Intravenous norepinephrine and oral ephedrine blunted the carotid sinus massage-induced drop in systolic pressure (-19±12 and -21±11 mm Hg) compared to pacing alone (-48±19 mm Hg; p<0.01).
Do atrioventricular sequential pacing or pharmacologic interventions prevent carotid sinus massage-induced vasodepressor responses in patients with carotid sinus hypersensitivity?
Alpha-adrenergic agonists like ephedrine, but not AV sequential pacing or muscarinic/beta-blockade, attenuate the vasodepressor response in carotid sinus hypersensitivity.
p-value: p=<.01
The basis of the vasodepressor response in patients with carotid sinus hypersensitivity (CSH) is unknown, and prevention of recurrent vasodepressor-induced hypotension in these patients has not been possible. In this study we assessed the effectiveness of atrioventricular sequential pacing and pharmacologic interventions in the prevention of carotid sinus massage (CSM)-induced vasodepressor responses in eight patients with CSH. Maintenance of constant heart rate (80 beats/min) and atrioventricular synchrony (atrioventricular interval 150 msec) with sequential pacing did not significantly alter mean CSM-induced fall in systolic pressure (CSM control, -60 +/- 12 mm Hg vs CSM with atrioventricular sequential pacing, -48 +/- 19 mm Hg). Similarly, neither pharmacologic muscarinic blockade nor combined muscarinic and beta-adrenergic blockade significantly attenuated CSM-induced fall in systolic pressure (CSM with atropine, -43 +/- 16 mm Hg; CSM with atropine plus propranolol, -47 +/- 18 mm Hg; both p = NS vs atrioventricular sequential pacing alone). On the other hand, intravenous norepinephrine and oral ephedrine blunted the CSM-induced drop in systolic pressure (CSM with norepinephrine, -19 +/- 12 mm Hg; CSM with ephedrine, -21 +/- 11 mm Hg; both p less than .01 vs atrioventricular sequential pacing alone). Thus, vasodepressor responses were not prevented by control of heart rate, maintenance of atrioventricular synchrony, pharmacologic muscarinic blockade, or combined muscarinic and beta-adrenergic blockade, but were attenuated by drugs believed to be predominantly alpha-adrenergic agonists. Consequently, atrioventricular sequential pacing alone may be inadequate to prevent hypotension in patients with pronounced vasodepressor responses, whereas administration of vasoconstrictors such as ephedrine may diminish symptoms.
Almquist et al. (Wed,) conducted a other in Carotid sinus hypersensitivity (n=8). Atrioventricular sequential pacing and pharmacologic interventions (atropine, propranolol, norepinephrine, ephedrine) vs. Carotid sinus massage control and pacing alone was evaluated on Carotid sinus massage (CSM)-induced fall in systolic pressure (p=<.01). Intravenous norepinephrine and oral ephedrine blunted the carotid sinus massage-induced drop in systolic pressure (-19±12 and -21±11 mm Hg) compared to pacing alone (-48±19 mm Hg; p<0.01).