Complications in Equine Surgery. Группа авторов
horses [77, 78]. Increases in circulating epinephrine and norepinephrine associated with hypercapnia underlies improved cardiovascular performance and the philosophy of “permissive hypercapnia” in the management of anesthetized horses. The exact level of hypercapnia that should be targeted for maximum benefit is not clear.
Although the terms mild, moderate, and severe have been used to describe different numerical values of arterial carbon dioxide tensions in different studies, horses with carbon dioxide values above 60–65 mmHg show increases in mean arterial pressure, stroke volume, and cardiac output with concurrent decreases in systemic vascular resistance. Slightly lower values (55–60 mmHg) may be associated with an increase in mean arterial pressure as a result of increases in vascular resistance but a lower cardiac output compared to normocapnic or more significantly hypercapnic horses. Therefore, the effects of carbon dioxide may be biphasic and higher values may be beneficial from the standpoint of improved cardiac output [77, 78].
However, severe hypercapnia is also associated with severe acidemia (arterial carbon dioxide of >85 mmHg correlated with a pH near 7.1 in the absence of metabolic changes), increases in intracranial pressure, increases in heart rate, anesthetic effects, and the potential for the development of arrhythmias [74, 79]. Additionally, experimental studies evaluating hypercapnia and cardiovascular function are limited to healthy horses, and the potential for further risks or benefits of hypercapnia in systemically compromised horses has yet to be explored.
With respect to retrospective analyses in horses undergoing colic surgery, one study of horses having surgery for correction of large colon volvulus showed that intraoperative hypercapnia (arterial carbon dioxide >70 mmHg) was a negative predictor of survival to hospital discharge (though anesthetic survival was unchanged) [80]. In another study, intraoperative hypocapnia (arterial carbon dioxide <40 mmHg) but not hypercapnia was a negative predictor for survival of anesthesia [81]. Whether these values simply reflect severity of underlying disease and management strategies used to correct concurrent problems (e.g. ventilation for hypoxemia) is not clear.
In human medicine, there is increasing use of permissive hypercapnia as a ventilation strategy, since it has been shown to reduce mortality in patients with acute respiratory distress syndrome irrespective of tidal volume. Hypercapnic acidosis appears to have a significant anti‐inflammatory effect, and benefits and risks of hypercapnia in critically ill humans are currently being investigated [82]. Data of this type is not available in horses.
Hypoxemia
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].