Output Dependent Anodal Capture: Case Report and Electrocardiographic Manifestations
- 10 (Oct.2005)
- Posted on: 5/1/08
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Heart failure is a progressive disorder that affects 6-10% of the population over the age of 65.1 Biventricular pacemakers are approved for use in patients with advanced heart failure that is refractory to medical therapy when cardiac contraction is dyssynchronous, manifested by QRS duration > 130 ms.2 They differ from conventional permanent pacemakers by virtue of having a third lead that is inserted into the epicardial surface of the left ventricle via the coronary venous system. Pacing stimulation of the right and left ventricles by the biventricular pacemaker resynchronizes ventricular activation,2 often with dramatic improvement in clinical CHF status. Anodal stimulation in biventricular pacemakers may negate the beneficial clinical outcome due to lack of left ventricular pacing. Anodal pacing makes it impossible to separate the timing of left ventricular and right ventricular pacing. Therefore, recognizing anodal stimulation is important in these cases. During echo optimization of biventricular pacing in particular, the knowledge of the chamber captured is essential. We present a case of amplitude-dependent anodal stimulation.
A 74-year-old male with a past medical history of coronary artery disease presented to the emergency department (ED) with complaints of shortness of breath, fatigue, dizziness, a non-productive cough, and increased pedal edema. In the emergency department, the patient was found to be markedly bradycardiac with a heart rate of 30 beats per minute (bpm) and low blood pressure (81/64 mmHg). The ECG revealed third degree heart block and left bundle branch block.
In the ED, the patient was stabilized with a dopamine drip, and temporary transcutaneous pacer pads were applied. Moderate decrease in ejection fraction of 45% was identified, and the decision was made to implant a biventricular pacemaker. During implantation, a QRS pattern of left ventricular capture was obtained during isolated left ventricular pacing (Figure 1) when low amplitude stimulation was used. However, when higher amplitude pacing (10 mA) was used to assess for diaphragmatic stimulation during left ventricular pacing, an ECG pattern similar to that seen with right ventricular pacing was noted (Figure 2). We switched to unipolar pacing of the LV (skin to LV lead) at various amplitudes and noted the LV paced QRS configuration only (Figure 3). We established the diagnosis of amplitude-dependent anodal stimulation. Since the anodal stimulation occurred only at unduly high pacing output and LV pacing thresholds were very low, we left the leads in that position and completed the implant.
Ventricular pacing is usually accomplished by cathodal stimulation, in which the electrode functioning as the cathode depolarizes the muscle cells immediately adjacent to it, while the anodal electrode is passive in regards to myocardial depolarization. Anodal stimulation can occur through hyperpolarization of surrounding tissue.3 This apparently paradoxical depolarization is known as anodal stimulation. Anodal stimulation can either occur during the stimulus pulse (make stimulation) or at the end of the pulse (break stimulation).3 When the anode is stimulated, the surrounding myocytes become more negative, hyperpolarizing these cells and creating a virtual anode. However, myocytes adjacent to this virtual anode have a resting membrane potential of normal negativity; thus, they are relatively more positive than those myocytes comprising the virtual anode. These adjacent myocytes, therefore, act as a virtual cathode. Together, they form the virtual electrode. For anode stimulation, a steady-state must develop between the hyperpolarized tissue at the anode and the depolarized tissue at the virtual cathode. At the end (or break) of the stimulus, the excitation propagates from the hyperpolarized tissue region as a result of depolarization extending from the virtual cathode.4 In conventional bipolar pacing leads, the anode and cathode are within the same chamber at a close distance. In this setting, there is little, if any, clinical impact from cathodal versus anodal stimulation. In current generation biventricular pacemakers and some biventricular defibrillators, the LV anode is in the right ventricle and the LV cathode is in the left ventricle. In this setting, pure anodal stimulation will negate the benefits of LV pacing and its attendant clinical improvement. Multilead monitoring at the time of LV capture testing is the only mechanism for clinical assessment of anodal capture.3
This case illustrates the occurrence of anodal capture only during high current ventricular stimulation. Since anodal stimulation is impossible with a unipolar system (anode at the skin incision, away from the myocardium), it is easy to test for anodal capture at implant by switching from bipolar pacing (LV cathode to RV anode) to unipolar pacing (LV cathode to skin anode). This case illustrates the relatively uncommon phenomenon of anodal pacing and its occurrence at only high outputs. Since it occurred during implantation, it was possible to isolate each electrode and demonstrate it incontrovertibly. It also illustrates how it is relatively easy to demonstrate LV versus RV capture if multiple ECG leads are used. Anodal pacing can be secondary to a hyperpolarization-activated current that is voltage dependent.5,6 It is possible that the reason for its occurrence in our patient at higher amplitudes was related to the voltage dependence of the hyperpolarization-activated current. There was no clinical implication for our patient given the large difference in the threshold for LV cathodal stimulation versus RV anodal stimulation. Had this difference been smaller, we would have had to look for alternative sites for LV stimulation. Should his LV pacing threshold increase significantly, we will have to be careful to assess for anodal pacing to keep the pacing output under that threshold.
1. Zei PC, Stevenson LW. Epidemiology and prognosis of heart failure. In: Ellenbogen KA, Kay GN, Wilkoff BL (ed). Device Therapy for Congestive Heart Failure. Philadelphia: WB Saunders Company, 2004: pp. 1-26.
2. Steinberg JS, Maniar PB, Higgins SL, et al. Noninvasive assessment of the biventricular pacing system. ANE 2004;9:58-70.
3. Ranjan R, Chiamvimonvat N, Thakor NV, et al. Mechanism of anode break stimulation in the heart. Byophysical Journal 1998;74:1850-1863.
4. Roth BJ. A mathematical model of make and break electrical stimulation of cardiac tissue by a unipolar anode or cathode. IEEE Trans Biomed Eng 1995;42:1174-1184.
5. Yu H, Chang F, Cohen IS. Pacemaker current i(f) in adult canine cardiac ventricular myocytes. J Physiol 1995;485:469-483.
6. Cerbai E, Pino R, Porciatti F, et al. Characterization of the hyperpolarization-activated current If in ventricular myocyte from human failing heart. Circulation 1997;95:568-571.