Small Animal Thoracic Surgery

E. Christopher Orton, Eric Monnet

• Publisher: Wiley-Blackwell
• Year: 2017
• ISBN:
  9781118943441
• Edition: 1
• Topic: Medicine
• Subtopic: Veterinary Medicine

A state-of-the-art reference for all aspects of thoracic surgery in dogs and cats

Written by two of the foremost experts in this area of surgery, Small Animal Thoracic Surgery encompasses both basic and advanced thoracic surgery for dogs and cats. It provides a host of well-illustrated techniques for thoracic surgery, including classic open surgery, minimally invasive surgery, thoracoscopy, and image-guided hybrid surgery. This comprehensive and detailed book will help improve outcomes of thoracic cavity operations in small animal patients.

Small Animal Thoracic Surgery provides the most current and complete information available on this challenging area of surgery. The book offers guidance for treating the many disorders that can affect the canine and feline thoracic cavity, including pleural effusions, pneumothorax, hernias, heart disease, and more.

Small Animal Thoracic Surgery:

• Presents step-by-step descriptions of thoracic surgeries ranging from basic to advanced
• Features high-quality illustrations that depict key steps for each procedure
• Covers emerging minimally-invasive procedures, including thoracoscopy
• Offers up-to-date information for surgical treatment of ailments of the heart and lungs
• Provides video clips of procedures on a companion website

An invaluable reference for veterinary surgeons, Small Animal Thoracic Surgery is also an ideal aid for general practitioners who perform some of the basic procedures in their clinics.

Section V

Cardiac Surgery

17
Pericardium

Eric Monnet and E. Christopher Orton

Structure and Function

The pericardium is a saclike structure that envelopes the heart and origins of the great vessels. It is divided into the parietal and visceral pericardium, with the pericardial cavity in between. The parietal pericardium consists of an outer fibrous portion that blends with the adventitia of the great vessels and an inner serous portion. The fibrous pericardium is around 2 mm thick, has low cellularity, and is composed of collagen and elastin fibers. The collagen fibers are wavy, allowing a degree of stretch until it reaches its elastic limit, after which it stiffens exponentially [1].

The serous pericardium forms a closed mesothelium-lined cavity consisting of the visceral pericardium, which forms the epicardium and the serous portion of the parietal pericardium that lines the inside of the fibrous pericardium. The stromal layer of the visceral pericardium (epicardium) consists predominately of elastic fibers. The apex of the fibrous pericardium is anchored to the ventral diaphragm and sternum by the sternopericardic ligament. The pericardium is supplied by pericardial arteries that course with the sternopericardic ligament and pericardiophrenic arteries that course with the phrenic nerves. Both are branches of the internal thoracic arteries.

The pericardium maintains the heart in its normal anatomic position in the thorax by its attachment to the sternal portion of the diaphragm. The pericardium also constrains cardiac filling and enhances diastolic ventricular coupling. By this mechanism, the pericardium prevents cardiac overdistention and helps balance the output of the right and left ventricles. At low cardiac volumes, intrapericardial pressure is zero or negative, and the pericardium exerts little effect on cardiac filling. An intact pericardium protects against atrial rupture in dogs with mitral insufficiency and myocardial hemorrhage induced by acute right-sided heart failure. It may also prevent the spread of infection or neoplasia from the pleural space to the heart.

The pericardium provides a gliding surface to accommodate heart motion. The pericardial cavity is filled with a variable amount of pericardial fluid. In dogs, fluid volumes range from 1 to 15 mL. Pericardial fluid is an ultrafiltrate of serum that contains phospholipids for lubrication, a protein content of 1.7 to 3.5 g/dL, and colloid osmotic pressure approximately 25% of that seen in serum [2]. Because the pericardium is noncompliant and has a small reserve volume, intrapericardial pressure rises rapidly when the volume increases acutely. Chronic stretching of the pericardium results in remodeling of the extracellular matrix and augmentation of the pericardial volume.

Pathophysiology

Capacitance of the pericardium is influenced by rate of fluid accumulation. Because parietal pericardium is fairly noncompliant, pericardial pressure begins to increase after 5 to 60 mL of fluid accumulates acutely within the pericardial sac. With slow accumulation, the pericardium stretches, permitting augmentation of pericardial volume and rightward shifting of the pressure-volume curve. As a result, the pericardium can accumulate a larger volume of fluid before pressure begins to increase. However, beyond a certain point, pressure increases quickly with small increases in volume. When the pericardium is thickened, as is the case with constrictive pericardial disease, a minor increase in volume causes a significant increase in pericardial pressure [3].

An increase in pericardial pressure increases diastolic pressure within the heart, which in turn reduces cardiac filling and stroke volume. Pericardial pressure first equilibrates with right ventricular filling pressure (right-sided heart tamponade) and then with left ventricular filling pressure (left-sided heart tamponade). With tamponade, cardiac output decreases and systemic venous pressure increases, stimulating activation of compensatory neuroendocrine responses to increase vascular volume and maintain blood pressure [3]. With activation of the renin-angiotensin-aldosterone system, sodium and water are retained. Sympathetic stimulation and adrenomedullary catecholamine release produce positive inotropic and chronotropic effects and vasoconstriction. Because atrial wall stretching is limited by tamponade, atrial natriuretic peptide is not released with pericardial effusion and is therefore not available to counteract the effects of the renin-angiotensin-aldosterone system. As a result, cardiac tamponade is associated with increases in systemic venous and portal pressures, causing jugular vein distention, liver congestion, ascites, and peripheral edema secondary to fluid transudation from systemic capillary beds. Although cardiac contractility is not directly affected by tamponade, compression of coronary arteries results in poor myocardial perfusion. When coupled with decreased cardiac output and arterial hypotension, cardiogenic shock and death may result.

Arterial pressures may vary paradoxically with respiration during severe cardiac tamponade. During inspiration, pericardial pressure and right ventricular pressure decrease, facilitating venous return to the right atrium and ventricle and pulmonary blood flow. However, because heart volume is limited by the pericardium, the intraventricular septum shifts to the left. Consequently, left ventricular end-diastolic volume, left heart output, and arterial pressure are decreased during inspiration, resulting in variation of systolic arterial pressures often greater than 10 mm Hg. This phenomenon, known as pulsus paradoxus, can also occur with obstructive lung disease, restrictive cardiomyopathy, constrictive pericarditis, or hypovolemic shock and is therefore not pathognomonic for cardiac tamponade [3–5].

Pericardial Effusion

Pericardial effusions are categorized by characteristics of the accumulated fluid. A transudative pericardial effusion may occur with congestive heart failure, peritoneopericardial diaphragmatic hernia, hypoalbuminemia, or increased vascular permeability [6–11]. An exudate (total protein >2.5 g/dL; total nucleated cell count >5000 cells/μL) results from infectious or noninfectious pericarditis, such as feline infectious peritonitis [12]. Infectious agents can be bacterial, fungal, or viral. Fungal pericarditis is uncommon, with the exception of Coccidioides immitis in dogs living in the southwestern United States [13]. Bacterial pericardial effusion has been reported in dogs and is suspected to be secondary to migration of plant materials [0012].

Causes of hemorrhagic pericardial effusion include trauma, neoplasia, anticoagulant intoxication, or rupture of the left atrium secondary to mitral valve disease [14,15]. If an underlying cause cannot be determined, it is classified as idiopathic pericardial effusion. Idiopathic pericardial effusion is considered by some authors to be the most common cause of acute or chronic hemorrhagic pericardial effusion in dogs [16]. Some dogs with idiopathic pericardial effusion may actually have a small undetected intrapericardial tumor or mesothelioma. Although infectious agents are an unlikely cause, influenza type A viral ribonucleic acid was detected in pericardial fluid of 1 in 14 dogs with idiopathic pericardial effusion [7].

The second most common cause of hemorrhagic pericardial effusion is neoplasia of the heart, heart base, or pericardium, with hemangiosarcoma of the right atrium being most common [15,17,18]. Hemangiosarcoma is sometimes multicentric, involving the spleen or liver at the time pericardial effusion is detected. Chemodectoma is the second most common cardiac tumor to cause pericardial effusion and is most often seen in brachycephalic dogs. Hemorrhagic pericardial effusion may also be caused by pericardial mesothelioma. This diffuse neoplasm of the pericardium and other serosal surfaces may be difficult to distinguish from idiopathic pericardial effusion even with pericardial histopathology and immunohistochemistry [19].

Diagnosis

Echocardiography is very sensitive for diagnosis of pericardial effusion and can detect as little as 15 mL of fluid.The classic echocardiographic finding in pericardial effusion is an anechoic space between the epicardium and parietal pericardium. Right and left ventricular dimensions are often diminished, and ventricular walls appear thicker than normal when pericardial effusion is severe and cardiac filling is impaired. Collapse of the right atrium or ventricle during diastole suggests significant increase in intrapericardial pressure and cardiac tamponade. Absence of these findings, however, does not exclude significant impairment of the cardiac function [20,21].

Echocardiograp...

Table of contents

• Cover
• Title page
• Copyright
• dedication
• Preface
• About the Companion Website
• Section I General Principles
• Section II Thoracic Approaches
• Section III Thoracic Wall and Pleural Space
• Section IV General Thoracic Surgery
• Section V Cardiac Surgery
• Index
• WILEY END USER LICENSE AGREEMENT