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Pericardial Diseases

The document discusses pericardial disease, focusing on types of pericarditis, their prevalence, risk factors, diagnostic methods, and treatments. It details the symptoms, diagnostic features, and treatment options for acute pericarditis and cardiac tamponade, as well as chronic constrictive pericarditis. The lecture aims to provide a comprehensive understanding of pericardial conditions for medical professionals.

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0% found this document useful (0 votes)
23 views41 pages

Pericardial Diseases

The document discusses pericardial disease, focusing on types of pericarditis, their prevalence, risk factors, diagnostic methods, and treatments. It details the symptoms, diagnostic features, and treatment options for acute pericarditis and cardiac tamponade, as well as chronic constrictive pericarditis. The lecture aims to provide a comprehensive understanding of pericardial conditions for medical professionals.

Uploaded by

Domeng Talks
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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“DON’T HEART ME"

PERICARDIAL DISEASE

DOMINGO B. AGREGADO JR. MD


LEVEL 3 INTERNAL MEDICINE RESIDENT
ADVENTIST MEDICAL CENTER-BACOLOD INC.
Learning Objectives:
• To explain and define the types of Pericarditis
• To discuss the prevalence and risks factors of patient
having Pericarditis
• To explain diagnostic modalities and treatments of
Pericarditis

Learning Disclosures:
 Source for this lecture is Harrisons Principles of Internal Medicine 21st
Edition
AZ 59/F Single Brgy. Taculing,
Bacolod
CC: Chest Pain
• About 1 week PTA, patient had onset of on and off PMH/Personal Hx
cough, non productive. No fever noted. No
medications taken and no consult done. • Hypertensive - Non
compliant
• 3 Days PTA, she had persistence of cough as
mentioned above. Despite being aware of the • DM - Non compliant
COVID protocols, she persisted to go to the salon to
get her hair rebonded. After having her hair • No history of
rebonded, she went to the dermatologist to have a previous MI
facial session. During the session, she manifested
chest pain which she noted to be intensified when • 10 pack-year
she was lying down and relieved by sitting up. She Smoker and
also noted that pain was aggravated when she was Occasional
coughing and radiating to the Trapezius area. Alcoholic Drinker (3
• ODA, Signs and symptoms mentioned above Long Neck Tanduay
persisted, thus went to the ER to seek consult and 2-3x/week)
AZ 59/F Single Brgy. Taculing, Bacolod
CC: Chest Pain

BP: 85/54 RR: 22


HR: 98 O2 Sat: 95% at RA
GENERAL APPEARANCE: Patient is conscious, coherent, oriented
HEENT: Pinkish conjunctivae, moist lips and tongue, non-enlarge , non-
hyperemic tonsils
CHEST/LUNGS: Symmetrical chest expansion with rales noted on basal LF, no
chest retraction
HEART: Rasping/Scratching upon auscultation, distended neck veins, muffled
heart sounds
ABDOMEN: Flat Abdomen, Normoactive bowel sounds, No mass palpated
EXTREMITIES: Full peripheral pulses, no cyanosis noted
SKIN: Good skin turgor, Capillary Refill time of <2s
ANATOMY AND PHYSIOLOGY
NORMAL FUNCTIONS OF THE PERICARDIUM

• Double-layered sac of the visceral


pericardium and parietal
pericardium
• Visceral pericardium is a serous
membrane that is separated from
the fibrous parietal pericardium
by a small quantity (15–50 mL) of
fluid
ACUTE PERICARDITIS
THE MOST COMMON PATHOLOGIC PROCESS INVOLVING THE
PERICARDIUM
CLASSIFICATION
4 PRINCIPAL DIAGNOSTIC FEATURES
ACUTE PERICARDITIS
1. CHEST PAIN
• Severe, retrosternal and/or left precordial
referred to neck, arms, or left shoulder
• Pleuritic, aggravated by inspiration and
coughing
• At times, it radiates to the trapezius ridge or
into either arm, and resembles that of
myocardial ischemia
• Intensified by lying supine and relieved by
sitting up and leaning forward
4 PRINCIPAL DIAGNOSTIC FEATURES
ACUTE PERICARDITIS

2. PERICARDIAL FRICTION RUB


• 85% of patients with acute pericarditis
• Described as rasping, scratching, or grating
• Heard most frequently at end expiration with
the patient upright and leaning forward
4 PRINCIPAL DIAGNOSTIC FEATURES
ACUTE PERICARDITIS
3. ECG Changes
• Without massive effusion usually displays
changes secondary to acute subepicardial
inflammation
• Typically evolves through four stages
4 PRINCIPAL DIAGNOSTIC FEATURES
ACUTE PERICARDITIS
3. ECG Changes in Comparison to AMI
• In AMI, ST elevations are upwardly convex, and
reciprocal depression is more prominent
• These changes may return to normal within a
day or two
• Q waves may develop, with loss of R-wave
amplitude, and T-wave inversions
• With acute pericarditis, these changes are
usually seen within hours before the ST
segments have become isoelectric
4 PRINCIPAL DIAGNOSTIC FEATURES
ACUTE PERICARDITIS
4. PERICARDIAL EFFUSION
• Usually associated with pain
• If the effusion is large, with electrical alternans
• Heart sounds may be fainter with large
pericardial effusion
• The base of the left lung may be compressed
by pericardial fluid, producing Ewart’s sign, a
patch of dullness, increased fremitus, and
egophony beneath the angle of the left scapula
ELECTRICAL ALTERNANS
DIAGNOSIS
• Echocardiography is the most widely used imaging technique. It is
sensitive, specific, simple, and noninvasive
• The presence of pericardial fluid is recorded by two-dimensional
transthoracic echocardiography as a relatively echo-free space
between the posterior pericardium and left ventricular epicardium
and/or as a space between the anterior right
• The diagnosis of pericardial fluid or thickening may be confirmed by
computed tomography (CT) or magnetic resonance imaging (MRI)
• MRI is also helpful in detecting pericardial inflammation
TREATMENT
Acute Pericarditis
• No specific treatment
• Bedrest
• Anti-inflammatory Drugs (1-2 weeks, then tapered over several
weeks), should be administered with gastric protection (Ex.
Omeprazole 20mg/day)
• Aspirin (2–4 g/d)
• Ibuprofen (600–800 mg tid)
• Indomethacin (25–50 mg tid)
• In addition, colchicine (0.5 mg qd [<70 kg] or 0.5 mg bid [>70 kg])
should be administered for 3 months
TREATMENT
Acute Pericarditis

• Anticoagulants should be avoided because their use could cause


bleeding into the pericardial cavity and tamponade
• Full-dose corticosteroids should be given for only 2–4 days and then
tapered
• In patients with multiple, frequent, and disabling recurrences that
continue for >2 years, are not prevented by continuing colchicine
and other NSAIDs, and are not controlled by glucocorticoids —>
azathioprine or anakinra (an interleukin 1β receptor antagonist)
CARDIAC TAMPONADE
Accumulation of fluid in the pericardial space in a
quantity sufficient to cause serious obstruction of the
inflow of blood into the ventricles
CARDIAC TAMPONADE
CAUSES

• Idiopathic pericarditis
• Pericarditis secondary to:
• Neoplastic Disease
• Tuberculosis
• Bleeding into the pericardial space after leakage from an aortic
dissection, cardiac operation, trauma or treatment with
anticoagulants
CARDIAC TAMPONADE
3 Principal Features (Beck’s Triad)
CARDIAC TAMPONADE
How to Identify at thse ER/Wards

High index of suspicion for cardiac tamponade is required


because in many instances no obvious cause for pericardial
diseases apparent
Unexplained sudden enlargement of the cardiac silhouette,
hypotension, and elevation of jugular venous pressure
Reductions in amplitude of the QRS complexes and electrical
alternans of the P, QRS, or T waves
CARDIAC TAMPONADE
Paradoxical Pulse

Greater than normal (10 mmHg) inspiratory decline in systolic


arterial pressure

Because both ventricles share a tight incompressible covering, i.e.,


the pericardial sac, the inspiratory enlargement of the right ventricle
causes leftward bulging of the interventricular septum, reducing left
ventricular volume, stroke volume, and arterial systolic pressure
CARDIAC TAMPONADE
Diagnosis

Echocardioagraphy

When pericardial effusion causes tamponade, Doppler ultrasound


shows that tricuspid and pulmonic valve flow velocities increase
markedly during inspiration

Pulmonic vein, mitral, and aortic flow velocities decrease (As with
Constrictive Pericarditis)

Late diastolic inward motion (collapse) of the right ventricular free


wall and the right atrium
CARDIAC TAMPONADE
Treatment: Pericardiocentesis
Pericardiocentesis using an apical, parasternal, or, most commonly,
subxiphoid approach must be carried out at once

Intravenous saline may be administered as the patient is being


readied for the procedure

If possible, intrapericardial pressure should be measured before fluid


is withdrawn and the pericardial cavity should be drained as
completely as possible

In developed nations, bloody fluid is most commonly due to


neoplasm, renal failure, or after cardiac injury

In developing nations, tuberculosis, may also cause exudative and/or


bloody effusion
POST-CARDIAC INJURY SYNDROME
• One common feature—previous injury to the myocardium with blood
in the pericardial cavity
• May develop after a cardiac operation (postpericardiotomy
syndrome), after blunt or penetrating cardiac trauma, and after
perforation of the heart with a catheter
• Principal symptom is the pain of acute pericarditis, which usually
develops 1–4 weeks after the cardiac injury
• The pericarditis may be of the fibrinous variety, or it may be a
pericardial effusion, which is often serosanguinous and rarely causes
tamponade
• Often no treatment is necessary aside from aspirin and analgesics
VIRAL OR IDIOPATHIC ACUTE PERICARDITIS
• Coxsackievirus A or B or the virus of influenza, echovirus, mumps,
Herpes simplex, varicella/zoster, adenovirus, or cytomegalovirus has
been isolated from pericardial fluid
• Frequently, a viral cause cannot be established, and the term
idiopathic acute pericarditis is appropriate
• Most common in young adult males and is often associated with
pleural effusion and pneumonitis
• Elevations of C-reactive protein and of the white blood cell count are
common
• The ST-segment alterations in the ECG usually disappear after 1 or
more weeks, but the abnormal T waves may persist for as long as
several years
• The most frequent complication is recurrent (relapsing) pericarditis
CHRONIC CONSTRICTIVE
PERICARDITIS
Results when the healing of an acute fibrinous or serofibrinous pericarditis or
the resorption of a chronic pericardial effusions followed by obliteration of
the pericardial cavity with the formation of granulation tissue
CHRONIC CONSTRICTIVE
PERICARDITIS
Epidemiology and Etiology

• In developing nations, a high percentage of cases are of tuberculous


origin
• May follow acute or relapsing viral or idiopathic pericarditis, trauma
with organized blood clot, or cardiac surgery of any type, or results
from mediastinal irradiation, purulent infection, histoplasmosis,
neoplastic disease (especially breast cancer, lung cancer, and
lymphoma), rheumatoid arthritis, SLE, or chronic renal failure treated
by chronic dialysis
• In many patients, the cause of the pericardial disease is
undetermined
CHRONIC CONSTRICTIVE
PERICARDITIS
Pathophysiology
• Inability of the ventricles to fill owing to the limitations imposed by the
rigid, thickened pericardium
• Ventricular filling is unimpeded during early diastole but is reduced
abruptly when the elastic limit of the pericardium is reached, whereas in
cardiac tamponade, ventricular filling is impeded throughout diastole
• In both conditions, ventricular end-diastolic and stroke volumes are
reduced and the end-diastolic pressures in both ventricles and the mean
pressures in the atria, pulmonary veins, and systemic veins are all
elevated to similar levels
• Right and left atrial pressure pulses display an M-shaped contour, with
prominent x and y descents
• The y descent, which is absent or diminished in cardiac tamponade, is the
most prominent deflection in constrictive pericarditis; it reflects rapid early
CHRONIC CONSTRICTIVE
PERICARDITIS
Clinical and Laboratory Findings
• Weakness, fatigue, weight gain, increased abdominal girth,
abdominal discomfort, and edema are common
• In advanced cases, anasarca, skeletal muscle wasting, and cachexia
may be present
• The neck veins are distended and may remain so even after
intensive diuretic treatment, and venous pressure may fail to decline
during inspiration (Kussmaul’s sign)
• The pulse pressure is normal or reduced. A paradoxical pulse can be
detected in about one-third of cases
• The apical pulse is reduced and may retract in systole (Broadbent’s
sign)
CHRONIC CONSTRICTIVE
PERICARDITIS
Clinical and Laboratory Findings
• ECG frequently displays low voltage of the QRS complexes and diffuse flattening
or inversion of the T waves
• Atrial fibrillation is present in about one-third of patients
• Congestive hepatomegaly is pronounced, may impair hepatic function, and may
cause jaundice
• Transthoracic echocardiogram often shows pericardial thickening, dilation of the
inferior vena cava and hepatic veins, and a sharp halt to rapid left ventricular
filling in early diastole, with normal ventricular systolic function and flattening of
the left ventricular posterior wall
• Doppler Echocardiography: During inspiration, there is an exaggerated reduction
in blood flow velocity in the pulmonary veins and across the mitral valve, and a
leftward shift of the ventricular septum; the opposite occurs during expiration.
Diastolic flow velocity in the inferior vena cava into the right atrium and across
the tricuspid valve increases in an exaggerated manner during inspiration and
declines during expiration
CHRONIC CONSTRICTIVE
PERICARDITIS
Differential Diagnosis
• Cor pulmonale: marked systemic venous hypertension, little
pulmonary congestion, a (left) heart that is not enlarged, and a
paradoxical pulse. However, in cor pulmonale, advanced
parenchymal pulmonary disease is usually apparent and venous
pressure falls during inspiration (i.e., Kussmaul’s sign is negative)
• Tricuspid Stenosis: congestive hepatomegaly, splenomegaly, ascites,
and venous distention. However, the characteristic murmur and that
of accompanying mitral stenosis are usually present
• Restrictive cardiomyopathy: similar pathophysiologic underpinning
(i.e., restriction of ventricular filling)
CHRONIC CONSTRICTIVE
PERICARDITIS
Treatment
• Pericardial resection is the only definitive treatment of constrictive
pericarditis and should be as complete as possible
• Coronary arteriography should be carried out preoperatively in
patients aged >50 years to exclude unsuspected accompanying
coronary artery disease
• The benefits derived from cardiac decortication are usually
progressive over a period of months
• Operative mortality is in the range of 5–10% even in experienced
centers; the patients with the most severe disease, especially
secondary to radiation therapy, are at highest risk
Thank You and God bless!

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