Vol. 21, No.
9 September 1999 V 20TH ANNIVERSARY
CE Refereed Peer Review
FOCAL POINT
★ Supraventricular tachycardias
(SVTs) are common in dogs
and cats and, if pathologic, are
most often associated with
cardiac diseases that cause
enlarged atria.
KEY FACTS
■ The most common SVT in dogs
and cats is sinus tachycardia,
which occurs as a normal
response to physiologic,
pathologic, or drug-induced
conditions.
■ In cats, atrial tachycardia most
often occurs in conjunction with
hyperthyroidism or hypertrophic
cardiomyopathy.
■ Atrial fibrillation is most common
in middle-aged male giant-breed
dogs and may be an incidental
finding; when associated with
congestive heart failure, however,
the prognosis is poor.
■ Junctional tachycardia, an
infrequent finding in dogs and
cats, is usually caused by digitalis
toxicity.
Supraventricular
Tachycardias in
Dogs and Cats*
The Ohio State University
Tamara Grubb, DVM, MS
William W. Muir, DVM, PhD
ABSTRACT: Supraventricular tachycardias (SVTs) in dogs and cats include sinus tachycardia,
unifocal and multifocal atrial tachycardia, atrial flutter, atrial fibrillation, atrioventricular acces-
sory pathway tachycardia, and junctional tachycardia. SVTs occur more often in dogs than in
cats and with greater frequency in patients with primary cardiac disease, especially diseases
that enlarge the atria. Digoxin is the drug of choice for treatment of many SVTs. Therapy also
commonly includes β-adrenergic and calcium-channel blockers. The prognosis for patients
with SVTs depends largely on the cause, ventricular response rate, presence or absence of
concurrent organic heart disease, and patient’s response to treatment.
S
upraventricular tachycardia (SVT) is any tachyarrhythmia that originates in
or requires atrial or atrioventricular (AV) junctional tissue as part of the
electric circuit.1,2 SVTs classified as atrial in origin include sinus tachycardia
(ST), unifocal (UAT) and multifocal (MAT) atrial tachycardia, atrial flutter
(AF), atrial fibrillation (AFib), sinus node reentry tachycardia (SNRT), and atri-
al reentry tachycardia (ART).1–3 SVTs classified as junctional include AV node
reentry tachycardia (AVNRT), AV accessory pathway tachycardia (AVAPT), and
junctional tachycardia (JT). All except SNRT, ART, and AVNRT have been re-
ported in veterinary medicine.4
Supraventricular tachycardias are more common in dogs than in cats and oc-
cur with greater frequency in dogs and cats with primary cardiac disease, espe-
cially diseases that cause enlarged atria.4 The diagnosis of specific SVTs (Figure
1; Table I) is based on recording and interpreting a diagnostically acceptable
electrocardiogram (ECG). Therapy (Figure 2) is designed to normalize the
electric activity of the heart and to improve hemodynamic function by elimi-
nating the arrhythmia or controlling the ventricular rate (VR) in order to opti-
mize cardiac output (CO) and blood flow. The prognosis for patients with
SVT depends on the presence or absence of concurrent heart disease, the pa-
tient’s response to antiarrhythmic therapy, and the stabilization of hemody-
namics.
*A companion article presenting an overview of supraventricular tachycardia appeared in
the May 1999 issue (Vol. 21, No. 5) of Compendium.
Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

IDENTIFICATION AND TREATMENT

OF ARRHYTHMIAS
Sinus Tachycardia
Sinus tachycardia is the most common
paroxysmal (intermittent) SVT in dogs and
cats and is generally a normal response to
physiologic (e.g., excitement), pathologic
(e.g., pain, anemia), or drug-induced (e.g.,
anticholinergic) conditions (see Causes of
Sinus Tachycardia).4–7 On ECGs, ST is char-
acterized by a rapid heart rate (HR) with
normal-appearing and appropriately timed
(in relation to the QRS complexes) P waves
(Figures 1 and 3; Table I). ST originates in
the sinus node and is characterized by a
regular rhythm with an HR faster than 140
beats/min in giant-breed dogs, 160 beats/
min in medium-sized dogs, 180 beats/min
in toy-breed dogs, 220 beats/min in pup-
pies, and 240 beats/min in cats.4,8,9 Most
SVTs do not require treatment, but under-
lying causes should be determined and cor-
rected. Depending on the cause and rate of
the ST, vagal manipulation by gradual ocu-
lar or carotid pressure may produce tran-
sient slowing of the HR but is often unsuc-
cessful.4,10,11
Cats with hyperthyroid disease com-
monly present with STs4,10,11 and, although Figure 1—Location and mechanisms of supraventricular tachycardias and the
hyperthyroidism should be treated with characteristic electrocardiographic tracings associated with each. (A) Sinus
medical or surgical interventions specific tachycardia, (B) atrial tachycardia, (C) multifocal atrial tachycardia, (D) atrial
fibrillation or flutter, and (E) junctional tachycardia (AV = atrioventricular;
for the disease, propranolol has been used
ECG = electrocardiogram; f = fibrillation; F = flutter; LAF = left anterior fasi-
in patients without myocardial dysfunction cle; LBB = left bundle branch; LPF = left posterior fasicle; P = P waves; P' and
for initial control of the HR.7,11 β-adrener- P* = P waves of different origin or configuration; RBB = right bundle branch;
gic blockers (e.g., propranolol) and the cal- SA = sinoatrial.
cium-channel blocker diltiazem have been
used judiciously to control HR in cats with
hypertrophic cardiomyopathy (HCM).6,7,10 Patients in from multiple sites produce MAT (Figure 5).12 P waves
heart failure (HF) should be treated with appropriate may not occur regularly during MAT, and at least three
drugs (e.g., furosemide, digoxin, angiotensin-convert- configurations may be present.12 In both forms, the HR
6,7,10
ing enzyme inhibitors). is faster than 160 beats/min in medium-sized dogs and
faster than 240 beats/min in cats.4 Rapid UAT or MAT
Unifocal and Multifocal Atrial Tachycardia can be hard to distinguish from AFib or AF, especially
Atrial tachycardia and AFib are the most common in cats. The lack of discernible P waves and irregular
sustained (continuous) SVTs in dogs and cats.4,7 The VRs (as indicated by variable R-R intervals) faster than
mechanism of AT is reentry or enhanced automaticity 300 beats/min during AFib or AF are used to differen-
of ectopic foci (Figure 1B).12–14 On ECGs, AT is charac- tiate these syndromes from AT.4,7 AT can also be diffi-
terized by three or more premature atrial contractions cult to distinguish from ST. AV block and QRS-com-
initiated at a site other than the SA node (Figure 4; plex alternans (QRS complexes of varying heights) are
Table I).4,12 P waves generally occur at regular intervals suggestive of AT. 7 AT can often be abolished or
during UAT but have a configuration different from changed to AV block with increased vagal tone (e.g.,
that of sinus P waves and are not always conducted ocular pressure), whereas ST is only slowed or does not
through the AV node. 4,6,12,13 Impulses that originate respond.6,10,11 Characteristic ECG changes during AF (F

HYPERTHYROID DISEASE ■ ELECTROCARDIOGRAPHIC TRACINGS ■ MULTISITE IMPULSES

Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

TABLE I
Common Supraventricular Tachycardias: Electrocardiographic Findings and Associated Causes or Signs
Supraventricular Tachycardia Electrocardiographic Findings Associated Causes or Signs

Sinus tachycardia Regular sinus rhythm; HR >160 beats/min Exercise, pain, fever, shock,
in medium-sized dogs, >180 in toy breeds, hyperthyroidism, anemia,
>220 in puppies, >240 in cats hypoxia, fear, anticholinergic
drugs

Unifocal atrial tachycardia HR >160 beats/min, P waves regular but Atrial enlargement (secondary to
of different configuration than normal, AV valvular insufficiency), atrial
sudden acceleration at initiation and disease, digitalis toxicity
deceleration at termination of arrhythmia

Multifocal atrial tachycardia HR >160 beats/min, at least 3 different Same as for Unifocal atrial
P wave configurations tachycardia, respiratory disease

Atrial fibrillation No apparent P waves, ventricular rate Atrial enlargement, congenital

rapid and irregular heart defects, digitalis toxicity,
may occur in species with large
hearts without concurrent cardiac
disease

Atrial flutter No apparent P waves but F waves Same as for Atrial fibrillation
present as coarse undulations of the
baseline, F wave rate may be up to 300
beats/min, ventricular rate depends on
state of AV conduction (e.g., 1:1, 4:1)

Accessory pathways
Normal P wave with short P-R interval Anatomic anomaly, generally
and prolonged QRS (delta wave; WPW not associated with altered
syndrome) or P waves inverted in ST physiologic or pathologic
segment or T wave with normal QRS conditions
duration (LGL syndrome), tachycardia
usually paroxysmal

Junctional tachycardia P waves buried in QRS or inverted in the Digitalis toxicity and cardiac
terminal QRS, ST, or T wave disease involving the AV node,
sick sinus syndrome

AV = atrioventricular; HR = heart rate; LGL = Lown-Ganong-Levine; WPW = Wolff-Parkinson-White.

waves), ST (P waves of normal morphology), and AT
(premature P waves of abnormal morphology) are help-
ful in differentiating each arrhythmia (Figure 1).
Hemodynamically, AT often produces compromise
because it generally occurs with cardiac disease. Clinical
signs of AT range from minor or unrecognizable (with
paroxysmal UAT) to acute collapse, which can lead to
sudden death (with sustained MAT). Both UATs and
MATs generally occur secondary to atrial enlargement
(e.g., enlargement from AV valvular insufficiency) in
dogs and cats.4,15 Other associated conditions include
myocarditis, congenital heart disease, cardiac neoplasia,
HCM, digitalis toxicity, hyperthyroidism, general anes-
thesia, and hypokalemia.4,7,8,15,16
Digoxin is generally the drug of choice for treating
AT if digitalis toxicity is not the cause of the arrhyth-
mia and if the patient is not a cat with HCM.4,6 Rapid
digitalization (intravenous administration or double
oral maintenance dose) may be necessary if the patient
is in congestive HF (CHF).6,11 A β-adrenergic blocker
(e.g., propranolol) or the calcium-channel blocker dilti-
azem can be added to digoxin if digoxin alone does not
control the arrhythmia.6,7,10 In patients that are not in
HF, atenolol, propranolol, esmolol, verapamil, or dilti-

ELECTROCARDIOGRAPHIC FINDINGS ■ ASSOCIATED CAUSES OR SIGNS ■ DIGOXIN

 Clinical Assessment

PATIENT STABLE PATIENT MARGINAL PATIENT CRITICAL

• Pulse quality good • Pulse quality weak • Pulse thready or absent
• Mucous membranes pink • Mucous membranes pale pink or white • Mucous membranes white or blue (cyanotic)
Small Animal/Exotics

• Pulse rhythm regular but rate rapid • Pulse rhythm irregular or very rapid • Pulse rhythm irregular or very rapid
• Low-intensity heart sounds • Very low–intensity heart sounds

Treatment may not be necessary

Begin emergency resuscitative therapy

Sinus tachycardia Atrial fibrillation/flutter Tachycardia of unknown origin

Identify and treat underlying cause Attempt to slow heart rate and make diagnosis
• Administer analgesics
IV fluids IV esmolol 0.25–0.50 mg/kg slowly
Potassium
Rapid ventricular response Controlled
IV diltiazem 0.25 mg/kg
Tranquilizers ventricular response
• Digoxin
• Vagal maneuvers Vagal maneuvers?
Dogs: IV loading dose 0.005 Treatment may not be
mg/kg/hr to effect, 0.02 mg/kg necessary if not in heart Adenosine?
If unresponsive, use β-adrenergic or max dose; oral loading dose two
calcium-channel blockers to slow failure 0.1 mg/kg; can repeat or increase to 0.2 mg/kg
times maintenance dose for 24–48 (clinical efficacy not confirmed in dogs and cats)
ventricular rate hr; begin maintenance dosing 12
hr after completion of loading dose Edrophonium?
• β-adrenergic blockers Dogs: 0.11–0.22 mg/kg IV
Cats: 0.007–0.01 mg/kg PO QOD
Propranolol Cats: 2.5 mg/cat IV
Dogs and cats: 0.02–0.06 mg/kg IV
over 5–10 min
If not in heart failure Assess QRS complex width if rate slows
Dogs: 0.2–1.0 mg/kg PO TID
20TH ANNIVERSARY

• Diltiazem: see Sinus tachycardia

Cats: 2.5–5.0 mg/kg PO TID
• β-adrenergic blockers
Atenolol
Propranolol
Dogs: 0.25–1.0 mg/kg PO SID or BID
Atenolol see Sinus tachycardia
Cats: 6.25–12.5 mg PO SID
Esmolol
Esmolol
• Quinidine
}
Dogs and cats: 250–500 mg/kg slow IV;
Dogs: 6–20 mg/kg IM or
50–200 mg/kg/min infusion
PO every 6–8 hr
• Calcium-channel blockers
Diltiazem
Dogs and cats: 0.25 mg/kg IV
If unresponsive
Dogs: 0.5–1.5 mg/kg PO every 8 hr
• Synchronized cardioversion
Cats: 0.5–2.0 mg/kg PO every 8–12 hr
100–400 W/sec extrathoracic
10–40 W/sec intrathoracic
Narrow QRS arrhythmias
Hemodynamic status?
Stable
• Digoxin: see Atrial fibrillation
• Diltiazem: see Atrial fibrillation
• β-adrenergic blockers: see Sinus
tachycardia
If refractory
• Procainamide: see Wide QRS
arrhythmias
• Amiodarone: 2–5 mg/kg IV over
1–8 hr, 10–20 mg/kg PO BID
• Synchronized cardioversion: see
Wide QRS arrhythmias
Wide QRS arrhythmias
• Lidocaine
Dogs: 2 mg/kg IV, repeat to effect, max
8 mg/kg over 10 min; 25–75 µg/kg/
min infusion
Unstable Cats: 0.25–0.75 mg/kg IV over 3–5 min
• Procainamide
• Rapid digitalization and vagal Dogs: 4 mg/kg IV, repeat to effect,
maneuvers to decrease heart
max 20 mg/kg over 30 min; 25–40
rate µg/kg/min infusion, 6–20 mg/kg IV
• Emergency supportive every 4–6 hr, 8–20 mg/kg PO every
therapy: IV fluids; oxygen 4–6 hr
supplementation Cats: 3–8 mg/kg IM
• Synchronized cardioversion
• Synchronized cardioversion 100–400 W/sec extrathoracic
may be necessary: see
10–40 W/sec intrathoracic
Wide QRS arrhythmias

Figure 2—Algorithm for differentiating and treating supraventricular tachycardias (BID = twice daily; IM = intramuscularly; IV = intravenously; PO = orally; QOD = every
other day; SID = once daily; TID = three times daily).
Compendium September 1999
Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

azem has been used to slow tained (continuous) SVTs in

the VR. 4,6,11 These drugs Causes of Sinus Tachycardia dogs and cats. 4,7 AFib is
have also been used often (but caused by circus movement
cautiously) as primary therapy Physiologic Pharmacologic of electric impulses (e.g., be-
in cats with HCM because Increased sympathetic Anticholinergics tween the vena cavae), reen-
the increased inotropic effects tone (atropine, try of multiple impulses, or
of digoxin can cause oxygen Decreased glycopyrrolate) unifocal or multifocal atrial
debt in hypertrophied myo- parasympathetic Catecholamines impulse formation (i.e., au-
cardium.4,6,7 tone (epinephrine, tomaticity) (Figure 1D).4,17
The calcium-channel block- Exercise norepinephrine, Development and mainte-
er verapamil produces po- Excitement dopamine) nance of Afib depend on a
tent negative inotropic ef- large critical atrial mass. Thus,
Fear β-adrenergic agonists
fects, may be reserved for normally large (e.g., equine
(isoproterenol)
refractory sustained AT,4 and atria) or pathologically enlarged
should always be used judi- (e.g., secondary to mitral in-
ciously.4,6 Lidocaine and pro- Pathologic sufficiency) atria are more
cainamide have been used to Anemia Hyperthyroid disease susceptible to AFib.18,19,20–22
4,6
treat AT. A forceful thump Hypoxia Congestive heart On ECGs, AFib is charac-
on the chest over the heart terized by the replacement
Hypercarbia failure
(left or right side, fourth to of normal P waves with os-
Hypotension Hypertrophic
fifth intercostal space), al- cillating fibrillating (f ) waves
though rarely effective, may Hypovolemia cardiomyopathy and rapid and irregular VRs
terminate the arrhythmia Pain Other cardiac diseases caused by rapid, irregular
and should be attempted if Pyrexia that lead to low stimulation of the AV node
treatment is not immediate- Shock cardiac output (Figure 6). VRs range from
ly accessible.4 For chronic ther- Hypokalemia 130 to 260 beats/min in dogs
apy, propranolol, atenolol, and 200 to 280 beatsmin in
diltiazem, or verapamil can cats.20,23 Hemodynamically,
10
be used alone or in combination with digitalis. Regard- AFib is characterized by rapid, uncoordinated atrial
less of whether the arrhythmia is converted to normal si- muscle contractions without effective atrial systole.24
nus rhythm, these drugs can slow the ventricular re- The lack of a coordinated atrial contribution to ventric-
sponse rate and improve hemodynamic stability. Under ular filling has minimal effects at rest but reduces CO
special circumstances, intracardiac pacing can be used to by as much as 30% during exercise and HF.24 AV valve
4
terminate ATs. closure is less efficient in the absence of coordinated
atrial contraction and can lead to AV insufficiency and
Atrial Fibrillation valvular regurgitation.25
Atrial fibrillation and AT are the most common sus- Atrial fibrillation is a grave arrhythmia associated

Figure 3A Figure 3B
Figure 3—Electrocardiographic tracings of (A) sinus rhythm and (B) sinus tachycardia recorded from dogs. Note that the P waves
are rounded and upright in both tracings, a P wave occurs for every QRS complex, and QRS complexes appear normal (narrow
complexes). The heart rate in A is 100 beats/min and 200 beats/min in B. The paper speed is 25 mm/sec.

CALCIUM-CHANNEL BLOCKERS ■ HEMODYNAMIC STABILITY ■ ATRIOVENTRICULAR INSUFFICIENCY

Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

I).4,20,23 Less common causes include untreated congeni-

tal defects, digitalis toxicity, heartworm disease, elec-
trolyte disorders (especially hyperkalemia), and cardiac
trauma.4,15,21,25 Anesthesia may induce or exacerbate
AFib,29,30 and the condition can occur in dogs with gas-
tric dilatation-volvulus.31
Atrial fibrillation occurs less often in cats and is gener-
ally associated with restrictive cardiomyopathy or
HCM.6,7,23,32 Castrated cats 4 to 17 years of age account
for more than 75% of the cases.23 Presenting signs include
Figure 4—Electrocardiographic tracing of unifocal atrial
rear leg weakness from aortic thromboemboli, coughing,
tachycardia recorded in a dog. Note the sinus P waves (P)
anorexia, weight loss, lethargy, cardiomegaly, hepato-
that occur at the end of the recording following multiple P
waves (P' ) generated at a site other than the sinoatrial node. megaly, pleural effusion, and pulmonary edema.23 The prog-
The heart rate initiated by P' is 170 beats/min, whereas that nosis is usually extremely grave, and the life span following
initiated by P is 120 beats/min. The paper speed is 25 diagnosis may be as short as 2 weeks.23
mm/sec. The urgency of treatment ultimately depends on the
VR and is primarily designed to both slow the VR and
control HF. Conversion of AFib to normal sinus rhythm
with high mortality in dogs and cats.20,23 Clinical signs rarely occurs in patients with cardiac disease. The opti-
range from mild (exercise intolerance) to severe (syn- mum resting VR is unknown, but a target rate of 100 to
cope, collapse) and can result in sudden death.20,23 Most 160 ventricular beats/min in dogs is recommended by
signs occur secondary to CHF and include weight loss, some cardiologists,10,11 whereas others recommend 70 to
weakness, exercise intolerance, collapse, syncope, as- 100 beats/min in dogs and 80 to 140 beats/ min in cats.6
cites, dyspnea, cardiomegaly, pulmonary edema, and Digoxin is usually the drug of choice for treating
pleural effusion.20,23 The most common presenting com- AFib, except in cats with HCM.4,10 However, the HR
plaint in dogs is persistent cough.23
Atrial fibrillation occurs most of-
ten in middle-aged male giant-
breed dogs (Table II) in which it
may be an incidental finding on
physical examination10,23 but is gen-
erally associated with clinical mani-
festations of cardiac disease.4,15,20,21,23,26–28
Occasionally, large dogs (similar to Figure 5—Electrocardiographic tracing of multifocal atrial tachycardia recorded in a
large animal patients and humans) dog. Note the three different P wave configurations (P, P ', and P*) and irregular P-R
may develop AFib without concur- and R-R intervals. The first three P waves are generated by the sinoatrial node (P). The
rent cardiac disease (as often occurs impulse initiated by the third P wave is blocked at the AV node, allowing a secondary
with systemic illness, trauma, or pacemaker (P') to generate the fourth QRS complex. The ventricular rate is approxi-
anesthesia) and may be converted to mately 160 beats/min. The paper speed is 25 mm/sec.
normal sinus rhythm.6,10 The prog-
nosis is especially grave in small and
medium-sized dogs because they are more likely to suf-
fer from AFib secondary to serious cardiac disease and
permanent conversion to normal sinus rhythm is rarely
successful.10,21 Mortality in dogs can be as high as 64%
within 3 months of diagnosis.18 In one study, more
than 50% of dogs diagnosed with AFib secondary to
congestive cardiomyopathy died or were euthanatized
within 1 week of diagnosis.23 Figure 6—Electrocardiographic tracing of atrial fibrillation
Conditions most often associated with AFib in dogs recorded in a dog. Note the lack of a discernible P wave, pres-
ence of fibrillation (f ) waves, and variable R-R interval. The
include dilated cardiomyopathy (DCM) (especially in
ventricular rate is approximately 200 beats/min. The paper
large- and giant-breed dogs) and AV valve insufficiency speed is 25 mm/sec.
or fibrosis with subsequent atrial enlargement (Table

CLINICAL SIGNS ■ PROGNOSIS AND MORTALITY ■ ATRIAL FIBRILLATION CONVERSION

Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

TABLE II
Population Statistics of Dogs with Atrial Fibrillation
Study
21
Statistic Bohn and Coworkers Bonagura and Ware 20

Total number of dogs in study population 30,663 ~12,000

Number of dogs with AFib 55 81
Number of males with AFib 48 66
Number of males in study 16,733 ~6000
Percent of males with AFib 87 82
Number of females with AFib 7 15
Number of females in study 13,930 6000
Percent of females with AFib 13 18
Age range in years (median) 1–13+ (6) 1–14 (6)
Weight range in kg (median) Not reported 9–80 (40)

Total Dogs with AFib Dogs with AFib

Number b
Breed Disposition a of Dogs Number Percent Number Percent

Giant breedsc 674 16 29 32 41

Great Dane 324 8 15 13 16
St. Bernard 273 4 7 13 16
Newfoundland 53 3 5 0
Irish wolfhound 24 1 4 6 7.4

Large or medium-sized breeds 28,913 39 71 48 59

German shepherd 3624 8 15 1 1
Mixed breed 7376 7 13 12 15
Doberman pinscher 382 3 5 14 17
Standard poodle 2840 3 5 1 1
Boxer 827 3 5 3 4
Collie 944 2 4 1 1
Afghan hound 55 1 2 2 2
Irish setter 181 1 2 2 2
Other breedsd 12,684 11 20 12 15

Toy breeds 1670 0 — 0 —

a Except for Newfoundlands, only breeds that appeared in both studies are included in this table.
b Totalsnot available for the Bonagura and Ware study.
cDefinition of giant-breed dogs from Bohn and coworkers.
d Other breeds for the Bohn and coworkers study included bloodhound (1), German shorthair pointer (1), whippet (1), cocker spaniel

(6), Boston terrier (1), and basset hound (1). Other breeds for the Bonagura and Ware study included Old English sheepdog (2), En-
glish bulldog (2), Great Pyrenees (2), beagle (1), golden retriever (1), komondor (1), mastiff (1), Scottish deerhound (1), sheltie (1),
and springer spaniel (1).
AFib = atrial fibrillation.

often does not decrease to an acceptable range with
digoxin alone and a β-adrenergic blocker (propranolol
or atenolol) or calcium-channel blocker (generally dilti-
azem) can be added to the treatment protocol 24 to 48
hours after digitalization was initiated. 4,6,10,11 These
drugs should be administered cautiously with digoxin
because of their negative inotropic effects and should
not be used alone in patients in HF.4,11 In patients not
in HF and in cats with HCM, propranolol, atenolol, or
diltiazem can be used without digoxin to control the
VR.4,6,7,10 Oral diltiazem reaches therapeutic blood con-
centrations more rapidly than does oral digoxin6 and

POPULATION STATISTICS ■ NEGATIVE INOTROPIC EFFECTS ■ ORAL DILTIAZEM

Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

can be instituted alone or si- The VR depends on AV con-

multaneously with oral duction, and ocular or carot-
digoxin as a practical and id sinus pressure may slow the
safe way to rapidly decrease VR by suppressing impulse
ventricular response rate. conduction through the AV
Although the technique is node.4
not very effective in dogs The hemodynamic conse-
and cats, low-voltage electric quences and clinical signs of
cardioversion can be at- Figure 7—Electrocardiographic tracing showing atrial flutter AF are similar to those de-
tempted in patients with (F) recorded in a dog. Note the lack of a discernible P wave, scribed for AFib. AF is asso-
clinical signs of HF and presence of F waves, and variable R-R interval. The atrial rate ciated with conditions that
rapid VRs.4,10 is approximately 450 beats/min, whereas the ventricular rate cause enlarged atria (e.g., AV
Atrial fibrillation may oc- is approximately 120 beats/min. The paper speed is 25 valvular insufficiency 4,15,27
casionally be converted to mm/sec. (From Tilley LP: Analysis of common canine and and DCM in dogs34) and is
normal sinus rhythm if the feline cardiac arrhythmias, in Tilley LP (ed): Essentials of Ca- a common occurrence dur-
AFib is an acute response to nine and Feline Electrocardiography: Interpretation and Treat- ing cardiac catheterization
trauma or recent illness or ment. Philadelphia, Lea & Febiger, 1992, p 144. Reprinted with in dogs with a large right
occurs in giant-breed dogs permission.) atrium.4,10 AF is uncommon
11
with no cardiac disease. in cats and is generally asso-
Normal sinus rhythm may be achieved in up to 80% of ciated with HCM.35
these patients.10 Conversion may occur spontaneously As with AFib, therapy is designed to control the VR
or may be facilitated by diltiazem therapy.6,10 In addi- and alleviate clinical signs of HF. Digoxin is the drug
tion, pharmacologic cardioversion can be attempted of choice, except in cats with HCM.4,11 Propranolol,
with intramuscular quinidine (four doses of 6 to 8 atenolol, diltiazem, or verapamil can be added to the
mg/kg every 6 hours); however, therapeutic concentra- therapeutic protocol if digoxin alone is ineffective at
tions of quinidine may cause increased sinus rate and controlling the VR.4,11 These drugs can be used alone if
10
enhanced AV conduction, resulting in increased VRs. the patient is not in HF, and propranolol is used alone
Thus, controlling the VR with digoxin before initiating in cats with HCM.4
10
quinidine therapy may be necessary. The concurrent Quinidine may produce pharmacologic cardiover-
use of quinidine and digoxin can result in elevated sion, but pretreatment with digoxin is often necessary
serum digoxin concentrations and potentially con- to control the VR. 4 AF has been terminated using
10
tribute to digoxin toxicity. Therefore, prolonged use drugs (e.g., procainamide, bretylium) that increase atri-
of quinidine and digoxin is not recommended.6,10 al refractoriness.33 Low-energy electric shock or a force-
Therapy is generally discontinued once sinus rhythm ful thump on the chest (as described for AT) may elim-
has been achieved; however, digoxin, quinidine, dilti- inate the arrhythmia and should be attempted in
azem, or propranolol has been used following car- hemodynamically unstable patients that are unrespon-
dioversion to prevent recurrence of AFib.4,10 Dogs with sive to traditional therapy or when traditional therapy
nonconverting AFib that is not associated with cardiac is unavailable.4
disease (a condition not uncommon in giant-breed Atrial flutter is an unstable rhythm in small animals
dogs) may not require therapy6,10 if the VR remains and commonly converts to normal sinus rhythm or de-
slower than 150 beats/min.6 teriorates to AFib.10 The latter scenario often occurs
with progression of organic cardiac disease and may oc-
Atrial Flutter cur during treatment of AF with quinidine.8 If AF dete-
10
Atrial flutter is uncommon in dogs and rare in cats. riorates to fibrillation, therapy should proceed as previ-
The mechanisms that cause AF are similar to those caus- ously described.
ing AFib (Figure 1), although AV node reentry has been
suggested to play a crucial role.33 On ECGs, AF is char- Atrioventricular Accessory Pathways
acterized by flutter (F) waves that are coarser, more saw- Abnormal conduction pathways (i.e., bypass tracts or
tooth in appearance, and more regular than are the f accessory pathways [APs]) may develop between the
waves produced in AFib (Figure 7). In all species, the VR atria and the ventricles and allow impulses to bypass the
is generally 300 to 500 beats/min. Conduction to the normal conduction system (i.e., the AV node) and cause
ventricles may be more regular than it is in AFib, result- ventricular preexcitation. There are four types of APs:
ing in a rapid but often regular ventricular response.4 bundle of Kent (AV pathway), James fibers (atrio-His

NORMAL SINUS RHYTHMS ■ APPEARANCE OF FLUTTER WAVES ■ ACCESSORY PATHWAYS

Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

pathway), Mahaim fibers (nodoventricular,

nodofascicular, or fasciculoventricular path-
way), and intranodal fibers (Figure 8).1,46
Wolff-Parkinson-White (WPW) syn-
drome (Figure 9) occurs when impulses are
conducted anterograde (atria to ventricles)
over Kent bundles, which are the most com-
Delta wave
mon path for ventricular preexcitation in
3,36,37 4,38,46 46 Mahaim fibers
humans, dogs, and cats. Antero- Nodoventricular
grade conduction through the AP during si- Nodofascicular
nus rhythm causes early excitation of the Fasciculoventricular
pathways
ventricles, resulting in a shortened P-R in- James fibers
(atrio-His pathway)
terval and prolonged QRS duration.2,4 Pro-
longation of the QRS complex is typified by
the presence of a delta wave, which appears Intraodal pathway
as a slurring in the initial upstroke of the
QRS complex.1,2,4 The duration of the P-R
interval in dogs with WPW syndrome is
generally less than 60 msec, with a QRS du- Kent fibers
ration of more than 60 msec.38 HRs faster (atrioventricular pathway)
than 300 beats/min may occur.4
Lown-Ganong-Levine syndrome (conduc-
tion via James fibers) is characterized by a
shortened P-R interval and a normal QRS
duration with no delta wave.39 Orthodrom- Figure 8—Diagram of locations of accessory pathways and characteristic elec-
ic atrioventricular reentrant tachycardia trocardiographic tracing of Wolff-Parkinson-White syndrome.
(OAVRT) is characterized by retrograde
(ventricles to atria) conduction and a QRS
complex that is normal in duration.2,38 The retrograde sary unless tachycardia occurs. Treatment is designed to
conduction causes inverted P waves that occur in the prolong conduction through the AP so that conduction
late portion of the ST segment or early T wave, result- through the AV node can be reestablished as the primary
ing in an R-P interval that is much shorter than the pathway. Lidocaine and procainamide are the treatment
corresponding P-R interval.38 of choice.4 Calcium-channel and β-adrenergic blockers
Atrioventricular APs occur sporadically in dogs and are alternatives46; however, these drugs can slow conduc-
16,38,40–53
cats. Although occasionally associated with tion through the AV node and thus encourage conduc-
congenital cardiac defects,4 ventricular preexcitation syn- tion over the AP.4 A combination of procainamide and
dromes are generally not caused by cardiac pathology in diltiazem or verapamil can simultaneously slow conduc-
humans3 or dogs4,38 but can result in tachycardia-induced tion through both the AP and the AV node. This combi-
HF. AVAPTs should be con- nation has been used success-
sidered in young patients that fully to treat SVT caused by
present with severe tachycar- OAVRT.38 Digitalis can dan-
dia and no evidence of heart gerously slow conduction
disease. Young Labrador re- through the AV node and ac-
trievers may have a predilec- celerate conduction over the
tion for OAVRT.38 AVAPTs AP and is not recommended
in cats are generally associat- as a sole therapeutic agent.4,11
4,46
ed with HCM. The hemo- Quinidine can occasionally
dynamic consequences of APs Figure 9—Electrocardiographic tracing of accessory pathway eliminate the tachycardia, as
are equivalent to those pro- tachycardia (Wolff-Parkinson-White syndrome) recorded in can low-voltage electric
a dog. Note the upstroke in the early part of the QRS com-
duced by other SVTs. shock.4 Abolition of the AP
plex (delta wave; arrow), shortened P-R interval, and long
Not all APs are associated QRS duration. The heart rate is 150 beats/min. The paper by surgical or catheter abla-
with tachycardia, and treat- speed is 50 mm/sec. tion is becoming the treat-
ment is generally not neces- ment of choice.1,38,53

WOLFF-PARKINSON-WHITE SYNDROME ■ LOWN-GANONG-LEVINE SYNDROME

Small Animal/Exotics 20TH ANNIVERSARY Compendium September 1999

Figure 10A Figure 10B

Figure 10—Electrocardiographic tracings of junctional tachycardia recorded in a dog. Note the inverted P waves. (A) Inverted P
waves following the QRS complexes. The heart rate is 165 beats/min. (B) Inverted P waves preceding the QRS complex. The
heart rate is 120 beats/min. The paper speed in both figures is 50 mm/sec. (Figure 10A from Tilley LP: Analysis of common ca-
nine and feline cardiac arrhythmias, in Tilley LP (ed): Essentials of Canine and Feline Electrocardiography: Interpretation and
Treatment. Philadelphia, Lea & Febiger, 1992, p 151. Reprinted with permission.)

Junctional Tachycardia secondary to digitalis toxicity and may restore normal

Junctional tachycardia (Figures 1E and 10; Table I) is sinus rhythm. Anticholinergics have occasionally been
an uncommon cause of SVT in dogs and cats. JT oc- used to increase normal si-
curs when an ectopic focus at the AV junction begins to nus rates and allow the SA ENDIU
MP
discharge at a rate faster than the rate of the SA node node to overdrive the junc-

M’
20th

CO

S

and faster than the inherent rate of the AV node (40 to tional focus.10 1 9 7
9 - 1
9 9 9

60 beats/min in dogs).2,4,54 Digitalis toxicity and prima- ANNIVERSARY

ry cardiac disease, especially diseases that cause enlarged PROGNOSIS

atria (e.g., chronic AV valvular insufficiency, patent
ductus arteriosis, HCM), can cause ectopic foci and
The prognosis for pa-
tients with SVTs depends
A LookBack
JT.1,2,4 Once manifest, the arrhythmia is most likely sus- largely on the VR and pres- When considering
tained by reentry.55 P waves are often absent because of ence or absence of concur- supraventricular tachycardia,
the lack of atrial activation or inapparent because of the rent organic heart disease
one of the greatest advancements
simultaneous occurrence of the P wave and the QRS (Table III). The presence of
in veterinary medicine during
complex. If present, P waves are generally inverted from heart disease (e.g., mitral
the past 20 years has been the
retrograde conduction or are dissociated from the QRS valve insufficiency, CHF)
continued development of
complexes, which are normal in appearance.1,54 The VR may be associated with a
poor prognosis, decreased therapeutic agents. β-adrenergic
is constant during JT, but the arrhythmia can be sus-
tained or paroxysmal. 1 Digitalis toxicity commonly ability to terminate the and calcium-channel blockers
causes JTs characterized by a slower HR (less than 160 SVT, decreased response to allow practitioners to control a
beats/min) than JTs caused by cardiac disease (greater pharmacologic therapy, and patient’s heart rate with
than 160 beats/min).4 JTs caused by digitalis toxicity increased chance that more minimal adverse side effects. In
have a gradual onset and termination and may be tem- than one drug will be need- addition, technologic
porarily slowed by vagal maneuvers. 4 JTs caused by ed to control the effects of achievements have enabled
heart disease have a rapid onset and termination and both the SVT and heart practitioners to locate and
may be abolished by vagal maneuvers.4 The hemody- disease.10 abolish certain tachycardias, such
namic consequences of JT are equivalent to those Sustained SVTs and as accessory pathway arrhythmia.
caused by other SVTs. MATs (originating from Today pharmacology and
Treatment of JT is designed to eliminate the underly- more than one site) carry a technology promote longer,
ing cause. Digitalis should be discontinued if the ar- worse prognosis than do healthier lives for patients with
rhythmia is caused by digitalis toxicity or supplemented paroxysmal tachycardia and supraventricular tachycardia.
with potassium if hypokalemia is the cause of digitalis UATs. Patients without
toxicity. If the JT is not caused by digitalis toxicity, heart disease but with SVTs
digoxin is the drug of choice except in cats with HCM that can be eliminated or
(which should be treated with propranolol). Propran- easily controlled have a fa-
olol, atenolol, and diltiazem are effective treatments for vorable prognosis. Of the
JT. Diphenylhydantoin (phenytoin) is used to treat JTs SVTs, ST is the most benign

DIGITALIS TOXICITY ■ JUNCTIONAL TACHYCARDIA TREATMENT ■ POOR PROGNOSIS

Compendium September 1999 20TH ANNIVERSARY Small Animal/Exotics

TABLE III digoxin alone does not effectively con-

Prognosis for Dogs with Supraventricular Tachycardia
Type Prognosis
Sinus tachycardia Excellent if the underlying cause is
eliminated; poor if tachycardia leads
to heart failure
Unifocal atrial tachycardia Fair if patient is hemodynamically stable;
poor if patient is not stable or if cardiac
disease is severe
Multifocal atrial tachycardia Grave to fair, depending on the severity
of cardiac disease
Atrial fibrillation Good for giant-breed dogs without
cardiac disease; grave to poor for all other
breeds and dogs with cardiac disease;
improvement may occur with appropriate
therapy
Atrial flutter Same as for Atrial fibrillation
trol the HR. β-adrenergic blockers and
calcium-channel blockers are very ef-
fective for slowing the HR but should
be used judiciously because of their
negative inotropic effects. Other drugs
with specific applications include
quinidine (treatment of AFib or AF),
phenytoin (treatment of digitalis-in-
duced arrhythmias), and procainamide
(treatment of WPW syndrome). The
prognosis for SVTs ranges from excel-
lent (no cardiac disease or hemody-
namic compromise) to grave (severe
cardiac disease).
ACKNOWLEDGMENT
The authors thank Tim Vojt, a
graphic artist at The Ohio State Uni-
versity, for his artistic contribution.

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About the Authors
Drs. Grubb and Muir are affiliated with the Department of
Veterinary Clinical Sciences, College of Veterinary Medi-
cine, The Ohio State University, Columbus, Ohio. Both
are Diplomates of the American College of Veterinary
Anesthesiologists, and Dr. Muir is also a Diplomate of the
American College of Veterinary Emergency and Critical
Care.