Acute Pericarditis

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Acute Pericarditis

• Yrd.Doç. Dr. Olcay ÖZVEREN

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Pericardial physiology includes 3 main functions.

• First, through its mechanical function, the
  pericardium 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.

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• 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

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• A pericardial friction rub is pathognomonic for
  acute pericarditis. 
• The rub has a scratching, grating sound similar
  to leather rubbing against 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.

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Cardiac Tamponad
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Pathophysiology

• 3 phases of hemodynamic changes in tamponade.1
• 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

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etiology

• 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

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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.

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• Normal inspirasyon esnasinda sistemik arteryel
  basinçta 5-8 mmHglik düsüs normaldir.
• Kalp tamponadinda sistolik arter basinci normal
  inspirasyonda 10 mmHg veya daha fazla düser, buna
  Pulsus Paradoksus denir ve tamponad için önemli
  bir bulgudur.
• Pulsus paradoksusun nabiz bulgusu olarak
  algilanabilmesi için ekspiryum-inspiryum
  arasindaki sistolik basinç farkinin 20 mmHgnin
  üzerinde olmasi gerekmektedir. Bu durumlarda
  hastanin abdomeni izlenir, inspirasyon ile
  abdomen yükseldigi anda radiyal nabiz zayiflar
  veya kaybolur.
• Pulsus paradoksus invaziv arteryel
  monitörizasyonla veya noninvaziv olarak
  degerlendirilebilir. Noninvaziv olarak tansiyon
  aletinin mansonu sistolik kan basincinin 15 mmHg
  üzerine kadar sisirilir, sonra sistolik seslerin
  ilk olarak duyuldugu noktaya kadar mansonun
  havasi yavas yavas indirilir. Daha sonra tüm
  atimlar devamli olarak duyuluncaya kadar
  indirmeye devam edilir. Ilk sistolik seslerin
  kesintili olarak duyuldugu nokta ile korotkoff
  seslerin devamli olarak duyuldugu nokta
  arasindaki fark pulsus paradoksusun büyüklügünü
  verir.
• Pulsus paradoksusun nedeni kalp tamponadinda
  inspirasyonda bir miktar azalan intraperikardiyal
  basinç, sag ventrikülün diyastol diyastol basinda
  hizla dolmasina izin verir ve bu dolusla iyice
  artan sag ventrikül diyastolik basinci
  interventriküler septumu sol ventriküle dogru
  iter. Septumun sola dogru kaymasiyla küçülen sol
  ventrikül kavitesinin diyastolik dolusu azalir.
  Buna inspirasyon sirasinda artan pulmoner venöz
  göllenme eklenir ve sonuçta sol ventrikül atim
  volümü, dolayisiyla sistolik kan basinci daha da
  düserek pulsus paradoksus meydana gelir.

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• Kalp tamponadinda venöz dönüsün ve kalp dolusunun
  engellenmesi boyun ven dolgunlugunun ileri
  derecede artmasina ve ven pulsasyonlarinda
  belirgin degisikliklere neden olur.

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• Normalde kalbe olan venöz dönüs, boyun venlerinin
  ventrikül sistolüne rastlayan X çöküntüsü ve
  atriyumlarin bosalmalarina rastlayan Y inisi
  süresince olur. Kalp tamponadinda ventrikül
  volümü hizli ejeksiyon esnasinda hizla küçüldügü
  için intraperikardiyal basinç ve sag atriyum
  basinci da hizla düser ve bunun sonucunda X
  çöküntüsü belirgin olur. Intraperikardiyal basinç
  yüksekligi nedeniyle ventrikül diyastolü tam
  olmadigi ve tüm diyastol boyunca kompresyon
  oldugu için Y inisi yavaslar, hatta kaybolur.

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ECG

• Elektrokardiyografi (EKG) normal olmakla birlikte
  siklikla nonspesifik degisiklikler özellikle de
  ST-T dalga degisiklikleri bulunur.
• Kalbin perikard sivisi içerisinde yüzmesine bagli
  olarak QRS kompleksinde nadiren de P ve/veya T
  dalgasini da kapsayacak sekilde üç veya dört
  atimda bir voltaj degisikligi izlenir ve bu durum
  elektriki alternans olarak adlandirilir.
• Hem P hem de QRS komplekslerinde elektriki
  alternans izlenmesi tamponad için spesifiktir.
• QRS voltajinda azalma izlenir.

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Telekardiyografi
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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
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management

• All patients should receive the following
• Oxygen
• Volume expansion with blood, plasma, dextran, or
  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

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• Positive-pressure mechanical ventilation should
  be avoided because it may decrease venous return
  and aggravate signs and symptoms of tamponade

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pericardiocentesis

• Removal of pericardial fluid is the definitive
  therapy for tamponade and can be done 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

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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 pericardio-peritoneal 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.

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Constrictive Pericarditis
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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

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• 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.

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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 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.

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Causes

• Idiopathic
• Infectious (tbc.bacterial . viral )
• Radiation-induced
• Postsurgical
• Neoplasms
• Uremia.
• Connective tissue disorders
• Drug-induced Procainamide and hydralazine
  Methysergide therapy
• Trauma

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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
  lt150 ng/L). BNP levels are generally higher in
  restrictive cardiomyopathy (diagnostic if gt650
  ng/L) and may be useful in differentiating these
  disorders .

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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
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Echocardiography

• an early diastolic septal notch or "septal bounce
• evidence of right-sided pressure overload such as
  atrial septal shifting to 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 (gt8
  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

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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)

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Right atrial pressure tracing showing marked y
descents in constrictive pericarditis.
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management

• medical considerations are as follows
• Subacute constrictive pericarditis may respond to
  steroids if 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

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Complete pericardectomy

• Results are generally better if the procedure is
  performed earlier in the 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

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