Disorders of the cardiovascular system



Disorders of the cardiovascular system



Part 1: The heart and blood vessels


Developmental disorders


Serious and/or complicated congenital defects of the circulation such as cardiac ectopia usually result in intrauterine death but some cardiac and vascular anomalies may only become evident after birth, and sometimes much later when the animal starts to work. Defects of structure in the heart usually arise within the first 50 days of gestation, when the rate of development of the heart is maximal.



Persistent neonatal pulmonary hypertension


If the ‘normal’ anatomical and physiological transitions from fetal to neonatal circulation do not occur, a condition of persistent pulmonary hypertension can arise. This has also been known as ‘persistent fetal circulation’.


This condition results in systemic arterial hypoxemia due to increased pulmonary vascular resistance and shunting of pulmonary blood to the systemic circulation. Failure of the pulmonary vascular resistance to lessen post partum despite alveolar expansion and alveolar oxygenation encourages continued variable shunting of blood through the ductus arteriosus and/or foramen ovale with resultant systemic arterial hypoxemia.


A progressive cyanosis is the most prominent clinical feature of this condition with stunting, poor (or extremely poor) exercise tolerance and a secondary polycythemia.





Patent ductus arteriosus (PDA) (Fig. 4.1)


The ductus arteriosus in the fetus normally shunts blood from the pulmonary artery to the aorta. It is regarded as physiologically normal for a foal to maintain some shunting of blood in the opposite direction (i.e. from aorta to pulmonary artery) for up to 72 hours after birth. A large persistent PDA typically results in enlargement of the left atrium and ventricle. Over time, if the pulmonary arterial pressure rises substantially, right-sided congestive heart insufficiency/failure may ensue.


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Figure 4.1 Schematic representation of a PDA. Reproduced from McAuliffe SB, Slovis NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.

The murmur is typically described as a loud, continuous (‘machinery’) murmur, accompanied by a detectable thrill which is most obvious over the left side at the base of the heart, or slightly above this point. However, by the time many of these foals present the continuous murmur may be absent and replaced by a systolic murmur. This is due to pulmonary hypertension which restricts the flow within the ductus during diastole.


Clinically, foals with persistent large bore PDAs may have increased peripheral pulse pressure. This increase in pulse pressure is often described as ‘bounding’ due to the left ventricular increased stroke volume +/− related systolic hypertension and decreased diastolic pressure from the aortic blood pushing into the pulmonary circulation via the PDA. The foal may grow reasonably, but most cases show considerable exercise intolerance and are often noted to be reluctant to play with other foals and lag behind the dam.




Ventricular septal defect (VSD) (Figs. 4.2–4.5)


Reportedly this is the most frequently occurring congenital cardiac defect in large animals. Foals with VSDs often have readily auscultable murmurs on both sides of the thorax. The majority are situated in the membranous portion of the septum in the left ventricular outflow tract immediately below the right coronary cusp of the aortic valve and the tricuspid valve. Most VSDs are not clinically significant and many are found as incidental findings. In those which are clinically significant there may be a history of lagging behind the dam or disinclination to play with other foals. Young foals with septal defects of clinical significance often show a characteristic exhaustion when suckling and sometimes collapse (faint) during feeding or after only slight exercise. A persistent dyspnea and weakness with an inability or disinclination to stand for reasonable periods of time are often noted.


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Figure 4.2 Schematic representation of a ventricular septal defect (VSD). Reproduced from McAuliffe SB, Slovis NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.

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Figure 4.3 VSD muscular. Welsh section A pony 2-year-old at presentation, lethargy and poor exercise tolerance. A VSD was diagnosed on ultrasound; no treatment was given, and there was no follow up.

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Figure 4.4 PM of VSD (VSD membranous). Post-mortem examination of a restrictive ventricular septal defect viewed from the left side, in a horse subjected to euthanasia for a non-responsive periocular tumor. The VSD measured approximately 1 cm in diameter in the perimembranous region of the ventricular septum immediately cranial to the septal leaflet of the tricuspid valve and adjacent to the right coronary leaflet aortic valve. Ante-mortem the VSD was associated with a grade 4/6 pansystolic murmur over the right heart apex and a grade 2/6 holosystolic murmur over the left heart base. The size of the VSD and velocity of shunt blood across the defect as detected by spectral Doppler ante-mortem (>5 m/s) supported the characterization of the defect as a restrictive VSD.

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Figure 4.5 Echogram of subaortic VSD. Right parasternal long-axis echocardiogram optimized for the left ventricular outflow tract from a 10-year-old Welsh Mountain pony gelding without exercise intolerance. A paramembranous VSD is present, adjacent to the right coronary cusp of the aorta and the septal leaflet of the tricuspid valve. The small size (<0.25 of the aorta diameter) of the defect and the high peak shunt velocity across the defect (> 4.8 m/s) are consistent with a restrictive VSD that is not hemodynamically important.



Diagnosis



• VSDs are usually associated with at least two murmurs. The shunt causes an obvious, loud, pansystolic murmur in the area of the aortic and tricuspid valves. The persistent, undulating, ‘machinery type’ murmur has a marked precordial vibration (thrill) which radiates widely and is audible on both sides of the chest, but is usually significantly louder on the right. The thrill can often be appreciated merely by palpation of the lower right thoracic wall. This murmur usually becomes more prominent with exercise and rising blood pressure. There is also frequently a second murmur associated with relative pulmonic stenosis. Although the right ventricular tract is normal there is an increased volume of blood leaving the right ventricle which results in a loud holosystolic crescendo–decrescendo murmur over the pulmonic valve in the left third intercostal space. This murmur is usually at least one grade lower than the VSD murmur.


• Peripheral signs of circulatory status and electrocardiographs are usually normal.


• Ultrasound studies including Doppler are the best diagnostic tools as they not only determine the presence and size of the defect and the shunt velocity but can also be helpful to assess the hemodynamic burden.


• Major septal defects, which shunt significant volumes of blood into the relatively lower-pressured right side, result in gross right-sided enlargement and this may be detected on percussion or, more precisely, by radiographic and ultrasonographic examination of the chest.



Treatment and prognosis



• Membranous defects that are smaller than 25 mm and demonstrate a shunt velocity of greater than 4 m/s may be exercise-tolerant.


• In smaller breeds of horses and ponies it is also useful to compare the size of the VSD with the diameter of the aortic root. Those which are less than one third of the aortic root carry a better prognosis.


• Muscular ventricular septal defects, defects with aortic insufficiency, or other anomalies are likely to be intolerant of strenuous exercise.


• Foals with membranous VSD larger than 35 mm in diameter or muscular VSDs tend to have decreased life expectancy. VSD may also be a component of complex cardiac anomalies carrying a poor prognosis.


• Treatment of significant defects is generally impractical and owners should be advised against using the horse for athletic purposes or breeding.



Atrial septal defect (ASD) (Fig. 4.6)


Atrial septal defects are uncommon in the equine neonate. Most are a component of complex congenital cardiac anomalies.


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Figure 4.6 Schematic representation of an atrial septal defect (ASD). Reproduced from McAuliffe SB, Slovis NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.

Three types of ASD are most described: ostium primum, ostium secundum and sinus venosus; however, a fourth, ‘unroofed coronary sinus’ which is a coronary sinus septal defect occurs less commonly.




Tetralogy of Fallot (Figs. 4.7 & 4.8)


Pulmonary valve stenosis, ventricular septal defect, overriding aorta and right ventricular hypertrophy make up this complex cardiac defect. If a patent ductus arteriosus also is present, then pentalogy of Fallot is present. Right-to-left shunting results in cyanosis and lethargy.


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Figure 4.7 Schematic representation of tetralogy of Fallot. Reproduced from McAuliffe SB, Slovis NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.

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Figure 4.8 Echocardiogram demonstrating an overriding aorta as part of tetralogy of Fallot.

Many of the affected foals are born dead or die shortly after birth, having shown marked respiratory distress, polypnea and cyanosis. The foals may appear to faint spontaneously and collapse at the slightest exertion. Exercise intolerance, difficulty nursing and dyspnea are frequently encountered. Frequently foals are presented for suspected respiratory disease and when questioned the owners frequently reveal a history consist with congenital cardiac abnormality.





Great vessel transposition (Fig. 4.9)


This condition consists of the aorta exiting the right ventricle and the pulmonary artery exiting the left ventricle. Foals born with this anomaly may survive for several days postpartum but are markedly cyanotic and frequently recumbent.


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Figure 4.9 Great vessel transposition. Reproduced from McAuliffe SB, Slovis NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.

Auscultation often reveals a louder right-sided systolic murmur compatible with VSD as well as the continuous, crescendo–decrescendo ‘machinery’-type left heart base murmur of the PDA.




Truncus arteriosus (Fig. 4.10)


Incomplete or failed septation of the embryonic truncus arteriosus leads to a common ‘trunk’ through which the aorta and pulmonary artery flow. A ventricular septal defect is also usually evident. This leads to mixing of oxygenated and non-oxygenated blood, variable cyanosis and often pulmonary vascular overload. Decreased PaO2, right heart insufficiency and pulmonary edema often ensue. Since pulmonary vascular resistance is lower than systemic vascular tone, blood is preferentially pushed into the pulmonary vascular system driving pulmonary vascular overload with resultant clinical signs.


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Figure 4.10 Truncus arteriosus. Reproduced from McAuliffe SB, Slovis NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.



Non-infectious disorders


Dysrhythmias: atrial fibrillation (Fig. 4.11)


Atrial fibrillation is the most common atrial arrthymia associated with poor performance and exercise intolerance. It may be found as an incidental finding in some horses or can occur in horses with concurrent EIPH, congestive heart failure, respiratory distress, pulmonary hemorrhage, ataxia or collapse and myopathy.


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Figure 4.11 Atrial fibrillation. Classic electrocardiogram of atrial fibrillation revealing no definitive P waves, F waves (flutter) of the atria and normal-appearing QRS complexes arising at irregular intervals.

It may be paroxysmal or sustained. The paroxysmal form is often associated with a single episode of poor performance and normally disappears spontaneously within 24–48 hours. Hypokalemia and other electrolyte abnormalities, which are frequently seen in horses with diarrhea or following furosemide therapy, predispose the equid to paroxysmal atrial fibrillation as can excessive resting vagal tone.


Sustained atrial fibrillation is less common but easier to diagnose. Some of these horses may have no other evidence of heart disease.




Diagnosis and treatment



• On auscultation it is classically described as an ‘irregularly irregular’ rhythm.


• Atrial fibrillation is easily identified on an ECG strip as multiple rapid atrial ‘f’ waves preceding regular QRS complexes. In horses with sustained atrial fibrillation an echocardiogram should be performed to determine whether there is any underlying cardiac disease.


• Laboratory studies for determination of electrolyte abnormalities may be useful for horses with paroxysmal atrial fibrillation.


• Therapy with β-blockers, class 1A antiarrhythmics (quinidine, procainamide, etc.), class 1C (flecainide, etc.), class III medications (amiodarone, etc.) and electroconversion should only be reserved for intractable or persistent atrial fibrillation (greater than 48 hours duration) without spontaneous conversion to normal rhythm or with clinical signs of exercise intolerance, lethargy, etc.




Premature atrial beats (PAB) (Fig. 4.12)


Premature atrial depolarizations arise within atrial foci not often associated with the SA node. Therefore, atrial p waves of often variable morphology occur earlier than expected in the ECG recording. Most have a normal QRS that follows. Infrequent premature atrial beats can be found in apparently normal horses. PABs are more likely to be clinically significant if:


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Figure 4.12 Premature atrial beats (arrows) in a 3-week-old foal. The foal had been bitten 3 days previously by a Western Diamond Back Rattlesnake. The foal had disseminated intravascular coagulation (DIC) and had to be hospitalized for 2 weeks; 6 weeks after initial presentation the arrhythmia resolved. Reproduced from McAuliffe SB, Slovis NM (eds). Color Atlas of Diseases and Disorders of the Foal (2008), with permission from Elsevier.




Diagnosis and treatment



• Auscultation reveals a regular sinus rhythm that is interrupted by an obviously premature beat. Confirmation is by electrocardiogram (ECG). Documentation during exercise may be required to demonstrate a relationship with poor performance.


• Therapy is not often recommended unless atrial tachycardia arises. Atrial tachycardia is defined as more than four consecutive premature atrial beats. Transient atrial tachycardia can occur in structurally normal hearts during exercise, catecholamine release, hypoxia, hypovolemia, electrolyte alterations and caffeine therapy due to increased automaticity or triggered activity.


• Quinidine or procainamide can be considered but are impractical for long-term use. Digoxin is an alternative therapy but its effectiveness in such cases has not been evaluated in large studies.


• Other considerations of therapy are maintenance of normal serum potassium levels and treatment of any underlying cardiac disease such as myocarditis.



Ventricular premature contractions (VPC) (Figs. 4.13 & 4.14)


These premature contractions arise within the myocardium of the ventricles. Reportedly, premature ventricular contractions can transiently occur in approximately 14% of clinically normal horses during a 24-hour monitoring period. Isolated or rare VPCs can also be observed occasionally in normal individuals immediately post-exercise. Premature ventricular contractions that occur during exercise or are occurring frequently (> 7 VPCs per minute) are abnormal. These VPCs can be caused by hypoxia, hypokalemia, hypomagnesemia, hypercalcemia, elevated catacholamines, adrenergic medications, endotoxemia/sepsis, and primary cardiac disease (myocardial, pericardial or contusive cardiac insults).


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Figure 4.13 Ventricular premature contractions (VPC). Characteristic ‘bizarre’ QRS complex with lack of preceding ‘P’ wave.

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Figure 4.14 Ventricular tachycardia.



Diagnosis



• Early beats can be heard via auscultation and pulse deficits are common.


• ECG findings reveal lack of p waves preceding wide and/or tall (‘bizarre’) QRS complexes. If the QRS complex morphology varies, these VPCs are considered polymorphic and are assumed to arise from multiple/variable foci within the ventricles indicative of more diffuse myocardial disease.


• A pronounced jugular pulse with the VPC may be observed due to atrioventricular asynchrony (cannon A wave) and the follow-up beat after a VPC may be stronger due to the increased left ventricular filling that occurs with a compensatory pause following the VPC. This is known as extrasystolic potentiation leading to greater intensity of this beat.


• A physical examination, complete blood count, serum chemistry, blood gas (arterial +/− venous), echocardiogram and ECG evaluations should be considered to define the inciting cause(s).


• Evaluation of electrolyte abnormalities, as well as measurement of ionized calcium and magnesium, is recommended. Hypokalemia and hypomagnesemia are frequent causes of VPCs and electrolyte derangements may affect the usefulness of specific antidysrhythmic agents such as lidocaine.


• Measurement of cardiac Troponin 1 and other cardiac enzymes can be used to document underlying cardiac disease; 95% of normal healthy foals in one study had cardiac Troponin 1 values <0.49 ng/ml. Values ≥1 ng/ml are highly suggestive of myocardial disease/inflammation.



Treatment



• The majority of horses with VPCs will have spontaneous resolution of the arrhythmia after 4–8 weeks of rest.


• Patients with abnormal VPCs should be closely monitored such that ventricular tachycardia (VT) does not arise, i.e. heart rate >100–120 beats per minute with the rhythm being initiated from below the bundle of His (ventricular origin). Although potassium imbalance (both hypo- and hyperkalemia), other electrolyte disorders (hypomagnesemia), toxicants, vitamin E/selenium deficiency and stimulants can lead to VT, primary myocardial disease is most associated with ventricular tachycardia.


• Therapy should be directed at the inciting cause with primary myocardial disease a likely complicating issue. Class I anti-arrhythmic medications (lidocaine, procainamide, quinidine, propafenone) are often effective in VT patients with clinical signs of cardiac insufficiency while at rest, if multimorphic VT is noted, R waves are superimposed onto T waves on ECG, or if the heart rate is excessive for the age group patient.


• Although not as rapidly acting as lidocaine, magnesium sulfate (2–4 mg/kg q 2 minutes) can be useful to control ventricular tachycardia with a total dose not to exceed 50 mg/kg.


• The use of corticosteroids may be indicated if primary cardiac disease is deemed to be the inciting cause.



Acquired valvular heart disease


Valvular pathology is probably the most common cause of significant murmurs in the horse. These are sometimes accompanied by physiological disturbances of blood flow and exert consequent effects on the well-being and exercise capacity of the horse. In particular, defects of the mitral valve appear somewhat more likely to result in clinically significant murmurs. Mild, chronic, progressive valvular disease resulting in systolic murmurs form the commonest group of acquired disorders of the equine heart. The murmurs are usually of low intensity, and the sounds remain localized over the affected valve. Serious valvular dysfunction results in poor exercise tolerance and prolonged recovery after exercise. There is usually a high resting heart rate which shows a poor recovery rate to normal resting levels following even limited exercise but some cases affected by apparently severe murmurs show no detectable clinical effect on either performance or well-being. Causes of valvular regurgitation are listed in Table 4.1. Further discussion of more common causes is given below.





Clinical signs



• Mitral regurgitation. The murmur of mitral insufficiency is holo- or pan-systolic, typically band-shaped and is loudest over the fifth intercostal space, radiating caudo-dorsally if it is severe. It may be an incidental finding or horses may show signs of poor performance or clinical signs of heart failure. The tolerance is often largely dependent on the type of work the horse is doing, with horses in vigorous training showing an expected poorer tolerance for the condition. In some horses the condition may be complicated by atrial fibrillation which further compromises cardiac function. Depending on the cause other clinical signs may be present such as fever, weight loss or polyarthritis which can occur in cases of bacterial endocarditis.


• Aortic regurgitation. The murmur of aortic insufficiency is typically pan, holo or early diastolic decrescendo and has its point of maximal intensity over the aortic valve in the left fifth intercostal space and radiates variable distances ventrally. It may be musical or have a ‘creaking’ quality in some horses. In most horses, aortic regurgitation (AR) is an incidental finding and commonly occurs as a result of valvular degeneration in horses greater than 10 years of age. The existing murmur can vary greatly in intensity and is not indicative of the prognosis. Although degenerative valvular changes are generally regarded as being slowly progressive, studies have indicated that horses with AR have a shorter survival time and are more prone to developing congestive heart failure or sudden death. The quality of the arterial pulses is a good indicator of the severity of the AR as bounding pulses are associated with volume overload and moderate to severe AR with a poorer prognosis.


• Tricuspid regurgitation. A soft, grade 2–3 pansystolic murmur with the point of maximal intensity on the right side of the tricuspid valve is most commonly found incidentally. Endocarditis less commonly affects the tricuspid valve and thus associated signs are not frequently seen. The prognosis for horses with TR is generally good.




Ruptured chordae tendinae (Figs. 4.15 & 4.16)


Loud, widely radiating murmurs with an abrupt onset and a marked thrill develop in cases where there is rupture of one or more of the chordae tendinae (tendinous strands running from the papillary muscles to the free borders of the atrio-ventricular valves). The mitral valve is most often affected. This elicits a pronounced mitral valve insufficiency +/− cardiac insufficiency (edema, atrial enlargement, arrhythmias) and in some cases collapse and death.


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Figure 4.15 Ruptured chordae tendinae. Echocardiogram obtained from the left side showing a long-axis view of the mitral valve. Note that the ruptured chordae (arrow) can be appear to “flap” with movements of the valve.

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Figure 4.16 Post-mortem image revealing a ruptured chordae tendinae from a horse that was found dead. Image courtesy of the Irish Equine Centre.



Endocarditis (Figs. 4.17–4.24)


Bacterial endocarditis can affect the endocardium and/or one or more valve components. It occurs sporadically and can be seen in horses of all ages. The aortic and mitral valves are most commonly affected with mural lesions less common. Although they do occur on the valves of the right side, the effects of emboli are likely to be less obvious, possibly even passing unnoticed. Bacterial invasion and colonization secondary to a bacteremia is the most likely pathogenic mechanism but pre-existing valvular disease or endocardial changes as a result of jet lesions may predispose to the condition. Microthrombi production during severe illness, i.e. sepsis, etc., can also lead to turbulent or traumatic endocardial damage which allows adhesion by transient bacteremic organisms and subsequent infective endocarditis. The organism involved is largely dependent on the origin of the bacteremia (gastrointestinal, respiratory, skin, oral cavity, surgical wound or intravenous catheter). Streptococcus sp., Actinobacillus sp., Pasteurella sp. and Staphylococcus aureus are most frequently isolated although many other bacteria and even fungi have been reported. Thrombophlebitis and catheter sepsis have been associated with the development of endocarditis in the horse.


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Figure 4.17 Endocarditis. This 1-year-old TB had a history of prior illness and subsequent poor growth. Valvular insufficiency was suspected on the basis of an auscultable murmur and echocardiography confirmed the presence of a vegetative endocarditis associated with valvular insufficiency.

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Figure 4.18 (A, B) Echocardiograms obtained from a Thoroughbred broodmare with endocarditis involving the aortic and mitral valves. The clinical findings at presentation were weight loss, lethargy, tachycardia, pyrexia, increased jugular pulses and grade 4/6 pansystolic and holodiastolic murmurs, loudest on the left side. Marked vegetative lesions involving all leaflets of the aortic (A) and mitral valves and valvular insufficiency were evident during B-mode and color flow Doppler imaging (B). Moderate mature neutrophilia, marked hyperfibrinogenemia and hyperglobulinemia were present, consistent with a marked inflammatory process. The horse was subjected to euthanasia without treatment and post-mortem examinations confirmed the ante-mortem diagnosis of endocarditis. No bacteria were cultured from blood or valvular tissue.

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Figure 4.19 Endocarditis with thickening of the mitral valve.

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Figure 4.20 Echocardiogram of the mitral valve showing marked thickening and shortening of the valve associated with endocarditis.

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Figure 4.21 Echocardiogram demonstrating an endocarditis lesion of the aortic valve (same mare as Fig. 4.20). She presented with a history of bilateral shifting hindlimb lameness with variable swelling of the hindlimbs and intermittent fevers. Both mitral and aortic valves were incompetent.

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Figure 4.22 Long-axis view of the aortic valve showing thickening of the left coronary cusp of the valve. This thickening often appears as an echogenic thickening parallel to the free edge of the valve leaflets and corresponds to parallel fibrous band lesions which are frequently noted at necropsy.

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Figure 4.23 (A, B) Necropsy images from horses with vegetative endocarditis. Note the marked thickening and shortening of valves with vegetative lesions of the valve cusps. Image courtesy of Irish Equine Centre.

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Figure 4.24 Mitral valve incompetence (color flow Doppler, ultrasound). Blood flow coded red, flowing from left ventricle (LV) to right atrium (LA) during systole. The signal has aliased, as shown by the central core change from blue through to red (i.e. traveling so fast that signal received as if traveling in the opposite direction).

Valvular inflammation results in ulceration and inflammation of the valve leaflets and although affected valves may not appear to be grossly thickened, there are serious consequences in relation to valve movement and the development of valvular endocarditis lesions which act as a focus for the accumulation of fibrin; extensive blood clots are commonly present attached to the damaged valves. Organization of the fibrinous accumulations (with the enclosed bacteria) produces friable vegetative lesions, from which infective emboli may be disseminated into the circulation. These have, therefore, considerable potential as sources of emboli, of both infective and non-infective types. Progressive organization of the inflammatory foci in the valve leaflets has profound effects on valve closure and the site and type of the lesion may be of great importance. Smooth, longstanding and well-organized thickening of the valve cusps typical of chronic valvular endocarditis is somewhat less likely to result in serious embolism than the more irregular, friable lesions associated with acute bacterial endocarditis.




Clinical signs



• Most horses with bacterial endocarditis present with intermittent pyrexia, weight loss, depression, malaise, intermittent lameness and clinical indications of cardiac insufficiency attributable to the chamber/side of heart affected.


• A predisposing condition or concurrent infection or the history of such may be present but many horses present with no other obvious signs of disease and no history of a prior disorder.


• Valvular lesions often incite regurgitant murmurs best heard over the valve involved. Therefore, atrioventricular valve endocarditis results in a systolic murmur whereas aortic or pulmonic valve endocarditis results in a diastolic murmur. Mural endocarditis and small vascular lesions may not produce heart murmurs, especially if the right side of the heart is affected. The quality or intensity of the murmur may change during subsequent examinations and arrythmias may also be present.


• Right-sided vegetative lesions that dislodge may create embolic pneumonia or focal pulmonary abscesses, whereas left heart vegetations can dislodge to spread septic emboli to other organ systems with swelling of joints and tendon sheaths commonly seen.





Pericarditis (Figs. 4.25–4.30)


Pericardial inflammation and/or infection is uncommon in the horse. It may, however, when it occurs lead to life-threatening cardiovascular compromise and is most commonly associated with pericardial effusion and fibrinous pericarditis. Viral and bacterial infections are most commonly implicated but primary pneumonia, pulmonary abscesses, trauma and neoplasia-associated cases have been reported. Not all cases of pericarditis are septic but given the consequences should be regarded as such until proven otherwise. Additionally, although sepsis is by far the most common cause of pericardial inflammation, culture from the fluid (or even from the pericardium at post-mortem examination) is frequently unrewarding. The pathogenesis of non-infective pericarditis is unknown.


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Figure 4.25 A ventrodorsal radiograph obtained from a 7-day-old foal with pericarditis that presented with a 2 day history of lethargy, inappetance and increased respiratory effort. There is a globoid enlargement of the cardiac silhouette due to marked pericardial effusion and scalloped lung margins asscociated with pleural effusion, most evident in teh right hemithorax. Concurrent septic conditions present in the foal were polyarthritis and omphalophlebitis, consistent with disseminated bacterial infection.

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Figure 4.26 (A, B) Jugular distension in a 16-year-old Thoroughbred gelding. The horse presented for weight loss and the signs of generalized venous congestion. Jugular pulses, ventral edema and cardiac cachexia were identified. Echocardiography confirmed the right-sided congestive heart failure was secondary to severe restrictive pericarditis. Euthanasia was recommended and the necropsy image is shown in Fig. 4.29.

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Figure 4.27 (A, B, C) Echocardiographic images showing marked accumulation of fluid within the pericardial sac consistent with pericarditis. Note the irregular surface of the myocardium consistent with fibrin deposition (C).

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Figure 4.28 Pericardial drainage in a foal with pericarditis. This septic foal was noted to have marked accumulation of fluid within the pericardial sac on routine thoracic ultrasound. He was treated by drainage and lavage of the pericardial sac in addition to systemic antibiotics and made a full recovery.

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Figure 4.29 (A, B) Post-mortem images. (A) Heart and lungs showing marked fibrin deposition on the myocardium following opening of the pericardium. (B) Fibrinous pericarditis.

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Figure 4.30 Pericardial accumulation of blood. Pericardial and myocardial laceration (arrow) caused by a severely displaced fractured rib resulted in pericardial accumulation of blood and death of this foal.

The clinical signs associated with the disorder vary according to the extent and nature of the exudate within the pericardial sac. Where the disease is secondary to respiratory tract disease, the respiratory signs may be prominent and the presence of concurrent pericarditis might easily be overlooked. Affected horses typically are pyrexic, partially to completely anorexic, lethargic and may be reluctant to move.


Extensive pericardial effusions result in diminished or muffled heart sounds and evidence of cardiac tamponade (compression of venous return to the heart due to increased volume of fluid in the pericardium). The signs of tamponade are those of right-sided cardiac failure, including prominent jugular distension and pulsation, tachycardia, poor pulse pressure (hypotension) and ventral edema. In some cases the apex beat of the heart may not easily be palpable, but a number of other conditions, including obesity and pleural effusions, may also produce the same result. A pericardial ‘rub’ is often present during auscultation of the ventrolateral thorax. Other clinical signs may be related to the underlying cause, e.g. infection or neoplasia.




Diagnosis



• Clinical signs may be suggestive but echocardiography is fundamentally diagnostic where the thickened pericardium and the presence of variable amounts and consistency of effusion will usually be obvious.


• Pericardiocentesis with fluid analysis and culture may be required to identify the causal agent and its susceptibility profile. Streptococcus spp., Actinobacillus equuli, Pseudomonas aeruginosa and Pasteurella sp. have all been reported. Pericardiocentesis may be performed between the fourth, fifth or sixth left intercostal space midway between the shoulder level and the sternum. This technique is relatively easy and safe. Simultaneous ultrasound may provide accurate guidance for the aspiration needle. Normal pericardial fluid is limited in volume and contains few cells and low protein levels, whereas in most cases of pericarditis, whether septic or not, both cell and protein content increase markedly.


• The electrocardiogram of horses affected with pericarditis shows a characteristically diminished QRS voltage and/or repeated variations in QRS amplitude, which may be attributable to the movement of the heart within the distended pericardial sac.


• Thoracic radiography may also be used to demonstrate an enlarged, rounded cardiac silhouette but is limited by any concurrent pleural fluid and the technical problems of thoracic radiography in all but the smaller horses.


• CBC results are variable with the majority of horses demonstrating a moderate to marked neutrophilic leukocytosis with elevated fibrinogen. Animals suffering from pericardial tamponade will frequently present with azotemia due to decreased cardiac output and subsequent reduced renal output. Central venous pressure (if routinely monitored) greater than 10–12 mmHg is suggestive of cardiac tamponade and should prompt further diagnostics/therapy.


• Post-mortem examination reveals a markedly thickened pericardial sac and the presence of exudate which may be purulent or partially organized and, in longstanding cases, fibrinous. There is commonly some intercurrent valvular endocarditis.



Treatment and prognosis



• Therapy is aimed at the inciting cause with broad-spectrum antibiotics and anti-inflammatory medications initially; specific culture results may dictate longer-term treatment.


• Pericardiocentesis is indicated in all cases of septic effusion and cases of cardiac tamponade. Electrocardiographic monitoring during the drainage procedure allows recognition of arrthymias.


• Pericardial lavage can be performed in cases of septic pericarditis. It should be repeated daily until the accumulation of fluid declines (<1 L in 12 hours for an adult), clinical signs have improved and the cytological characteristics of the fluid indicate the presence of less inflammatory cells.


• Surgery is rarely required but could be considered in cases of constrictive pericarditis that are non-responsive to other therapies.


• Traditionally the prognosis for horses affected by pericarditis has been poor, however, there have been recent reports of successful outcomes.

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Feb 27, 2017 | Posted by in EQUINE MEDICINE | Comments Off on Disorders of the cardiovascular system

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