8.3.2 Cardiovascular causes of collapse
8.3.2 Cardiovascular causes of collapse

Severe cardiac disease may result in collapse of an animal at rest, but more frequently it occurs during exercise. Animals which collapse due to a sudden fall in cardiac output may show no signs of motion when on the ground and in effect show flaccid paralysis. This often lasts only a few seconds.

Collapse during exercise

Poor athletic performance is usually the first clinical sign associated with cardiac disease and is therefore seen before any condition is sufficiently severe to result in collapse. Intermittent arrhythmias, or myocardial or valvular disease of recent onset may result in collapse because the animal may be worked hard without knowledge of the presence of disease. Severe valvular heart disease can cause collapse during exercise, but this is remarkably uncommon. In addition, it would be a mistake to assume in every case in which a cardiac murmur associated with pathological change is detected, that cardiac disease is the cause of collapse. Severe myocardial disease or pericardial disease may also cause collapse at exercise, but these conditions are uncommon. Echocardiographic examination should be performed to assess their severity.

By far the most important cardiovascular causes of collapse during exercise are dysrhythmias. The development of AF during exercise may result in an animal suddenly tiring and collapsing or falling. Atrial or ventricular tachycardias may produce similar sudden reductions in cardiac output resulting in unexpected tiring or collapse. Usually there will be some evidence of these conditions when the animal is examined at rest. However, a diagnosis is often difficult in horses which develop paroxysmal AF because sinus rhythm may be present by the time that a veterinary examination is performed.

Some respiratory conditions can result in collapse during exercise. Exercise induced pulmonary haemorrhage can cause collapse and even death in horses usually just after the end of exercise. This only occurs if the condition is very severe, in which case epistaxis will be evident. Only rarely do exercise-induced upper respiratory tract obstructions result in collapse, although they frequently result in a sudden tiring of the animal, which may predispose it to falling.

Occasionally acute musculo-skeletal problems such as bilateral fractures or rhambdomyolysis result in collapse during exercise. Stumbling or falling, with subsequent winding must also be considered.

Collapse may also occur during the immediate post-exercise period. This may be due to exhaustion, dehydration, heat stress, haemorrhage; or musculo-skeletal problems, but is unlikely to be primarily due to cardiac disease. Unforan ECG is seldom recorded at these times so it is difficult to exclude the possibility of an arrhythmia. It is also unlikely that this diagnostic dilemma will ever be resolved. Similar problems occur in man and are frequently undiagnosed.

Collapse at rest

The majority of horses which are presented for investigation of a collapsing episode have collapsed while at rest. Reaching a definitive diagnosis in these cases is often extremely difficult because the intermittent nature of the problem means that the animal will be normal when it is examined.

Animals with severe valvular heart disease may collapse, but usually they will have been showing clinical signs of severe heart disease for some time and congestive heart failure will be present. Some of these horses collapse because of the sudden development of a dysrhythmia, or because of rupture of a major vessel such as the pulmonary artery. Tachydysrhythmias may develop as a result of systemic disease, and these may cause a sudden reduction in cardiac output and resultant collapse. Pericardial disease will result in a severe limitation of the preload and therefore limit cardiac output so that collapse may ensue if there is an increased demand, for example on excitement. Severe myocardial disease may have a similar effect.

Bradycardias

Bradydysrhythmias, including extreme forms of vagally mediated arrhythmias such as 2~AVB and sinus arrest/block, are very seldom responsible for collapse. Usually, light exercise will result in the abolition of these arrhythmias. Sinus bradycardia is more commonly a pathological situation and may result in colHowever, it is common for animals with this arrhythmia to show signs of systemic disease of which the arrhythmia is a secondary feature.

Collapse is likely to be one of the prominent presenting signs in horses with third degree atrioventricular block (30AVB or complete heart block). This condition is usually persistent and results in collapse when the animal is first exercised because of an inability to increase heart rate to meet the demands for increased cardiac output 30AVB is very rare in horses. Treatment is with a pacemaker (see section 7.8.15).

If an intermittent bradycardia or tachycardia is suspected to be the cause of a collapsing episode, 24-hour and/or radiotelemetric ECG recording may be worthwhile. However, if the collapsing episodes are infrequent, it may not be possible to identify the cause of collapse even with this technique.

Vaso-vagal syncope

Vaso-vagal syncope is a cause of episodic collapse which is well-recognised in humans, but is poorly documented in animals. In people it is associated with fear, i.e. a classic 'fainting attack' and is most commonly found in very highly strung individuals. Although horses are not entirely analogous, it seems likely that a similar mechanism may occur in this species. Usually the animals affected are at rest and are then suddenly excited by a precipitating event. Recognised causes are grooming of the head or tightening of the girth, although other events may be responsible and should be identified if possible. In some cases the inciting cause will be a sudden, unexpected event. The mechanism of vaso-vagal syncope is thought to involve an inappropriate combination of sympathetic and pararesponses. In the 'flight-fight' mechanism, animals which are excited have an increased heart rate, myocardial contractility and central arterial tone, resulting in an increase in blood pressure. This is required to counteract a marked vasodilation in the skeletal musculature. These changes allow muscular perfusion to increase dramatically, enabling the animal to respond rapidly. In vaso-vagal syncope, baroreceptors in the left ventricle, carotid sinuses and aorta may be over-sensitive and, when stroke volume is increased, a reflex may cause a vagally mediated bradycardia, or prevent the heart rate rising in an appropriate manner. The imbalance due to the lack of increased cardiac output and pervasodilation results in a precipitous drop in blood pressure to the brain and collapse ensues. The drop in blood pressure is only momentary and cormechanisms result in the animal rapidly regaining consciousness and standing, unless serious trauma has occurred.

It should be emphasised that the existence of this mechanism in horses is conjecture. There is no specific treatment; however, it is very unlikely that the episode will occur once the heart rate has risen while the horse is being ridden. If there is a specific inciting cause, it is wise to take steps to avoid it being repeated, if possible. In preparation for exercise it may be worthwhile lunging these animals, or trotting them in hand, so that a mild tachycardia is present before the horse is ridden.