Equis ISSN 2398-2977

Heart: ventricular premature complex

Contributor(s): Christopher Brown, Wendy Furness, Lesley Young

Introduction

  • Cause: abnormal premature impulses originating from tissue below the atrioventricular node, ie the AV junction, His-Purkinje network or the ventricular myocardium.
  • Signs: if an isolated finding there may be no clinical signs; if persistent and numerous, or associated with cardiac disease or other systemic disease, there may be cardiovascular collapse and exercise intolerance in addition to signs related to the primary disease process.
  • Diagnosis: auscultation, ECG.
  • Treatment: in primary cases, rest should be advised and steroids have been advocated. In secondary cases, treatment should focus on treatment of the underlying disease and correction of fluid metabolic and electrolyte disturbances. If life-threatening, VPCs can sometimes be controlled with lidocaine, quinidine gluconate, popafenone or procainamide.
  • Prognosis: related to the severity of the underlying disease process if VPCs are isolated and there are no clinical signs then prognosis is fair to good. It is much more guarded if there is evidence of myocardial damage or severe cardiac disease.

Pathogenesis

Etiology

  • Hypoxia.
  • Ventricular myocardial disease.
  • Elecytrolyte and metabolic disturbances.
  • Elevated sympathetic tone.
  • Pyrexia.
  • Toxemia.

Pathophysiology

  • Normal sinus rhythm is interrupted by a premature depolarization that originates from below the AV junction   Heart: ventricular premature complex 01 - ECG  .
  • As the atria are electrically isolated from the AV junction and ventricles, there is no retrograde conduction of the premature beat and the sinus node and atria are unaffected.
  • AV dissociation is the hallmark of ventricular or junctional premature beats.
  • The normal sinus P wave is still present at the normal rate, but it may be buried in the QRS complex of the ectopic beat, or be visible in isolation   Heart: ventricular premature complex 04 - ECG    Heart: ventricular premature complex 05 - ECG  .
  • Usually the sinus impulse does not then result in ventricular contraction as the ventricular tissue is still refractory and cannot respond. This results in a compensatory pause before the next sinus complex which follows exactly 2P-P intervals after the last conducted sinus beat.
  • As ventricular depolarization does not follow the normal pathway, the QRS complex of an ectopic beat is altered from the normal sinus beats. If the pulse eminates from the myocardium, the complexes will be wide and bizarre   Heart: ventricular premature complex 01 - ECG    Heart: ventricular premature complex 03 - ECG    Heart: ventricular premature complex 04 - ECG  . If, however, it comes from within the AV junction, or conduction tissues, it will only be subtly different from the normal complexes   Heart: ventricular premature complex 01 - ECG      Heart: ventricular premature complex 02 - ECG      Heart: ventricular septal defect 05 - echocardiograph  .
  • If the ectopic beat is times such that it falls on the T wave of the preceding beat, the myocardial cells are stimulated during their relative refractory period and are highly vulnerable to the development of ventricular fibrillation. This is the R on T phenomenon and is potentially very dangerous.

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.
  • Pipers F S (1995) Equine cardiovascular medicine - past, present and future. Equine Vet J Suppl 19, 3-4 PubMed.
  • Reimer J M, Reef V B & Sweeney R W (1992) Ventricular arrhythmias in horses, 21 cases (1984-1989). JAVMA 201 (8), 1237-1243 PubMed.
  • Glendinning S A (1977) The clinician's approach to equine cardiology. Equine Vet J (4), 176-177 PubMed.

Other sources of information

  • Reef V B (1999) Arrhythmias. In: Cardiology of the Horse. Ed: Marr C M. W B Saunders, UK. Chapter 12pp 179-209.


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