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Manual of Equine Anesthesia and Analgesia


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of the PR interval until a dropped beat occurs. The ECG shows a P wave not followed by a QRS complex.Often associated with increased vagal tone and is common with administration of α2 agonists.Normal sinus rhythm can be restored with this type of arrhythmia by exciting or exercising the horse to increase sympathetic tone and decreasing parasympathetic tone. Elevation of the HR above 60–80 beats/min may be required to resolve the block.

       Type 2 (Mobitz type 2)Regular PR interval and then sudden absence of a QRS after a P wave.Persistence of the heart block, despite exercising the horse to increase the sympathetic tone, may indicate a pathologic condition such as disease of the AV node, which is often the case for this type of block.

       Atria are not contracting in a coordinated manner.

       It is relatively common in horses due to their large atria and high degree of vagal tone.There is a higher incidence in Standardbreds, Draft horses and Warmbloods.

       Paroxysmal atrial fibrillation has been reported in Thoroughbreds during racing, and sinus rhythm returns spontaneous within 72 hours. In most cases however, atrial fibrillation does not spontaneously convert to sinus rhythm.

       No “P” waves are present. Fibrillation (f) waves are evident and they may have a frequency up to 500 beats/min, but few are conducted through the AV node to the ventricle.The f wave morphology can be course or fine.

       The RR interval is irregularly irregular and QRS complexes are normal if there is no underlying disease.

       Cardiac function can be relatively normal at rest or during mild to moderate exercise if the finding is incidental.

       Decreased cardiac function occurs if there is associated heart disease or at high levels of performance.

       Treatment of atrial fibrillation

       If cardiac function is otherwise normal, atrial fibrillation can generally be converted to sinus rhythm with quinidine. Prognosis for conversion is poor if atrial fibrillation has been present for over four months.

       Transvascular electrical conversion under general anesthesia is reported to have good success in converting atrial fibrillation of longer duration.

      E Atrial flutter

       Similar to atrial fibrillation but less common in horses.

       Baseline sinusoidal wave with more frequent “f” waves, referred to as saw‐tooth pattern, between two consecutive QRS complexes.

       Uncommon in horses.

       Treatment is the same as for atrial fibrillation.

      F Premature atrial contractions (PACs)

       A normal QRS complex appears before expected; therefore, the R–R interval is shorter between the previous normal beat and the premature beat.

       The “P” wave can be absent (hiding) if the PAC occurred to soon after the normal beat.

       Can be incidental or associated with heart disease that has caused enlarged atria, or myocarditis or hypokalemia.

       A solitary PAC is not likely to be significant if not associated with clinical signs and does not occur during exercise.

Photo depicts atrial fibrillation.

       Treatment

       Not necessary to treat unless the PACs become frequent and the horse develops clinical signs or atrial fibrillation is triggered.

       Quinidine can be used to terminate the arrhythmia.

       Digoxin can be used to control the arrhythmia if there is underlying cardiac disease.

       Large, abnormal morphology QRS complexes that appear before a normal beat was expected. Therefore, the R–R interval is shorter.

       The depolarization from the PVC travels retrograde and blocks the next impulse from the SA node, which can result in a compensatory pause after the abnormal beat.Note: Singular to several PVCs are often identified in normal horses.

       The PVC is not conducted via the normal conduction pathway; hence, its morphology is different and it is of longer duration than a normal QRS complex.

       The PVC is not associated with the preceding P wave.

       Runs of PVCs are of concern and may result in weakness, syncope, ventricular tachycardia and death.

       PVCs do not allow for complete and normal filling of the ventricle, which affects the SV and results in a lower cardiac output and/or hypotension.

       Treatment of single PVCs

       Treatment should be administered if PVCs:Are multifocal.Are frequent and the pulse quality is poor.Figure 3.6 Premature ventricular complex.Figure 3.7 Ventricular bigeminy; every other complex is ventricular in origin.Figure 3.8 Ventricular tachycardia.Are on top of the preceding T wave, as this scenario may result in ventricular fibrillation.

       Administer lidocaine (0.5–2 mg/kg, IV).

       Treatment of multiple PVCs

       Lidocaine (0.5–2 mg/kg, IV) for immediate control of PVCs.

       Treat underlying cause (e.g. hypoxia, electrolyte abnormalities [K+, Ca++, Mg++]).

       Quinidine gluconate (1.1–2.2 mg/kg, IV) for short‐term control of PVCs.

       Lidocaine (25–50 μg/kg/min) for longer term control.

       A group of four or more consecutive PVCs.

       Characterized by abnormal QRS complexes that are not associated with P waves.P waves, if present, may be hidden in the QRS complexes.

       VT may be paroxysmal or sustained for minutes or hours and may lead to ventricular fibrillation.

       The ventricular rate may be slow (slightly above normal rate) or fast (up to 200 beats/min).

       The QRS complexes may be monomorphic or polymorphic.

       SV is decreased especially if the