1.8 Pericardial Disease & Acute Aortic Syndromes

1. Pericardial Diseases

Acute Pericarditis

• Clinical Presentation: Sharp, retrosternal, pleuritic chest pain that is worsened by deep inspiration, coughing, and lying supine, and relieved by sitting upright and leaning forward. A superficial, scratchy, high-pitched pericardial friction rub is the pathognomonic physical sign (best heard with the diaphragm at the LLSB on full expiration while leaning forward).
• Diagnostic Criteria (Requires >=2 of 4 features):
  1. Typical pleuritic, positional chest pain.
  2. Pericardial friction rub.
  3. Characteristic ECG changes: Widespread, concave upward ST-segment elevation with PR-segment depression across multiple leads, accompanied by reciprocal ST depression and PR elevation in lead aVR.
  4. New or worsening pericardial effusion on echocardiography.
• First-Line Pharmacotherapy:
  • High-Dose NSAIDs: Ibuprofen 600-800 mg PO TID or Indomethacin 50 mg PO TID for 1-2 weeks until symptom resolution; or Aspirin (650-1000 mg PO TID; preferred in post-MI pericarditis [Dressler syndrome]).
  • PLUS Colchicine: 0.5-0.6 mg PO daily (if weight <70 kg) or BID (if >=70 kg) for 3 months. Colchicine halves the recurrence rate (ICAP trial).
• Role of Systemic Corticosteroids (Prednisone): Second-line therapy reserved strictly for NSAID contraindications, NSAID failures, or specific autoimmune/uremic etiologies. Corticosteroids are independent risk factors for recurrent pericarditis and must be tapered very slowly.

Cardiac Tamponade

• Pathophysiology: Accumulation of pericardial fluid under high pressure exceeding normal pericardial compliance, causing compression of all cardiac chambers, impairment of diastolic filling, equilibration of diastolic pressures, and catastrophic reduction in stroke volume and cardiac output.
• Clinical Features:
  • Beck's Triad: (1) Hypotension; (2) Jugular Venous Distension (JVD) with loss of the y-descent (diastolic filling blunted); (3) Distant, muffled heart sounds.
  • Pulsus Paradoxus: An exaggerated inspiratory decrease in systolic blood pressure > 10 mmHg during normal breathing. Measured using a manual sphygmomanometer by noting the difference between the pressure at which Korotkoff sounds are first heard only during expiration and the pressure at which sounds are heard throughout the entire respiratory cycle.
• Diagnostic Workup:
  • ECG: Low QRS voltage and electrical alternans (beat-to-beat variation in QRS amplitude and axis caused by the heart swinging within the large pericardial effusion).
  • Echocardiography (Gold Standard): Diastolic collapse of the right atrium (late diastole) and right ventricle (early diastole); dilated, plethoric inferior vena cava (IVC) without inspiratory collapse; >25% respiratory variation in mitral inflow velocity.
• Emergency Treatment: Emergency pericardiocentesis under echocardiographic or fluoroscopic guidance with indwelling catheter drainage. Temporary bridge: IV crystalloid bolus (1-2 liters) to increase intravascular filling pressures. Avoid positive-pressure mechanical ventilation, which dramatically reduces venous return and precipitates immediate cardiac arrest.

Constrictive Pericarditis

• Pathophysiology: Chronic fibrotic thickening, scarring, and calcification of the pericardium causing rigid casing that limits diastolic expansion of the ventricles in mid-to-late diastole.
• Clinical Signs: Predominant right-sided heart failure symptoms (anasarca, ascites, hepatomegaly, jaundice, peripheral edema) out of proportion to pulmonary symptoms.
  • Kussmaul's Sign: Paradoxical rise (or lack of fall) in jugular venous pressure during inspiration due to inability of the right heart to accommodate increased inspiratory venous return.
  • Pericardial Knock: High-pitched early diastolic sound occurring just after S2 (earlier than S3) caused by sudden arrest of ventricular filling against the rigid pericardium.
• Diagnostics: Chest X-ray or CT showing heavy pericardial calcification; Cardiac MRI showing thickened pericardium (>4 mm); Cardiac catheterization demonstrating ventricular interdependence (discordance of LV and RV peak systolic pressures during respiration) and the classic dip-and-plateau ("square root sign") on ventricular pressure tracings.
• Treatment: Diuretics for symptomatic congestion; definitive curative therapy is surgical pericardiectomy (pericardial stripping).

2. Acute Aortic Syndromes

Thoracic Aortic Dissection

• Pathophysiology: A tear in the aortic intima allows pressurized blood to enter the media, creating a false lumen that propagates proximally or distally.
• Classification:
  • Stanford Type A (65%): Involves the ascending aorta (proximal to the brachiocephalic artery). Surgical Emergency.
  • Stanford Type B (35%): Involves only the descending thoracic aorta (distal to the left subclavian artery). Primarily medical management.
• Clinical Presentation: Sudden-onset, excruciating, "tearing," "ripping," or "sharp" chest pain radiating to the back/interscapular region. Associated with pulse deficits / blood pressure differential > 20 mmHg between arms, acute aortic regurgitation murmur (Type A extending into aortic root), acute hemopericardium/tamponade, or stroke/paraplegia from branch vessel occlusion.
• Diagnostic Modality: CT Angiography (CTA) of the chest, abdomen, and pelvis is the diagnostic modality of choice in hemodynamically stable patients. Transesophageal Echocardiography (TEE) is preferred in unstable patients or severe renal failure.
• Emergency Medical Management (Anti-Impulse Therapy):
  • Step 1 — IV Beta-Blockers First: Administer IV Esmolol infusion (or IV Labetalol) to achieve a target heart rate < 60 bpm and decrease the rate of change of aortic pressure (dP/dt, aortic shear stress).
  • Step 2 — Vasodilators Second: Only after heart rate is strictly controlled to <60 bpm, add IV Nitroprusside or Nicardipine if needed to achieve a target Systolic Blood Pressure < 120 mmHg (ideally 100-110 mmHg).
  • (CRITICAL RULE: Never initiate vasodilators before beta-blockers, as reflex tachycardia increases shear stress and accelerates aortic dissection propagation and rupture!)
• Definitive Treatment:
  • Stanford Type A: Immediate open surgical repair with graft replacement of the ascending aorta +/- aortic valve resuspension/replacement.
  • Stanford Type B (Uncomplicated): Medical therapy with strict long-term BP and HR control. Complicated Type B (end-organ malperfusion, refractory pain, uncontrolled HTN, rapid aneurysmal expansion, rupture) requires Thoracic Endovascular Aortic Repair (TEVAR).

Abdominal Aortic Aneurysm (AAA)

• USPSTF Screening Recommendation (Grade B): One-time screening abdominal ultrasound for men aged 65 to 75 who have ever smoked (>=100 lifetime cigarettes).
• Surgical / EVAR Thresholds: Elective repair (Endovascular Aneurysm Repair [EVAR] or open surgical repair) is indicated for: (1) AAA diameter >= 5.5 cm in men or >= 5.0 cm in women; (2) Rapid expansion rate (>0.5 cm in 6 months or >1.0 cm in 1 year); or (3) Any symptomatic AAA regardless of diameter.