Cardiac murmurs are very common in horses; reduced athletic performance is also very common. However cardiovascular disease is an uncommon cause of poor performance (PP) in horses (<2% of cases) and in these cases it is usually a cardiac arrhythmia that is the underlying problem. There is usually no association between the presence of a cardiac murmur and lack of athletic performance unless the murmur is very severe and the horse is no longer able to compensate for the abnormal flow. 

Causes of poor performance 

1. Musculoskeletal problems (see lameness lectures)

2. Conditions of the Respiratory Tract (see Lectures Alterations in respiratory

function)

3. Lack of fitness.

4. Owner’s unrealistic expectations of ability (horse or rider).

5. Inappropriate training.

6. Cardiovascular abnormalities

7. Others (medical, neurological etc) 

General Approach to a poor performance horse 

Obtain a detailed history of the nature of the poor performance (PP). Poor jumping performance rather than poor exercise tolerance is more likely to be due to a musculoskeletal problem than a cardiac one. Cardiac murmurs are often an incidental finding in horses with PP caused by orthopaedic and respiratory diseases.

Horses have a massive cardiac reserve being able to increase cardiac output (Qt) from 35 L min-1 to 350 L min-1 during exercise. Reductions in cardiac reserve caused by cardiac disease will first become apparent during intense exercise. Horses will start to tire when their cardiac output is no longer able to meet the requirements of the tissues. Classically this will be obvious during fast work up hill or during racing (towards the end of the race).

In more severe cases horses may show exertional weakness (hindlimbs) and rarely syncope. Gradually as cardiac disease progresses signs of poor performance will become apparent at less intense exercise and ultimately signs of heart failure will be evident at rest. 

Observe the whole horse at rest

• Count respiratory rate do not guess. Tachypnoea will be present in horses with

  pulmonary oedema caused by pulmonary venous hypertension as a result of left

  sided cardiac failure.

•   Observe respiratory rhythm/effort, will be increased with pulmonary oedema.

•   Observe nares. In horses in congestive left sided failure, rarely a white frothy

  bilateral discharge may appear at the nostrils. This may only have been present at the onset of the condition, therefore carefully question the owners. Commonly horses will swallow oedema fluid and a nasal discharge will not be obvious.

•   Coughing is NOT a sign of cardiac failure (unlike in other species) unless there is secondary bacterial infection as a result of pulmonary oedema. 

Observe the degree of Jugular filling.

•   Jugular distension above the lower 1⁄4 to 1/3 of its length with the head held up

  indicates elevated central venous pressure. Causes include

  •   cranial thoracic obstruction/mass (heart rate likely to be normal, not necessarily

    any murmurs)

  •   pericardial effusion (muffled heart sounds or friction rubs present)

  •   right sided failure (should have murmur of tricuspid regurgitation). Primary right

    sided failure is rare, it more commonly develops secondary to left sided failure.

•   Reduced filling indicates hypovolaemia or low output failure

• 2. Look for subcutaneous oedema (indicative of right sided congestive failure, raised central venous pressure). NB The location of cardiogenic oedema due to right sided failure is species specific: Dogs tend to develop ascites; large animals accumulate subcutaneous oedema and pleural effusions; bovidae develop submandibular and brisket oedema; horses develop subcutaneous oedema in a plaque along the ventral thorax and occasionally extending to the cranial abdomen. In severe cases in horses subcutaneous oedema may extend to the upper fore limbs. Subcutaneous oedema of the lower limbs is usually non cardiac in origin. NB right sided cardiac failure often develops secondary to left sided failure, due to the increased right ventricular workload caused by pulmonary hypertension. Although right ventricular failure may not be the primary problem, the clinical signs of right sided failure may be the first thing to be noticed by the owner.

  3. c)  Assess weight loss and loss of muscle mass (cardiac cachexia).

  4. d)  Observe the filling of superficial veins (e.g. saphenous filling may be unequal in

     aortoiliac thrombosis)

  3. 3)  Locomotor system (See orthopaedic lectures for approach to clinical

     examination).

  4. 4)  Training.

     Is the body weight appropriate for degree of training – fat horses rarely win races. 

•  

0.  Clinical examination of the cardiovascular system : palpate the pulse 

Palpate pulse

 Count heart rate (do not guess), assess rhythm and pulse quality

•   Heart rate will be elevated (60-70 beats per minute) and there will be no

  evidence of vagal tone (e.g. sinus or atrioventricular block) in a horse in congestive heart failure. Remember fit horses have a low resting heart rate and in the early stages of decompensated cardiac disease there may only be a moderate increase in heart rate, and the heart rate may still remain within the normal range for all breeds.

•   Abnormalities of heart rhythm may be easier to detect from the arterial pulse (atrial fibrillation is the commonest cardiac cause of poor performance in horses). Cardiac arrhythmias may be a primary cause of cardiac dysfunction or may occur secondary to the development of myocardial ischaemia (decreased oxygen delivery and increased demand) or chamber dilatation as a result of other cardiac disease. Atrial dysrhythmias (e.g. atrial fibrillation) may develop secondary to left atrial enlargement caused by mitral regurgitation (MR).

 Assess pulse quality

•   The pulse pressure is the difference between systolic and diastolic pressure.

  Assessing deviation from normality in the pulse pressure is subjective due to differences in skin thickness and hair coat between breeds and variability due to normal physiologic changes in sympathetic tone. However with experience some worthwhile information can be obtained e.g. a bounding arterial pulse may indicate severe aortic insufficiency (AI), in a horse with a diastolic murmur that is not excited. In AI systolic pressure is raised due to the increased stroke volume and diastolic pressure is low due to run off into the left ventricle during diastole.

•   Assess mean pressure. Apply three fingers to the arterial pulse; determine how much pressure is needed in the upstream finger to occlude the pulse. This is often reduced in horses with colic and gives some idea of heamodynamic compromise.

•   Assessing the area under the pressure waveform or the volume of the pulse to give a subjective assessment of stroke volume. 

Observe mucous membranes 

In cardiac failure mucous membranes may be pale due to reduced cardiac output (Qt) and vasoconstriction. Cyanosis is uncommon (unless there is right to left shunting (complex congenital cardiac abnormalities). Reduced capillary refill time will occur with reduced Qt.

• Find the apex beat (provides landmark for cardiac auscultation). See tutorial notes on cardiac auscultation). Count heart rate and assess rhythm especially if this was not possible from the arterial pulse.

•   Feel for the normal heart sounds and precordial thrills. Thrills indicate significant cardiac disease. A diastolic thrill on the left hemithorax is most likely caused by aortic insufficiency, systolic thrill left hemithorax Mitral regurgitation, systolic thrill right hemithorax Tricuspid regurgitation or ventricular septal defect. 

Auscultatecardiacarea

See tutorial notes on cardiac auscultation.
e) Continue examination of Respiratory system See Lectures Alterations in respiratory function.
Increased lung sounds may be apparent as a result of pulmonary oedema (caused by pulmonary venous hypertension and left sided failure) however these are very difficult to hear, unlike in small animals.
f) Continue examination of Orthopaedic System (see orthopaedic lectures) Palpate lower limbs (and other extremities) will be cold in cardiac failure (forward failure) due to low cardiac output (NB care as lower limbs are often cold).
g) FurtherTests

•   Be guided by history and clinical findings towards more detailed medical

  examination or examination of locomotor and respiratory systems.

•   Cardiac abnormalities may require further evaluation by echocardiography and

  ECG (during exercise or 24hr).

•   Blood analysis (e.g cardiac isoenzymes). 

Cardiac arrhythmias are very common in athletic horses due to their high resting vagal tone.

Second degree AV Block is present in approximately 15%-18% of horses during the recording of a resting ECG but up to 44% when the ECG is recorded using an ambulatory Holter monitor.

Sinus block is also common. However these normal arrhythmias would be considered abnormal if the heart rate cannot increase in response to exercise.

Similarly ventricular premature beats common in the initial slowing period following exercise are considered abnormal if they occur during exercise when they may result in PP or increase the risk of exercise associated sudden cardiac death. Atrial fibrillation is the commonest cause of PP in Thoroughbred racehorses.

Cardiac murmurs

Cardiac murmurs due to valvular dysfunction are very common in athletic horses. Mitral regurgitation is present in 7% of flat racing Thoroughbreds (Flat), and 21% of National Hunt Thoroughbreds (NH), Tricuspid regurgitation (Flat 12%, NH 54%), Aortic regurgitation (Flat 0 %, NH 4%). Horses will commonly develop tricuspid and mitral regurgitation in response to training. Cardiac murmurs due to valvular disease rarely affect performance for racing and horses will continue to compensate for the abnormal flow. However when horses start to decompensate performance will be effected.

These are poorly understood in horses. Myocarditis secondary to viral and bacterial infections is suspected to be a cause of poor performance.
Dilated cardiomyopathy does occur and will cause poor performance with secondary mitral and tricuspid regurgitation. Cardiomyopathy will also occur as part of a generalised myopathy.
Toxic damage to the myocardium by salinomycin and monensin has been reported. Monensin ingestion (coccidiostat in poultry feed) causes acute myocardial necrosis leading to fibrosis. Clinical signs and outcome depend on amount consumed.
Horses present in various stages of heart failure, +/- murmurs and arrhythmias. Diagnosis is confirmed by demonstrating reduced myocardial contraction by echocardiography and raised cardiac isoenzymes (Cardiac troponin I). Prognosis is poor. 

Isolated pericardial effusions occur sporadically in horses although outbreaks have been reported. The main forms of pericardial disease are idiopathic fibrinous and idiopathic effusive pericarditis however neoplasia, traumatic haemorrhage or septic disease can occur sporadically as in any other species. The volume of the effusion can vary up to approx 6 litres and in most cases is serofibrinous, but eosinophilic and histeocytic effusions have been reported. 

• right sided heart failure, as the pressure in the pericardial sac compresses the less muscular right side of the heart and prevents filling. NB. Must differentiate from a cranial thoracic mass (e.g. thymic lymphosarcoma) which will also lead to jugular distention. Cases may also present with thoracic pain which may be mistaken for colic. 

• may change on a daily basis depending on the type and volume of fluid in the pericardial space. Initially friction rubs are audible as the inflamed epicardium and pericardium rub against each other. These rubs can occur whenever the heart moves. Therefore they may be audible during atrial contraction (between S4 and S1), during ventricular contraction (between S1 and S2) and during ventricular relaxation (between S2 and S3). This causes the classic triphasic pericardial friction rub. However the sounds may not be present during every phase and may therefore be monophasic or biphasic. As fibrin is deposited and fluid builds up the rubs may disappear and the heart sounds may become muffled. 

• s based on the presence of some of the above findings. Echocardiography (two-dimensional) is the method of choice for diagnosis. In the fibrinous or effusive forms the heart can be clearly seen surrounded by the anechoic (black) effusion. Fibrous bands may be seen floating in the effusion and the epicardium will have a shaggy appearance.

  • This condition is rare however when it occurs, pericardiocentesis and drainage can be lifesaving. NB Furosemide will not reduce the effusion, it will however decrease right atrial filling pressures and further reduce Qt. Drainage and lavage can be successful. In non-septic cases drainage and corticosteroid therapy is recommended. In septic cases aggressive treatment with antibiotics both systemic and into the pericardial sac, combined with pericardial lavage and the use of indwelling drains has proved to be successful. Echocardiography is useful to select the optimum site for drainage. The drain is inserted via the left 5th intercostal space, below a line level with the point of the shoulder and above the lateral thoracic vein. It is recommended that an ECG is recorded during pericardiocentesis and an intravenous catheter placed. Local analgesia is infiltrated beneath the skin and into the underlying muscle. A 20 - 28 French catheter with trocar should be used due to problems of blockage with fibrin clots. The pericardial sac may be lavaged with 2 litres of saline which can be left in place for 30 -- 60 minutes before removal. If antimicrobial or steroids are to be given a further 1-2 litres of saline, combined with antibiotics (penicillin/gentomycin) and steroids are flushed into the pericardial sac and left for 12 hours before draining. Indwelling catheters are ideal for this procedure. 

   

Diseases of the vessels 

The most important syndromes associated with vascular disorders are sudden death (see lecture) due to rupture of a major artery, colic due to cranial mesenteric arteritis or thrombosis and progressive exercise induced hind limb lameness due to aortico iliac thrombosis (See orthopaedic lectures). 

The diagnosis of cardiac arrhythmias 

requires an ECG examination. In horses, the base-apex lead is most commonly used. This lead system produces large complexes, which are easy to identify, and is less affected by movement artefacts than the limb leads. In contrast to small animal electrocardiography, the different depolarisation process in horses results in the ECG providing no information about chamber size or muscle mass. The ECG however is useful for assessing heart rate and rhythm. To record a base-apex lead the positive left arm electrode is positioned at the cardiac apex, and the negative right arm electrode is placed two thirds of the way down the jugular groove on the right. The third electrode is placed in a remote position away from the heart. The ECG is recorded from lead 1 on the ECG machine.

Atrial Fibrillation aetiology 

• Atrial fibrillation is one of the most common cardiac causes of poor

  performance in large hunters and Thoroughbreds. It is re-entrant rhythm, initiated by a premature atrial contraction and maintained as a result of the horses’ large atrial mass and high vagal tone. It may be caused by atrial dilatation secondary to valvular dysfunction or there may be no obvious underlying pathology (lone AF). Large horses are predisposed to the development of atrial fibrillation due to their large atrial size. Atrial fibrillation can develop secondary to electrolyte abnormalities or medical conditions e.g. peritonitis. NB It may also be associated with the administration of alpha2agonist drugs which increase vagal tone (Always auscultate heart before sedating any horse to inform owner if the dysrhythmias is already present), and may occur during or in the recovery phase of general anaesthesia. 

• If there is no other underlying cardiac disease the horse will continue to perform well during low intensity exercise only showing signs of poor performance during maximum exertion. The atria contribute up to 15-20% to ventricular filling, but in most horses at rest the loss of the atrial contraction has little effect on Qt. During exercise any decrease in Qt caused by the decreased stroke volume is offset by slight elevations in heart rate, however heart rate maximum will be attained at a lower exercise intensity and they will fatigue sooner. At high heart rates, diastole is short, reducing the time for ventricular filling and this is when the atrial contraction is most needed to maintain Qt. Despite attaining maximum heart rates in excess of 280 beats per minute (bpm) (normal heart rate max is about 225 bpm), affected horses fail to wholly compensate for their reduced ventricular filling. Some horses with AF develop heart rates in excess of 300 beats per minutes during exercise. Such cases are at risk of fatal ventricular arrhythmias and are not safe to ride. An ECG should be recorded during exercise in any horse with AF that continues in ridden work. If AF develops suddenly during racing the horse may pull up abruptly, and be very distressed due to the sudden decrease in Qt. Depending on the work load of the horse AF may be identified as an incidental finding. Reduced performance may not be detected if the horse is only used for low level athletic activity e.g. dressage. Rarely horses may present with epistaxis. AF usually develops in large breed horses or athletes with a large heart. If AF develops in a small non athletic animal, severe underlying heart disease that has caused atrial enlargement, should be suspected. 

• may suspect by auscultation but must confirm by ECG

  •   Auscultation Irregular rhythm. If there is no underlying cardiac disease the

    heart rate may be normal; there will be long pauses greater than 2 preceding cardiac cycles with occasional beats occurring earlier than normal. The third heart sound may be loud. There will be no 4th heart sound, however if a le lubb sound is audible; before diagnosing profound atrioventricular block with the occasional premature beat do an ECG examination as the le lubb may be due to a split first sound (i.e. tricuspid and mitral valves closing asynchronously). The slow heart rate in athletic horses with no other underlying heart disease is due to the high vagal tone blocking conduction at the AV node (resulting in 2oAV block) or at the sinus node (resulting in sinus block). If only a cursory auscultation is performed, the subtle irregularity in a case with slow AF may be missed and a diagnosis of profound atrioventricular block made. If the atrial fibrillation has occurred due to dilatation of the atria secondary to mitral regurgitation, and the horse is in heart failure, the heart rate will be elevated.

  •   ECG Irregularly irregular rhythm, no ‘p’ waves, fluctuating isoelectric line ‘f waves’ which may be coarse or fine. QRS morphology is normal unless fibrillation is due to underlying heart disease.

     

The underlying cause of the fibrillation must be determined before treatment is attempted. Treatment should not be attempted in horses if there is evidence of cardiac failure and if there is no compromise to athletic ability. Treatment may not be successful where there is atrial dilatation secondary to valvular disease. Horses should not be treated during the first 3-4 days following diagnosis as they may spontaneously revert to normal sinus rhythm. Horses with underlying medical or electrolyte conditions should be treated for their underlying problem and the cardiac arrhythmia will then usually resolve. 

Anti arrhythmic drugs

All antiarrhythmic drugs are also proarrhythmic and should only be used if the above criterion have been met and the owners are advised of the potential risks.

Quinidine Sulphate
Quinidine is administered at 20 mg/kg per os via indwelling nasogastric tube. This dosage is repeated every 2 hours until sinus rhythm is restored, signs of toxicity develop, or a maximum total dose of 60-80 g (120mg/kg) is achieved.
Signs of toxicity include urticaria diarrhoea, anorexia, weakness, ataxia and tachycardia. Laminitis has also been reported, but appears to be rare. Sudden death can occur in a small minority of cases, sometimes without any premonitory signs. ECG recordings should be made prior to each treatment, and the QRS interval measured. A 25% increase in the width of the QRS interval has been suggested to be an index of quinidine toxicity. Nasal oedema with stertorous breathing, and depression are commonly observed after only a few doses. Horses receiving quinidine should not be moved, due to the possibility of hypotension and the potential for producing rapid supraventricular or ventricular tachycardia. If a horse starts to show mild signs of toxicity the next dose of quinidine should be delayed for up to 6 hours to allow time for the side effects to resolve.
Heart rate and rhythm must be monitored throughout treatment and, when necessary, it has been suggested that supraventricular tachycardia (SVT) can be treated by the intravenous administration of 0.002 mg/kg digoxin IV, alternatively an alpha2agonist can be given.
In suspected quinidine toxicity sodium bicarbonate can be used (0.5-1.0 mEq per kg intravenously) to decrease plasma quinidine levels. Intravenous fluids and phenylephrine (0.01mg/kg) IV can also be used to treat severe hypotension, if present. 

Owners should be warned that the success rate for conversion of AF to normal sinus rhythm is only 87% and that sudden death is a rare but clinically relevant side effect. Horses that fail to revert to sinus rhythm during an initial treatment regimen often respond to a second treatment following a 24-hour period without drug administration. If the horse still fails to respond, quinidine administration should be continued at six hourly intervals. It has also been suggested that digoxin (0.01 mg/kg orally) should be given every 12 hours until sinus rhythm is restored.
It has also been suggested that following conversion to normal sinus rhythm and return to a normal resting heart rate, the horse should be checked for the presence of atrial premature systoles using 24-hour Holter monitoring. The presence of premature atrial systoles is believed to indicate an increased risk of recurrence of atrial fibrillation. When a large number of atrial premature beats are identified, it has been suggested that the horse should be rested for 1-2 months +/- anti-inflammatory therapy. In practice however, financial pressures only usually justify such measures when a horse repeatedly reverts to AF or when atrial premature beats are identified by auscultation. 

Electric defibrillation or cardioversion for atrial fib. 

This technique consists of the application of a direct current shock under general anaesthesia to stop the atrial fibrillation. It requires right heart catheterisation via the jugular vein, to allow electrodes to be placed in the pulmonary artery and right atrium. A pacing catheter is also placed as sinus arrest or atrioventricular block may occur following complete depolarisation of the ventricles. The technique is not without risk; the shock itself is pro arrhythmic and must be timed to coincide with the R wave of the ECG, there is the risk of general anaesthesia and the drugs used to sedate a horse prior to anaesthesia increase vagal tone, one of the predisposing factors to atrial fibrillation. However a number of studies have reported the success of this technique. The catheters are expensive and when compared to the ease of converting AF in some horses (after 2-3 doses of quinidine) the latter may still remain the best option. However the terminal and sporadic side effects of quinidine and the difficulties involved in treating some cases may make electrocardioversion the treatment of choice in certain cases especially in those horses that develop abnormally high heart rates during exercise or those in which AF has been present for a long time.

Premature systoles aetiology 

Premature systoles may be atrial or ventricular in origin. The underlying aetiology is often difficult to identify. Premature systoles may be associated with hypoxia, myocardial disease, electrolyte and metabolic disturbances, elevated sympathetic tone, fever and toxaemia. When all noncardiac causes have been ruled out, a primary myocardial lesion must be suspected.

Atrial premature systoles are detected fairly frequently in horses in training and affect performance only if they produce excessive heart rates during exercise. More commonly the premature excitatory focus is over-ridden as sinus nodal rate increases, and the extrasystoles disappear. At a prepurchase examination these cases probably should not be passed outright and should be investigated further as they may predispose to atrial fibrillation. Unfortunately further investigations to determine the cause of the premature beats, including evaluation of electrolyte status, are usually unrewarding, but remain necessary to ensure that the horse can continue in its chosen career. Affected animals may still be suitable for many owners following more extensive investigations.
Ventricular premature systoles will also affect performance only if they produce a tachycardia during exercise. This dysrhythmia is of more concern due to the risk of sustained ventricular tachycardia predisposing to ventricular fibrillation. This situation is likely to be exacerbated during exercise when sympathetic tone increases. Ventricular premature complexes (VPC) also occur frequently in the immediate cardiac slowing period following fast exercise and in the absence of concurrent cardiac disease are often considered to be a normal finding. In all cases of persistent ectopic activity, evaluation of electrolyte status and assessment of other body systems should preclude expensive cardiac examinations. Dysrhythmias should only be treated when there is significant effect on cardiac function, or the rhythm is likely to degenerate into a more sinister life-threatening arrhythmia. 

The ECG trace shows P waves which occur earlier than expected from the underlying P-P interval. If the P wave occurs after the refractory period of the ventricles, it is conducted and a normally configured QRS complex follows earlier than expected from the underlying R-R rhythm. If the P wave occurs during the refractory period of the ventricles the P wave is not conducted. The P wave of the premature complex may have a different configuration to the normal P waves. Premature P waves may be 'lost' in the previous T wave causing an abnormal configuration of the T wave. 

The premature QRS complexes may have a wide bizarre configuration, as ventricular depolarisation does not follow the normal conduction pathways. However if the PVC occurs from a site close to the normal conduction pathways, the shape of the PVC may be very similar to a normally conducted QRS. If the premature depolarisations are occurring from the same site the abnormal QRS complexes are of uniform configuration (unifocal or uniform VPCs). If there are multiple sites of ectopic activity, the abnormal QRS complexes will be of differing morphology (multifocal or multiform VPCs). If the premature QRS complex occurs during the preceding T wave, the vulnerable period of the cells, this may result in the development of ventricular fibrillation. This R on T phenomena indicates a poor prognosis.

Treatment of atrial & ventricular premature complexes

Usually specific anti-arrhythmic treatment is not indicated, as the premature beats are usually too infrequent to significantly affect cardiac output at rest. However it is important to establish what happens to heart rhythm during exercise. In many cases with atrial premature complexes (APC’s) when sinus rate exceeds the ectopic firing rate, cardiac rhythm & rate become normal. Isolated and multiple ventricular ectopic beats which occur during the immediate early slowing period after maximal exercise, rarely seem to be associated with primary cardiac disease and probably should not be over-interpreted as a cause for poor performance. However if they occur during exercise they may well affect performance and may pose a risk to the rider as the horse may develop ventricular fibrillation. If PVC’s are identified during the exercise period the underlying cause should be sought and treated if possible, the horse and the horse should be retired from ridden work.
Arrhythmias due to non-infectious myocardial disease may respond to treatment with anti-inflammatory agents. However the efficacy of this treatment is not proven. In cases of active myocardial disease a period of rest (2-3 months) may result in resolution of the arrhythmia with or without steroid treatment. In severe life- threatening ventricular tachycardia e.g. during anaesthesia or intensive care, lidocaine, a class 1b antiarrhythmic drug is the drug of choice to control ventricular rhythm. 

Bradydysrhythmias 

Although bradydysrhythmias are common and may be of no clinical significance, if maintained during exercise, cardiac output will be inadequate and performance will be limited. Abnormalities include 3rd and 2nd degree AV block, sinus block.

Diagnosis - bradydysrhythmias  

Sinus block and AV block are normal findings in horses therefore diagnosis of abnormality is based on ECG evidence of an inappropriate heart rate response during exercise. Pathological second degree AV block and profound sinus bradycardia occur rarely in horses. Affected horses have an inappropriately slow resting heart rate and may present with collapse and/or exercise intolerance. Pathological sinus bradycardia is found most commonly in elderly ponies and donkeys. Occasionally horses affected with profound 2nd degree AV block and sinus badycardia respond favourably to daily oral administration of alpha2 adrenoreceptor agonist drugs e.g. clenbuterol. The prognosis however remains guarded to poor. Third degree AV block indicates total block in conduction at the AV node and is always a pathological finding, thought to be associated with inflammation or degeneration of the AV node. ECG examination shows multiple p waves not associated with QRS complexes. Atropine administration results in increased p wave frequency with little or no increase in ventricular rate. A slow junctional or ventricular escape rhythm will be evident. If the escape beats originate high up in the His- purkinje network the QRS configuration will be normal and the rate will be approximately 20 -30 beats per minute. If the escape rhythm originates in the ventricles the QRS complexes will have a bizarre configuration and the rate will be slow (10 -20 beats per minute).

Treatment for bradydysrhytmias 

In most species third degree AV block is permanent and transvenous pacing is required. However some cases have resolved spontaneously or after treatment with anti-inflammatory drugs. In some cases that resolve spontaneously pathological first degree AV block remains.