Pericardial disease

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Pericardial disease

• Emma Rees,
• Tutor in Cardiology,
• Biomedical Studies

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Learning Outcomes

• Outline the aetiology, prevalence and mechanism
  of pericardial disease
• Describe the effects of the pathology on the
  patient
• Identify investigations used in the diagnosis
• Explain how investigation results aid in
  diagnosis
• Detail the treatment and prognosis of the
  pathology

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Introduction

• Pericardial disease is potentially curable
• Accounts for 7 of all hospitalizations in Africa
• Spectrum of the disease is determined by
  epidemiological setting of patient
• Western countries largely idiopathic
• Developing countries tuberculous
• But there are a large number of diseases that can
  cause it.

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What do you know about the pericardium?

• What is it?
• Where is it?
• What is its function?

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What is it?

• Fibrous sac surrounding heart-dense network of
  collagen fibres
• Serous membrane two continuous layers separated
  by a small amount of fluid lubricant (10-20mls
  straw coloured)
• Layers are called visceral and parietal
• Visceral is inner layer (epicardium)
• Parietal is continuous with diaphragm and outer
  walls of great arteries

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Where is it?

• Surrounds the heart
• Continuous with the great arteries and the
  diaphragm

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What is its function?

• Stabilises the position of the heart within the
  chest
• Prevents friction between the moving heart and
  adjacent structures
• Allows for small acute changes in size and shape
  but limits ventricular filling (not the case in
  chronic setting)

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Pericardial disease

• May be primary and acute
• or
• Chronic
• - Constrictive
• - Effusive
• - Or constrictive-effusive

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Acute pericarditis
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Causes

• Idiopathic (idio and pathy) 86
• Infective (viral or bacterial) 7
• Following a myocardial infarction or cardiac
  surgery (Dresslers syndrome)
• Radiation therapy
• Neoplastic disease (commonly lung or breast) 6
• Connective tissue disease
• Figures from Permanyer-Miralda et al 1985

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Signs, Symptoms and Investigations

• Think about how an inflamed, thickened
  pericardium might affect the hearts function
  how can we diagnose this?
• Clinical examination
• Auscultation
• Chest x-ray
• ECG
• Echo
• Catheter laboratory investigations

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Clinical Examination

• Retrosternal chest pain sharp worse on insp and
  lying flat
• Friction rub (high pitched scratching noise)
• Raised jugular venous pressure

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ECG (acute pericarditis)
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ECG differential diagnosis - MI

• What leads is the ST elevation in?
• What shape is the elevation?
• Are there Q waves?
• Do the ST T changes evolve with time?
• History of the patient
• Cardiac enzymes etc
• But remember that you can get more than one
  pathology at the same time!

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Clinical signs differential diagnosis - pleurisy

• Pleuritic pain has similar sharp quality but is
  usually more specific in location
• Pleural rub is heard over the area where the pain
  occurs

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Diagnosis of pericarditis

• Patient will have 2 or more of the following
• Characteristic chest pain
• Pericardial friction rub (auscultation)
• ECG showing characteristic ST elevation (caused
  by epicardial injury)

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Treatment

• NB. Search for the underlying disease
• No good evidence from randomised controlled
  trials
• Patients require bed rest
• NSAID (aspirin, indomethacin) are generally
  accepted as effective for relieving symptoms of
  chest pain
• NSAID ketorolac tromethamine rapid results
• Colchicine may be a useful adjunct in those who
  do not respond to NSAIDs alone

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Prognosis

• Pericarditis is usually a benign disorder
• Diagnosis relates to underlying cause
• But any cause can lead to an effusion and
  tamponade which can lead to death
• Pericarditis can also progress to pericardial
  constriction and heart failure

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Chronic constrictive pericarditis
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Causes

• Tuberculous constrictive pericarditis was common
  cause of constriction pre 1960 decline in
  incidence.
• Post-radiotherapy constriction features
  prominently today along with post-surgical
  causes.
• Needs to be differentiated from restrictive
  cardiomyopathy when making diagnosis.

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Investigations

• As for acute pericarditis
• Clinical examination prime symptoms likely to
  be RHF and SOB
• ECG may not show characteristic ST elevation
• CXR may see calcification and helps to rule out
  coexisting effusion
• Echo to identify haemodynamic effects on heart
  and coexisting effusion
• Auscultation may reveal a friction rub
• MRI/CT scan data about the thickness of the
  pericardium. Cine CT is a new technique which
  also gives info about the effects of physiology
  as well.

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Kussmauls sign

• Normal subjects inspiration causes a decrease
  in chest pressure. Increase in venous return
  JVP falls
• Constrictive pericarditis Increased venous
  return cannot be accommodated in RV because of
  high EDP
• So JVP rises on inspiration

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Chest x-ray

• Occasionally calcification noted
• More useful to determine whether there is a
  coexisting effusion (fluid accumulation)

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Echo findings

• Normal subjects increase in TV flow velocity on
  inspiration, and decrease in MV flow
• Due to increased vascular capacity of lungs
  venous return and RV output increases while
  return to LA is reduced
• This is exaggerated in tamponade/sig constriction
  RV output cant increase because of high EDP
  pulmonary return is reduced further

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Treatment

• The only effective treatment for chronic
  constrictive pericarditis is complete surgical
  resection of the pericardium.
• Mortality for procedure ranges from 5-16
• Symptomatic improvement in 90
• 5 year survival rate is 74-87 depending on
  co-morbidities pre-op

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Pericardial effusion (may be acute or
chronic,Global or localised)
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Pericardial effusion

• Spectrum of causes of effusion is similar to
  acute pericarditis
• More likely than constriction following MI and
  cardiac surgery
• Can coexist with acute pericarditis and chronic
  constrictive disease

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Causes

• Major causes are post cardiac surgery and
• Neoplastic disease
• Gradual accumulation of fluid (chronic) permits
  progressive stretching of pericardium
• Patient may develop a substantial fluid without
  significant increase in intrapericardial pressure

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• Rapid accumulation of fluid (acute) leads to
  critical elevation of intrapericardial pressure

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Pathophysiology

• Significantly increased intrapericardial pressure
  impedes diastolic filling of the ventricles
• Therefore in order for the ventricles to fill the
  end-diastolic pressure must exceed the
  pericardial pressure
• Global effusion pericardial pressure is equal
  around heart
• Therefore both ventricles have to increase EDP to
  same amount for ventricles to fill

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• Normal difference in diastolic pressures between
  RV and LV is lost
• As the pericardial effusion worsens the EDP
  cannot raise significantly to maintain cardiac
  output

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Investigations and clinical signs

• Clinical examination SOB, orthopnoea,
  tachycardia (varying degrees)
• Auscultation may have muffled heart sounds
• ECG may show low amplitude QRS complexes and
  alternating axis
• CXR globular appearance to heart and therefore
  increased cardiothoracic ratio
• Echo size of effusion and haemodynamic effect
  of it

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Pericardial effusion
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Echocardiography
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Cath lab- diastolic equalization of left and
right heart pressures
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High RA pressures
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Treatment

• Depends on the cause and nature
• If acute the cause is treated and the patient
  monitored
• If persistent problem or life threatening more
  dramatic action is called for

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Cardiac tamponade
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Cardiac tamponade(complication of pericardial
effusion)

• This is a clinical diagnosis
• - It is based upon the patients symptoms
• Investigations may be performed to confirm the
  suspected cause of the symptoms (pericardial
  effusion).

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• Occurs when the fluid accumulation around the
  heart impairs filling to such an extent that
  there is haemodynamic compromise.
• It is a medical emergency and must be treated
  promptly.
• Risk of death depends upon speed of diagnosis,
  treatment and underlying cause of the tamponade.

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How much fluid is a problem?

• Depends on rate of accumulation and compliance of
  the pericardium
• 150ml that accumulated quickly could cause a
  problem
• 1000ml that accumulates very slowly may be
  tolerated fairly well

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Signs and symptoms

• Acutely unwell
• Significant SOB, rapid breathing
• Tachycardia
• Orthopnoea
• Cold, clammy extremities because of poor
  perfusion
• Kussmauls sign

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Investigations (used to confirm only)

• CXR globular heart
• ECG (findings are suggestive not diagnostic)
• - Sinus tachycardia
• - Low voltage QRS complexes
• - Electrical alternans (not always)
• Echo
• - Size and location of effusion
• - Any evidence of diastolic collapse
• - Swinging of the heart
• - Decrease of insp. flow across MV

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Treatment

• Medical emergency intensive care environment
  needed.
• Oxygen
• Volume expansion
• Bed rest with leg elevation
• Inotropic drugs if necessary

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Pericardiocentesis

• Pericardiocentesis is the definitive therapy to
  remove the excessive fluid
• Commonly performed in the cath lab but may be
  done blind in an intensive care environment

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Pericardiocentesis
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How is it done?

• Patient lies on the table with the upper body
  elevated to a 60 degree angle. Limb ECG leads
  attached.
• Xyphisternum puncture site is cleaned with an
  antiseptic solution and local anaesthetic is
  injected to numb area.
• Patient is instructed to remain still
• Physician inserts a large needle with syringe
  attached into chest wall until pericardial sac is
  reached

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• The needle is then pushed through the tough
  pericardial sac (patient may experience some
  pain/pressure at this point)
• A guidewire is inserted through the needle and
  the needle withdrawn
• A catheter can then be passed over the guidewire
  and into the pericardial space
• This can be used for continuous drainage.

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Case study

• Mr B. 64 years old
• Recent course of radiotherapy for lung tumour
• History of chest pain over the last week,
  shortness of breath and ankle oedema.
• What else do you want to know?
• How would you investigate him?

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Extra information

• Sharp chest pain worse on deep inspiration
• No added heart valve murmurs, pericardial
  friction rub
• Elevated JVP

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Echo findings

• Medium sized pericardial effusion 1.5cm along
  anterior and inferior RV free wall.
• IVC dilated with reduced insp. collapse
• RVSP estimated at 40mmHg JVP.
• No obvious signs of respiratory variation in
  LV/RV filling patterns

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What do you want to do with this patient?

• Admit. Bed-rest.
• NSAIDs to relieve the pain
• Effusion does not need draining unless cardiac
  tamponade develops
• Monitor - does pain ease with treatment
• Needs repeat echo to assess effusion size

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What happened next

• Mr B deteriorated over following 2 days
• Became acutely unwell
• Severe sob, tachypnoea
• Tachycardia
• Hypotensive
• Cold and clammy extremities
• What do you want to do?

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Treatment

• Give oxygen
• monitor ECG and BP
• Elevate legs
• Consider volume expansion
• Seek expert help!
• Consider moving to an intensive care environment
• Urgent echo
• Assess need for Pericardiocentesis

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Follow-up

• Monitor for signs of recurrence
• May develop signs of constrictive pericarditis in
  future

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Learning outcomes revisited!

• Outline the aetiology, prevalence and mechanism
  of pericardial disease
• Describe the effects of the pathology on the
  patient
• Identify investigations used in the diagnosis
• Explain how investigation results aid in
  diagnosis
• Detail the treatment and prognosis of the
  pathology

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References

• Timmis (1997) Essential Cardiology
• Rimmington Chambers (1998) Echocardiography A
  Practical Guide for Reporting
• Yusuf et al. (Eds.) (2003) Evidence-Based
  Cardiology
• Levick (2003) An Introduction to Cardiovascular
  Physiology
• Jenkins Gerred (1997) ECGs by Example
• Martini (2004) Fundamentals of Anatomy and
  Physiology
• Website www.emedicine.com