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 all over the world.
The heart is located in the thoracic cavity, its apex (tip of the heart) is directed backwards and slightly to the left; the base is directed forwards. Like other small animals, the rabbit heart is formed by 4 chambers, 2 atria and 2 ventricles separated by inter-auricular and inter-ventricular septa, but it also possesses some anatomical and physiological particularities.
Atria are thin walled chambers that receive blood, while the ventricles are thick walled muscular structures that pump the blood out of the atrium, back into the blood system.
When the left ventricle is not able to pump the blood out of the left atrium, or when the mitral valve is not working properly, the blood will accumulate in the lungs (left sided-heart failure). These become congested, leading to pulmonary edema (accumulation of fluids). As a consequence, the oxygen uptake and its movement from the lungs to the heart will be impaired, causing tiredness. It is often accompanied by labored breathing (dyspnea).
When the right ventricle is not able to function properly, or the tricuspid valve is defective, the blood pressure will rise, leading to fluid accumulation in body tissues, mainly the abdomen and the lower body parts.
The main cause for congestive heart failure is a malfunctioning of the left ventricle. Regularly it also is caused by a lack of movement or a diet deficiency (vitamin and mineral deficiencies) in rabbits. Further causes leading to this disorder include:
· 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.
Signs of congestive heart failure include tiredness, weakness, loss of appetite, intolerance to exercice, persistent coughing or wheezing, dyspnea.
Various clinical tests (see: Cardiology and techniques to detect cardiac diseases in rabbits) will often reveal an enlarged heart, increased heart rate, arrhythmia, and the presence of (lung) edema.
The treatment of congestive heart failure will not heal the problem, but helps keeping it under control. It includes the treatment of the underlying disease (e.g., pneumonia, treated with appropriate antibiotics), and the inset of medication that will prevent further deterioration of the heart function.
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 drugs (e.g., nitroglycerin) will help reduce the strain on the heart. Sometimes, therapeutic pleurocentesis is needed in a rabbit suffering from pleural effusion
and severe dyspnea. The cause(s) should be investigated, by means of echocardiography (ultrasound) for instance.
In rabbits, long-term management of congestive heart failure includes the use of:
· Angiotensin converting enzyme (ACE) inhibitors (e.g., enalapril) smoothen the blood vessels so that blood can flow more easily through them or give rest to the heart, in the hope that it will decrease in size and respiration will become easier. Enalapril has a slight little advantage over the other available drugs.
· Diuretics (e.g., furosemide) help reduce fluid buildup in the body. Increased excretion of water and sodium will reduce the symptoms of heart failure. Their dosage is based on the body weight. Indeed, to much will lead to dehydration and potential kidney failure, while to little will not bring the expected relief or improvement of the symptoms. The side effects of diuretics may be a low potassium blood level.
· Inotropic agents (e.g., digoxin) are used to stimulate a stronger heart beating 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). These drugs should only be used if a regular monitoring of the hydration state, body weight, appetite, and serum levels of electrolytes, BUN, and creatinine is possible.
Many thanks to Tom Chlebecek, DVM, (Makai Animal Clinic, Kailua, HI) and to Frossie Economou, for giving the permission to use the ultrasound picture.
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 Zooligical 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.