Ancillary Procedures

Electrocardiography

The electrocardiogram (ECG) is essential for definitive categorization of arrhythmias in cattle. Vector analysis of ECG tracings to determine cardiac chamber enlargements and other pathology seldom is used in cattle because ventricular myocardial depolarization tends to be rapid and diffuse rather than organized, as in some other species. ECG is also indicated when cattle have variation in heart sound intensity, require monitoring for anesthesia or treatment of cardiac arrhythmias, or show signs of heart failure. Cardiac ultrasound, however, has superseded the ECG as a diagnostic tool in determining chamber enlargement and other cardiac pathology.

The base-apex lead system is most commonly used in cattle. The base-apex lead system results in an ECG with large wave amplitude and is sufficient for evaluating most arrhythmias. The positive electrode is placed on the skin over the left fifth intercostal space at the level of the elbow; the negative electrode is placed on the skin over the right jugular furrow roughly 30 cm from the thoracic inlet; and the ground electrode is attached to the neck or withers. The resultant ECG recorded through the base-apex lead system has a positive P wave with a single peak, a QRS complex with an initial positive deflection followed by a large negative deflection, and a variable (positive or negative) T wave (Figure 3-3, A to C).

Figure 3-3 A, Normal sinus rhythm with a heart rate of 60 beats/min recorded from a 4-year-old Holstein cow. B, Sinus bradycardia with heart rate of 36 beats/min recorded from a 6-year-old Brown Swiss cow sick with abomasal ulcers. C, Sinus tachycardia with heart rate of 108 beats/min recorded from a 2-year-old Holstein with an acute leg injury.

Echocardiography

Two-dimensional echocardiography and Doppler echocardiography have greatly enhanced our ability to assess cardiac function and visualize anatomic variations and pathologic lesions in cattle. Valvular, myocardial, pericardial, congenital, and acquired lesions can be visualized in real time, measured, and monitored. Qualitative and quantitative assessment of the impact of congenital anomalies and monitoring treatment response of endocarditis, pericarditis, or other myocardial lesions are possible with the appropriate equipment and people trained to conduct and interpret a systematic cardiac examination. In short, echocardiography is now an essential component of a cardiology workup. Sector scanners utilizing a 3.5-mHz (or lower) transducer are most useful for adult cattle. A 5.0-mHz transducer may be helpful when evaluating neonatal calves suspected of having congenital anomalies or other cardiac conditions. Although some clinicians may lack the equipment or expertise with echocardiography, current graduates are being trained in the technique, and continued competition among manufacturers may allow more veterinarians to own this equipment. In any event, referral for echocardiography is indicated for valuable cattle whenever cardiac disease is apparent but a specific diagnosis is lacking. In most cattle, a systematic examination can be conducted from the right parasternal window to provide a long axis four-chamber view of the heart, a long axis view of the left ventricular outflow tract, and a short axis view of the left ventricle just ventral to the mitral valve and at the papillary muscle level. From the same window, all four heart valves can be visualized, chamber sizes can be measured, myocardial functional measurements can be made, and abnormalities of the pericardium can be seen. Congenital lesions like ventricular septal defect (VSD) (Figure 3-4) and acquired pericarditis (Figure 3-5) are easily visualized by echocardiogram.

Figure 3-4 Echocardiogram of heifer calf with congenital ventricular septal defect.

Figure 3-5 Echocardiogram of adult dairy cow with traumatic reticulopericarditis.

White Muscle Disease

Myocardial damage from vitamin E and selenium deficiency may occur at any site in the heart and may be focal, multifocal, or diffuse (Figure 3-6). Signs may develop at any time from birth to 4 years of age but are more common in calves less than 3 months of age. Specific cardiac signs are variable and include arrhythmias, murmurs, exercise intolerance, cyanosis, dyspnea, congestive heart failure signs, and acute death. Signs may be subtle or dramatic, depending on the magnitude and locations of myocardial damage. Sudden death can occur spontaneously or following exercise or restraint. Other signs of white muscle disease such as stiffness, difficulty in prehension or swallowing, inhalation pneumonia, and myoglobinuria may or may not be present. Dyspnea may be directly related to the cardiac lesions or may be caused by Zenker’s degeneration in the diaphragm or intercostal muscles. Tachycardia (.120 beats/min) and arrhythmias are the most common specific cardiac signs, but murmurs may be present as well.

Figure 3-6 A pale focal area of Zenker’s degeneration of myocardium from a calf that died of diffuse white muscle disease.

Diagnosis can be confirmed by measuring blood selenium values, urine dipstick testing to look for positive “blood” (myoglobin) and protein, and serum biochemistry to evaluate creatine kinase (CK) and aspartate aminotransferase (AST) enzymes. If the heart is the only muscle involved, serum enzymes may not be greatly elevated; however, the heart seldom is the only area involved.

Treatment should be instituted immediately with vitamin E and selenium injected at the manufacturer’s recommended dosage. Although some commercial preparations include label instructions that include IV use, it is suggested that vitamin E/selenium be given intramuscularly (IM) or subcutaneously to avoid the occasional life-threatening anaphylactic-type reaction seen with these products. The calf should be kept in a small box stall, straw bale enclosure, or hutch, so it can move about but not run freely, lest further muscle damage be precipitated. If pulmonary edema is present, furosemide (0.5 to 1.0 mg/kg) may be given once or twice daily. Concurrent aspiration pneumonia would require intense antibiotic therapy. Vitamin E and selenium injections are repeated at 72-hour intervals for three or four total treatments. Herd selenium status and preventive measures to address the problem should be discussed. Calves that survive for 3 days following diagnosis have a good prognosis.

Hyperkalemia

Cardiac arrhythmias or bradycardia associated with hyperkalemia is primarily observed in neonates having severely acute diarrhea. Enterotoxigenic E. coli causing secretory diarrhea, metabolic acidosis, low plasma bicarbonate values, and hyperkalemia appears to be the most common causative organism. Rotavirus or coronavirus also may be involved in calf diarrhea, but they seldom produce as profound a metabolic acidosis as E. coli.

Less common causes of hyperkalemia include severe diffuse white muscle disease involving heavy musculature of the limbs, ruptured bladders, renal failure, urinary obstructions, and nonspecific shock.

Hyperkalemia reduces the resting membrane potential, which initially makes cells more excitable, but gradually (with further elevation in potassium and further reduction in resting membrane potential) the cells become less excitable. Atrial myocytes seem more sensitive to these effects than those within the ventricles. Cardiac conduction is affected, and several characteristic ECG findings evolve in a typical sequence that correlates well with increasing K⁺ values: ECG changes include peaking of the T wave, shortening and widening of the P wave, prolongation of the PR interval, eventual disappearance of the P wave, widening of the QRS complex, and irregular R-R intervals (Figure 3-7). Atrial standstill characterized by bradycardia and absence of P waves may occur and has been documented in association with hyperkalemia in diarrheic calves. Further progression may lead to AV block, escape beats, ventricular fibrillation, asystole, and death.

Figure 3-7 Base-apex lead ECG recording in a calf with a K of 8.6 mEq/L; despite the tachycardia of 130 beats/min, the peaked T waves and flattening of the P waves is very apparent.

In neonates, hypoglycemia is the major differential diagnosis when bradycardia is present. Septic myocarditis or white muscle disease also may be considered if an arrhythmia is present.

Calves less than 2 weeks of age that have developed acute diarrhea, are recumbent, dehydrated, and have bradycardia or arrhythmia should be suspected of being hyperkalemic. Obviously only an acid-base and electrolyte analysis of blood and an ECG can confirm this. However, these may not be available in the field. The consequences of underestimating the life-threatening importance of the heart and K⁺ relationship in these patients are severe.

Calves suspected to be hyperkalemic based on history, physical signs, and arrhythmia or bradycardia should receive alkalinizing fluids and dextrose. Being neonates, hypoglycemia may contribute to bradycardia when this sign is present. One way to treat metabolic acidosis and hyperkalemia is by IV infusions of 5% dextrose solution containing 150 mEq NaHCO₃/L. Usually 1 to 3 L is necessary, depending on the magnitude of the metabolic acidosis and bicarbonate deficit. Glucose and bicarbonate help transport K⁺ back into cells, and the glucose also treats or prevents potential hypoglycemia. Once the acute crisis has been resolved, the calf may be safely treated with balanced electrolyte solutions containing potassium. Calves with diarrhea, despite having plasma hyperkalemia, have total body potassium deficits and require potassium supplementation. This may be true even in the acute phase of disease, but when serum K⁺ is 5.0 to 8.0 mEq/L there is no time to worry about a “total body potassium deficit.” We have treated hundreds of calves as suggested above, and those with a venous blood pH of 7.0 or greater have a good to excellent prognosis unless they have had failure of passive transfer of immunoglobulins and subsequent septicemia. Specific insulin therapy as an adjunct to bicarbonate and glucose to correct hyperkalemia is not necessary in calves.

Congenital Heart Disease

Virtually all types of congenital cardiac anomalies occur in cattle. Most congenital anomalies appear to be sporadic, but inheritance may play a part in some of the most common anomalies. The most common congenital anomalies in cattle appear to be VSDs (Figure 3-8), tetralogy of Fallot, atrial septal defects, and transpositions of great vessels.

Figure 3-8 Image obtained at necropsy of a calf with VSD.

Most congenital cardiac defects cause distinct murmurs. Calves affected with the most common defects such as VSDs, atrial septal defects, tetralogy of Fallot, or aortic or pulmonic stenosis usually have systolic murmurs. Patent ductus arteriosus, which is rare as a single defect in calves, can cause a systolic or continuous murmur.

Most calves with congenital cardiac defects appear normal at birth but eventually are noticed to have dyspnea, poor growth, or both. Many calves with congenital heart defects are eventually examined by a veterinarian because of persistent or recurrent respiratory signs or generalized ill thrift. The respiratory signs may be real in the form of pulmonary edema associated with heart failure and shunts or be caused by opportunistic bacterial pneumonia secondary to pulmonary edema and compromise of lower airway defense mechanisms. The owners may already have treated the calf one or more times for coughing, dyspnea, and fever, only to have the signs recur. Usually only one calf is affected, thus making enzootic pneumonia an unlikely diagnosis. Regardless of whether pulmonary edema or pneumonia plus pulmonary edema are present, veterinary examination usually detects the cardiac murmur that allows diagnosis. Venous pulsation and distention of the jugular veins may be present, but calves seldom show ventral edema as distinctly as adult cattle with heart failure.

Calves with congenital heart defects that do not develop respiratory signs usually show stunting compared with herdmates of matched age. The degree of stunting varies directly with the severity of the congenital lesions in regard to blood oxygenation but usually becomes apparent by 6 months of age and is very dramatic in calves that survive to yearlings. Some cattle with small defects survive and thrive as adults, but this is rare.

VSDs are the most common defects in dairy calves and are found in all breeds. In Guernseys and Holsteins, VSD may be linked to ocular and tail anomalies. Microphthalmos and tail defects, including absence of tail, wry tail, or short tail, frequently signal VSD (Figure 3-9). Sometimes ocular, tail, and cardiac defects all are present in the same calf, but it is more common to find tail or ocular pathology plus VSD. Depending on the size of the VSD, affected calves have a variable life span. Prognosis for most is hopeless because of eventual respiratory difficulty and stunting. However, calves do, in rare instances, survive to productive adult states. The genetics of these multiple defects (eye, tail, and heart) have not been investigated in Holsteins but have been assumed to be a simple recessive trait in Guernseys.

Figure 3-9 Congenital absence of the tail in a 1-day-old Holstein heifer that also had a VSD.

Tetralogy of Fallot and other multiple congenital defects that allow right to left shunting of blood provoke marked exercise intolerance, cyanosis, and dyspnea and may lead to polycythemia secondary to hypoxia. Prognosis for long-term survival is grave in these calves. Ectopia cordis in a calf creates a dramatic sight, with the heart beating under the skin in the neck, but is extremely rare.

Neoplasia

The heart is one of the common target sites of lymphosarcoma in adult dairy cattle. Many cattle with multicentric lymphosarcoma have cardiac infiltration based on gross or histologic pathology, but fewer of these cattle have clinically detectable cardiac disease. When the heart is a major target site, cardiac abnormalities are more obvious. The heart seldom is the only organ affected with lymphosarcoma. Therefore detection of cardiac abnormalities coupled with other suspicious lesions (e.g., enlarged peripheral lymph nodes, exophthalmos, melena, and paresis) simply helps to make a lymphosarcoma diagnosis more definite.

Depending on the anatomic location and magnitude of the tumors, cattle with cardiac lymphosarcoma may have arrhythmias, murmurs, jugular venous distention, jugular venous pulsations, or muffling caused by diffuse cardiac or pericardial involvement. Muffling and splashing sounds are possible if a pericardial transudate or exudate is present. The most common site of tumor involvement is the right atrium, but nodular or infiltrative tumors can be found anywhere in the myocardium or pericardium (Figure 3-10). The color and consistency of the tumors may vary. Mediastinal lymph nodes also are commonly involved. Cattle with signs of heart disease should be thoroughly examined for other lesions consistent with lymphosarcoma. When multiple lesions exist, the diagnosis is easy. However, cattle examined because of vague signs such as hypophagia and decreased milk production that are found to have tachycardia or other cardiac abnormalities can present diagnostic challenges. Although ECG and thoracic radiographs have seldom helped make a definitive diagnosis, ultrasound may be very helpful to image nodular or large masses of lymphosarcoma. Thoracocentesis and pericardiocentesis to obtain fluid for cytologic evaluation are the most helpful ancillary aids when cardiac lymphosarcoma is suspected. A complete blood count (CBC) and assessment of bovine leukemia virus (BLV) antibody status are indicated, but a positive BLV agar gel immunodiffusion (AGID) or radioimmunoassay (RIA) test does not ensure an absolute diagnosis because most positive cattle never develop tumors (see the section on Lymphosarcoma in Chapter 15). Therefore simply assuming a cow with a positive BLV test and heart abnormality detected on physical examination has lymphosarcoma may be an incorrect assumption. A double line-positive BLV-AGID may add further weight to the suspected diagnosis, as would the finding of a persistent lymphocytosis in a set of CBC results. Clinical identification of masses in other locations or cytology from thoracocentesis or pericardiocentesis provides the best means of definitive diagnosis.

Figure 3-10 Lymphosarcoma in the heart of a cow that died as a result of multicentric lymphosarcoma. Multifocal areas of yellow-red friable tumor infiltrate are present scattered over the epicardium, great vessels, and right atrium.

Fever usually is absent in cattle with cardiac lymphosarcoma. Occasional cattle with large tumor masses in the thorax or abdomen may have fever because of tumor necrosis or nonspecific pyrogens produced by neoplasms. Secondary bacterial infections of the lungs or other body systems also may lead to fever, which confuses the diagnosis.

Prognosis is hopeless for cattle with cardiac lymphosarcoma, and most cattle with the disease die from cardiac or multisystemic disease within a few weeks to a few months. Successful attempts at chemotherapy have not been reported to our knowledge. One author has successfully prolonged life up to 6 months in a few cattle with cardiac lymphosarcoma that had significant pericardial fluid accumulations by intermittent pericardial drainage. Occasionally valuable cattle may justify such treatment to allow a pregnancy to be completed or to be superovulated. However, as with many catabolic conditions, owners should be cautioned that maintaining the dam with advanced heart disease for more than a few weeks may produce a gestationally dysmature fetus even if the pregnancy is carried to term, or may seriously affect the cow’s ability to superovulate or even produce viable oocytes for in vitro fertilization. There is also the risk of vertical transmission of BLV from dam to fetus in utero, which is greater should the dam have clinically apparent tumors. In one late pregnant cow with severe pericardial effusion caused by lymphosarcoma, we were able to maintain the cow for several weeks by surgically opening the pericardial sac into the pleural cavity, which significantly improved venous return to the heart and the overall condition of the cow. The cow was also treated with isoflupredone.

Neurofibroma, although uncommon, frequently causes arrhythmia and variable intensity of heart sound in affected cattle and bulls. Further the cardiac arrhythmia may coexist with paresis or paralysis caused by neurofibroma masses in the spinal canal. Because lymphosarcoma more commonly causes paresis coupled with cardiac disease, this combination of signs is most suggestive that lymphosarcoma is present. Although perhaps a moot point because both diseases are fatal, further medical workup of neurofibroma patients fails to provide confirmation of lymphosarcoma. To date, postmortem examination has been the only means of definitive diagnosis for cardiac neurofibroma. Examiners talented in ultrasound may be able to diagnose these lesions based on the typically gnarled, raised cords of tumor involving the cardiac nerves.

Myocardial Disease

Endocarditis

Etiology

Bacterial endocarditis is the most common valvular disease or endocardial disease in adult dairy cattle. It also is one of the few treatable heart conditions of cattle. Therefore early suspicion, diagnosis, and appropriate treatment improve the prognosis.

Cattle with chronic infections such as septic musculoskeletal conditions, hardware disease, abscesses, lactic acid indigestion, chronic pneumonia, metritis or mastitis, and thrombophlebitis are at risk for bacterial endocarditis. In addition, cattle with long-term IV catheters have increased risk of endocardial infections. Bacteremia appears essential to the pathophysiology of bacterial endocarditis in cattle.

A. pyogenes is the most common organism isolated from the blood and endocardial lesions of cattle affected with endocarditis, but Streptococcus sp., Staphylococcus sp., and gram-negative organisms may also cause the disease. The right AV valve (tricuspid) is the most commonly infected valve with the left AV (mitral) being the second most common (Figure 3-11). Other valves or the endocardium adjacent to valves may also occasionally be the site of infection (Figure 3-12). Owner complaints regarding affected cattle include recurrent fever, weight loss, anorexia, poor production, and sometimes lameness.

Figure 3-11 Bacterial valvular endocarditis with vegetative lesions in a cow.

(Photo courtesy Dr. John M. King.)

Figure 3-12 Large vegetative endocarditis lesion involving the valves and adjacent endocardium in the ventricle.

(Photo courtesy Dr. John M. King.)

Diagnosis

Early signs of reduced appetite and production, fever, and tachycardia certainly are not specific for endocarditis. A pounding heart or systolic murmur should suggest the diagnosis and dictate further workup. Diagnosis may be overlooked because of more obvious primary problems such as abscesses, infected digit or other musculoskeletal infection, suspected hardware disease, or thrombophlebitis because these conditions may also cause fever and nonspecific signs of illness. Therefore heart murmurs, a pounding heart, or early signs of heart failure in addition to tachycardia merit consideration of a diagnosis of endocarditis. Lameness and stiffness may be difficult to differentiate from primary musculoskeletal disease or painful stance caused by peritonitis but can be important clinical signs that aid diagnosis. Because of fever, tachycardia, and sometimes polypnea, cattle having endocarditis often are misdiagnosed with pneumonia or traumatic reticuloperitonitis.

Diagnosis of endocarditis usually is based on the patient’s history and clinical signs. However, a positive blood culture and echocardiography allow definitive diagnosis. Blood cultures, as mentioned previously, may or may not be successful; however, when positive, they allow appropriate selection of antibiotics. Definitive diagnosis based on two-dimensional echocardiography has proven to be one of the most impressive uses of ultrasound since its widespread use in diagnostics began 10 years ago. Veterinarians trained in echocardiography now have a tool to confirm bacterial endocarditis in most patients (Figure 3-13).

Figure 3-13 Echocardiographic image of endocarditis of the tricuspid valve of a cow.

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