The use of concurrently administered medications such as the alpha‐2 adrenergic agonist drugs can help improve blood pressure due to their effects on vascular smooth muscle receptors. Following a single dose of intravenously administered drug in both the standing and anesthetized horse, the duration of this vasoconstrictive effect is drug dependent [38, 39], but when given by a constant rate infusion, the effect is sustained with all these drugs [40–42]. Whether used as part of an injectable [40] or inhalation [43] protocol, heart rate is likely to decrease with a corresponding decrease in cardiac output; second‐degree heart block, sinus pauses, and occasionally ventricular escape beats may also be evident following administration of alpha‐2 agonist drugs. This effect is most notable after high‐dose intravenous administration. The consequence of a significant decrease in cardiac output in the face of increased vascular resistance (and thus normal blood pressure) on organ function has not been fully elucidated for the horse.
Expected outcome
Hypotension during anesthesia can range from mild and short‐lived to prolonged and life‐threatening. Horses that experience sustained hypotension are at risk for end‐organ dysfunction as a result of poor perfusion.
Documentation of the deleterious consequences of hypotension are available in humans, where low mean arterial blood pressure (<55 mmHg) for as little as 10–20 minutes during anesthesia is associated with an increased risk of acute kidney injury, myocardial damage, and 30‐day mortality [44]. Although data of this kind is not available in horses, it is prudent to consider that the same physiological consequences are possible and thus hypotension should be treated.
Specific to horses, an early landmark experimental study showed that myopathy associated with hypotension (mean blood pressure of 55–65 mmHg for over 3 hours) during inhalation anesthesia in horses contributes negatively to recovery from anesthesia and survival [45]. In addition, a long duration of hypotension poses a greater risk for the development of myopathy in clinical cases [46]. Since this time, the widespread use of the positive inotrope dobutamine to maintain mean arterial pressure above 70 mmHg has significantly reduced the severity of post‐anesthetic myopathy cases [47].
Additionally, it has been shown that (direct) blood pressure monitoring reduces the risk of cardiac arrest death in horses [58, 49], possibly because hemodynamic problems are detected and corrected earlier in their time course.
Cardiac Arrhythmias
Definition
Resting heart rate for horses ranges from 28–44 beats per minute and some variation in heart rhythm, such as second‐degree atrioventricular (AV) block, is considered normal in athletic animals. Interestingly, it is not clear how low a heart rate is too low when considering treatment of the same in the perianesthetic period, but experienced anesthesiologists will often express concern with rates below 18–20 beats per minute. While it is common to see premature atrial contractions in anesthetized horses, they seem to be of no particular consequence. Atrial fibrillation, which is occasionally observed during anesthesia, can cause cardiovascular compromise depending on the ventricular rate. In general, a rate similar to the normal heart rate for the horse allows for better cardiac filling and maintenance of cardiac output and blood pressure.
Risk factors for bradycardia/bradyarrythmias
Horses with high fitness levels
Use of alpha‐2 adrenergic agonists
Underlying cardiac disease
Risk factors for tachycardia/tachyarrhythmias
Use of anticholinergics
Use of positive inotropes, especially at high doses or more than one at a time
Surgical procedure of a highly innervated area
Hypovolemia, endotoxemia, sepsis, systemic inflammatory response syndrome
Underlying cardiac disease
Pathogenesis
Bradycardia and bradyarrythmias are commonly seen in horses with the use of alpha‐2 adrenergic agonists as a result of both central decreases in sympathetic tone and a baroreceptor‐mediated response to hypertension. These are also common as vagally‐mediated physiological arrhythmias in normal horses and should disappear during physical activity [50]. Pathological high‐grade second‐degree or third‐degree AV block as a result of toxicities, electrolyte derangements, or AV nodal dysfunction occurs but is rare in horses [51, 52].
Tachycardia and ventricular tachydysrhythmias, while not common during equine anesthesia, may occur with concurrent use of sympathomimetics and anticholinergics or with the combined use of two sympathomimetics in an effort to improve blood pressure. Ventricular arrhythmias can also be observed in medically compromised horses, especially if anesthetized prior to adequate fluid resuscitation. As compared to adult horses, foals tend to respond to inotropes with an increase in heart rate, which in turn results in an increase in cardiac output [30]. This is thought to result from the inability of the foal to increase contractility due to immature cardiac muscle development. Tachycardia can occur as a response to the underlying disease process, such as sepsis or endotoxemia associated with bowel disease. Tachycardia may also occur in response to noxious stimulation and is anecdotally observed with surgical interventions in well innervated areas, for example during surgical neurectomies. Large volume hemorrhage commonly results in tachycardia as a response to hypovolemia in other species, but this response may not be seen in anesthetized horses until volume loss is near‐fatal [53].
Atrial fibrillation can be considered “lone” (occurring in the absence of underlying structural cardiac disease), and this is seen not uncommonly in racehorses and draft horses. Atrial fibrillation can occur for the first time under anesthesia in a horse with no signs of cardiac disease [54], or it can develop in horses with cardiac disease and/or cardiac failure with atrial enlargement.
While structural cardiac disease‐causing arrhythmias is common in humans and small animals, arrhythmias seen in horses are more commonly associated with systemic disease or as a result of drugs used during anesthesia. Normal horses have supraventricular arrhythmias or AV block, whereas horses with colic also have ventricular arrhythmias [55]. Endotoxemia associated with colic is thought to be a primary cause of myocardial injury, which results in the development of ventricular arrhythmias. Cardiac troponin I is used as a biomarker for myocardial damage in humans, dogs, and horses. Its concentrations are elevated in septicemic foals and adult horses with both experimentally‐induced endotoxemia and naturally occurring colic [56]. Horses presenting for colic with high cardiac troponin I concentrations are more likely to have a strangulating lesion (thus requiring surgery), have ventricular arrhythmias, and experience a poorer outcome than horses in which is cardiac troponin I is normal [57, 58].
Monitoring
A three‐lead electrocardiogram (ECG) can be used during anesthesia for the diagnosis and monitoring of cardiac rhythm disturbances. A commonly used configuration of ECG leads used by cardiologists is to place the negative electrode in the right jugular groove, the positive electrode on the thorax near the left elbow, and the remaining electrode somewhere away from the heart. This ECG is then recorded in lead 1 (base–apex configuration) [51]. However, there are multiple combinations of lead locations that will project an acceptable ECG in the anesthetized horse, and lead placement will often be dictated by the position of the horse and the surgical procedure.
Treatment
Anticholinergics in horses are not considered a routine tool in treating bradycardia and second‐degree heart block in horses. Unlike in dogs where the combined use of alpha‐2 agonists and anticholinergics is well studied and not recommended due to the increase in heart work, studies using the same combination of drugs in horses are limited [59, 60]. Hyoscine‐n‐butylbromide