Pericardial Surgery
World Small Animal Veterinary Association World Congress Proceedings, 2011
Peter Vogel, VMD, DACVS
Southern California Veterinary Specialty Hospital, USA

Pericardium

 Sac that envelopes the heart, root of aorta and pulmonary artery, termination of vena cava, pulmonary veins, and azygous vein

 Thin layer of fibrous tissue covered by pleura of the mediastinum

 Visceral layer consists of mesothelium

 Maintains the heart in normal anatomic position

 Prevents cardiac over-distention

 Acts as a barrier between pleural space and the heart

 Usually filled with small amount of fluid (serum ultrafiltrate)

 Non-compliant with small reserve volume

Pericardial Effusion

Categorized by clinical pathologic features:

 Transudate:

 Congestive heart failure

 PPDH

 Hypoalbuminemia

 Increased vascular permeability

 Exudate:

 Infectious or non-infectious pericarditis

 FIP

 Feline cardiomyopathy

 Fungal (Coccidioides)

 Hemorrhage:

 Trauma

 Neoplasia

 Rodenticide intoxication

 Aneurysmal rupture

 Idiopathic

Cardiac Tamponade

 Pericardial pressure increases after 50–60 mL of fluid accumulates

 Slower fluid accumulation allows pericardium to hypertrophy to some degree

 Elevation of pericardial pressure increases diastolic pressure within the heart, reducing stroke volume

 First equilibrates with right ventricular filling pressure, and the left ventricular filling pressure, significantly reducing cardiac output

 Activation of renin-angiotensin-aldosterone system

Diagnosis

 Clinical signs depend on rate of fluid accumulation and rise in intraperitoneal pressure

 Acute pressure increases result in hypotension, weakness, dyspnea, collapse, and cardiogenic shock

 Chronic effusion presents with exercise intolerance, lethargy, anorexia, dyspnea and weakness. Gradual onset of abdominal distention is reported.

 Classic sign is muffled heart sounds, weak femoral pulses, and distended veins

 Radiographs reveal a large, globoid shaped heart

 ECG often reveals electrical alternans and decreased R wave amplitude

 Echocardiography reveals a large accumulation of fluid within the pericardial sac

Treatment

 Ultrasound guided or blind pericardiocentesis can alleviate the acute crisis

 Sample submitted for cytologic exam and fluid analysis, C&S, etc.

 Pericardectomy

 Curative for idiopathic effusions (however, in my experience most idiopathic effusions are actually non-diagnosed neoplasia)

 Palliative for others

 Subtotal, partial, thorascopic pericardial window

 Subtotal via median sternotomy

 Able to remove most of pericardium

 Complete has no advantage of sub-total

 Partial via right lateral thoracotomy

 Thorascopically guided pericardial window

 Just as effective in palliation

 Minimal invasive

 Performed in dorsal recumbency

 Selective intubation not necessary, but helpful

 One port placed transdiaphragmatically (for scope)

 2 additional ports placed in the 4th and 7th intercostal space on the right (for instruments)

 Graspers and Metzenbaum scissors are utilized to remove a window (3 cm X 3 cm) of pericardium at the level of the ventricles

Constrictive Pericarditis

 Nondistensible, thickened, fibrotic pericardium

 Parietal pericardium usually more effected

 Severe adhesions may be present

 Effusive-constrictive pericarditis may occur

Pathophysiology

 Affects late diastole

 Limits ventricular filling in late diastole

 Elevated pulmonary wedge pressure, right atrial pressure, left ventricular diastolic pressure

 Diminished cardiac output

 Fluid retention and signs of right heart failure

Diagnosis

 Exercise intolerance, weakness, dyspnea, and collapse

 Signs of right sided heart failure on PE

 Globoid heart shape on radiographs

 Echocardiography for DDx

Treatment

 Subtotal or complete pericardectomy is treatment of choice

 Good outcome if only pericardium affected

 Decortication of affected epicardium necessary if affected

 Laceration of coronary artery, PTE, arrhythmias can occur

  

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Peter L. Vogel, VMD, DACVS
Southern California Veterinary Specialty Hospital
USA


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