Dysrhythmias: cardiac pacing and electrical cardioversion

Chapter 14 Dysrhythmias

cardiac pacing and electrical cardioversion


Cardiac cells, due to their excitable properties, are capable of being depolarized by an external stimulus such as an electrical pulse. Such depolarization will only occur if the external stimulus has sufficient strength to reach the threshold for stimulation and provided that the stimulus is not delivered while the cell is in a refractory period.1,2 As atria and ventricles act as a pseudosyncytium, depolarization of a few atrial or ventricular cells leads to depolarization of the whole atrium or ventricle, respectively. As such, by delivering electrical stimuli at a precise location in or around the heart, one can selectively induce atrial or ventricular contractions at a specific rate and this is called atrial or ventricular pacing. Certain pacing techniques can be performed in the standing, unsedated horse without being sensed as the required electrical stimuli are of relatively low intensity.

It is possible to depolarize nearly the whole atrium or ventricle at once using a high-energy direct current shock from a capacitor discharge. The whole myocardium is instantaneously brought into a refractory state, and this technique can be used to treat certain tachyarrhythmias such as atrial or ventricular fibrillation. This procedure is called electrical defibrillation (in case of ventricular fibrillation) or electrical cardioversion (in case of other tachyarrhythmias). Required energy levels are high and render the technique impossible to be performed without general anaesthesia. It is critical that the clinician is aware that delivery of an electrical pulse or shock with inappropriate amplitude, duration or timing may induce unwanted or even dangerous arrhythmias.


During pacing, current pulses with specific amplitude, duration and interval are transmitted to the atrium or ventricle via appropriately positioned electrodes. Only when the current is able to reduce the resting potential of the cardiac cell by a critical amount and within a critical time, will “capture” be achieved, which means that a depolarization of that chamber will follow. The intensity of the electrical pulse required to reach the threshold for stimulation is determined mainly by the position of the electrodes in relation to the heart. This intensity is expressed by the pacing amplitude (strength, V) and the pulse width (duration, ms) of the electrical stimulus. A stimulus that is large in amplitude requires a shorter duration to reach threshold, and vice versa. At a given pulse duration, the corresponding threshold amplitude can be easily determined by the stimulus reduction method. With a fixed pulse duration, pacing is started at a high amplitude, which results in consistent capture. Every few beats the amplitude is gradually reduced until, finally, capture is lost. The lowest amplitude resulting in capture represents the threshold value for that pulse duration. Similarly, the threshold pulse duration can be determined for a fixed pulse amplitude. Threshold values describe a hyperbolic-like strength-duration curve (Fig. 14.1), which is a means of verifying that a given electrode position is likely to achieve safe and effective cardiac pacing.2 Two important features of the strength-duration curve are the rheobase and chronaxie. The rheobase is the lowest voltage that results in capture at “infinitely” long pulse duration (usually less than 1.5 ms). The chronaxie is the required pulse width when pacing at two times the rheobase voltage. When two random points of the strength-duration curve are determined, the rheobase, the chronaxie and the remaining points of the curve can be calculated using the following equation3:


where I is the stimulus intensity (voltage or current), t the pulse width, Ir the rheobase and tc the chronaxie.

It is critical that a stimulus is not delivered near the end of the refractory period, i.e. the “vulnerable” period, because this might initiate fibrillation4 and is extremely dangerous in case of ventricular stimulation. For this reason, most pulse generators (pacemakers) are able to “sense” each cardiac depolarization, thereby temporarily inhibiting the pacing function.


Cardiac pacing techniques can be subdivided depending on: (1) the polarity of the electrodes (unipolar or bipolar), (2) the location of the electrodes (transcutaneous, transoesophageal, epicardial, endomyocardial) and (3) the duration of pacing (temporary or permanent).

An electrical current flows between two electrodes, the cathode and the anode. The number of electrodes in contact with or close to the heart determines whether unipolar or bipolar pacing is performed. The electrode nearest to the myocardium should be the cathode (negative) because cathodal stimulation is less likely to induce arrhythmias.5 For unipolar pacing, one electrode, the cathode, is in contact with the heart while the second electrode is at a remote site of the heart. In case of bipolar pacing, cathode and anode are, within a short distance of each other, in contact with the heart. Unipolar pacing results in a much larger pacing artifact on the surface ECG and is more likely to induce skeletal muscle stimulation (near the anode) than bipolar pacing. Finally, recording an intracardiac ECG through a unipolar lead is more susceptible to muscle potential artifacts than bipolar recordings.

Electrode size and especially location determine which cardiac chamber will be stimulated and which pulse intensity will be required to reach the threshold for stimulation. Electrodes at remote distance from the heart, such as transcutaneous electrodes, will require a rather high pulse intensity. As such, pacing will be sensed by the patient rendering the technique inapplicable in conscious horses. There is no available information regarding transoesophageal pacing in horses, but most likely, the technique is not applicable in the conscious horse, due to the larger distance between oesophagus and atrium or ventricle compared to humans. Electrodes in close contact with the heart (epicardial or endomyocardial) will require such little intensity to achieve consistent capture that stimulation is not sensed by the patient and this method has been most widely applied in equine cardiology.

During right atrial pacing, electrodes located near the phrenic nerve can result in hiccups during atrial pacing, especially at higher pacing thresholds. As the nerve cannot be easily identified by ultrasonography, testing stimuli should be applied at higher strength-duration values to determine whether diaphragmatic stimulation occurs, and if so, the right atrial electrode must be repositioned.

The most suitable and safest approach for atrial and ventricular pacing in horses utilizes a lead or catheter with electrodes on its tip, inserted transvenously and positioned in the respective right cardiac chambers, to allow stimulation of the endomyocardium.6 Due to the close contact between electrode and myocardium, a minimal amount of energy, usually between 0.5 and 7.5 V and 0.3 and 1.2 ms, is sufficient to achieve consistent capture. Therefore, pacing will not be sensed by the patient. Positioning of the electrode is guided by fluoroscopy and echocardiography. In addition, the electrode position is verified by recording the intracavitary electrogram from the lead simultaneously with a surface ECG.6 During transvenous insertion of the lead the intracavitary electrogram will successively show: (1) no or minimal deflections during passage through the vein, (2) a deflection simultaneous with the P wave from the surface ECG during right atrial positioning (Fig. 14.2A) and (3) a deflection simultaneous with the QRS complex when located in the right ventricle (see Fig. 14.2B). Additionally, electrode position is verified by connecting the lead with a pacing device and applying testing stimuli of sufficient strength. An intravenous position will not result in capture, while an atrial or ventricular position will produce a P wave or QRS complex, respectively.

Temporary pacing is achieved with a temporary lead or catheter that possesses (at least) two closely spaced electrodes at the tip to obtain bipolar pacing. The lead is transvenously inserted and the external part of the lead is connected with an external pacing device from which pacing rate and pulse strength and duration can be adapted. On the other hand, permanent pacing requires permanently implanted pacing device (pacemaker) and leads. It is crucial for this system that the electrodes remain in a secure position. To maintain transvenously inserted endocardial electrodes in a stable position, implantable leads have a fixation mechanism to preserve endocardial contact. Available options are either active fixation leads that invade the endomyocardium with a screw or small jaw or passive fixation leads that have little tines of fins to enhance entanglement in trabeculae of the myocardium. In horses, the atrial lead should have active fixation because in the large equine right atrium, a passive fixation lead is very likely to drop ventrally towards the right ventricle, resulting in loss of atrial capture. Although it is also advisable to use an active fixation lead for the equine ventricle, the ventrally located lead tip in the right ventricular apex can remain in position even with a passive fixation tip.


Permanent pacing

Bradydysrhythmias such as third-degree AV block and sick sinus syndrome are the major indications for permanent pacing, requiring implantation of an artificial pacemaker.7 The pacemaker is a multi-programmable and implantable battery-powered pacing device. It is connected with one or more leads towards the right atrium or ventricle (single chamber pacemaker) or towards both (dual chamber pacemaker) to stimulate a specific chamber at a specific rate (e.g. 35 bpm) so that symptomatic bradycardia is avoided. However, because an intrinsic atrial and/or ventricular rhythm might still be present, pacemakers have the ability to sense this intrinsic rate via the implanted leads and can be programmed to respond in a specific way to an intrinsic beat. Besides the treatment of bradydysrhythmias, in humans, pacemaker implantation is also used to prevent induction of certain tachydysrhythmias.8 However, this technique has never been used in horses.

Pacemaker types are described using a three-letter code, with an optional fourth or even fifth letter. The first and second position indicate the chamber being paced and sensed, respectively: A (atrium), V (ventricle), D (double, both) or O (none). Manufacturers occasionally use the S to indicate that the device is capable of pacing/sensing only a single chamber. The third position denotes the reaction of the pacemaker when an intrinsic beat is sensed: I (inhibited) when pacing is inhibited by a sensed beat, T (triggered) when pacing is triggered, D (dual, both) for a dual mode of response, or O (none) when the pacemaker does not react on a sensed signal. The fourth position of the code may reflect the programmability of the device but is most frequently used to indicate that the pacemaker incorporates a sensor for rate modulation (R). Such a sensor detects changes in pressure, temperature, oxygen saturation, ventilation or detects patient activity and is capable of adapting the pacing rate towards an upper or lower limit. The fifth letter is rarely used and is restricted to antitachycardia functions: P (antitachycardia pacing), S (direct current shock), D (dual, P+S), or O (none). After implantation multiple pacing and sensing parameters can be adapted by telemetric (transcutaneous) programming of the pacemaker. Telemetric access requires the pacemaker to be implanted at a short distance from the skin at a location where it does not get damaged or hamper the animal to move or lie down.

Depending on the kind of dysrhythmia, different types of pacemakers can be applied. If the cause of bradycardia is a depressed or absent AV node conduction, a “simple”, single chamber (ventricular) pacemaker can be implanted. When this pacemaker is programmed to the VVI mode, with a minimal ventricular rate of, for example, 35 beats per minute, syncope will be prevented by preserving this minimal heart rate. However, no adaptation of heart rate to the physical needs (e.g. exercise) will occur. Rate-modulation, for example, based upon an activity sensor, is achieved with a VVIR pacemaker. However, much more efficient in case of a third-degree AV block, is to implant a dual chamber pacemaker. Such a pacemaker can be programmed to prevent a too slow atrial and ventricular rate but also to “look for” (sense) an intrinsic atrial depolarisation and to deliver (trigger) a ventricular stimulus for each sensed atrial signal, which is achieved in the DDD function (Fig. 14.3). As sinus node function in an animal with third-degree AV block is usually intact, a fairly normal paced ventricular rate, which adapts with stress or exercise, can then be obtained. If bradycardia is caused by an abnormal sinus node function, adaptation of pacing rate with exercise can only be achieved by using a pacemaker with an incorporated sensor (e.g. VVIR, DDIR).

In horses, both epicardial and transvenous lead placement has been described. The epicardial lead placement requires general anaesthesia and thoracotomy, which implies a risk, especially in an animal with a compromised cardiovascular system.9,10 This method has successfully been applied in a healthy pony and in two donkeys with third-degree AV block for implantation of a single chamber or dual chamber pacemaker.11,12,13 The pacemaker device was inserted underneath the pectoral muscle or, subcutaneously, caudal to the left elbow. In the donkeys, successful pacing was obtained for 6 weeks in one and more than 1 year in the other. During an attempt to place an epicardial lead in a mature horse with third-degree AV block, the horse developed ventricular fibrillation during general anaesthesia and died.14

Transvenous lead placement is a much safer and simpler procedure to achieve cardiac pacing and is widely used in human and small animal medicine. It requires a vein that is located relatively close to the heart (maximal lead length is around 110 cm), that is large enough to introduce one or two leads and that can be ligated permanently. A standardized approach has been described to implant a dual chamber pacemaker via the cephalic vein.6 As the whole procedure can be performed in the standing, sedated horse, the additional risk of anaesthesia can be avoided. During the implantation procedure, an atrial and a ventricular active fixation lead are inserted through a surgically exposed cephalic vein. Lead placement is guided by both echocardiography and by measuring the electrical characteristics of the lead. After permanent ligation of the vein a pacemaker pocket is created between the lateral pectoral groove and the manubrium sterni. Successful clinical application of transvenous lead placement was first reported by Reef et al.,15 implanting a single chamber (ventricular) pacemaker in a horse with third-degree AV block. Under general anaesthesia, a passive fixation lead was inserted in the jugular vein and placed in the right ventricular apex under echocardiographic guidance. The pacemaker pocket was created dorsal to the jugular vein. Although the horse remained asymptomatic, 16 months later, a second lead with active fixation was implanted in the right atrium and the pacemaker was updated to a dual chamber model, allowing AV sequential pacing of the ventricles. Consequently, a physiological rate response to exercise and stress occurred. With the dual chamber pacemaker the horse was able to perform exercise with a maximal achievable heart rate of 150 beats per minute. About 3 years after the initial implantation, however, the horse suddenly died due to a suppurative endocarditis and suspected terminal bacteraemia.16 Implantation of a dual chamber rate-adaptive pacemaker has also been used in a horse with post-exercise bradycardia and syncope due to sinus node dysfunction.17 At 7-year follow-up, proper dual chamber pacing was still achieved.

Temporary pacing

Short-term therapeutic pacing is generally applied as a temporary solution for bradydysrhythmias, e.g. prior to the implantation of a permanent pacemaker and during neonatal cardiopulmonary resuscitation. On rare occasions, it can also be used to terminate certain tachydysrhythmias. Temporary pacing is achieved with an external, temporary pacing device, connected to two electrodes (bipolar pacing) which are positioned near the heart, usually near the ventricles, in order to accelerate ventricular rate. The closer the electrodes are positioned to the heart, the smaller the pulse intensity required to elicit a ventricular depolarization, and thus the better pacing will be tolerated. Although little information is available in equine medicine, transcutaneous and transoesophageal pacing are likely to be poorly tolerated in the conscious adult horse and therefore only applicable during general anaesthesia, but transcutaneous temporary pacing can be used successfully in sick, obtunded foals. (image SBR)

A transvenously inserted catheter, electrode or lead within the right atrium or right ventricle can directly stimulate the endomyocardium, requiring only low pulse intensity, and is a safe and effective means to obtain consistent cardiac pacing. As the pacing stimuli are not sensed by the horse the technique can be used without sedation or anaesthesia. Temporary transvenous pacing has been used in horses with symptomatic bradycardia to avoid syncope prior to the permanent implantation of a pacemaker.1315,17,18 Transvenous temporary pacing has also been used to treat transient asystole following electrical cardioversion of atrial fibrillation (AF) in a horse.19

In human beings, temporary pacing is also used to terminate tachydysrhythmias such as atrial flutter, AV node tachycardia and sustained ventricular tachycardia.7 During such a transvenous overdrive pacing procedure, a train of electrical pulses is repeatedly given at a fixed rate in excess of the basic natural rhythm. The purpose is to entrain and interrupt the tachydysrhythmia by depolarizing regions of the excitable gap of the re-entry cycle.8,20 This technique has been successfully applied in a horse with persistent, medically resistant atrial flutter.21 In this horse, right atrial pacing at a rate slightly higher (300 ms cycle length) than the atrial flutter rate (365 ms cycle length) terminated the re-entry phenomenon and re-established sinus rhythm. The procedure was performed in the standing unsedated horse and was well tolerated. However, because overdrive pacing can accelerate tachycardia and result in fibrillation, the technique is not recommended for ventricular tachycardia in horses.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Dysrhythmias: cardiac pacing and electrical cardioversion
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