Heart

Chapter 48


Heart



Heart disease is common in cats but there are few feline cardiac conditions that are treated surgically. Of these, patent ductus arteriosus (PDA) and symptomatic, medically unresponsive bradycardias are the most frequent indications for performing cardiac surgery. Both conditions are rare in cats.


The commonest cardiac surgical procedure performed in cats is subtotal pericardectomy; the commonest indication for performing this procedure is chylothorax, which has a number of potential underlying causes, only one of which is cardiac disease.


The basic requirements for anesthesia and postoperative care for cats undergoing cardiac surgeries, and many of the potential postoperative complications are as for patients undergoing sternotomy or thoracotomy for other reasons. Specific postoperative requirements will depend on the underlying disease and the patient’s clinical status. In this chapter the most commonly performed surgical cardiac procedures are discussed.



Surgical anatomy


There is little variability in normal thoracic conformation and heart shape between cat breeds. The normal feline heart is slender in appearance on a lateral thoracic radiograph and it appears more horizontal in its orientation within the thorax than in the dog; with increasing age this can become more marked.1 The heart lies within the mediastinum in the mid thorax, approximately between the 3rd and 6th intercostal spaces.


The right atrium and ventricle form the craniodorsal part of the heart. The right atrium receives blood from the cranial and caudal vena cavae, and from the coronary vessels via the coronary sinus. The right atrial appendage arises from the cranial aspect of the right atrium and extends ventrally. The right ventricle is arciform in cross section; it lies cranial and ventral to the left ventricle. Blood is ejected from the right ventricle through the pulmonic valve into the pulmonary trunk. The initial part of the pulmonary trunk is within the pericardium, the ventral, lateral and caudal surfaces are covered by serous pericardium, and this portion of the pulmonary trunk is usually masked by fat. The pulmonary trunk contacts the aorta along its entire medial surface. The pulmonary trunk divides into the right and left pulmonary arteries. The fibrous pericardium attaches to the distal fourth of the pulmonary trunk and the terminal portion of the pulmonary trunk can be examined without opening the pericardium.


The left atrium and ventricle form the caudodorsal part of the heart. The left atrium forms the left dorsocaudal part of the base of the heart. The left atrial appendage is a cranial extension of the left atrium. It is located caudal to the pulmonary trunk and lies along the right atrial appendage, caudal to and separated from it by the pulmonary trunk. Blood enters the left atrium from the pulmonary veins, which open into its dorsal aspect; the individual pulmonary veins may fuse but usually remain separate and enter the left atrium separately. The left ventricle is cone shaped and its apex forms the apex of the heart. Blood is ejected from the left ventricle through the aortic valve into the aorta, near the center of the heart base. The initial part of the aorta, the ascending portion, is mainly located within the pericardium. It continues for a short distance cranially before passing dorsocaudally and to the left by forming a U-bend, the aortic arch. Two great vessels leave the aortic arch to supply the head, neck, and thoracic limbs: the brachiocephalic trunk and the left subclavian artery. The ligamentum arteriosum, the connective tissue remnant of the fetal ductus arteriosus, arises near the bifurcation of the pulmonary trunk and passes to the aorta. The aorta then continues caudally as the descending aorta.


The right and left vagus nerves pass caudally in the dorsal mediastinal pleura. The left vagus nerve passes over the ligamentum arteriosum, and is a landmark used during the surgical treatment of PDA. The left recurrent laryngeal nerve leaves the left vagus nerve just cranial to the ductus and it passes around the caudal aspect of the ductus.


The pericardium forms a double layered sac that surrounds the heart, the initial portion of the ascending aorta, pulmonary trunk, termination of the vena cavae, and the pulmonary veins. It attaches near/at the base of the heart to the aortic arch, pulmonary trunk, left atrium at the level of the pulmonary veins and dorsal to the interatrial groove on the right side. The outer fibrous layer is termed the parietal pericardium, the inner serous membrane the visceral pericardium, which is adherent to the epicardium. At its apex the pericardium is continued as a flattened band, the caudoventral mediastinal reflection, which attaches to the ventral part of the muscular insertion of the diaphragm. The right and left phrenic nerves run across the dorsal third of the pericardium and must be identified and preserved during pericardectomy. Paired pericardiophrenic blood vessels from the internal thoracic arteries run with the phrenic nerves. Pericardial blood vessels, also arising from the internal thoracic arteries, run within the pericardium passing in a caudoventral direction. With pericardial disease or pericardial and/or pleural effusion the pericardium can become thickened and these vessels will become more prominent.



General considerations


Specific investigations will depend on the patient’s history, clinical signs, findings on clinical examination, and differential diagnoses but will usually include a minimum of hematology, serum biochemistry, and thoracic radiography. Specific blood tests to assess for infections such as feline coronavirus, leukemia, and immunodeficiency viruses may be indicated. For investigation of suspected cardiac disease electrocardiography (ECG), echocardiography and, uncommonly, angiography are indicated. Pleural and/or pericardial effusions should be sampled for biochemistry, cytology, and bacterial and/or fungal culture as appropriate. Blood coagulation screen should be performed if a hemorrhagic effusion is identified. Advanced imaging of the thorax using computed tomography may be appropriate in cases (e.g., chylothorax or other pleural effusions) where intrathoracic neoplasia is a differential diagnosis.



Surgical diseases



Patent ductus arteriosus


The ductus arteriosus carries blood from the pulmonary artery to the aorta in the fetus. Within hours of the birth the ductus normally closes in response to an increase in the oxygen tension of the blood; failure of closure allows continual shunting of blood between the left and right sides of the heart. After birth, the blood pressure in the pulmonary artery reduces and the systemic blood pressure increases. Typically this pressure differential is such that blood shunts continuously through the cardiac cycle, from the higher pressure aorta to the lower pressure pulmonary artery (i.e., left to right shunting) if the ductus remains patent. The secondary changes that occur with increased blood flowing in the pulmonary artery are pulmonary over-circulation, left atrial dilatation, left ventricular dilatation with eccentric hypertrophy, dilatation of the aortic arch to the level of the origin of the PDA, and dilatation of the pulmonary trunk. As a consequence of the left to right shunting and left-sided volume overload, left-sided congestive heart failure (CHF) commonly develops. The size of the shunt will determine volume of blood shunting, which in turn determines the onset and severity of secondary consequences. As a sequel to the increased blood flow in the pulmonary vessels, resistance to blood flow and pulmonary hypertension can develop. If the pulmonary arterial pressure is greater than the aortic pressure for some or all of the cardiac cycle, blood flow through the PDA will reverse. Blood will then flow from the pulmonary artery into the aorta (i.e., right to left shunting). Right to left shunting can also occur from birth, and usually occurs when the ductus is large and tubular without narrowing at the pulmonary ostium, and this may reflect retention of fetal pulmonary vasculature. Right to left shunting, termed Eisenmenger’s physiology, is rarely reported in cats,2,3 although it is suggested that it is more likely to develop over time in cats than dogs.4 Surgical treatment of the PDA is contraindicated in patients with right to left shunting.


PDA is a rarely diagnosed congenital heart disease in the cat, with few cases of this condition reported in the English language veterinary literature so it is difficult to make conclusions about the presentation, investigative findings, and the outcome with medical or surgical treatment. This contrasts with dogs, where PDA is one of the more commonly diagnosed congenital heart diseases5,6 and it is well documented.


Most dogs are diagnosed as puppies, whilst the condition is asymptomatic, by auscultation of a pathognomic continuous murmur. It is suggested that the situation may be similar in cats, and certainly the majority of cats reported with PDAs are less than one year of age. However, in an abstract reporting 21 cases of PDAs in cats approximately two-thirds had a continuous murmur but the remainder were described to have systolic murmurs and approximately only one-third of the cats in the study were asymptomatic at presentation. Their presenting complaints included abnormal respiration, exercise intolerance/lethargy, stunted growth, and poor weight gain.7


The murmur is well described in dogs; it may be accompanied by a thrill felt at the heart base, and by hyperkinetic pulses. The point of maximal intensity of the murmur lies over the main pulmonary artery at the dorsocranial heart base and may radiate cranially to the thoracic inlet and to the right heart base. It is suggested that in cats the continuous murmur of a PDA may be best heard slightly more ventrally than this typical location in dogs. Femoral pulses may be more difficult to assess in cats;8 hyperkinetic pulses may be noted.



Diagnosis


Thoracic radiographic changes are variable and will depend on the size of the PDA and any consequential left-sided heart failure. Cardiomegaly, shifting of the cardiac apex to the left, a ductus aneurysmal bump, and pulmonary over-circulation are all common radiographic findings. If the patient presents in left-sided heart failure, pulmonary venous congestion and pulmonary edema will be present.


Diagnosis is usually confirmed with echocardiography using a right parasternal short axis or left parasternal cranial window (Fig. 48-1). Initially, there may be no changes in chamber size or myocardial contractility but eventually the consequences of left to right shunting may result in dilatation of the left atrium, aorta, and main pulmonary artery and dilatation and hypertrophy of the left ventricle, all recognizable on echocardiography (Fig. 48-2). Left ventricular systolic function may become impaired. If a left-to-right shunting PDA is identified, Doppler studies can be performed and will show characteristic high velocity turbulent flow from the aorta, through the ductus and into the main pulmonary artery (Fig. 48-3). This PDA peak velocity will decrease if pulmonary pressures increase, prior to exceeding systemic pressures. However, note that this decrease may be reactive pulmonary hypertension as a consequence of the pulmonary over-circulation and closure of the PDA may resolve the mild pulmonary hypertension when assessed after surgery. Mild increase of velocity in the left ventricular outflow tract and mild aortic and pulmonic insufficiency may also be recognized. Mitral regurgitation is secondary to the left-sided dilation and may be significant.





Thorough echocardiography should be performed in cats because concurrent, but unspecified, congenital heart defects may be present; these were found in 29% of cats in one study.7


If the diagnosis of suspected PDA cannot be confirmed by echocardiography, or the presence of other congenital heart anomalies is suspected, cardiac catheterization and angiocardiography may be helpful, but this investigative procedure is rarely required to confirm diagnosis of PDA.


ECG is non-specific; it usually shows tall R waves and wide P waves due to atrial enlargement. Arrhythmias such as atrial fibrillation, supraventricular or ventricular arrhythmias, and ventricular premature complexes may be present.




Pericardial disease


Congenital pericardial diseases are infrequently diagnosed and most have an excellent prognosis with surgical treatment. The most common condition in dogs and cats is peritoneopericardial diaphragmatic hernia (PPDH);9 it is more common in cats (see Chapter 45).



Intrapericardial cysts


Intrapericardial ‘cysts’ are rarely reported.10–14 These are usually not true cysts but encapsulated adipose tissue or organizing cystic hematomas. The cyst may be attached to the apex of the pericardium by a pedicle. They may arise if a PPDH containing herniated omentum or falciform fat closes before birth, trapping the fat within the pericardial sac. Cystic changes of herniated and incarcerated liver tissue may also occur in association with PPDH in cats. Intrapericardial cysts cause clinical signs either directly associated with their presence, or due to an associated effusion causing cardiac tamponade. Diagnosis can usually be made by radiography (Fig. 48-4) and/or ultrasound examination of the cranial abdomen and heart. Treatment is by subtotal pericardectomy (see Box 48-4), removal of the cyst (and pedicle if present), and repair of the PPDH (Chapter 45, 45.4.3) if present.



Congenital pericardial defects are very rare. Clinical signs may develop if the size of the defect is such that a portion of the heart can herniate through the defect, as cardiac function will then be compromised. This condition is treated by subtotal pericardectomy.



Pericardial effusion


The commonest acquired pericardial disease in both cats and dogs is pericardial effusion (PE), but the incidence, presentation and underlying causes have differences between these species. Clinically significant PE is very uncommon in cats, and this species rarely presents with cardiac tamponade. In both species PEs remain asymptomatic if the effusion is small and the pericardium remains slightly compliant, or if a larger effusion accumulates slowly allowing the pericardial sac to accommodate to some extent. Cardiac tamponade results when the amount of fluid (or cyst/mass) reaches a volume such that it exerts a pressure equal to or greater than normal cardiac diastolic pressures. The heart is compressed externally and cannot fill effectively during diastole. Right ventricular filling is reduced first, and may progress to compromise left ventricular filling and cardiac output. Systemic venous pressure and capillary hydrostatic pressure increase whilst cardiac output is reduced. Cats with cardiac tamponade usually develop pleural effusion and present with tachypnea and increased respiratory effort.


PE in cats is most commonly part of a more generalized disease (Box 48-1). Myocardial disease is the commonest underlying cause.15 Small volume clinically insignificant PEs have been reported in approximately 45% of cats with CHF,16,17 while PEs are rarely reported in dogs with CHF. The other most frequent underlying cause of PE in cats is feline infectious peritonitis. The commonest causes of PE in dogs are idiopathic hemorrhagic pericardial effusion (IPHE), which is unreported in the cat, and cardiac-related neoplasia. In dogs, hemangiosarcoma, usually of the right side of the heart, is the most common neoplastic cause of PE, aortic body tumors also occur with some frequency, mesotheliomas occur less commonly, and other tumors are also reported. These tumors are rarely diagnosed as a cause of PE in cats; lymphoma is the most common underlying tumor associated with the effusion.



The classic radiographic appearance of PE is general cardiomegaly (globoid heart) and sharp borders to the cardiac silhouette (Fig. 48-5). If the PE has accumulated rapidly without time for adaptation, cardiac tamponade may occur without the classic radiographic signs being present. Pleural effusion is usually present in cats with significant PE and may partly obscure the cardiac silhouette.



A definitive diagnosis of PE is made by echocardiography, which allows cardiac disease or mass lesions to be excluded. The pericardial fluid is seen as an anechoic/slightly anechoic circular region surrounding the heart, within the thin hyperechoic line representing the pericardium. Although an uncommon cause of PE in cats, mass lesions affecting the heart may be seen on ultrasound examination. A thorough examination of the heart should be performed prior to pericardiocentesis because masses are most likely to be identified whilst surrounded by fluid (Fig. 48-6).


Sep 6, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Heart
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