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200  Section 3  Cardiovascular Disease

            arrhythmias, usually within 72 hours. Dogs with single   Ventricular premature depolarizations  can occur  in
  VetBooks.ir  VPCs and underlying myocardial disease may or may not   patterns such as ventricular bigeminy (every other beat is
                                                              a VPC) and ventricular trigeminy (every third beat is a
            need to be treated. More often, the presence of VPCs in
            a patient with underlying heart disease indicates the
                                                              with severity or potential malignancy of a ventricular
            need to further investigate the arrhythmia (e.g., with     VPC). This type of pattern, however, does not correlate
            24‐hour ambulatory ECG [Holter] analysis) to determine   rhythm.  More  important  characteristics  of  potentially
            if more serious arrhythmias are occurring at other times   dangerous ventricular arrhythmias include the rate of
            (Figure 20.1).                                    firing of a VPC and the morphology of a ventricular
             An example would be a Doberman pinscher with     rhythm. If a VPC fires rapidly and occurs close to the
            dilated cardiomyopathy, who is already receiving therapy   peak of the preceding T‐wave (so‐called R‐on‐T phe-
            but is found to have a newly discovered ventricular   nomenon), depolarization during this time may predis-
            arrhythmia. Immediate introduction of antiarrhythmic   pose to ventricular fibrillation (Figure 20.4).
            therapy in this case may or may not be appropriate and   Ventricular rhythms can be monomorphic (one
            further evaluation with Holter monitoring would be rec-    morphology) or polymorphic (several different mor-
            ommended. Patients with VPCs do not show clinical   phologies), with the polymorphism generally considered
            signs associated with only single premature beats. Even   to imply multiple origins or pathways for the arrhythmia,
            with ventricular tachycardia, if the rate of the ventricular   thus increasing the potential for degeneration into a
            is below 200–220 bpm, no clinical signs may be present.   malignant arrhythmia (Figure 20.5).
            The rate at which a ventricular tachycardia will cause   A ventricular couplet is two consecutive VPCs, a
            clinical signs will depend on many underlying factors     ventricular triplet is three consecutive VPCs, and ven-
            such as rate, underlying myocardial  function,  species,   tricular tachycardia is >3 consecutive VPCs occurring at
            and/or breed. Typically, however, when the rate of the   a rate of >170–180 bpm. Ventricular tachycardia is
            ventricular tachycardia is rapid (greater than 250 bpm),     considered sustained if it lasts >30 seconds and nonsus-
            signs of poor cardiac output will be present and syncope   tained if it lasts <30 seconds. A ventricular rhythm that is
            may occur. Clinical signs will also be influenced by the   less than approximately 140–170 bpm is not truly a
            degree of underlying heart disease. Thus, the patient     tachycardia and is therefore best termed an accelerated
            with systolic dysfunction and ventricular arrhythmias   idioventricular rhythm (sometimes referred to as slow
            may exhibit clinical signs at a slower ventricular rate than   ventricular tachycardia) (Figure 20.6).
            a patient without underlying myocardial disease and   Accelerated  idioventricular rhythms  are seen com-
            ventricular tachycardia. Patients with more serious ven-  monly in hospitalized patients in association with noncar-
            tricular arrhythmias (ventricular tachycardia, ventricu-  diac diseases as mentioned in the beginning of the chapter.
            lar fibrillation) and compromised/diminished myocardial   These are often benign, the rate is too slow to cause  clinical
            function may have a history of exercise intolerance,   signs and they often do not require therapy.
            shortness of breath, syncope or near syncope.

                                                                Therapy
              Diagnosis
                                                              Prior to discussing specific therapeutic interventions, it is
            Two basic ECG characteristics of VPCs are that they   important to review the main objectives of treating a ven-
            are premature in their timing (earlier than the sinus   tricular arrhythmia: (1) to improve hemodynamics in order
            beat) and they are wide and bizarre in morphology   to alleviate clinical signs and (2) to prevent sudden death.
            compared to the sinus beat (Figures  20.2 and 20.3).   When making the decision to treat or not, it is impor-
            They appear wide and bizarre because VPCs originate   tant to attempt to determine whether the arrhythmia is
            below  the bundle  of His and  therefore cannot take   causing hemodynamic compromise. A healthy heart can
            advantage of the specialized conduction system. They   tolerate  many  types  of  VA  whereas  a  diseased  heart
            therefore must depolarize the ventricles muscle cell to     cannot. Therefore, the presence or absence of underlying
            muscle cell. This is relatively slow and produces a wide   cardiac disease is an important factor in this decision.
            and bizarre complex. QRS complexes can be positive or   Evaluation of the peripheral pulse quality, mucous mem-
            negative in lead II, depending on the site of origin of the   brane color, attitude of the patient, and arterial blood
            VPC, and they have no relationship to the P‐waves.   pressure can be helpful in determining whether hemody-
            Because depolarization occurs in an abnormal fashion,   namics are being affected. Sustained ventricular tachy-
            repolarization is also abnormal and there is typically a   cardia at a high rate is more likely to cause hemodynamic
            large and bizarre T‐wave which is opposite in polarity   compromise than an idioventricular rhythm or a ven-
            to the VPC.                                       tricular tachycardia firing at slower rates.
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