Congestive heart failure in rabbits

 

 

Esther van Praag, Ph.D. 

 

MediRabbit.com is funded solely by the generosity of donors.

Every donation, no matter what the size, is appreciated and will aid in the continuing research of medical care and health of rabbits.

Thank you  

 

 

The heart is located in the thoracic cavity. Its apex (the tip of the heart) is directed backwards and slightly to the left, while its base is directed forwards. The rabbit heart is similar to the hearts of other small animals in that it is formed by four chambers: two atria and two ventricles. These chambers are separated by inter-auricular and inter-ventricular septa. However, the rabbit heart also possesses some anatomical and physiological particularities.

Anatomy of the rabbit heart

Atria are thin-walled chambers that receive blood. In contrast, ventricles are thick-walled muscular structures that pump blood out of the atrium and back into the blood system.

In cases where the left ventricle is unable to expel blood from the left atrium, or when the mitral valve is malfunctioning, blood accumulation in the lungs can occur, leading to left-sided heart failure. Congestion of this nature can lead to pulmonary edema (the accumulation of fluids in the lungs). Consequently, the body's oxygen uptake and its movement from the lungs to the heart will be impaired, leading to tiredness. It is frequently accompanied by labored breathing, also known as dyspnea.

Impaired right ventricular function or tricuspid valve defects can lead to elevated blood pressure, resulting in fluid accumulation in body tissues, particularly in the abdomen and lower extremities.

Causes

The primary cause of congestive heart failure is a malfunctioning of the left ventricle. In many cases, this issue is caused by a lack of movement or a diet deficiency (vitamin and mineral deficiencies) in rabbits. There are additional factors that contribute to this disorder, including:

·         Arrhythmia (abnormal heart beat);

·         Bicuspid or mitral valve defect, either of congenital origin, or caused by an infection (viral or bacterial), or other diseases;

·         Coronary disease;

·         Myocardia related disorders, inflammation or cardiomyopathy;

·         Anemia or low red blood cell count;

·         Lung diseases, e.g., pneumonia.

Clinical signs

Indications of congestive heart failure may include generalized fatigue and weakness, anorexia, exercise intolerance, persistent coughing or wheezing and/or dyspnea.

Various clinical tests (see: Cardiology and techniques to detect cardiac diseases in rabbits) often reveal an enlarged heart, increased heart rate, arrhythmia, and the presence of (lung) edema.

Michel Gruaz

The presence of foam in the nasal cavity (arrow) in this Belgian bearded rabbit that died suddenly is the sign of a mixed pulmonary and cardiac distress.

.

Michel Gruaz

During the autopsy, heart of the same Belgian bearded rabbit, with dark heart auricles (arrows), after a heart attack and sudden death. 

Treatment

While there is no cure for congestive heart failure, treatment can help manage the condition. The treatment plan includes addressing the underlying disease, such as pneumonia, with appropriate antibiotics, as well as the administration of medication to prevent further deterioration of heart function.

Tom Chlebecek

“Two chamber view” ultrasound of a rabbit heart (LV = left ventricule, LA = left auricle), which permits evaluation of the motion of the anterior and inferior left ventricular myocardial segments. The mid-portion of the mitral valve motion is also evident.

Acute treatment of congestive heart failure consists of oxygen administration and rest in a quiet place. The use of diuretics will help relieve the sodium and fluid retention. Nitrate-based medications (e.g., nitroglycerin) can help reduce cardiac strain. Therapeutic pleurocentesis is indicated in rabbits with pleural effusion and severe dyspnea. The cause(s) should be investigated using echocardiography (ultrasound), for example.

In rabbits, long-term management of congestive heart failure includes the use of:

·           Angiotensin converting enzyme (ACE) inhibitors such as enalapril, are medications used to treat high blood pressure. These medications work by relaxing the blood vessels, which allows blood to flow more easily. They also reduce the workload on the heart, which can help it to decrease in size and improve respiration. Enalapril has a slight advantage over the other available drugs.

·           Diuretics, for example, furosemide is an effective medication that can help reduce fluid buildup in the body. It increases the excretion of water and sodium, which can lead to a reduction in the symptoms associated with heart failure. Dosage is determined by body weight. It can indeed lead to dehydration and potential kidney failure, while insufficient intake may not provide the anticipated relief or improvement in symptoms. Potential side effects of diuretics include low potassium levels in the blood.

·           Inotropic agents (e.g., digoxin) are used to stimulate a stronger heartbeat and slightly increase the amount of blood pumped out of the left ventricle at each contraction. In rabbits, they are used to control sub-acute and chronic disorders of the myocardium, supraventricular arrhythmia, or valve regurgitation (leakage of blood from the ventricle back into the atrium during systole). The use of these medications is contingent upon adequate monitoring of the hydration status, body weight, appetite, and serum electrolyte, BUN, and creatinine levels.

Acknowledgement

I would like to express our gratitude to Tom Chlebecek, DVM (Makai Animal Clinic, Kailua, HI), Frossie Economou, and Michel Gruaz (Switzerland) for granting me permission to use their pictures on this MediRabbit webpage.

Further information

M.V. Bray MV, WE. C. Weir EC, D. G. Brownstein, M. L. Delano, (1992) Endometrial venous aneurysms in three New Zealand white rabbits. Lab Anim Sci.; 42(4):360-2.

Farkas, A. J. Batey, S. J. Coker (2004) How to measure electrocardiographic QT interval in the anaesthetized rabbit. J Pharmacol Toxicol Methods.; 50:175-85. 

L.C. St John, F. P. Bell (1990) Arterial fatty acid-binding protein activity associated with dietarily-induced and spontaneously occurring atherosclerosis in the rabbit (Oryctolagus cuniculus). Comp Biochem Physiol B.; 97(1):123-7. 

C. Kozma, W. Macklin, L. M. Cummins, R. Mauer (1974) The anatomy, physiology and biochemistry of the rabbit, in The Biology of the Laboratory Rabbit (Weisbroth et al., eds), pp 50-69.

L. I. Kupferwasser, M. R. Yeaman, S. M. Shapiro, C. C. Nast, A. S. Bayer (2002) In vitro susceptibility to thrombin-induced platelet microbicidal protein is associated with reduced disease progression and complication rates in experimental Staphylococcus aureus endocarditis: microbiological, histopathologic, and echocardiographic analyses. Circulation; 105:746-52.

C. J. Orcutt (2000) Cardiac and respiratory disease in rabbits. Proceedings of the British veterinary Zoological Society (Autumn meeting).

K. E. Quesenberry, J. W. Carpenter, P. Quesenberry (2004) Ferrets, Rabbits and Rodents: Clinical Medicine and Surgery Includes Sugar Gliders and Hedgehogs, Elsevier Health, pp 211-216.

R. S. Simons (1996) Lung morphology of cursorial and non-cursorial mammals: lagomorphs as a case study for a pneumatic stabilization hypothesis. J Morphol. 1996; 230(3):299-316.

F. Harcourt-Brown Textbook of Rabbit Medicine, Oxford, UK: Butterworth-Heinemann, 2001.

 

 

e-mail: info@medirabbit.com