title: Increasing tidal volumes and pulmonary overdistention adversely affect pulmonary vascular mechanics and cardiac output in a pediatric swine model.
abstract: OBJECTIVE
  In a pediatric swine model, the effects of increasing tidal volumes and the subsequent development of pulmonary overdistention on cardiopulmonary interactions were studied. The objective was to test the hypothesis that increasing tidal volumes adversely affect pulmonary vascular mechanics and cardiac output. An additional goal was to determine whether the effects of pulmonary overdistention are dependent on delivered tidal volume and/or positive end-expiratory pressure (PEEP, end-expiratory lung volume).
  
  
  METHODS
  Prospective, randomized, controlled laboratory trial.
  
  
  METHODS
  University research laboratory.
  
  
  METHODS
  Eleven 4- to 6-wk-old swine, weighing 8 to 12 kg.
  
  
  METHODS
  Piglets with normal lungs were anesthetized, intubated, and paralyzed. After median sternotomy, pressure transducers were placed in the right ventricle, pulmonary artery, and left atrium. An ultrasonic flow probe was placed around the pulmonary artery.
  
  
  RESULTS
  The swine were ventilated and data were collected with delivered tidal volumes of 10, 15, 20, and 25 mL/kg and PEEP settings of 5 and 10 cm H2O in a random order. Pulmonary overdistention was defined as a decrease in dynamic compliance of > or =20% when compared with a compliance measured at a baseline tidal volume of 10 mL/kg. At this baseline tidal volume, airway pressure-volume curves did not demonstrate pulmonary overdistention. Tidal volumes and airway pressures were measured by a pneumotachometer and the Pediatric Pulmonary Function Workstation. Inspiratory time (0.75 sec), FIO2 (0.3), and minute ventilation were held constant. We evaluated the pulmonary vascular and cardiac effects of the various tidal volume and PEEP settings by measuring pulmonary vascular resistance, pulmonary characteristic impedance, and cardiac output. When compared with a tidal volume of 10 mL/kg, a tidal volume of 20 mL/kg resulted in a significant decrease in dynamic compliance from 10.5 +/- 0.9 to 8.4 +/- 0.6 mL/cm H2O (p = .02) at a constant PEEP of 5 cm H2O. The decrease in dynamic compliance of 20% indicated the presence of pulmonary overdistention by definition. As the tidal volume was increased from 10 to 20 mL/kg, pulmonary vascular resistance (1351 +/- 94 vs. 2266 +/- 233 dyne x sec/cm5; p = .004) and characteristic impedance (167 +/- 12 vs. 219 +/- 22 dyne x sec/cm5; p = .02) significantly increased, while cardiac output significantly decreased (951 +/- 61 vs. 708 +/- 48 mL/min; p = .001). Each of these effects of pulmonary overdistention were further magnified when the tidal volume was increased to 25 mL/kg. The tidal volume-induced alterations in pulmonary vascular mechanics, characteristic impedance, and cardiac output occurred to a greater degree when the PEEP was increased to 10 cm H2O. Pulmonary vascular resistance and characteristic impedance were significantly increased and cardiac output significantly decreased for all tidal volumes studied at a PEEP of 10 cm H2O as compared with 5 cm H2O.
  
  
  CONCLUSIONS
  Increasing tidal volumes, increasing PEEP levels, and the development of pulmonary overdistention had detrimental effects on the cardiovascular system by increasing pulmonary vascular resistance and characteristic impedance while significantly decreasing cardiac output. Delivered tidal volumes of >15 mL/kg should be utilized cautiously. Careful monitoring of respiratory mechanics and cardiac function, especially in neonatal and pediatric patients, is warranted.
authors.affiliation: Department of Pediatrics, Duke University Medical Center, Durham, NC, USA.
authors.forename: I M
authors.initials: IM
authors.lastname: Cheifetz
authors.forename: D M
authors.initials: DM
authors.lastname: Craig
authors.forename: G
authors.initials: G
authors.lastname: Quick
authors.forename: J J
authors.initials: JJ
authors.lastname: McGovern
authors.forename: M L
authors.initials: ML
authors.lastname: Cannon
authors.forename: R M
authors.initials: RM
authors.lastname: Ungerleider
authors.forename: P K
authors.initials: PK
authors.lastname: Smith
authors.forename: J N
authors.initials: JN
authors.lastname: Meliones
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output / Q000502:physiology*; D008168:Lung / Q000098:blood supply*; D008170:Lung Compliance / Q000502:physiology*; D008954:Models, Biological; D011175:Positive-Pressure Respiration; D011651:Pulmonary Artery / Q000502:physiology; D013552:Swine; D013990:Tidal Volume / Q000502:physiology*; D014655:Vascular Resistance