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(TM)) (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.

Circulating adrenaline concentrations in posturally induced vasovagal faints rise more rapidly in vasovagal fainters than in comparably posturally stressed non-fainters, and were significantly greater in fainters prior to either detectable haemodynamic compromise or diminution of circulating Norepi levels. These findings suggest that a premonitory rise in adrenaline concentrations occurs in vasovagal fainters unassociated with an evolving circulatory crisis.

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Abstract-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, ␤-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. (Circulation. 1999;100:1242-1248.)Key Words: syncope Ⅲ nervous system Ⅲ pharmacology Ⅲ Cardiovascular Drugs N eurally mediated (neurocardiogenic) syncope comprises a number of clinical conditions in which symptomatic systemic hypotension occurs as a result of a transient disturbance of neural reflex cardiovascular control (Table 1). [1][2][3] The vasovagal faint, carotid sinus syndrome, and postmicturition syncope are the most common forms of the neurally mediated faint. Others, including cough syncope and postexertional syncope, are less frequently encountered.This communication focuses on the pharmacological options that have been proposed for preventing neurally mediated faints, and especially the vasovagal faint, because it has been the most thoroughly studied. The objective is to provide an overview of the pharmacology and pertinent proposed modes of action of those agents that may be of benefit. Drug Therapy of Neurally Mediated Syncope: Basic PrinciplesMost individuals who experience a neurally mediated faint (particularly vasovagal fainters) require no additional therapy beyond education (ie, recognition of premonitory symptoms, avoidance of triggering events, and awareness of useful evasive actions) and reassurance regarding the non-lifethreatening nature of the condition. On occasion, stress and anxiety management may be warranted. Various more aggressive nonpharmacological (eg, support hose, extended exposure to upright posture, pacemakers) and pharmacological treatment options are usually reserved for those relatively few individuals who experience frequent syncope and/or when symptoms cause excessive lifestyle difficulties, threaten employment, or result in unacceptable risk of physical injury to the patient or others.Currently, drugs are used for both diagnostic and therapeutic purposes in the patient with neurally mediated syncope. [1][2][3] In terms of diagnostic applications, agents such as isoproterenol, edrophonium, nitroglycerin, and adenosine have been reported to be helpful during tilt-table testing (ie, so-called pharmacolog...

Compared with individuals who do not manifest VVS during HUT, VVS prone individuals appear to demonstrate functional diminution of baroreceptor responsiveness. This altered response may undermine the normal expected compensatory response to evolving systemic hypotension. The basis for this transient disturbance in baroreceptor responsiveness is currently unknown.