normal
epicardial-pericardial space
Apical views are laterally displaced
Congenital Absence of the Pericardium
Doppler echo
Reductions in the systolic flow in the SVC and the
systolic/diastolic flow ratio in the pulmonary veins
Most likely due to the reduction in the negative intrapericardial pressure
generated by the pericardium during systole with and absent pericardium
CT/CMR
Interposition of lung tissue in spaces typically covered by the
pericardium, including the anterior space between the aorta and
pulmonary artery or between the diaphragm and the base of the
heart.