Abstract
Objective
To evaluate the bronchodilatory effect of propofol constant rate infusion (CRI) on PaO2 and PaCO2 in dogs with suspected bronchoconstriction.
Methods
In this retrospective, observational study, anesthetic records from August 2022 through July 2023 at the Seoul National University Veterinary Medical Teaching Hospital were reviewed. Dogs with PaO2 < 300 mm Hg and PaCO2 > 45 mm Hg during mechanical ventilation under inhalation anesthesia receiving a propofol CRI were included. Ventilatory parameters and arterial blood gas results were extracted, reported as median (range). Arterial partial pressure of oxygen and PaCO2 values before and after propofol CRI were compared.
Results
7 client-owned dogs were identified. Bronchoconstriction was suspected postintubation based on ventilatory parameters (tidal volume of 8.1 [6.0 to 9.3] mL/kg; compliance respiratory system of 0.6 [0.4 to 0.8] mL/cm H2O/kg) and arterial blood gas results. Despite immediate interventions, including optimizing mechanical ventilation, deepening anesthesia, and drug therapy, PaO2 remained < 300 mm Hg. Thus, a propofol CRI (12 to 14 mg/kg/h) was initiated. Arterial partial pressure of oxygen increased following propofol CRI, rising from 153.0 (75.5 to 233.0) mm Hg to 284.0 (183.0 to 386.0) mm Hg at 30 minutes (mean difference, 130.9 mm Hg; 95% CI, 21.4 to 240.3) and to 331.5 (236.0 to 458.0) mm Hg at 60 minutes (mean difference, 168.0 mm Hg; 95% CI, 93.0 to 244.5). Arterial partial pressure of carbon dioxide levels were similar without improvement. Postoperatively, 4 dogs exhibited hypoxemia, taking 60 to 135 minutes to recover.
Conclusions
In dogs with perioperative gas exchange problems, PaO2 increased after propofol CRI, though PaCO2 levels remained unchanged.
Clinical Relevance
Propofol CRI improved oxygenation in dogs with suspected bronchoconstriction and may serve as a bronchodilatory treatment option.
Bronchoconstriction, also known as bronchospasm, is a phenomenon where bronchial smooth muscle constricts, mediated by the vagus nerve. It can manifest as an independent condition or as part of another issue, such as anaphylaxis, and is often triggered by specific maneuvers, particularly in patients with preexisting airway diseases, like asthma.1 Although reports on this phenomenon in dogs are limited, this reversible reflex can be activated by a noxious stimulus, such as tracheal intubation during inhalation anesthesia.2
The bronchodilatory effects and irritation potential of inhalational anesthetics vary; for example, sevoflurane is less pungent compared to other inhalants.3 However, in cases of bronchoconstriction, the ability to increase the vaporizer setting to induce airway relaxation is limited as severe bronchoconstriction can impair the delivery of inhalants and carrier gases. Severe bronchoconstriction leads to gas exchange problems and can be managed either mechanically by optimizing ventilation or chemically by drug therapy to ameliorate pulmonary collapse.4 However, mechanical treatments, such as the alveolar recruitment maneuver, could result in pulmonary barotrauma, so drugs with bronchodilatory effects can be considered. While halogenated inhalational anesthetics can produce airway relaxation, their effectiveness varies. In cases where bronchoconstriction is severe enough to impair the delivery of the inhalant and carrier gases despite pharmacologic intervention, another IV anesthetic, such as propofol, should be required for bronchodilation.5
Propofol, a short-acting injectable anesthetic, has been reported to produce anticholinergic effects on the airway, preventing bronchoconstriction induced by tracheal intubation in humans.6 It also produces bronchodilation in chronic obstructive pulmonary disease in patients under mechanical ventilation.7 This bronchodilatory effect of propofol has been experimentally shown in various species, including dogs,8 sheep,9 and guinea pigs,10 but there are no clinical case reports in dogs proving its effectiveness in perioperative situations. The objective of this retrospective study was to determine whether propofol constant rate infusion (CRI) exerts a bronchodilatory effect that improves oxygenation and ventilation, as indicated by changes in PaO2 and PaCO2, in isoflurane-anesthetized dogs suspected of bronchoconstriction unresponsive to conventional interventions. The hypothesis was that propofol CRI would result in a clinically significant improvement in both PaO2 and PaCO2, suggesting a bronchodilatory effect in dogs with suspected bronchoconstriction.
Methods
Case selection
Anesthetic records of dogs presented to the Seoul National University Veterinary Medical Teaching Hospital and anesthetized from August 2022 through July 2023 were reviewed. Patients that showed gas exchange problems (PaO2 < 300 mm Hg and PaCO2 > 45 mm Hg)11 during mechanical ventilation under inhalation anesthesia and were receiving a propofol CRI were included. Patients with arterial blood gas (ABG) values (PaO2 ≥ 300 mm Hg) were excluded. All patients had ABG analysis (ABL90 Flex; Radiometer) performed perioperatively. Animals were identified by searching for “propofol infusion” or “bronchoconstriction” in the anesthetic record archive system. Other information regarding patients’ history and laboratory examinations was searched via the electronic medical record system (e-Friends, version 5.1; Woorien Co Ltd). Written, informed consent to pursue publication of this case report was provided by the owner.
Anesthetic procedure
Food was withheld from dogs for 6 hours, with water allowed. Preanesthetic examinations, including physical examination, CBC, serum chemistry, and thoracic radiography, were conducted preoperatively.
Anesthetic premedications were administered to the animals IV in the cephalic vein. All dogs were premedicated with remifentanil (0.5 to 1 μg/kg, IV) and midazolam (0.1 mg/kg, IV), followed by CRI of remifentanil (0.17 μg/kg/min), midazolam (0.02 mg/kg/h), and ketamine (0.3 mg/kg/h), which are suggested infusion rates for isoflurane-anesthetized dogs.12 Induction was achieved with either alfaxalone (1 to 2 mg/kg, IV) or propofol (2 to 6 mg/kg, IV) administered to effect. Dogs were then intubated, and general anesthesia was maintained with isoflurane in oxygen (inspired oxygen concentration of approx 95%). A 24-gauge, 0.75-inch cannula was placed in the dorsal pedal artery for arterial blood pressure monitoring and ABG analysis. The catheter was connected to an electronic transducer (TruWave; Edwards Lifesciences) via noncompliant, saline-filled tubing with a pressurized (300 mm Hg) 3-way stopcock. The transducer was zeroed to atmospheric pressure and positioned at the level of the right atrium, aligning with the shoulder/manubrium in dorsal recumbency and the xiphoid process in lateral recumbency.13,14 To assess system accuracy, a square wave test was performed by activating the fast-flush device, with a normal dynamic response defined as 1 to 2 oscillations following the flush.15
Electrocardiography, hemoglobin oxygen saturation, and temperature were measured using a multiparametric monitor (Carescape B650; GE Healthcare). End-tidal isoflurane (FE′Iso) and end-tidal carbon dioxide (PE′CO2) were measured using a sidestream infrared gas analyzer of the patient monitor. Peak airway pressure, tidal volume (VT), and respiratory system compliance (CRS) were monitored using a D-lite Sensor (GE Healthcare). Monitoring parameters were recorded every 5 minutes, except spirometry parameters, which were recorded every 15 minutes.
After intubation, volume-controlled mechanical ventilation was initiated, and ventilator settings were adjusted based on PE′CO2 and spirometry parameters. Normal ranges were defined as PE′CO2 between 35 and 45 mm Hg, VT ≥ 10 mL/kg,16 and CRS (VT/[plateau pressure – positive end-expiratory pressure (PEEP)]) ≥ 1.3 mL/cm H2O/kg.17 Arterial blood gas analysis was performed if at least 1 of these parameters remained outside the normal range despite ventilatory adjustments. Simultaneously, the endotracheal tube was evaluated for potential misplacement (eg, endobronchial or esophageal), kinking, or obstruction due to factors such as mucus plugs or cuff herniation. The breathing circuit was also inspected for blockages.18 Additionally, cardiovascular and cutaneous signs were assessed to rule out anaphylactic or allergic reactions as potential sources of the abnormality. If abnormalities in PE′CO2 or spirometry parameters persisted despite ventilatory adjustments, those differential diagnoses were performed. If these potential causes were ruled out, nonallergenic bronchoconstriction was suspected.
Following the differentiation process, immediate management was initiated at the anesthesiologist’s discretion. Ventilatory support (manual bag ventilation, adjustment of mechanical ventilation, and adjustment of PEEP) was implemented first, followed by IV drug therapy for bronchodilation (administration of anticholinergics) and the use of alternative agents (aminophylline and anesthetic agents for deepening anesthesia). After immediate management, ABG analysis was repeated. If no improvement was observed, a propofol CRI was started, and the vaporizer settings and the rate of remifentanil-midazolam-ketamine CRI for perioperative analgesia were adjusted based on mean arterial pressure (decreased if < 60 mm Hg and increased if > 100 mm Hg). Serial ABG analyses were performed after propofol CRI until the end of the surgical procedures.
During the recovery period, the patient was placed in sternal recumbency and extubated upon regaining the gag reflex. The oxygen supply was discontinued once the patient raised their head. After 5 minutes, ABG samples were collected while breathing room air, and if abnormalities (PaO2 < 80 mm Hg) were detected, patients received supplemental oxygen via a mask or flow-by in the ICU, with ABG analysis repeated approximately every 30 minutes to monitor progress.
Follow-up
The dogs were followed up for postoperative respiratory symptoms for at least 6 months. Thoracic radiography was performed after surgery on those that exhibited respiratory symptoms postoperatively, including cough, cyanosis, and abnormal respiratory sounds, such as stridor or stertor.
Statistical analysis
Demographic data, clinical signs, and diagnostic imaging regarding the respiratory system, surgery type, procedure duration, anesthetic agents, respiratory parameters, and ABG results were extracted from the records. All numeric data are reported as median (range).
The normality test was performed using the Shapiro-Wilk test for continuous variables. Arterial partial pressure of oxygen and PaCO2 values before and after propofol CRI, measured repeatedly, were compared using a linear mixed model. In the model, PaO2 and PaCO2 values were dependent numeric variables, time points were independent variables, and individual dogs were included as a random effect. If significance was observed between individual dogs’ PaO2 and PaCO2 values, a post hoc pairwise comparison was conducted using Bonferroni correction. End-tidal isoflurane before and after propofol CRI were compared using a paired t test. The SPSS software (version 26.0; IBM Corp) was used for the analysis. Statistical significance was defined as P < .05. Results were reported with P values, mean differences (effect sizes), and 95% CIs.
Results
Case selection
Initially, 8 dogs were identified through the anesthetic record archive system during this period. Of these, 7 dogs with gas exchange problems potentially caused by bronchoconstriction were included for analysis. Demographic data, respiratory symptoms, diagnostic imaging regarding the respiratory system, and type and duration of surgery in 7 dogs are described in Table 1.
Demographic data (including age, American Society of Anesthesiologists [ASA] grade, body condition score, weight, sex, and breed), respiratory symptoms (cough, cyanosis, and stertor), tracheal collapse (TC) and bronchial collapse (BC) diagnosed via fluoroscopy, type of surgery, and duration of surgery in 7 dogs.
| Value | |
|---|---|
| Age (y) | 13 (7–17)a |
| ASA grade (5-point scale) | 3 (2–3)a |
| Body condition score (9-point scale) | 6 (5–7)a |
| Weight (kg) | 4.7 (3.0–5.9)a |
| Sex | |
| Female | 2b |
| Spayed female | 2b |
| Male | 0b |
| Castrated male | 3b |
| Breeds | |
| Bichon Frise | 2b |
| Maltese | 1b |
| Miniature Pinscher | 1b |
| Pomeranian | 1b |
| Poodle | 1b |
| Yorkshire Terrier | 1b |
| Respiratory symptoms | 5b |
| TC and BC diagnosed via fluoroscopy | 4b |
| Type of surgery | |
| Abdominal | 2b |
| Dental | 1b |
| Ophthalmic | 3b |
| Neurological | 1b |
| Duration of surgery (min) | 224 (139–273)a |
Diagnostics
For intubation, alfaxalone (1 to 2 mg/kg, IV) was administered to 3 dogs and propofol (2 to 6 mg/kg, IV) to 4 dogs. After induction, despite adjustments of the ventilator settings based on the patients’ respiratory status, VT was 8.1 (6.0 to 9.3) mL/kg at a peak inspiratory pressure (PIP) of 14 (12 to 17) cm H2O, CRS was 0.6 (0.4 to 0.8) mL/cm H2O/kg, PE′CO2 was 41 (34 to 55) mm Hg (5.5 [4.5 to 7.3] kPa), and PaCO2 was 60.1 (51.0 to 71.8) mm Hg (8.0 [6.8 to 9.6] kPa), indicating hypoventilation despite ventilatory support. Serial ABG analysis also revealed low PaO2 values at an inspired oxygen concentration of approximately 95% (Table 2). There were no remarkable issues with the position of endotracheal tube, the integrity of the breathing circuit, or cardiovascular and cutaneous signs.
Arterial partial pressure of oxygen/PaCO2 values (at an inspired oxygen concentration of approx 95%) at the time of intubation (TIB), suspected bronchoconstriction (TBC), before propofol infusion (TP0), 30 minutes after propofol infusion (TP30), and 60 minutes after propofol infusion (TP60) in dogs.
| Case | TIB (mm Hg [kPa]) | TBC (mm Hg [kPa]) | TP0 (mm Hg [kPa]) | TP30 (mm Hg [kPa]) | TP60 (mm Hg [kPa]) |
|---|---|---|---|---|---|
| Dog 1 | 231.0/53.9 (30.8/7.2) | 79.3/71.8 (10.6/9.6) | 75.5/62.2 (10.1/8.3) | 183.0/51.3 (24.4/6.8) | 328.0/58.2 (43.7/7.8) |
| Dog 2 | — | 182.0/61.2 (24.3/8.2) | 133.0/60.6 (17.7/8.1) | 327.0/52.3 (43.6/7.0) | 348.0/50.1 (46.4/6.7) |
| Dog 3 | — | 85.2/59.0 (11.4/7.9) | 99.4/43.9 (13.3/5.9) | 386.0/43.6 (51.5/5.8) | — |
| Dog 4 | 360.0/44.7 (48.0/6.0) | 114.0/51.0 (15.2/6.8) | 167.0/43.0 (22.3/5.7) | — | 236.0/45.4 (31.5/6.1) |
| Dog 5 | 411.0/63.4 (54.8/8.5) | — | 153.0/36.1 (20.4/4.8) | 305/53.6 (40.7/7.1) | 281.0/43.0 (37.5/5.7) |
| Dog 6 | 433.0/59.0 (57.7/7.9) | 252.0/70.0 (33.6/9.3) | 212.0/53.0 (28.3/7.1) | 263.0/58.0 (35.1/7.7) | 335.0/54.0 (44.7/7.2) |
| Dog 7 | 107.0/77.0 (14.3/10.3) | 209/56.9 (27.9/7.6) | 233.0/45.0 (31.1/6.0) | 227.0/51.4 (30.3/6.9) | 458.0/49.3 (61.1/6.6) |
— = No data.
Treatment
All dogs received immediate management, including optimizing mechanical ventilation, deepening anesthesia, and drug therapy based on the anesthesiologist’s discretion (Table 3). Despite these efforts, PaO2 remained below 300 mm Hg in all cases. Consequently, a propofol CRI was initiated at 0.2 mg/kg/min in 6 dogs and 0.23 mg/kg/min in 1 dog. Arterial partial pressure of oxygen and PaCO2 values at the times of intubation, suspected bronchoconstriction, and before and after (at an average of 30 and 60 minutes) the propofol CRI are presented in Table 2. After 30 minutes of propofol CRI, VT, CRS, and PE′CO2 were 9.5 (6.9 to 12) mL/kg, 0.6 (0.3 to 0.7) mL/cm H2O/kg, and 41 (28 to 46) mm Hg (5.5 [3.7 to 6.1] kPa) at a PIP of 16 (14 to 17) cm H2O, respectively. After 60 minutes of propofol CRI, VT, CRS, and PE′CO2 were 10.0 (6.9 to 12.3) mL/kg, 0.7 (0.5 to 1.0) mL/cm H2O/kg, and 37 (27 to 50) mm Hg (4.9 [3.6 to 6.7] kPa) at a PIP of 15 (10 to 18) cm H2O, respectively. The vaporizer settings were adjusted based on mean arterial pressure and assessment of anesthetic depth, which included eye position, palpebral reflex, jaw tone, and movement. The FE′Iso before and after the propofol CRI were 1.4 (1.1 to 1.5) and 1.0% (0.7% to 1.5%), respectively, representing a statistically significant decrease (P = .040; mean difference, 0.2%; 95% CI, −0.03 to 0.4), although the modest magnitude of this difference may limit its clinical relevance.
Interventions prior to propofol infusion for suspected bronchoconstriction in dogs.
| Case | Interventions for suspected bronchoconstriction |
|---|---|
| Dog 1 | PEEP, 4 cm H2O; aminophylline, 10 mg/kg; ketamine, 0.4 mg/kg; midazolam, 0.1 mg/kg; alfaxalone, 1.7 mg/kg; medetomidine, 2 μg/kg |
| Dog 2 | Glycopyrrolate, 10 μg/kg; aminophylline, 10 mg/kg; midazolam, 0.1 mg/kg |
| Dog 3 | Glycopyrrolate, 5 μg/kg; aminophylline, 10 mg/kg |
| Dog 4 | PEEP, 4 cm H2O; glycopyrrolate, 5 μg/kg; aminophylline, 10 mg/kg; alfaxalone, 1 mg/kg |
| Dog 5 | Glycopyrrolate, 10 μg/kg; aminophylline, 10 mg/kg; propofol, 0.7 mg/kg |
| Dog 6 | Aminophylline, 10 mg/kg; propofol, 0.3 mg/kg |
| Dog 7 | Glycopyrrolate, 15 μg/kg; aminophylline, 10 mg/kg |
PEEP = Positive end-expiratory pressure.
Treatments for suspected bronchoconstriction were described in the following order: adjustment of mechanical ventilation, administration of anticholinergics, and alternative agents (aminophylline; anesthetic agents for deepening of anesthesia). Treatments were used at the anesthesiologist’s discretion and were not described in chronological order. All drugs were administered IV.
Arterial partial pressure of oxygen values were increased after the propofol CRI (P < .001), rising from 153.0 (75.5 to 233.0) mm Hg (20.4 [10.1 to 31.1] kPa) to 284.0 (183.0 to 386.0) mm Hg (37.9 [24.4 to 51.5] kPa) after 30 minutes (P = .001; mean difference, 130.9 mm Hg; 95% CI, 21.4 to 240.3) and further to 331.5 (236.0 to 458.0) mm Hg (44.2 [31.5 to 61.1] kPa) after 60 minutes (P = .014; mean difference, 89.0 mm Hg; 95% CI, 93.0 to 244.5). Arterial partial pressure of carbon dioxide levels were similar without improvement (P = .572), measuring 45.0 (36.1 to 62.2) mm Hg (6.0 [4.8 to 8.3] kPa) before the propofol CRI, 51.9 (43.6 to 58.0) mm Hg (6.9 [5.8 to 7.7] kPa) after 30 minutes, and 49.7 (43.0 to 58.2) mm Hg (6.6 [5.7 to 7.8] kPa) after 60 minutes.
Recovery period
After extubation, 3 dogs had severe hypoxemia (PaO2 < 60 mm Hg), 1 had mild hypoxemia (PaO2 < 80 mm Hg), and 3 had normoxemia (PaO2 > 80 mm Hg). Despite limitations in ABG analyses as patients awoke, the majority showed improved oxygen tension over time. Arterial partial pressure of oxygen improved to mild hypoxemic levels after 60 and 135 minutes from the first ABG while breathing room air in dogs with severe hypoxemia, and PaO2 improved to normoxemia after 90 minutes in the dog with mild hypoxemia. All dogs were normocapnic except 1 (PaCO2, 46.1 mm Hg [6.1 kPa]).
Follow-up
Among the 5 dogs with preoperative respiratory symptoms (Table 1), 3 exhibited persistent symptoms, including cough, nasal discharge, and hemoptysis, postoperatively. Thoracic radiography was performed, but no significant radiographic changes were observed compared to the preoperative examination. However, fluoroscopy revealed tracheal collapse in 1 dog. All 3 dogs showed improvement following at least 2 weeks of pharmaceutical treatment, with follow-up at 25, 18, and 17 months showing no signs of progressive worsening. The remaining 4 dogs did not exhibit any postoperative respiratory symptoms.
Discussion
This retrospective study presents dogs with perioperative acute respiratory failure, characterized by inadequate oxygenation (PaO2 < 300 mm Hg) and impaired carbon dioxide elimination (PaCO2 > 45 mm Hg).11 These cases were successfully managed with propofol CRI, which we consider to have a bronchodilatory effect during inhalation anesthesia. Since there were improvements in PaO2, VT, and CRS values in similar ventilatory settings before and after propofol CRI, it is assumed that propofol induced bronchodilation in these patients. Arterial partial pressure of oxygen significantly improved in this case series, whereas PaCO2 did not show a significant decrease. This may result from too small of a sample size to show sufficient improvement, or when pulmonary shunt occurs perioperatively, oxygen, which is less soluble in the blood-gas barrier, is primarily decreased compared to carbon dioxide, which has little diffusion limitation.19
In mechanically ventilated patients, perioperative acute respiratory failure based on the ABG analysis can be induced by multifactorial causes, including alveolar dysfunction (eg, pulmonary edema), shunting (eg, atelectasis), and ventilation-perfusion (V/Q) mismatch (eg, pulmonary aspiration).20 In the present cases, none of the patients were diagnosed with preexisting pulmonary disease or showed evidence of alveolar dysfunction in the preanesthetic examinations. Intraoperative atelectasis can affect oxygenation but typically resolves with ventilatory adjustments.21 Pulmonary conditions, such as asthma, chronic obstructive pulmonary disease, pneumonia, and aspiration, can all contribute to V/Q mismatch to varying degrees, but postoperative radiographic evaluations did not reveal abnormalities indicative of these pulmonary conditions in these patients. Furthermore, low CRS (low VT and/or high PIP) can be observed in inadequate anesthetic depth or restrictive thoracic diseases22 and bronchoconstriction. Anesthetic depth was promptly adjusted by administering additional anesthetics following ventilator optimization, which was performed immediately after detecting abnormal values. A review of the preanesthetic examinations revealed no radiographic or fluoroscopic signs of restrictive thoracic diseases, and none of the patients had documented conditions commonly associated with it, such as obesity, scoliosis, muscular dystrophy, or autoimmune diseases, like systemic lupus erythematosus. Consequently, bronchoconstriction remained a possibility. Unfortunately, bronchoconstriction was not confirmed in these cases using diagnostic methods such as CT, bronchoscopy, or possibly intraoperative thoracic radiography. While other causes of V/Q mismatch cannot be entirely ruled out, the suspicion of bronchoconstriction was primarily supported by the significant increase in PaO2 following the propofol CRI.
Bronchoconstriction caused by anaphylactic or allergic reactions should also be considered, though these commonly occur during the maintenance stage.1 Additionally, no cutaneous or cardiovascular signs were observed in these cases; thus, the condition was attributed to vagally mediated, nonallergenic bronchoconstriction. This phenomenon primarily occurs during induction (44%) and is predominantly caused by endotracheal intubation (64%), which triggers vagal tone in humans.1,4 In this study, patients’ conditions worsened toward the end of the induction phase, shortly after intubation, a pattern consistent with vagally mediated bronchoconstriction. Mechanical stimulation, including intubation2 or bronchoscopy,23 has been suggested as a potential contributing factor for bronchoconstriction in dogs. Notably, during manual ventilation at this point, lung inflation felt restricted, indicating inadequate lung expansion. This observation was suggestive of bronchoconstriction as a possible cause. Whether preoperative bronchoconstriction-related respiratory symptoms, such as cough and cyanosis, affect intraoperative respiratory events cannot be determined based on the available data. However, given the relatively high proportion of patients exhibiting preoperative respiratory signs, careful perioperative monitoring may be warranted to promptly detect and manage potential respiratory complications. Arterial blood gas analysis revealed a lower-than-expected PaO2, with all but 2 cases demonstrating values exceeding 100 mm Hg. Clinically, a PaO2 above 100 mm Hg during anesthesia is generally not indicative of an immediately critical condition. However, these values can fluctuate in real time and may deteriorate, posing a potential risk for worsening hypoxemia. In addition, considering the potential need for recovery time from such hypoxemia after extubation, prompt intervention and vigilant monitoring remain essential.
Perioperative bronchosconstriction can be managed mechanically or pharmaceutically. Adjusting mechanical ventilation can be initially achieved by increasing PIP, PEEP, or alveolar recruitment maneuver. However, ventilator-induced lung injury is widely reported in both humans24 and dogs.25 Ventilatory support as the first response in some patients did not show improvement in gas exchange status; thus, pharmaceutical management was performed. This primarily includes β-2 agonists, anticholinergics, and alternative agents. Short-acting β-2 agonists (eg, terbutaline and salbutamol) are crucial agents4 but are not readily available in IV form. Anticholinergics can reduce vagal tone for bronchodilation but may cause tachycardia and hypertension in anesthetic contexts. Alternative agents, including corticosteroids, aminophylline, and anesthetic agents for deepening anesthesia, which were used based on patients’ hemodynamic status and the anesthesiologist’s discretion, can be options. In particular, inadequate anesthetic depth at the time of airway stimulation, such as intubation, can increase vagal tone, leading to reflex bronchoconstriction, especially in the presence of airway irritants, like isoflurane or desflurane.26 Deepening anesthesia mitigates this risk by suppressing airway hyperreactivity and enhancing ventilatory stability. In 1 dog, a mild PaO2 increase was shown after immediate management before propofol CRI. However, immediate management (Table 3) regarding bronchoconstriction was insufficient (PaO2 < 300 mm Hg; Table 2); thus, propofol CRI was initiated.
Experimentally in dogs, propofol 2 mg/kg produced a significant bronchodilatory effect in histamine-induced bronchoconstriction, unlike lower doses (0.2 mg/kg).8 Similarly, in the present study, low doses of propofol bolus (0.3 and 0.7 mg/kg) administered to 2 dogs did not improve PaO2. If bronchoconstriction occurs during surgery, halting the procedure is not always a feasible option. In such cases, propofol CRI could be a viable alternative, and this approach necessitates adjustment of the dosages of concurrent inhalational agents or analgesic infusions as evidenced by the reduction in the mean FE′Iso value following propofol administration. Several studies27,28 have reported using propofol CRI for maintenance in dogs, with dosages ranging from 0.3 to 0.5 mg/kg/min, alongside various induction doses. The doses of 0.2 to 0.23 mg/kg/min used in this study effectively increased PaO2, suggesting a bronchodilatory effect.
One limitation of this study is the small number of cases presented, which may not fully represent the broader population of dogs with perioperative bronchoconstriction. Specifically, the lack of standardized protocols for the mechanical and pharmaceutical management of perioperative acute respiratory failure in veterinary medicine results in varied treatment approaches across patients. Consequently, differences in timing and application of propofol CRI may lead to variable effects observed among individual cases. Additionally, although bronchoconstriction was suspected based on the ABG values and clinical presentations that responded to the bronchodilatory effect of propofol, a definitive diagnosis via CT or bronchoscopy was not performed. Therefore, future prospective studies with a larger population and definitive diagnoses are needed to further validate the clinical utility of propofol CRI in dogs.
In conclusion, the improvement in arterial oxygenation and spirometry results after the propofol CRI in this study suggests that this treatment can be an effective option for managing patients with suspected bronchoconstriction in intubated dogs. While bronchoconstriction cannot be definitely identified as the sole cause, it should be considered as a potential differential diagnosis in dogs experiencing perioperative low VT and gas exchange problems. In such clinical scenarios, when conventional methods prove ineffective, propofol CRI could be a viable alternative due to its bronchodilatory effect. All patients recovered without severe complications; however, close monitoring and oxygen supplementation are recommended due to the risk of hypoxemia. In hypoxemic patients, pulmonary oxygenation improved within approximately 1 to 2 hours.
Acknowledgments
None reported.
Disclosures
The authors have nothing to disclose. No AI-assisted technologies were used in the composition of this manuscript.
Funding
This research was supported by the Basic Science Research Promotion program through the National Research Foundation of Korea funded by the Ministry of Education, Science, and Technology (2021R1F1A104546013); the New Faculty Startup Fund from Seoul National University; and the BK21 FOUR program and Research Institute of Veterinary Science, College of Veterinary Medicine, Seoul National University.
ORCID
W. G. Son https://orcid.org/0000-0001-5431-3254
References
- 1.↑
Westhorpe RN, Ludbrook GL, Helps SC. Crisis management during anaesthesia: bronchospasm. Qual Saf Health Care. 2005;14(3):e7. doi:10.1136/qshc.2002.004457
- 2.↑
Kim MH, Choi JH, Lee IH, Son WG. Intubation-related reflex atelectasis of lung lobes during computed tomography in two dogs. Vet Anesth Analg. 2024;51(5):566–568. doi:10.1016/j.vaa.2024.05.002
- 3.↑
TerRiet MF, DeSouza GJ, Jacobs JS, et al. Which is most pungent: isoflurane, sevoflurane or desflurane? Br J Anaesth. 2000;85(2):305–307. doi:10.1093/bja/85.2.305
- 4.↑
Dewachter P, Mouton-Faivre C, Emala CW, Beloucif S. Case scenario: bronchospasm during anesthetic induction. Anesthesiology. 2011;114(5):1200–1210. doi:10.1097/ALN.0b013e3182172cd3
- 5.↑
Freeman BS, Berger JS. Bronchospasm. In: Freeman BS, Berger JS, eds. Anesthesiology Core Review. Part Two: Clinical Sciences. 2nd ed. McGraw-Hill Education; 2024. Accessed April 8, 2025. https://accessanesthesiology.mhmedical.com/content.aspx?bookid=3399§ionid=282996527
- 6.↑
Wu RS, Wu KC, Sum DC, Bishop MJ. Comparative effects of thiopentone and propofol on respiratory resistance after tracheal intubation. Br J Anaesth. 1996;77(6):735–738. doi:10.1093/bja/77.6.735
- 7.↑
Conti G, Dell’Utri D, Vilardi V, et al. Propofol induces bronchodilation in mechanically ventilated chronic obstructive pulmonary disease (COPD) patients. Acta Anaesthesiol Scand. 1993;37(1):105–109. doi:10.1111/j.1399-6576.1993.tb03609.x
- 8.↑
Hirota K, Sato T, Hashimoto Y, et al. Relaxant effect of propofol on the airway in dogs. Br J Anaesth. 1999;83(2):292–295. doi:10.1093/bja/83.2.292
- 9.↑
Brown RH, Greenberg RS, Wagner EM. Efficacy of propofol to prevent bronchoconstriction: effects of preservative. Anesthesiology. 2001;94(5):851–855. doi:10.1097/00000542-200105000-00024
- 10.↑
Gleason NR, Gallos G, Zhang Y, Emala CW. Propofol preferentially relaxes neurokinin receptor-2-induced airway smooth muscle contraction in guinea pig trachea. Anesthesiology. 2010;112(6):1335–1344. doi:10.1097/ALN.0b013e3181d3d7f6
- 11.↑
Mirabile VS, Shebl E, Sankari A, Burns B. Respiratory failure in adults. In: StatPearls. StatPearls Publishing; 2026.
- 13.↑
Deflandre CJ, Hellebrekers LJ. Clinical evaluation of the Surgivet V60046, a non invasive blood pressure monitor in anaesthetized dogs. Vet Anaesth Analg. 2008;35(1):13–21. doi:10.1111/j.1467-2995.2007.00346.x
- 14.↑
Garofalo NA, Teixeira Neto FJT, Alvaides RK, de Oliveira FA, Pignaton W, Pinheiro RT. Agreement between direct, oscillometric and Doppler ultrasound blood pressures using three different cuff positions in anesthetized dogs. Vet Anaesth Analg. 2012;39(4):324–334. doi:10.1111/j.1467-2995.2012.00711.x
- 15.↑
Strugess DJ, Watts RP. Hemodynamic monitoring. In: Oh TE, ed. Oh’s Intensive Care Manual. 3rd ed. Elsevier; 2019:135–136.
- 16.↑
Balakrishnan A, King LG. Updates on pulmonary function testing in small animals. Vet Clin North Am Small Anim Pract. 2014;44(1):1–18. doi:10.1016/j.cvsm.2013.08.007
- 17.↑
Asorey I, Pellegrini L, Canfrán S, Ortiz-Díez G, Aguado D. Factors affecting respiratory system compliance in anaesthetised mechanically ventilated healthy dogs: a retrospective study. J Small Anim Pract. 2020;61(10):617–623. doi:10.1111/jsap.13194
- 19.↑
Wayman M, Errington D. Respiration: gas transfer. Anaesth Intensive Care Med. 2011;12(11):481–484. doi:10.1016/j.mpaic.2011.08.008
- 20.↑
Summers C, Todd RS, Vercruysse GA, Moore FA. Acute respiratory failure. In: Newman MF, Fleisher LA, Kahn CR, eds. Perioperative Medicine. Elsevier; 2022:576–586. doi:10.1016/B978-0-323-56724-4.00039-3
- 21.↑
Ray K, Bodenham A, Paramasivam E. Pulmonary atelectasis in anaesthesia and critical care. Contin Educ Anaesth Crit Care Pain. 2014;14(5):236–245. doi:10.1093/bjaceaccp/mkt064
- 22.↑
Pandya CM, Hardin KA. Sleep loss associated with medical conditions and diseases. In: Kushida CA, ed. Encyclopedia of Sleep. Vol 1. Academic Press; 2013:281–286. doi:10.1016/B978-0-12-378610-4.00058-9
- 23.↑
Cooper ES, Schober KE, Drost WT. Severe bronchoconstriction after bronchoalveolar lavage in a dog with eosinophilic airway disease. J Am Vet Med Assoc. 2005;227(8):1257–1262. doi:10.2460/javma.2005.227.1257
- 24.↑
Slutsky AS. Ventilator-induced lung injury: from barotraumas to biotrauma. Respir Care. 2005;50(5):646–659.
- 25.↑
Wang RL, Xu K, Yu KL, Tang X, Xie H. Effects of dynamic ventilatory factors on ventilator-induced lung injury in acute respiratory distress syndrome dogs. World J Emerg Med. 2012;3(4):287–293. doi:10.5847/wjem.j.issn.1920-8642.2012.04.009
- 26.↑
Gavel G, Robert WMW. Laryngospasm in anaesthesia. Contin Educ Anaesth Crit Care Pain. 2014;14(2):47–51. doi:10.1093/bjaceaccp/mkt031
- 27.↑
Hall LW, Chambers JP. A clinical trial of propofol infusion anaesthesia in dogs. J Small Anim Pract. 1987;28(7):623–627. doi:10.1111/j.1748-5827.1987.tb01277.x
- 28.↑
Nolan A, Reid J. Pharmacokinetics of propofol administered by infusion in dogs undergoing surgery. Br J Anaesth. 1993;70(5):546–551. doi:10.1093/bja/70.5.546
