When AF is associated with WPW, which ONE of the following statements is TRUE?
Answer: D In AF, the conducted QRS complexes are usually narrow except in patients where AF is associated with a bundle branch block or an accessory pathway. In WPW, when the accessory pathway exhibits a very short antegrade refractory period, very rapid conduction from atria to ventricles may occur. AF in this situation can be a dangerous arrhythmia. Conduction across the accessory pathway during AF in patients with WPW can result in very rapid ventricular rates. In this broad QRS complex (>0.12 second) AF, the heart rate can be higher than 250/min. This rapid ventricular response can degenerate into ventricular fibrillation (VF) and lead to potential death.
In AF not related to preexcitation syndromes, the relatively long refractory period in the AV node protects the ventricle from achieving very high rates, therefore preventing AF degenerating into VF. Calcium channel blockers, beta-blockers and digoxin prolong the refractory period in AV node and this slows down AV nodal conduction. The resultant increase in the impulse transmission through the accessory pathway causes a rapid ventricular rate. Although calcium channel blockers, beta-blockers and digoxin are beneficial in the treatment of non-WPW AF, they should not be used in WPW AF because of the risk of precipitating VF.
Treating a stable patient with broad-complex AF known or suspected to be caused by WPW should be aimed at prolonging the refractory period of the accessory pathway for antegrade conduction and this will allow impulses to traverse through the AV node, slowing down the ventricular rate. Amiodarone and procainamide appear to be the drugs of choice. An unstable patient with very rapid ventricular rates should be cardioverted.
References:
Regarding recognition of atrial flutter on a 12-lead ECG, which ONE of the following statements is TRUE?
Answer: A: Identification of atrial flutter on a 12-lead ECG can be challenging. In atrial flutter, the atrial complexes (flutter waves) are precisely regular. There should not be any variability. The rate of the atrial complexes are between 215 and 350/min and in adults it will not exceed >350/min. There is absolutely no flat or isoelectric segment between atrial complexes (flutter waves) and therefore they have a saw-tooth appearance. Usually these waves are visible in one lead system only – mainly in limb leads but can appear in a single other lead. There is a unique appearance at the junction between a flutter wave (atrial complex) and the QRS complex. Here the two waves always intersect above the baseline. Flutter waves disappear into the QRS complex and reappear on the other side of the complex, maintaining the precise regularity.
Reference:
Regarding artificial pacemaker code, which ONE of the following is INCORRECT?
Answer: C: ‘T’ stands for triggered, and indicates that pacing is triggered in response to sensed cardiac activity. The first letter refers to the chamber paced, the second letter refers to the chamber sensed, the third letter to the response to sensing, the fourth letter to programmability and the fifth letter, if present, to the antiarrhythmic function (pacing, shock or dual).
‘R’ in the fourth position refers to the ability of the pacemaker to modulate its response to sensing depending on rate.
Which ONE of the following statements is FALSE regarding failure of electrical and mechanical capture in a patient with a pacemaker?
Answer: D: In a patient with a pacemaker, failure to pace may be due to a lack of pacemaker output or failure to capture.
There are a few reasons that can contribute to failure to capture. If the energy in the pacemaker is insufficient to generate an adequate impulse to successfully depolarize the myocardium this may lead to failure to capture myocardium electrically and mechanically. This can happen in pacemaker battery failure. A local inflammatory reaction in the initial few weeks following the insertion of pacemaker, can cause a local fibrosis in the myocardium to occur. This can increase the resistance at the electrode– myocardial interface, leading to failure to capture. Lead problems such as lead fracture or dislodgement, cardiac perforation and faulty connections of leads can cause failure to capture. High levels of antiarrhythmic drugs can cause failure to capture. Flecainide is known to cause failure to capture at therapeutic levels.
As expected, a prolonged refractory period of the myocardium causes failure to capture. Electrolyte abnormalities may be a cause for a prolonged refractory period of myocardium.
Regarding artificial pacemakers, when the pacemaker fails to provide output, which ONE of the following statements is FALSE?
Answer: C: Oversensing, therefore inappropriate inhibition of the pacemaker, may cause failure of pacemaker output. Oversensing of P and T waves and skeletal muscle activity by the pacemaker can occur, causing failure of output. The depolarizing muscle relaxant suxamethonium causes muscular fasciculation during rapid sequence induction, hence it may cause pacemaker failure during this time.
When pacemaker output fails, a pacemaker-dependent patient should exhibit signs of hypoperfusion. There will be no pacemaker spikes visible in the ECG and on the monitor. Unipolar electrodes are more likely to oversense normal electrical and muscle activity than modern bipolar electrodes.
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