PERICARDITIS

Question 1

RED FLAGS

Question 2

DIFFERENTIALS

Answer 2

• ACS
• PE
• Pneumonia (pleuritic chest pain)
• Thoracic aortic aneurism
• AAA.

Lack of cardiac ischaemic features suggests good perfusion & decreases suspicion of ACS (not pale, diaphoretic, SOB, nauseous).

Question 3

CAUSE

Answer 3

Virus (common caused by COX B, COVID 19, tuberculosis), malignancy, autoimmune disorder (HIV), bacterial due to thoracic surgery, uraemia.

Question 4

DEFINITON

Answer 4

Inflammation of the pericardium.

Question 5

PATHOPHYSIOLOGY

Answer 5

Virus enters circulation & infects the pericardium  Acute inflammation of the pericardial sack  progress to myocardial inflammation + pericardial effusion, cardiac tamponade (inflammation  permeability  Fluid shift  effusion (if fills slow) + tamponade (if fast fill).
- Tamponade manifestations = Bex triad: low BP, JVD, muffled heart sounds.

• Acute: Develops quickly, causing inflammation of the pericardial sac & often pericardial effusion. Inflammation can extend to the epicardial myocardium. Adverse hemodynamic effects & rhythm disturbance are rare, although cardiac tamponade is possible.
• SubacutE: occurs within weeks to months of an inciting event.
• Chronic: pericarditis persisting > 6 months.

Question 6

MANIFESTATIONS

Answer 6

• Chest pain: sharp, pleuritic, improved with sitting up/leaning forward/inspiration. Hard to differentiate between ACS & pericarditis.
• Pain in trapezius due to increase in intrathoracic pressure on inspiration.
• Pericardial friction rub: Pericardium has lubricant that prevents friction rub  pericarditis impairs this production.
• Fever/flu-like symptoms.
• ECG: global (concave, convex in STEMI) ST-elevation + PR-depression (early stages)
• Dx: (2 out of 4 to diagnose) pleuritic chest pain, ST elevation, friction rubbing, & effusion.

Question 7

TREATMENT

Answer 7

Primary survey: DRAB: O2 to reduce anxiety? C: IV access + fluids, ECG. D: Analgesia (Paracetamol, Fentanyl), Aspirin (can’t rule out ACS), Fentanyl (CCP, low dose). E: reassurance, position of comfort.
Secondary Survey: Thorough CVA + reassessments.

Question 8

ROLE OF PARAMEDICS

Answer 8

Provisionally Dx pericarditis, attempt to rule out ACS but maintain high suspicion.

Question 9

PHARMACOLOGY

Answer 9

NSAIDs  decrease inflammation & reduce fluid accumulated in the pericardium. Ibuprofen inhibits prostaglandin synthesis  reducing inflammatory response. It interferes with the action of cyclooxygenase (enzyme that catalyses the conversion of arachidonic acid to prostaglandic acid).
There is evidence to support the use of opiate-based drugs, in addition to Ibuprofen. Some Ambulance Committees advocate the use of Morphine for the management of cardiac chest pain, specifically the use the IV morphine to reduce pain & anxiety & lower cardiac preload. QAS prefer the use of Fentanyl for chest related pain.
Fentanyl is a mu (opioid) receptor agonist which reduce GABAergic neurotransmission & increase parasympathetic activity. GABA release  hypopolarisation  CNS depression, activation of dopaminergic pathways in CNS  change perception from pain + euphoria. The inhibition of nociceptive afferent neurons in the PNS impairs transmission of pain message.

Question 10

DEFINITIVE CARE

Answer 10

Assessments:
- Echocardiogram – for effusion and tamponade. Chest radiography (for Pneumonia, pneumothorax). Troponin. Check for bacterial infection by inflammatory markers (CRP, WBC). CT scan to rule out PE. Blood gases. Assess Lipase to rule out pancreatitis.
Treatment:
- Pericardiocentesis/drainage- can drain but typically don’t, typically take NSAID for 7days & reassess. Steroids to decrease inflammation. Antibiotics if bacterial. Colchicine – reducing likelihood of recurrence of pericarditis.
- Lasix (diuretics)