Nemer Samniah

Improving Standard Cardiopulmonary Resuscitation with an Inspiratory Impedance Threshold Valve in a Porcine Model of Cardiac Arrest

To improve the efficiency of standard cardiopulmonary resuscitation (CPR), we evaluated the potential value of impeding respiratory gas exchange selectively during the decompression phase of standard CPR in a porcine model of ventricular fibrillation. After 6 min of untreated cardiac arrest, anesthetized farm pigs weighing 30 kg were randomized to be treated with either standard CPR with a sham valve (n = 11) or standard CPR plus a functional inspiratory impedance threshold valve (ITV™) (n = 11). Coronary perfusion pressure (CPP) (diastolic aortic minus right atrial pressure) was the primary endpoint. Vital organ blood flow was assessed with radiolabeled microspheres after 6 min of CPR, and defibrillation was attempted 11 min after starting CPR. After 2 min of CPR, mean ± sem CPP was 14 ± 2 mm Hg with the sham valve versus 20 ± 2 mm Hg in the ITV group (P < 0.006). Significantly higher CPPs were maintained throughout the study when the ITV was used. After 6 min of CPR, mean ± sem left ventricular and global cerebral blood flows were 0.10 ± 0.03 and 0.19 ± 0.03 mL · min−1 · g−1 in the Control group versus 0.19 ± 0.03 and 0.26 ± 0.03 mL · min−1 · g−1 in the ITV group, respectively (P < 0.05). Fifteen minutes after successful defibrillation, 2 of 11 animals were alive in the Control group versus 6 of 11 in the ITV group (not significant). In conclusion, use of an inspiratory impedance valve during standard CPR resulted in a marked increase in CPP and vital organ blood flow after 6 min of cardiac arrest.

Pharmacotherapy of Neurally Mediated Syncope

A wide variety of pharmacological agents are currently used for prevention of recurrent neurally mediated syncope, especially the vasovagal faint. None, however, have unequivocally proven long-term effectiveness based on adequate randomized clinical trials. At the present time, beta-adrenergic receptor blockade, along with agents that increase central volume (eg, fludrocortisone, electrolyte-containing beverages), appear to be favored treatment options. The antiarrhythmic agent disopyramide and various serotonin reuptake blockers have also been reported to be beneficial. Finally, vasoconstrictor agents such as midodrine offer promise and remain the subject of clinical study. Ultimately, though, detailed study of the pathophysiology of these syncopal disorders and more aggressive pursuit of carefully designed placebo-controlled treatment studies are essential if pharmacological prevention of recurrent neurally mediated syncope is to be placed on a firm foundation.

Feasibility and effects of transcutaneous phrenic nerve stimulation combined with an inspiratory impedance threshold in a pig model of hemorrhagic shock

ObjectiveIntrathoracic pressure changes are of particular importance under hypovolemic conditions, especially when central venous blood pressure is critically low. Accordingly, the purpose of this study was to assess the feasibility of transcutaneous phrenic nerve stimulation, used in conjunction with an inspiratory impedance threshold, on hemodynamic variables during hemorrhagic shock. DesignProspective, randomized laboratory investigation using a porcine model for measurement of hemodynamic variables, left and right ventricular diameter, and transmitral, transpulmonary, and transaortic blood flow employing transesophageal echo-Doppler technique. SettingUniversity hospital laboratory. SubjectsThirteen female pigs weighing 28–36 kg. InterventionsThe anesthetized pigs were subjected to profound hemorrhagic shock by withdrawal of 55% of estimated blood volume over 20 mins. After a 10-min recovery period, the diaphragm was stimulated with a prototype transcutaneous phrenic nerve stimulator at a rate of ten per minute while the airway was intermittently occluded with an inspiratory threshold valve between positive pressure ventilations. Hemodynamic variables were monitored for 30 mins. Measurements and Main ResultsPhrenic nerve stimulation in combination with the inspiratory threshold valve significantly (p < .001) improved right and left ventricular diameter compared with hypovolemic shock values by 34 ± 2.5% and 20 ± 2.5%, respectively. Moreover, phrenic nerve stimulation together with the inspiratory threshold valve also increased transaortic, transpulmonary, and transmitral valve blood flow by 48 ± 6.6%, 67 ± 13.3, and 43 ± 8.2%, respectively (p < .001 for comparisons within group). Mean ± sem coronary perfusion and systolic aortic blood pressures were also significantly (p < .001) higher compared with values before stimulation (30 ± 2 vs. 20 ± 2 mm Hg, and 37 ± 2 vs. 32 ± 3 mm Hg, respectively). ConclusionsThis feasibility study suggests that phrenic nerve stimulation with the inspiratory threshold valve may improve cardiac preload and, subsequently, key hemodynamic variables in porcine model of severe hemorrhagic shock.

Atrioventricular dissociation exacerbating posturally-induced syncope.

We report a case of an 85-year-old patient with posturally-induced syncope in whom symptoms were reproduced during tilt table testing in conjunction with development of an accelerated junctional rhythm with isorhythmic atrio-ventricular (AV) dissociation. That loss of AV synchrony was crucial to development of hypotension and syncope was demonstrated during electrophysiologic testing in which both an accelerated junctional rhythm and an inducible atypical AV nodal re-entrant tachycardia (AVNRT) were induced. The accelerated junctional rhythm was accompanied by moderate hypotension with the patient in the supine posture, whereas blood pressure was well maintained during atypical AVNRT despite a much faster ventricular rate. Thus, symptomatic hypotension due to AV dissociation, presumably the result of transient autonomic disturbance, may be another manifestation of neurally-mediated syncope.

Unusual Cause of Supraventricular Tachycardia After Acute Myocardial Infarction

A 43-year-old white female with a history of diabetes mellitus, hypertension, heavy cigarette smoking, and hypercholesterolemia suffered an inferoposterior wall myocardial infarction (MI) and was treated with primary angioplasty of the right coronary artery. A week later she developed, for the first time, recurrent palpitations associated with chest pain and dyspnea. These episodes occurred several times every day, were of abrupt onset and offset, and lasted up to 2 hours. Physical examination was unremarkable. The echocardiogram demonstrated diminished left ventricular ejection fraction (0.40) with normal right ventricular function. Repeat coronary angiogram confirmed patency of the right coronary artery. Holter monitoring revealed frequent symptomatic episodes of supraventricular tachycardia (SVT) with a rate of 130 beats/min. Most episodes of SVT were closely associated with a preceding premature ventricular contraction (PVC) (Fig. 1). The tachycardia was unaffected by carotid sinus massage, valsalva maneuver, or treatment with atenolol and/or verapamil. The working diagnosis at this time was primary atrial tachycardia complicating myocardial infarction. Electrophysiology testing was performed using light sedation with intravenous fentanyl and medazolam to ascertain the nature of the arrhythmia. Five electrode catheters were introduced percutaneously via the femoral veins, and recordings were obtained from sites along the crista terminalis and the intraatrial septum (A), the His bundle (H), coronary sinus (C), and right ventricular apex. A narrow QRS complex tachycardia (cycle length of 495 ms) was readily induced by spontaneous PVCs. Following positioning of electrode catheters the tachycardia became incessant. Attempts to terminate the tachycardia were accompanied by immediate reinitiation by a PVC. At this point, an explanation for an apparently new onset paroxysmal SVT was unclear.

Midodrine for Treatment of Vasovagal Syncope

Most vasovagal fainters who seek medical attention require no more than the reassurance that their physician understands the basis of their symptoms, and education regarding both the nature of the problem and techniques which may avert recurrences. However, when spells are frequent, or are associated with physical injury, or threaten to compromise occupational status, prophylactic treatment measures become a consideration. Unfortunately, the optimum treatment approach remains uncertain.

Atrial fibrillation: defining potential curative ablation targets.

The concept that atrial fibrillation (or at least certain forms of the arrhythmia) may be amenable to reversal or amelioration by transcatheter ablation techniques has become increasingly accepted in recent years. As yet, however, the techniques being studied for ablation of atrial fibrillation address neither known critical anatomic elements nor well defined electrophysiologic markers. The approaches, although essentially empirical, are conceptually based on the ‘multiple wavelet’ or ‘focal origin’ hypotheses. To date, addressing ‘focal origin’ atrial fibrillation by transcatheter ablation has been the more encouraging. However, as technology evolves, both in terms of catheter design and possibly endocardial mapping techniques, approaches to wavelet or rotor mechanisms may become similarly effective. This communication examines concepts regarding the manner in which atrial fibrillation is initiated and maintained. The goals are to better understand the encouraging success of empirical ablation methods, and possibly derive insights which may help refine ablation targeting in the future.