title: Enhanced left ventricular contractility in autonomic failure: assessment using pressure-volume relations.
abstract: Severe autonomic failure is usually characterized by both supine hypertension and orthostatic hypotension. Inadequate preload reserve, insufficient arterial resistance and abnormal cardiac performance have been postulated to contribute to the hypotension. To clarify these mechanisms, left ventricular performance and contractility were assessed using radionuclide ventriculography and systolic pressure-volume relations when supine and with graded head-up tilt in 11 patients with autonomic failure. Results were compared with those of 12 normal subjects, using phenylephrine infusion for pharmacologic afterload augmentation after autonomic blockade with atropine and propranolol. In a subset of four patients with autonomic failure, systolic pressure-volume relations were similar by both the tilt and phenylephrine methods. In autonomic failure, end-diastolic volume, end-systolic volume and stroke volume decreased with progressive degrees of tilt (p less than or equal to 0.007 for each). The supine radionuclide ejection fraction and cardiac output were similar to those of normal subjects (69% versus 68% and 5.4 versus 4.9 liters/min, respectively, p = NS). However, the slopes of the pressure-volume relations and the supine pressure/volume ratio in autonomic failure were much greater than normal (8.8 versus 2.5, and 6.3 versus 3.6 mm Hg/ml, respectively, p less than or equal to 0.04 for both). The baseline total peripheral resistance was greater than normal (24.9 versus 17.4 mm Hg.min-1/liter, p = 0.01), but the resistance at maximal tilt failed to increase (20.8 +/- 6.1 units). Plasma norepinephrine concentrations were lower than normal. Thus, patients with autonomic failure had hypercontractile left ventricular performance when assessed by pressure-volume relations, and their hearts were well matched to the elevated peripheral resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.
authors.forename: M W
authors.initials: MW
authors.lastname: Kronenberg
authors.forename: M B
authors.initials: MB
authors.lastname: Forman
authors.forename: J
authors.initials: J
authors.lastname: Onrot
authors.forename: D
authors.initials: D
authors.lastname: Robertson
mesh_terms: D000328:Adult; D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004837:Epinephrine / Q000097:blood; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D009638:Norepinephrine / Q000097:blood; D010656:Phenylephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D013670:Sodium Pertechnetate Tc 99m; D014655:Vascular Resistance / Q000502:physiology; D015646:Ventriculography, First-Pass
chemical_list: D010656:Phenylephrine; D011433:Propranolol; D013670:Sodium Pertechnetate Tc 99m; D009638:Norepinephrine; D004837:Epinephrine