Constrictive Pericarditis

Fixed, rate-dependent output - Stroke volume is fixed by the constricting shell, so cardiac output depends on heart rate — avoid bradycardia and keep a normal-to-high rate.

Preserve preload and contractility - These hearts need adequate filling; avoid hypovolemia, myocardial depression, and abrupt falls in venous return (careful with high airway pressures and vasodilating agents).

Maintain afterload and sinus rhythm - Avoid drops in systemic vascular resistance and preserve sinus rhythm (both rate and atrial contribution matter).

Pericardiectomy is high-risk - The surgery can involve major bleeding and, on release of the constriction, sudden hemodynamic shifts (ventricular dilation or failure); have blood, access, and inotropes ready.

Monitoring - Arterial line and often central access; this physiology is unforgiving.

Echo answers constriction versus restriction - Both give a stiff, non-dilated ventricle with preserved systolic function, so hunt for ventricular interdependence, which only constriction produces: septal bounce with an abrupt leftward septal shift on inspiration, transmitral inflow falling on inspiration while transtricuspid inflow rises, and a plethoric IVC that does not collapse. Tissue Doppler seals it — the lateral mitral annulus is tethered to the diseased pericardium, so lateral e' drops below medial e' (annulus reversus), the reverse of normal.

Cath tracings and BNP when the echo is equivocal - The ventricular tracing shows the dip-and-plateau (square root sign): rapid early filling that stops dead when the pericardium hits its elastic limit, with end-diastolic pressures equalized in all four chambers. Equalization by itself does not discriminate — tamponade does it too. What discriminates is discordant respirophasic filling on simultaneous high-fidelity RV and LV catheters. On labs, an S3 and a high BNP point to restrictive cardiomyopathy, while a BNP under 100 alongside a pericardial knock, pericardial calcification on chest film, and pericardial thickening on imaging points to constriction. Kussmaul's sign shows up in both, so it does not sort them, and endomyocardial biopsy has a low yield here.

Effusive-constrictive disease - Draining the fluid does not fix the physiology, because the visceral pericardium is constricting underneath it. The hallmark is a right atrial pressure that stays elevated after the pericardial fluid comes off, with a prominent x and blunted y before drainage converting to the dip-and-plateau after. It accounts for 2.4% to 14.8% of pericarditis series and 3% to 14% of tuberculous pericarditis. Expect only a partial hemodynamic win from a window or a centesis and expect the patient back for pericardiectomy — both the visceral and parietal layers have to come out.

A normal-looking pericardium does not rule it out - Pericardial thickness over 4 mm on CT predicts constriction, but up to 20% of patients with constriction have a normal-thickness pericardium, about 18% have no thickening at all, and calcification is absent in up to 20%. CT reads calcium best; MRI distinguishes a small effusion from thickening and separates active edema from scar. The imaging finding that should change your expectations is myocardial atrophy or fibrosis on CT or MRI — that predicts a poor surgical result.

Not every constriction goes to the OR - A subset is transient and resolves. If the patient is hemodynamically stable without the stigmata of chronic constriction, cardiology may run up to three months of anti-inflammatory therapy (NSAIDs, colchicine, corticosteroids) with close monitoring before committing to surgery. Those agents slow further scarring but will not reverse established fibrosis or calcification. Patients on interleukin-1 blockade (anakinra) for an incessant pericardial syndrome have had it continued straight through pericardiectomy to prevent rebound inflammation — confirm the plan with cardiology and the surgeon rather than holding it by reflex.

Know the operation you are staffing - Median sternotomy in the large majority (94% in one 47-patient series), with thoracotomy and one-lung ventilation chosen for some cases — ask before you pick a tube. Total resection beats partial: total pericardiectomy gives better long-term survival and functional recovery than partial, so the surgeon is peeling calcified pericardium off epicardium across both ventricles, phrenic nerve to phrenic nerve. That dissection plane is where the bleeding and the ventricular injury come from. Many are done beating-heart off pump (79% in that series, with CPB needed in 21%), but the pump and perfusionist stay on standby and bypass is used deliberately when it is the only way to get a complete biventricular decortication.

Low cardiac output after decortication - Low cardiac output syndrome after pericardiectomy is a named postoperative entity carrying high morbidity and mortality, and it is not confined to the moment the constriction is released. A ventricle squeezed for years is atrophic and stiff, and freeing it does not mean it can immediately handle the preload it suddenly receives. The support requirement runs for days in the ICU rather than ending when the chest closes; levosimendan, where it is available, shortened intubation, vasopressor duration, and ICU stay in a small retrospective post-pericardiectomy cohort.

The postoperative course outruns the operation - In a contemporary series 30-day mortality was 6% while sepsis hit 13% and dialysis-requiring renal failure 8.5%, with a mean ICU stay near four days — the operation is survivable and the recovery is where patients are lost. Risk tracks preoperative NYHA class (III-IV do markedly worse), renal dysfunction, pulmonary hypertension, advanced age, and liver failure. Etiology sets the ceiling: seven-year survival was 88% for idiopathic constriction, 66% after cardiac surgery, and 27% after mediastinal radiation. Needing bypass marks a sicker patient — in effusive-constrictive series mortality reached 50% when CPB was required versus 0% when it was not.

Congestive hepatopathy is a real coagulopathy - Years of venous congestion give a firm, tender, pulsatile liver and a measurable hepatic injury pattern: total bilirubin elevated in about 70% (indirect, rarely above 3 mg/dL), serum albumin low in about 40% (rarely below 2.5 g/dL), and prolonged coagulation times, with the INR climbing in the severe ischemic-injury cases. Send a preoperative PT/INR, albumin, and LFTs and treat a prolonged INR as genuine synthetic dysfunction heading into an operation that bleeds. The ascites is congestive by gradient (SAAG over 1.1) but protein-rich (often over 2.5 g/dL) from lymphatic leak, and a tense abdomen splints the diaphragm — build that into the ventilation plan and expect it post-induction. If they are on warfarin, the congested liver changes the dose they tolerate.

Protein-losing enteropathy - Constriction raises intestinal interstitial and lymphatic pressure, so protein leaks into the gut. The tell is low albumin AND low globulins together, since loss here is independent of molecular weight (nephrotic loss spares globulins); confirmation is alpha-1 antitrypsin clearance above 27 mL/24 h. They lose immunoglobulins and lymphocytes with it, so treat them as immunocompromised for line and airway technique and expect opportunistic infection, and let the hypoalbuminemia inform how you dose highly protein-bound drugs. Pericardiectomy can reverse it, which is part of the argument for operating.

Constrictive pericarditis is a rigid, fibrotic, sometimes calcified pericardium that encases the heart and prevents diastolic filling. Filling is abruptly limited in mid-to-late diastole, cardiac output becomes fixed and rate-dependent, and filling pressures equalize across the chambers.

Patients are preload-dependent and cannot augment stroke volume, so they lean on heart rate and adequate volume to maintain output. It resembles restrictive cardiomyopathy and tamponade physiologically; definitive treatment is pericardiectomy.

Constriction is how the pericardium heals badly. Granulation tissue obliterates the pericardial space after an episode of fibrinous pericarditis or after a chronic effusion resorbs, then contracts and calcifies over months to years. About 9% of acute pericarditis progresses, but the cause sets the odds: per 1000 person-years the incidence runs 0.76 for viral or idiopathic disease, 4.40 for connective tissue disease and pericardial injury syndromes, 6.33 for malignant, 31.65 for tuberculous, and 52.74 for purulent pericarditis. Worldwide tuberculosis leads, with roughly half of tuberculous pericardial effusions going on to constrict despite antitubercular therapy; mediastinal radiation does it in 2% to 30% of those treated. Across surgical series the mix runs idiopathic or viral 42% to 49%, prior cardiac surgery 11% to 37%, radiation 9% to 31%, connective tissue disease 3% to 7%, and tuberculous or infectious 3% to 6%.

The rigid shell also uncouples the heart from the chest. Inspiratory drops in intrathoracic pressure no longer reach the cardiac chambers, so pulmonary venous pressure falls while left atrial pressure does not, left-sided filling drops, and the septum shifts left so the right ventricle fills only at the left ventricle's expense. That ventricular interdependence is the fingerprint of constriction and the basis for nearly every test that separates it from restrictive cardiomyopathy. It is also why venous pressure rises rather than falls with inspiration (Kussmaul's sign).

Long-standing disease leaves marks well outside the chest: hepatic congestion progressing to cardiac cirrhosis, hepatomegaly and ascites, protein-losing enteropathy from bowel edema, atrial fibrillation from chronically elevated atrial pressures, and in advanced cases muscle wasting and frank cachexia. Untreated the trajectory is multiorgan dysfunction and death, with mortality over 90% reported when the diagnosis is missed.