To eliminate the impact of variable FiO2 on the assessment of ventilation‐perfusion relationship in the lung, the arterial/alveolar ratio of oxygen can be calculated.Normal PaO2/PAO2 ratio should be >0.75 regardless of FiO2.

       In blood, O2 exists in two forms:Dissolved in plasma.Combined with hemoglobin.

       O2 is poorly soluble, so the majority of O2 in the blood is carried in combination with hemoglobin (Hb).

       Oxygen content of the blood (CaO2) is calculated as the sum of the O2 bound by Hb and that dissolved in the plasma. Note: PaO2 is expressed in mmHg.

       Oxygen delivery to tissues (DO2) is a function of the arterial O2 content (CaO2) and cardiac output.DO2 (ml/min) = Cardiac Output (l/min) x CaO2 (ml/l)Note: it is important to convert CaO2 to (ml/l)

       Several factors can influence the binding of O2 to hemoglobin.

       The O2‐Hb dissociation curve demonstrates the relationship between PO2 and saturation of Hb with oxygen (SO2) (see Figure 4.5).A left‐shift to the curve indicates a higher affinity of Hb for O2 and thus a higher saturation at a given PaO2.A right shift in the curve results from a lower affinity of Hb for oxygen.

       The position of the curve is usually described by the position at which Hb is 50% saturated (P50).P50 is approximately 24 mmHg in the adult horse.

       Intrapulmonary shunts can result in the delivery of poorly oxygenated blood into the pulmonary venous blood.

       The fraction of cardiac output that passes through a shunt is expressed as the shunt fraction (Qs/Qt), and can be calculated using the Berggren equation:

       CcO2 = the O2 content in pulmonary capillary blood (Calculated based on PaO2, assuming 100% saturation of Hb).CaO2 and CvO2 = the O2 content in arterial and mixed venous blood (obtained from a pulmonary artery catheter), respectively.In order for this calculation to be accurate, measurements must be performed when the horse is breathing 100% O2.Figure 4.5 The oxy‐hemoglobin dissociation curve illustrates the relationship between the partial pressure of oxygen in arterial blood and the percent of hemoglobin that is bound by oxygen. The sigmoid shape of the curve illustrates the cooperative binding of oxygen to hemoglobin. The P50 indicates the partial pressure of oxygen at which hemoglobin is 50% saturated.Estimates of (Qs/Qt) can be determined using the F‐shunt equation where a fixed arterial to mixed venous oxygen content difference [C(a‐v) O2] of 3.5 ml/dl is assumed.

       Normal shunt fraction is <5%.Clinically insignificant shunts are 10–19%.Clinically significant shunts are 20–30%.Potentially fatal shunts are >30%.

       Physiologic shunts are the most common type of shunt and they arise secondary to atelectasis or consolidation of alveoli.

       Anatomic shunts include bronchial, mediastinal, pleural, and coronary veins.

       Pathologic anatomic shunts include shunts secondary to congenital or traumatic anomalies and intrapulmonary tumors.

       Shunts and V/Q inequalities have a greater impact on O2 uptake than CO2 removal from the lungs due to the shapes of their respective dissociation curves.Specifically, blood passing under‐ventilated alveoli tends to retain its CO2, and blood passing over‐ventilated alveoli gives off an excessive amount of CO2.The amount of the retained CO2 and the excessively lost CO2 are proportional due to the relatively linear relationship of CO2 to VA.On the other hand, blood passing under‐ventilated alveoli does not take up enough O2, and blood passing over‐ventilated alveoli cannot take up a proportionately increased amount of O2 owing to the flatness of the O2‐Hb dissociation curve in this region.

       In the horse, the effects of sedatives on lung function are relatively minor although differences do exist among agents.

       In general, with acepromazine and α2 adrenergic agonists, ventilation changes include a decrease in rate and an increase in tidal volume.

       α2 agonists increase the work of breathing.Due to a decrease in tone of the abductor muscles of the upper respiratory tract, thus leading to collapse of the external nares and/or laryngeal structures during inspiration.The effects of increased work of breathing are insignificant in the normal horse, but may be significant in the horse with airway obstruction.Heavy sedation with α2 agonists (e.g. detomidine 0.01 mg/kg, IV) decreases the gas exchange function of the lungs.The decrease in oxygenation with detomidine sedation is due, in part, to an increase in the V/Q maldistribution within the lung.

       General anesthesia dramatically alters the function of the respiratory system.

       Changes result from the direct effects of the anesthetic drugs on the respiratory system and the indirect effects of recumbency.

       In the anesthetized recumbent horse, PaO2 can markedly decrease, and arterial CaO2 and DO2 may become critically impaired.These changes are greatest for horses in dorsal recumbency.Recumbency without anesthesia does not impair gas exchange to the same degree, indicating the role of the anesthetic drugs in this process.

       The magnitude of the decrease in gas exchange function of the lung does not vary greatly among anesthetic protocols.

       V/Q mismatching and intrapulmonary shunting are the major mechanisms responsible for the decrease in oxygenation during anesthesia.The distribution of ventilation changes in dorsal or lateral recumbency due to a decrease in FRC and regional differences in pleural pressures.Perfusion of the lungs changes due to a decrease in cardiac output, regional changes in vascular resistance, and inhibition of hypoxic pulmonary vasoconstriction.

       As the degree of right‐to‐left intrapulmonary shunting increases within the lung, the effect of increasing FiO2 on PaO2 decreases.

       A decrease in arterial CO2 removal from the lungs (e.g. with hypoventilation) with a resulting increase in PaCO2 is typically observed under general anesthesia.

       In general, with injectable and inhalational anesthetics, the minute ventilation and VT are decreased, while the f may be increased or decreased.

       The degree of respiratory depression with anesthetic agents is dose‐dependent and results from drug‐induced effects on the respiratory control centers.

      1 Clerbaux, T., Serteyn, D., Willems, E., and Brasseur, L. (1986). Determination de la courbe de dissociation standard de l'oxyhemoglobine du cheval et influence, sur cette courbe, de la temperature, du pH et du diphosphoglycerate. Can. J. Vet. Res. 50: 188–192.

      2 Drabkova, Z., Schramel, J.P., and Kabes, R. (2018). Determination of physiological dead space in anesthetized horses: a method‐comparison study. Vet. Anaesth. Analg. 45: