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VETERINARY CLINICAL CARDIOLOGY
CARDIOLOGY CONCEPTS
Electrocardiology
Tachycardias
1. What is sinus tachycardia?

It is a sinus rhythm (see above) with an increased sinus nodal rate, and therefore ventricular rate.

  • Dog (<20 kg) with heart rate >180 bpm
  • Dog (>20 kg) with heart rate >160 bpm
  • Cat with heart rate >240 bpm

Example of Sinus Tachycardia in a Dog (HR 214 bpm)


(25 mm/sec)

Examples of etiologies include:

  1. Pain
  2. Fever
  3. Anemia
  4. Hypovolemia
  5. Reduced cardiac output (and resultant hypotension)
  6. Hyperthyroidism
  7. Excitement or stress

Consequences:

  1. If HR is excessive, cardiac output may fall due to reduced diastolic filling time
  2. Coronary perfusion decreases, also due to shorter diastole
  3. Increased myocardial oxygen consumption per beat
  4. The above are generally only significant if sustained for long period of time

Treatment: Treat the underlying cause.

2. What are supraventricular premature beats/contractions?

ECG Findings:

  1. Premature beats (beats that come earlier than expected)
  2. The morphology of these beats usually looks identical or very similar to the normal sinus beats
  3. The duration of the QRS complexes are usually normal
  4. They may or may not have an identifiable premature P wave associated with them

Example of Supraventricular Premature Beats in a Dog

Etiology:

  1. These beats may originate within ectopic foci in the atria (atrial premature beats) or they may originate in the peri-AV nodal tissue
  2. The causes of both origins of supraventricular beats are identical:
    • Due to disorders that result in enlargement of the atria (e.g. AV valve insufficiency)
  3. Due to inflammation, infection, ischemia, or neoplasia affecting the atria
  4. Drugs (digitalis, anesthetics)
  5. Extra-cardiac causes such as pain, other causes of catecholamine stimulation, intra-thoracic disease

Consequences:

  1. Several isolated premature beats are of no hemodynamic significance
  2. However, when enough of these beats are present, a reduction in cardiac output may result

Treatment:

  1. Several isolated beats do not warrant therapy. However, such individuals should be frequently monitored for exacerbation of their rhythm disturbance. In addition, attention should be directed toward identification and management of the underlying disorder.
  2. Criteria for therapy include:
    1. If the animal is symptomatic during the arrhythmia
    2. If paroxysms of sustained tachycardia develop such as a run lasting greater than 30 sec (see SVT below)
    3. Drugs used may include beta blockers (e.g. propranolol, metoprolol, atenolol), calcium channel blockers (diltiazem), sotalol, or digoxin.
3. What is supraventricular tachycardia?

ECG Findings:

  1. A run of at least 4 supraventricular premature beats in a row (see above).
  2. Often occurs as paroxysms (bursts).

Example of Supraventricular Tachycardia in a Dog (first third of ECG)

Etiology: The same as for supraventricular premature beats (see above)

Consequences: Paroxysms of supraventricular tachycardia can result in weakness, syncope, and heart failure when sustained and untreated

Treatment:

  1. Efforts to increase the parasympathetic tone and thereby reduce A-V nodal conduction may be useful in slowing the ventricular response, assisting in detecting atrial activity (P waves on ECG), and differentiating supraventricular tachycardia from ventricular tachycardia. This may be accomplished by:
    • Vagal maneuvers such as ocular pressure or carotid sinus massage
    • Reflex induced increase in vagal tone using phenylephrine
  2. Anti-arrhythmics including beta blockers (e.g. propranolol, metoprolol, atenolol), calcium channel blockers (diltiazem), sotalol, or digoxin.
4. What is atrial fibrillation?

Atrial fibrillation is a supraventricular arrhythmia associated with many microfoci of atrial myocardium acting as ectopic foci or serving as small reentrant pathways and activating the adjacent atrial myocardium. Only the ectopic foci that manage to depolarize close to the A-V node successfully penetrate the A-V node to activate the ventricles. There is no coordinated atrial contraction, and the ventricles are activated at a fast rate and at irregular intervals.

ECG Findings:

  1. Typically rapid and always irregular ventricular rhythm.
  2. No distinct P waves; at times the baseline may show very fine baseline undulations which are called fibrillation waves. However sometimes these fibrillation waves are not apparent.
  3. The QRS complexes are supraventricular in origin thus the QRS complexes tend to look of normal morphology. They may be wide if there is underlying ventricular myocardial disease.

Example of Atrial Fibrillation in a Dog

Another Example of Atrial Fibrillation in the Dog - Place cursor on the image to see examples of the ECG Findings

The hallmark ECG findings are the presence of an irregular rhythm and absence of P waves. As the heart rate becomes very rapid, the rhythm approaches a regular rhythm; however, a slight irregularity remains present. Although the heart rate is usually rapid, it can be slow if:

  1. A giant breed of dog is involved
  2. A-V nodal disease co-exists
  3. Medication such as digitalis, beta-blocker, or calcium channel blocker therapy is on board

Etiology:

  1. Due to a very high number of microfoci or small reentrant pathways in the atria. They are competing to activate the A-V node.
  2. Due to disorders associated with atrial dilation.
    1. A-V valvular insufficiency
    2. Cardiomyopathy
    3. Congenital heart disease
  3. May occur in the absence of organic heart disease (often giant breed dogs). These patients usually have slow to normal ventricular rates.

Consequence:

  1. The rapid ventricular rhythm results in a fall in cardiac output due to excessive heart rate.
  2. Cardiac output also falls due to a loss of atrial contraction. At rapid rates, the atrial component to ventricular filling can account for up to 30% of ventricular filling. At slower rates, the atria contribute relatively little to ventricular filling.
  3. The rapid heart rates also result in an increase in myocardial oxygen consumption. This can result in more myocardial hypoxia which causes a reduction in inotropy and exacerbation of dysrhythmias.

Treatment options:

  1. Convert the rhythm to a sinus rhythm
    • Although direct current electrical cardioversion is possible, most individuals revert back to atrial fibrillation because of the underlying atrial pathology
  2. Slow the ventricular rate - reduce the tachycardic effect on cardiac output and the effect of loss of atrial filling
  3. Calcium channel blocker - diltiazem is often a drug of choice to slow the heart rate
  4. Beta blocker – e.g. propranolol, metoprolol, atenolol
  5. Digoxin
    • Combination of diltiazem and digoxin - a study of 18 dogs with advanced cardiac disease and atrial fibrillation showed that better rate control was achieved with the combination of diltiazem and digoxin compared with either drug on its own (Gelzer et al. JVIM 2009;23:499-508).
  6. Amiodarone – not only may slow rate, but may result in conversion to sinus rhythm in some cases, however associated with a significant adverse side effect profile
  7. The target heart rate in hospital for most canine patients is 120-150 bpm, though this is very patient dependent (some patients require higher heart rate than others to maintain adequate cardiac output). Note that both calcium-channel blockers and beta blockers are negative inotropes as well as negative chronotropes. Beta blockers in particular require starting at low doses and up-titrating gradually.

5. What are ventricular premature contractions?

Ventricular premature contractions (VPCs) are depolarizations from an ectopic focus in the ventricular myocardium.

ECG Findings:

  1. The QRS complexes are usually wide and bizarre.
  2. If several ectopic foci are present, the morphology of the QRS will vary with each focus (multi-form VPCs).
  3. Most VPCs are accompanied by a pause or delay after, prior to the onset of the next sinus beat. A time measurement that includes the pause can be used to discriminate between VPCs and SVPCs. For a representation please see diagram under question 33.
  4. VPCs may occur as fusion and as interpolated beats.
    • A fusion beat is a QRS with a morphology that is neither identical to the sinus QRS, nor to a typical VPC. It is also a QRS which occurs on time (i.e. it is not premature). It represents a fortuitous situation wherein part of the ventricular mass was depolarized as a result of the sinus beat and the remainder of the ventricular mass was depolarized as a result of the ectopic ventricular focus.
  5. An interpolated beat is a special form of VPC wherein the presence of the VPC did not interrupt the underlying sinus rhythm.

Example of Ventricular Premature Contractions in a Dog

Etiology:

  1. Myocardial disease causing ventricular concentric hypertrophy or eccentric hypertrophy
  2. Hypoxemic states as anemia, gastric dilation volvulus, heart failure
  3. Metabolic derangements such as acidosis or hypokalemia
  4. Trauma (traumatic myocarditis)
  5. Circulating cytokines in neoplastic and systemic inflammatory disorders
  6. Drugs such as digoxin, barbiturates, some antiarrhythmic agents

Consequence:

  1. If enough premature beats are present, cardiac output may fall due to dyssynergy of contraction and high heart rate.
  2. May predispose to ventricular fibrillation.

Treatment:

  1. If IV anti-arrhythmic therapy is necessary, choices include lidocaine, procainamide, beta blockers, or in some cases amiodarone, with lidocaine being the first choice.
  2. Oral anti-arrhythmic choices include mexiletine (lidocaine analog), sotalol, pure beta blockers, or amiodarone
  3. The intravenous drug of choice for treatment of ventricular tachycardia is typically lidocaine. The first choice for oral therapy of VPCs is often sotalol, however this depends on the case and underlying disease process.

6. When should I begin therapy for premature ventricular contractions?

This decision must be approached individually for each case, however some general guidelines include:

  1. If the patient is symptomatic due to the dysrhythmia (syncopal or weak or in heart failure due to the fast heart rate)
  2. If you believe the patient's rhythm is in imminent danger of degenerating to ventricular fibrillation
  3. If you believe the patient is at risk of sudden death (either due to severity of the arrhythmia or the presence of underlying structural heart diseases associated with sudden death, like DCM in Dobermans or ARVC in Boxers)

There is often little difficulty in determining if condition #1 is present. Determining if condition #2 or 3 is present is more challenging. In determining the significance of ventricular arrhythmias, heart rate is likely one of the more important criteria. If VPCs occur at a fast heart rate (i.e. >170 bpm), this potentially represents a more clinically significant condition, whereas if they occur at a more normal heart rate, this situation may not represent as significant of a risk. The definitive importance of heart rate in the presence of VPCs remains to be determined.

Why not institute anti-arrhythmic therapy in any case just to be safe? The issue is that all anti-arrhythmics have the potential to be pro-arrhythmic, some more than others. Therefore, follow-up to assess efficacy is critical in any patient in which anti-arrhythmic therapy is initiated.

7. What is ventricular tachycardia?

Ventricular tachycardia (VT) refers to runs of more than 3 VPCs in sequence. As above for VPCs, QRS complexes are wide and bizarre, and there is lack of association with P waves (A-V dissociation). VT may markedly reduce cardiac output (through dyssynergy of contraction and high heart rate). Etiology is as for premature ventricular contractions (see above). VT is treated as described above under premature ventricular contractions. Again, the presence of clinical signs, the presence of an underlying heart disease known to be associated with sudden death, and high heart rate are likely the most important criteria for treatment. Slow VT (VT rate from 80 - 140 bpm in dogs) frequently has minimal hemodynamic consequences and therefore warrants observation but not necessarily anti-arrhythmic therapy.

Example of Ventricular Tachycardia in a Dog

8. What criteria assist in the differentiation of supraventricular and ventricular premature beats?

While the differentiation of SVPCs and VPCs may often be straightforward, it can also be a challenge in that SVPCs may conduct with aberrancy (abnormally) resulting in bizarre and wide QRS morphology. Since clinical significance, therapy, and prognosis for one may be very different than for the other, it is important to attempt to differentiate these abnormalities.

Supraventricular Premature Beats (SVPBs) Ventricular Premature Beats (VPBs)
1. Morphology of QRS is usually similar to the sinus beats 1. Morphology of QRS is bizarre vs the sinus beats
2. QRS is usually narrow 2. QRS is usually wide
3. SVPBs can't occur as fusion beats 3. VPBs may occur as fusion beats
So if the beat in question occurs as a fusion beat it must be a VPB
4. SVPBs can't occur as interpolated beats 4. VPBs may occur as interpolated beats
So if the beat in question occurs as an interpolated beat it must be a VPB
5. Atrial (P wave) and ventricular (QRS) activation are associated 5. A-V dissociation is usually present
In either case, often the P waves cannot be visualized in the presence of tachycardia because they are buried in the QRS or T waves.
6. Non-fully compensatory pause is present 6. Fully compensated pause is present
If the background rhythm is irregular (as with sinus arrhythmia or atrial fibrillation) this criterion can’t be used because the duration of 2 normal R to R intervals cannot be predicted with precision.
7. When supraventricular tachycardia occurs it tends to be very regular 7.When ventricular tachycardia occurs it may be slightly irregular
8. A premature beat that follows a premature P wave is always a SVPC 8. A premature beat that follows a premature P is never a VPC
The absence of a premature P does not discriminate between an SVPC and a VPC

A refers to the time between two normal sinus beats close to the premature beat. B refers to the time between the sinus beat just before the premature beat to the sinus beat just after the premature beat.

If A > B (this is called a non-compensatory pause), indicates the premature beat is a supraventricular beat.

If A < B (this is called a compensatory pause), indicates the premature beat is a ventricular beat.

Example of an Interpolated VPC

production