PERICARDIAL INVOLVEMENT

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PERICARDIAL INVOLVEMENT
IN CRITICAL ILLNESS
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KEY POINTS

• Pericardial disease should be considered in any
  patients with low cardiac output and elevated
  right atrial pressure
• Understanding the events of ventricularfilling
  is the key to distinguish betweencardiac
  tamponade and constrictivepericarditis
• Echocardiogram is the best noninvasivetool for
  evaluation the presence and significance of
  effusive pericardial disease

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KEY POINTS

• There is no general consensus as to which
  drainage procedure is best used to
  treateffusive pericardial disease
• Pericardial disease is not a contraindicationto
  anticoagulation
• Purulent pericarditis is exceedingly uncommon,
  even in immunocompromisedpatients

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Differential Diagnosis

• Cardiac Tamponade
• Constrictive Pericarditis
• Effusive-Constrictive Pericarditis

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Differential Diagnosis

• To determine the potential cause for concern
• To be able to address the issues
  ofanticoagulation, ischemia, and infection in
  patients with pericardialeffusion or acute
  pericarditis

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Hemodynamic Effects ofPericardial Disease

• The pericardial disease interferes withcardiac
  filling- rapidly in effusive disease- slowly in
  constrictive disease- chronic pericardial
  disease also can deteriorate rapidly
• Parietal and visceral pericardium encaseatrium
  and ventricle influence theircompliance

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V ventricular contraction A atrial
contraction Y descent early diastole passive
ventricular filling X descent isovolemic
atrial relaxation
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Pericardial Pressure

• Pericardial pressure is distributed amongall
  chambers in a manner which equalizesthe
  intracavity pressures
• This effect is present at all chamber volumes,
  thereby reducing the gradient forblood flow
  between the chambers throughout diastole in small
  amount ofpericardial effusion

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1.Transmural pressure intracavity -
pericardial pressure2.Distending pressure-Stroke
volume is according to Frank-Starling priciple
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Hemodynamics in Cardiac Tamponade

• If pericardial pressure exceeds the pressureto
  distend the chamber, cardiac filling cannot
  occur
• Equalization of the diastolic pressures onboth
  sides of the heart right atrial a wave pressure
  (RA pressure) RVEDP (right ventricular
  end-diastolic pressure) pulmonary wedge a wave
  (LA pressure) LVEDP (left ventricular
  end-diastolic pressure)

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Equalization of Pressures
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Absence of Y Descent Wavein Cardiac Tamponade

• Because of equalization of four chambers
  pressures, no blood flow crosses the
  atrio-ventricular valve in early diastole
  (passive ventricular filling, Y descent) except a
  wave (atrial contraction)

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Absence of Y Descent Wavein Cardiac Tamponade
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Reduced Passive Filling in Cardiac Tamponade
Slow Rise in Ventricular Pressure in Early
Diastole
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Tamponade Physiology
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Summary in Cardiac Tamponade

• Elevated diastolic pressure
• Equal end-diastolic pressure in RV and LV
• Absence of ventricular filling early in diastole
• Absent Y decent in the atrial tracings

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Hemodynamics in Constrictive Pericarditis

• During constriction, pericardium encasesthe
  heart like a box, and the heart can onlydistend
  to an certain extent then stops
• The rapid early diastolic filling and abrupthalt
  gives rise to the classic dip and
  plateauconfiguration
• In the atrial pressure tracing, rapid ventricular
  filling (passive atrial emptying)resulting in a
  rapid Y descent with a nadir and sharp rise in
  atrial pressure as the ventricle cannot expand
  further

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Hemodynamics in Constrictive Pericarditis

• Similarly, following atrial systole the fallin
  atrial pressure, or x descent is rapid, witha
  quick rise in atrial pressure--- M shape in
  right atrial tracing
• Because the overall volume of pericardiumis
  fixed, it will result in identical LVEDPand
  RVEDP once the limitation of chamberenlargement
  are met

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Dip and Plateau Configuration
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M Shape Atrial Tracing in CP
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Equalization of Pressures
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Pressure Tracings in Constrictive Pericarditis
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Kussmauls Sign

• Mechanism 1) Increase venous pressure due to
  reduced compliance of pericardium and heart
  ? venous return may stop abruptly during
  inspiration due to impaired cardiac
  filling 2) Increase abdominal presssure during
  inspiration with elevated venous pressure
  
• Clinical presentation inspiratory engorgementof
  jugular vein
• Also seen in cardiomyopathy, pulmonaryembolism,
  and right ventricular infarction

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Summary in Constrictive Pericarditis (CP)

• Elevated diastolic pressure
• Equal diastolic pressure in RV and LV
• Completion of ventricular filling early
  indiastole recognized as the dip and plateau in
  the ventricular tracing
• Rapid x and y descents in the atrial tracings
• Presence of the Kussmauls sign

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Paradoxical Pulse
During inspiration, the drop of blood pressure
is more than 10 mmHg --- Meachanism
Inspiration -gt Increase RA venous return -gt RA,
RV pressure and volume increase -gt Compress
septum to left -gt Compress LV -gt Decrease LV
cardiac output --- Also seen in severe
myocardial failure, effusive constrictive
pericarditis, and constrictive pericarditis
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EFFUSIVE-CONSTRICTIVEPERICARDITIS

• Presentation - The combination of cardiac
  tamponade and constrictive pericarditis
• Most common seen in Malignancy
• Clinical presentation is tamponade
  beforepericardial fluid is removed
• After pericardial fluid was removed,
  constric-tion is considered if no improvement of
  hemodynamics

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Diagnostic Consideration

• CXR water bottle appearance
• ECG sinus tachycardia, electrical alternans,
  T wave abnormality, low voltage in
  ECG leads (tamponade) ST elevation, PR
  segment depression (acute pericarditis)
  
• 2D echocardiography best noninvasivediagnostic
  tool in diagnosis pericardialeffusion or
  tamponade
• CT or MRI identify pericardial thickening

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ECG in Cardiac Tamponade
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ECG in Acute Pericarditis
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Pericardial Effusion
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Pericardial Effusion
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Respiratory Variation in Cardiac Tamponade
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Respiratory Variation in Constrictive
Pericarditis
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Respiratory Variation in Constrictive
Pericarditis
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Respiratory Variation in Constrictive
Pericarditis
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M Mode in CP
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M Mode in CP
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RA Diastolic Collapse
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RV Diastolic Collapse
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RV Diastolic Collapse
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Pericardial Calcification
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Pericardial Thickening
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Treatment Options

• Medical treatment fluid administration
• Pericardiocentesis
• Subxiphoid pericardiotomy
• Complete pericardium removal post.Effusion

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Nonhemodynamic onsiderations

• Anticoagulation
• Management of effusion in renal failure
• Purulent pericarditis
• Pericardial effusion following cardiac surgery
• Acute pericarditis and ischemia

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Anticoagulation

• Anticoagulation should not be stopped inpatients
  with pericardial effusion whichneed short or
  long term anticoagulation
• Anticoagulation in patient with AMI,pulmonary
  embolism, or ventricularthrombus does not
  increase the amount ofpericardial effusion and
  incidence of pericarditis or cardiac tamponade

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Effusion in Renal Disease

• Up to 40 of patients with renal failurewill
  develop pericardial effusion
• Not limited to predialysis but also occurrsafter
  hemodyalysis
• Pericardial effusion has no evident
  relation-ship with heparin use
• Intensive hemodialysis has highest chance to
  clear pericardial effusion noted
  beforehemodialysis or early in the course after
  treatment ( several weeks)
• Pericardial effusion more than 200 to 250 ml(gt
  1cm in M mode) should be drained

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Purulent Pericarditis

• Common seen in patients with empyema,mediastiniti
  s, endocarditis, burn, and post-pericardiodectomy
  
• Diagnosis ECG, echocardiography, Gallium67 scan
  with SPECT, Gallium67 andTc99 scan
• Primary purulent pericarditis is rare, evenin
  immunocompromised host

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Pericardial Disease after Cardiac Surgery

• First few hours after surgery hemopericar-dium
  or hemomediastinum leads to cardiactamponade (gt
  60)
• Several weeks after op postpericardiectomysyndro
  me with fever, chest pain, and friction rub
  (10-20)
• 6 weeks to years after op constrictive
  pericarditis ( 1)

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Acute Pericarditis or ischemia ?

• Pericarditis fever, CPK and ESR
  elevation,pluritic pain and friction rub,
  concave STelevation in all leads except V1 and
  aVR,PR segment depression
• AMI or Prizmentals angina Convex STelevation
  in regional leads, series evolution-al change in
  ECG, Q wave noted finally