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Pacemaker Syndrome: an Iatrogenic Condition Br Heart J 1992;68:163-6 163 VIEWPOINT Pacemaker syndrome: an iatrogenic condition Christopher M Travill, Richard Sutton Pacemaker syndrome was first described in inhibited (VVI) pacing was used. In the re- 1969 by Mitsui when it was referred to as the maining 20 patients with no history of pacemaking syndrome.' The name pacemaker pacemaker syndrome or ventriculoatrial con- syndrome was first coined by Erbel (using the duction Doppler derived cardiac output German Schrittmacher syndrom) in 1979.2 It improved by 14% when pacing was changed can present with symptoms as severe as to DDD from VVI.8 syncope, presyncope, oedema, dyspnoea, and chest pain, or more moderately and subtly as lethargy, palpitation, or an awareness of Haemodynamics of pacemaker venous pulsation all of which may occur when syndrome there is atrial systole during ventricular sys- Contraction of the atria against closed atrio- tole. This is most frequent when there is ventricular valves during ventricular systole ventriculoatrial conduction from the paced leads to raised atrial pressures, loss of atrial ventricle to the atrium usually via the contribution to ventricular filling, and a con- atrioventricular node.34 The symptoms can be sequent fall in cardiac output which causes a identical to those prompting implant.5 fall in arterial pressure if the baroreceptor Occasionally pacemaker syndrome can occur mediated rise in systemic vascular resistance is in the absence of ventriculoatrial conduction insufficient.9 In a study on 20 open-chest dogs when ventricular pacing is in competition with experimental complete heart block left with sinus rhythm.6 atrial angiography showed retrograde blood flow into the pulmonary venous system at Incidence of pacemaker syndrome atrioventricular intervals of -50 and The incidence of pacemaker syndrome varies - 100 ms. Therefore in addition to the loss of with the vigour with which it is sought and it atrial contribution to ventricular filling there is probably affects 7% of all ventricularly paced a "negative atrial kick" further compromising patients in its severe form in which it is haemodynamic function.'0 In three patients essential to revise the pacemaker. If mild to studied by Alicandri et al" there was an moderate symptoms are considered it affects absent or smaller rise in peripheral resistance 20% of the ventricularly paced. This group in response to a fall in cardiac output. The too can benefit clinically from pacemaker mechanism was thought to be due to vaso- upgrade.7 All too often the symptoms and dilatation in response to activation of atrial signs of the syndrome are not sought and stretch receptors by atrial cannon waves patients who previously experienced syncope, which dominated over the baroreceptor now relieved, complain little. This leads to a mediated increase in resistance that occurs widespread impression that the syndrome is secondary to the fall in systemic arterial pres- rare. sure. Similar findings were observed in a group of 20 patients studied haemodynam- ically more than 24 hours after coronary Clinical diagnosis of pacemaker artery bypass grafting or aortic valve re- syndrome placement. Hypotension with ventricular pac- The diagnosis is made by reproduction of ing occurred only in those patients with left symptoms during ventricular pacing and atrial cannon waves.'2 It has been suggested depends on the history and the search for that patients with left ventricular disease, hypotension, signs of congestive cardiac especially hypertrophy of any cause, are more Department of failure, and venous cannon waves associated sensitive to the correct timing of atrial systole Cardiology, with ventricular pacing. Usually the diagnosis and are, therefore more liable to be sympto- Westminster Hospital, can be made without recourse to with atrioventricular con- London clinically matic retrograde C M Travill special investigations. However, Doppler duction.7 R Sutton echocardiography can be useful in its A recent study of a large group of patients Correspondence to diagnosis: Doppler ultrasound measurement with intact ventriculoatrial conduction Dr R Sutton, Department of of cardiac output in nine patients with showed similar results, with peripheral resis- Cardiology, Westminster Hospital, Dean ventriculoatrial conduction or symptoms con- tance failing to rise in seven patients requiring Ryle Street, London SWIP sistent with pacemaker syndrome showed a upgrade to dual chamber mode because of 2AP. 30% when fully automatic of whereas it Accepted for publication improvement symptoms pacemaker syndrome 12 February 1992 (DDD) pacing rather than ventricular rose during ventricular pacing in the symptom 164 Travill, Sutton free group.'3 The difference between the re- identified during 800 head up tilt than with the sponse of the cardiac output between the two patient supine. In those patients in whom the groups was negligible and the authors argued interatrial conduction delay exceeded 150 ms that the behaviour of the blood pressure was (three of 16 patients) a programmed atrioven- crucial. They advised that a cuff recording of tricular delay of 150 ms resulted in left atrial blood pressure should be made at the onset of activation after the ventricular spike, yielding ventricular pacing during pacemaker implant left atrial contraction during left ventricular and that a fall in systolic pressure of greater systole. The temporal difference between sens- than 25 mm Hg should be regarded as predic- ing of spontaneous right atrial activation and tive for the possible development of right atrial pacing is such that at a given pacemaker syndrome and they recommended atrioventricular interval, the sequence between dual chamber pacing.'3 We suggest that if atrial and ventricular contraction is longer in clinicians allow their choice of pacing mode to the atrial synchronous ventricular inhibited be guided by haemodynamic variables during (VDD) than in the atrioventricular sequential temporary ventricular pacing before implant, mode (DVI). Some pacemakers now take this they must assess the patient in the upright delay into account as a programmable feature. posture (600 head up tilt with appropriate The DDI mode has been recommended for safety restraint) before considering it appro- patients with carotid sinus syndrome, malig- priate to implant a VVI unit.'4 nant vasovagal syndrome, and sick sinus syn- drome who do not require atrial tracking (ven- tricular pacing as a result of atrial sensing) and Pacemaker syndrome in different pacing who often have ventriculoatrial conduction.2224 modes In this mode it is impossible for pacemaker In a small group of patients, paced in VVI mediated tachycardia to occur but pacemaker mode and presenting with symptoms of syndrome can occur with non-conducted pacemaker syndrome, changing the mode from premature atrial beats or with retrograde con- VVI to atrial inhibited (AAI) relieved symp- duction from premature ventricular beats.25 toms and was associated with a fall in both the Either of these events will inhibit atrial output mean right atrial and pulmonary capillary if they occur outside the post ventricular atrial wedge pressures as well as a rise in cardiac refractory period. They are then followed by a output."' In view of the high prevalence of ventricular stimulus at the programmed ven- ventriculoatrial conduction in patients with tricular rate which may be conducted sinus node disease, AAI pacing with the pos- retrogradely if the atrium has had sufficient sible addition of a sensor-driven facility for time to recover. Ventricular pacing will only those patients who do not show an increase in then be inhibited if the sinus rate recovers and sinus rate on exertion (chronotropic incom- is normally conducted. In patients with petence) is advocated by some for all patients in documented ventriculoatrial conduction the whom atrioventricular conduction is sound.'6 atrial refractory period in DDI should be Two large randomised controlled trials to programmed long enough to include the compare ventricular and dual chamber pacing retrograde conduction interval. Thus sensing in patients with sinus rhythm identified of a retrograde P wave and atrial output inhibi- improved well-being even in "asymptomatic" tion is avoided. It is suggested that the atrial patients when the dual chamber mode was refractory period be set to 325 ms at program- used.'718 However, ventricular pacing is the med rates of 55-85 pulses per minute (ppm), preferred mode in patients with symptomatic shorter for faster rates, and longer for slower bradycardia in the presence ofatrial fibrillation. rates. Although the early dual chamber pacing mode (atrial synchronous ventricular inhibited (VDD)) was an improvement over the atrio- Pacemaker syndrome in rate responsive ventricular sequential (DVI) mode, it was still pacing associated with pacemaker syndrome in those Sensor driven ventricular pacing (VVIR) patients whose sinus rate dropped below the would be expected to result in pacemaker programmed lower rate at which point the syndrome at resting heart rates in the same way pacing mode effectively became VVI."9With the as non-sensor driven ventricular pacing. In advent of fully automatic dual chamber pacing patients with sinus node chronotropic incom- systems (DDD) it became apparent that petence, a group of patients who are often pacemaker syndrome can still occur in properly considered suitable for the VVIR mode, ven- functioning dual chamber pacing systems in tricular pacing is often programmed so as to be the DDD
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