Pulse oximetry and oxygenation assessment in small animal practice

Oxygen is essential for the cellular respiration of all aerobic organisms so it is important that the amount of oxygen present within the circulation can be measured. In clinical veterinary practice, a non-invasive method of measuring oxygen saturation of arterial blood is necessary for the rapid, reliable assessment of a patient's oxygen status, whether anaesthetised or in the intensive care unit. Pulse oximetry is considered to be essential for the safe conduct of anaesthesia by the Association of Anaesthetists of Great Britain and Ireland, and the American Society of Anesthesiologists, because a failure to recognise hypoxaemia is a major cause of preventable death. This article describes how oxygen is carried within the blood and the basic technology behind the pulse oximeter, together with some of its pitfalls and limitations

Review of hypoxaemia in the anaesthetized horse: predisposing factors, consequences and management

Objectives: To discuss how hypoxaemia might be harmful and why the horse is particularly predisposed to developing it. To review the strategies that are used to manage hypoxaemia in anaesthetised horses, to describe how successful these strategies are and the adverse events associated with them. Databases used: Google Scholar and PubMed using the search terms – horse; pony; exercise; anaesthesia; hypoxaemia; oxygen; mortality; morbidity; ventilation perfusion mismatch. Conclusions: Although there is no evidence that hypoxaemia is associated with increased morbidity and mortality in anaesthetised horses, most anaesthetists would agree that it is important to recognise and prevent or treat it. The favourable anatomical and physiological adaptations of the horse for exercise, adversely affect gas exchange once the animal is recumbent. Hypoxaemia is recognised more frequently than in other domestic species during general anaesthesia, although its incidence in healthy horses remains unreported. The management of hypoxaemia in anaesthetised horses is challenging and often unsuccessful. Positive pressure ventilation strategies to address alveolar atelectasis in humans have been modified for implementation in the recumbent anaesthetised horse, but are often accompanied by unpredictable and unacceptable cardiopulmonary adverse effects, and some strategies are difficult or impossible to achieve in adult horses. Furthermore, the anticipated beneficial effects of these techniques are inconsistent. Increasing the inspired fraction of oxygen during anaesthesia is often unsuccessful since much of the impairment in gas exchange is a direct result of shunt. Alternative approaches to the problem involve the manipulation of pulmonary blood away from atelectatic regions of lung to better ventilated areas. However, further work is essential, with particular focus upon survival associated with general anaesthesia in the horse, before any technique can be accepted into widespread clinical use

Cardiac output affects the response to pulsed inhaled nitric oxide in mechanically ventilated anesthetized ponies determined by CT angiography of the lung

OBJECTIVE To measure changes in regional lung perfusion using CT angiography in mechanically ventilated, anesthetized ponies administered pulsed inhaled nitric oxide (PiNO) during hypotension and normotension.ANIMALS 6 ponies for anesthetic 1 and 5 ponies for anesthetic 2.PROCEDURES Ponies were anesthetized on 2 separate occasions, mechanically ventilated, and placed in dorsal recumbency within the CT gantry. Pulmonary arterial, right atrial, and facial arterial catheters were placed. During both anesthet-ics, PiNO was delivered for 60 minutes and then discontinued. Anesthetic 1: hypotension (mean arterial pressure < 70 mmHg) was treated using dobutamine after 30 minutes of PiNO delivery. Following the discontinuation of PiNO, dobutamine administration was discontinued in 3 ponies and was continued in 3 ponies. The lung was imaged at 30, 60, and 105 minutes. Anesthetic 2: hypotension persisted throughout anesthesia. The lung was imaged at 30, 60, and 90 minutes. At all time points, arterial and mixed venous blood samples were analyzed and cardiac output (Qt) was measured. Pulmonary perfusion was calculated from CT image analysis.RESULTS During PiNO delivery, perfusion to well-ventilated lungs increased if ponies were normotensive, leading to increased arterial oxygenation, reduced alveolar dead space, and reduced alveolar to arterial oxygen tension gradient. When PiNO was stopped and dobutamine administration continued, alveolar dead space and venous admixture increased, in contrast to when dobutamine and PiNO were both discontinued.CLINICAL RELEVANCE If PiNO is administered to mechanically ventilated, anesthetized ponies with concurrent hypotension and low Qt, this must be supported to achieve favorable redistribution of pulmonary perfusion to improve pulmonary gas exchange

Behavioral and cardiopulmonary effects of dexmedetomidine alone and in combination with butorphanol, methadone, morphine or tramadol in conscious sheep

Objective: To compare cardiopulmonary and sedative effects following administration of dexmedetomidine alone or with butorphanol, methadone, morphine or tramadol in healthy sheep. Study design: Randomized crossover study. Animals: Six Santa Inês sheep, five females, one male, aged 12–28 months and weighing 40.1 ± 6.2 kg. Methods: Sheep were assigned treatments of dexmedetomidine (0.005 mg kg−1; D); D and butorphanol (0.15 mg kg−1; DB); D and methadone (0.5 mg kg−1; DM); D and morphine (0.5 mg kg−1; DMO); or D and tramadol (5.0 mg kg−1; DT). All drugs were administered intravenously with at least 7 days between each treatment. Rectal temperature, heart rate (HR), respiratory rate (fR), invasive arterial pressure, blood gases and electrolytes were measured prior to administration of drugs (baseline, T0) and every 15 minutes following drug administration for 120 minutes (T15–T120). Sedation was scored by three observers blinded to treatment. Results: HR decreased in all treatments and fR decreased in DM at T30 and DMO at T30 and T45. PaCO2 was increased in D, DB and DM compared with baseline, and PaO2 decreased in D at T15 and T45; in DB at T15 to T75; in DM at T15 to T60; in DMO at T15; and in DT at T15, T30 and T75. There was a decrease in temperature in D, DB and DM. An increased pH was measured in D at all time points and in DT at T30–T120. inline image and base excess were increased in all treatments compared with baseline. There were no statistical differences in sedation scores. Conclusions and clinical relevance: The combination of dexmedetomidine with butorphanol, methadone, morphine or tramadol resulted in similar changes in cardiopulmonary function and did not improve sedation when compared with dexmedetomidine alone

Optimising pulmonary gas exchange in anaesthetised horses : unravelling the role of pulsed inhaled nitric oxide using computed tomography angiography of the lung

Mortality rates in healthy, anaesthetised horses are higher than in most other species. Hypotension, hypoxaemia and hypoventilation are implicated as risk factors, which develop due to the combined effects of general anaesthesia and recumbency. Hypoxaemia is largely a consequence of ventilation perfusion (V̇ /Q̇ ) mismatch. When horses are recumbent, dependent areas of lung become compressed and collapse. These atelectatic lung regions receive a large proportion of pulmonary blood, do not participate in gas exchange and contribute significantly to venous admixture. Whilst the hypercapnia associated with hypoventilation is easy to manage, treatment of hypoxaemia is more challenging. Mechanical ventilation (MV) is often employed, but can have detrimental effects, and the response to it is unpredictable. Pulsed inhaled nitric oxide (PiNO), has been used successfully to manage hypoxaemia in anaesthetised horses. The presumptive mechanism of action is via redistribution of pulmonary perfusion, from dependent areas of lung, to better ventilated, non-dependent lung regions. This movement of blood occurs due to the selective, pulmonary vasodilatory effect of PiNO. However, it necessary to further elucidate the mechanism of action of PiNO. The aims of these studies were to: develop a CT method to quantify regional pulmonary perfusion in the equine lung; measure changes in regional pulmonary perfusion when PiNO is administered, during spontaneous breathing (SB) and MV and; measure changes in pulmonary perfusion in response to PiNO during SB and MV in hypotensive and normotensive horses. The CT method could reliably measure changes in aerated and atelectatic regions of lung, and compared well to previously reported values measured using microspheres. During SB and MV in the normotensive horse, PiNO caused a redistribution of blood to non-dependent lung regions which led to improvements in gas exchange. Unexpectedly, PiNO was ineffective during MV if horses were hypotensive. However, during SB, the response to PiNO was similar regardless of blood pressure. By developing a new CT method with angiography for studies of the distribution of pulmonary perfusion, these experiments have shown that PiNO is an effective and safe treatment option for hypoxaemic horses, but blood flow and blood pressure must be supported if horses are mechanically ventilated

Clinical effects of midazolam or lidocaine co-induction with a propofol target-controlled infusion (TCI) in dogs

Objective: To evaluate the propofol requirement, cardiovascular and respiratory variables using midazolam or lidocaine with a propofol target-controlled infusion (PTCI) for induction of anaesthesia in healthy dogs. Study design: Prospective, randomized, controlled blinded clinical trial. Animals: Sixty client-owned dogs [American Society of Anesthesiologists (ASA) I–II] undergoing surgical procedures. Methods: Thirty minutes after premedication with acepromazine (0.03 mg kg−1) and morphine (0.2 mg kg−1), PTCI was started and maintained at a plasma target concentration of 1 μg mL−1. Three minutes later, dogs (n = 20 per group) received either 5 mL 0.9% sodium chloride (SG), 2 mg kg−1 of lidocaine (LG) or 0.2 mg kg−1 of midazolam (MG) intravenously (IV) as a co-induction agent. Two minutes later, suitability for endotracheal intubation was assessed. If intubation was not possible, the propofol target was increased by 0.5 μg mL−1 every 60 seconds until it was successfully achieved. Heart rate (HR), respiratory rate (fR), and oscillometric systolic arterial pressure (SAP), mean arterial pressure (MAP) and diastolic arterial pressure (DAP) were recorded immediately prior to commencing PTCI (B0), prior to intubation (BI), immediately after (T0), and at 3 (T3) and 5 (T5) minutes post-intubation. End-tidal partial pressures of carbon dioxide (Pe′CO2) were recorded at T0, T3 and T5. The occurrence of excitement at any time point was noted. Results: The median (range) propofol target concentration for endotracheal intubation was significantly lower in MG, 1.5 (1.0–4.0) μg mL−1 compared with LG, 2.5 (1.5–4.5) μg mL−1 or SG, 3.0 (2.0–5.0) μg mL−1. Heart rate, MAP, fR and Pe′CO2 were similar in the three groups at all time points. No excitement was reported in any dog. Conclusions and clinical relevance: Midazolam, but not lidocaine, provided a significant reduction in PTCI requirement for induction of anaesthesia thereby allowing successful intubation. However, cardiovascular and respiratory effects were not different between the groups