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Ventricular Fibrillation

 

Ventricular fibrillation (see figure 9B) is a terminal arrhythmia, uniformly requiring rapid initiation of emergency measures.
ventricular flutter

Ventricular flutter(see figure 9B) with loss of consciousness and rapid unstable VT may be clinically equivalent to VF and is treated identically when accompanied by the clinical picture of cardiac arrest. Ventricular fibrillation occurs commonly in the setting of acute ischemic events (see figure 70) or unpredictabley in advanced chronic ischemic heart disease. Moreover, it is the mode of death in 25 to 50 percent of fatalities among patients with cardiomyopathies (see figures 39A, 39B, 39C, 39D, 39E, 39F, 39G, 43B, 73, 74, 75, 76, 77A, 77B) . It may also develop during hypoxia, atrial fibrillation with rapid ventricular responses in WPW syndrome (see figure 3A, 3B), R-on-T pacing or cardioversion, or improper grounding of electrical devices or as proarrhythmic (see figure 13) effects of antiarrhythmic drugs. A particularly high risk setting for VF is acute myocardial infarction with right or left bundle branch block.

Ventricular fibrillation may occur de novo, but among patients with out-of –hospital cardiac arrest, VT commonly precedes the onset of VF. The right coronary artery is a common site of isolated coronary-artery spasm leading to cardiac arrest due to ventricular fibrillation (figure 9d).

The electrocardiographic pattern of VF is that of gross disorganization without identifiable repetitive waveforms or intervals (see figure 9B). At the onset, VF may be “coarse” in pattern, but over time, it loses its amplitude and becomes “fine” (<0.2 mV) (see figure 9B, parts D and E). Successful defibrillation and survival rates are decreased in patients with the fine pattern of VF (see figure 9B, part E). In ventricular flutter, a sine wave configuration is present, having a cycle length in the range of 200 to 240 ms (see figure 9B, part C). Rapid polymorphic VTs may be difficult to distinguish from ventricular fibrillation or flutter.

MALFUNCTION OF INTERNAL CARDIOVERTOR DEFIBRILLATORS

Here are devices currently available, incorporating both the pacemaker(VVI pacing) as well as the implantable cardioverter defibrillator to treat those patients with a history of chronic sinus bradycardia,A-V conduction system disease,or severe postshock bradyarrhythmias.

The malfunctioning ICD may be caused by lead fracture or migration,premature battery depletion,and generator malfunction.

All units usually are modified temporarily by placing a magnet over the pulse generator.Tachycardia detection and therapy are temporarily suspended by magnet placement.

Appropriate ,undesirable discharges may sometimes be difficult to distinguish from appropriate,desirable shocks(atrial fibrillation with a rapid ventricular rate exceeding the programmed rate cutoff may trigger an appropriate (although undesirable)discharge and may account for repetitive discharges experienced in close succession.

Devices with second look features that require arrhythmia reconfirmation immediately prior to shock delivery have largely eliminated the problem of undesirable discharges due nonsustained ventricular tachycardia.Sensing lead malfunction( oversensing) resulting from lead fractures may be the cause of inappropriate discharges triggered by sensing artifact.

Lead disruption may be diagnosed on the basis of over pentrated x'ray findings,by analyzing audible tones emitted in synchrony with the sensed events, or examing the telemetered records of stored or real-time intracardiac electrograms.Discharge during sinus rhythm is strong evident for sensing malfunction.Analysis of electrograms or rate intervals recorded by the newer devices during sinus rhythm and at time of therapy has allowed for better correlation between arrhythmic events and device responses and has greatly facilitated the diagnosis of lead or pulse generator malfunction.

In suspected pacemaker malfunction in cases with the pacer as well as the ICD,long strips of several ECG leads should be taken.The ECG must be recorded in the base (synchronous) and magnet(asynchronous) modes.Because of competitive rhythms when using a magnet, most manufacturers use a magnet rate between 90 and 100 pulses per minute to override spontaneous rhythms.With single chamber pacing systems the ECG in the synchronous or asynchronous modes should confirm normal pacing,The stimulus artifact of the bipolar lead system is often impossible to see on the surface ECG.In these cases.polarity programming with verification of pacing in the unipolar mode is very useful.For confirmatiom of pacemaker sensing in patients with consistent pacing,the patient can be exercised to accelerate the intrinsic rate or the pacing rate reduced by programming until the intrinsic rate emerges.

The runaway pulse generator of the pacemaker is a rare problem(referring to an increase in pacing rate beyond 150 pulses/minute with sufficient output to capture the heart).