title: Respiratory, metabolic and hemodynamic effects of clonidine in ventilated patients presenting with withdrawal syndrome.
abstract: OBJECTIVE
  To investigate the respiratory, metabolic and hemodynamic effects of clonidine in ventilated patients presenting with withdrawal syndrome after sedation interruption.
  
  
  METHODS
  Prospective, interventional, single-center study in 30 ventilated ICU patients.
  
  
  METHODS
  Metabolic [oxygen consumption (VO(2)), CO(2) production (VCO(2)), resting energy expenditure (REE)], respiratory [minute ventilation (V (E)), tidal volume (V (T)), respiratory rate (RR)] and hemodynamic (HR, SAP, MAP) parameters were measured in 30 ventilated ICU patients. Measurements were performed first under sedation with remifentanil-propofol, then after sedation interruption, and finally after clonidine administration (0.9-1.8 mg of clonidine in two doses of 10 min interval).
  
  
  RESULTS
  Sedation interruption produced significant increases in the hemodynamic parameters (SAP and MAP by 33%, HR by 37%), and metabolic rate (increase in VO(2) by 70%, VCO(2) by 88% and REE by 74%), leading to high respiratory demands (increase in V (E) from 9 to 15 l/min). The V (E) was increased due to a twofold increase in the RR; V (T) remained constant. In 25 out of 30 patients, clonidine administration decreased the hemodynamic (SAP, MAP and HR), metabolic (VO(2), VCO(2), REE) and respiratory parameters to values close to those observed with sedation. Clonidine induced mild sedation and patients became more cooperative with the ventilator. All patients responding to clonidine were weaned from the ventilator in 2 days (median, range 1-18 days).
  
  
  CONCLUSIONS
  Patients with withdrawal syndrome had significantly elevated hemodynamic, metabolic and respiratory demands. Clonidine significantly decreased these demands, induced mild sedation and facilitated patient cooperation with the ventilator, enabling ventilator weaning.
authors: ICU, Papageorgiou General Hospital, Thessaloniki, Greece.
authors: Domniki
authors: D
authors: Liatsi
authors: Basilis
authors: B
authors: Tsapas
authors: Smaro
authors: S
authors: Pampori
authors: Matthew
authors: M
authors: Tsagourias
authors: Ioannis
authors: I
authors: Pneumatikos
authors: Dimitrios
authors: D
authors: Matamis
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology* / Q000627:therapeutic use*; D000328:Adult; D002153:Calorimetry, Indirect; D002245:Carbon Dioxide / Q000378:metabolism*; D003000:Clonidine / Q000494:pharmacology* / Q000627:therapeutic use*; D004562:Electrocardiography; D004734:Energy Metabolism; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D006993:Hypnotics and Sedatives; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects*; D010880:Piperidines / Q000008:administration & dosage; D015742:Propofol / Q000008:administration & dosage; D011446:Prospective Studies; D000077208:Remifentanil; D012121:Respiration, Artificial / Q000379:methods*; D012131:Respiratory Insufficiency / Q000453:epidemiology / Q000628:therapy*; D012146:Rest; D013375:Substance Withdrawal Syndrome / Q000453:epidemiology* / Q000209:etiology*; D013610:Tachycardia / Q000188:drug therapy*; D015300:Ventilator Weaning
chemical_list: D000316:Adrenergic alpha-Agonists; D006993:Hypnotics and Sedatives; D010880:Piperidines; D002245:Carbon Dioxide; D003000:Clonidine; D000077208:Remifentanil; D015742:Propofol