Cardiophile MD Archive » Electrophysiology

Purely subcutaneous implantable defibrillator (ICD)

Johnson Francis — Thu, 13 May 2010 14:15:28 +0000

Conventional implantable defibrillators have a subcutaneous device and lead which is placed within the heart, through the venous system. Bardy GH et al has evaluated an entirely subcutaneous ICD and reported the preliminary results in NEJM. Initially they compared the thresholds for various configurations in 78 patients and later the best configuration in 49 patients to determine the defibrillation threshold with conventional ICD implants. Then they went on to a pilot study of long term use in 6 patients and finally a trial involving 55 patients. The best configuration was found to be one with a parasternal electrode and an ICD can location in the left lateral thoracic region. It was effective in terminating ventricular fibrillation with a higher energy requirement compared to transvenous lead systems (36.6±19.8 J vs. 11.1±8.5 J).Ventricular fibrillation was successfully detected in all the episodes induced. Two cases of pocket infection and four lead revisions were required in the trial. During the follow up period of 10 months, 12 episodes of spontaneous sustained ventricular tachyarrhythmias were detected and treated. Larger randomised studies of longer duration are needed to see if this entirely subcutaneous ICD will become a viable option for patients with life threatening arrhythmias. If it shown to be useful, it will avoid a lot of problems due to trans venous leads which could occur during the implantation as well as on long term follow up. Though transient back up pacing is available in an entirely subcutaneous system, long term antibradycardia pacing is not feasible in this system. Similarly anti-tachycardia pacing (for slower ventricular tachycardias) is also not available.

Ideal site for right ventricular pacing

Johnson Francis — Fri, 07 May 2010 05:00:16 +0000

Right ventricular apical pacing has been found to have certain disadvantages like progressive left ventricular dysfunction leading to heart failure and associated morbidity and mortality as well as a propensity for atrial fibrillation. Hence attempts were made to simulate the natural sequence of ventricular activation by alternate site ventricular pacing. Right ventricular sites which were evaluated include outflow tract, and septum. The presumption was that pacing the septal aspect of the right ventricle would initiate as normal a sequence of ventricular contractions as possible. But the studies gave conflicting results, probably because most of the pacing which was done in the right ventricular outflow tract was not actually on the septal aspect, but the free wall aspect. Right ventricular free wall is one of the last regions to be activated in the normal activation sequence. So if a right ventricular outflow tract pacing causes early activation of the right ventricular free wall, it would not be expected to give the results simulating a normal activation sequence.

The disadvantage in earlier studies was also due to the difficulty in actually pacing the septal aspect of the right ventricular outflow tract. Now special types of stylets are available to direct the lead to the septal aspect of the right ventricular outflow tract which is posteriorly situated. But we will have to wait for the results of the randomized trials which are currently going on to finally conclude whether high septal pacing is indeed superior to right ventricular apical pacing in terms of long term preservation of left ventricular function and preventing heart failure.

EP tracing of ventricular premature complex

Johnson Francis — Mon, 22 Mar 2010 06:31:18 +0000

EP tracing of ventricular premature complex

The first two complexes are sinus beats. The A in these beats seen the coronary sinus electrode channels (CS910 to CS12) preced the V recorded in the HISP (His bundle proximal) channel. The QRS complexes of these beats are narrow as seen in the surface ECG recordings at the top (I, AVF, V1, V6). The third complex (VPC) is a ventricular premature complex. It is not preceded by A in the coronary sinus channels. Instead there is atrial activity after the V, indicating retrograde activation sequence (A’).

EP tracing of ventricular premature complex

EP tracing during ventricular pacing

Johnson Francis — Mon, 22 Mar 2010 05:19:30 +0000

EP tracing during ventricular pacing

(Click on the image for a larger view)

EP tracing during ventricular pacing showing atrial ventricular activation. The CS 910 electrode is in the proximal coronary sinus while the CS12 electrode is in the distal coronary sinus. ‘A’ represents atrial activation and ‘V’ represents ventricular activation. The pacing stimulus is delivered from the HISD electrode as evidenced by the polarization artefact seen in this lead. But the electrode does not seen to be in the region of the His bundle as neither the His bundle activity nor the atrial activity is seen as is usual. It seems that the lead has been pushed into the ventricle during the EP study for ventricular pacing. This is sometimes done to minimise the total number of electrodes being used during an EP study. The RFD and RFP electrodes do not seem to be connected to the recorder as these electrodes are not recording any electrical activity of the heart. The initial QRS is narrow while the subsequent two QRS complexes preceded by pacing spikes are wide. The first one is a sinus beat conducted to the ventricles while the latter two are paced beats. The atrial activity picked up by the coronary sinus leads show almost the same sequence of activation as the sinus beat, though it is retrogade activation. But the retrograde interval is longer for the second paced beat compared to the first paced beat.

Hypersensitive carotid sinus syndrome

Johnson Francis — Sat, 20 Mar 2010 13:27:03 +0000

Hypersensitive carotid sinus syndrome is an exaggerated response to stimulation of the barorecptors in the carotid sinus and leads to bradycardia / hypotension and syncope. Three types of responses have been described: cardioinhibitory, vasodepressor and mixed. In cardioinhibitory type there is only bradycardia, and there is no fall in blood pressure. The cardioinhbitory type is the commonest variety contributing to about three fourth of the cases. In vasodepressor type there is only hypotension, but no bradycardia. It is the least common type. In the mixed variety there is both bradycardia and hypotension. Mixed type occurs in about one fifth to one fourth of cases. Though baroreceptor function decreases with age, the Hypersensitive carotid sinus syndrome is more common in older males. In some even trivial stimuli like a tight collar or shaving the neck may be enough to cause a sycope.

Hypersensitive carotid sinus syndrome can be spontaneous or induced. The former occurs spontaneously while the latter is brought on by carotid sinus massage during the evaluation of a syncope. Spontaneous variety may present with fractures or other injuries, especially in the elderly. Vasovagal syncope and postural hypotension have to be excluded in this setting.

While trying to reproduce carotid sinus syncope, extreme care is needed, especially in the elderly. Careful assessment of carotids for bruit or obstruction on either side is needed to prevent the potential for dislodgement of atherosclerotic plaques and causing embolic stroke. ECG and blood pressure has to be monitored through out. Initial evaluation should be in the supine position and gentle. If negative in the supine position, carotid massage may have to be repeated in the standing position, to improve the sensitivity, if the clinical suspicion is high. But it will be ideal to conduct it with the patient strapped to a tilt table in order to prevent injuries due to a fall. The massage is done for five seconds on each side with a one minute interval. Recent stroke, transient ischemic attacks and myocardial infarction are reasons to avoid a carotid sinus massage.

Midodrine, fludrocortisone and volume supplementation are the methods tried in the treatment of vasodepressor variety of carotid sinus hypersensitivity. If the cardioinhibitory variety is symptomatic with recurrent syncope, permanent pacemaker implantation is a Class I indication as per American Heart Association guidelines.

Ashman phenomenon

Johnson Francis — Sat, 20 Mar 2010 00:50:15 +0000

Ashman phenomenon is a form of aberrancy which was described by Gouaux and Ashman in atrial fibrillation [Gouaux JL, Ashman R. Auricular fibrillation with aberration stimulating ventricular paroxysmal tachycardia. Am Heart J. 1947;34:366]. Ashman phenomenon is aberrancy due to the change in refractory period with varying cycle length. The refractory period increases with the preceding cycle length and vice versa. Hence if a short cycle follows a long cycle, aberrancy can result. The aberrancy is usually of the right bundle branch (RRBB) type because the refractory period of the right bundle is more than that of the left bundle branch. The aberrancy can be maintained in subsequent beats due to a concealed trans septal conduction which keeps the right bundle refractory. This rather fast sequence of wide QRS complexes in the setting of atrial fibrillation mimic a run of ventricular tachycardia. But the differentiating features are the initiating long short sequence and the irregularity in the RR intervals during the tachycardia.

Recognition of Ashman phenomenon in a strip with atrial fibrillation can be clinically important. If the person is on digoxin, occurrence of Ashman phenomenon does not call for dose reduction, but if it is ventricular ectopy, dose reduction is needed. Same applies in a more sinister way to a run of wide QRS complex tachycardia.

Fish C has proposed a few criteria for the diagnosis of Ashman phenomenon [Fisch C. Electrocardiography of arrhythmias: from deductive analysis to laboratory confirmation--twenty-five years of progress. J Am Coll Cardiol. 983;1:306-16]:

1. Long-short sequence terminating in the wide QRS. Occasionally a reverse sequence has also been reported. Though RBBB aberrancy is more common, LBBB aberrancy can also occur.

2. RBBB aberrancy has a normal initial QRS vector.

3. Varying coupling intervals of the aberrant QRS complexes

4. Full compensatory pause is not seen as the underlying rhythm is atrial fibrillation.

Richard Ashman was a physiologist at Louisiana State University School of Medicine in New Orleans [Kennedy LB, Leefe W, Leslie BR. The Ashman phenomenon. J La State Med Soc. 2004;156:159-62].

Pacemaker syndrome

Johnson Francis — Fri, 19 Mar 2010 15:06:26 +0000

Mitsui et al was the first to describe pacemaker syndrome in 1969 as a symptom complex associated with right ventricular pacing [Mitsui T, Hori M, Suma K, Wanibuchi Y, Saigusa M. The “pacemaking syndrome.” In: Jacobs JE, editor. Proceedings of the Eighth Annual International Conference on Medical and Biological Engineering. Chicago, Illinois: Association for the Advancement of Medical Instrumentation; 1969:29-33]. In general it is due to loss of AV synchrony and it is relieved by AV sequential pacing. But of late, the role of V-V synchrony (loss of) has also been highlighted so that efforts to minimise right ventricular pacing have been promoted.

Patients with pacemaker syndrome may present with exertional dyspnoea, hypotension, syncope or even syncope. Syncope occurs in the setting of a drop of systolic blood pressure more than 20 mm Hg at the onset of ventricular pacing. Easy fatigability, sensation of fullness and pulsations in the head and neck are also features of pacemaker syndrome. When an intact V-A conduction is present, the pacemaker syndrome may be more severe due to the reverse atrial kick associated with every cardiac cycle. Venous pressure elevation as a result of atrial contraction against a close A-V valve causes reflex peripheral vasodilation and hypotension by stimulating the vagal afferents.

The reported incidence of pacemaker syndrome varies widely. In those trials in which a dual chamber pacemaker was implanted and programmed to single chamber mode for the study purpose, the change over rates to dual chamber mode for suspected pacemaker syndrome was high. But in those trials in which a surgical revision was required for a mode change, the reported incidence was low. This may indicate a lower threshold for the diagnosis of pacemaker syndrome when surgical revision is not required.

Pulseless electrical activity (PEA)

Johnson Francis — Thu, 18 Mar 2010 15:58:24 +0000

Pulseless electrical activity (PEA) refers to any cardiac rhythm in which there is no palpable pulse, but the ECG shows cardiac activity. The earlier terminologies for PEA were electromechanical dissociation (EMD) and non-perfusing rhythm. It is due to the inability of the heart to generate sufficient force of contraction in response to depolarization. Severe hypoxia is probably the most common cause of PEA. The causes of PEA are remembered by the AHA (American Heart Association) mnemonic of several conditions beginning with H and T:

Hypovolemia
Hypoxia
Hydrogen ions (acidosis)
Hypothermia
Hyperkalemia or Hypokalemia
Hypoglycemia
Toxins
Tamponade, cardiac
Tension pneumothorax
Thrombosis (Myocardial infarction / Pulmonary embolism)
Trauma

Pulseless electrical activity is treated like a cardiac arrest with cardiopulmonary resuscitation (CPR) after a quick evaluation for the reversible causes. Bedside echocardiography is useful in confirming cardiac tamponade, which should prompt immediate pericardiocentesis. Echocardiography will also show features of right ventricular enlargement and pulmonary hypertension in pulmonary embolism. Mechanical complications of a myocardial infarction can also be sought on echocardiography.

An intercostal drain is inserted in case of tension pneumothorax. Intravenous access for correction of hypovolemia and administration of drugs is of top priority. Epinephrine, vasopressin and atropine are the important drugs which may be given. Intubation and ventilation with 100% oxygen is useful in correcting the hypoxia.

Public access AED success in Japan

Johnson Francis — Thu, 18 Mar 2010 12:58:07 +0000

AEDs are automatic external defibrillators which give instructions to the lay operators and can be used by the lay public for resuscitating a person in cardiac arrest. AEDs are kept in public places where large number of people arrive as in airports. Japan is a country with nation wide access to AEDs. A recent study published in the New England Journal of Medicine [Kitamura Tet al, NEJM 362:994-1004] evaluated the benefit of these devices in Japan. They included 312,319 adults who had an out of hospital cardiac arrest over a period of two years in this study. Of these, 12,631 had ventricular fibrillation and a witnessed cardiac arrest due to cardiac cause. Four hundred and sixty two of them received AED shocks administered by lay persons. While 14.4% of those with a witnessed cardiac arrest due to ventricular fibrillation was alive at one month with minimal neurological deficit, 31.6% of those who received AED shocks had a similar status. All those who received early defibrillation regardless of whether it was administered by a paramedic or a bystander, there was good neurologic outcome. The figures improved as the number of public access AEDs increased from 1 per square kilometer of inhabited area to 4 or more.

NCX inhibitors (Na+ / Ca2+ exchange) inhibitors to limit ischemic injury

Johnson Francis — Tue, 09 Mar 2010 07:06:47 +0000

Elevation of calcium levels in the cells is an important mechanism of ischemic cellular injury and death. Na⁺ / Ca²⁺ exchanger (NCX) has the main role in elevating calcium levels within the myocardial cells during ischemia and reperfusion. Hence NCX inhibitors have been considered to be potential novel agents for limiting hypoxic cell injury.

Three genes encoding for NCX in the human genome are NCX1, NCX2 and NCX3. NCX1 is present in heart, brain and kidney. NCX2 and NCX3 are seen in brain and skeletal muscle. It is interesting to note that while NCX1 knockout is embryonically lethal, NCX2 knockout increases hippocampal long term potentiation and improves performance on learning and memory tests.

Though homozygous NCX1 knockouts are embryonic lethal, heterozygote NCX1 knockouts are viable. These transgenic mice have reduced NCX protein levels and have lesser rise of calcium levels within the cells after hypoxia and have a reduced susceptibility to ischemic injury.