Technician Update

Shock to the Heart: TVEC in the Equine Practice

By Signe Mullen, LVT

When cardiac output is decreased, it affects the blood flow to the body, which can decrease oxygen to the muscles and organs. If a patient has reduced cardiac output for a prolonged period, it may result in muscle and organ dysfunction.

Signs of atrial fibrillation (AFib) that you may see in an equine patient are shortness of breath, lethargy, decreased or poor performance, and coughing or nasal discharge. It is also possible that the patient will be asymptomatic, and AFib may only be detected on auscultation.

There are 2 ways to treat AFib: quinidine and transvenous electrical cardioversion (TVEC). Quinidine is an antiarrhythmic drug that can be given through a nasogastric tube every 2 hours until the patient converts to a normal sinus rhythm. Quinidine may have side effects, including ataxia, nasal edema, colic, hives and laminitis.

TVEC entails putting the patient under general anesthesia and placing electrodes into the heart. In human and small animal medicine, paddles are used to convert the patient to a normal sinus rhythm. However, due to the large muscle mass of horses, the shock will not reach the heart, so shocks administered directly to the heart are the most efficient.

The electrodes are inserted through the jugular vein and into the right atrium and the pulmonary artery. Electrode placement is confirmed via ultrasound and radiographs. Once the electrodes are placed, the patient is put under general anesthesia and shocks are administered via the electrodes to convert the heart back into a normal sinus rhythm. The shocks are timed so that they are given during the QRS complexes.

There are always risks involved when putting a horse under general anesthesia, so that must be a consideration before performing the procedure.

The patient in this case study is a 16-year-old, 1,402-lb (636-kg) Holsteiner gelding that was evaluated originally by his primary care veterinarian for an unresolving cough. Initial examination disclosed an irregular heart rhythm consistent with AFib. The primary care veterinarian also observed that the patient had asymmetrical musculature of the hind end. Further cardiac workup showed a heart rate of 60 to 80 beats per minute (bpm) and an irregularly irregular rhythm.

Blood chemistry and cardiac troponin levels were within normal limits. The referring veterinarian attempted a conversion with quinidine. The patient suffered a syncopal episode and collapsed shortly after administration, and the quinidine treatment was discontinued. The patient was then referred to a cardiologist for an examination.

During evaluation by the cardiologist, the patient’s heart rate was 64 to 72 bpm with weak pulses. An electrocardiogram (ECG) revealed an “irregularly irregular” rhythm with no P waves, but there were F waves consistent with AFib. Echocardiography showed minimal structural changes of the heart, indicating the patient was a suitable candidate for a TVEC procedure.

The patient was then referred to Pilchuck Veterinary Hospital for a TVEC that would be performed with both the Pilchuck and the cardiology teams. Preoperative blood work showed CBC and chemistry were within normal limits.

On the day of the procedure, the patient was sedated in the stocks, and a 14-gauge IV catheter was placed in the left jugular vein. Two 10-gauge × 3-inch catheters were placed in the right jugular vein, 4 to 5 inches from each other. A 7-French transvenous electroconversion catheter was inserted into the jugular vein and placed in the pulmonary artery via the caudal catheter. A second 7-French transvenous electroconversion catheter was inserted in the jugular vein and placed in the right atrium via the cranial catheter. The 10-gauge IV catheters were removed from the jugular vein, and the transvenous catheters were sutured to the skin. The electrode placement was confirmed via ultrasound.

The electrodes were then taped to the patient’s neck to keep them in place during the induction process. The patient was walked to the induction stall, and xylazine IV and butorphanol IV were administered. Once the patient was at an adequate plane of sedation, he was induced with ketamine and midazolam. The patient was then intubated with a 30-mm cuffed endotracheal tube. Hobbles were placed around the patient’s pasterns, and the patient was transported to the operating room with a hoist.

He was placed in left lateral recumbency and his legs were loosely tied to the table to minimize movement during shock administration. Mechanical ventilation was started, and the patient was maintained on isoflurane throughout the procedure. An arterial catheter was placed in the right facial artery. IV fluids and CRI dobutamine and xylazine were initiated, and monitoring was performed via ECG, blood pressure readings, blood gas analysis, pulse oximetry and capnography. Thoracic radiographs were obtained to confirm that the catheter positions remained stable, and minor adjustments were performed.

The defibrillator was attached to the patient to begin monitoring and to ensure appropriate sensing of the QRS complexes, and the team ensured that no person or metal objects were touching the patient to avoid accidental shocks. Once the patient was positioned safely and his head and limbs were protected, shocks were administered.

A series of 7 shocks were given in the following order: 100 J, 125 J, 150 J, 175 J, 200 J, 250 J and 300 J. Unfortunately, the series of 7 shocks did not convert the heart to a normal sinus rhythm. An amiodarone infusion was started, and 1,800 mg was given during 1 hour. Amiodarone is an antiarrhythmic medication that helps to lower the threshold needed for a conversion.

During the amiodarone infusion, echocardiography disclosed evidence that the catheter within the pulmonary artery had doubled over within the artery, so the electrode was repositioned sterilely. Thoracic radiographs were then obtained to confirm placement.

A series of 3 sequential shocks were then delivered in the following order: 125 J, 200 J and 300 J. Unfortunately, the series of shocks failed to convert the heart to a normal sinus rhythm, and the AFib persisted.

A final advancement of the left pulmonary artery catheter was performed to the full depth of the catheter. The cardiologists, internist and referring veterinarian conferred to consider administering one more shock. This shock would be 1 shock above the published high-end normal. The choices were to administer 1 more shock or to wake the patient and re-attempt the procedure another day. After consideration of the amiodarone infusion, the final adjustment of the catheter, and the fact that the owner would not pursue another attempt, there was a uniform consensus to administer 1 last shock. A final shock was administered at 300 J, and a normal sinus rhythm was achieved.

After the conversion to a normal sinus rhythm, the anesthesia team noted an immediate increase in the patient’s systemic blood pressure. There was also a clear arterial pressure waveform, where it was noted previously to be a poor/weak waveform. The patient was monitored for an additional 15 minutes in a normal sinus rhythm before he was moved to the recovery stall. The TVEC catheters were removed, and pressure wraps were applied to the sites for the recovery period.

After the patient was transported to the recovery stall, continued monitoring with an ECG was performed until the patient started to move. A head bumper and leg wraps were placed to help protect the patient during the recovery process. He was extubated once he was breathing consistently, and intranasal phenylephrine was administered to assist with any nasal edema. Postoperative IV xylazine was administered after eye signs were present. The patient then recovered on an inflatable pillow.

Pulmonary edema due to being in lateral recumbency for a prolonged period—a risk when undergoing general anesthesia—was observed.

IV dexamethasone and furosemide were administered after the patient was standing in recovery. Results of cardiac troponin testing 1 day after the procedure were normal, indicating that the extra shock did not damage the myocardium. The patient remained in the hospital for an extra 3 days on supportive care after the pulmonary edema was observed. He was maintained on IV fluids for 48 hours, IV antibiotics for 3 days, and furosemide for 24 hours. ECGs were performed daily while the patient was hospitalized, and he maintained a normal sinus rhythm.

The patient was discharged 4 days after the procedure, and he did well for a few months afterward. About 6 months after the TVEC, he had another episode of AFib. Due to the patient’s decline in health, the owner elected for humane euthanasia.

In this patient’s case, it is unknown how long the horse was initially in AFib. He was also considered an older patient who was noted to have decreased musculature on exam when the AFib was first observed. Because the length of the AFib was unknown, he may have had damage to his tissue or organs due to a prolonged decrease in cardiac output.

This shows the importance of yearly exams and wellness checks, as certain conditions may be caught and treated early.
This was the first time that TVEC was performed at my hospital and with the cardiology clinic with which we work closely. It was a great learning experience for all of us, and we can perform it on more horses in the future. MeV

Teaching Points
This case study discusses transvenous electrical cardioversion (TVEC), which is a method of treating atrial fibrillation (AFib). Before reading the case, here is a brief overview of the difference between a normal sinus rhythm and atrial fibrillation.

A normal sinus rhythm contains a P wave, a QRS complex and a T wave:

• The P wave represents atrial depolarization and contraction of the atria.
• The QRS complex represents the ventricular depolarization and contraction
  of the ventricles.
• The T wave represents ventricular repolarization and recovery of the
  ventricles.

In a normal sinus rhythm, all beats appear to have a similar pattern, are equally spaced, and contain a P wave, a QRS complex and a T wave. The intervals between the QRS complexes are the same.

AFib is an electrical disorder of the heart in which electrical impulses do not fire in a regular pattern. Instead, many electrical impulses fire rapidly at the same time. This causes a fast and chaotic rhythm and pace, which prevents the atria from pumping blood efficiently to the ventricles and causes the ventricles to contract irregularly.

AFib is the only “irregularly irregular” heart rhythm, meaning that the beats are not spaced evenly, and there is no discernible pattern. If an irregularly irregular rhythm is heard on auscultation, then it is AFib.

On an electrocardiogram, there will be no P waves. There will instead be F waves—fibrillations caused by the atria quivering and not fully contracting. AFib can cause cardiac output to be significantly decreased.