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Chapter 18: Arrhythmias and Other Electrocardiographic Abnormalities  233


              devastating  proportion  of  feline  cardiomyopathy   ing cause eliminated, or monthly, or even more often if
              patients, either spontaneously or in association with a   overt  clinical  signs  such  as  syncope  are  present).  The
              stressful episode such as general anesthesia. Stratification   purpose of follow-up is to update the history (has the
              of risk of life-threatening episodes such as these is poorly   client observed a change in clinical signs?) and physical
              understood in cats at the present time. The presence of   examination; perform an ECG to identify new arrhyth-
              clinical signs (dyspnea, lethargy, hiding, or other signs   mias if present; and perform diagnostic tests (blood or
              of  congestive  heart  failure;  syncope;  pulselessness  or   radiographic  examinations)  as  indicated  by  history  of
              other signs of aortic thromboembolism) and the degree   clinical  signs,  current  medications,  etc.  Subsequent
              of ventricular distortion (hypertrophy or other change)   rechecks  similarly  evaluate  these  parameters  at  a
              probably are negative general prognostic indicators with   minimum and include follow-up telemetry or Holter/
              PVCs,  markers  that  may  occur  more  commonly  in   event monitoring if done previously.
              arrhythmic cats that have a somewhat worse long-term
              prognosis.  Long-term  clinical  studies  are  needed  to   Accelerated Idioventricular Rhythm
              confirm  these  suspicions,  and  currently  a  markedly   A  rhythm  that  consists  of  4  or  more  PVCs  occurring
              worse  prognosis  (and  ensuing  decision  not  to  pursue   consecutively but where the rate is less than the defined
              treatment  or  to  euthanize)  for  PVCs  cannot  be  sup-  rate for ventricular tachycardia (VT; 240 beats/minute)
              ported  by  degree  of  concurrent  echocardiographic   is  called  accelerated  idioventricular  rhythm  (AIVR)
              change,  for  example:  there  are  likely  too  many  other   (see  Figure  18.15).  Initially  termed  “slow  ventricular   Arrhythmias
              variables  to  pin  a  prognosis  on  these  parameters     tachycardia”—a  contradiction  in  terms—AIVR  occurs
              alone  and  a  great  deal  of  overlap  exists  between  cats    for the same reasons as PVCs and VT. The major differ-
              that do well despite these parameters and cats that do   ence is that the slower rate of AIVR provides more time
              poorly.                                            for diastolic ventricular filling, and therefore is a more
                 A likely prelude to syncope or sudden cardiac death   hemodynamically effective rhythm than VT. AIVR and
              is PVCs, and one of the greatest misconceptions in car-  VT likely represent different parts of one continuum, and
              diology is that proactive control or elimination of ven-  the lower end of this continuum is approximately 120
              tricular  arrhythmias  with  antiarrhythmic  medications   beats/minute in the cat; ventricular rhythms lower than
              could  reduce  the  risk  of  sudden  death.  Indeed,  as  in   this rate are in fact a ventricular escape rhythm, beneficial
              human cardiology, “rendering treatment to suppress a   expressions of spontaneous ventricular activity that save
              risk factor [asymptomatic PVCs] because of the tempta-  the heart from catastrophic bradycardia or asystole (see
              tion  to  equate  causality  with  association  between  the   the discussion of third-degree AV block, below). AIVR is
              risk  factor  and  a  putative  clinical  outcome  has  never   generally  well-tolerated,  and  treatment  is  therefore
              been more misguided than with nonsustained ventricu-  directed at the underlying cause; antiarrhythmic medica-
              lar tachycardia (Marinchak et al. 1997).” Thus, in feline   tions  are  not  considered  unless  management  of  the
              heart disease, the prognosis associated with PVCs is not   underlying cause is ineffective at abolishing the arrhyth-
              conclusively  worse  than  that  of  normal  sinus  rhythm   mia and the rate increases to the point that the criteria for
              given that both can occur with cardiomyopathy, and no   VT are met.
              study has evaluated the benefit or harm associated with
              treating  ventricular  arrhythmias  with  antiarrhythmic   Ventricular Tachycardia
              drugs in asymptomatic cats. Certainly, treating inciden-  As mentioned earlier, ventricular tachycardia (VT) is the
              tally  discovered  PVCs  in  asymptomatic  humans  has   occurrence of 4 or more PVCs consecutively at a rate of
              been shown conclusively to be harmful with several anti-  240 beats/minute or greater (Figure 18.17). Accordingly,
              arrhythmic  drugs  (causing  worsening  arrhythmias  or   a major difference between PVCs and VT is that PVCs,
              “proarrhythmia”) (Echt et al. 1991; Cardiac Arrythmia   since they occur as only 1 or a few at a time, have little
              Suppression Investigators 1992)). In cats, the prognosis   or no negative hemodynamic impact. Organ perfusion
              of the concurrent cardiomyopathy is likely the dominant   and oxygen delivery are not affected to a clinically mean-
              factor rather than the prognosis of the arrhythmia. Cats   ingful extent by individual PVCs. Conversely, VT may
              with PVCs but no associated signs of syncope or collapse   occur for any length of time and at any rate, including
              should  be  treated  with  medications  that  reverse  or   rapid VT (>280 beats/minute) wherein diastolic filling
              correct  triggers  that  exist  (e.g.,  concurrent  hyperthy-  of the ventricles is compromised and a reduced, possibly
              roidism, hypokalemia, or other), and followed up rou-  inadequate, cardiac output occurs.
              tinely: typically within 1–2 weeks of diagnosis at first,   The causes, mechanisms, associated conditions, sig-
              and  then  as  dictated  by  clinical  signs  (e.g.,  every  3–6   nalment, differential diagnoses, and diagnostic evalua-
              months if the arrhythmia is asymptomatic and underly-  tion of patients with VT are the same as for PVCs (above)
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