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Hypoventilation

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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 in healthy anesthetized 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.

Complications in Equine Surgery

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