Anesthetic Case Management of a Canine Patient With Severe Subaortic Stenosis Using Dexmedetomidine

Subaortic stenosis (SAS) is one of the most common congenital cardiac diseases in dogs; overall estimated prevalence is 0.3% in the general population and approximately 5% in dogs with cardiac disease.¹ Commonly affected breeds include bullmastiffs, Bouvier des Flandres, Dogues de Bordeaux, golden retrievers, Newfoundlands, and Rottweilers.²

In patients with SAS, fibromuscular cartilage causes a partial left ventricular outflow tract obstruction below the aortic valve.¹ That impedance decreases cardiac output and can lead to a host of negative sequelae, including exercise intolerance, syncope, arrhythmias, congestive heart failure, and sudden death.

Prognosis for patients with SAS depends on the severity of the disease. Dogs with severe SAS have an average lifespan of 19 months, which may improve if β-blocker therapy (e.g., atenolol, carvedilol) is initiated.¹ β-Blocker therapy is aimed at reducing heart rate and decreasing myocardial oxygen demands.

Signalment, History, and Presentation

An 11-month-old intact male Staffordshire bull terrier crossbreed was presented to a private veterinary referral center for surgical consultation. A review of the patient’s medical record revealed a previous diagnosis of severe SAS. Echocardiography performed 7 days previously showed a heart rate of 200 beats per minute (bpm), normal sinus rhythm, normal and synchronous pulse strength, and pressure gradient of 196 mm Hg (blood pressure was not noted). After echocardiography, carvedilol, a β-blocker, was prescribed (0.5 mg/kg PO q12h). The patient was not being given any other medications, and the patient had never been anesthetized. No other clinical symptoms, diseases, or comorbidities were noted in the record.

Initial Assessment

The patient was bright, alert, and responsive with the following vital signs: heart rate, 132 bpm; respiratory rate, 24 breaths per minute; temperature, 38.4 °C (101.2 °F); pink mucous membranes; capillary refill time, < 2 seconds; body weight, 23 kg (50.7 lb); and body condition score, 5/9. Physical examination revealed a grade 4/6 systolic left apical heart murmur and a ring of prolapsed urethral mucosa at the tip of the glans penis.

After consultation, the client elected to pursue surgical castration and urethral prolapse correction. Surgery was scheduled for the following week, and presurgery pharmaceuticals were dispensed to the owner.

Patient Management

Anesthesia/Analgesia

The owners administered maropitant (2 mg/kg PO), gabapentin (10 mg/kg PO), trazodone (5 mg/kg PO), and carvedilol (0.5 mg/kg PO) the morning of the surgery. Upon arrival at the veterinary clinic, the patient’s mentation was noted to be quiet, alert, and responsive. Preoperative vital signs were collected (TABLE 1) and blood work was performed; no abnormalities were identified.

The patient was premedicated with butorphanol (0.3 mg/kg IM) and dexmedetomidine (2 µg/kg IM). Within 15 minutes, the patient was laterally recumbent in its kennel. The patient was placed on a padded gurney and transported to the surgery department. A 20-gauge catheter was placed in the right cephalic vein. During catheter placement, peripheral oxygen saturation (Spo₂), oscillometric noninvasive blood pressure (NIBP), and electrocardiography were monitored. During this time, the patient received flow-by oxygen supplementation (3 L/min for 10 minutes via facemask). The patient’s eyes were lubricated to prevent corneal drying and ulceration.

General anesthesia was induced by slowly administering lidocaine (1 mg/kg IV) followed by a titration of propofol (1.4 mg/kg IV). Endotracheal intubation was performed with a 7-mm endotracheal tube; correct tube placement was verified using direct visualization and capnography. General anesthesia was maintained by isoflurane (initial vaporizer setting of 1.5%) in 100% oxygen via an adult rebreathing circuit with a 2-L reservoir bag. An initial oxygen flow rate of 2 L/min (87 mL/kg/min) was used to rapidly achieve appropriate anesthesia depth. The patient was rotated to dorsal recumbency. After surgical preparation, a testicular block with lidocaine (1 mg/kg per testicle) was performed.

The patient was transported to the operating room. Fluid therapy was initiated using lactated Ringer’s solution (3 mL/kg/hr IV). Hydromorphone (0.05 mg/kg IV) was administered for primary systemic analgesia. An additional dose of lidocaine (1 mg/kg IV) was slowly administered for adjunct analgesia.

Surgery

The initial surgical incision was made, and anesthetic depth was deemed appropriate based on cranial reflex assessment (absence of palpebral blink, loose jaw tone, and ventromedial eye position). Due to the absence of observed nociception and use of a multimodal analgesia plan, the isoflurane vaporizer setting was reduced to 1% and oxygen flow rate was reduced to 0.5 L/min (22 mL/kg/min) for the remainder of surgery. No instances of tachycardia, bradycardia, hypertension, hypotension, hypoxia, or cardiac arrhythmias were observed during the perioperative period. Surgical castration and correction of urethral prolapse were performed without complication. The total anesthesia time was 46 minutes.

Recovery and Outcome

After discontinuation of inhalant anesthesia, the patient was transported to a recovery ward and placed in sternal recumbency with pulse oximetry, NIBP, and electrocardiography monitoring. Carprofen (4 mg/kg SC) was administered, and a cold pack was applied to the incision for 20 minutes. Fluid therapy was discontinued (total volume infused, 42 mL). The patient was extubated 25 minutes after isoflurane discontinuation without complication. Postoperative vital signs were taken every hour for the next 3 hours; no abnormal parameters were observed.

The patient was discharged from the hospital 5 hours after extubation without complication. Postoperative at-home care instructions included gabapentin (10 mg/kg PO q8h), trazodone (5 mg/kg PO q8h), carprofen (2.2 mg/kg PO q12h starting 24 hours after subcutaneous injection), cold packs on incision every 6 hours, and carvedilol (0.5 mg/kg PO q12h).

Discussion

Anesthetic management of patients with SAS can be challenging. Primary anesthesia goals include decreasing myocardial work (i.e., avoiding tachycardia, minimizing perioperative stress, maintaining normal sinus rhythm), minimizing vasodilation and hypotension, maintaining preload, and maintaining systemic vascular resistance.³ Unfortunately, these goals can be difficult to achieve given current anesthetic and analgesic options. For example, ketamine and anticholinergics should be used with caution given their effects of increasing heart rate and myocardial oxygen demands. The lowest effective dose of injectable and inhalant anesthetics should be used to minimize their vasodilatory and negative inotropic effects. Acepromazine should be used with caution due to its vasodilating effect. Benzodiazepines have minimal effect on the cardiovascular system,⁴ but their efficacy as a sedative in young otherwise healthy animals is poor.^5,6

Dexmedetomidine is a reversible α₂ agonist that provides reliable sedation, anxiolysis, visceral and somatic analgesia, and significant minimum alveolar concentration reduction. The drug can have profound cardiovascular effects, including vasoconstriction, reflexive bradycardia, and decreased cardiac output. Those effects have led to a general mistrust and avoidance of dexmedetomidine in small animal patients with cardiac disease. However, given the anesthetic goals of SAS management along with the lack of viable alternatives, dexmedetomidine may be an ideal anesthetic/analgesic for this specific patient population. The potential advantages of dexmedetomidine administration include decreased heart rate, decreased myocardial work, and decreased oxygen demands in addition to increased systemic vascular resistance and increased cardiac preload. The potential disadvantages of dexmedetomidine administration include decreased cardiac output and increased cardiac afterload. However, an increase in afterload may not be clinically significant because SAS creates a relatively fixed increase in afterload.³

This theoretical and pharmacological argument is bolstered by the field of human anesthesiology. Dexmedetomidine is commonly used in humans with cardiac disease,^7-12 including those undergoing transcatheter aortic valve implantation.^13,14 Moreover, the notion of utilizing dexmedetomidine in patients with cardiac disease is not completely foreign to veterinary medicine. For example, dexmedetomidine has been successfully used in patients with pulmonic stenosis undergoing balloon valvuloplasty,¹⁵ and medetomidine has been successfully used in cats with dynamic left ventricular outflow tract obstruction secondary to hypertrophic cardiomyopathy.¹⁶

Further studies, especially those utilizing advanced cardiovascular monitoring equipment (e.g., invasive blood pressure, echocardiography, direct cardiac output), are needed to fully evaluate the efficacy and safety of this drug in veterinary patients with SAS.

Summary

The use of dexmedetomidine in this patient may strike many readers as odd or even medically inappropriate. There is widespread mistrust of this drug throughout veterinary medicine, especially when cardiac disease is present. However, the author believes many of these fears are unfounded or exaggerated.

The objective of this case report is to suggest that low doses of dexmedetomidine can, and maybe should, be used in patients with SAS. The effects of dexmedetomidine complement the anesthetic goals for SAS patients. Although there is substantial literature on this subject in human medicine, research in the veterinary community is scant. The author hopes this article will begin a conversation about the safe and efficacious use of dexmedetomidine in novel situations such as SAS.