Dr. Mozhgan ParsaeeDepartment of Echocardiography

Shahid Rajaei Cardiovascular Center

Pericardial Disease

Normal Function of Pericardium

Fibrous sac surrounding heart-dense network of collagen fibres.

Serous membrane – two continuous layers separated by a small amount of fluid lubricant , ultrafiltration of plasma (10-50 mL).

Layers are called visceral and parietal Visceral is inner layer (epicardium) Parietal is continuous with diaphragm and

outer walls of great arteries.

Normal Function of Pericardium

Limit cardiac dilatation

Limit cardiac displacement

Reduce friction to cardiac movement

Barrier to inflamation

Not needed to sustain life

Acute Pericarditis

Acute Pericarditis

Acute pericarditis, defined as symptoms or signs resulting from pericardial inflammation of no more than 1 to 2 weeks in duration.

Serous Fibrinous Purulent Hemorrhagic

Etiology

Infectious pericarditisA.Viral : coxackievirus A&B, echovirus,

mumps,HIV, adenovirus, hepatitis

B. Pyogenic: pneumococcus, streptococcus, staphylococcus

C. Fungal: histoplasma, candida

Etiology

Non infectious pericarditisA. acute MIB. UremiaC. Cancer (commonly lung or breast) D. TraumaE. MyxedemaF. PostirradiationG. Aortic dissectionH.Acute idiopathicI. Connective tissue disease

Etiology

Pericarditis related to hypersensivity or autoimmunity

A. Rheumatic fever

B. Collagen vascular disease(SLE, RA)

C.Drug induced (phenytoin, procainamide, hydralazine, isoniazide, minoxidil, anticoagulant)

D.Post cardiac injury (posttraumatic, Dressler’s syn, post pericardiotomy)

Signs, Symptoms and Investigations

How can we diagnose this?

Clinical examinationAuscultationChest x-rayECGEchoCatheter laboratory investigations

Acute Pericarditis

Chest pain

Pericardial friction rub

ECG changes

Pericardial effusion

Chest Pain

Usually present in the acute infectious types and in many of the forms related to hypersensivity and autoimmunity

Often absent pain in slowly developing TB, post irradiation, cancer, or uremic pericarditis

Chest Pain

The pain of acute pericarditis is often severe, retrosternal and left precordial and reffered to the neck, arms or the left shoulder; the most characteristic radiation is to the trapezius ridge.

Almost always the pain is pleuritric (sharp and aggravated by inspiration, coughing, and changes in body positions).

Pain may be relieved by sitting up and leaning forward and is intensified by lying supine.

Pericardial Friction Rub

Pericardial friction rub is audible in 85% of patients.

Is high pitch and scratching.

Has three components per cardiac cycle presystolic rub during atrial filling ventricular systolic rub (loudest) ventricular diastolic rub (after A2P2)

Pericardial Friction Rub

Most frequently is audible at end-expiration with the patient upright and leaning forward.

is audible when the diaphragm of the stethoscope is applied firm to the chest wall at the LLSB.

The rub is often inconstant.

Clinical signs differential diagnosis - pleurisy

Pleuritic pain has similar sharp quality but is usually more specific in location

Pleural rub is heard over the area where the pain occurs

A pericardial rub is heard throughout the respiratory cycle, while a pleural rub disappears when respiration is suspended.

ECG differential diagnosis - MI

What leads is the ST elevation in?What shape is the elevation?Are there Q waves?Do the ST –T changes evolve with time?History of the patientCardiac enzymes etcBut REMEMBER that you can get more

than one pathology at the same time!

ECG Features

ECG display changes secondary to acute subepicardial inflammation and shows typically four stages.

Stage I (first hours to days)Diffuse up sloping ST elevation with

reciprocal ST depression(aVR,V1)PR depression in the inferolateral leadsPR elevation in aVR

ECG Features

Stage II (after several days)Normalization of the ST and PR segments

Stage IIIDiffuse T wave inversions, generally after the ST

segment have become isoelectric, however, this phase is not seen in some patients

Stage IVECG may become normal or the T inversion may

persist indefinitely

ECG in AMI

ST elevation are convex

Reciprocal depression is usually more prominent

QRS changes occurs (development of Q wave and loss of R-wave amplitude)

T wave inversion are seen within hours before the ST segment have become isoelectric.

ECG in Early Repolarization

Early repolarization is a normal variant and may also associated with widespread ST-T segment elevation, most prominent in left precordial leads.

T wave are usually tall.

ST/T ratio is <0.25 (this ratio is higher in pericarditis)

ST/T ratio in Pericarditis

ECG in Early Repolarization

Diagnosis of pericarditis

Patient will have 2 or more of the following;

Characteristic chest pain

Pericardial friction rub (auscultation)

ECG showing characteristic ST elevation (caused by epicardial injury)

Treatment

Search for the underlying disease

Patients require bed rest

NSAIDs: Iboprofen (600 to 800 mg orally three times daily) with discontinuation if pain is no longer present after 2 weeks

Reliable patients with no more than small PE who respond well to NSAIDs need not to be admitted to the hospital.

Indication for Hospital Admission

Patients who do not respond well initially to NSAIDs

Patients have larger effusion

Patients have a suspected cause other than idiopathic pericarditis

Should be hospitalized for additional observation, diagnostic

testing, and treatment as necessary

Prognosis

Pericarditis is usually a benign and self-limited disease (usually over 1 to 3 weeks) without significant complication or recurrence in 70% to 90% of patients

Diagnosis relates to underlying causeBut any cause can lead to an effusion and

tamponade which can lead to deathPericarditis can also progress to pericardial

constriction and heart failure

Management

In young women, it is not unreasonable to test for SLE.

However, low ANA titers appear to be common in patients with recurrent idiopathic pericarditis who do not meet other criteria for SLE.

Thus, the significance of low ANA titers in the setting of an initial presentation in somewhat uncertain.

Cardiac Enzymes

Cardiac troponin I was detectable in 49% and above 1.5 ng/ml−1 in 22%.

Elevated troponin values were felt to reflect superficial myocardial inflammation and were not an adverse prognostic marker after a mean follow‐up of 24 months.

Pericarditis of Renal Failure

Occurs in to one-third of patients (uremic pericarditis)

Occurs in patients undergoing chronic dialysis with normal level of BUN, CR (dialysis associated pericarditis)

Pain is absent or mild.

The ECG does not usually show the typical ST and T wave elevation.

Treatment: NSAID, intensification of dialysis.

Early Post-MI Pericarditis

It is associated with large, transmural MIs, but it is almost invariably a benign process that does not affect in-hospital mortality.Treatment is based on symptoms.

Augmentation of usual post-MI aspirin doses (650 mg TID or QID for 2-5 days) or acetaminophen is usually effective.

Because significant hemopericardium is rare with early post-MT pericarditis and there is no evidence that heparin or other antithrombotic drugs increase its risk, their administration need not be modified.

Pericardial Effusion

Pericardial Effusion

It is important clinically when it develops within a relatively short time as it may lead to tamponade.

Heart sounds may be fainter with PE.

The friction rub may disappear.

Apex impulse may vanish.

Pericardial Effusion: Symptoms

Dull constant left chest acheDyspnea (shortness of breath)Less common: Hiccups (phrenic

nerve)Hoarseness (recurrent laryngeal

nerve)Dysphagia (esophageal compression)

Pericardial Effusion

Ewart’s sign: the base of the left lung may be compressed by

PE, a patch of dullness and increased fremitus (egophony) beneath the angle of the left scapula.

CXR: - Enlargemnt of cardiac silhouette (effusion>250

mL) - Water bottle configuration of the cardiac

cilhouette.

Pericardial Effusion

Echo:Is the most effective imaging.A echo free space between the posterior

pericardium and LV epicardiumIn the latter, the heart may swing freely within

the pericardial space.(electrical alternans)

CT,MRI:Loculated PE, pericardial thickening and mass

Myxedema

25-35% of patients with severe hypothyroidism develop PE.

PE has a high concentration of protein-cholestrole and like other serous effusions ,its pathogenesis is not fully understood (accumulation of mucopolysaccharides or a combination of extravasation of albumin and decreased lymph flow( .

The effusion gradually resolve with thyroid replacement.

PE occasionally occur in subclinical hypothyrodism.Rarely, PE can occur in hyperthyrodism.

PE in hypothyroidy

May cause of large chronic pericardial effusion (rarely is massive and lead to tamponade).

Management of Pericardial Effusion

The management of small or moderate pericardial effusions, without tamponade, is usually conservative.

The routine diagnostic pericardiocentesis in the absence of cardiac tamponade is not indicated.

If the pericardial effusion is likely to be purulent then it should be drained.

If the effusion is felt to be malignant, pericardiocentesis is recommended if confirmation would change management and can be performed safely.

Taomponade

Tamponade

Tamponade is life-threatening, slow (2000 mL) or rapid (150-200 mL) compression of the heart due to the pericardial accumulation of the fluid.

There are limitation of ventricular filling and reduction of cardiac output.

The causes of Raised Intra Pericardial Pressure

Raised intrapericardial pressure can occur by 3 main mechanisms:

1.Increased fluid within the intrapericardial space (PE)

2.Increased volume of the cardiac chambers (PTE)

3.Increased stiffness of the pericardium (CP)

Consequences of raised IPP

Raised intrapericardial pressure has 3 potential adverse effect on the heart:

1.A compressive effect with limits diastolic filling of the heart

2.Increased diastolic filling pressure3.Reduced stroke volume and cardiac output

Etiology

Causes of tamponade :CancerIdiopathic pericarditis (receive anticoagulant)Renal failureCardiac operationTraumaPCIInsertion PPM

Tamponade

The clinical manifestation of tamponade may be resemble of heart failure (dyspnea, orthopnea, hepatic engorgement)

When tamponade more slowly a high index of suspicious is necessary because sometimes no obvious cause for pericardial disease is apparent

It should be considered in any patient with hypotention and increased JVP.

Suspicious to Tamponade

Hypotention+increased JVP

Unexplained enlargement of the cardiac silhouette

Reduction in amplitude of the QRS complex

Electrical alternance of the P,QRS,T

Beck’s triad

Hypotension

Soft or absent heart sounds

Jugular venous distention (prominent x)

Ventricular interdependence

Normal subjects – there is normally small augmentation of right-sided transvalvular flows accompanying inspiration.

Explanation – combination of increased venous return due to decreases intrathoracic

pressure fall in PVR

Enhanced Ventricular interdependence in Tamponade

Pulse paradox

A more than 10 mmHg (normal) inspiratory decline in systolic arterial pressure

When severe, it may be detected by palpating weakness or disappearance of the arterial pulse during inspiration.

DD: RVMI, 1/3 patients with constrictive pericarditis, hypovolemic shock, PTE, acute and chronic obstructive lung disease

How to measure Pulsus Paradoxus

When severe, it may be detected by palpating weakness or disappearance of the arterial pulse during inspiration.

Ask the subject to breath normally Auscultate Korotkoff’s sounds as the BP cuff is

slowly lowered. Time respiration simultaneously Mark when BP sounds are heard only in expiration Mark when BP sounds are heard both in expiration

& inspiration. Korotkoff’s sounds seem to double at this point.

The difference is the measured pulsus paradoxus

Echocardiography

Both ventricles is a tight incompressible covery (pericardial sac)

Inspiratory enlargement of the RV in tamponadeCompress and reduce LV volume due to left

ward bulging of the IVSNormal inspiratory augmentation of RV volume

causes an exaggerated reciprocal reduction in LV volume

Respiratory distress increases the fluctuation in transthoracic pressure

Ventricular interdependence in Tamponade

Echocardiography

% respiratory variation= E exp- E ins E exp

Echocardiography

An exaggerated respiratory variation in inflow and outflow velocities:

MV:25% increase with expiration (normally 15%)

TV :50% increase with inspiration (normally 25%)

AV :14% increase with expiration (normally 4%)

PV :16% increase with inspiration (normally 5%)

Echocardiography

Doppler ultrasound shows the TV and PV flow velocities increase markedly in inspiration

MV and AV and PVs flow velocities diminish

RA and RV collapse in late diastole

Management

In patient with clinical finding of tamponade if there is RV collapse , immediate therapy is needed

In patient without clinical finding of tamponade if there is RV collapse it means intrapericardial pressure is greater than RV pressure and there is potential for acute hemodynamic deterioration, urgent therapy is needed

Management

Medical emergency – intensive care environment needed.

OxygenVolume expansionBed rest with leg elevationInotropic drugs if necessary

Management

Pericardiocentesis is the definitive therapy to remove the excessive fluid

Commonly performed in the cath lab but may be done ‘blind’ in an intensive care environment

Constrictive Pericarditis

Chronic constrictive pericarditis

Tuberculous constrictive pericarditis was common

cause of constriction pre 1960 – decline in incidence.

Post-radiotherapy constriction features prominently today along with post-surgical causes.

Needs to be differentiated from restrictive cardiomyopathy when making diagnosis.

Chronic constrictive pericarditis

Formation of granulation tissue after desorption of effusion or healing of a acute fibrinous pericarditis.

The ventricles are enable to fill because of the limitations imposed by rigid, thickened pericardium

Ventricular filling is only in early diastole and is reduced abruptly when the elastic limit of the pericardium is reached

In tamponade ventricular filling is impeded throughout diastole

Investigations

Clinical picture– prime symptoms weakness, fatigue, weight gain, edema, ascitis, exertional dyspnea, ortopnea (not severe)

The cervical veins are distended and may remain so even after intensive diuretic treatment

Auscultation may reveal a pericardial knock(0.09-0.12 after AV closure) , audible in apex, it occurs due to abrupt cessation of ventricular filling

Investigations

Heart sounds may be distant

Audible systolic murmur due to TR

Congestive hepatomagaly that cause LFT impairment and jaundice

Broadbent’s sign: reduced apical pulce and sometimes retract in systole

Kussmaul’s sign

Normal subjects – inspiration causes a decrease in chest pressure. Increase in venous return – JVP falls

Constrictive pericarditis – Increased venous return cannot be accommodated in RV because of high EDP

So JVP rises on inspiration

D.D: tricuspid stenosis, RVMI, RCM

Investigations

ECG may not show characteristic ST elevation, display low voltage of the QRS complexes and diffuse flattening or inversion of the T waves, AF is present in one-third of patients

CXR may see calcification(23-50%), calcification in CXR is more common in TB and there is normal or only mild enlarged heart that helps to rule out coexisting effusion

Echo to identify hemodynamic effects on heart and coexisting effusion

Respiratory Variation in CP

Ventricular interdependence is found in CP but not RCM

Respiratory Variation in CP

Echo Finding

Normal subjects – increase in TV flow velocity on inspiration, and decrease in MV flow

Due to increased vascular capacity of lungs venous return and RV output increases while return to LA is reduced

This is exaggerated in tamponade/sig constriction – RV output can’t increase because of high EDP + pulmonary return is reduced further

Septal Bounce

TDI of the Mitral Annulus

CP RCM

CT/MRI

MRI/CT scan – data about the thickness of the pericardium and display calcification.

Pericardial thickening and even calcification are not synonymous with CP since they may occur without seriously impairing ventricular filling.

Normal Right Atrial Pressure Tracing

• “a” wave– Atrial systole

• “x” descent– Relaxation of RA– Downward pulling of

tricuspidannulus by RV contraction

• “v” wave– RV contraction

• “y” descent– TV opening and RA emptying

CVP Tracing in Normal Subjects

Bimodal with x > y

Constrictive Pericarditis

Constrictive Pericarditis vs. Tamponade

Tamponade CP

Dip and Plateau in Diastolic Waveform

No respiratory variation in RCM

Treatment

The only effective treatment for chronic constrictive pericarditis is complete surgical resection of the pericardium.

Mortality for procedure ranges from 5-16%

Symptomatic improvement in ~90%

5 year survival rate is 74-87% depending on co-morbidities pre-op

Treatment

Radiation-induced disease is considered a relative contraindication for pericardiectomy.

Healthy older patients with very mild constriction may also be managed nonsurgically (salt restriction and diuretics consumption).

Pericardial cyst

Appear as rounded or lobulated deformities of the cardiac silhouette, most commonly at the right cardiophernic angle

No symptom

May be confused by tumor, ventricular aneurysm, or cardiomegaly

Management is conservative

The End Result