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and in one study were shown to reverse detomidine‐induced bradycardia and increase cardiac index as a result of the increase in heart rate (tachycardia). However, hypertension was noted at the doses studied [60]. This along with tachycardia caused by the anticholinergics has the potential to increase myocardial work. There is also concern for the development of ileus and signs of colic with the use of anticholinergics, although reported effects on gastrointestinal motility are mixed. In addition, despite mild to moderate bradycardia, many horses maintain acceptable hemodynamic parameters during anesthesia when treated with inotropes.

      The authors therefore suggest the cautious use of anticholinergics in horses when a low heart rate is cause for concern (e.g. the horse is concurrently hypotensive), reversal of medications causing the decrease is not possible, and where other treatment efforts have not been successful. When considering anticholinergics, use of sympathomimetic drugs should be discontinued temporarily to avoid potential for serious cardiac dysrhythmias as reported in halothane anesthetized horses [61]. It is also prudent to monitor these horses for signs of gastrointestinal stasis in the recovery period and intervene if necessary.

When long acting alpha‐2 adrenergic agonists are used as anesthetic pre‐medication, concurrent administration of acepromazine results in a higher heart rate than that seen with the alpha‐2 agonist alone [62] because the vasodilatory properties of acepromazine offset the baroreceptor‐induced bradycardia from the alpha‐2 agonist. Additionally, acepromazine use has been shown to reduce the prevalence of arrhythmias during the anesthesia period [63].

      Pathologic arrhythmias in horses (e.g. high‐grade second‐degree AV block and third‐degree AV block) are treated via pacemaker implantation [64]. In these horses, elective procedures should not be performed until the cardiac rhythm disturbance has been successfully treated.

      For tachyarrhythmias in anesthetized horses, treatment should be focused on the underlying cause (volume replacement; management of potassium, calcium, and magnesium levels; correction of underlying bowel disease). Intravenous lidocaine may be used as a non‐specific treatment of ventricular tachycardia, though horses may convert spontaneously to sinus rhythm.

      Heart rate increases associated with the use of dobutamine will usually resolve shortly after the infusion is discontinued. For longer acting sympathomimetics (e.g. ephedrine), the effect may be sustained for up to an hour. When vasoconstrictive drugs (e.g. phenylephrine, norepinephrine, vasopressin) are used in the management of hypotension, heart rate typically drops when vascular resistance increases.

      Atrial fibrillation can be managed in anesthetized horses via electrical cardioversion. In many horses with atrial fibrillation, the purpose of anesthesia is to perform the cardioversion procedure. Therefore, knowledge of the anesthetic management of this condition is useful, and approaches have been thoroughly reviewed.

       Expected Outcome

      Many arrhythmias common to horses are relatively inconsequential (e.g. atrial premature contractions, physiologic bradyarrhythmias) and do not affect outcome in the anesthetic period. Some less‐common arrhythmias cause significant hemodynamic disturbances and could be fatal.

      Hypoventilation

       Definition

      Ventilation is the means by which the lungs remove carbon dioxide, a product of metabolism, from the body. Carbon dioxide regulation is also important in the maintenance of normal pH, as an elevation in carbon dioxide of about 20 mmHg from normal will reduce the pH by approximately 0.1 unit. Hypoventilation or increased arterial carbon dioxide tension is the most commonly seen ventilatory aberration in anesthetized horses. For the unsedated, calm, air‐breathing horse at sea level, arterial carbon dioxide values range between 45 and 50 mmHg. These values are somewhat higher than those reported for dogs and humans [68].

       Risk factors

       Use of respiratory depressant drugs (e.g. inhalant anesthetics)

       Abdominal distention (e.g. unfasted horse, pregnant mare, colic with gas‐filled bowel)

       Thoracic injury or pleural space disease

       Laparoscopic procedures with carbon dioxide insufflation [69]

       Use of neuromuscular blockade (paralytics) in the absence of mechanical ventilation

       Pathogenesis

      The newer inhalation anesthetics (isoflurane, sevoflurane, and desflurane) dependently influence ventilation such that arterial carbon dioxide values may reach 65–75 mmHg with a corresponding decrease in pH in the unstimulated horse at a surgical plane of anesthesia 70–73].

      The absence of fasting, gastrointestinal or abdominal distention, and recumbency can further compromise the horse’s ability to ventilate. At extreme carbon dioxide tensions (> 90 mmHg), increases in intracranial pressures and sedative and anesthetic effects can further compound respiratory depression [74, 75].

       Monitoring

      The anesthetist can sometimes intuit a hypercapnic horse due to the presence of bright red mucus membranes that occur as a result of carbon dioxide induced vasodilation, but monitoring of arterial carbon dioxide tensions via blood gas analysis is the gold standard for assessing ventilation in horses. Blood gas analysis also provides useful information about blood pH.

      Capnography, while useful, may not always accurately represent arterial carbon dioxide values. Large gradients develop in anesthetized horses between the carbon dioxide measured at the end of an expired breath and that measured in arterial blood. The gradient results from ventilation of alveolar dead space and is not necessarily consistent over the course of the anesthesia. The gradient is wider in larger horses and those being mechanically ventilated [76]. Therefore, the measurement of a normal end‐tidal carbon dioxide does not preclude the presence of arterial hypercapnia.

       Treatment

      Mechanical ventilation is commonly used to control carbon dioxide tensions in anesthetized horses, though it is not necessary to routinely ventilate the horse to values considered normal in other species (i.e. as low as 35–45 mmHg). Rather ventilation to arterial carbon dioxide values of 55–60 mmHg will still maintain pH within an acceptable range in healthy horses and minimize the negative influences of ventilation on cardiovascular function.

      Under circumstances of normal carbon dioxide production, ventilation guidelines enable one to correlate easily observed parameters and arterial carbon dioxide. Normal minute ventilation is 100–200 ml/kg/minute in the large animal patient. This is a product of tidal volume and respiratory rate. Normal tidal (per breath) volume ranges between 10 and 20 ml/kg and respiratory rate may range from 4–8 breaths per minute. Tidal volume may be estimated by excursions of the rebreathing bag whereas respiratory rate is easily obtained by looking at the rebreathing bag or the animal’s chest. Recording tidal volume and respiratory rate over one minute provides minute ventilation.

      It is important to remember that ventilation and certain ventilation strategies are often employed in an attempt to prevent or treat hypoxemia. Correction of hypercapnia may not be the direct goal, but arterial carbon dioxide levels will drop as minute ventilation is increased.

       Expected outcome

      Moderate hypercapnia in healthy anesthetized horses has been shown to improve cardiovascular performance with no reported negative side effects [77]. Hypercapnia in an anesthetized patient with concurrent metabolic acidemia (e.g. a strangulating colic) can cause pH to drop well below the normal range. Whether this degree of acidosis is a primary factor in short‐ or long‐term survival in horses is not known because it is difficult to separate intraoperative pH from a number of outcome‐modulating variables related to the severity of the horse’s underlying disease.

      There are good studies describing the cardiovascular effects of hypercapnia

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