Pericarditis, Effusion and Tamponade Flashcards

1
Q

What is the anatomy and function of the pericardium?

A

2x layers:

  • Outer = fibrous
  • Inner = serous

Contained between is serous fluid
- c. 50mls

both layers are innervated by the phrenic nerve
- C4 (C3 + C5)

The pericardium:

  • Limits dilatation, aids atrial filling
  • Protects the heart by reducing external friction and a barrier to external malignancy
  • Fixes the heart anatomically with ligaments
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2
Q

What is the aetiology of pericarditis?

A

Viral infection:

  • Most common
  • e.g. Coxsackieviruses, echoviruses, influenza viruses, adenoviruses, mups, HIV, hepatitis

Other infections:

  • TB - most common cause of constrictive pericarditis in developing world
  • Other bacterial, fungal and parasitic causes

Inflammatory conditions:

  • RA
  • SLE, scleroderma, sarcoidosis, granulomatosis with polyangiitis etc.

Metabolic:

  • Uraemia (so patients with CKD pre-dialysis)
  • Hypothyroidism

Cardiovascular:

  • MI - either during (transmural infarcts or persistent ST elevation = common) or post (Dressler’s syndrome)
  • Aortic dissection

Neoplastic:

  • Relatively common
  • Metastatic disease (lung, breast and haematological)

Drugs:

  • Doxorubicin, cyclophosphamide
  • Methyldopa, isoniazid, hydralazine (all can cause drug induced SLE)
  • Small pox vaccine
  • Dantrolene
  • Phenytoin
  • Minoxidil
  • Irradiation

Idiopathic = Most common overall; a portion of these will likely be due to undiagnosed viral causes

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3
Q

What is the pathophysiology of pericarditis?

A

Inflammation of the pericardium:

  • Can be fibrinous (dry) OR
  • Effusive - serous, haemorrhagic or purulent

Acute:
- <4-6wks

Chronic:

  • Chronic effusive pericarditis - due to long term accumulation of fluid in pericardium
  • Chronic constrictive pericarditis - a thickening of the pericardium and symptomatic even after drainage of fluid

Pathogenesis suggests a clinical continuum initiated by acute pericarditis and progressing through pericardial effusion, chronic effusive pericarditis, effusive-constrictive pericarditis to chronic constrictive pericarditis

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4
Q

What is Dressler’s syndrome?

A

An autoimmune response to myocardial tissue
- Antimyocardial antibodies (though not known if these are the cause or consequence of the syndrome)

1-6 wks following an MI; can be as late as 3/12

c.1% of patients post MI

Can follow a relapsing course

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5
Q

How does acute pericarditis present?

A

Chest pain

  • Usually central
  • Sudden onset
  • Sharp/stabbing (but may be more dull and steady like an MI)
  • May radiate to L neck or trapezius ridge
  • Exacerbated by coughing, breathing, lying down
  • Alleviated with sitting up or leaning forward

Breathlessness
- Also exacerbated by the same things as above

Palpitations

Other symptoms depending on cause
- E.g. fever, cough - from a viral infection

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6
Q

What are the examination findings in acute pericarditis?

A

Pericardial friction rub:

  • Classical/most important
  • Specific but not that sensitive
  • Heard best with the diaphragm of stethoscope at the L sternal border, when supine and at the end of an exhalation (not held as noise made by movement)
  • Squeaky or scratching sound resembling leather surfaces rubbing against each other or boots walking over fresh snow

Triad of pericardial tamponade:

  • Tamponade = compression of heart due to fluid in sac
  • Hypotension
  • Muffled heart sounds
  • Jugular venous distension

Tachycardia

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7
Q

How do you investigate acute pericarditis?

A

ECG:
- Characteristic changes

Bloods:

  • Troponin - to rule out MI (but may be raised if myocardial concurrent myocarditis)
  • FBC - leukocytosis if infection
  • ESR/CRP - raised
  • U+E - uraemia?
  • TFT - hypothyroidism?
  • Rheumatoid factor + other autoimmune biomarkers
  • HIV etc. serology

Echo:
- Important to detect pericardial effusion

CXR:
- Usually normal, sometimes cardiomegaly, signs of pleural effusions, malignancy, TB etc.

Chest CT/cardiac MRI:
- More detail of pericardial involvement, thickness, fluid volume etc

Pericardialcentesis/biopsy:
- Fluid sent for MC+S

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8
Q

What are the characteristic ECG changes in acute pericarditis?

A

4 Stages:
- (though <50% progress through all 4 stages and evolution may not follow classical pattern)

  • *1) Occurs over <14 days
  • Widespread saddle-shaped/concave ST elevation AND PR depression in most of limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6)
  • Reciprocal ST depression and PR elevation in lead aVR (+/- V1)
  • Sinus tachy = common due to pain/pericardial effusion

2) Occurs over 1-3 wks
- Normalisation of ST changes
- Generalised T wave flattening

3) Occurs over 3-several wks
- Inversion of T waves

4) Several weeks +
- Normalisation of ECG

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9
Q

What are they key steps to differentiate acute pericarditis from STEMI?

A
  • Is there ST depression in a lead other than AVR or V1? This is a STEMI
  • Is there convex up or horizontal ST elevation? This is a STEMI
  • Is there ST elevation greater in III than II? This is a STEMI
  • Now look for PR depression in multiple leads… this suggests pericarditis (especially if there is a friction rub!)

Serial ECG is very useful if there is diagnostic uncertainty as things may become clear with time (though should not substitute good clinical judgement)

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10
Q

What are the key diagnostic factors for acute pericarditis?

A

At least 2x of the following:

  • Chest pain
  • Pericardial rub
  • ECG changes consistent with pericarditis
  • (at least a) small pericardial effusion on echo

+/- presence of risk factors

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11
Q

How do you manage acute pericarditis?

A

NSAIDs:
- Ibuprofen = first choice
(+ PPI if needed)

+ Colchicine:
- If unresponsive or persistent

+ Corticosteroids if still unresponsive

Treat underlying cause if known
- e.g. TB treatment

For massive effusion +/- tamponade:
- Therapeutic pericardiocentesis

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12
Q

How does chronic pericarditis present?

A

Effusive:

  • Dyspnoea, esp on exertion
  • Chest pain
  • Syncope, light-headedness
  • Palpitations
  • Possible cough, hoarseness, hiccough
  • Hypotension + raised JVP + diminished heart sounds (= Beck’s triad/ acute compression triad)

Constrictive:

  • Gradual onset (usually months)
  • Signs of right heart failure e.g. dyspnoea, peripheral oedema, JVP elevated +/- doesn’t fall with inspiration, pulsatile hepatomegaly
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13
Q

How do you investigate chronic pericarditis?

A

CXR:
- Calcification of pericardium strongly suggests constrictive pericarditis in patients with heart failure

Echo:
- Can help differentiate from restrictive cardiomyopathy

MRI:
- Can estimate thickness of pericardium

Pericardial biopsy:
- esp. if infective, malignant or granulomatous causes suspected

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14
Q

How do you mange chronic pericarditis?

A

Effusive:

  • Catheter pericardiocenteis or surgical drainage
  • Pericardectomy

Constrictive:

  • Some causes are reversible through anti-inflammatory meds so if stable enough can trial
  • If ineffective, gold standard is complete pericardectomy
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15
Q

What are pericardial effusions?

A

Collections of fluid in the pericardial space:
- Transudate (hydropericardium), exudate (pyopericardium) or haemopericardium

Can be of varying sizes and presentation will depend on how quickly effusion accumulates

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16
Q

What are the causes of pericardial effusions?

A
Idiopathic 
Infectious pericarditis 
Acute MI
Malignancy 
- Hypothyroidism 
- Trauma 
- Ruptured TAA with leakage into pericardial sac
- Post-radiotherapy 
- Post-cardiac surgery 
- Autoimmune disease + drugs (same as pericarditis)
17
Q

How do you clinically differentiate pericardial effusion from cardiac tamponade?

A

Pulsus paradoxus:

  • The exaggeration of the normal decrease in systemic blood pressure during inspiration
  • A pulsus paradoxus = a drop >10 mmHg systolic
  • On physical examination, one can detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse (the accentuated drop in BP means radial pulse cannot be felt)
  • May also be accompanied by an increase in JVP = Kussamul’s sign

When present in a patient with known/suspected pericardial effusion, it is indicative of tamponade

18
Q

How might a large pericardial effusion show up on CXR?

A

Increased cardiothoracic ratio (i.e. cardiomegaly)
- ‘globular’ cardiomegaly with sharp margins or ‘water bottle’ sign

Pericardial fluid is suggested by lucent lines within the cardiopericardial shadow

19
Q

How do you manage pericardial effusions?

A

Treat the underlying condition
- e.g. NSAIDs, TB treatment

A good portion will tamponade spontaneously

  • If persists for >1/12 or if symptoms of R-sided heart collapse
  • Then should be drained
  • Either using long needles, or surgery if necessary

Surgery may involve:

  • Cutting a pleuropericardial window (to allow drainage of fluid into pleura where can be easily reabsorbed)
  • Baloon pericardotomy - inflation of a balloon by catheter placed into pericardial space, drains fluid to pleural space
  • Pericardial sclerosis using chemical agents e.g. tetra/doxycycline, cisplatin
20
Q

How do you manage cardiac tamponade?

A

Oxygen

Improve venous return:
- Bed rest + leg elevation

Fluids:
- Small boluses

Positive inotropes:
- e.g. dobutamine

Echo-guided pericardiocentesis e.g. emergency subxiphoid percutaneous drainage

21
Q

What is the difference between pericardial rub and a pleural rub on examination?

A

Pericardial friction rub may have one, two, or three audible components, whereas the similar pleural friction rub ordinarily has two audible components.

Also, a pleural rub can only be heard during inspiration, whereas the pericardial rub can be heard even after cessation of breathing