Canis ISSN: 2398-2942

Heart: ventricular septal defect

Synonym(s): VSD

Contributor(s): Serena Brownlie, Daniel Schrope, Rachel Blake

Introduction

Pathogenesis

Etiology

  • Embryological - may be inherited - failure of closure of interventricular septum.
  • Most commonly defect is in membranous portion of ventricular septum (upper region); under septal leaflet of tricuspid valve; and in left ventricular outflow tract below aortic valve. Rarely defect is in lower, muscular region of septum.

Predisposing factors

General
  • Heredity; ?breed lines.

Specific

  • Polygenic in Keeshond Keeshond.
  • Autosomal dominant with incomplete penetrance or polygenic in English Springer Spaniel.
  • Autosomal recessive in Beagle.

Pathophysiology

  • Embryological failure of interventricular septum, leaving conduit between left ventricle and right ventricle → left ventricular pressure exceeds normal right ventricular pressure in systole → systolic left-to-right shunting occurs across the defect.
  • Large defects in lower part of septum (less common) → volume overload of right ventricle, pulmonary circulation, left atrium and left ventricle.
  • Defects higher in septum (more common) → discharge into the pulmonary artery → overloaded pulmonary circulation, left atrium and left ventricle.
  • Majority of shunting occurs in systole when blood is leaving right heart out pulmonary artery → increased blood volume out pulmonary artery → volume overloaded pulmonary circulation → increased pulmonary venous return to left atrium (dilates) and left ventricle (dilation and eccentric hypertrophy), volume overloaded left heart → eventually left-sided congestive heart failure Heart: congestive heart failure.
  • Magnitude of flow through VSD depends on size of defect and systemic and pulmonary vascular resistance.
  • Small defects, where the small orifice is 'restricting' left-to-right shunting, are known as restrictive VSDs. Restrictive VSD prevents transmission of left ventricular pressures to right ventricle, so pressure gradient between right and left ventricle remains high.
  • Higher pressure gradient between right and left ventricle with smaller defects mean smaller defects have louder murmurs; degree of murmur not related to severity of disease.
  • Large defects are associated with loss of the pressure gradient between the left and right ventricles and shunt from left to right may even be laminar (so low grade murmur). Large defects may have diastolic bidirectional shunting, even with systolic left-to-right shunting. Therefore, can have continuous murmur.
  • The aortic valve may prolapse into the VSD, resulting in aortic regurgitation during diastole which can contribute to left ventricular overload.
  • Small VSDs carry a good prognosis, and may close completely due to scar tissue forming across the defect, or a portion of the septal leaflet of the tricuspid valve may seal the defect.
  • Right ventricular dilation can occur with large VSDs that allow significant flow left to right during diastole. Right ventricular volulme overload may also occur with more apically located VSD.
  • If the left-to-right shunt is severe, pulmonary hypertension Pulmonary Arterial Hypertension (PHT) can uncommonly develop (4% of cases). This can cause an increase in right heart pressures leading to right ventricular hypertrophy and right-to-left shunting. This may manifest as cyanosis, dyspnea, and polycythemia. This is called 'Eisenmenger's Syndrome'.

Timecourse

  • From birth.
  • Progression or development of clinical signs depends on size of defect and presence of concurrent defects.
  • If large defect, clinical signs may be seen <2 years of age.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bomassi E, Misbach C, Tissier R et al (2015) Signalment, clinical features, echocardiographic findings, and outcome of dogs and cats with ventricular septal defects: 109 cases (1992-2013). JAVMA 247 (2), 166-175 PubMed.
  • Schrope D P (2015) Prevalence of congenital heart disease in 76,301 mixed-breed dogs and 57,025 mixed-breed cats. J Vet Cardiol 17 (3), 192-202 PubMed.
  • Shimizu M, Tanaka R, Hoshi K et al (2006) Surgical correction of ventricular septal defect with aortic regurgitation in a dog. Aust Vet J 84 (4), 117-121 PubMed.
  • Rausch W P & Keene B W (2003) Spontaneous resolution of an isolated ventricular septal defect in a dog. JAVMA 223 (2), 219-220 PubMed.
  • Eyster G E (1994) Atrial septal defects and ventricular septal defect. Semin Vet Med Surg (Sm Anim) (4), 227-233 PubMed.
  • Sisson D, Luethy M & Thomas W P (1991) Ventricular septal defect accompanied by aortic regurgitation in five dogs. JAAHA 27 (4), 441-448 VetMedResource.
  • Eyster G E, Whipple R D, Anderson L K et al (1977) Pulmonary artery banding for ventricular septal defects in dogs and cats. JAVMA 170 (4), 434-438 PubMed.

Other sources of information

  • Kittleson M D (2005) Ventricular Septal Defects. In: Small Animal Cardiovascular Medicine. 2nd edn (e-edition) Kittleson M D & Kienle R D (eds). Mosby.
  • Bonagura J D & Lehmkuhl L B (1999)Congenital heart disease.In:Textbook of Canine and Feline Cardiology.2nd edition. Fox P R, Sisson D, Moise N S (eds). W B Saunders, Philadelphia. pp 471-535.
  • Brown W (1995)Ventricular Septal Defects in the English Springer Spaniel.In:Kirk's Current Veterinary Therapy XII.Bonagura J D (ed). W B Saunders, Philadelphia. pp 827-830.


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