Sunday, July 24, 2011

Notes from July 2011 St. Louis AVMA Conference-Arythmias

These are papers from the July 2011 St. Louis AVMA conference.  I’ve edited them to delete some of the vet only jargon and for space considerations.  If you see (…) that means that information has been deleted due to these considerations.  The ones listed here include HCM, and other heart related papers, treatments, papers on x-rays and echos, thrombosis, kidney disease, idiopathic cystitis, pain management, anesthesia and cardiac disease, supplements and other hazards for pets, and some other basic information I hope is helpful.

Emergency Management of Arrhythmias

Deborah M. Fine, DVM, MS, DACVIM (Cardiology)

University of Missouri

Arrhythmias requiring urgent therapy may result from a variety of conditions including

underlying cardiac disease, trauma, anesthesia, electrolyte abnormalities, and hypoxia. Of

these, cardiac disease is the common cause of life-threatening arrhythmias. Determining the

specific nature of the underlying cardiac disease ultimately determines the likelihood of

successful short and long-term management of an arrhythmia.

The first decision that must be made in arrhythmia management is deciding if an arrhythmia

requires therapy. Important considerations in this decision include:

1. Is the arrhythmia hemodynamically significant (i.e. causing clinical signs)?

If the answer to this question appears to be “no”, then emergency therapy is not

indicated. The exception to this occurs if the next consideration appears likely.

2. Does the arrhythmia appear likely to degenerate into a less stable rhythm?

3. Can a correctable underlying cause for the arrhythmia be identified?

If this is the case, then successfully treating the underlying abnormality is likely to result

in resolution of the arrhythmia.

4. What are the risks of beginning therapy?

All anti-arrhythmic therapies have the potential to be pro-arrhythmogenic. Many of them

also have profound effects on cardiovascular function. Therefore the potential benefit

associated with therapy must outweigh the potential risks.


Drug therapy and complications of anesthesia are the most common non-cardiac causes of

pathologically slow heart rates. Cardiovascular depression can result from sedatives,

analgesics, anesthetic agents, and hypothermia. Appropriate therapy includes reversal agents

(e.g. naloxone for opioids), decreasing the rate or dose of anesthetic administration,

administration of atropine, and warming the patient. Less common causes of bradycardia

include head trauma/brain tumors, and malignant systemic hypertension. (These

abnormalities ultimately mediate their effects by increasing vagal tone; however the underlying

mechanisms are quite different.)

The most common bradyarrhythmias requiring emergency therapy are:

1. Severe second degree atrioventricular heart block

ECG features: intermittent and frequent failure of the P wave to be conducted to the

ventricles. Therefore some P waves are not followed by a QRS complex. This results

in the ventricular rate being slower then the atrial rate.

Etiology: can be the result of increased vagal tone, cardiomyopathy, or idiopathic

degeneration of the AV node.

2. Third degree atrioventricular heart block

ECG features: complete failure of the P waves to be conducted to the ventricles. There

is complete dissociation between P waves and QRS complexes. The ventricular rate is

much slower then the atrial rate (30 to 60 bpm).

Etiology: most commonly the result of idiopathic degeneration of the AV node, or

cardiomyopathy. Other less common causes include cardiac glycoside toxicity (e.g.

digoxin, Lilly of the Valley, oleander, bufo toads), infectious myocarditis (e.g. Ehrlichia,

Bartonella), and infiltrative cardiac neoplasia.

3. Sick sinus syndrome

ECG features: prolonged periods of asystole (no P waves or QRS complexes), often

alternating with periods of tachycardia. This arrhythmia is often intermittent and the

patient may have a completely normal rhythm between episodes.

Etiology: most commonly idiopathic, and most commonly seen in female miniature


4. Atrial standstill

ECG features: complete absence of P waves preceding any of the QRS complexes.

Etiology: hyperkalemia (e.g. urethral blockage, Addisonian crisis), or idiopathic atrial

cardiomyopathy (seen most often in Springer Spaniels).

In the absence of a treatable underlying cause such as hyperkalemia, most symptomatic

bradycardias require implantation of a permanent transvenous or transdiaphragmatic

pacemaker for alleviation of clinical signs. Medical therapy with atropine, theophylline, or

propantheline may improve symptoms; however improvement is usually temporary.

5. Asystole

ECG features: flat-line in multiple leads (must rule-out artifact caused by lead


Etiology: occurs when the heart’s electrical system fails to generate a depolarization. It

may occur as a severe vagal reflex during ocular manipulation, or with vomition. More

commonly it occurs due to severe myocardial hypoxia subsequent to ventricular

fibrillation, and commonly occurs after unsuccessful attempts at defibrillation.

Treatment: atropine, epinephrine, and vasopressin; but the outcome is almost always



Most clinically significant tachycardias occur in the context of underlying heart disease.

Therefore, long-term prognosis for patients presenting with symptomatic tachycardia is usually

guarded. Nonetheless, therapy can be rewarding and may result in marked improvement in

clinical signs, even if only temporarily. There is no absolute number which defines a

hemodynamically significant tachycardia. Holter evaluation of dogs shows that the sinus node

can depolarize at rates of 250 bpm during periods of extreme excitement. Blood pressure

measurement can help assess the hemodynamic consequences of a tachyarrhythmia.

Tachyarrhythmias requiring medical therapy are much more common in dogs then in cats.

The most common tachyarrhythmias requiring emergency therapy are:

1. Atrial or AV nodal tachycardia

ECG features: persistent or intermittent bursts of supraventricular tachycardia

(“supraventricular” refers to normal, narrow appearing QRS complexes, indicating the

depolarization is being conducted via the normal conduction system). P waves may be

absent, abnormal in appearance, or buried in the preceding T wave

Etiology: may occur subsequent to cardiac disease causing atrial enlargement. Atrial

enlargement and fibrosis serve as a substrate for abnormal pacemaker activity. This is

more common in older animals. In younger animals, this form of tachycardia is often

the result of accessory conduction tissue. These bypass tracts allow abnormally fast

conduction between the atria and the ventricles.

Treatment: calcium channel blockers (diltiazem, verapamil) are the first choice if systolic

dysfunction is present. Beta blockers (esmolol, atenolol) will decrease systolic function

and should be used very cautiously in patients with myocardial dysfunction. Digoxin is

rarely used for emergency control of supraventricular tachyarrhythmias, but rapid

digitalization is sometimes necessary for patients with systolic dysfunction in which

calcium channel blockers or beta blockers is initially unsafe.

2. Ventricular Tachycardia

ECG features: persistent or intermittent bursts of wide QRS complexes with no visible P

waves present. The depolarization originates in the ventricular myocardium, and

therefore is not propagated through the normal conduction system. As a result the QRS

complexes are bizarre in shape and prolonged in duration. The T wave is large and

usually of opposite polarity to the QRS complex, and the flat ST segment is absent.

Sustained ventricular tachycardia may degenerate into fibrillation if not corrected.

Etiology: usually occurs in the presence of severe underlying heart disease.

Ventricular tachycardia can also be induced by marked metabolic disturbances,

toxicities, and trauma, but these abnormalities are more likely to cause an accelerated

idioventricular rhythm (see below).

Treatment: intravenous lidocaine is the treatment of choice; if patients are nonresponsive

then IV procainamide can be tried.

3. Ventricular Fibrillation

ECG features: rapid, irregular undulations of the ECG which may be coarse or fine.

There is a complete absence of recognizable P waves or QRS complexes.

Hemodynamically this is disastrous; death ensues rapidly if not corrected.

Etiology: severe end-stage cardiac disease or other abnormality which results in

profound myocardial hypoxia.

Treatment: electrical defibrillation is the only reliable therapy. The probability of

successful defibrillation declines by 50% for every 3 – 5 minute delay. Drug therapy can

be used to reduce the energy required to electrically defibrillate the heart. Intravenous

amiodarone, bretylium, and magnesium have been used in animals that are refractory

to repeated attempts at electrical defibrillation.

4. Atrial fibrillation

This is the most common tachyarrhythmia seen in veterinary medicine; however it rarely

requires emergency therapy.

ECG features: supraventricular QRS complexes (narrow), irregularly irregular R to R

intervals, absence of P waves, +/- fine baseline fibrillation waves (“f waves”)

Etiology: severe atrial enlargement and myocardial fibrosis are the substrates.

Increased circulating catecholamines associated increase action potential propagation

and decrease the refractory period allowing perpetuation of the arrhythmia.

Treatment: most patients will present with heart rates that are elevated, but not to the

same extent as the arrhythmias listed above. Therefore, in most instances initiating oral

therapy will be adequate for controlling clinical signs. However, in dogs with atrial

fibrillation and dilated cardiomyopathy, rapid intravenous digitalization may help to

control signs of heart failure in the acute setting.

Accelerated idioventricular rhythm is the most common ventricular arrhythmia seen in

veterinary medicine and is often mistaken for ventricular tachycardia. Consequently patients

presenting with this arrhythmia are often inappropriately treated with lidocaine. Accelerated

idioventricular rhythms also have wide bizarre biphasic ventricular complexes; however the

rate is usually less then 180 bpm. The patients usually do NOT have underlying cardiac

disease. Rather, accelerated idioventricular rhythms are secondary to a vast array of noncardiac

abnormalities including neoplasia, GDV, trauma, sepsis, autoimmune disease, and

end-stage organ failure. This arrhythmia is not hemodynamically significant, but is important

because it is a marker of an underlying abnormality. Anti-arrhythmic therapy is rarely

necessary, and rarely successful. Successful treatment of the underlying abnormality will

result in resolution of this arrhythmia.

Ventricular tachycardia is distinguished from an accelerated idioventricular rhythm by

examination of the ECG.

Ventricular Tachycardias show the following features:

1. Rate is significantly higher than the underlying sinus rhythm (usually > 220 bpm)

2. Onset is always premature; that is the R-R interval of the last normal sinus complex to the

first abnormal ventricular complex is shortened compared to the normal sinus R-R interval.

3. Associated with significant underlying cardiac disease

4. Respond to intravenous lidocaine

Accelerated Idioventricular rhythms show the following features:

1. Rate is only slightly higher than the underlying sinus rhythm (typically about 10% faster)

2. Onset is variable; it can start with a premature complex, or it can start after a pause. It can

even start at the same time as a sinus complex is depolarizing the ventricle, in which case a

fusion beat will result (a fusion beat is intermediate in appearance between a sinus origin

complex and a ventricular origin complex)

3. Associated with underlying systemic disease

4. Resolves with resolution of the underlying disease. Almost never requires antiarrhythmic

therapy as it is not hemodynamically significant of itself. Does not typically respond to



All hospitalized patients should have emergency drug doses calculated on admission. The

dose sheet should be kept in an easily accessible location (i.e. chart or cage door). It is

impossible to memorize the dose of all emergency drugs that may potentially be used, and

looking up drug dosages during an emergency is extremely inefficient. There are a number of

drug calculators available on the web that only require entering the patient’s species and

weight, and the doses are automatically calculated.

References available upon request.

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