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  • “viral” or “idiopathic” (>80%)
  • post-infarction regional pericarditis (PIRP)
    • occurs in the days following transmural STEMIs as the epicardium is involved with subsequent inflammation of the pericardium
    • this results in either:
      • persistent ST elevation with upright T waves > 48hrs post-STEMI
      • gradual reversion of inverted T waves to upright Twaves within 48-72hrs post-STEMI in association with well formed Q waves
    • these patients are at risk of:
      • myocardial rupture causing cardiac tamponade or, if it is a septal AMI, an acute VSD with L-to-R shunt and APO/cardiogenic shock
      • LV aneurysm and mural thrombus
  • auto-immune (7%)
  • purulent (<1%)
  • chylopericardium is a rare disorder that may be primary (ie, idiopathic) or, more often, secondary to injury to the thoracic duct such as in trauma or post-operative
    • chylothorax, with or without chylopericardium, is much more common than isolated chylopericardium. Most cases are nontraumatic, with the major cause being malignancy, particularly lymphoma.

clinical features

  • anterior chest pain
    • typically sharp, worse on inspiration and on lying down
    • may be dull
    • may radiate to shoulders
  • may have a pericardial friction rub
    • highly specific but low sensitivity as they are quite variable from hour to hour, and may not be heard if there is an effusion
    • superficial scratchy or squeaking quality that is best heard with firm pressure of the diaphragm of the stethoscope, with patient leaning forwards or resting on elbows and knees so that contact between visceral and parietal pericardium is maximised
    • ask patient to stop breathing to differentiate from a pleural rub
  • may have a pericardial effusion
    • 40% do NOT have a pericardial effusion
    • of the remainder, ~80% have a small effusion and 10% have a moderate effusion
    • 5% develop life threatening cardiac tamponade2)
  • may have recent or current viral infection
  • 15% also have evidence of viral myocarditis hence called myopericarditis but this is usually benign 3)
    • diagnosed by either:
      • raised troponin (does not appear to have any prognostic value)
      • impaired LV ejection fraction on echo
    • risk factors include:
      • arrhythmias (odds ratio (OR) = 17.6, 95% confidence interval (CI) 5.7 to 54.1; p<0.001)
      • male gender (OR = 6.4, 95% CI 2.3 to 18.4; p = 0.01)
      • age <40 years (OR = 6.1, 95% CI 2.2 to 16.9; p = 0.01)
      • ST elevation (OR = 5.4, 95% CI 1.4 to 20.5; p = 0.013)
      • recent febrile syndrome (OR = 2.8, 95% CI 1.1 to 7.7; p = 0.044)

Diagnostic criteria

  • generally required to have at least 2 of the 4 features:
    • pericardial chest pain
    • pericardial friction rubs
    • new ECG changes of widespread ST-segment elevation or PR depression (< 60% have these)
    • new or worsening pericardial effusion (<60% have this)

ECG changes in acute pericarditis

classic four stages

  • 1st described by Spodick et al
  • less than half of all patients evolve through all stages
  • the evolution of ECG changes in acute pericarditis is heterogeneous with a significant variation between patients
  • a normal ECG does NOT exclude pericarditis as it may be normal at initial presentation and at 12-48hrs after that!
  • ECG changes are dynamic and can evolve rapidly during the disease course and are influenced by several factors
  • the classic ECG patterns of widespread ST-segment elevation or PR depression can be seen in less than 60% of patients, and often only at the initial phase (stage 1) of the acute pericarditis, and are more common in younger male patients, particularly in the presence of concomitant involvement of the adjacent myocardium (myopericarditis) 4)
  • ECG changes are due to inflammation of the epicardium
  • tachycardia may be the only ECG finding if ST elevation has resolved & T waves remain normal
  • stage 1:
    • lasts hrs-days
    • diffuse PR depression leads I,II,III,aVL, aVF, V2-6 (esp. II, aVF, V4-6) with reciprocal elevation in aVR, V1
      • NB. PR depression may also occur in benign repolarisation (but is usually < 0.8mm and there is no ST depression in V1 and ST:T height ratio is < 25% in benign repolarisation) and in AMIs involving the atrium
    • widespread ST elevation, 2-5mm concave & upward in leads I, II, III, aVF & V2-5 (may be confined to II, V5,6 where it tends to be greatest) and reciprocal depression if present, only in aVR & V1
      • ST elevation limited to the anterior leads is more likely to be early repolarization than pericarditis
    • PR changes often co-exist with ST changes but may be isolated and may precede ST changes
    • slight elevation of PR segment in aVR
    • if T-wave inversion antedates pericarditis, concomitant ST elevation and T-wave inversion may be seen once pericarditis develops
  • stage 2:
    • a few days later
    • ST & PR segments become isoelectric with flattened or upright T waves
    • HOWEVER, 40% of patients develop a notched or biphasic positive-negative T wave before full return of the ST segment to the baseline
  • stage 3:
    • diffuse T wave inversion
  • stage 4:
    • lasts days - weeks
    • T waves normalise, but rarely, remain normal

distinguish acute pericarditis from early repolarization

  • ST elevation occurs in BOTH limb leads and precordial leads in pericarditis whereas 50% with early repolarization have no ST deviations in the limb leads
  • PR and ST/T wave evolutionary changes do not occur in early repolarization
  • ratio of ST elevation to T wave amplitude in lead V6 > 0.24 indicates pericarditis 5)

ECG changes in chronic pericarditis

  • usually related to the presence of either:
    • pericardial effusion
      • ⇒ low voltage amplitude in all leads
      • ⇒ electrical alternans may occur with large effusions or tamponade
    • constrictive pericarditis
      • ⇒ low voltage amplitude in all leads but no electrical alternans
      • ⇒ left atrial abnormalities
  • NB. myxoedema also causes low voltages but usually bradycardia as well whereas pericarditis tends to cause tachycardia

High risk factors which suggest need for admission

  • fever >38 degrees C (HR 3.56, 95% CI 1.82 to 6.95; P<0.001)
  • subacute onset (HR 3.97, 95% CI 1.66 to 9.50; P=0.002)
  • immunosuppression
  • trauma
  • oral anticoagulant therapy
  • myopericarditis
  • large pericardial effusion (HR 2.15, 95% CI 1.09 to 4.23; P=0.026)
  • raised troponin
  • failure to respond to aspirin or NSAID Rx (9% develop constriction vs 0.5% of those who respond to aspirin, HR 2.50, 95% CI 1.28 to 4.91; P=0.008) )6) 7)

ED Mx of suspected acute "viral" pericarditis or recurrent pericarditis

  • exclude other potential causes of chest pain if Dx is not clear
  • CXR to help exclude a large effusion or evidence of LVF
  • ECG
  • FBE, U&E, troponin
  • consider CRP
  • viral studies are NOT indicated
  • consider need to test for tuberculosis (TB), HIV / AIDS, and auto-immune disorders (eg. consider ANA)
  • if low risk:
  • if high risk
    • admit
    • urgent echo
    • emergency therapeutic pericardiocentesis if cardiac tamponade is present
    • diagnostic pericardiocentesis should be considered if:
      • suspect a malignant or bacterial etiology, or,
      • in patients with an effusion refractory to medical therapy
    • patients who fail to respond to NSAIDs after 2 weeks may benefit from colchicine or corticosteroids
pericarditis.txt · Last modified: 2024/02/03 11:11 by gary1

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