title: Central-to-peripheral arterial pressure gradient during cardiopulmonary bypass: relation to pre- and intra-operative data and effects of vasoactive agents.
abstract: A significant central-to-peripheral arterial pressure gradient may exist during and after cardiopulmonary bypass (CPB). The etiology and mechanisms of this phenomenon remain controversial. We studied the pressure gradient between aorta, brachial artery and radial artery in 68 patients, scheduled for elective coronary artery bypass surgery. We evaluated whether choice of cardioprotection during CPB (use of cold cardioplegic solution or use of intermittent crossclamping under protection with lidoflazine), and choice of pulsatile or nonpulsatile flow during the course of CPB, affected the magnitude and duration of the systolic pressure gradient. We also studied whether central-to-peripheral pressure gradient was influenced by administration on CPB of different vasoactive drugs with different mode of action: sodium nitroprusside (direct action on the vessels), droperidol (alpha-adrenergic blocking action), ketanserin (5-hydroxytryptamine antagonist) and phenylephrine (selective alpha 1-agonist). It appeared that central-to-peripheral gradient occurred early during CPB and remained constant throughout the course of CPB. The gradient disappeared within 60 min after weaning from CPB. We found the main pressure gradient to occur between the brachial and the radial artery. There was no relation between magnitude of the gradient and sex, weight, length or age of the patient. There was also no relation between magnitude of the pressure gradient and type of cardioprotection, choice of pulsatile vs nonpulsatile flow on CPB and duration of CPB. We also found no relation between pressure gradients and changes in temperature, haematocrit and systemic vascular resistance. The pressure gradient was not affected by any of the vasoactive drugs.
authors.affiliation: Department of Anesthesia, University Hospital Antwerp, Edegem, Belgium.
authors.forename: S G
authors.initials: SG
authors.lastname: De Hert
authors.forename: K M
authors.initials: KM
authors.lastname: Vermeyen
authors.forename: M M
authors.initials: MM
authors.lastname: Moens
authors.forename: V L
authors.initials: VL
authors.lastname: Hoffmann
authors.forename: K J
authors.initials: KJ
authors.lastname: Bataillie
mesh_terms: D000368:Aged; D001011:Aorta / Q000502:physiology; D001790:Blood Physiological Phenomena; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D001831:Body Temperature; D001916:Brachial Artery / Q000502:physiology; D002314:Cardioplegic Solutions / Q000008:administration & dosage; D002315:Cardiopulmonary Bypass / Q000379:methods*; D003250:Constriction; D004329:Droperidol / Q000494:pharmacology; D005260:Female; D006400:Hematocrit; D006801:Humans; D007430:Intraoperative Care; D007650:Ketanserin / Q000494:pharmacology; D008013:Lidoflazine / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011300:Preoperative Care; D011673:Pulsatile Flow; D017534:Radial Artery / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D002314:Cardioplegic Solutions; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D007650:Ketanserin; D008013:Lidoflazine; D004329:Droperidol