• Definition: failure of conduction from the atria to the ventricles, resulting in a ventricular escape rhythm.
• Cause: often unknown. Leading differentials are structural AV node diseases, such as degeneration and myocarditis. Other rare differentials include neoplasia, neurodegenerative disorders, infectious, anti-arrhythmic therapy, trauma, and aortic endocarditis.
• Signs: depends on the block’s underlying ventricular escape rate and cause. This condition needs to be better defined in rabbits. Based on other species which can have high ventricular rates of escape, eg cats, low ventricular escape rates (<100 bpm reported in cats) can lead to syncope, weakness, lethargy, anorexia and congestive heart failure. Patients with high ventricular escape rates >120 bpm (in cats) may be asymptomatic. Other symptoms associated with endocarditis, myocarditis, and neuromuscular disorders may be seen.
• Diagnosis: electrocardiogram shows AV disassociation, ie non-conducting P waves with a ventricular escape rhythm.
• Treatment: poorly defined in rabbits. Medical management in other species is often not successful. Pacemaker implantation is gold-standard treatment.
• Prognosis: poorly defined in rabbits. Often present with severe hypotension and bradycardia with immediate prognosis as guarded. In other species, the prognosis is good with pacemaker implantation. Medical therapy of symptomatic patients is guarded. If left untreated and the patient is symptomatic, the prognosis is poor and guarded if they are asymptomatic.

• Syncope.
• Weakness/lethargy.
• Anorexia.
• Congestive heart failure.
• Ventricular fibrillation or Torsade de Pointes.
• Signs associated with underlying etiology.
• None – incidental finding.

• Sudden onset of presenting signs.
• Sudden death.

• Not reported in rabbits; in other species, degenerative causes are usually seen in older animals, while myocarditis is generally seen in younger animals.

• None reported.
• In one study of 59 cases of pet rabbits with cardiovascular disease, four (21.1%; 95% CI, 6.1% to 45.6%) had atrioventricular block, but the type/degree is not described.

Diagnostic workup

• Electrocardiography.
• Echocardiography
• Biochemistry and hematology, urinalysis. Troponin-I is used in other species, but more data is needed in rabbits.
• Thoracic radiographs.
• Endomyocardial biopsies can be performed during pacemaker implantation (reported in other species).

Treatment

• Medical management with sympathomimetic drugs.
• Transvenous endomyocardial pacemaker implantation vs epicardial pacemaker implantation.

Rechecks

• Medical management: recheck ECGs with dose titration at two weeks, one month, then every 6 months (or as often as deemed necessary to control rhythm).
• Pacemaker interrogation at 2 weeks, one month, then every 6 months.

• Cardiac output is significantly compromised, and blood pressure may be critically low, requiring emergency treatment.

Anesthesia

• Anesthesia pacemaker implantation is high risk due to the compromised cardiac output.
• The main goals of anesthesia are to improve cardiac output, avoid exacerbation of bradycardia, avoid accidental induction of ventricular fibrillation or Torsades de Pointes, and avoid hypotension.

⚠️Transcutaneous (external pacemaker) or transvenous temporary pacing should be in place during anesthetic induction so that the patient’s rhythm can be controlled through external pacing, as the premedication/induction can terminate the ventricular escape rhythm supporting cardiac output.  

• Drugs that increase afterload, thus reducing cardiac output, such as alpha2-agonists (dexmedetomidine, xylazine, medetomidine), should be avoided.
• Ventricular escape complexes should be addressed as these keep the patient alive.

• Although no specific information exists in rabbits, the etiology can be extrapolated by what is commonly seen in other species.
• Degenerative lesions interrupt the conduction pathways. These tend to be progressive and non-reversible.
• Congenital: it is primarily genetic in some species (no available data in rabbits) or secondary to other defects such as VSD or aortic stenosis.
• Inflammatory: myocarditis is more commonly seen in younger animals
• Infectious: primary infection associated with the AV system, eg trichinosis, vs secondary, such as aortic bacterial endocarditis, which diffuses into the AV node.
• Electrolyte: severe hyperkalemia.
• Idiopathic.
• Trauma: chest trauma or secondary to other surgical or intra-cardiac interventions.
• Neoplasia: neoplasia associated with the AV node, bundle of His and His-Purkinje system
• Neuromuscular disease, eg myasthenia gravis, muscular dystrophies, eg Duchene, etc.
• Endocrine, eg hypothyroidism.
• Iatrogenic: secondary to medications such as ß-blockers.
• Toxin: cardiac glycoside ingestion, eg digitalis.
• Myocardial infarction, eg occlusion of terminal branches of the left and right coronary arteries.

General

• Exercise and excitement can lead to syncope in 3^rd degree AV block.

• A pathological lesion occurs at the AV node, bundle of His, or the His-Purkinje branches.
• The structural lesion interrupts the specialized conduction pathways, infiltrating them with non-conductive cell populations and thus preventing the conduction of the depolarization wave from the atrial myocardium.
• Ventricular pacemaker cells below the AV node produce a ventricular or junctional escape rhythm that controls ventricular contraction.
• Lack of conduction through the atria into the ventricles results in an electrical disassociation of the two chamber groups, leading these to contract independently from one another.
• Ventricular and junctional pacemaker cells depolarize slower than the sino-atrial node, resulting in bradycardia and reduced cardiac output, which can result in syncope during increased cardiovascular demands.
• Sudden death may occur due to asystole or the development of malignant tachyarrhythmias.
• Canon jugular waves may be seen when the atrium contracts on a closed AV valve.
• Patients can be asymptomatic if the ventricular intrinsic rate is high enough (seen in other species, such as cats; no data is available in rabbits).

• Progressive in the case of degenerative and neoplastic with no reported timeline.
• Acute in the presence of trauma, inflammation, infection.

• Underreported in rabbits.
• Breed predispositions are seen in other species but not reported in rabbits.

Refereed papers

• Recent references from PubMed and VetMedResource.
• Machida N, Sasaki T, Kimura Y & Hirakawa A (2023) The anatomical basis of third-degree atrioventricular block in dogs with atrioventricular valve endocardiosis. J Comp Pathol 201, 63-69 VetMedResource.
• Machida N, Sasaki T & Kimura Y (2022) Histological features of the atrioventricular conduction system in cats with high-grade atrioventricular block. J Comp Pathol 190, 36-44 PubMed.
• Maneval K L, Karlin E T, Dos Santos L & Priest K (2022) Third-degree atrioventricular block secondary to infiltrative cardiac hemangiosarcoma in a dog. J Vet Cardiol 42, 43-46 PubMed.
• Ozawa S, Guzman D S, Keel K & Gunther-Harrington C (2021) Clinical and pathological findings in rabbits with cardiovascular disease: 59 cases (2001–2018). J Am Vet Med Assoc 259 (7), 764-776 PubMed.
• Sasaki T, Saeki C, Hirakawa A & Machida N (2020) Pathological features of complete atrioventricular block in dogs with lymphocytic myocarditis. J Comp Pathol 174, 18-25 PubMed.
• Gallay J, Bélanger M C, Hélie P et al (2011) Cardiac leiomyoma associated with advanced atrioventricular block in a young dog. J Vet Cardiol 13 (1), 71-77 PubMed.
• Lord B, Boswood A & Petrie A (2010) Electrocardiography of the normal domestic pet rabbit. Vet Rec 167 (25), 961-965 PubMed.
• Onuma M, Ono S, Ishida T et al (2010) Radiographic measurement of cardiac size in 27 rabbits. J Vet Med Sci 72 (4), 529-531 PubMed.
• Sanchez-Migallon Guzman D, Mayer J, Melidone R et al (2006) Pacemaker implantation in a ferret (Mustela putorius furo) with third degree atrioventricular block. Vet Clin North Am Exot Anim Pract 9 (3), 677-687 PubMed.
• Tsuji Y, Opthof T, Yasui K et al (2002) Ionic mechanisms of acquired QT prolongation and Torsades de Pointes in rabbits with chronic complete atrioventricular block. Circulation 106 (15), 2012-2018 PubMed.
• Opthof T, Coronel R, Rademaker H M E et al (2000) Changes in sinus node function in a rabbit model of heart failure with ventricular arrhythmias and sudden death. Circulation 101 (25), 2975-2980 PubMed.
• Hackett T B, Van Pelt D R, Willard M D et al (1995) Third degree atrioventricular block and acquired myasthenia gravis in four dogs. J Am Vet Med Assoc 206 (8), 1173-1176 PubMed.
• James T N (1967) Anatomy of the cardiac conduction system in the rabbit. Circ Res 20 (6), 638-648 PubMed.

Other sources of information

• Quesenberry K E, Orcutt C J, Mans C & Carpenter J W (2020) Cardiovascular Disease. In: Ferrets Rabbits & Rodents. Eds: Orcutt C L & Malakoff R. Elseviery, USA.  pp 250–257 SciDirect.