Download ACCELERATED IDIOVENTRICULAR RHYTHM

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ACCELERATED
IDIOVENTRICULAR
RHYTHM
Authored by
Nick Schroeder, D.V.M.
DACVIM (Cardiology)
Ventricular rhythms that are faster than ventricular escape, but
slower than classical ventricular tachycardia are termed accelerated
ventricular rhythms. Most ventricular escape rhythms have an
inherent heart rate of 20-45 beats-per-minute (bpm) in the dog.
Ventricular tachycardia is present if the rhythm is ventricular and the
heart rate is arbitrarily over 180 bpm. Everything in between (heart
rate 45-180 bpm) is considered to be accelerated, and usually the
result of increased normal or abnormal automaticity occurring in
the Purkinje fibers of origin. This may be the result of ischemia
with subsequent reperfusion, hypoxia, electrolyte abnormalities
as well as drugs (digitalis intoxication). The term accelerated
idioventricular rhythm is used if atrioventricular dissociation is
present. If ventriculoatrial association is present, then the term
accelerated ventricular rhythm is used. This means the ventricular
focus completely depolarizes the atrioventricular node retrogradely,
capturing the atrial myocardium and sinus node from the bottom
up. Most of the time, atrioventricular dissociation is present, and
thus the prefix idio- is retained.
Atrioventricular dissociation is a condition that refers to the atria
and the ventricles beating independently of one another. This is a
broad category that involves multiple different electrocardiographic
phenomena. This means that “atrioventricular dissociation” is
not an electrocardiographic diagnosis, but rather a symptom of
an underlying arrhythmic mechanism. Ventricular tachycardia,
accelerated idioventricular rhythm, automatic junctional tachycardia
and accelerated idiojunctional rhythm (both types of supraventricular
tachycardia), block/acceleration dissociation and third degree
atrioventricular block all may create atrioventricular dissociation.
Atrioventricular dissociation is termed “incomplete” (or
“interference” atrioventricular dissociation) if fusion complexes or
capture beats occur. A ventricular fusion complex is the result of
an impulse originating at or above the atrioventricular node that
merges with a depolarization initiated in the ventricle. The resultant
QRS complex is intermediate in morphology between that of the
supraventricular (usually sinus) focus and that of the ectopic focus
in the ventricles and is preceded by a P wave, often with a short
P-R interval. A capture beat is the first supraventricular beat (again,
usually sinus) that occurs following a run of ectopic rhythm. If
atrioventricular dissociation is incomplete, then the atrioventricular
node is still capable of impulse transmission only if it is no
longer refractory. Often the sinus rhythm is irregular (i.e. a sinus
arrhythmia), and as it slows down a focus in the ventricles may take
over until the sinus node outcompetes it again. Whichever focus
is faster will dominate the rhythm. Atrioventricular dissociation is
termed “complete” if no fusion complexes or capture beats occur,
and the atrioventricular node is incapable of impulse transmission.
This really only occurs in the setting of 3rd degree atrioventricular
block, when the atrioventricular dissociation occurs by default.
FROM VETERINARY SPECIALISTS
OF SOUTH FLORIDA
Phone: (954) 437-9630
www.vetspecialistsofsfl.com
Paper speed 50 mm/s, 1 cm/mV, lead II, canine with right atrial mass and pericardial effusion. Sinus arrhythmia, incomplete atrioventricular dissociation
secondary to usurpation by accelerated idioventricular rhythm. A right ventricular focus (producing a left bundle-branch block pattern) captures the rhythm
before the second sinus beat is conducted, resulting in an accelerated idioventricular rhythm. The 5th complex is a sinus capture beat, and accelerated
idioventricular rhythm resumes after the 6th beat. The 11th beat is another capture (the P wave is hiding in the T wave of the last ventricular complex). The
sinus rate is approximately 111-150 bpm, and the rate of the ventricular focus is similar at 130 bpm.
Paper speed 25 mm/s, 1 cm/mV, lead II, canine with immune-mediated hemolytic anemia. Sinus arrhythmia, incomplete atrioventricular dissociation secondary
to usurpation by accelerated idioventricular rhythm. A left ventricular focus (producing a right bundle-branch block pattern) captures the ventricles with the
3rd complex (which is a fusion beat). The resulting accelerated idioventricular rhythm is hemodynamically well-tolerated by the dog since the sinus rate and
the rate of the ventricular focus are both at around 125-150 bpm.
Paper speed 25 mm/s, 1 cm/mV, lead II, canine. Sinus arrhythmia, incomplete atrioventricular dissociation secondary to usurpation by accelerated
idioventricular rhythm. The idioventricular rhythm is interrupted by periods of sinus rhythm. Note that the ventricular focus takes over when the sinus rate
slows. This patient had a splenic infarction following a gastric dilatation/volvulus and surgical gastropexy. Accelerated idioventricular rhythm is very common
following this kind of surgery and is typically well-tolerated by the patient, poorly-responsive to antiarrhythmics, and self-limiting. Persistent arrhythmias and
colic in this patient more than 72 hours post-operative indicated an unresolved problem. Timely splenectomy resulted in resolution of the arrhythmias.
It is important to distinguish whether atrioventricular dissociation
is occurring secondary to usurpation or by default. A rapid ventricular
or junctional focus that outpaces the sinus node and takes control
of the ventricles often results in atrioventricular dissociation. This
is also termed atrioventricular dissociation due to usurpation, and
the atrial (usually sinus) rate is normal or fast, but still less than
that of the ventricles. Automatic junctional tachycardia, accelerated
idiojunctional rhythm, ventricular tachycardia and accelerated
idioventricular rhythm all may cause atrioventricular dissociation
via usurpation. If atrioventricular dissociation is secondary to
usurpation and the ventricular rate becomes unacceptably fast
and hemodynamically compromising (i.e. during ventricular
tachycardia with a HR of 250-300 bpm), then intervention is clearly
indicated. Slowing of the sinus rate, sinus arrest, atrial standstill
and atrioventricular block may result in atrioventricular dissociation
by default, in which case a junctional or ventricular escape rhythm
may take over. When atrioventricular dissociation occurs by default,
suppression of the rescuing focus may result in life-threatening
bradycardia.
Otherwise known as “slow ventricular tachycardia,” accelerated
idioventricular rhythm is usually monomorphic and only rarely
polymorphic, irregular or associated with R on T phenomenon. If
a premature beat depolarizes the ventricles again (producing an R
wave) right when the ventricles are repolarizing from the previous
beat (during the T wave), then ventricular fibrillation can result. This
is termed “R on T,” and since it only happens when the heart rate
is fast, it is uncommonly associated with accelerated idioventricular
rhythm. The QRS complexes are typically prolonged at 0.06s or
greater. The on and off-set of accelerated idioventricular rhythm
is commonly associated with various degrees of ventricular fusion,
occasionally confusing the examiner with multifocal ventricular
arrhythmias. In the hospital setting, these arrhythmias are often
described as “runs of ventricular premature complexes.” Arguably
the most overtreated arrhythmia in veterinary medicine, accelerated
idioventricular rhythm is quite common among our patients that
have gastric-dilatation/volvulus, hemoabdomen from ruptured
splenic or hepatic neoplasia (usually hemangiosarcoma), pericardial
effusion (post-pericardiocentesis, usually secondary to ruptured
right atrial mass from hemangiosarcoma), immune-mediated
hemolytic anemia, or traumatic myocarditis (hit-by-car). Typically,
NOT associated with excessively fast tachycardia or hemodynamic
compromise, accelerated idioventricular rhythm responds poorly
to typical antiarrhythmic therapy for ventricular tachycardia, is
secondary to non-cardiac issues, and often will resolve on its own
following correction of the underlying disorder.
While it is important to monitor patients with ventricular
arrhythmias, especially while hospitalized, pharmacologic
intervention in patients with accelerated idioventricular rhythm is
almost never warranted. Generally if the heart rate is under 200
bpm and the patient’s blood pressure is within normal limits, then
antiarrhythmic therapy is of no real value. The most commonly used
intravenous medication for ventricular tachycardia is the sodiumchannel blocker lidocaine, which is frequently administered to
patients with accelerated idioventricular rhythm. Lidocaine actually
works well for ventricular tachycardia when the arrhythmia is
secondary to reentry in patients with structural heart disease (i.e.
dilated cardiomyopathy in Boxers and Doberman Pinschers). This
is because the drug preferentially acts on diseased myocardial cells.
When patients have accelerated idioventricular rhythm, the cytokines
circulating in the bloodstream that are the presumed root cause
tend to persist until the underlying problem is resolved. An apparent
therapeutic success is often attributed to lidocaine in such patients
as the patients naturally go in and out of sinus rhythm as the sinus
node competes for control of the heart with the focus producing the
accelerated idioventricular rhythm. The best approach is to place
these patients on telemetry, monitor the arrhythmias and continue to
search for and treat the underlying problem until it resolves.
OUR TEAM.
Cardiology
Emergency and Critical Care Services 24/7/365
Kathleen Kersey, D.V.M.
Nick A. Schroeder, D.V.M.
Practice Limited to Emergency & Critical Care Medicine
Diplomate, A.C.V.I.M.(Cardiology)
Dr. Kersey received her DVM degree from the University of Illinois
in 2007. She then completed a small animal medicine and surgery
internship at Veterinary Specialists of South Florida. Dr. Kersey then
completed a three year residency in Emergency & Critical Care
Medicine with Veterinary Specialists of South Florida in July 2011.
Her professional interests include sepsis and septic peritonitis,
trauma, and immune-mediated disease. In her free time, Dr. Kersey
enjoys running, going to the beach, and spending time with her
family.
Dr. Schroeder received his D.V.M. from Kansas State University College of
Veterinary Medicine, served his internship here at VSSF, and completed
his cardiology residency under the guidance of renowned Cardiologist
and author, Dr. Steve Ettinger at California Animal Hospital. He has
also lectured locally and nationally. Dr. Schroeder offers a full range of
services in cardiology and pulmonary medicine.
24/7 EMERGENCY CRITICAL CARE SERVICES
Surgery
Jason Horgan, D.V.M.
David Spranklin, D.V.M.
Diplomate, A.C.V.E.C.C.,
Diplomate, A.C.V.S.
Practice Limited to Surgery
Dr. Horgan is a South Florida native who grew up in Hollywood.
He received his doctorate in veterinary medicine at the Ohio State
University. Dr. Horgan joined VSSF for a small animal emergency/
critical care residency, which he completed in July 2008. He
received his board certification in Emergency/Critical Care Medicine
in October of 2009. Dr. Horgan is VSSF’S ICU Medical Director
and will continue to maintain the cutting edge medical care VSSF
has always provided. He will also be attending to emergency and
critical care cases personally and offering dialysis, endoscopy and
long term ventilation.
Radiology, Radiation Oncology
Ronald L. Burk, DVM, MS, MBA
Diplomate, A.C.V.R. (Radiology, Radiation Oncology)
9410 Stirling Road Cooper City, FL 33024
Telephone: (954) 437-9630 Fax: (954) 437-7207
www.vetspecialistsofsfl.com
Hours by Appointment Only
Dr. Burk received his DVM from Purdue University, served his internship
at the Henry Bergh Memorial Hospital of the ASPCA and completed his
MS and residency in Veterinary Radiology at the University of Missouri.
The American College of Veterinary Radiology has certified him in both
Diagnostic Radiology and Radiation Oncology. Dr. Burk served as Chief
of Radiology and Radiation Oncology as well as Assistant Chief of Staff at
the Animal Medical Center in New York City for 13 years. Dr. Burk provides
diagnostic imaging services (including ultrasound, fluoroscopy, CT and
MR scan), radiation therapy for cancer, and radioiodine therapy for feline
hyperthyroidism. Dr. Burk has served as Chief of Staff of VSSF since 1994.
Dr. Spranklin is a fifth generation veterinarian. He received his D.V.M.
from Virginia-Maryland Regional College of Veterinary Medicine and
completed his internship at Mississippi State University College of
Veterinary Medicine. Dr. Spranklin completed his surgical residency
at Washington State University in Pullman, Washington. Dr. Spranklin
performs soft tissue, orthopedic, oncologic and neurosurgery with a
special interest in minimally invasive surgery (laparoscopy, thoracoscopy,
and arthroscopy). He is a board certified member of the American College
of Veterinary Surgeons (ACVS) as well as a member of the AVMA and
BCVMA. Dr. Spranklin works to provide the newest techniques and
procedures in veterinary surgery to offer our patients both state-of-theart and personalized care.
Jason Horgan, D.V.M.
Diplomate, A.C.V.E.C.C.,
Practice Limited to Surgery
Dr. Horgan has completed his surgical residency and has joined Dr.
Spranklin as one of VSSF staff surgeons. Dr. Horgan performs soft tissue,
orthopedic, neurological, oncological and minimally invasive surgery. His
unique background, being trained in two specialties that often go hand
in hand, make him particularly qualified to deal with difficult surgical
patients. Most important to Dr. Horgan is spending time with his wife,
Robin, “little man” Rylee, canine girls “Hannah” and “Maddie” and the
rest of his family.