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Objective: To compare adequacy of oxygen delivery and severity of shock during maintenance of anaesthesia with isoflurane or alfaxalone infusion in greyhounds experiencing blood loss. Study design: Prospective, randomised study. Animals: Twenty-four greyhounds (ASA I). Methods: All greyhounds were premedicated with methadone (0.2 mg kg-1) intramuscularly. Anaesthesia was induced with alfaxalone 2.5 mg kg-1intravenously. Following endotracheal intubation, the dogs were connected to an anaesthetic circle circuit delivering oxygen. Dogs were allocated to receive inhaled isoflurane or an intravenous infusion of alfaxalone for maintenance of anaesthesia. Isoflurane was initially administered to achieve an end-tidal concentration of 1.4% and alfaxalone was initially administered at 0.13 mg kg-1 minute-1. The dose of isoflurane or alfaxalone was adjusted during instrumentation to produce a clinically equivalent depth of anaesthesia. All dogs were mechanically ventilated to normocapnia (PaCO2 35-40 mmHg; 4.67-5.33 kPa). Passive warming maintained core body temperature between 37 and 38 °C. Measured and calculated indices of cardiovascular function, including mean arterial blood pressure (MAP), cardiac index (CI), systemic vascular resistance index (SVRI), oxygen delivery index (ḊO2I), oxygen consumption index (V̇O2I) and oxygen extraction ratio (OER), were determined at baseline (60 minutes after start of anaesthesia) and after removal of 32 mL kg-1and 48 mL kg-1of blood. Results: In all dogs, blood loss resulted in a significant decrease in MAP, CI, ḊO2, and a significant increase in SVRI, V̇O2I, and OER. The changes in each of the indices did not differ significantly between dogs receiving isoflurane and dogs receiving alfaxalone. Conclusion and clinical relevance: No difference in oxygen delivery or severity of shock was observed when either inhaled isoflurane or intravenous alfaxalone infusion was used for maintenance of anaesthesia in greyhounds experiencing blood loss

Objective: To describe sudden onset of generalized pulmonary atelectasis following thoracic lavage in 3 dogs. Series Summary: Thoracic lavage was performed following ligation of a patent ductus arteriosus in case 1, prior to closure of a large traumatic full thickness wound in the chest wall in case 2, and during investigation of an idiopathic spontaneous pneumothorax in case 3. In each case anesthesia and surgery were uneventful until thoracic lavage was performed, after which sudden generalized pulmonary atelectasis was observed. The atelectasis was visualized and was associated with oxyhemoglobin desaturation, decreased end-tidal carbon dioxide partial pressure (ETCO 2), and a marked increase in the peak inspiratory pressure (PIP) required to achieve visible lung inflation. Occlusion of the endotracheal tube and cervical trachea was directly eliminated as the cause of atelectasis in cases 1 and 2, and indirectly eliminated in case 3. Improvement in pulmonary function occurred in all cases in response to increased PIP ± positive end expiratory pressure (PEEP). New or Unique Information Provided: Generalized atelectasis should be considered a possible complication of thoracic lavage performed during thoracotomy. In the cases presented here, it is suspected that pre-existing reduction in lung volume (due to inadequate ventilation, surgical compression, absorption atelectasis) was exacerbated by the addition of the lavage fluid to the thoracic cavity. This pre-existing lung collapse is believed to have resulted in reduction of lung volume and that further reduction below the critical closing volume occurred following instillation of saline into the thorax resulting in the subsequent development of generalized atelectasis. The performance of regular arterial blood gas analyses and different ventilation protocols may have prevented the marked atelectasis that was observed in these cases.

Objective: To describe sudden onset of generalized pulmonary atelectasis following thoracic lavage in 3 dogs. Series Summary: Thoracic lavage was performed following ligation of a patent ductus arteriosus in case 1, prior to closure of a large traumatic full thickness wound in the chest wall in case 2, and during investigation of an idiopathic spontaneous pneumothorax in case 3. In each case anesthesia and surgery were uneventful until thoracic lavage was performed, after which sudden generalized pulmonary atelectasis was observed. The atelectasis was visualized and was associated with oxyhemoglobin desaturation, decreased end-tidal carbon dioxide partial pressure (ETCO 2), and a marked increase in the peak inspiratory pressure (PIP) required to achieve visible lung inflation. Occlusion of the endotracheal tube and cervical trachea was directly eliminated as the cause of atelectasis in cases 1 and 2, and indirectly eliminated in case 3. Improvement in pulmonary function occurred in all cases in response to increased PIP ± positive end expiratory pressure (PEEP). New or Unique Information Provided: Generalized atelectasis should be considered a possible complication of thoracic lavage performed during thoracotomy. In the cases presented here, it is suspected that pre-existing reduction in lung volume (due to inadequate ventilation, surgical compression, absorption atelectasis) was exacerbated by the addition of the lavage fluid to the thoracic cavity. This pre-existing lung collapse is believed to have resulted in reduction of lung volume and that further reduction below the critical closing volume occurred following instillation of saline into the thorax resulting in the subsequent development of generalized atelectasis. The performance of regular arterial blood gas analyses and different ventilation protocols may have prevented the marked atelectasis that was observed in these cases.