Surgery of the Cardiovascular System

Chapter 28

Surgery of the Cardiovascular System

General Principles and Techniques


Cardiac surgery includes procedures performed on the pericardium, cardiac ventricles, atria, venae cavae, aorta, and main pulmonary artery. Closed cardiac procedures (i.e., those that do not require opening major cardiac structures) are most commonly performed; however, some conditions require open cardiac surgery (i.e., a major cardiac structure must be opened to accomplish the repair). Open cardiac surgery necessitates that circulation be arrested during the procedure by inflow occlusion or cardiopulmonary bypass. Venous inflow occlusion provides brief circulatory arrest, allowing short procedures (less than 4 minutes) to be performed. Longer open cardiac procedures require establishing an extracorporeal circulation by cardiopulmonary bypass to maintain organ perfusion during surgery.

Preoperative Management

Animals requiring cardiac surgery often have prior cardiovascular compromise that should be corrected or controlled medically when possible before anesthetic induction (Box 28-1). Congestive heart failure (CHF), particularly pulmonary edema, should be managed with diuretics (e.g., furosemide) and angiotensin-converting enzyme (ACE) inhibitors (e.g., enalapril, benazepril, lisinopril) and an inodilator (pimobendan) before surgery. Cardiac arrhythmias should be recognized and treated (see also later discussion in the “Postoperative Care and Assessment” section). Ventricular tachycardia should be suppressed before surgery with class I antiarrhythmic drugs (i.e., lidocaine and procainamide). Other antiarrhythmic drugs to consider include sotalol and amiodarone. Lidocaine is effective for management of ventricular tachyarrhythmias during and immediately after surgery. Supraventricular tachycardia may require digoxin, β-adrenergic blockers (e.g., esmolol, propranolol, atenolol), or calcium channel–blocking drugs (e.g., diltiazem) before surgery. Atrial fibrillation should be controlled before surgery with a β-blocker or a calcium channel blocker with or without digoxin to lower the ventricular response rate to below 140 beats per minute. Alternatively, amiodarone may be used to control the ventricular response rate, and in a small percentage of cases, to convert atrial fibrillation to normal sinus rhythm. Animals with bradycardia should undergo an atropine or glycopyrrolate response test before surgery. If bradycardia is not responsive to atropine or glycopyrrolate, temporary transvenous pacing or constant intravenous infusion of isoproterenol (see management of bradycardia on p. 901) may be required.

image Box 28-1   Selected Drugs Used in the Management of Animals with Cardiac Disease

*Use 0.05 mg/kg in cats.

All animals should undergo a complete echocardiographic evaluation before cardiac surgery; an incomplete or inaccurate diagnosis can have devastating consequences. With the advent of Doppler echocardiography, cardiac catheterization is no longer routinely necessary before cardiac surgery.


Anesthesia of the patient with cardiac compromise has risks that vary depending on the cause of the underlying disease. For example, the anesthetic protocol that is safest for the patient with mitral regurgitation can be dangerous for the patient with aortic stenosis. The pathophysiology of the patient’s cardiac condition needs to be fully understood. Likewise, the practitioner needs to have a working knowledge of the pharmacology of the drugs used to manipulate heart rate and blood pressure. Although cardiac surgery is typically performed at veterinary teaching hospitals and referral institutions, veterinarians from a variety of practices are required to anesthetize the patient with heart disease. See p. 870 for a discussion of anesthesia in patients with mitral regurgitation and p. 881 for information on anesthesia in the patient with subaortic stenosis (Tables 28-1 to 28-3). See also the discussion of anesthesia for the patient with cardiac tamponade on p. 892.

Preanesthetic medication is appropriate for most animals undergoing cardiac surgery. Parenteral opioids (i.e., hydromorphone, butorphanol, buprenorphine, and fentanyl) induce sedation with minimal cardiovascular effects; however, all opioids can produce respiratory depression and/or bradycardia. α2-Agonists (e.g., demedetomidine) and acepromazine should be avoided in cardiac patients owing to significant alterations in hemodynamic parameters associated with their administration. Anticholinergics (i.e., atropine and glycopyrrolate) should be administered only as needed. Carefully consider whether an elevated heart rate will assist or hinder forward flow of blood in the individual patient. Benzodiazepines (e.g., diazepam 0.2 mg/kg, midazolam 0.2 mg/kg) have minimal cardiopulmonary effects and enhance sedation when given alone or combined with opioids. Some patients may have an unpredictable behavioral response (e.g., excitation, aggressiveness) to benzodiazepine administration. Therefore, they are often used in combination with an opioid.

Induction of anesthesia should be undertaken with caution in animals with cardiopulmonary compromise. Thiobarbiturates should be avoided in patients with significant cardiac disease because they result in dose-dependent cardiac depression and are arrhythmogenic. Propofol (Diprivan or Rapinovet) produces rapid induction but causes essentially the same cardiovascular compromise as thiobarbiturates. The addition of fentanyl decreases propofol requirements in healthy dogs with minimal alteration in cardiovascular parameters (Covey-Crump and Murison, 2008). Ketamine combined with diazepam may be appropriate for induction of compromised patients. It should be avoided in animals with mitral insufficiency because it increases the regurgitant fraction by increasing peripheral vascular resistance. However, it is the induction agent of choice in animals with pericardial constriction. Opioids can be used for induction of very sick and compromised dogs; however, opioids do not induce hypnosis, so intubation may be difficult. Etomidate is not arrhythmogenic, maintains cardiac output, and offers rapid induction, although it is associated with longer and poorer recoveries (Sams et al, 2008). Mask induction is discouraged in all patients with cardiopulmonary disorders because the patient’s reduced cardiac output will cause an increased time to achieve adequate induction. Additionally, inhalants cause marked hypotension, which is often undesirable. A balanced anesthetic approach using benzodiazepine, opioids, and modest amounts of inhalant is generally much safer. Atracurium (Box 28-2) is a short-acting muscle relaxant that is not dependent on metabolism or excretion to terminate its action; it may be used if further muscle relaxation is needed (it must be used with intermittent positive-pressure ventilation [IPPV]).

Thoracic surgery always requires controlled ventilation. Controlled ventilation can be achieved by manually squeezing the reservoir bag or by attaching a mechanical ventilator to the anesthetic machine. Ideally, mechanical ventilation should achieve a tidal volume of 6 to 10 ml/kg of body weight at an inspiratory pressure of less than 20 cm of water. Ensuring adequate ventilation is accomplished by optimizing tidal volume, inspiratory pressure, and respiratory rate to achieve ventilation with the least risk of causing pulmonary injury or cardiovascular compromise. Ultimately, the goal of mechanical ventilation is to maintain normocapnia. Ventilation can be monitored by measurement of end-tidal CO2 by capnography, or of arterial CO2 by blood gas analysis.

Successful inflow occlusion requires meticulous anesthesia. Intraoperative and postoperative care may be complicated and may require multiple vasoactive medications. For further discussion of anesthesia techniques for these patients, the reader is referred to a cardiac anesthesia text. Balanced anesthetic techniques that minimize inhalation anesthetic agents are indicated (e.g., fentanyl citrate plus atracurium besylate combined with isoflurane [see Box 28-2]). Administration of a single dose of dexamethasone (see Box 28-2) after induction may be beneficial in reducing cardiac damage and improving postoperative outcomes (Yared et al, 2007). Mild hypothermia (32° C to 34° C) reduces basal metabolic rate, allowing lengthening of occlusion time; however moderate hypothermia (<32° C) is associated with spontaneous ventricular fibrillation. Animals should be hyperventilated for 5 minutes before inflow occlusion. Ventilation is discontinued during inflow occlusion and is resumed immediately upon reestablishment of blood flow. Drugs and equipment for full cardiac resuscitation must be available immediately after inflow occlusion. Gentle cardiac massage may be necessary after inflow occlusion to reestablish cardiac function. Digital occlusion of the descending aorta during this period helps direct available cardiac output to the heart and brain. If ventricular fibrillation occurs, immediate internal defibrillation is necessary as soon as inflow occlusion is discontinued. Constant intravenous infusion of lidocaine (see Box 28-2) should be initiated before inflow occlusion and continued as necessary. Epinephrine, administered as a constant rate infusion, should be given as the animal is being weaned off inflow occlusion or a pump (see Box 28-2). If long-term inotropic support is necessary, dobutamine or amrinone should be given (see Boxes 28-1 and 28-2 and Tables 28-1 through 28-3).

Transesophageal echocardiography (TEE) can be an invaluable tool for assessing both cardiac function and volume status in the cardiac patient. Its use intraoperatively and immediately postoperatively can guide the choice of pharmacologic intervention and can assist in assessing the effectiveness of therapy. Central venous pressure measurements have been shown to poorly correlate with volume status. When TEE is used, ventricular filling can be visualized and volume replacement modified accordingly.

Surgical Anatomy

The heart is the largest mediastinal organ. It generally extends from the third rib to the caudal border of the sixth rib; however, variations have been noted among breeds and between individuals. The heart base (i.e., the craniodorsal aspect [from where the great vessels originate]) faces dorsocranially, whereas the apex (i.e., formed by muscles of the left ventricle) points caudoventrally. Except for a portion of the right side of the heart (cardiac notch), most of its surface is covered by lung. The right ventricular wall accounts for approximately 22% of the total heart weight; the left ventricular wall accounts for nearly 40%.

The right atrium receives blood from the systemic circulation. The coronary sinus enters the left caudal aspect of the atrium, ventral to the caudal vena cava. The caudal vena cava returns blood from the abdominal viscera, the pelvic limbs, and a portion of the abdominal wall (Fig. 28-1). The cranial vena cava returns blood to the heart from the head, neck, thoracic limbs, and ventral thoracic wall, and from a portion of the abdominal wall. The azygos vein usually enters into the cranial vena cava; it carries blood from the lumbar regions and the caudal thoracic wall. The brachycephalic trunk is the first large artery from the aortic arch. The common carotid arteries usually arise from it as separate vessels. The left subclavian artery arises from the aortic arch distal to the brachycephalic trunk (the right subclavian is a branch of the brachycephalic trunk). The vertebral arteries, costocervical trunk, internal thoracic arteries, and axillary arteries branch from the subclavian vessels.

The pericardium is a thick, two-layer sac composed of outer fibrous and inner serous layers. The pericardial cavity is located between two layers (visceral and parietal) of serous pericardium and normally contains a small amount of fluid. The fibrous pericardium blends with the adventitia of the large vessels, and its apex forms the sternopericardiac ligament. Phrenic nerves lie in a narrow plica of pleura adjacent to the pericardium at the heart base. Complete pericardiectomy requires that these nerves be elevated to avoid incising them. The vagus nerves lie dorsal to the phrenic nerve. They divide to form dorsal and ventral branches that lie on the esophagus in the caudal thorax. The left recurrent laryngeal nerve leaves the vagus and loops around the aortic arch distal to the ligamentum arteriosum to run cranially along the ventrolateral tracheal surface.

Surgical Technique

Cardiac surgery is not fundamentally different from other types of general surgery, and similar principles of good surgical technique (i.e., atraumatic tissue handling, good hemostasis, and secure knot tying) apply. Consequences of poor surgical technique are often devastating. Cardiac surgery differs from other surgeries in that motion from ventilation and cardiac contractions adds to the technical difficulty of performing these procedures. Approaches that provide limited access to dorsal structures (e.g., median sternotomy; see p. 967) require that surgeons incise, suture, and/or ligate structures located deep within the thorax. Ligature placement using hand ties (see p. 76) is useful in such situations, and the ability to place hand-tied knots (vs. instrument tying) should be considered a fundamental skill for cardiac surgeons. Secure knot tying is critically important for successful cardiac surgery. Hand tying of knots is fast and produces tighter and more secure knots than instrument tying. The one-handed knot tie technique (see p. 78) is best suited to the fine sutures used in cardiac surgery. Tight knots are facilitated by throwing the first two or three throws in the same direction before finishing with square knots for security.

Closure of cardiovascular structures requires precise suturing techniques and good instrument handling skills to minimize hemorrhage. Using fine suture with swaged-on atraumatic needles (see discussion on suture materials on p. 865) and carefully following the needle contour when suturing (to minimize the size of needle tracts) are important. “Palming” of needle holders is a good skill for fast suturing but should be avoided when suturing inside the thoracic cavity. Finer control is gained by grasping instruments with fingers placed in the instrument rings.

Inflow Occlusion

Inflow occlusion is a technique used for open heart surgery in which all venous flow to the heart is temporarily interrupted. Because inflow occlusion results in complete circulatory arrest, it allows limited time to perform cardiac procedures. Ideally, circulatory arrest in a normothermic patient should be less than 2 minutes, but it can be extended to 4 minutes if necessary. Circulatory arrest time can be extended up to 8 minutes with mild, whole-body hypothermia (32° C to 34° C). Temperatures below 32° C may predispose to spontaneous ventricular fibrillation and should be avoided. The advantage of inflow occlusion is that it does not require specialized equipment; however, the limited time available to perform the surgery requires that the procedure be well planned and executed with speed and expertise.

Depending on the cardiac procedure that is being done, perform a left or a right thoracotomy (see p. 964) or a median sternotomy (see p. 967). With a right thoracotomy or median sternotomy, occlude the cranial and caudal vena cava and the azygos vein with vascular clamps or Rumel tourniquets (Fig. 28-2). Make a Rumel tourniquet by passing umbilical tape around the vessel, then thread the umbilical tape through a piece of rubber tubing that is 1 to 3 inches long. When the umbilical tape has been adequately tightened to occlude the vessel, place a clamp above the rubber tubing to hold it securely in place. Take care to prevent injuring the right phrenic nerve during placement of the clamps or tourniquets. For left thoracotomies, pass separate tourniquets around the cranial and caudal venae cavae. Then, while dissecting dorsal to the esophagus and aorta, occlude the azygos vein by placing a tourniquet around it (Fig. 28-3).

Healing of Cardiovascular Structures

Vascular structures heal quickly, forming a fibrin seal within minutes. Epithelialization and early endothelial regeneration occur in veins used for grafts. Thrombosis commonly occurs in small veins that have been traumatically occluded for short periods of time; however, thrombosis of large veins occluded during inflow occlusion or cardiac bypass procedures has not been a clinically recognized problem. To prevent thrombosis of vascular structures, they should be handled gently, because trauma may lead to the deposition of platelets, fibrin, and red cells on the intimal surface. If the torn intima is lifted upward, a flap may develop that partially or completely occludes the distal lumen. This in turn can lead to accumulation of blood within the vessel wall, vascular sludging, and thrombosis.

Suture Materials and Special Instruments

Polypropylene (Prolene, Surgipro) and braided polyester (Ticron, Mersilene) suture are the standard sutures used for cardiovascular procedures. The sizes most commonly used are 3-0, 4-0, and 5-0, although smaller sizes may be needed for vascular anastomoses. Sutures should be available with swaged-on taper-point cardiovascular needles in a variety of sizes. Some procedures require that the suture be double-armed (i.e., with needles at both ends). Teflon pledgets are useful for buttressing mattress sutures in ventricular myocardium or great vessels.

Successful cardiac surgery requires proper surgical instrumentation. Most of the basic instruments required for general surgery can be used for cardiac surgery; however, a few specialized instruments are desirable for thoracic surgery. The standard thoracic retractor is a Finochietto retractor (Fig. 28-4, A). It is helpful to have retractors of at least two sizes to accommodate animals of different sizes. Self-retaining orthopedic retractors can substitute as thoracic retractors in small dogs and cats. The standard tissue forceps for thoracic surgery is a DeBakey tissue forceps (Fig. 28-4, B). At least two DeBakey forceps should be available, and it is helpful if one has a carbide inlay for grasping suture needles. Metzenbaum scissors are the standard operating scissors for cardiac surgery. Curved Metzenbaum scissors are more versatile than the straight design. Potts scissors (45-degree angle) are desirable for some cardiac surgery procedures (see Fig. 28-4, B). Needle holders should be long and available in different sizes to accommodate a variety of suture needle sizes. Mayo-Hegar, Crile-Wood, and Castroviejo needle holders represent a good selection of sizes for thoracic surgery in animals. Angled thoracic forceps are an important instrument for cardiac surgery and should be available in a variety of sizes (see Fig. 28-4, B). Vascular clamps are noncrushing clamps used for temporary occlusion of cardiovascular and pulmonary structures. They come in a variety of sizes and shapes, including straight, angled, curved, and tangential (Fig. 28-5). The most versatile shape for most cardiac surgery procedures is a medium-width tangential clamp.

Postoperative Care and Assessment

Patient monitoring and postoperative care are the cornerstones of successful cardiac surgery. The level of supportive care required for cardiac surgeries depends on the patient and the surgical procedure performed. A working knowledge of cardiopulmonary function and good patient observation skills are as important to successful patient management as advanced monitoring devices.

Evaluation of ventilation is important after any thoracic surgery. Poor ventilatory efforts may first be noted in the period after surgery, when the influence of anesthetic drugs is still present but ventilatory support has been discontinued. Hypoventilation may also result from uncontrolled pain. Total ventilation can be assessed directly by measuring the volume of expired gas with a respirometer. Tidal volume should be at least 10 ml per kg of body weight. Ultimately, the best measure of alveolar ventilation is arterial CO2 tension (PaCO2). Alveolar hypoventilation is present when PaCO2 is increased to above 40 mmHg. Treatment of hypoventilation should be directed at correcting its underlying cause if possible. Drugs that are known to depress ventilation (i.e., opioids and muscle relaxants) should be used with caution in the perioperative period, and the risk of ventilatory depression weighed against the risk of hypoventilation due to pain (see p. 961 for analgesia after thoracotomy). Pleural air or fluid should be evacuated if present. Injury or dysfunction of the neuromuscular ventilatory apparatus should be corrected, if possible. If hypoventilation is severe and the cause is not immediately correctable, positive-pressure ventilation is indicated. If necessary, keep the animal intubated and ventilated postoperatively until partial pressure of arterial oxygen (PaO2), partial pressure of arterial carbon dioxide (PaCO2), pH, blood pressure (BP) and heart rate (HR) indicate that the patient is stable enough to extubate. Constant-rate infusions of fentanyl and propofol can assist in keeping the patient comfortable until complications such as significant ventilation/perfusion (image) mismatch or acidosis have improved. If necessary, vasopressors may be administered to correct hypotension caused by propofol.

Under physiologic conditions, gas exchange between the alveolus and the pulmonary capillary blood is efficient, and alveolar oxygen tension (PAO2) and arterial oxygen tension (PaO2) are nearly equal. In patients with impaired gas exchange, hypoxemia occurs because PAO2 and PaO2 are not equal. The most common cause of impaired pulmonary gas exchange in the postoperative setting is ventilation/perfusion (image) mismatch with formation of pulmonary shunts secondary to alveolar collapse. The importance of image ratios relates to how well the lungs resaturate venous blood with O2 and eliminate CO2. During procedures involving circulatory arrest or cardiopulmonary bypass, ventilation is temporarily ceased and the remaining oxygen is absorbed, resulting in collapsed alveoli (absorption atelectasis). With reperfusion of collapsed pulmonary tissues, blood passes through the lungs without becoming oxygenated. The result can be large shunts of deoxygenated blood returning to the left side of the heart. Patients with shunts are not responsive to higher concentrations of oxygen. Instead, they need assisted ventilation and positive end-expiratory pressure (PEEP). Therefore, response to supplemental oxygen therapy must be evaluated for each individual patient, preferably by arterial blood gas analysis. The therapeutic goal of supplemental oxygen should be to keep PaO2 above 80 mmHg. Ventilation and PEEP are indicated for patients with severe gas exchange impairment that is not responsive to supplemental oxygen therapy alone.

Maintaining an adequate PaO2 in a patient is important because it is the soluble oxygen that crosses membranes. Total oxygen content of the blood is the sum of the oxygen in solution (PaO2) plus that carried by hemoglobin. The major determinant of hemoglobin oxygen saturation (SaO2) is hemoglobin. SaO2 can be measured by pulse oximetry. The therapeutic goal should be to maintain SaO2 at or above 90%. Oxygen content of the blood is a function of SaO2 and hemoglobin concentration. Thus maintenance of adequate oxygen content requires not only adequate pulmonary function, but also an adequate hemoglobin concentration. Maintenance of the packed cell volume above 30% is an important therapeutic goal for animals undergoing cardiac surgery, especially if cardiopulmonary compromise is present.

Systemic blood pressure is directly proportional to cardiac output and systemic vascular resistance. Measurement of blood pressure provides a good assessment of cardiovascular function, especially during and immediately after surgery. Indirect techniques for measuring blood pressure include the oscillometric method, which serves as the basis of monitors such as the Dinamap, or Doppler, method. Doppler technique provides only systolic pressure but is useful for evaluating blood pressure trends during and after surgery. Indirect methods of blood pressure assessment are less invasive, but are also less accurate than direct measurements. Direct measurement of blood pressure requires placement of an arterial catheter. Arterial catheters have the additional advantage of providing access for arterial blood gas analysis. An arterial catheter can be placed percutaneously into a dorsal pedal artery. Direct blood pressure measurement also requires a pressure transducer and a monitor, or a manometer. The therapeutic goal is to maintain a mean blood pressure above 65 mmHg and systolic blood pressure above 90 mmHg. Blood pressure can be elevated by increasing cardiac output or systemic vascular resistance. In many instances (depending on the cause), a more appropriate therapeutic strategy to correct hypotension is to improve cardiac output. Maintenance of adequate vascular volume is the most important aspect of maintaining adequate cardiac output. Central venous pressure should be maintained at between 5 and 10 cm of water. If echocardiography is available, evaluation of ventricular filling is a more reliable way to detect hypovolemia. Indications for arterial pressor therapy are rare. Inotropic and pressor support can be obtained by constant intravenous infusion of epinephrine (see Box 28-2). Long-term inotropic support is maintained with dobutamine (see Box 28-2).

Monitoring the electrocardiogram for disturbances in cardiac rhythm is important for animals undergoing cardiac surgery. Sinus tachycardia is the most common rhythm disturbance in surgery patients. Therapy for sinus tachycardia should be directed at correction of its underlying cause (e.g., hypovolemia, pain, anxiety, acidosis, hypotension, anemia, hypoxemia, drug-induced) and improvement in cardiac output. Ventricular dysrhythmias, including premature ventricular complexes (PVCs) and nonsustained or sustained ventricular tachycardia, are frequently encountered during and after cardiac surgery. Frequent PVCs, particularly when they occur with a short coupling interval (i.e., R-on-T phenomena), and rapid ventricular tachycardia should be suppressed in the perioperative period. Continuous intravenous infusion of lidocaine is effective in most instances. Ventricular fibrillation is a form of cardiac arrest that requires immediate electrical defibrillation. If cardiac surgery is performed, equipment for defibrillation should be available. Recommendations for postoperative analgesics are provided in Chapter 12 (see Table 12-3 on p. 141 and Box 31-2 on p. 992).


The major complication associated with cardiac surgery is hemorrhage. Severe hemorrhage may be encountered intraoperatively or postoperatively. Materials for blood transfusion should be available (see Box 4-1 and Table 4-5 on pp. 30 and 34, respectively). Fresh whole blood should be collected as close as possible to the time that it is needed and should not be cooled because this may reduce platelet content. If possible, a compatible donor should be identified by cross-matching the patient before surgery. Cell Saver autologous blood recovery systems (Haemonetics, Braintree, Mass.) are available for collection and processing of blood for procedures in which rapid bleeding or high-volume blood loss may occur. They can also be used to sequester platelets and plasma from a patient immediately before surgery, thereby reducing the need for donor blood.

Special Age Considerations

Most animals undergoing surgery for congenital cardiac defects are young. Special care must be given to these animals during and after surgery. Young animals should not have food withheld for longer than 4 to 6 hours before surgery and should be fed as soon as they are fully recovered from anesthesia. If they cannot be fed, blood glucose concentration should be maintained by adding glucose to intravenous fluids; blood glucose concentrations should be monitored intraoperatively. Hypothermia is common in young patients during thoracotomy and is protective during cardiac procedures. However, the temperature should be monitored closely, and patients should be actively rewarmed postoperatively.

Specific Diseases

Mitral Regurgitation

General Considerations and Clinically Relevant Pathophysiology

MR is the most common form of acquired heart disease in dogs. Approximately 75% of dogs with chronic heart disease have MR attributable to MVD. It commonly occurs as the result of myxomatous degeneration of the valve and may be associated with one or more of the following: thickening and billowing of the leaflets, dilation of the mitral annulus, thickening and lengthening or rupture of the chordae tendineae, and flattening of the papillary muscles with left ventricular dilation. Morphologic changes associated with MVD in dogs are similar to those observed in humans with mitral valve prolapse. Tissue swelling occurs on the edge of valve leaflets, the chordae tendineae, and the chordal-papillary muscle junction. Damage to the valve complex endothelium is unevenly distributed. On rare occasions, annular dilation and MR occur without significant disease of the chordae or leaflets. Congenital valve dysplasia and dilated cardiomyopathy are other causes of mitral regurgitation.

The clinical presentation and progression of MVD are variable. Most dogs remain asymptomatic for their lifetime. For dogs that do have progression of disease, volume overload of the left ventricle occurs when blood regurgitates through the mitral valve, causing left atrial and left ventricular hypertrophy. As the mitral valve annulus dilates, MR typically becomes more severe, and left-sided CHF typically ensues. Atrial fibrillation may be associated with left atrial dilation, especially in large and giant breeds of dogs with sufficient atrial mass to sustain the arrhythmia. A classification system has been proposed (Box 28-4) to aid identification of dogs with cardiac disease, and to link the extent of clinical signs with appropriate treatment and monitoring recommendations.


Clinical Presentation

Physical Examination Findings

Affected animals typically have a holosystolic murmur heard best at the left cardiac apex. The intensity of the murmur may be correlated with the severity of disease in some dogs (usually small breeds) (Ljungvall et al, 2009). Pulmonary crackles may be heard if pulmonary edema is present. Electrocardiographic evidence of left atrial and/or left ventricular enlargement may be manifested by a P wave duration greater than 0.04 second (P mitrale) or tall R waves (>2 to 2.5 mV), respectively, in lead II.

Diagnostic Imaging

Consensus guidelines from the American College of Veterinary Internal Medicine (ACVIM) regarding dogs with MVD recommend thoracic radiographs for all dogs with suspected MVD to assess the hemodynamic significance of the murmur, as well as to obtain a baseline image when the dog is asymptomatic. Echocardiography should be performed to confirm the suspected cause of an identified murmur and to document the presence or absence of cardiac chamber enlargement.

Left atrial and left ventricular enlargement may be evident on thoracic radiographs. When CHF develops, additional radiographic features include pulmonary venous congestion and pulmonary parenchymal infiltrate, typically with a perihilar or caudal and dorsal distribution.

Differential Diagnosis

Other causes of heart failure and cardiac murmur in mature dogs include dilated cardiomyopathy and previously undiagnosed or unrepaired congenital heart disease (patent ductus arteriosus [PDA], ventricular septal defect [VSD], mitral dysplasia, subvalvular aortic stenosis [SAS]). Primary differentials include chronic bronchitis, heartworm disease, tracheal collapse, pneumonia, and primary or metastatic pulmonary neoplasia.

Medical Management

Few data suggest that medical intervention before the onset of clinical signs of heart failure is beneficial, and the topic remains controversial (Atkins et al, 2009). In fact, several placebo-controlled trials have demonstrated that therapy with ACE inhibitors or inodilators has no effect on the symptom-free interval (time to onset of heart failure) in asymptomatic patients, although benazepril was shown to have a beneficial effect in certain breeds in an uncontrolled retrospective study (Atkins et al, 2007; Quellet et al, 2009; Pouchelon et al, 2008).

Once CHF is documented, treatment with diuretics (e.g., furosemide; see Box 28-1), ACE inhibitors (i.e., enalapril or benazepril; see Box 28-1), and inodilators (pimobendan, see Box 28-1) is indicated. Additional diuretics (e.g., spironolactone, hydrochlorothiazide) and vasodilators (e.g., hydralazine, amlodipine) should be considered in refractory cases. The use of β-blockers in dogs with MVD is controversial because they can exacerbate unstable CHF; a recent study found quality of life and functional class improvement in a small number of dogs, although echocardiographic variables were unchanged (Marcondes-Santos et al, 2007). Further investigation is warranted.

Surgical Treatment

Mitral valve replacement and repair have been reported in dogs. For mitral valve replacement, a mechanical or bioprosthetic heart valve is typically used. Disadvantages of these valves are that the animal must be placed on lifelong anticoagulation therapy, and early pannus formation and calcification occur with bioprosthetic valves (bioprosthetic). Valvular replacement requires cardiopulmonary bypass. Mitral valve repair may offer advantages over valve replacement in that long-term anticoagulation is not required and myocardial function is better preserved. However, results are variable and are highly dependent on the surgeon’s experience.


The goal of managing the patient with mitral regurgitation while the patient is under anesthesia is to maximize forward flow of blood and minimize the regurgitant fraction (see Tables 28-1 and 28-2). To do this, heart rate needs to be kept at high normal values and blood pressure needs to be normal to 20% below normal. A slower heart rate allows for larger filling volumes, potentially leading to left ventricular distention and dilation of the mitral annulus. This can result in a larger regurgitant fraction. Treat bradycardia with anticholinergics (i.e., atropine, glycopyrrolate). Patients with mild or moderate disease usually have adequate left ventricular function and normal end-diastolic ventricular pressures, especially in mild to moderate disease. Therefore they are able to perfuse the myocardium with low-normal systemic blood pressures. With lowering of systemic vascular resistance (SVR), the pressure gradient across the aortic valve favors forward flow of blood into the aorta. This reduces the regurgitant fraction, increases cardiac output, and increases blood pressure. High systemic blood pressure should be avoided. If it does occur, hypertension should be treated immediately by deepening the anesthesia with an inhalational agent and giving a rapidly acting opioid (i.e., fentanyl). If the initial treatment is inadequate, nitroglycerin or nitroprusside may be titrated to effect as a constant rate infusion.

Several drugs should be avoided in patients with mitral regurgitation. The α2-agonists are contraindicated in affected animals. Hypertension can cause a marked increase in the regurgitant fraction, resulting in a decrease in cardiac output and potentially cardiovascular collapse. Although acepromazine causes a decrease in systemic vascular resistance, many of these patients are geriatric with hepatic congestion, and its metabolism may be prolonged. Therefore acepromazine should be used very cautiously and probably only in patients with mild valvular disease. Propofol causes a decrease in systemic vascular resistance that accounts for part of the hypotension seen with its use. However, it also causes a decrease in myocardial contractility. This is undesirable in patients with moderate to severe MR. In patients with mild valvular dysfunction, propofol may be slowly titrated to effect as an induction drug. In moderate to severe cases of MR, etomidate is a better choice for induction. Because ketamine maintains sympathetic tone and thus systemic vascular resistance, it is a poor choice for induction in MR patients.

If hypotension needs to be treated while the patient is under anesthesia, ephedrine is a good choice and can be titrated in increments of 2.5 to 10 mg, depending on the degree of hypotension and the size of the patient. Because ephedrine causes stimulation of β-receptors in the heart, it also causes a mild increase in contractility, heart rate, and blood pressure. Phenylephrine in low doses causes venoconstriction with a subsequent increase in preload. However, at higher doses, the increase in systemic vascular resistance caused by phenylephrine is undesirable. For this reason, epinephrine is often the vasopressor of choice. It has less effect on systemic vascular resistance and a greater effect on both heart rate and contractility.

To avoid increases in pulmonary vascular resistance (PVR) and worsening pulmonary hypertension, avoid acidosis, nitrous oxide, hypoxemia, hypoventilation, and hypercarbia. Refer to Tables 28-1 and 28-2 for anesthetic recommendations for patients with mitral regurgitation undergoing cardiac or noncardiac procedures.

Surgical Anatomy

The right and left coronary vessels (Fig. 28-6) arise from the aortic bulb immediately distal to the aortic valve. The right coronary artery arises from the right sinus of the aorta and curves to the right and ventrocranially, lying in the fat of the coronary groove. Its initial part is bounded by the pulmonary trunk and the conus arteriosus craniolaterally; dorsally it is covered by the right auricle. The left coronary artery is a short trunk about 5 mm long and nearly as wide. It terminates in the circumflex and paraconal interventricular branches. The circumflex branch lies in the coronary groove as it extends to the left. On approaching the dorsal interventricular groove, it turns toward the apex of the heart and is known as the subsinuosal interventricular branch. The combined length of the circumflex and subsinuosal branches is approximately 8 cm in the dog. The paraconal interventricular branch is approximately 1.5 mm wide and 7 cm long. It winds obliquely and distally from left to right across the sternocostal surface of the heart in the paraconal interventricular groove.

Postoperative Care and Assessment

Postoperative pain should be treated with systemic opioids and local anesthetic techniques (see Box 31-2 on p. 992 for post-thoracotomy analgesia). Animals should be monitored for pulmonary edema after surgery. If pulmonary edema occurs, it should be treated with furosemide (see Box 28-1). Left ventricular failure should be treated as outlined in the “Medical Management” section.


MVD is a common cardiac condition, but most dogs remain asymptomatic during their lifetime. For dogs with progressive disease and heart failure, prognosis is related to cardiac size and severity of MR, type of pharmacologic and adjunctive therapy, cardiac cachexia, complications, and other concomitant disease (Borgarelli et al, 2008).

Mitral valve replacement with a mechanical valve prosthesis was shown to have a median survival after surgery of 4.5 months (Orton et al, 2005). Although most dogs survived the surgery, a high incidence of prosthetic valve thrombosis was reported. Experimental studies with the current generation of bioprosthetic valves show improved antithrombogenicity, but further investigation is warranted (Takashima et al, 2008). Mitral valve repair (e.g., circumferential annuloplasty, placement of artificial chordae, chordal fenestration, papillary muscle splitting, edge-to-edge repair) successfully resolved signs of CHF in 75% of dogs that survived surgery, for a median period of 1 year (range, 4 months to 3 years) after surgery (Griffiths et al, 2004).


Atkins, C, Bonagura, J, Ettinger, S, et al. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med. 2009;23:1142.

Atkins, CE, Keene, BW, Brown, WA, et al. Results of the veterinary enalapril trial to prove reduction in onset of heart failure in dogs chronically treated with enalapril alone for compensated, naturally occurring mitral valve insufficiency. J Am Vet Med Assoc. 2007;231:1061.

Borgarelli, M, Savarino, P, Crosara, S, et al. Survival characteristics and prognostic variables of dogs with mitral regurgitation attributable to myxomatous valve disease. J Vet Intern Med. 2008;22:120.

Griffiths, LG, Orton, EC, Boon, JA. Evaluation of techniques and outcomes of mitral valve repair in dogs. J Am Vet Med Assoc. 2004;15:224.

Ljungvall, I, Ahlstrom, C, Höglund, K, et al. Use of signal analysis of heart sounds and murmurs to assess severity of mitral valve regurgitation attributable to myxomatous mitral valve disease in dogs. Am J Vet Res. 2009;70:604.

Marcondes-Santos, M, Tarasoutchi, F, Mansur, AP, Strunz, CM. Effects of carvedilol treatment in dogs with chronic mitral valvular disease. J Vet Intern Med. 2007;21:996.

Orton, EC, Hackett, TB, Mama, K, et al. Technique and outcome of mitral valve replacement in dogs. J Am Vet Med Assoc. 2005;226:1508.

Ouellet, M, Bélanger, MC, Difruscia, R, et al. Effect of pimobendan on echocardiographic values in dogs with asymptomatic mitral valve disease. J Vet Intern Med. 2009;23:258.

Pouchelon, JL, Jamet, N, Gouni, V, et al. Effect of benazepril on survival and cardiac events in dogs with asymptomatic mitral valve disease: a retrospective study of 141 cases. J Vet Intern Med. 2008;22:905.

Takashima, K, Soda, A, Tanaka, R, et al. Long-term clinical evaluation of mitral valve replacement with porcine bioprosthetic valves in dogs. J Vet Med Sci. 2008;70:279.

Patent Ductus Arteriosus

General Considerations and Clinically Relevant Pathophysiology

PDA is one of the most common congenital heart defects of dogs; it occurs infrequently in cats. PDA typically causes a left-to-right shunt that results in volume overload of the left ventricle and produces left ventricular dilation. Progressive left ventricular dilation distends the mitral valve annulus, causing secondary regurgitation and additional ventricular overload. This severe volume overload leads to left-sided CHF and pulmonary edema, usually within the first year of life. Atrial fibrillation may occur as a late sequela because of notable left atrial dilation.

Rarely, dogs with PDA develop suprasystemic pulmonary hypertension that reverses the direction of flow through the shunt, causing severe hypoxemia and cyanosis (Eisenmenger’s physiology). Right-to-left PDA can occur as a late sequela (6 months) to untreated PDA. When right-to-left PDA is noted in very young animals, it may be due to persistent pulmonary hypertension after birth. Reversal of right-to-left PDA lessens the risk for developing progressive left-sided heart failure but causes severe debilitating systemic hypoxemia, exercise intolerance, and progressive polycythemia.


Physical Examination Findings

The most prominent physical finding associated with PDA is a characteristic continuous (machinery) murmur heard best at the high left heart base or left axillary region. The left apical cardiac impulse is prominent and is displaced caudally, and a palpable cardiac “thrill” often is present. Femoral pulses are strong or hyperkinetic (water hammer pulse) owing to a wide pulse pressure caused by diastolic runoff of blood through the ductus. Tall R waves (>2.5 mV in lead II) or wide P waves on a lead II electrocardiogram are supportive of the diagnosis, but they are not always present. Atrial fibrillation or ventricular ectopy may occur in advanced cases.

Physical examination findings in animals with right-to-left or reverse PDA differ from findings in those with left-to-right shunts. “Differential” cyanosis is typically present (i.e., cyanosis is most apparent in the caudal mucous membranes), but cyanosis may also be noted in the cranial half of the body in some animals. Cyanosis occurs because a mixture of nonoxygenated blood (from the pulmonary artery) with oxygenated aortic blood is present. Femoral pulses are normal. A systolic cardiac murmur, rather than a machinery murmur, is often present. However, a murmur may not be auscultated if polycythemia is present, if left- and right-sided pressures are nearly equal, and if shunting of blood through the ductus is minimal.

Diagnostic Imaging

Thoracic radiographs typically show left atrial and ventricular enlargement, pulmonary vasculature overcirculation, and characteristic dilation of the descending aorta and sometimes the main pulmonary artery on the dorsoventral view. With right-to-left PDA, thoracic radiographs show evidence of biventricular enlargement, notable dilation of the main pulmonary artery segment, and enlargement and tortuosity of lobar pulmonary arteries. Nuclear scintigraphy can be used to quantitate left-to-right shunts and to diagnose right-to-left shunts.


Echocardiography provides information that further confirms PDA and helps exclude concurrent cardiac defects, but it is not invariably required to establish the diagnosis. Echocardiographic findings that support a diagnosis of PDA include left atrial enlargement, left ventricular dilation, pulmonary artery dilation, increased transaortic and transmitral flow velocities, and a characteristic reverse turbulent Doppler flow pattern in the pulmonary artery. Echocardiographic features of right-to-left PDA typically include right ventricular dilation and thickening, dilation of the main pulmonary artery, and flattening of the interventricular septum. A right-to-left PDA can be documented by performing a saline microbubble contrast echocardiogram. Observing microbubbles in the descending aorta, but not in any left-sided cardiac chamber, is diagnostic.


Angiographic studies determine the ductal morphology and the minimal ductal diameter (MDD) of the PDA (Box 28-5). This information is helpful for predicting procedural feasibility with intravascular coils or ductal occluders.

Differential Diagnosis

The characteristic physical examination findings (i.e., continuous murmur and bounding arterial pulses) make diagnosis of PDA straightforward in most affected animals. Rarely, a combination of aortic stenosis and/or aortic insufficiency (see p. 879), or VSD and/or aortic insufficiency (see p. 882), causes a to-and-fro murmur that may be difficult to differentiate from continuous PDA murmurs. In animals in which the diastolic component of the PDA murmur is difficult to detect, other differentials would include subaortic stenosis, pulmonic stenosis (PS), atrial septal defect (ASD), and VSD. Differentials for dogs with right-to-left PDA include tetralogy of Fallot, right-to-left shunting, ASD or VSD, and other rare complex forms of cyanotic heart disease.

Medical Management

Animals with pulmonary edema should be given furosemide (see Box 28-1) for 24 to 48 hours before surgery. If atrial fibrillation is present, the ventricular response rate should be controlled with a β-adrenergic blocker or a calcium channel blocker (with or without digoxin) or amiodarone before surgery. If hemodynamically significant arrhythmias are present, they must also be controlled. Complete resolution of clinical signs of CHF may be difficult or impossible with medical management alone. Long-term medical management of dogs with right-to-left PDA has been described in only a small number of dogs using phlebotomy or hydroxyurea.

Surgical Treatment

Intravascular coils, vascular plugs, and duct occluders are now used routinely for closure of patent ductus arteriosus (Fig. 28-7). These techniques have the advantage of not requiring a thoracotomy and have less risk for major complications; however, mortality rates are comparable between transcatheter arterial occlusion and surgical ligation. Transversus coil embolization has been reported in dogs weighing fewer than 3 kg (Henrich et al, 2011). Ductal occlusion is most commonly performed from access through the femoral artery, although recently coil embolization through the carotid artery has been described, as has a transvenous approach through the femoral vein (Blossom et al, 2010; Miller and Thomas, 2009). The coil(s) or occluders are placed in the ductus under fluoroscopic guidance, and complete occlusion is verified by injection of contrast agent into the aorta (Fig. 28-8).

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Sep 11, 2016 | Posted by in SMALL ANIMAL | Comments Off on Surgery of the Cardiovascular System

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