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Acute Pericarditis
Yrd.Doç. Dr. Olcay ÖZVEREN
Pericardial physiology includes 3 main functions.
• First, through its mechanical function, the pericardium
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promotes cardiac efficiency by limiting acute dilation,
maintaining ventricular compliance with preservation of
the Starling curve, and distributing hydrostatic forces.
The pericardium also creates a closed chamber with
subatmospheric pressure that aids atrial filling and
lowers transmural cardiac pressures.
Second, through its membranous function, the
pericardium shields the heart by reducing external
friction and acting as a barrier against extension of
infection and malignancy.
Third, through its ligamentous function, the pericardium
anatomically fixes the heart.
• Chest pain is the cardinal symptom.
• The quality of the pain may be sharp, dull,
aching, burning, or pressing.
• Intensity varies from barely perceptible to
severe.
• Pain is usually precordial with referral to the
trapezius ridge.
• It is worse during inspiration, when lying flat,
or during swallowing and with body motion
• A pericardial friction rub is pathognomonic for acute pericarditis.
• The rub has a scratching, grating sound similar to leather rubbing against
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leather.
Auscultation with the diaphragm of the stethoscope over the left lower
sternal edge allows the best detection of the rub.
Auscultation during end expiration with the patient sitting up and leaning
forward increases the likelihood of observing this physical finding.
Serial examinations may be necessary for detection.
More than 50% of rubs are triphasic. They are composed of (1) an atrial
systolic rub that precedes S1, (2) a ventricular systolic rub between S1 and
S2 and coincident with the peak carotid pulse, and (3) an early diastolic rub
after S2 (usually the faintest).
The biphasic to-and-fro rub is less common (24%). It can occur with
tachycardia and is due to summation of the atrial and early diastolic rub.
Monophasic rubs (the ventricular systolic) are the least common but may
occur in patients with atrial fibrillation.
Especially when it is monophasic, the pericardial friction rub can be
mistaken for a systolic murmur. Pericardial rubs may be differentiated if
the rub does not change with usual respiratory or positional maneuvers, if 3
components are present, and if the findings on the ECG are typical.
Cardiac Tamponad
Pathophysiology
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3 phases of hemodynamic changes in tamponade.1
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Phase I: The accumulation of pericardial fluid causes
increased stiffness of the ventricle, requiring a higher
filling pressure. During this phase, the left and right
ventricular filling pressures are higher than the
intrapericardial pressure.
Phase II: With further fluid accumulation, the
pericardial pressure increases above the ventricular
filling pressure, resulting in reduced cardiac output.
Phase III: A further decrease in cardiac output occurs,
which is due to equilibration of pericardial and left
ventricular (LV) filling pressures.
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• Rapid accumulation of pericardial fluid
may cause elevated intrapericardial
pressures with as little as 80 mL of fluid,
while slowly progressing effusions can
grow to 2 L without symptoms
etiology
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Infectious
viral.
Pyogenic
Tuberculous
Fungal (histoplasmosis, coccidioidomycosis, Candida)
Other infections (syphilitic, protozoal, parasitic)
Neoplasia
Postoperative/postprocedural
Uremia
Myxedema
Severe pulmonary hypertension
Radiation therapy
Acute myocardial infarction,
Aortic dissection,
Trauma
Familial Mediterranean fever
Systemic lupus erythematosus
Drug-associated (eg, procainamide, hydralazine, isoniazid,
minoxidil, phenytoin, anticoagulants, methysergide
Physical findings
• The Beck triad or acute compression triad
• Described in 1935, this complex of
physical findings refers to
• increased jugular venous pressure,
• hypotension,
• and diminished heart sounds.
• Normal inspirasyon esnasında sistemik arteryel basınçta 5-8 mmHg’lık düşüş
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normaldir.
Kalp tamponadında sistolik arter basıncı normal inspirasyonda 10 mmHg veya
daha fazla düşer, buna “Pulsus Paradoksus” denir ve tamponad için önemli bir
bulgudur.
Pulsus paradoksusun nabız bulgusu olarak algılanabilmesi için ekspiryuminspiryum arasındaki sistolik basınç farkının 20 mmHg’nın üzerinde olması
gerekmektedir. Bu durumlarda hastanın abdomeni izlenir, inspirasyon ile
abdomen yükseldiği anda radiyal nabız zayıflar veya kaybolur.
Pulsus paradoksus invaziv arteryel monitörizasyonla veya noninvaziv olarak
değerlendirilebilir. Noninvaziv olarak tansiyon aletinin manşonu sistolik kan
basıncının 15 mmHg üzerine kadar şişirilir, sonra sistolik seslerin ilk olarak
duyulduğu noktaya kadar manşonun havası yavaş yavaş indirilir. Daha sonra tüm
atımlar devamlı olarak duyuluncaya kadar indirmeye devam edilir. İlk sistolik
seslerin kesintili olarak duyulduğu nokta ile korotkoff seslerin devamlı olarak
duyulduğu nokta arasındaki fark pulsus paradoksusun büyüklüğünü verir.
Pulsus paradoksusun nedeni; kalp tamponadında inspirasyonda bir miktar azalan
intraperikardiyal basınç, sağ ventrikülün diyastol diyastol başında hızla dolmasına
izin verir ve bu doluşla iyice artan sağ ventrikül diyastolik basıncı interventriküler
septumu sol ventriküle doğru iter. Septumun sola doğru kaymasıyla küçülen sol
ventrikül kavitesinin diyastolik doluşu azalır. Buna inspirasyon sırasında artan
pulmoner venöz göllenme eklenir ve sonuçta sol ventrikül atım volümü,
dolayısıyla sistolik kan basıncı daha da düşerek pulsus paradoksus meydana
gelir.
• Kalp tamponadında venöz dönüşün ve kalp
doluşunun engellenmesi boyun ven
dolgunluğunun ileri derecede artmasına ve
ven pulsasyonlarında belirgin değişikliklere
neden olur.
• Normalde kalbe olan venöz dönüş, boyun
venlerinin ventrikül sistolüne rastlayan X
çöküntüsü ve atriyumların boşalmalarına
rastlayan Y inişi süresince olur. Kalp
tamponadında ventrikül volümü hızlı ejeksiyon
esnasında hızla küçüldüğü için intraperikardiyal
basınç ve sağ atriyum basıncı da hızla düşer ve
bunun sonucunda X çöküntüsü belirgin olur.
İntraperikardiyal basınç yüksekliği nedeniyle
ventrikül diyastolü tam olmadığı ve tüm diyastol
boyunca kompresyon olduğu için Y inişi yavaşlar,
hatta kaybolur.
ECG
• Elektrokardiyografi (EKG) normal olmakla birlikte
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sıklıkla nonspesifik değişiklikler özellikle de ST-T
dalga değişiklikleri bulunur.
Kalbin perikard sıvısı içerisinde yüzmesine bağlı
olarak QRS kompleksinde nadiren de P ve/veya
T dalgasını da kapsayacak şekilde üç veya dört
atımda bir voltaj değişikliği izlenir ve bu durum
“elektriki alternans” olarak adlandırılır.
Hem P hem de QRS komplekslerinde elektriki
alternans izlenmesi tamponad için spesifiktir.
QRS voltajında azalma izlenir.
Telekardiyografi
ekokardiyografi
Pericardial efusion
Early diastolic collapse of the right ventricular free wall
Late diastolic compression/collapse of the right atrium
Ivc pleathore
Swinging heart
A greater than 40% relative inspiratory augmentation of right-side flow
A greater than 25% relative decrease in inspiratory flow across the mitral valve
management
• All patients should receive the following:
• Oxygen
• Volume expansion with blood, plasma, dextran, or
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isotonic sodium chloride solution, as necessary to
maintain adequate intravascular volume:
Sagrista-Saauleda et al noted significant increase
in cardiac output after volume expansion.14
Bed rest with leg elevation: This may help
increase venous return.
Inotropic drugs (eg, dobutamine): These can be
useful because they do not increase systemic
vascular resistance while increasing cardiac
output
• Positive-pressure mechanical ventilation
should be avoided because it may
decrease venous return and aggravate
signs and symptoms of tamponade
pericardiocentesis
• Removal of pericardial fluid is the definitive therapy for tamponade and can be done
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by the following 3 methods.
Emergency subxiphoid percutaneous drainage: This is a life-saving bedside
procedure. The subxiphoid approach is extrapleural; hence, it is the safest
for blind pericardiocentesis. A 16- or 18-gauge needle is inserted at an
angle of 30-45° to the skin, near the left xiphocostal angle, aiming
towards the left shoulder. When performed emergently, this procedure is
associated with a reported mortality rate of approximately 4% and a
complication rate of 17%.
Echocardiographically guided pericardiocentesis (often performed in the
cardiac catheterization laboratory): This is usually performed from the left
intercostal space. First, mark the site of entry based on the area of
maximal fluid accumulation closest to the transducer. Then, measure the
distance from the skin to the pericardial space. The angle of the transducer
should be the trajectory of the needle during the procedure. Avoid the
inferior rib margin while advancing the needle to prevent neurovascular
injury. Leave a 16-gauge catheter in place for continuous drainage.
Percutaneous balloon pericardiotomy: This can be performed using an
approach similar to that for echo-guided pericardiocentesis, in which the
balloon is used to create a pericardial window
surgical
• Surgical creation of a pericardial window: This involves the
surgical opening of a communication between the
pericardial space and the intrapleural space. This is usually
a subxiphoidian approach with resection of xiphoid.
Recently, a left paraxiphoidian approach with preservation
of xiphoid has been described. Open thoracotomy and/or
pericardiotomy3 may be required in some cases, and these
should be performed by an experienced surgeon.
• Pericardiocentesis or sclerosing the pericardium: This is a
therapeutic option for patients with recurrent pericardial
effusion or tamponade. Through the intrapericardial
catheter, corticosteroids, tetracycline, or antineoplastic
drugs (eg, anthracyclines, bleomycin) can be instilled into
the pericardial space.
• Pericardio-peritoneal shunt: In some patients with
malignant pericardial effusions, creation of a pericardioperitoneal shunt helps prevent recurrent tamponade.
• Pericardiectomy: Resection of the pericardium
(pericardiectomy) through a median sternotomy or left
thoracotomy is rarely required to prevent recurrent
pericardial effusion and tamponade.
Constrictive Pericarditis
Pathophysiology
• The normal pericardium is composed of 2 layers: the
tough fibrous parietal pericardium and the smooth
visceral pericardium. Usually, approximately 50 mL of
fluid (plasma ultrafiltrate) is present in the
intrapericardial space to minimize friction during cardiac
motion.
• Acute and subacute forms of pericarditis (which may or
may not be symptomatic) may deposit fibrin, which may,
in turn, evoke a pericardial effusion. This often leads to
pericardial organization, chronic fibrotic scarring, and
calcification, most often involving the parietal
pericardium
• This thickened fibrotic pericardium, regardless of cause,
impedes normal late diastolic filling, distinguishing
constrictive from restrictive pericarditis. Since
the myocardium is unaffected, early ventricular filling during
the first third of diastole is unimpeded, but afterwards, the stiff
pericardium affects flow and hemodynamics. In other words,
the ventricular pressure decreases rapidly early (producing a
steep y descent on right atrial pressure waveform tracings) and
then increases abruptly to a level that is sustained until systole
("dip-and-plateau waveform" or "square root sign" seen on
right or left ventricular pressure waveform tracings).
• The clinical symptoms and classic hemodynamic findings can
be explained by early rapid diastolic filling and elevation and
equalization of the diastolic pressures in all of the cardiac
chambers restricting late diastolic filling, leading to venous
engorgement and decreased cardiac output, all secondary to a
confining pericardium.
Physical findings
• Constrictive pericarditis presents with a myriad of symptoms,
making a diagnosis based solely on clinical history virtually
impossible. Additionally, these symptoms may develop slowly
over a number of years such that patients may not be aware of all
of their symptoms until questioned.
• Dyspnea tends to be the most common presenting symptom and
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occurs in virtually all patients. Fatigue and orthopnea are common.
Lower-extremity edema and abdominal swelling and discomfort
are other common symptoms. Nausea, vomiting, and right upper
quadrant pain, if present, are thought to be due to hepatic
congestion, bowel congestion, or both.
The initial history may be more compatible with liver disease
(cryptogenic cirrhosis) than with pericardial constriction because of
the predominance of findings related to the venous system.
Chest pain, presumably due to active inflammation, may be
present, although this is observed in a minority of patients.
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muscle wasting, cachexia, or jaundice.
pleural effusion, hepatomegaly, or ascites.
Elevated jugular venous pressures
Sinus tachycardia
The apical impulse is often impalpable, and the patient may have
distant or muffled heart sounds.
A pericardial knock, which corresponds with the sudden cessation
of ventricular filling early in diastole, occurs in approximately
half the cases and may be mistaken for an S3 gallop. However, a
knock is of higher frequency than an S3 and occurs slightly earlier
in diastole
The Kussmaul sign (ie, elevation of systemic venous pressures
with inspiration) is a common nonspecific finding, but this sign is
also observed in patients with right ventricular failure, restrictive
cardiomyopathy, right ventricular infarction, and tricuspid
stenosis, although, importantly, not in patients with cardiac
tamponade.
Causes
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Idiopathic
Infectious (tbc.bacterial . viral )
Radiation-induced
Postsurgical
Neoplasms:
Uremia:.
Connective tissue disorders:
Drug-induced: Procainamide and hydralazine
Methysergide therapy
Trauma:
Lab.
• The level of brain natriuretic peptide
(BNP), a cardiac hormone released in
response to increased ventricular wall
stretch, is often mildly increased in
constrictive pericarditis (usually <150
ng/L). BNP levels are generally higher in
restrictive cardiomyopathy (diagnostic
if >650 ng/L) and may be useful in
differentiating these disorders .
radiology
Pericardial thickening of more than 4 mm
assists in differentiating constrictive disease
from restrictive cardiomyopathy, and a
Thickening of more than 6 mm adds
even more specificity for constriction
Echocardiography
• an early diastolic septal notch or "septal bounce
• evidence of right-sided pressure overload such as atrial septal shifting to
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the left with inspiration or dilated inferior and superior vena cavae and
hepatic veins
Respiratory variation is usually greater in constriction than in restriction
(probably because of the normal intraventricular septum), usually with over
25% changes. With restriction, often the E/A ratio is more than 2, the
deceleration time is less than 150 ms, and the relaxation time is less than
60 ms. Unfortunately, when such Doppler findings are not present, the
diagnostic reliability decreases. If a concomitant pericardial effusion is
present, it may account for some respiratory variation .
Tissue Doppler echocardiography, measures the actual endocardial and
epicardial tissue velocities. Since myocardial relaxation itself is preserved in
pure constrictive pericarditis, the early relaxation myocardial velocity (Ea,
also known as Em) is normal, whereas it is abnormal with restriction (when
intrinsic myocardial disease is present). For example, given that a normal
Ea is more than 10 cm/s, a near-normal (>8 cm/s) Ea supports constriction,
whereas a much lower Ea supports restriction.16 The newer method of
speckle tracking of B-mode images measures cardiac longitudinal and
circumferential deformation. Patients with constrictive pericarditis were
found to have constrained circumferential deformation rather than the
longitudinal constraint found in patients with restrictive cardiomyopathy
Right heart catheterization
• Elevated left and right ventricular diastolic pressures equalized within 5
mm Hg
• Right ventricular systolic pressure less than 55 mm Hg
• Mean right arterial pressure greater than 15 mm Hg
• Right ventricular end-diastolic pressure greater than one third of the right
ventricular systolic pressure (narrow pulse pressure)
Right atrial pressure tracing showing marked y descents in
constrictive pericarditis.
management
• medical considerations are as follows:
• Subacute constrictive pericarditis may respond to steroids if
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treated before pericardial fibrosis occurs.
Diuretics are commonly used to relieve congestion if
ventricular filling pressures are clinically elevated. However,
this may decrease cardiac output and requires careful
monitoring.
Any therapy directed toward the causative disease is
appropriate, such as antituberculosis medication.
Complications, such as atrial arrhythmias, require their own
therapy as needed.
In general, beta-blockers and calcium channel blockers should
be avoided because the sinus tachycardia that commonly
occurs in constrictive pericarditis is compensatory in nature,
maintaining cardiac output in a setting of fixed stroke volume
(secondary to fixed diastolic filling
Complete pericardectomy
• Results are generally better if the procedure is performed earlier in the
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course, when less calcification is present and when the chance of abnormal
myocardium or advanced heart failure is reduced.
Some judgment is required because patients who are asymptomatic (NYHA
class I) or who have early NYHA stage II symptoms may be clinically
stable for years.
The published surgical mortality rates range from 5-15%
Even though the symptoms following a pericardiectomy are commonly
improved, evidence of abnormal diastolic filling (which can be correlated
with clinical status) often remains. Only 60% of patients have complete
normalization of cardiac hemodynamics
Cardiac mortality and morbidity seems to be related to presurgical
myocardial atrophy or fibrosis, which can be detected using CT.
Excluding these patients keeps the mortality rate at the lower end of
the range (5%).
Postoperative low cardiac output can be treated in the usual
fashion, including vasoactive pressors and intra-aortic balloon pump
(IABP), if necessary