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Definition

Normal values for arterial oxygen tension in air breathing horses (presuming normal ventilation) at sea‐level (barometric pressure ~760 mmHg) range between 80 and 100 mmHg [83]. When horses are maintained with fractional inspired oxygen fractions greater than 90%, as is common during anesthesia, oxygen values under similar conditions should approximate 500 mmHg [73]. The alveolar gas equation may be used as needed to predict arterial oxygen tensions over a wide range of inspired oxygen fractions.

Hypoxemia is defined in many ways. When considering ideal lung function, an arterial oxygen tension that is lower than that predicted by the alveolar gas equation by 20% or more reflects some degree of hypoxemia. An arterial oxygen tension of less than 60 to 80 mmHg is a value more universally considered hypoxemic and one that is likely to result in tissue hypoxia.

Risk Factors

 Low fraction of inspired oxygen

 Dorsal recumbency

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

 Pulmonary, pleural space, or cardiac disease

Pathogenesis

Suboptimal oxygenation (arterial oxygen tension below 500 mmHg in a horse on a high fraction of inspired oxygen) is not uncommon during general anesthesia in horses, especially those positioned in dorsal recumbency, and is often explained by postural influences on ventilation perfusion matching [84]. In healthy standing horses, ventilation and perfusion are relatively evenly matched [85]. When placed under anesthesia in dorsal recumbency, a large portion of the lung is compressed under the diaphragm and abdominal contents. Atelectasis of these lung fields leads to the development of physiological right to left shunts, which decrease arterial oxygen tensions. Shunt fraction is higher in heavier horses and in dorsal compared to lateral recumbency [84].

True hypoxemia (arterial oxygen below 60–80 mmHg), while sometimes seen in healthy horses anesthetized on high fractions of inspired oxygen, more commonly results when positioning is compounded by disease processes that create further alveolar collapse (e.g. abdominal distention) and low cardiac output states. Hypoxemia is also common in horses anesthetized in the field where supplemental oxygen is not provided or those placed into the recovery stall after inhalant anesthesia and allowed to breathe room air [83, 86].

Monitoring

The arterial oxygen tension, similar to carbon dioxide and pH, is measured using a blood gas analyzer. The measurement of oxygen tension from an arterial blood sample, though costly, provides useful information about the patient’s oxygenation. Blood samples are easily obtained in the horse either by percutaneous puncture of a peripheral artery or preplaced arterial catheter.

Measurement of oxygen saturation using a pulse oximeter provides a means of continuously monitoring the patient’s oxygenation at a lesser cost. While it may not provide information pertaining to lung function, it can inform when circumstances will result in compromise to the animal. Values should range between 98 and 100% during anesthesia, and in this range reflect an arterial oxygen tension greater than 100 to 120 mmHg. A saturation value of approximately 90% corresponds to an arterial oxygen tension of about 60 mmHg, which as mentioned previously can contribute to tissue hypoxia. The ease of application and portability of pulse oximetry makes this a useful and user‐friendly tool for monitoring oxygenation during equine anesthesia. Pulse oximeter probes fall into two categories, transmittance and reflectance. The former probes are more common and typically attached to the horse’s tongue. The lip, nasal mucosa, ear, or vulvar/penile mucous membranes may be used as alternative sites.

The anesthetist may be able to detect hypoxemia via the presence of cyanosis of the mucous membranes, though this is not evident until hypoxemia is severe and even then may not be obvious in the presence of vasoconstrictive drugs or anemia. Hypoxemic horses may demonstrate hypoxic ventilatory drive and breathe rapidly, deeply, or around the ventilator. In addition, they can be tachycardic and hypertensive. This is easily misinterpreted as a light plane of anesthesia, therefore these signs should be considered in light of the entire clinical presentation when monitoring anesthesia.

Prevention

Pre‐oxygenation using a nasal cannula and oxygen flow rate of 15 liters per minute for 3 minutes has been shown to improve arterial oxygen tensions immediately after anesthetic induction in healthy horses undergoing elective procedures [87]. It is the authors’ experience that if the horse is well‐sedated, tolerance of the nasal insufflation tubing is good and the tubing can be maintained in place throughout the induction period.

A demand valve can be used to provide ventilation with 100% oxygen immediately after induction, particularly in horses at high risk of hypoxemia (e.g. colic with distended abdomen). Use of a demand valve also provides optimal oxygen tensions in recovery from anesthesia as compared to oxygen insufflation alone [83].

Horses are more likely to become hypoxemic in dorsal recumbency. When a choice is available, from the standpoint of oxygenation, horses should be placed in lateral recumbency for surgical procedures as ventilation/perfusion matching is improved compared to dorsal recumbency [88].

Initiation of positive pressure ventilation at the beginning of anesthesia (but not after an extended period of spontaneous ventilation) will lessen the severity of decreases in arterial oxygen tensions caused by positioning and subsequent development of physiological right to left shunts. [88, 89].

To help decrease the weight of the gastrointestinal contents on the diaphragm and thus pressure opposing pulmonary expansion, the surgical table can be adjusted such that the front end of the horse is tilted upward. However, the degree to which this can be performed depends on the nature of the surgical procedure.

Treatment

While many strategies are attempted to counter arterial hypoxemia, no method is consistently successful. Hence in the circumstances when hypoxemia does not respond to treatment strategies, it is best to minimize anesthesia time if possible. When this is not possible, the anesthetist should try to compensate for the decreased oxygen content by increasing cardiac output with use of fluids and inotropes if appropriate.

A high fraction of inspired oxygen (>95%) improves arterial oxygen tensions in anesthetized horses. Although using a low fraction of inspired oxygen during anesthesia has the theoretical benefit of reducing pulmonary shunts created by adsorption atelectasis, horses anesthetized using low inspired oxygen fractions are at greater risk of hypoxemia and arterial oxygen tensions increase dramatically with oxygen supplementation, even though shunt fraction does increase [90, 91].

Application of recruitment maneuvers consists of creating high peak inspiratory pressures (60–80 mH₂O) for a prolonged inspiratory hold during several breaths. This in combination with the use of positive end expiratory pressure (PEEP) can be successful in improving arterial oxygen tensions in horses [92–94]. These techniques, however, have detrimental effects on cardiac output. When cardiac output is significantly decreased, oxygen delivery to tissues is reduced and thus the benefits of having higher oxygen tensions may be negated.

Bronchodilators have been used with mixed results to improve oxygenation. Early studies used intravenous clenbuterol, which was successful but had undesirable systemic side effects such as sweating and tachycardia [95]. Inhaled salbutamol has been used more recently with success, improving arterial oxygen tensions without causing tachycardia, though sweating was still noted and a small percentage of horses failed to respond to treatment. In order to deliver the drug, an inhaler and endotracheal tube adapter are used [96].

Horses should routinely be provided with high flow oxygen insufflation (15 liters per minute) in the recovery stall [97]. Horses entering the recovery stall already hypoxemic, despite high fractions of inspired oxygen during anesthesia, may benefit from the use of a demand valve as described earlier.

Expected Outcome

Despite the fact that oxygen is essential for cellular processes and it would seem that hypoxemia should influence survival, there are few data on the effect of hypoxemia on clinical outcome in horses. Two studies in horses undergoing colic surgery failed to link intraoperative hypoxemia and negative outcome [80, 81]. Regardless, studies reflect that serum biochemical changes do occur in experimental horses when arterial oxygen is low over a period of several hours [98].

Additionally, horses with suboptimal oxygenation on high fractions of inspired oxygen during anesthesia have the potential to become severely hypoxemic when moved to the recovery stall and provided a lower oxygen fraction in addition to drugs that depress ventilation (e.g. post‐anesthetic sedation). Severe hypoxemia in experimentally apneic horses is associated with rapid progression to cardiovascular collapse [99], and this scenario in a clinical case is certainly possible.

Horses undergoing colic surgery, in which recruitment maneuvers and positive end expiratory pressure were used to maintain arterial oxygen tensions over 400 mmHg, had fewer attempts to stand and shorter recoveries with a higher (though statistically insignificant) median recovery quality score compared to controls that were ventilated conventionally [94], which would suggest that aggressive attempts to correct arterial oxygen are of benefit at least to recovery from anesthesia. However, as stated earlier, the cardiovascular effects of these ventilation strategies are not benign. In a horse presenting with hemodynamic instability, efforts should be made to augment cardiovascular function prior to and during attempts to improve arterial oxygen tensions.