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Pacing

• unipolar commonly used for permanent pacing: metal case of pacemaker used as neutral lead. Oversensing of electromagnetic interference or skeletal muscle potentials may be a significant problem
• bipolar has two conducting wires surrounded by a layer of insulation. Current passes down one wire to an electrode (usually distal) and back up other wire. Method of choice for temporary pacing. If one limb fails the system can be converted into a unipolar system by connecting active pole (usually +ve) to functioning limb and other pole (usually -ve) to a skin ECG electrode

• most common site. Pacing wire passed into RA, RV or rarely into coronary sinus (to pace LA)

• mainly used following cardiac surgery. Leads attached directly to epicardial surface of atrium and/or ventricle

• use of larger electrodes Þ improved patient tolerance
• can sense and deliver adequate adjustable current outputs (50-150 mA) and stimuli of long duration (10-40 msec)
• some patients still experience significant pain
• temporary measure
• has rendered prophylactic temporary transvenous pacing redundant in most situations

• dangerous and unreliable

• safe and effective in refractory atrial flutter. Probably be replaced by transcutaneous pacing in most situations

• in practice three-position code is adequate to describe emergency temporary pacing and most forms of permanent pacing in ICU

• indicated for sinus bradycardia provided AV conduction is intact. Has the advantage of maintaining AV synchrony

• most commonly used mode
• mode of choice in life threatening bradyarrhythmias

• AV sequential pacing
• if AV conduction is successful ventricular output of pacemaker is inhibited. Otherwise a ventricle is paced after a delay
• AV synchrony maintained as long as pacemaker discharge rate is greater than spontaneous atrial rate (no atrial sensing)
• asynchronous atrial pacing can precipitate AF
• self inhibition ("cross-talk") can occur: inappropriate detection of atrial pacing stimulus by ventricular channel. If there is no escape rhythm this leads to asystole
• indicated for impaired AV conduction with atrial bradycardia. No value in the presence of atrial tachycardia

• atrial synchronous ventricular inhibited
• sensed P wave triggers ventricular pacing
• indicated for high degree AV block with normal sinus rhythm
• re-entry pacemaker mediated tachycardias possible. Commonly initiated by a ventricular premature beat which is conducted retrogradely to the atria. Here it is sensed by the atrial channel and ventricle is paced. This impulse in turn is conducted to the atria. Conversion to asynchronous (non-sensing) mode or increasing the pacemaker atrial refractory period will prevent this problem

• P wave inhibits atrial output. If it is conducted normally then ventricular output is also inhibited. If not then ventricle is paced after a delay
• If there is no P wave atrium is paced with ventricular pacing occurring after a delay if the atrial pacing impulse is not conducted to the ventricle
• upper rate limit needs to be set to prevent the pacemaker from following excessive atrial activity with paced ventricular responses
• self inhibition can be prevented by introducing a ventricular blank (refractory) period coinciding with atrial pacing stimulus
• re-entry pacemaker mediated tachycardia possible (see above)

DDD pacing. ECG demonstrates sensed p waves with ventricular pacing , atrial pacing spikes with normal conduction, atrial pacing spikes with failure of conduction and subsequent ventricular pacing spikes

• recently introduced and is available in some external pacemakers
• useful in patients with SA node dysfunction and episodes of atrial tachyarrhythmias. During atrial tachyarrhythmias pacemaker paces ventricle at back-up rate and will not track tachyarrhythmia
• re-entry pacemaker mediated tachycardia not possible

• designed so that pacemaker can mimic response of normal heart rate to increased metabolic need
• most commonly used systems incorporate sensors of respiratory rate (changes in thoracic impedance) or movement and therefore in many cases will not increase rate appropriately in response to critical illness

• during single chamber ventricular pacing the atria and ventricles contract asynchronously. Sometimes this leads to significant regurgitation of blood into pulmonary and systemic circulations with serious haemodynamic compromise which may lead to syncope
• can be eliminated by atrial or dual chamber pacing
• dual chamber pacemakers require the AV interval to be set as close as possible to normal PR interval (140-200 msec). Traditionally it is arbitrarily set at 150-200 msec. If interatrial (ie RA to LA) conduction time is significantly prolonged the LV may contract before or at the same time as the LA. As a result LA contracts against a closed mitral valve with resulting fall in stroke volume and hence cardiac output: DDD pacemaker syndrome. If there is evidence of inadequate cardiac output or impaired oxygen delivery the AV interval may need to be increased appropriately (ideally titrated against cardiac output or echo findings).

• ideally ventricular threshold should be £ 1 V and atrial £ 1.5 V
• set pacemaker output at 2-3 times threshold to allow reasonable safety margin
• after acute MI the amplitude should not be set higher than necessary as inadvertent pacing during the vulnerable period of the cardiac cycle may result in VT or VF

• set pacing amplitude to zero
• set pacing rate lower than spontaneous rate of tested cardiac chamber
• decrease sensitivity until there is competition between paced and spontaneous cardiac rhythms
• set sensitivity at twice threshold value (ie at half the voltage)
• do not attempt this method in pacemaker-dependent patients
• assessment of sensing particularly important in inf MI with RV involvement: intracardiac ventricular signal may be very small and not sensed. Resultant competition between pacemaker and spontaneous cardiac rhythm may initiate VT or VF

• those associated with CVP line insertion
• RV perforation. Rarely results in cardiac tamponade
• undersensing with pacemaker induced arrhythmias

• oversensing with pacemaker inhibition and loss of pacing stimuli

• failure to capture. Usually due to device defects, unstable lead position, increasing pacing threshold and RV perforation
• diaphragmatic pacing. May be associated with RV perforation
• thrombus formation. Uncommon
• Complication rate should be very low

• If life threatening situation develops as a result of failure to pace:
• increase output to maximum setting (usually 20 mA or 10 V)
• select VOO (ie fixed rate ventricular pacing) mode to prevent oversensing
• check all leads and connections (faulty leads and connections are most common causes of pacemaker failure
• consider replacing pacemaker or batteries
• transcutaneous pacing until new system can be placed
• CPR and positive chronotropes (eg atropine, adrenaline) may be necessary

• failure of drug therapy
• recurrent arrhythmias
• contraindication for DC cardioversion (eg digoxin toxicity)
• aid to arrhythmia diagnosis (eg to distinguish wide complex SVT from VT)

• AVNRT
• AVRT
• atrial flutter
• VT

Can be programmed to function in a sequential manner so that overdrive pacing is attempted first when VT is sensed, followed if necessary by low and then high energy DC shock. Systems with transvenous leads are now available. Mortality is reduced but remains high.

©Charles Gomersall, May, 2013 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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