When the av node acts as pacemaker, the slower heartbeat has what type of rhythm?

Bradyarrhythmias

The SA and AV nodes are the most sensitive areas to (physiological) functional block because the speed of conduction is largely dependent on calcium channel currents.1 Parasympathetic tone inhibits calcium channel opening and reduces the speed of conduction, while β-adrenergic agonists increase these currents. The release of acetylcholine from parasympathetic nerve endings at the SA node also affects potassium ion channels resulting in hyperpolarization of the tissues, and release of inhibitory factors which reduce the inward pacemaker current and slow conduction.

Functional block resulting in bradyarrhythmias is common in horses because of high vagal tone. If SA node discharge is affected, they result in sinus bradycardia, sinus block or arrest. The distinction between block and arrest is largely academic because it is unclear whether an impulse is formed but fails to escape from the node or whether its formation is depressed. In horses, increased vagal tone results in a delay in conduction through the AV node much more commonly than it causes sinus bradycardia. A variation in the P–R interval is so common that it is difficult to define first-degree AV block. However, second-degree AV block is found in around 20% of horses, and is probably more common than this in undisturbed animals.17 It has been shown that when arterial blood pressure reaches a certain level an episode of second-degree AV block may occur.24 The blocked beat results in a reduction in arterial pressure, followed by a gradual increase in the arterial pressure with each subsequent beat until the same maximum pressure level is reached and second-degree AV block occurs again. This “staircase effect” appears to be a normal homeostatic mechanism to control blood pressure. (

Variation in vagal tone can also cause sinus arrhythmia, in which there is a cyclical alteration in sinus rate, or a wandering pacemaker, when the exact site of formation of the impulse in the SA node and/or its conduction through the atria varies, altering P wave morphology. Sinus arrhythmia is not very common at rest, but is frequently found during the recovery period after exercise when there is a change from sympathetic to vagal tone.17 Extreme postexercise bradycardia and syncope has been reported in a horse and was treated with the implantation of a dual-chamber rate-adaptive pacemaker.25

Structural abnormalities affecting conduction through the AV node and major conduction pathways are rare in horses. Third-degree AV block has been reported rarely26,27 and the precise cause is seldom identified. Bundle branch block is extremely uncommon and may also be difficult to recognize in horses due to their ventricular depolarization pattern.

D Atrioventricular Node

The cells of the a–v node generate APs that are quite similar to the APs of the s–a node. Thus, these cells fire Ca2+-dependent APs and also display phase 4 depolarization (and, hence, are automatic). However, the rate of the phase 4 depolarization in a–v nodal cells is much slower than the rate of phase 4 depolarization in s–a nodal cells. Thus, the s–a node cells reach threshold and fire APs before the a–v node cells reach their threshold and fire. This is why the s–a node cells are the normal pacemaker cells of the heart; that is, they fire APs first.

Third-Degree Atrioventricular Block (Complete Heart Block)

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All conduction through the AV node is blocked. Atrial and ventricular depolarizations are no longer coordinated and occur independently of one another. Ventricular depolarization is initiated by discharge of a ventricular escape focus.

Electrocardiographic features (see Figure 3-12, D)

There is no association between P waves and QRS-T complexes.

P waves are of normal morphology and usually occur at a normal rate.

QRS complexes are of ventricular origin morphology.

Ventricular rate is typically 30 to 50 bpm.

Causes include fibrosis of the AV node, drug-induced (digoxin), infiltrative disease, Rickettsial myocarditis, hyperkalemia.

Usually associated with clinical signs of weakness or collapse. Complete AV block warrants implantation of a permanent pacemaker in most cases.

Therapy

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AF is an AV node–independent arrhythmia, caused by multiple simultaneous intra-atrial reentrant circuits. Medical conversion of AF to sinus rhythm with drugs is very difficult and rarely achieved in canine patients. In most cases, ventricular rate control via slowing of AV node conduction with diltiazem and or digoxin is the goal (drug dosages are listed in Table 16-1). The veterinary literature also cites atenolol as effective for rate control of AF. The authors do not have much personal experience with atenolol for this purpose. The reluctance to use atenolol for rate control stems in part from the concomitant degree of advanced myocardial failure in many patients with AF. In our experience diltiazem XR is very well tolerated even in dogs with severe systolic myocardial dysfunction.

Dogs with normal cardiac function or only mild dysfunction and normal to moderately elevated ventricular response rates may be candidates for electric cardioversion of AF to sinus rhythm.

Medical management varies with the initial average heart rate and overall condition of the dog (Figures 16-2 through 16-4). Treatment can be tailored to the patient based on the approximate average heart rate. The authors prioritize treatment according to three general categories of ventricular response rate: (1) fast (Figure 16-2: average heart rate faster than 180 bpm), (2) moderate (Figure 16-3: average heart rate 130 to 160 bpm) and (3) slow (Figure 16-4: heart rate around 100 bpm). The dosages for the drug listed in Figures 16-2, 16-3 and 16-4 are provided in Table 16-1.

Treatment of AF in cats is challenging. There is usually significant underlying heart disease present, resulting in markedly enlarged atria and very rapid AF. Medical management for rate control with a target heart rate of 130 to 150 bpm may be achieved using either CCB or BB (for drug dosages for antiarrhythmic drugs in cats see Table 16-3).

Occasionally, the administration of narcotics has been associated with the induction of AF in large dogs. This is likely caused by the increased vagal tone that occurs with narcotics. Treatment with 2 mg/kg lidocaine IV within 4 hours of onset has been demonstrated to restore sinus rhythm. Vagolytic drugs (atropine) should prevent onset or recurrence of AF in such cases.

Key Point

Digoxin monotherapy does not control the ventricular response rate adequately during times of excitement, stress or exercise. Thus, dogs with AF and moderate to fast heart rates will require combination therapy of digoxin with diltiazem or atenolol.

Etiology and Pathophysiology

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Etiology

Structural lesions of the AV node (fibrosis, inflammation, degeneration) that may be associated with endocarditis, myocarditis, or infiltrative processes

Severe hyperkalemia

Intoxication (rattlesnake envenomation)

Immediately after delivery of an intracardiac direct current electrical shock (eg, treatment of atrial fibrillation), a temporary high-degree AV block may occur

Idiopathic

Pathophysiology

Clinical signs of weakness and intermittent syncope are related to the ability of the ventricles to generate their own (slow) escape rhythm.

The escape rhythm may emanate from pacemaker cells from the distal AV node, His bundle, or ventricle.

Bradycardia results in low blood pressure and a reflex increase in the atrial rate (commonly 60–120/min).

Lifting the horse's head seems to further decrease blood flow to the brain and may elicit syncope.

First and second degree atrioventricular (AV) block

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Delays of impulse conduction at the atrioventricular (AV) node are classified as first, second, and third degree (or complete) AV block. Second degree AV block is the most common physiological arrhythmia in horses. Third degree AV block is considered pathological and will be discussed below.

First-degree AV block occurs when the PQ interval exceeds the upper normal limit while the atrial impulse still transmits through the AV conduction system and activates the ventricle, causing a normal QRS-T complex on the ECG.

Diagnosis of first-degree AV block is difficult by auscultation, although a prolongation of the interval between the fourth (S4) and first (S1) heart sound may be heard.

During second-degree AV block, some P waves are not conducted to the ventricles, resulting in occasional P waves not followed by a QRS-T complex on the ECG. The underlying rhythm is usually a normal sinus rhythm (Figure 7.4).

Auscultatory findings include a regular underlying rhythm with intermittent pauses during which the fourth heart sound (S4) may be audible.

Up to one in three beats may be blocked in normal horses.

Occasionally, two or more consecutive second-degree AV blocks are observed in presence of a normal or slow sino-atrial rate.

Second-degree AV block following progressive prolongation of the PQ interval is classified as Mobitz type I (Wenckebach) block (Figure 7.4). Conversely, the AV block is termed Mobitz type II if the PQ interval is constant.

First- and second-degree AV block are considered normal variations in the horse. These rhythms are most often associated with high vagal tone and may be seen in normal, resting horses with a normal or low-normal heart rate. Furthermore, second-degree AV block can be seen during the recovery phase immediately after exercise (so called phase of autonomic imbalance) or in an anxious horse after a brief surge of sinus tachycardia.

If second-degree AV block persists despite excitement, exercise, or vagolytic drugs, structural AV node disease should be suspected. Persistent high-grade second-degree AV block may progress into complete AV block over time.

Definition and Causes

I.

Atrioventricular reciprocating tachycardia travels a circuit through the AV node and an accessory pathway (that can conduct impulses from the atria to the ventricles directly), and bypasses the AV node and the His Purkinje system.

During typical orthodromic AV reciprocating tachycardia (OAVRT), electrical activity proceeds from the atria to the ventricles through the AV node and then moves back up to the atria in a retrograde direction via the accessory pathway (bypass tract).

An accessory pathway can behave like a two-way street for electrical conduction.

During early activation of the ventricle via the accessory pathway (if it conducts in an antegrade direction), a delta wave may be seen on the ECG.

Antegrade conduction is uncommon in the dog.

Accessory pathways are embryonic, muscular remnants that allow conduction from the atria to the ventricles and bypass the normal pathway of activation.

Labrador retrievers with tricuspid valve dysplasia occasionally have accessory pathways and OAVRT.

Junctional and ventricular arrhythmias

Cardiac arrhythmias that originate in or below the AV node are classified as junctional (AV node or bundle of His) or ventricular (ventricular conducting tissues or myocardium), respectively. Determining the exact origin of the abnormal impulse can be difficult but occasionally may be achieved by careful inspection of the QRS complex. Junctional impulses are more likely to result in a narrow, relatively normal-appearing QRS complex (Figure 3-34). Complexes that originate in the ventricles, by contrast, are conducted abnormally and more slowly, resulting in wide, morphologically abnormal QRS and abnormal T waves (Figures 3-35 and 3-36). Some junctional tachycardias may be conducted aberrantly, resulting in wide and morphologically bizarre QRS complexes. Junctional and ventricular ectopic rhythms may produce abnormal ventricular activation patterns that can be electrically destabilizing deteriorating ventricular flutter or fibrillation (see Figure 3-36, E).

The normal heart contains latent (subsidiary) cardiac pacemakers within the AV and ventricular specialized tissues. The activity of these potential pacemakers may become manifest during periods of sinus bradycardia (see previous paragraphs) or AV block (see following paragraphs), leading to escape complexes or escape rhythms. Escape rhythms are characterized by slow ventricular rates, often between 15 to 25 beats/min (see following paragraphs and Figure 3-34, B). Specific antiarrhythmic drug suppression of escape rhythms generally is not necessary and is contraindicated because these rhythms may serve as the only rescue mechanism for the initiation of ventricular contraction. Management of escape rhythms should be toward determination of the cause of sinus bradycardia or AV block.

Occasionally the normal subsidiary pacemakers may be enhanced and discharge at a rate that is equal to or slightly above the SA rate (usually between 60 and 80 beats/min). The resulting rhythm is commonly referred to as accelerated idionodal or idioventricular rhythm or slow ventricular tachycardia (see Figure 3-36, B). Conditions that favor the development of accelerated idioventricular rhythms include endotoxemia, autonomic imbalance, acid-base disturbances, and electrolyte abnormalities.254 Some combinations of preanesthetic drugs such as xylazine and detomidine and anesthetic drugs (halothane) suppress SA function, potentially resulting in sinus bradycardia while enhancing the effects of catecholamines on latent junctional and ventricular pacemakers.255 Idioventricular rhythms are often quite regular and can be misdiagnosed as sinus tachycardia during auscultation or palpation of peripheral pulses. Persistent, unexplained mild–to-moderate tachycardia should prompt an ECG evaluation to correctly determine cardiac rhythm. Most idioventricular rhythms generally are of little clinical (electrophysiologic and hemodynamic) significance and resolve spontaneously with appropriate treatment or resolution of the underlying disease. Electrolyte supplementation (potassium, magnesium) and correction of fluid deficits and acid-base disturbances may be beneficial. Lidocaine therapy is sometimes administered as an intraoperative adjunct to general anesthesia or as a prokinetic drug in the management of postoperative ileus (see Chapter 22).

Junctional and ventricular complexes that arise early relative to the next normal cardiac cycle are designated as premature junctional or ventricular complexes (see Figures 3-34, A, and 3-35, A). They are often associated with administration of drugs (i.e., catecholamines, digoxin, halothane), sympathetic stimulation, electrolyte disturbances (i.e., hypokalemia, hypomagnesemia), acid-base disorders, ischemia, or inflammation. Premature complexes may occur as single events, couplets (pairs), triplets, or short runs. A cardiac rhythm characterized by sinus beats followed at a fixed coupling interval by premature ventricular beats is referred to as ventricular bigeminy (see Figure 3-36, A). Repetitive ectopic complexes that occur in short bursts or runs are termed nonsustained or paroxysmal ventricular tachycardias. Sustained junctional and ventricular tachycardias may also occur (see Figures 3-35, C and D, and 3-36, C). Ventricular tachycardias are referred to as uniform (monomorphic) if the QRS-T morphology of the ectopic beats is consistent throughout the recording and as multiform (polymorphic) if two or more abnormal QRS-T configurations can be identified (see Figure 3-36, D). Torsades de pointes represent a specific form of polymorphic ventricular tachycardia characterized by progressive changes in QRS direction, leading to a steady undulation in the QRS axis. Ventricular flutter and fibrillation are characterized by a chaotic ventricular activation pattern, leading to uncoordinated undulations of the electrical baseline (Figure 3-36, E).

Ventricular premature complexes and junctional arrhythmias are usually considered abnormal in the horse, although isolated ventricular ectopic complexes may be more common than recognized from routine ECG studies.127,256 The clinical significance of an occasional junctional or ventricular premature complex in the horse is difficult to ascertain. Persistent or repetitive junctional or ventricular rhythms are indicative of heart disease, systemic disease, or a drug-induced abnormality of cardiac rhythm. Ventricular tachycardia may be life threatening if the arrhythmia is rapid (e.g., above 180 beats/min), multiform (polymorphic, including torsades de pointes), or characterized by a short coupling interval and R-on-T phenomenon (R-on-T refers to premature complexes occurring on the peak of the preceding T wave). Ventricular tachycardia can progress into ventricular flutter or ventricular fibrillation, rhythms that commonly indicate terminal events (see Figure 3-36, E).

Accelerated idionodal or idioventricular rhythms and junctional or ventricular tachycardias usually cause interference with AV conduction of normal SA impulses while leaving atrial activation unaffected. The resulting (independent) coexistence of the SA activity (P wave) and the ectopic ventricular activity (QRS-T) is commonly referred to as AV dissociation (see Figures 3-34, A and B, 3-35, C and D, and 3-36, B). The P waves may appear to “march in and out” of the QRS complex when the independent atrial and ventricular pacemaker foci discharge at similar rates. This phenomenon is called isorhythmic AV dissociation and is occasionally observed in adult horses during inhalation anesthesia; it rarely requires therapy because the ventricular rate is maintained near normal values. It is important to note that escape rhythms associated with sinus bradycardia or complete AV block also cause AV dissociation (Figure 3-37, C). Thus AV dissociation is a purely descriptive term of an ECG finding and neither characterizes the type and pathophysiologic mechanism of the arrhythmia nor determines the therapeutic approach.

The identification of nonconducted P waves is common during sustained junctional or ventricular tachycardias (see Figure 3-36). Some P waves may be buried in the ectopic QRS-T complexes (especially during faster heart rates), making their identification difficult. The use of ECG calipers helps determine the P-P interval and can greatly facilitate the identification of P waves. Occasionally atrial impulses may be conducted normally, leading to capture beats or fusion beats. Capture beats are characterized by a normal P-QRS-T configuration, resulting from normal ventricular activation occurring before the ectopic focus discharges (see Figure 3-36, C). Fusion beats are seen when both the conducted impulse and an ectopic impulse cause simultaneous ventricular activation. The QRS-T morphology of a fusion beat represents the summation of a normal and an ectopic beat (see Figure 3-36, B).

The ECG should be monitored closely during induction and throughout the maintenance of anesthesia in horses with junctional or ventricular arrhythmias (see Chapter 8). Sedatives and anesthetic drugs should be chosen carefully to avoid administration of proarrhythmic drugs (e.g., halothane). Antiarrhythmic drugs should be available (see Table 3-10).194,211,257 Junctional and ventricular arrhythmias that develop intraoperatively should be treated when premature complexes are frequent, multiform (polymorphic), or rapid (>100 to 120 beats/min); they show R-on-T characteristics; or there is evidence of hypotension. Lidocaine is commonly used as treatment for junctional or ventricular arrhythmias in horses. Lidocaine is usually well tolerated, but bolus doses should not exceed 2 mg/kg intravenously. Excessive doses of lidocaine can produce neurotoxic side effects (disorientation, muscle fasciculations, and convulsions) or hypotension in anesthetized horses. Fluid therapy and especially maintenance of normal serum potassium concentration (4 to 5 mEq/L) are essential for antiarrhythmic therapy to be effective. Magnesium supplementation (e.g., 25 to 150 mg/kg/day intravenously, diluted in polyionic isotonic solution) may be beneficial. Therapeutic doses of magnesium are considered the treatment of choice for torsades de pointes (see Table 3-10). Procainamide or quinidine gluconate is potentially effective therapy for the treatment of ventricular tachyarrhythmias resistant to lidocaine and magnesium. Both drugs can cause hypotension and reduced myocardial contractility and must be administered cautiously. The risk-benefits of preoperative or intraoperative antiarrhythmic treatment should be considered carefully before initiating therapy.120,122,194

Prognosis is favorable for infrequent single ectopic ventricular complexes, particularly in the absence of other signs of cardiac disease. The prognosis for sustained junctional or ventricular tachycardia is usually guarded, especially when there is evidence of significant structural heart disease or congestive heart failure. The prognosis for multiform ventricular tachycardia or torsades de pointes is usually poor.

Basic Information

Disease Forms/Subtypes

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First-degree AV block: slowing of conduction through the AV node, represented by a prolonged PR interval on the ECG (the expected PR interval in a ferret is 0.03 to 0.06 second)

Second-degree AV block: occasional or regular nonconduction through the AV node represented by P waves not followed by a QRS (ventricular) complex on the ECG. Second-degree AV block may be further subcategorized as follows:

Mobitz type I (Wenckebach phenomenon): the PR interval becomes progressively prolonged, culminating in a nonconducted P wave (uncommon in ferrets)

Mobitz type II: the PR interval is constant, but some P waves are not conducted to the ventricles (not followed by a QRS complex). If nonconducted P waves occur in regular repetitions, this pattern can be described by using a ratio of P waves to QRS complexes (e.g., 3 : 1). This type of AV block may be further described as “high grade” if it occurs with three or more consecutive nonconducted P waves.

Third-degree AV block: complete failure of the AV node to convey the atrial electrical impulse to the ventricles, leading to complete dissociation of P waves and QRS complexes on an ECG. With this bradyarrhythmia, P waves occur regularly and at a rate faster than the ventricular escape rate (rate of QRS complexes). QRS complexes are typically wide and bizarre in appearance owing to their ventricular origin, although they may appear narrow if originating high in the ventricle or at the AV junction.