VETgirl October 2024 Beat e-Magazine

The VETgirl Beat is a quarterly publication available to all subscribed members of VETgirl. The digital newsletter features highlighted webinars (small animal, large animal, veterinary technician, leadership), tech tips, provider spotlights, and recent happenings.

QUARTERLY BEAT / OCTOBER 2024 ISSUE 22 • OCTOBER 2024 BEAT

EMAGAZINE

MATTERS OF THE HEART

TECH TIPS

TO PEE OR NOT TO PEE?

20 MIND MASSAGE RECAP

WHAT'S ON THE CALENDAR? 35

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beat ISSUE 20 • APRIL 2024 TABLE OF CONTENTS

04 WEBINAR HIGHLIGHTS: TO PEE OR NOT TO PEE? THAT IS THE QUESTION:

14 WEBINAR HIGHLIGHTS:

22 TECH TIPS

NO, IT'S NOT HEART FAILURE: A THORACIC RADIOGRAPHIC CASE SERIES

WHEN AND HOW TO MAKE A URETHROSTOMY IN MALE DOGS AND CATS

WEBINAR HIGHLIGHTS: AUTHENTIC WELLBEING: IT’S [NOT] WHAT’S TRENDING 18

06 WEBINAR HIGHLIGHTS: CANINE NOISE PHOBIA AND THE ANXIETY PATIENT

24 TEAM SPOTLIGHT

08 BLOG HIGHLIGHTS: RATE AND RHYTHM DURING ANESTHESIA

20 MIND MASSAGE

26 WHAT'S ON

THE CALENDAR

MATTERS OF THE HEART: IMPORTANCE OF HEART

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Other complications include reobstruction without stricture due to larger stones, bleeding from the surgery site, and increased risk of UTIs. A less common but potentially serious complication occurs when urine tracks subcutaneously, resulting in inflammation or even large areas of sloughed skin. P ost - op care It is CRITICAL that cats not lick at the urethrostomy site so an e-collar is mandatory for two weeks post-op. I prefer non-clumping litter so that it doesn’t clump on the surgery site. Owners can gently dab the surgery site but should not aggressively clean for fear of disrupting the mucosal healing. I usually get the cats back in two weeks post-op, examine the site, and pass an 8 fr red rubber tube (can almost always be done without sedation) to make sure stoma is adequate size. C at urethrostomies when a PU has failed or is not adequate : T ranspelvic and antepubic urethrostomies If a urethrostomy strictures, the first option is to move further cranially in the urethra to make a new PU. This is much easier if the PU was not adequately cranial the first time! If moving further cranially in the urethra is not possible then we go to a plan B. Two other urethrostomies can be considered, both performed with the cat in dorsal recumbency. My preference is a transpelvic urethrostomy. For this procedure, the urethra is tracked caudally to the caudal ischium. A 1-2 cm long x 5-8 mm wide rectangle of ischium is removed using rongeurs to localize the intrapelvic urethra. A longitudinal incision is made into the ventral aspect of this portion of the urethra (a catheter pass from a cystotomy can assist with locating this) and the urethrostomy is performed similar to a PU using both similar suture and suture pattern to make a stoma in the intra pelvic urethra. The second option, an antepubic or prepubic urethrostomy is performed by transecting the urethra as far caudally as possible from an abdominal approach. The urethra is then brought through a paramedian incision in the abdominal body wall. The end of the urethra is spatulated and a stoma is created to the ventral abdominal skin. C omplications and post - op care Both of these salvage options are technically challenging and have higher complication rates than a PU. The antepubic urethrostomy particularly has a high risk of peristomal dermatitis and stricture. The antepubic also has a high rate of recurrent UTIs and urinary incontinence due to the shorter length of the urethra and potential damage to the nervous plexus supplying it. The transpelvic has lower risk of incontinence but still risk for peristomal dermatitis and stricture as well at UTI. Owners need to be counseled carefully when these options are selected.

FELINE PERINEAL URETHROSTOMY I ndications Most common indication is repeated urethral obstructions. May also be indicated in cats that cannot be unblocked or for caudal urethral tears. S urgical technique Position can be either sternal with legs hanging over the table or dorsal (allowing for concurrent cystotomy or conversion to transpubic or antepubic urethrostomy). Pass a tomcat or other catheter into the urethra if possible. Incise the skin around the prepuce and scrotum and continue the dissection cranially to the level of the ischium. Transect the ischiocavernosus muscles from the ischium using bipolar cautery or sharp dissection. Sever the attachments of the penile tissue to the floor of the ischium sharply to allow the penis to be mobilized dorsally and caudally. It is helpful to clamp a hemostat or Allis tissue forceps to the penis and prepuce to maintain orientation and allow easier tissue manipulation during the dissection. Resect the retractor penis muscle off of the penis back to a level cranial to the bulbourethral glands. Make a longitudinal incision near the caudal end of the penile urethra over the tomcat catheter and back the catheter out slowly until the tip exits through this defect. Introduce a second tomcat catheter into the cranial portion of the urethra and the bladder. Use an 11-blade vertically to make a longitudinal incision in the urethra. The author finds that this is most easily done without jagged stops and starts by holding the blade vertically resting on the dorsal portion of the tomcat catheter. As the tomcat catheter is pushed cranially along the urethra, use the 11-blade to make a smooth cut in the dorsal urethra. Continue this cut to a level cranial to the bulbourethral glands. At this level the urethra should accommodate the thick part of a tomcat catheter or a mosquito hemostat to the boxlocks (hinge). Construct the stoma by placing 5 or 7 simple interrupted sutures around the dorsum of the skin incision and cranial urethral incisions. It is critical to suture the urethral mucosa to the skin. The author likes to use 4-0 or 5-0 Monocryl for the sutures, which are left to absorb, however, some surgeons prefer non-absorbable, which are eventually removed. Following construction of the dorsal stroma, the “drainboard” of the remaining urethral mucosa is constructed using the same suture in a simple continuous pattern down each side. Once 1-2 cm of drainboard has been completed, the remaining penis is amputated, and remaining skin defect is closed. The bladder should be flushed thoroughly with sterile saline post-op and express the bladder to make sure the cat has a good urine stream. C omplications and surgical errors Stricture is the most common and devastating complication, typically due to one of the following: 1. Failure to suture mucosa to skin; 2. Failure to dissect cranial to the bulbourethral glands where the urethra is wider; or 3. Cats grooming the site prior to healing. These patients must have an e-collar during recovery.

TO PEE OR NOT TO PEE? THAT IS THE QUESTION: WHEN AND HOW TO MAKE A URETHROSTOMY IN MALE DOGS AND CATS

DR. CHRIS RALPHS DACVS Ocean State Veterinary Specialists

In this VETgirl Webinar To Pee or Not to Pee? That is the Question: When and How to Make a Urethrostomy in Male Dogs and Cats on June 12, 2024, Dr. Chris Ralphs, DACVS reviews all you need to know about becoming a derm rockstar! In case you missed the webinar, watch it again HERE or read the cliff notes below!

side to avoid excessive bleeding and to be centered on the urethra to maintain mucosa on each side for closure. The penile mucosa is then sutured to the skin on either side of the incision to form the stoma using 4-0 or 5-0 absorbable monofilament such as Monocryl in a simple interrupted or simple continuous pattern. The author prefers 5 simple interrupted sutures at the caudal edge closest to the bladder and then simple continuous down each side. These sutures are typically left to be absorbed. Pass a catheter from the stoma to the bladder to ensure patency and then close any remaining skin defects. C omplications and surgical errors Strictures are gratifyingly uncommon in this surgery. However, hemorrhage is very common and annoying. Make sure owners are aware that there will likely be bleeding from the site for a week or more. If bleeding continues past two weeks it may require a revision. If too much scrotal skin is left, there can be irritation of the skin. Some dogs may urinate on their legs and are more prone to UTIs. P ost - op care E-collar for two weeks. Owners should gently dab, not scrub, at the surgery site if cleaning is needed.

MALE CANINE URETHROSTOMY I ndications Canine urethrostomy is performed less commonly than feline and can be performed for several reasons including stricture, persistent stone formation (e.g., dalmatians and bichon frise), trauma, or neoplasia. L ocation The most common location to perform a urethrostomy is scrotal because the urethra is wide and superficial at this level. It can also be performed prescrotal, if the dog is not to be neutered, or perineal, although the urethra is deeper and more vascular at the perineal location so this is less common. T echnique An ellipse of scrotal skin is excised over the urethra to avoid urine scald. The retractor penis muscle and other subcutaneous adventitia is moved off to the side of the urethra at this site. An 8-10 fr red rubber catheter can be passed to aid in identification and safe incision into the urethra. A 2 to 4 cm longitudinal incision is made on the ventral surface of the urethra caudal to the os penis. Care is taken to not incise into the tunica on either

WEBINAR HIGHLIGHTS

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Pheromones play a significant role in canine communication and can provide comfort and security. Products like ThunderEase® diffusers and collars have been used successfully to help dogs adapt to stressful situations. Pheromones are species-specific semiochemicals that trigger innate, subconscious responses and are not the same as olfactory cues. They are a critical part of non-pharmaceutical intervention strategies and can significantly improve clinical outcomes. In conclusion, managing canine noise phobia and anxiety requires a comprehensive approach involving environmental management, behavioral therapy, and medication. Effective intervention can enhance the quality of life for both dogs and their owners, making it essential to understand and apply these multifaceted strategies.

Desensitization and counterconditioning are considered the gold standard for the management and treatment of canine noise phobia. This involves controlled exposure to noise below the stress response threshold and gradually increasing intensity, paired with positive reinforcement, as the threshold level and emotional response of the animal improves. Timing is critical to ensure the intervention is neither too soon nor too late to be effective. Medication options include maintenance or situational/event- specific drugs. Maintenance medications are better suited for frequent, unpredictable triggers and require weeks to months for onset, while situational drugs act quickly for predictable, infrequent triggers. Common medications include fluoxetine, paroxetine, sertraline, clomipramine, trazodone, clonidine, gabapentin, buspirone, amitriptyline, and benzodiazepines.

CANINE NOISE PHOBIA AND THE ANXIETY PATIENT

CHRISTOPHER PACHEL DVM, DACVB, CABC (IAABC) Animal Behavior Clinic Portland, OR, USA

WEBINAR HIGHLIGHTS

In this VETgirl webinar Canine Noise Phobia and the Anxiety Patient on June 20, 2024, Dr. Christopher Pachel, DACVB, CABC (IAABC) reviews canine noise phobia and the anxious patient. Learn about the most comprehensive approach to enhancing the quality of life for your patients and their owners! In case you missed the webinar, watch it again HERE or read the cliff notes below!

while passive coping involves autonomic inhibition and increased neuroendocrine responses when the threat is inescapable. Individual differences in learning history and experiences, socialization, and stimulus exposure context can significantly influence the development of these and other coping strategy variations. Medical conditions such as endocrine disorders, pain, gastrointestinal dysfunction, pruritic conditions, sensory loss, age-related dementia, and seizure disorders can contribute to anxiety and phobia. A recent study identified a connection between pain and noise phobia, especially in situations in which the onset of noise aversion occurs later in life and with a generalized anxiety component. Thus, a comprehensive assessment is essential to identify underlying medical issues to ensure appropriate treatment of contributing conditions. Intervention strategies involve identifying the stimulus or context and avoiding uncontrolled exposure. Controlled exposure should be set up to create positive associations, and aversives (e.g., unpleasant stimuli) should be avoided in favor of humane approaches. Medication or supplements may be used if necessary. Avoidance strategies include providing access to secure, comfortable locations and using acoustic strategies like white noise, loud music, or calming music. Product options like ThunderShirts®, Happy Hoodies®, and iCalmPet TM music can be beneficial.

Canine noise phobia and anxiety are prevalent behavioral disorders that significantly impact the quality of life of affected dogs and their owners. Fear, as defined in this context, is a distressing emotional response to a perceived threat that is identifiable and shaped by individual experiences, serving as an adaptive response essential for survival. However, phobias, specifically noise phobias, represent non-adaptive, excessive fears towards specific stimuli such as fireworks, thunderstorms, and gunshots. These phobias often generalize to predictive cues, leading to anxiety characterized by an apprehensive anticipation of a threat. Anxiety is more likely to be experienced by the animal in situations in which the perceived threat occurs unpredictably or when the animal doesn’t have the opportunity to avoid or control their exposure. Understanding the continuum from normal to pathological responses is crucial. Natural adaptive responses can become pathological when they interfere with an animal's coping abilities, leading to altered body functions, disrupted sleep patterns, and abnormal gastrointestinal functions. The severity, intensity, and duration of these responses can vary from acute to chronic stress, significantly impacting the immune system and contributing to the compromised welfare of an affected animal. Coping strategies in dogs can be categorized into active and passive responses. Active coping involves sympathetic activation and is utilized when escape is perceived as possible,

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HOW DOES THE HEART RATE AFFECT PERFUSION?

pressure is measured to aid in the assessment of patient well- being. When heart rate increases excessively, stroke volume is compromised resulting in decreased cardiac output and potentially low blood pressure. Inversely, low heart rates may decrease cardiac output resulting in low blood pressure when there is reduced systemic vascular resistance.

Heart rate is just one variable that influences the adequacy of cardiovascular circulation (Figure 1). A common reference range for canine heart rates is 60 – 160 beats per minute; however, this wide range of heart rates fails to ensure adequate perfusion across all canine patients in various clinical situations. 1 The heart rate and rhythm in tandem influence optimal stroke volume and cardiac output. Coupled with systemic vascular resistance, blood

MATTERS OF THE HEART: IMPORTANCE OF HEART RATE AND RHYTHM DURING ANESTHESIA

FIGURE 1. CARDIOVASCULAR CIRCULATION

AMANDA M. SHELBY RVT, VTS (Anesthesia & Analgesia)

Ever wonder why ALL your patients under sedation and anesthesia should have an ECG on (plus a pulse oximeter and blood pressure monitoring to boot!)? Read why in this VETgirl blog , where our newest VETgirl team member Amanda M. Shelby , RVT, VTS (Anesthesia & Analgesia) reviews the importance of heart rate and rhythm monitoring in our veterinary patients. Whether you’re a small animal or large animal veterinarian or veterinary technician, you’ll want to read more to learn about the importance of heart rate’s effect on cardiac output!

The body is a complex network of systems working in tandem to optimize survival. In sedated or anesthetized patients, monitoring of the cardiopulmonary systems is paramount. The pulmonary system functions optimally to provide ventilation (i.e., elimination of carbon dioxide) and oxygenation (i.e., oxygen saturation of blood) while the cardiovascular system provides circulation—movement of blood through the body. Working optimally, the cardiopulmonary systems provide perfusion,

the delivery of oxygen to tissues. Perfusion is challenging to directly measure in clinical settings. Subjectively, capillary refill time and mucous membrane color provide indications of perfusion and oxygenation. Objective methods of monitoring oxygenation, ventilation and circulation are provided in Table 1. Regardless, ensuring adequate perfusion to the tissues is a primary goal of patient monitoring and assessment, in conscious or unconscious patients.

Figure 1. Cardiovascular Circulation; Figure Courtesy of Amanda M. Shelby, RVT, VTS (Anesthesia & Analgesia)

DOES NORMAL BLOOD PRESSURE EQUAL ADEQUATE PERFUSION?

TABLE 1. MONITORING METHODSª

a compensatory increase in heart rate can also produce a state of low blood pressure and reduced perfusion. However, some reduction in systemic vascular resistance could increase blood flow to tissues, increasing perfusion. Blood pressure is often viewed as a quantitative variable, obtainable in clinical situations. However, given the many variables identified in Figure 1 that influence blood pressure, a qualitative approach using the data collected from the whole patient assessment requires interpretation by a dedicated, trained anesthetist to make conclusions on perfusion.

The assumption commonly made is that patients with normal blood pressure (i.e., systolic arterial pressure [SAP] over 90- 160 mmHg, mean arterial pressure [MAP] over 60-80 mmHg) have adequate perfusion. 1 Adequate blood pressure does not always ensure adequate perfusion. In states of excessive vasoconstriction, an increase in systemic vascular resistance occurs and low SpO2 values from the pulse oximeter are common. This demonstrates vasoconstriction could result in decreased perfusion. Conversely, excessive vasodilation resulting in decreased afterload, reduced stroke volume without

OXYGENATION

VENTILATION

CIRCULATION

INVASIVE NON-INVASIVE INVASIVE NON-INVASIVE INVASIVE

NON-INVASIVE

· Arterial blood · Gas

· MMC · Pulse

· Arterial or venous · Blood gas

· Capnography · RR & effort

· Direct arterial · Blood pressure · CO monitoring · CVP

· Non-invasive blood pressure · Oscillometric device · Doppler/Cuff/Sphygmomanometer · HR & Rhythm (ECG)

oximetry · RR & effort

· PR & Palpation · Capnography · CRT a MMC = mucous membrane color; RR = respiratory rate; CO = cardiac output; CVP = central venous pressure; HR = heart rate; ECG = electrocardiogram; PR = pulse rate; CRT = capillary refill time Table 1. Monitoring Methods; Table Courtesy of Amanda Shelby, RVT, VTS (Anesthesia & Analgesia)

KEY CONCEPT: BLOOD PRESSURE ≠ PERFUSION

BLOG HIGHLIGHTS

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EFFECT OF HEART RATE & RHYTHM ON BLOOD PRESSURE The heart is a smart organ. Baroreceptors present in the heart respond to changes in variables within the Figure 1 equation. For example, in states of hypotension resulting from hypovolemia (i.e., reduced afterload and preload), the heart rate increases to increase cardiac output and maintain blood pressure—think about patients in hypovolemic shock. The heart’s electrical rhythm influences its mechanical function. Arrhythmias are disruptions in the electrical pathway with or without heart rate abnormality. During arrhythmias patients are at increased risk for reduced cardiac contractility, cardiac output, blood pressure, and potential perfusion. As the heart rate increases, the phase of diastole is minimized. When diastole is shortened, perfusion to the myocardium, ventricular filling, and resulting stroke volume during systole are reduced. This decreased cardiac output because of tachycardia (high heart rates), with or without a tachyarrhythmia, contributes to hypotension and potentially poor perfusion. Similarly, bradycardia (low heart rates), with or without bradyarrhythmias, can also result in decreased cardiac output and blood pressure. Figure 2 demonstrates the relationship of bradyarrhythmia impact on blood pressure in a cat.

HEART RATE & ANESTHETIC DRUGS Most drugs used in the peri-anesthetic period have a dose- dependent effect on heart rate. Table 2 details common peri-anesthetic drugs and their effect on cardiovascular variables seen in Figure 1. As heart rate increases so does myocardial oxygen consumption, along with the incidence of tachyarrhythmias. Extreme increases in heart rate decrease ventricular filling time and stroke volume resulting in decreased cardiac output and blood pressure. Figure 3 is a video that shows a patient in a tachyarrhythmia with resulting pulse pressure variance on the arterial waveform and plethysmograph. Although not hypotensive, stroke volume for some of the cardiac contractions is compromised. Anticholinergics increase heart rate and as a result, increase cardiac output and blood pressure. Conversely, most opioids cause bradycardia. When bradycardia is excessive, cardiac output decreases resulting in reduced blood pressure. Buprenorphine, a partial mu opioid agonist, does not have profound cardiovascular effects at clinical doses. Alpha2 adrenergic agonists cause a reduction in heart rate as a reflex response to an increase in systemic vascular resistance, vasoconstriction. While blood pressure increases due to vasoconstriction, perfusion often decreases. When alpha2 adrenergic agonists are used as premedication agent prior to halogenated inhalants, which cause a decrease in contractility and vasodilation, and opioids, which augment bradycardia, this results in a reduced cardiac output and hypotension. Acepromazine causes a reduction in systemic vascular resistance and a resulting decrease in blood pressure with a potential increase in perfusion. In combination with other peri-anesthetic drugs, hypotension could result. The important concept to recognize is that blood pressure and perfusion do not have a linear relationship. WHAT IS THE ‘IDEAL’ HEART RATE UNDER ANESTHESIA? The ideal heart rate under anesthesia for dogs and cats is a heart rate that maintains blood pressure and optimizes tissue perfusion. The author prefers to perform a pre-anesthetic assessment of each patient to identify the patient’s specific resting heart rate and blood pressure prior to the administration of any peri-anesthetics, when possible, to maintain a heart rate within 20-30% of the patient’s specific resting heart rate. With the use of alpha2 adrenergic agonists, this general guideline often requires allowances for heart rates lower than 20-30% less than the patient’s specific resting heart rate. When this occurs, blood pressure is used to assist the anesthetist in

TABLE 2: COMMON PERI-ANESTHETIC DRUGS USE IN CATS AND DOGS ON CARDIOVASCULAR PARAMETERS (2)

EFFECT ON CARDIOVASCULAR PARAMETERS*

PERI-ANESTHETIC DRUG CLASSIFICATION

PERI-ANESTHETIC

CONTRACTILITY

SVR

Atropine/glycopyrrolate

Anticholinergic

NC**

/NC

Morphine, hydromorphone, methadone, fentanyl

Full agonist opioid

Butorphanol 3

Opioid agonist (kappa)/ antagonist(mu)

/NC

Acepromazine 4

Phenothiazine

Dexmedetomidine/ medetomidine/xylazine 5

Alpha2 agonist

/NC

Propofol 6

Non-barbiturate sedative/ hypnotic

/NC /NC

Aflaxalone 7-9

Neurosteroid, non- barbiturate sedative/ hypnotic

Ukn***

Ketamine

Dissociative agent

Midazolam/diazepam

Benzodiazepine

Etomidate 9

Imidazole derivative, non-barbiturate sedative/ hypnotic

/NC /NC

/NC

Isoflurane/sevoflurane

Halogenated inhalants

*A drug effect on cardiovascular parameters is often dose dependent where higher doses generally produce more significant change; NC** = no change; Ukn*** = unknown Table 2. Common Peri-Anesthetic Drugs Use in Cats and Dogs on Cardiovascular Parameters. Table courtesy of Amanda M. Shelby, RVT, VTS (Anesthesia & Analgesia)

determining if the heart rate requires a treatment response. If a patient experiences hypotension with a low heart rate, an anticholinergic may be used to increase heart rate and cardiac output resulting in improved blood pressure. Conversely, when bradycardia is associated with hypertension because of administration of an alpha2 adrenergic agonist, treatment is often not warranted. When tachycardia with hypotension under anesthesia is experienced, identifying the contributing cause of hypotension is prioritized. Rarely does the tachycardia require direct treatment with a beta blocker or calcium channel blocker.

Regardless of brady- or tachycardia, electrocardiographic (ECG) evaluation should be performed. Heart rates with accompanying dysrhythmias often have a negative impact on cardiac output, blood pressure, and perfusion. With arrhythmias, priority is given to identification of the arrhythmia, resolving the underlying cause, and returning to normal electrical rhythm and rate.

Figure 2. Impact of Bradyarrhythmia on Blood Pressure; Photo courtesy of Amanda M. Shelby, RVT, VTS (Anesthesia & Analgesia)

BLOG HIGHLIGHTS

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anticholinergic may be used to increase heart rate and cardiac output resulting in improved blood pressure. Conversely, when bradycardia is associated with hypertension because of administration of an alpha2 adrenergic agonist, treatment is often not warranted. When tachycardia with hypotension under anesthesia is experienced, identifying the contributing cause of hypotension is prioritized. Rarely does the tachycardia require direct treatment with a beta blocker or calcium channel blocker. Regardless of brady- or tachycardia, electrocardiographic (ECG) evaluation should be performed. Heart rates with accompanying dysrhythmias often have a negative impact on cardiac output, blood pressure, and perfusion. With arrhythmias, priority is given to identification of the arrhythmia, resolving the underlying cause, and returning to normal electrical rhythm and rate. WHAT ABOUT CATS? Unlike dogs, domesticated cats are relatively similar in size and metabolic rate. This minimizes variation in accepted normal ranges. Slight variations in reference manuals exist but the normal heart rate in cats is 100-250 bpm.(1) Bradycardia in cats has been identified as heart rates under 100 bpm. (1) Tachycardias have been identified over 250 bpm.(1) While species variation in response to peri-anesthetic drugs do exist, target blood pressure values for cats are comparable to dogs. Like dogs, evaluating the whole patient prior to the administration of peri-anesthetics is ideal. While not always possible in cats, evaluating heart rate with blood pressure and tissue perfusion in the context of the patient’s physical examination history aides the veterinary professional in identification of heart rate and rhythm disturbances that could result in increased morbidity and mortality.

SUMMARY Heart rate is one of the measurable variables veterinary professionals can use to assess the cardiovascular system. In conjunction with arterial blood pressure and subjective means of evaluating perfusion (i.e., capillary refill time, mucous membrane color), ensuring a normal heart rate and rhythm helps ensure the cardiovascular system is working optimally. Additionally, in anesthetized patients using heart rate, rhythm, and blood pressure to evaluate circulation, along with the use of pulse oximetry to evaluate oxygenation and capnography to assist in the evaluation of ventilation, by a dedicated, trained veterinary professional can optimize patient outcomes.

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REFERENCES

1. Shelby AM, McKune CM. Small Animal Anesthesia Techniques. 2 ed. Hoboken, NJ: John Wiley & Sons, Inc.; 2023. 2. Muir W. Cardiovascular System. In: Tranquilli W, Thurmon J, Grimm K, editors. Lumb & Jones’ Veterinary Anesthesia and Analgesia. Ames, IA: Blackwell Publishing; 2007. p. 61-116. 3. Greene SA, Hartsfield SM, Tyner CL. Cardiovascular effects of butorphanol in halothane-anesthetized dogs. Am J Vet Res 1990;51(8):1276-9. 4. Farver TB, Haskins SC, Patz JD. Cardiopulmonary effects of acepromazine and of the subsequent administration of ketamine in the dog. Am J Vet Res 1986;47(3):631-5. 5. Pagel PS, Hettrick DA, Kersten JR, et al. Dexmedetomidine produces similar alterations in the determinants of left ventricular afterload in conscious dogs before and after the development of pacing-induced cardiomyopathy. Anesthesiology 1998;89(3):741- 8. 6. Henao-Guerrero N, Riccó CH. Comparison of the cardiorespiratory effects of a combination of ketamine and propofol, propofol alone, or a combination of ketamine and diazepam before and after induction of anesthesia in dogs sedated with acepromazine and oxymorphone. Am J Vet Res 2014;75(3):231-9. 7. Muir W, Lerche P, Wiese A, et al. Cardiorespiratory and anesthetic effects of clinical and supraclinical doses of alfaxalone in dogs. Vet Anaesth Analg 2008;35(6):451-62. 8. Muir W, Lerche P, Wiese A, et al. The cardiorespiratory and anesthetic effects of clinical and supraclinical doses of alfaxalone in cats. Veterinary Anaesthesia and Analgesia 2009;36(1):42-54. 9. Rodríguez JM, Muñoz-Rascón P, Navarrete-Calvo R, et al. Comparison of the cardiopulmonary parameters after induction of anaesthesia with alphaxalone or etomidate in dogs. Veterinary Anaesthesia and Analgesia 2012;39(4):357-65.

KEY CONCEPT: NORMAL HEART RATES IN DOGS AND CATS

100-250 BPM

60-160 BPM

Figure courtesy of Amanda M. Shelby, RVT, VTS (Anesthesia & Analgesia)

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WEBINAR HIGHLIGHTS

primary pulmonary diseases. Finally, a single dose of a diuretic can shrink pulmonary vessels in less than 30 minutes, which will mask this normally present and important clue in dogs. Unfortunately, cats love to be very different than dogs in many ways. First, cardiomegaly may only be mild in the face of fulminant L-CHF. When present, cardiomegaly is often generalized without appreciable chamber enlargement. A valentine-shaped cardiac silhouette is commonly seen on DV or VD radiographs and is most often caused by left atrial enlargement. 2 Second, the presence of enlarged pulmonary lobar veins is inconsistent in cats and further masked with a single dose of a diuretic. Third, pleural and pericardial effusion commonly occur with L-CHF in cats because their visceral pleura is drained by pulmonary veins. In the dog, pleural and pericardial effusion are primarily associated with right- sided CHF. Finally, cardiogenic pulmonary edema will sometimes increase pulmonary opacity only around the bronchi in cats, which creates a reticulonodular pattern, mimicking the appearance of a bronchial pulmonary pattern that occurs with inflammatory airway disease. Without cardiac or pulmonary lobar venous enlargement, the findings of a pulmonary pattern with or without pleural effusion are very nonspecific and caused by other etiologies such as neoplasia and infectious disease. PULMONARY HYPERTENSION The etiology and pathophysiology of pulmonary hypertension (PH) is well reviewed elsewhere. 3 However, it is worth noting that it is a common sequela to other causes of dyspnea. In dogs and cats, PH is most commonly caused by heartworm or other parasitic disease, L-CHF, or chronic airway disease. Thromboembolic disease, shunts, and idiopathic PH are uncommon causes. Although echocardiography is needed to definitively diagnosis PH, several radiographic features help differentiate this disease from L-CHF in dogs. Cardiomegaly is common, but typically right sided in nature. 4,5 Right ventricular enlargement causes increased width and sternal contact of the cardiac silhouette on lateral projections and rounding of the right side of the cardiac silhouette on the VD/DV. Many dogs will also have a bulge in the region of the main pulmonary artery, located around the 1-2 o’clock region (when imagining a clockface superimposed over the cardiac silhouette) on the VD/DV projection. Variably pulmonary lobar artery enlargement with or without tortuosity occurs, more commonly affecting the caudal vasculature. A recent study demonstrated that comparing the artery to its corresponding vein may be helpful to detect enlargement. 6 A caudal pulmonary lobar artery to vein ratio of 1.1 demonstrated 91% specificity and 31% sensitivity in predicting PH. In other words, seeing pulmonary lobar arterial enlargement supports the diagnosis of PH but its absence cannot rule out the disease. Pulmonary infiltrates are seen in approximately 2/3 of cases, most often as a patchy or diffuse unstructured interstitial or alveolar pulmonary pattern. Unfortunately, the appearance and distribution of pulmonary infiltrates with PH is identical to diseases such as L-CHF, non-

radiographs as they only evaluate the pleural space, heart, and surface of the lungs. 1 Large lesions or regions of abnormal lung can easily be missed by ultrasound due to the negative effects of reverberation artifact that results from gas within the pulmonary parenchyma. Additionally, thoracic radiographs provide a global view of the thorax, evaluating structures that may influence interpretation of cardiopulmonary or pleural space pathology. As a result, thoracic radiographs are essential and should be acquired when safe to do so. A complete thoracic radiographic study involves acquiring three projections: right lateral, left lateral, and either ventrodorsal (VD) or dorsoventral (DV) projections. A DV projection is likely safer in most patients with dyspnea as it maximizes ventilation. It also makes the caudal pulmonary lobar vessels easier to see. The only downside is that if pleural effusion is present, it is more likely to decrease visualization of the cardiac silhouette on a DV projection as compared to a VD. The author prefers to start with the DV (or VD) projection for all thoracic studies as it will decrease the odds of atelectasis from lateral recumbency causing increased opacity throughout the pulmonary parenchyma on lateral projections that could be confused with true disease. Finally, it is prudent to keep in mind that each lateral projection only evaluates the pulmonary parenchyma of the opposite side because of recumbent atelectasis. For example, when looking at a right lateral radiograph, only the left cranial and caudal lung lobes are evaluated. Beyond imaging, other routine diagnostics helpful during the initial work up of dyspneic patients include a complete blood count, a chemistry profile, urinalysis, retrovirus testing (for cats), and heartworm antigen/antibody testing. More advanced testing includes echocardiography, diagnostic thoracic ultrasound, and computed tomography with contrast.

NO, IT'S NOT HEART FAILURE: A THORACIC RADIOGRAPHIC CASE SERIES

MARC SEITZ Marc Seitz, DVM, DACVR, DABVP (Canine and Feline Practice) College of Veterinary Medicine, Department of Clinical Sciences Mississippi State University, Mississippi State, MS, USA

In this VETgirl webinar, No, it’s Not Heart Failure: A Thoracic Radiographic Case Series on August 21, 2024, Dr. Marc Seitz, MS, DACVR, DABVP (canine and feline) uses a case series to review the radiographic diagnosis of non-cardiogenic pulmonary edema, chronic lower airway disease, pulmonary hypertension, pulmonary thromboembolism, atypical appearing metastatic neoplasia, and pulmonary hemorrhage. Tune in HERE and learn what key radiographic findings can help you to get a diagnosis!

Dyspnea of any cause is a common reason dogs and cats present acutely unstable. While heart failure is common, it tends to get overdiagnosed in patients presented with dyspnea if the heart appears big and an abnormal pulmonary pattern is present. Unfortunately, many breeds of dog have a larger but still normal cardiac silhouette relative to their thoracic cavity and most causes of respiratory distress cause an abnormal pulmonary pattern. Imaging is a vital part of diagnosing the underlying cause of dyspnea. However, triaging and stabilizing patients is imperative before pursuing imaging studies as stress and non-sternal recumbency can alter ventilation, disrupting the delicate balance that comes with compensation for hypoxemia. This is especially true for pleural space disease and hypoventilation. All patients benefit from remaining in sternal recumbency and some form of oxygen therapy. Many patients benefit from a mild sedative (e.g., butorphanol) or an anxiolytic drug. If pleural space disease is present, thoracocentesis should be performed prior to radiographs as it will improve evaluation of the pulmonary parenchyma and make the study safer. Other stabilization therapies should be tailored to triage exam findings. For example, bronchodilators can be given to patients with suspected lower airway disease. A diuretic like furosemide can be given to patients with suspected heart failure. Furosemide can also function like a diagnostic test in that lack of radiographic improvement following diuretic therapy makes heat failure unlikely. A clinical response to furosemide is not

pathognomonic for heart failure as patients with airway disease will respond to the drug’s bronchodilatory effects.

POCUS AND THORACIC RADIOGRAPHS

LEFT SIDED CONGESTIVE HEART FAILURE

Thoracic point-of-care ultrasound (POCUS) is an imaging technique that can safely be performed after the initial triage exam and while patient stabilization is being performed. Thoracic POCUS is easily performed with the patient standing or in sternal recumbency. A detailed description of various techniques and interpretation is beyond the scope of this presentation and well-reviewed elsewhere (references below). However, POCUS is invaluable at rapidly diagnosing pleural effusion, pericardial effusion, and alveolar-interstitial disease. When combined with the history, signalment, and physical exam findings, results from a POCUS exam can help localize the cause of dyspnea as well as guide stabilization therapies and further diagnostics. Thoracic POCUS ultrasound findings can also be used to complement radiographic findings. Specific examples include confirming the presence of pleural effusion, guiding diagnostic or therapeutic thoracocentesis, and differentiating cardiogenic pulmonary edema secondary to left sided congestive heart failure (L-CHF) from lower airway disease. Although thoracic POCUS findings are rapid and quite useful, they are never a replacement for thoracic

Left sided congestive heart failure (L-CHF) is most commonly caused by mitral valve disease in small-breed dogs, dilated cardiomyopathy in large-breed dogs, and hypertrophic cardiomyopathy in cats. CHF is a clinical diagnosis that is made based on physical exam and radiographic findings. Echocardiography is rarely needed for the diagnosis. In dogs, the classic triad of findings includes left-sided cardiomegaly, pulmonary lobar venous enlargement, and an unstructured interstitial to alveolar pulmonary pattern. The distribution of the pulmonary pattern varies and depends on the direction and symmetry of the mitral valve jet. Pulmonary patterns are most commonly patchy to diffuse and most severe caudodorsally. The pulmonary pattern can be either symmetric or asymmetric. Contrary to popular belief, a perihilar pattern is less common. In dogs with dilated cardiomyopathy, cranioventral distributed patterns are common, which can mimic aspiration pneumonia. Pulmonary patterns associated with L-CHF tend to be less severe as compared to

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in distribution according to the underlying cause. Patterns are often asymmetric and related to the location of trauma that caused hemorrhage to occur. Although the pulmonary pattern is relatively nonspecific, numerous other thoracic radiographic changes are common, including pleural effusion, increased mediastinal soft tissue opacity or widening due to effusion or hematoma, tracheal narrowing, and tracheal collapse. 12,13 The presence of these other thoracic changes combined with an absence of cardiomegaly or pulmonary lobar venous enlargement makes differentiating hemorrhage from L-CHF easier than the aforementioned causes. METASTATIC NEOPLASIA Most neoplasms typically cause a structured interstitial pulmonary pattern when they metastasize to the lungs, resulting in multifocal pulmonary nodules or masses. However, lymphoma, hemangiosarcoma, and mammary adenocarcinoma commonly cause a patchy to diffuse, unstructured interstitial pulmonary pattern when they metastasize. The absence of obvious nodules/masses in the presence of an unstructured interstitial pulmonary pattern can be confusing if a patient presents for dyspnea and happens to have cardiomegaly as a normal breed variant or occult cardiac disease such as mitral valve degeneration. The key to differentiating diffuse pulmonary neoplasia from L-CHF is to identify other findings that would support a diagnosis of cancer. For example, finding a mammary mass in the case of mammary adenocarcinoma, finding a splenic/ hepatic masses, a hemoabdomen, or pericardial effusion in the case of hemangiosarcoma, or finding lymphadnomegaly, hepatosplenomegaly, visceral masses, or unexplained cavitary effusions in the case of lymphoma. As has been the theme, failure to respond to a furosemide trial is always an important clinical clue to rule out L-CHF.

cardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage. For this reason, a lack of radiographic improvement to other supportive therapies such as furosemide or antibiotics in the face of right sided cardiomegaly and pulmonary lobar artery enlargement should raise suspicion for PH. In contrast, acute improvement or resolution of pulmonary infiltrates with sildenafil is strongly supportive of PH and will not interfere with the diagnosis of the disease via echocardiography. 7 If patients develop right-sided CHF secondary to severe pulmonary hypertension, other radiographic findings may be seen, including pleural effusion, caudal vena cava enlargement, hepatomegaly, and peritoneal effusion. 4 While pulmonary hypertension is less commonly reported in cats, radiographic findings appear to be similar to those reported in the dog. CHRONIC LOWER AIRWAY DISEASE AND PULMONARY FIBROSIS Chronic lower airway disease is usually easily distinguished from L-CHF in that it primarily affects young to middle-aged dogs and cats and typically manifests radiographically as a mild to moderate bronchial pulmonary pattern without cardiomegaly. Early in the disease, pulmonary infiltrates are not seen and the cardiac silhouette and pulmonary lobar vasculature are expected to be normal. As the disease progresses, pulmonary infiltrates become more likely, usually resulting from concurrent pneumonia, pulmonary fibrosis, and/or pulmonary hypertension secondary to cor pulmonale. In the case of the later, right-sided cardiomegaly commonly occurs. Even more confusing, some dogs and cats will have stable/occult cardiac disease (mitral valve disease in dogs, cardiomyopathy in cats) that causes left-sided cardiomegaly. The presence of pulmonary infiltrates with or without cardiomegaly is when chronic lower airway disease can be confused with heart failure. As previously discussed, failure to respond radiographically to furosemide, a lack of pulmonary lobar venous congestion, a lack of cardiomegaly, or right-sided cardiomegaly should all decrease suspicion for L-CHF. Patients with chronic lower airway disease usually respond acutely well to bronchodilators and oxygen therapy.

neurogenic causes (e.g., seizures and head trauma), electrocution injury, anaphylaxis, toxin exposure, and acute lung injury. Regardless of the cause, NCPE presents as a multifocal to diffuse, unstructured interstitial or alveolar pulmonary pattern, often most severe in the periphery of the caudodorsal lung fields. A perihilar distribution is also reported. Pulmonary patterns are usually bilaterally symmetric, but can also be asymmetric. In one study, if the radiographic pattern was asymmetric, 86% of cases were most severe in the right caudodorsal lung field. 9 In that same study, the most common cause of an asymmetric pulmonary pattern was airway obstruction. The radiographic pattern itself is very similar to that associated with L-CHF. However, oftentimes patients are presented with a history that strongly supports a diagnosis of NCPE, such as dyspnea localized to the upper airways, near- drowning, seizures, or head trauma. Additional clues that decrease the likelihood of L-CHF include the absence of a heart murmur, cardiomegaly, or pulmonary lobar vasculature enlargement, as well as a lack of response to furosemide. PULMONARY THROMBOEMBOLISM Pulmonary thromboembolism (PTE) is uncommon in dogs and cats, but most often secondary to an underlying process that has disrupted Virchow’s triad of coagulation: stasis of blood flow, endothelial injury, and hypercoagulability. In veterinary medicine, underlying causes of PTE are numerous and well- reviewed elsewhere. 10 Idiopathic PTE is rare in dogs and cats. Unfortunately, radiographic findings are inconsistent and often not present. Depending on the size and number of vessels affected as well as the underlying cause, two main radiographic patterns are possible. Small or multifocal PTEs will cause a focal or multifocal unstructured interstitial or alveolar pulmonary pattern. 11 The pulmonary lobar arteries among or adjacent to this pattern will be small to absent. In contrast, if a large pulmonary lobar artery is affected, regional oligemia will cause hyper lucency and small to absent pulmonary lobar arteries within the affected lung lobe/region. Adjacent lung lobes/regions will receive increased blood flow, resulting in a patchy to diffuse unstructured interstitial pulmonary pattern with or without pulmonary lobar artery enlargement. Unfortunately, radiographs are often unremarkable and more advanced diagnostics are needed, such as radiographic or computed tomographic angiography. Pulmonary thromboembolism should be prioritized over L-CHF anytime a patient with a predisposing cause for PTE develops an acute but moderate to severe dyspnea (or even sudden death) in the face of underwhelming thoracic radiographic findings. PULMONARY HEMORRHAGE Pulmonary hemorrhage is uncommon in dogs and cats. When it occurs, it is most often caused by anti-coagulant rodenticide toxicity, other coagulopathies, thrombocytopenia, or large vessel rupture secondary to trauma. The pulmonary pattern associated with pulmonary hemorrhage is usually a patchy to diffuse, unstructured interstitial to alveolar pulmonary pattern that varies

6. Lee SK and Choi J. Caudal pulmonary artery to vein ratio on radiography can predict pulmonary hypertension in dogs with mitral regurgitation. Vet Radiol Ultrasound 2023;64(1): 18-27. 7. Kellihan HB, Waller KR, Pinkos A, et al. Acute resolution of pulmonary alveolar infiltrates in 10 dogs with pulmonary hypertension treated with sildenafil citrate: 2005-2014. J Vet Cardiol 2015;17(3):182-191. 8. Unger K and Martin LG. Noncardiogenic pulmonary edema in small animals (clinical practice review). J Vet Emerg and Crit Care 2023;33(2):156-172. 9. Bouyssou S, Specchi S, and Desquillbet et al. Radiographic appearance of presumed noncardiogenic pulmonary edema and correlation with the underlying cause in dogs and cats. Vet Radiol Ultrasound 2017;58(3):259-265. 10. Goggs R, Benigni L, and Fuentes VL, et al. Pulmonary thromboembolism (state-of-the-art review). J Vet Emerg Crit Care 2009;19(1):30-52. 11. Fluckiger MA and Gomez JA. Radiographic findings in dogs with spontaneous pulmonary thromboembolism. Vet Radiol Ultrasound 1984;25(3):124-131. 12. Berry CR, Gallaway A, Thrall De, et al. Thoracic radiographic features of anticoagulant rodenticide toxicity in fourteen dogs. Vet Radiol Ultrasound 1993;34(6):391-396. 13. Thomer AJ and Beer KAS. Anticoagulant rodenticide toxicosis causing tracheal collapse in 4 small breed dogs. J Vet Emerg Crit Care 2018;28(6):573-578.

ADDITIONAL REFERENCES

1. Bahr, R. Chapter 35: Canine and Feline Cardiovascular System. In: Thrall DE (eds). Textbook of Veterinary Diagnostic Radiology. 7th eds. St Louis, MO: Elsevier, 2018, pp 684 – 709. 2. Boysen SR. Chapter 189: AFAST and TFAST in the intensive care unit. In: Silverstein, DC and Hopper, K. Small Animal Critical Care Medicine, 2nd ed. 2015:988-994. 3. Dickson D, little CJL, Harris J, et al. Rapid assessment with physical examination in dyspnoeic cats: the RAPID cat study. J Small Anim Pract 2018;59:75-84. 4. Geyer NE, Reichle JK, Valdes-Martinez A, et al. Radiographic appearance of confirmed pulmonary lymphoma in cats and dogs. Vet Radiol Ultrasound 2010;51(4):386-390. 5. Guglielmini C, Toaldo MB, Poser H, et al. Diagnostic accuracy of the vertebral heart score and other radiographic indices in the detection of cardiac enlargement in cats with different cardiac disorders. J Fel Med Surg. 6. Lisciandro GR and Gambino JM (eds). Diagnostic imaging: point-of-care ultrasound. Vet Clin Smal Anim 2021;51(6). 7. Louvet A and Bourgeois, JM. Lung ring-down artifact as a sign of pulmonary alveolar-interstitial disease. J Vet Radiol Ultrasound 2008;49(4):374-377. 8. Sleeper MM, Roland R, and Drobatz KJ, et al. Use of the vertebral heart scale for differentiation of cardiac and noncardiac causes of respiratory distress in cats: 67 cases (2002-2003). J Am Vet Med Assoc 2013;242(3):366-371. 9. Thrall, DE. Chapter 36: Canine and Feline Lung. In: Thrall DE (eds). Textbook of Veterinary Diagnostic Radiology. 7th eds. St Louis, MO: Elsevier, 2018, pp 710 - 734.

SELECT REFERENCES

1. Cole L, Pivetta M, and Humm K. Diagnostic accuracy of a lung ultrasound protocol (VetBLUE) for detection of pleural fluid, pneumothorax and lung pathology in dogs and cats. J Small Anim Pract 2021;62(3):178-186. 2. Oura TJ, Young AN, Keene BW, et al. A valentine-shaped cardiac silhouette in feline thoracic radiographs is primarily due to left atrial enlargement. Vet Radiol Ultrasound 2015;56(3):245-250. 3. Reinero C, Visser LC, Kellihan HB, et al. ACVIM consensus statement guidelines for the diagnosis, classification, treatment, and monitoring of pulmonary hypertension in dogs. J Vet Intern Med 2020;34:549-573. 4. Johnson L, Boon J, and Orton EC. J Vet Intern Med 1999;13:440-447 5. Adams DS, Marolf AJ, and Martinez AV, et al. Associations between thoracic radiographic changes and severity of pulmonary arterial hypertension diagnosed in 60 dogs via Doppler echocardiography: A retrospective study: Vet Rad Ultrasound 2017;58(4):363-489.

NON-CARDIOGENIC PULMONARY EDEMA

Non-cardiogenic pulmonary edema (NCPE) is a less common cause of dyspnea in dogs and cats and includes any process that alters pulmonary vascular permeability. In some etiologies, aberrancies in hydrostatic pressure also play a role. The result is the accumulation of proteinaceous fluid within the interstitial or alveolar spaces without the presence of a cardiac or iatrogenic fluid therapy cause. 8 This is in contrast to cardiogenic pulmonary edema which causes non-proteinaceous fluid accumulation via increased hydrostatic pressure, most commonly caused by L-CHF, fluid therapy, or blood product administration. Causes of NCPE are numerous and include but are not limited to airway obstruction,

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