Successful cardiopulmonary resuscitation and use of short-term mechanical ventilation following inadvertent ketamine overdose in a cat

Objective: To describe the clinical manifestations and successful outcome following an inadvertent overdose of ketamine to a cat. Case summary: A 4‐year‐old neutered male domestic shorthair cat was evaluated for a urethral obstruction. Because of an inadvertent miscalculation of ketamine, 20 times the intended dose was administered intravenously, which resulted in cardiopulmonary arrest. Cardiopulmonary‐cerebral resuscitation was successful, and short‐term mechanical ventilation, fluids and intensive monitoring were utilized to achieve full recovery and subsequent discharge of the animal. New or unique information provided: Ketamine is a common anesthetic agent used in cats that is considered to have a wide therapeutic index and minimal cardiopulmonary depressant effects at recommended doses. Successful management of inadvertent ketamine overdose has been reported in children, but not in cats. Prompt CPCR and short‐term mechanical ventilation may be necessary to treat a significant ketamine overdose. In cats, yohimbine may act as a partial antagonist of ketamine.     

Cardiopulmonary resuscitation with vasopressin in a dog

That endogenous vasopressin levels in successfully resuscitated human patients were significantly higher than in patients who died pointed to the possible benefit of administering vasopressin during cardiopulmonary resuscitation (CPR). Several CPR studies in pigs showed that vasopressin improved blood flow to vital organs, cerebral oxygen delivery, resuscitability and neurological outcome when compared with epinephrine. In a small clinical study, vasopressin significantly improved short-term survival when compared with epinephrine indicating its potential as an alternative pressor to epinephrine during CPR in human beings. As there was little clinical data available at that time, its recommended use was limited to adult human beings with shock-refractory ventricular fibrillation. In this report, we present the case of a dog in which the successful management of intraoperative asystolic cardiac arrest involved vasopressin. Unexpected cardiac arrest occurred during anaesthesia for the surgical removal of multiple mammary adenocarcinomata in a 11-year-old Yorkshire terrier. Despite an ASA physical status assignation of III, the dog was successfully resuscitated with external chest compressions, intermittent positive pressure ventilation and vasopressin (2 doses of 0.8 IU kg(-1)) and was discharged 3 days later without signs of neurological injury. We believe vasopressin contributed to restoring spontaneous circulation. It may prove increasingly useful in perioperative resuscitation in dogs.     

Successful cardiopulmonary cerebral resuscitation incorporating defibrillation in a filly with neonatal maladjustment syndrome following a routine anaesthetic procedure

A 10-h-old 56-kg Thoroughbred filly was presented for treatment of partial failure of passive transfer of immunity and presumed neonatal maladjustment syndrome (NMS). The filly was hospitalised, and supportive care initiated. On Day 5 of hospitalisation, seizures were observed and were controlled with IV administration of diazepam. Due to progression of clinical signs of NMS, magnetic resonance imaging of the filly's brain was performed. During the early anaesthetic recovery period, the filly exhibited cardiopulmonary arrest (CPA) at which point cardiopulmonary cerebral resuscitation (CPCR) was performed for a total of 48 min. During this time, ventricular fibrillation (VF) was observed on ECG and the filly was defibrillated three times at 1–2-min intervals using 2–4 J/kg of monophasic electrical defibrillation. The filly successfully recovered from CPCR, was discharged 5 days later and was reported healthy 12 months post-discharge.     

Efficacy of Low‐ and High‐Dose Trilostane Treatment in Dogs (< 5 kg) with Pituitary‐Dependent Hyperadrenocorticism

Background

Trilostane is commonly used to treat pituitary‐dependent hyperadrenocorticism (PDH) in dogs. There are differing opinions regarding the dose and frequency of trilostane administration in dogs with PDH.

Objectives

To compare the efficacy of 2 trilostane protocols in the treatment of dogs with PDH.

Animals

Sixteen client‐owned dogs with PDH and a body weight <5 kg.

Methods

Prospective observational study. Group A (n=9; low‐dose treatment group) received 0.78 ± 0.26 mg of trilostane/kg PO every 12 h and group B (n = 7; high‐dose treatment group) 30 mg of trilostane/dog PO every 24 h. All of the dogs were reassessed at 2, 4, 8, 12, 16, and 24 weeks after the initiation of treatment.

Results

An improvement in both ACTH‐stimulated serum cortisol concentrations and clinical signs occurred more slowly in group A than in group B; however, after 20 weeks of treatment, 2/7 dog in group B had clinical signs and abnormal laboratory findings consistent with hypoadrenocorticism. At 24 weeks, an improvement in the clinical findings of all of the dogs in both groups was detected.

Conclusions and clinical importance

In dogs with PDH, twice‐daily administration of low‐dose trilostane is an effective approach to the management of PDH. In addition, our results suggest fewer potential adverse effects if trilostane is administered twice daily in the lower dose.     

Use of recombinant human factor VIIa in 2 patients with postoperative noncompressible,abdominal hemorrhage

Objective

To describe the clinical presentation, clinical course, and successful management of noncompressible, abdominal hemorrhage with recombinant human factor VIIa (rFVIIa) in 2 postoperative patients.

Case Summary

A 14-year-old neutered female Border Terrier and a 9-year-old neutered male domestic shorthair were treated with rFVIIa to treat noncompressible abdominal hemorrhage in the postoperative period. The dog presented for a septic abdomen following endoscopic intestinal biopsies 10 days prior and was found to have a jejunal perforation along with a fractured liver lobe and hepatic lymphoma at the time of exploratory laparotomy. The cat presented for a spontaneous hemoabdomen associated with hepatic amyloidosis. Clinically significant hemorrhage occurred in the perioperative and postoperative period and both patients received massive transfusions and antifibrinolytic therapy. Despite these interventions, the patients continued to have ongoing abdominal hemorrhage and surgical attempts at hemostasis were not attempted due to the friable nature of the liver at the time of surgery. Both patients received rFVIIa intravenously every 3 hours at a dose between 70 and 90 μg/kg as indicated by the clinical picture, which subsequently decreased transfusion requirements.

New or Unique Information Provided

This case report describes the use of rFVIIa in a cat and a dog with severe, noncompressible abdominal hemorrhage in combination with standard hemostatic interventions.     

Delayed embolization of an Amplatz® canine duct occluder in a dog

A 5-year old, 5.8 kg, castrated male Pomeranian was diagnosed with a type IIa patent ductus arteriosus (PDA) with a minimal ductal diameter of 3.5 mm and ampulla width of 7.1 mm based on angiographic assessment. A 6 mm Amplatz^® Canine Duct Occluder (ACDO) was deployed within the PDA. Once deployed, the device assumed it's native shape and back-and-forth maneuvering was performed with the delivery cable to assess device stability. Device position and complete occlusion were confirmed with both angiography and transesophageal echocardiography prior to and after release of the device. The device location was confirmed within the ductus arteriosus by echocardiography prior to discharge. The dog was discharged with instructions for strict activity restriction. Two days after discharge, the dog was left unsupervised in the backyard and shortly afterwards was found coughing with severe respiratory distress. The dog was evaluated at an emergency hospital and thoracic radiographs documented embolization of the ACDO to the main pulmonary artery along with a severe alveolar pattern throughout the right lung fields. Shortly after obtaining thoracic radiographs, the dog experienced cardiopulmonary arrest with unsuccessful resuscitation. This case describes a possible complication of transcatheter PDA occlusion with an ACDO, which has not been previously reported. An incident report, or catalog of adverse events with these devices, may prove useful in identifying additional fatal complications that others may have encountered, but are not reported in the literature. The report of this complication emphasizes the importance of strict activity restriction after device placement in dogs.     

Successful resuscitation from cardiac arrest associated with extradural lidocaine in a dog

BACKGROUND: Extradural lidocaine exerts several adverse effects which are seldom fatal. While cardiac arrest following extradural lidocaine injection has been reported in human beings, it has not hitherto been reported in dogs. OBSERVATIONS: The emergency management of a dog with complete urethral obstruction is described. We intended to perform vaginoscopy and cystostomy under extradural lidocaine anaesthesia, but cardiac asystole occurred a few minutes after injection. Resuscitation was successful. About 20 minutes later cardiac arrest recurred, and was treated successfully. The dog remained hypothermic for approximately 7 hours. Complete recovery without neurological deficit occurred the next day and the dog remained normal for at least 3 months. The probable cause of the problem was cranial lidocaine dispersion causing a drop in cardiac preload and cardiac arrest. The successful neurological outcome was attributed to early diagnosis and effective treatment. Hypothermia may have conferred cerebral protection during ischemia. CONCLUSIONS: Extradural local anaesthetic administration is not without risk and the technique should be tailored to individual animals. Constant monitoring is required to detect potentially fatal complications and increase the likelihood of successful outcome.     

Questionnaire‐based Analysis of Owner‐reported Scratching and Pain Signs in Cavalier King Charles Spaniels Screened for Chiari‐like Malformation and Syringomyelia

Background

Chiari‐like malformation (CM) and syringomyelia (SM) cause a pain syndrome in Cavalier King Charles spaniels (CKCS). Clinical signs are not consistently apparent on neurologic examination, and owner reporting of signs provides vital clinical history. However, owner questionnaires for this disease are not well developed.

Objectives

To develop a tool to capture owner‐reported clinical signs for use in clinical trials and to compare owner‐reported signs with the presence of pain on neurologic examination and SM on magnetic resonance imaging (MRI).

Animals

Fifty client‐owned CKCS.

Methods

Owners completed a questionnaire and pain/scratch map. Each dog underwent a neurologic examination and craniocervical magnetic resonance imaging (MRI). Questionnaire responses were developed into scores, area of shading for pain/scratch maps was measured, and consistency of responses between these tools was assessed. Owner‐reported findings were compared with neurologic examination findings and presence and severity of SM on MRI.

Results

Thirty‐three dogs were symptomatic and 17 asymptomatic; 30 had SM. The most common sign of pain was crying out when lifted (n = 11). Extent of shaded areas on maps positively correlated with questionnaire scores for pain (r² = 0.213, P = 0.006) and scratch (r² = 0.104, P = 0.089). Owner‐reported findings were not significantly associated with presence or severity of SM or neurologic examination findings. Owner‐reported lateralization of signs was significantly associated with SM lateralization (P < 0.0001).

Conclusions

The questionnaire and maps may be useful for clinical trials. Lack of association of owner‐reported signs with SM highlights our lack of understanding of the pathophysiology of pain in this disease.     

Successful cardiopulmonary resuscitation in an adult horse following cardiovascular collapse on recovery from general anaesthesia in the Trendelenburg position

Equine anaesthesia is associated with a high risk of perioperative morbidity and mortality, particularly in the recovery period. Cardiovascular collapse and cardiopulmonary arrest (CPA) have been reported to account for one-third of anaesthesia-related perioperative deaths in the horse. This case report describes the successful cardiopulmonary resuscitation of a healthy adult Thoroughbred mare that developed cardiovascular collapse and subsequent CPA following positioning in the recovery box after general anaesthesia in the Trendelenburg position. Cardiopulmonary resuscitation (CPR) was instigated and included thoracic compressions, intermittent positive pressure ventilation and adrenaline administered via the intravenous and intra-tracheal routes. Return of spontaneous circulation (ROSC) was detected 5 min and 50 s after the start of CPR. A stable stance was achieved approximately 100 min after ROSC. The mare was discharged from the hospital 3 days later with no known complications. To the authors’ knowledge, this is the first case report documenting CPA following general anaesthesia in the Trendelenburg position in a horse, with subsequent successful CPR. The precise cause of the CPA is unknown but a number of plausible hypothesis are discussed including hypoventilation and a Bezold-Jarisch reflex.     

Causes of cardiopulmonary arrest, resuscitation management, and functional outcome in dogs and cats surviving cardiopulmonary arrest

Objective: To describe the functional outcome of canine and feline survivors of cardiopulmonary arrest (CPA) and the clinical characteristics surrounding their resuscitation. Design: Retrospective study. Setting: Veterinary teaching hospital. Animals: Client‐owned dogs (15) and cats (3) with CPA. Interventions: None. Measurements and main results: Eighteen animals were identified to have survived to discharge following CPA. Cardiopulmonary arrest was associated with anesthesia with or without pre‐existing disease in 10 animals, cardiovascular collapse in 5 animals, and chronic disease with an imposed stress in 3 animals. All CPAs were witnessed in the hospital. The most common initial rhythm at CPA was asystole (72%). Return of spontaneous circulation (ROSC) was achieved in less than 15 minutes from the onset of cardiopulmonary cerebral resuscitation (CPCR) in all animals. No animals had a recurrence of CPA after the initial CPA. Animals were of a wide range of ages (0.5–16 years) and breeds. Two animals were neurologically abnormal at discharge, one of which was normal at 2 months following CPA. Conclusions: A good functional recovery after CPCR was documented in the small number of CPA survivors presented in this study. This may be due to the reversible nature of their inciting cause of CPA, early detections of CPA (‘witnessed’), and/or the animal's underlying normal health status.     

Intraosseous injection during cardiopulmonary resuscitation in dogs

Five mixed breed dogs were used to investigate the feasibility of femoral intraosseous injection during cardiac arrest. The intraosseous route was evaluated in the anaesthetised dogs after induction of cardiac arrest. Fluorescein dye was injected through pre-placed intraosseous catheters during cardiac massage. The dye was detected at the membrana nictitans five to 12 seconds later indicating successful transfer from the femoral marrow cavity to the systemic circulation during cardiopulmonary resuscitation (CPR). The clinical value of intraosseous injection during CPR is discussed and compared with the endotracheal administration of drugs.     

Hybrid balloon valvuloplasty for management of severe mitral stenosis in four symptomatic,adult dogs

Four adult dogs weighing <10 kg presented for the evaluation of severe mitral valve stenosis with clinical signs. Owing to the size of the dogs, a hybrid surgical and interventional approach was utilized for balloon valvuloplasty. A left lateral thoracotomy was performed to allow direct entry through the left atrial wall. Transesophageal echocardiography was utilized for the entirety of the procedure in all dogs, and fluoroscopy was additionally used in two dogs. One dog had mild to moderate intra-operative bleeding from the left atrial wall during the procedure, but no other intra-operative complications were observed. No dogs developed a clinically relevant amount of worsened mitral regurgitation. Based on mitral leaflet mobility and transmitral flow profiles, there was perceived improvement in all four dogs. One dog died 6 h after extubation due to respiratory arrest. The remaining dogs survived to discharge and had resolution of clinical signs at home and discontinuation of heart failure medications. One dog died of an unknown cause at five months and another developed atrial fibrillation, and the owners elected to euthanize at ten months after the procedure. One dog continues to do well six months after the procedure as of the time of this writing. Hybrid balloon valvuloplasty can be a viable management option for small breed dogs with severe mitral stenosis exhibiting clinical signs, and both transesophageal echocardiography and fluoroscopy can be used intra-operatively to assist in successful procedural outcomes.     

The use of vasopressin for treating vasodilatory shock and cardiopulmonary arrest

Objective – To discuss 3 potential mechanisms for loss of peripheral vasomotor tone during vasodilatory shock; review vasopressin physiology; review the available animal experimental and human clinical studies of vasopressin in vasodilatory shock and cardiopulmonary arrest; and make recommendations based on review of the data for the use of vasopressin in vasodilatory shock and cardiopulmonary arrest. Data Sources – Human clinical studies, veterinary experimental studies, forum proceedings, book chapters, and American Heart Association guidelines. Human and Veterinary Data Synthesis – Septic shock is the most common form of vasodilatory shock. The exogenous administration of vasopressin in animal models of fluid‐resuscitated septic and hemorrhagic shock significantly increases mean arterial pressure and improves survival. The effect of vasopressin on return to spontaneous circulation, initial cardiac rhythm, and survival compared with epinephrine is mixed. Improved survival in human patients with ventricular fibrillation, pulseless ventricular tachycardia, and nonspecific cardiopulmonary arrest has been observed in 4 small studies of vasopressin versus epinephrine. Three large studies, though, did not find a significant difference between vasopressin and epinephrine in patients with cardiopulmonary arrest regardless of initial cardiac rhythm. No veterinary clinical trials have been performed using vasopressin in cardiopulmonary arrest. Conclusion – Vasopressin (0.01–0.04 U/min, IV) should be considered in small animal veterinary patients with vasodilatory shock that is unresponsive to fluid resuscitation and catecholamine (dobutamine, dopamine, and norepinephrine) administration. Vasopressin (0.2–0.8 U/kg, IV once) administration during cardiopulmonary resuscitation in small animal veterinary patients with pulseless electrical activity or ventricular asystole may be beneficial for myocardial and cerebral blood flow.     

Rebound hyperkalemia in a dog with albuterol toxicosis after cessation of potassium supplementation

Objective

To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog.

Case Summary

A 3-year-old female neutered mixed-breed dog was presented for albuterol toxicosis that led to a severe hypokalemia, hyperlactatemia, and hyperglycemia. The dog also experienced sinus tachycardia and generalized weakness. Treatment was instituted with intravenous fluid therapy and potassium supplementation, and the dog was monitored with a continuous electrocardiogram. Resolution of hypokalemia was documented 12 hours after initial presentation, at which time fluid therapy and potassium supplementation were discontinued. There were no further periods of sinus tachycardia, but instead the dog developed ventricular ectopy with rapid couplets (instantaneous rates of 300/min). An echocardiogram revealed normal cardiac size and function. Twenty-four hours after presentation, the patient developed severe hyperkalemia, despite discontinuation of fluids and potassium supplementation for 12 hours. Serial venous and urinary electrolytes were performed for determination of the fractional excretion of electrolytes. These data confirmed rebound hyperkalemia (7.0 mmol/L), consistent with a markedly increased fractional excretion of potassium, and secondary to the release of potassium from inside the cells. Fluid therapy with dextrose supplementation was provided until 36 hours postpresentation. The hyperkalemia resolved, and the dog was discharged after 44 hours of hospitalization.

New or Unique Information Provided

This case documents rebound hyperkalemia following treatment of albuterol toxicosis in a dog. This case highlights the importance of understanding the distribution of total body potassium when treating serum hypokalemia. Transcellular shifts of potassium, as in the case of albuterol toxicosis, can lead to rebound hyperkalemia even after discontinuation of potassium supplementation. This case further explores the utility of fractional excretion of electrolytes in elucidating the etiology and management of electrolyte disturbances.     

Cardiopulmonary cerebral resuscitation in neonatal foals

Cardiovascular or pulmonary system failure in neonatal foals requires rapid recognition and initiation of cardiopulmonary cerebral resuscitation (CPCR). Foals may require resuscitation immediately after birth or after arrest from progression of a disease process such as severe sepsis or septic shock. Initial treatment is aimed at establishing an airway and providing ventilation. Circulation is provided by closed-chest compressions. Circulatory access is important to provide intravenous fluid and pharmacologic therapy for cardiovascular support. Ventricular fibrillation and pulseless ventricular tachycardia are arrhythmias not commonly recognized with arrest in foals, whereas asystole and cardiovascular collapse are frequently encountered. Training of personnel, preparation of supplies, and organization during CPCR is essential to a successful outcome.Most of the information used for CPCR in neonatal foals is derived from human medical research and clinical medicine. As new advances are made in human neonatal and pediatric CPCR, many of these treatments and techniques can be applied to foals. This article reviews currently available CPCR guidelines in foals and highlights new perspectives in human medicine that may be applicable to foals.     

Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991).

Outcomes of cardiopulmonary arrest and resuscitation in clinically affected dogs and cats have not been adequately studied. We examined the records from 200 dogs and 65 cats that had received cardiopulmonary resuscitation for respiratory or cardiopulmonary arrest; none of the animals had been anesthetized or intubated at the time of arrest, and all had been hospitalized in a veterinary critical care facility. Cardiopulmonary arrest was found to be more common than respiratory arrest in dogs and cats. Hospital discharge rates for animals with cardiopulmonary arrest ranged from 4.1% for dogs to 9.6% for cats, and were consistent with those reported from studies of human beings with cardiopulmonary arrest. Hospital discharge rates for dogs and cats with respiratory arrest were 28% and 58.3%, respectively.     

Refractory shock,hypercoagulability, and multiorgan thrombosis associated with hypertrophic osteodystrophy in a dog

Objective

To describe the clinical findings and case progression in a dog presenting with severe systemic inflammatory response, refractory shock, progressive metabolic acidosis, and respiratory failure that was ultimately diagnosed with hypertrophic osteodystrophy (HOD).

Case Summary

A 4-month-old male intact Mastiff presented with a 24-hour history of lethargy and generalized ostealgia. On examination, the dog was recumbent, febrile, and tachycardic with pain on palpation of the abdomen, right femur, and mandible. Appendicular joint radiographs showed changes consistent with osteochondrosis and ulnar-retained cartilaginous cores, with no overt evidence of HOD. Initial treatment included IV fluid therapy, multimodal analgesia, and broad-spectrum antimicrobials. Vasopressor therapy was initiated following hemodynamic decompensation. Synovial fluid cytological analysis and culture revealed nonseptic suppurative inflammation and no bacterial growth, respectively. Blood and urine cultures also yielded no growth. Viscoelastic testing was consistent with hypercoagulability. The dog initially had a metabolic acidosis with appropriate respiratory compensation that progressed to a mixed metabolic and respiratory acidosis despite aggressive therapies that included antimicrobials, vasopressors, positive inotropes, and corticosteroids. Humane euthanasia was elected approximately 32 hours after admission. Necropsy yielded a diagnosis of HOD.

New or Unique Information Provided

This is the first report detailing the occurrence of refractory shock and hypercoagulability associated with HOD in a dog without evidence of another identified comorbidity. HOD should be considered in any young, large-breed dog with generalized ostealgia and signs of systemic illness, even in the absence of classic radiographic abnormalities. Further investigation of coagulation status in dogs with HOD and a secondary systemic inflammatory response is warranted.     

Prevalence and factors associated with initial and subsequent shockable cardiac arrest rhythms and their association with patient outcomes in dogs and cats undergoing cardiopulmonary resuscitation: A RECOVER registry study

Objective

To report the prevalence of initial shockable cardiac arrest rhythms (I-SHKR), incidence of subsequent shockable cardiac arrest rhythms (S-SHKR), and factors associated with I-SHKRs and S-SHKRs and explore their association with return of spontaneous circulation (ROSC) rates in dogs and cats undergoing CPR.

Design

Multi-institutional prospective case series from 2016 to 2021, retrospectively analyzed.

Setting

Eight university and eight private practice veterinary hospitals.

Animals

A total of 457 dogs and 170 cats with recorded cardiac arrest rhythm and event outcome reported in the Reassessment Campaign on Veterinary Resuscitation CPR registry.

Measurements and Main Results

Logistic regression was used to evaluate association of animal, hospital, and arrest variables with I-SHKRs and S-SHKRs and with patient outcomes. Odds ratios (ORs) were generated, and significance was set at P < 0.05. Of 627 animals included, 28 (4%) had I-SHKRs. Odds for I-SHKRs were significantly higher in animals with a metabolic cause of arrest (OR 7.61) and that received lidocaine (OR 17.50) or amiodarone (OR 21.22) and significantly lower in animals experiencing arrest during daytime hours (OR 0.22), in the ICU (OR 0.27), in the emergency room (OR 0.13), and out of hospital (OR 0.18) and that received epinephrine (OR 0.19). Of 599 initial nonshockable rhythms, 74 (12%) developed S-SHKRs. Odds for S-SHKRs were significantly higher in animals with higher body weight (OR 1.03), hemorrhage (OR 2.85), or intracranial cause of arrest (OR 3.73) and that received epinephrine (OR 11.36) or lidocaine (OR 18.72) and significantly decreased in those arresting in ICU (OR 0.27), emergency room (OR 0.29), and out of hospital (OR 0.38). Overall, 171 (27%) animals achieved ROSC, 81 (13%) achieved sustained ROSC, and 15 (2%) survived. Neither I-SHKRs nor S-SHKRs were significantly associated with ROSC.

Conclusions

I-SHKRs and S-SHKRs occur infrequently in dogs and cats undergoing CPR and are not associated with increased ROSC rates.     

Hypereosinophilic syndrome with cardiac infiltration and congestive heart failure in a cat

Hypereosinophilic syndrome is an uncommon disorder in the cat. It is a heterogeneous group of conditions defined by a persistent hypereosinophilia associated with organ damage directly attributable to tissue hypereosinophilia. A seven-year-old castrated domestic shorthair cat presented to the emergency service for dyspnea. Initial physical examination identified the presence of a grade III/VI systolic left parasternal murmur with no gallop or arrhythmia. A snap N-terminal-pro hormone brain natriuretic peptide was abnormal, and a point-of-care ultrasound revealed mild pleural effusion, scant pericardial effusion, and an enlarged left atrium. There was leukemia (72.35 K/uL, reference range 4.5–15.7 K/uL) predominated by eosinophilia (33.84 K/uL; reference range 0–1.9 K/uL). On echocardiogram, there was concentric hypertrophy of the left ventricular walls with irregular endocardial borders. The left atrium was enlarged with evidence of spontaneous echogenic contrast. The mitral valve was thickened with a vegetative lesion on the anterior leaflet. Despite treatment, the patient experienced cardiopulmonary arrest, and cardiopulmonary resuscitation was unsuccessful. Complete necropsy with histopathology revealed eosinophilic infiltrates in multiple organs and the presence of a severe, acute-on-chronic, fibrinous, and eosinophilic-granulomatous endomyocarditis with mural thrombosis and marked endocardial fibrosis. This case represents an unusual presentation of the hypereosinophilic syndrome in the cat with cardiac involvement and congestive heart failure as a primary clinical sign.