Definition 0 f pericardial diseases

PERICARDIAL DISEASES

Functions of pericardium:

PERCARDITIS

Essential for diagnosis

ESSENTIALS OF DIAGNOSIS_ Anterior pleuritic chest pain that is worse supine than upright. Pericardial rub. Fever common.Erythrocyte sedimentation rate usually elevated. ECG - diffuse ST segment elevation with associated PR depression.

1 MAGDI AWAD SASI PERICARDIAL DISEASES 2013

Pericaditis refers to an inflammation of a visceral pericardium which is a membranous sac enveloping the heart .

Pericarditis can be acute or chronic. Acute pericarditis(< 2 weeks) occurs due to complications of infections or may be due to systemic diseases (autoimmune syndromes, uremia), neoplasm, radiation, drug toxicity, hemopericardium, postcardiac surgery, or contiguous inflammatory processes in the myocardium or lung. In many of these conditions, the pathologic process involves both the pericardium and the myocardium.Chronic pericarditis is however less common a form of constrictive pericarditis. It can also be a primary illness which develop as a result of medical and surgical disorders .

More common in men

Occurs between the ages of 20 to 50 years

Pathology:

Depends on underlying cause and severity of inflammation

Serous pericarditis

Serofibrinous pericarditis

Suppurative (purulent) pericarditis

Hemorrhagic pericarditis


AETIOLOGY:

I. INFECTIVE A.viral illness

Coxsackie A & B((the commonest)), Echovirus, Hepatitis B ,HIV, Influenza ,Mononucleosis ,Mumps ,Varicella ,EBV ,Adeno.

B.Bacterial infections-

Stab wounds, pneumonia, endocarditis, sepsis, surgical contamination,

Tuberculosis, Diphtheria, Staphylococcus, pneumococus.

C .Fungal- Candida D. Parasitic- Amoeba

II. AUTOIMMUNE

1. Systemic lupus erythematosus (SLE)

2. Drug-Induced lupus (e.g. Hydralazine, Procainamide, ioniazide. minoxidil, penicillins, clozapine)

3. Rheumatoid Arthritis

4. Post Cardiac Injury Syndromes i.e. postmyocardial Infarction (Dressler's) Syndrome, postcardiotomy syndrome, Trauma

III. NEOPLASM 1. Primary mesothelioma 2. Secondary, metastatic breast cancer, renal cell carcinoma, Hodgkin disease, and lymphomas

3. Direct extension from adjoining tumorIV. RADIATION PERICARDITISV. RENAL FAILURE (uremia)

VI. TRAUMATIC CARDIAC INJURY1. Penetrating - stab wound, bullet wound2. Blunt non-penetrating - automobile steering wheel accident

VII. Chemotherapy VIII IDIOPATHIC (exclude others 1s)


Pericarditis & AMI

• If occurs within 2 – 7 days following an AMI

– Considered a pericardial inflammatory response to the AMI.

• Dressler Syndrome

– May occur 2 weeks to several months after the event after myocardial infarction or open heart surgery, may be recurrent

– Autoimmune response to myocardial necrosis involving both the pleura and the pericardium.

– Patients present with typical pain, fever, malaise, and leukocytosis. Occasionally, the syndrome will occur within days of surgery. Rarely, other symptoms of an autoimmune disorder, such as joint pain and fever, may occur. Tamponade is rare with Dressler syndrome after myocardial infarction but not when it occurs postoperatively.

PATHOPHYSIOLOGY

ACUTE

In acute pericarditis when microbes are inhaled or ingested, they migrate to myocardium and cause inflammation. So when these membranes are inflamed, they rub against each other and cause classic sounds of which the patient complains of severe chest pains which increases when the patient lies supine and decreases when in sitting position.

This acute inflammation causes accumulation of fluid in the pericardial sac called pericardial effusion. The fluid may be serous which accompanies heart failure, purulent accompanying tuberculosis and haemorrhage accompanying trauma in the heart.

The excessive accumulation of fluid in the sac causes compression of the heart, resulting in decrease venous retain of the heart resulting in ventricular filling and a decrease in stroke volume. These events will eventually lead to cardiac failure( right 1st), shock and death.


CHRONIC

Chronic pericarditis occurs when the layers adhere to each other causing fibrosis of the pericardial sac due to surgery which later restricts movement of the heart. So the fibrotic pericardium tightens the heart decreasing cardiac filling and output and later patient may report symptoms of heart failure.

CLINICAL MANIFESTATION:

The presentation and course of inflammatory pericarditis depend on its cause, but most syndromes have associated chest pain.Sharp chest pain- with a rapid onset that worsens with breathing, coughing and changes position(( pleuritic in nature)) , relief obtained by sitting upright and leaning forward((postural chest pain)).

The pain is substernal /? radiate to the neck, shoulders, back, or epigastrium.OFTEN- fever of 37.5 to 38 degrees and precede the chest pain.

o Bacterial percarditis- toxic and are often critically ill.o Uremic pericarditis can present with or without symptoms;

fever is absent.o Often neoplastic pericarditis is painless, and the presenting symptoms

relate to hemodynamic compromise or the primary diseaseo Chills, Night sweats

Dyspnea, cough

PERICARDIAL RUB------------to-and-fro rubbing be heard over the entire precordial region or a very small area.

It may be heard in both phases of the cardiac cycle. Pericardial friction rub is unaffected by respiration and is thus differentiated from a pleural friction rub. It is also increased as pressing the stethoscope firmly against the patient’s chest wall. A rub may be readily heard at one moment and be absent several minutes later. The intensity of the rub is usually increased when the subject is sitting upright and leaning forward.


Tuberculous Pericarditis

4-10% of All Acute Pericarditis is Caused by TB (Reported up to 80% in Some 3rd World Countries) Lymphatic or haematogenous spread.

Nonspecific symptoms (fever, night sweats, fatigue) may be present for days to months.

1-8% of Patients with TB Have Pericardial Involvement

Etiology of 20% of Constrictive Pericarditis

Cases 93% of all Pericardial Effusions in HIV Patients

Four Pathologic Stages of TB Pericarditis

I-Dry: Fibrin Deposition & Granulomatous Reaction. Clinically Silent

II-Effusive: Serous Fluid Accumulation Caused by Hypersensitivity to Tuberculoprotein and Impaired Resorption

III- Absorptive: Effusion Resolves and Fibrous Tissue Replaces Granulomas, Pericardium Thickens


IV-Constrictive: Parietal Pericardial Calcification

Presentation

Dyspnea 45-90% Rub 30-85%

Chest Pain 40-75% Cough 50-95%

Orthopnea 20-65% Fever 80-100%

Distant Heart Sounds 25-55%

50% of Patient Have Slowly Progressive Insidious Presentation

95% Have Cardiomegally, 30% Have Active Pulmonary TB, 39-71% Have Pleural Effusions L>R. Bilateral Pleural Effusions More Common than Rub.

“Because of the variable and nonspecific features of TB pericarditis, establishing the diagnosis on clinical grounds alone is impossible.

Diagnosis by Pericardial Fluid or Biopsy: Positive AFB Smear, Culture, Caseating Granulomas, TB DNA PCR

Treatment

Antibiotics: Isoniazid, Rifampin, Pyrazinamide, Ethambutol

Corticosteroids: Reduces Mortality and Need for Subsequent Pericardiocentisis

DIAGNOSTIC EVALUATIN STUDIES OF PERICARDITIS:

The diagnosis of viral pericarditis is usually clinical, and leukocytosis is often present. Rising viral titers in paired sera may be obtained for confirmation but are rarely done.

12-Lead EKG

• Most definitive test in acute pericarditis


• The ECG usually shows generalized ST and T wave changes and may manifest a characteristic progression beginning with diffuse ST elevation, followed by a return to baseline and then to T wave inversion.

• Atrial injury is often present and manifested by PR depression especially in the limb leads.

• ST-segment elevation(saddle shaped) in most leads except V1 and AVR.

• NO RECIPROCAL CHANGES OR T INVERSION IN ACUTE DURATION.

• PR segment depressed

• Electrical alternans

– QRS varies from beat to beat(( IN PERICARDIAL EFFUSION))

• Atrial dysrhythmias common( IF EXTEND TO MYOCARDIUM))


• Four stages of EKG changes

Stage 1 S-T elevation seen globally, but more prominent in the precordial leads

Stage 2 S-T segment starts to normalize and T-wave increases in amplitude

Stage 3 Normal S-T segments and inverted T-waves

Stage 4 Resolution of repolarization abnormalities

Chest X-Ray


• The chest radiograph is frequently normal.

• Cardiac silhouette enlarged if there is pericardial effusion, As well as signs of related pulmonary disease. Mass lesions and enlarged lymph nodes may suggest a neoplastic process.

– If more than 250 ml is present

Echocardiogram

Evaluates hemodynamic changes associated with cardiac tamponade

Transesophageal Echocardiogram (TEE)

Pericarditis is a clinical diagnosis, not an Echo diagnosis! The echocardiogram is often normal or reveals only a trivial amount of

fluid during the acute inflammatory process. The diagnosis of tuberculous pericarditis can be inferred if acid-fast bacilli are found elsewhere. The tuberculous pericardial effusions are usually small or moderate but may be large.

Helpful in evaluating the size of an effusion & compromised ventricular

Filling


Large pericardial effusions and accompanying pleural effusions are frequent.

Labs

1.Erhythrocyte Sedimentation Rate (ESR) & Complete Blood Count (CBC)

– Non-specific elevation

2. Cardiac Profile (CK-MB, troponins)---Rule out AMI /raised Troponin

Cardiac enzymes may be slightly elevated, reflecting an epicardial myocarditis component.3. PPD, HIV-AIDS screening

4.Rheumatoid factors (RF), Antinuclear Antibodies (ANA)

5.CT scan / MRI – locate neoplastic lesions

Biopsy of pericardium to obtain tissue sample for culture and microscopic examination

If bacterial pericarditis is suspected on clinical grounds, diagnostic pericardiocentesis may be of value. In uremic patients not on dialysis, the incidence of pericarditis correlates roughly with the level of blood urea nitrogen (BUN) and creatinine. The pericardium is characteristically “shaggy” in uremic pericarditis, and the effusion is hemorrhagic and exudative.

The diagnosis of neoplastic pericarditis can occasionally be made by cytologic examination of the effusion or by pericardial biopsy, but it may be difficult to establish clinically if the patient has received mediastinal radiation within the previous year. Neoplastic pericardial effusions develop over a long period of time and may become quite huge (> 2 L).

Clinical Management

Uncomplicated Viral Pericarditis

• Treatment of viral pericarditis is generally symptomatic. Aspirin (650 mg every 3–4 hours) or other nonsteroidal agents (eg, indomethacin, 100–150 mg daily in divided doses) are usually effective.


• Indomethacin & Colchicine --Allergy to NSAIDs or aspirin

• Narcotic analgesia

• Corticosteroids may be beneficial in unresponsive cases.

Complicated pericarditis• In general, symptoms subside in several days to weeks. The major early

complication is tamponade, which occurs in less than 5% of patients. There may be recurrences in the first few weeks or months.

• Rarely, acute pericarditis may lead to constrictive pericarditis, which may necessitate pericardial resection

• Uremic pericarditis usually resolves with the institution of aggressive dialysis. Tamponade is common, and partial pericardiectomy (pericardial window) may be necessary.

• Whereas anti-inflammatory agents may relieve the pain and fever associated with uremic pericarditis, indomethacin and systemic corticosteroids do not affect its natural history.

• The prognosis with neoplastic effusion is dismal, with only a small minority surviving 1 year. If it is compromising the clinical comfort of the patient, the effusion is initially drained percutaneously. Early attempts at ballooning the pericardium from a subxiphoid approach have been mostly abandoned in favor of surgical approaches. A pericardial window, either by a subxiphoid approach or via video-assisted thoracic surgery, allows for partial pericardiectomy. Instillation of chemotherapeutic agents or tetracycline may occasionally be used to reduce the recurrence rate.

• Relapses do occur and may require slow withdrawal of anti-inflammatory therapy over several months. Colchicine may be required for months to help prevent recurrences.

• Post-MI Pericarditis • Avoid use of corticosteroids and anti-inflammatory agents

– May cause rupture of the infarcted area

Pericarditis (recurrent pain or connective tissue disorders)

• Corticosteroids are most effective


Medication-Related Pericarditis Stop the medication

Pericardial Effusion

• Accumulation of excessive fluid in the pericardial space

• May happen slowly over time and the pericardial sac accommodates.

• The fluid may press on the heart enough to limit its movement within the sac.

• Rapid fluid accumulation results in Cardiac Tamponade.

Pericardial effusion causes an enlarged heart shadow that is often globular shaped (transverse diameter is disproportionately increased).

A lateral film and close-up of a pericardial effusion showing the anterior mediastinal fat (blue arrows) and epicardial fat (red arrows) separated by a


soft tissue stripe ( "fat pad" sign) reflecting the pericardial effusion seen edge-on.

The speed of accumulation determines the physiologic importance of the effusion. Because the pericardium stretches, large effusions (> 1000 mL) that develop slowly may produce no hemodynamic effects. Conversely, smaller effusions that appear rapidly can cause tamponade. Tamponade is characterized by elevated intrapericardial pressure (> 15 mm Hg), which restricts venous return and ventricular filling. As a result, the stroke volume and pulse pressure fall, and the heart rate and venous pressure rise. Shock and death may result.

AETIOLOGY: Any cause for pericarditis can cause pericardial effusion and temponade.

S&S:Pericardial effusions may be associated with pain if they occur as part of an acute inflammatory process OR may be painless, as is often the case with neoplastic or uremic effusion. Dyspnea and cough are common, especially with tamponade. Other symptoms may result from the primary disease. A pericardial friction rub may be present even with large effusions.

Diagnosis

Same line of investigations for pericarditis.

CXR , ECG, ECHO, CTSCAN CHEST ,CBC,ESR,ANA,TB TEST

CHEST X RAY

Although an effusion is often described as producing a globular-shaped heart, it is usually not possible to differentiate a pericardial effusion from cardiac enlargement on a chest radiograph.

May appear normal in acute situations.

Approximately 250 ml of fluid must be in the pericardium to lead to a detectable change in the size of the heart shadow on PA CXR


small effusions (100–200 mL) may not cause cardiomegaly even though they can cause tamponade when they accumulate rapidly or when the pericardial membrane is stiffened from fibrosis.

Pericardial effusion can be definitively diagnosed with either echocardiography (can be bedside in the emergency department in the critically ill patient patient) or CT chest.

ECG

The ECG often reveals nonspecific T wave changes and low QRS voltage. Electrical alternans is present uncommonly but is pathognomonic. It is due to the heart swinging within the large effusion.

ECHOEchocardiography is the primary method for demonstrating pericardial effusion and is quite sensitive.

Cardiac CT and MRI also demonstrate pericardial fluid and any associated

contiguous lesions.

Diagnostic pericardiocentesis or biopsy is often indicated for microbiologic and cytologic studies; a pericardial biopsy may be performed relatively simply through a small subxiphoid incision.

Unfortunately, the quality of the pericardial fluid rarely leads to a diagnosis, and any type of fluid (serous, serosanguinous, bloody, etc) can be seen in most diseases


Treatment

Small effusions can be followed clinically by careful observations of the JVP and by testing for a paradoxical pulse.

Serial echocardiograms are indicated if no intervention is immediately contemplated.

Continued or repeat drainage may be indicated, especially in malignant effusions. Pericardial windows via video-assisted thorascopy have been particularly effective in preventing recurrences. Additional therapy is determined by the nature of the primary process. Recurrent effusion in neoplastic disease and uremia, in particular, may require partial pericardiectomy as noted earlier.

Trivial pericardial effusions are common, especially in CHF, and need not be referred.

• Hypotension or a paradoxical pulse suggesting the pericardial effusion is hemodynamically compromising the patient should prompt an immediate referral.

_


Cardiac Tamponade

It is an impairment of ventricular filling during diastole due to some external pressure on the heart by pericardial effusion. Tamponade is characterized by elevated intrapericardial pressure (> 15 mm Hg), which restricts venous return and ventricular filling. As a result, the stroke volume and pulse pressure fall, and the heart rate and venous pressure rise. This leads to obstructive shock. Shock and death may result.Tamponade can occur acutely (eg, due to rupture of the heart or aorta, trauma, or as a complication of catheter or pacemaker procedures) or subacutely (eg, due to neoplasm, uremia, or idiopathic pericarditis).

Accumulation of fluid under high pressure: compresses cardiac chambers & impairs diastolic filling of both ventricles

¯ SV venous pressures

¯ CO systemic& pulmonary congestion

Hypotension/shock JVD rales

Reflex tachycardia Hepatomegaly

Ascites

Peripheral edema


Symptomatology of Cardiac Tamponade:

((Low cardiac output symptoms with heart failure))

Acute: (trauma, LV rupture)

profound hypotension-Fatigue, dizziness, syncope, lose of effort

confusion/agitation

Slow/Progressive large effusion (weeks)

Fatigue (¯CO)

Dyspnea

JVD

1. LVF:

.Chest pain _oppressive precordial , positional as it is preceded by pericarditis, stabbing in quality.

.Fullness in chest pushing on her heart

.Dyspnea on exertion , at rest , PND

.Cough dry irritant positional( more on laying )

2. RVF:

. Abdominal pain , dysphagia

.Early statiety

. Abdominal distention

. Nausea hoarsness


.Edema or ascites are rarely present; these signs favor a more chronic process.

Clinical Signs of Cardiac Tamponade:

Tamponade has a spectrum of presentations ranging from circulatory collapse to mildly reduced cardiac output with symptoms of dyspnea and chest or abdominal discomfort depending on the rate of fluid collection.

• General

o Anxious

o Apprehensive

o Ashen gray facies

o Cool perspiration

• Tachycardia

• Tachypnea

• Jugular venous distension-NO Y DESCENT IN RA/RV

• Peripheral Cyanosis

• Quiet precordium with both inspection and palpation

• muffled heart sounds

• Rub

• Right upper quadrant tenderness

• The venous pressure tracing shows absence of diastolic y descent (i.e. there is a deep x descent but y descent is absent) . Cardiac tamponade also causes a raised JVP, Kussmaul’s sign and pulsus paradoxus.

• Summary signs of cardiac tamponade are: 1. Rapid x descent 2. Kussmaul’s sign


3. Pulsus paradoxus

• Bamberger-Pins-Ewart sign

o Variable dullness and bronchial breathing at one or both bases most frequently the left below the 9th rib and between the mid scapular line and the spine(( lung collapse)).

o Beck's triad (1) systemic hypotension

(2) elevated systemic venous pressure

(3) muffled heart sounds is typical of acute tamponade which may be due to abrupt intrapericardial hemorrhage from penetrating trauma, invasive cardiac procedures, or rupture of an ascending aortic dissection or myocardial infarction. The complete triad is rarely present

• Pulsus Paradoxus

o First described by Kussmaul in 1873 as a palpable decrease or absence of the radial pulse during inspiration.

o Physiological bases (in normal person)

o Intrapericardial pressure (IPP) tracks intrathoracic pressure.

o Inspiration:

o Negative intrathoracic pressure is transmitted to the pericardial space.

o ¯ IPP blood return to the right ventricle

o ¯ jugular venous and right atrial pressures


o right ventricular volume à interventricular septum shifts towards the left ventricle ¯ left ventricular volume

o ¯ LV stroke volume

o Þ ¯ blood pressure (<10mmHg is normal) during inspiration

o Pulsus paradoxicus, an accentuated fall in the systolic pulse pressure (>10 mm Hg) during inspiration, is not present in one-quarter of patients with tamponade.

o A greater than10 mm Hg decline in systolic pressure during inspiration due to further impairment of LV filling—is the classic finding

• Place the patient in a position of comfort and conduct manometric studies

• Raise sphygmomanometer pressure until Korotkoff sounds disappear.

• Lower pressure slowly until first Korotkoff sounds are heard during early expiration with their disappearance during inspiration.

• Record this pressure.

• Very slowly lower pressure until Korotkoff sounds are heard throughout the respiratory cycle with even intensity and Record this pressure.

• The difference B/W the two recorded pressures is the Pulsus Pardoxus.

• Significant pulsus paradox is greater than or equal to 10% of the pressure at which all Korotkoff sounds are heard with even intensity.

• Pulsus Paradoxus is felt to be present when the paradoxus is greater than 10% of the pressure at which all Korotkoff sounds are heard with even

intensity(( > 10 mm Hg drop in BP with inspiration)).

Conditions in which Cardiac Tamponade presents without a Pulsus Paradoxus

• Septal Defect


• Severe Aortic Stenosis

• Severe Left Ventricular Dysfunction

o Cardiomyopathy

o Myocardial infarction

SUMMARY:

i. Acute cardiac tamponade is generally sudden in onset, may be associated with chest pain and dyspnea, and is life-threatening if not promptly treated. The central venous pressure is typically markedly elevated, while hypotension is common due to the decline in cardiac output. The heart sounds are often muted.

ii. Subacute cardiac tamponade is a less dramatic process. Patients may be asymptomatic or may complain of dyspnea, chest discomfort or fullness, peripheral edema, fatiguability, or other symptoms referable


to increased filling pressures and limited cardiac output. The physical examination in subacute tamponade may reveal hypotension with a narrow pulse pressure, reflecting the limited stroke volume. However, patients with preexisting hypertension may remain hypertensive due to increased sympathetic discharge.

DIAGNOSIS:

ECG FINDING

EKG in the setting of tamponade often shows sinus rhythm with low voltage (QRS amplitude in the limb leads <5 mm) suggestive of tamponade physiology.

Electrical alternans, a more specific sign of tamponade occurs when there is a very large pericardial effusion in which the heart swings during cardiac contraction causing a beat-to-beat variation in the ECG axis (QRS amplitude).

Electrical alternans

Low voltage

P-R depression

Etiologies of Electrical Alternans:

1.Pericardial effusion


2. Constrictive pericarditis 3. Tension pneumothorax 4. Myocardial dysfunction

– Severe cardiomyopathy

– Myocardial infarction

Echocardiographic

• If tamponade is present, the high intrapericardial pressure may collapse lower pressure cardiac structures, such as the RA and RV. In tamponade, the normal inspiratory reduction in LV filling is accentuated due to RV/LV interaction and there is a > 25% reduction in maximal mitral inflow velocities.

• Pericardial effusion,Right atrial collapse,Right ventricular diastolic collapse,Swinging heart

• Respiratory variation of tricuspid and mitral valve flow velocities.

• Right ventricular diastolic collapse is a highly sensitive and specific indicator of Cardiac Tamponade.

• Right atrial collapse although specific for Cardiac Tamponade was less sensitive for the detection of Cardiac Tamponade.

• Right heart collapse may not be seen in patients with pulmonary HTN and Cardiac Tamponade


CONCLUSIONS:

• The gold standard for the diagnosis of pericardial effusion is echocardiography.

• The diagnosis of Cardiac Tamponade is based solely on PHYSICAL EXAM.TREATMENT:When tamponade is present, urgent pericardiocentesis is required. Because the pressure– volume relationship in the pericardial fluid is curvilinear and up sloping, removal of a small amount of fluid often produces a dramatic fall in the intrapericardial pressure and immediate hemodynamic benefit; but complete drainage with a catheter is preferable.Surgical Care

• Pericardiocentesis: • Indicated in pt’s

• With effusions > 250 mL or • Effusion increases despite intensive dialysis for 10-14 days or • Evidence of tamponade.


•• Pericardial window is a modification of balloon valvuloplasty:

In which an uninflated balloon is passed inside the pericardial space, where it is opacified, inflated, and then pulled through the pericardium to create a window through which pericardial fluid drains into the peritoneal or pleural space

• Subxiphoid pericardiotomy:• Is performed under local anesthesia and has a lower risk of

complications compared to pericardiectomy. Consider subxiphoid pericardiotomy for large effusions that do not resolve.

• Pericardiectomy:• Is the most effective procedure managing large effusions because it

has the lowest associated risk of recurrent effusions. • It requires general anesthesia & thoracotomy; therefore, should be

considered only if pericardiotomy cannot be performed or has been unsuccessful.

EDIAGNOSIS Constrictive PericarditisESSENTIAL FOR DIAGNOSIS

Evidence of right heart failure with an elevated JVP, edema, hepatomegaly, and ascites.No fall or an elevation of the JVP with inspiration (Kussmaul sign). Echocardiographic evidence for septal bounce and reduced mitral inflow velocities with inspiration. Catheterization evidence for RV-LV interaction, a “square root” sign, equalization of diastolic pressures, normal pulmonary artery pressure, and narrow RV pressure tracing that increases with inspiration.


PATHOPHYSIOLOGY:Inflammation can lead to a thickened, fibrotic, adherent pericardium that restricts diastolic filling and produces chronically elevated venous pressures. In the past, tuberculosis was the most common cause of constrictive pericarditis, but the process now more often occurs after radiation therapy, cardiac surgery, or viral pericarditis; histoplasmosis is another uncommon cause

Fibrous scar formationFusion of pericardial layers

Calcification further stiffens pericardiumRigid, scarred pericardium encircles heart:

Systolic contraction normal Inhibits diastolic filling of both ventricles

¯ SV venous pressures

¯ CO Systemic & pulmonary congestion

Hypotension/shock JVD Rales Reflex tachycardia Hepatomegaly

Ascites Peripheral edema

Clinical FindingsA. Symptoms and Signs:

The principal symptoms are slowly progressive dyspnea, fatigue, and weakness. Chronic edema, Right hypochondrial pain or fullness, abdominal distention, lose of apetite are common symptoms.

Physical finding-HR, ¯BPascites, edema, hepatomegaly Hepatic congestion and ascites are usually present. Ascites often seems out of proportion to the degree of peripheral edema.


The examination reveals these signs and a characteristically elevated jugular venous pressure with a rapid y descent. This can be detected at bedside by careful observation of the jugular pulse and noting an apparent increased pulse wave at the end of systole (due to accentuation of the v wave by the rapid y descent).

Kussmaul sign—inspiration: ¯intrathoracic pressure, venous return to thorax

¯intrathoracic pressure not transmitted though to RV Þ No pulsus paradoxus!( unusual).

No inspiratory augmentation of RV filling (rigid pericardium) Intrathoracic systemic veins become distended ÞJVP rises with inspiration (normally falls)

Definition-a failure of the JVP to fall with inspiration—is also a frequent finding. The apex may actually retract with systole and a pericardial “knock” may be heard in early diastole.((sudden cessation of ventricular diastolic filling imposed by rigid pericardial sac)).Atrial fibrillation is common.

Summary = RT HEART FAILURE + JVP + PERICARDIAL KNOCK.

DIAGNOSIS

At times constrictive pericarditis is extremely difficult to differentiate from restrictive cardiomyopathy. When unclear, the use of noninvasive testing and cardiac catheterization is required to sort out the difference.

1. CHEST X RAY:

The chest radiograph may show normal heart size or cardiomegaly. Pericardial calcification is best seen on the lateral view and is uncommon. It rarely


involves the LV apex, and finding of calcification at the LV apex is more consistent with LV aneurysm.

2. Cardiac CT and MRI are only occasionally helpful. Pericardial thickening of > 4 mm must be present to establish the diagnosis, yet no pericardial thickening is demonstrated in 20–25% of patients with constrictive pericarditis

3. Echocardiography—Echocardiography rarely demonstrates a thickened pericardium. A septal “bounce” reflecting the rapid early filling is common, though. RV/LV interaction may be demonstrated by a reduction in the mitral inflow pattern of > 25%, much as in tamponade.

4. Cardiac catheterization-Because of the need to demonstrate RV/LV interaction, cardiac catheterization should include simultaneous measurement of both the LV and RV. Hemodynamically, patients with constriction have equalization of end-diastolic pressures throughout their cardiac chambers, there is rapid early filling then an abrupt increase in diastolic pressure (“square-root” sign), the RV end-diastolic pressure is more than one-third the systolic pressure, simultaneous measurements of RV and LV systolic pressure reveal a discordanceWith inspiration (the RV rises as the LV falls), and there is usually a Kussmaul sign (failure of the RA pressure to fall with inspiration).


The width (or area) of the RV pressure tracing may also be less in expiration and greater during inspiration, reflecting the variability in filling of the RV with respiration.In restrictive cardiomyopathy, the LV diastolic pressure is usually greater than the RV diastolic pressure by 5 mm Hg, there is pulmonary hypertension, and simultaneous measurements of the RV and LV systolic pressure reveal a concordant drop in the peak systolic pressure in both with inspiration .

Aetiology

Tuberculous Pericarditis Cardiac Sarcoidosis Cardiac Amyloidosis Giant Cell Myocarditis Radiation Post-surgery Neoplasm

TREATMENT:

Diuretics- Initial treatment consists of diuresis. As in other disorders of right heart failure, the diuresis should be aggressive, using loop diuretics (torsemide if bowel edema is suspected), thiazides ,and aldosterone antagonists (especially if ascites is present).Surgical pericardiectomy should be done when diuretics are unable to control symptoms. symptoms are usually dramatically improved.Most experts recommend earlier rather than later pericardiectomy if symptoms are present



Health & Medicine

Definition 0 f pericardial diseases