Mechanical ventilation may increase susceptibility to the development of bacteremia

Crit Care Med. 2003 May;31(5):1429-34. doi: 10.1097/01.CCM.0000063449.58029.81.

Abstract

Objective: We examined the hypothesis that mechanical ventilation with a potentially injurious strategy would predispose animals to the detrimental effects of subsequent instillation of bacteria.

Design: Interventional animal study.

Setting: A university hospital research laboratory.

Subjects: Fifty Sprague-Dawley male rats.

Interventions: Rats were anesthetized and randomized to receive a protective (tidal volume 7 mL/kg, positive end-expiratory pressure 5 cm H(2)O, n = 25) or an injurious ventilatory strategy (tidal volume 21 mL/kg, zero positive end-expiratory pressure, n = 25). Hemodynamics were similar during the 1-hr ventilation period in the two groups. Animals were then disconnected from the ventilator and Pseudomonas aeruginosa was instilled intratracheally before extubation. Thereafter, animals breathed spontaneously; mortality rate was assessed up to 48 hrs, at which time the animals were killed.

Measurements and main results: The 48-hr mortality rate was 28% in the protective group and 40% in the injurious group (p = not significant). A positive bacterial culture from the lung was obtained in 56% of the surviving rats in the low tidal volume group and 67% in the high tidal volume group (p =.059). A positive blood bacterial culture was found in 11% of the low tidal volume group and 33% in the high tidal volume group (p <.05). The absolute bacterial count in the blood was lower in the low tidal volume group compared with the high tidal volume group (p <.05). Concentrations of blood tumor necrosis factor-alpha and macrophage inflammatory protein-2, and lung macrophage inflammatory protein-2 at 48 hrs were significantly higher in the low tidal volume group than in the high tidal volume group.

Conclusions: An injurious ventilatory strategy predisposes animals to subsequent bacteremia associated with an impaired host defense reflected by cytokine response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Airway Resistance
  • Animals
  • Bacteremia / blood
  • Bacteremia / etiology*
  • Bacteremia / immunology
  • Bacteremia / mortality
  • Blood Gas Analysis
  • Blood Pressure
  • Causality
  • Chemokine CXCL2
  • Cross Infection / blood
  • Cross Infection / etiology*
  • Cross Infection / immunology
  • Cross Infection / mortality
  • Disease Models, Animal*
  • Disease Susceptibility
  • Heart Rate
  • Lung / chemistry
  • Male
  • Monokines / analysis
  • Monokines / blood
  • Positive-Pressure Respiration / adverse effects*
  • Positive-Pressure Respiration / methods
  • Pseudomonas Infections / blood
  • Pseudomonas Infections / etiology*
  • Pseudomonas Infections / immunology
  • Pseudomonas Infections / mortality
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Respiration, Artificial / adverse effects*
  • Respiration, Artificial / methods
  • Tidal Volume
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Chemokine CXCL2
  • Monokines
  • Tumor Necrosis Factor-alpha