Hemodynamic recovery during simulated ventricular tachycardia: role of adrenergic receptor activation.
Ventricular tachycardia (VT) produces a wide variety of hemodynamic outcomes. Variations in autonomic nervous system response were studied in an animal model of VT. In 18 dogs anesthetized with chloralose VT was simulated by ventricular pacing (rate 240 bpm). Dynamic changes in left ventricular (LV) function were assessed during sinus rhythm and after VT was initiated, under variable autonomic conditions: ganglionic blockade with hexamethonium (n = 5), alpha-adrenergic blockade with terazosin (n = 7; 0.3 mg/kg), and beta-adrenergic blockade with propranolol (n = 6; 2 mg/kg). Micromanometers were used to measure LV pressure, and endocardial piezo crystals assessed changes in cavity size. Sinus interval, an index of autonomic tone, was determined immediately after tachycardia was terminated. Under control conditions the onset of simulated VT was accompanied by severe hypotension, with a decline in LV systolic pressure from 113 +/- 5 to 67 +/- 4 mm Hg within 10 seconds (p less than 0.05). Subsequently, during persistent tachycardia peak LV pressure recovered to sinus values, and maximum +dP/dt exceeded sinus values by 20 seconds (2604 +/- 413 vs 2112 +/- 184 mm Hg/sec; 20 seconds for VT vs sinus rhythm). Diastolic pressures were unchanged, and sinus rate accelerated. Ganglionic blockade with hexamethonium resulted in persistent hypotension, blunted +dP/dt, no change in diastolic pressures, and failure of the sinus rate to accelerate after the tachycardia. After beta blockade there was sustained hypotension (LV systolic pressure 78 +/- 4 vs 120 +/- 5 mm Hg; 20 seconds for VT vs sinus rhythm), maximum +dP/dt was blunted, and minimum diastolic ventricular pressure rose. This was due to an upward shift in the diastolic pressure-dimension relationship associated with prolongation of the time constant of LV relaxation. The sinus interval did not change. In contrast, tachycardia during alpha blockade produced a sustained fall in peak LV pressure; however, maximum +dP/dt recovered (2194 +/- 328 vs 2154 +/- 153 mm Hg/sec; 20 seconds for VT vs sinus rhythm), minimum diastolic LV pressure remained low, and sinus rate accelerated after ventricular tachycardia. Hemodynamic recovery during ventricular tachycardia is mediated by the response of the autonomic nervous system and requires both alpha-adrenergic vasoconstriction and beta-adrenergic augmentation of contraction and relaxation.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D002304:Cardiac Pacing, Artificial / Q000379:methods; D004195:Disease Models, Animal; D004285:Dogs; D005260:Female; D005725:Ganglia, Autonomic / Q000187:drug effects; D006352:Heart Ventricles; D006439:Hemodynamics / Q000187:drug effects; D006584:Hexamethonium Compounds / Q000494:pharmacology; D007022:Hypotension / Q000209:etiology; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D011224:Prazosin / Q000031:analogs & derivatives / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D013610:Tachycardia / Q000503:physiopathology*
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D006584:Hexamethonium Compounds; C041226:Terazosin; D011433:Propranolol; D011224:Prazosin