INTRODUCTION

Mechanical ventilation is being used with increasing frequency to support veterinary patients with respiratory failure secondary to impaired oxygenation or ventilation (see Chapter 213, Basic Mechanical Ventilation).^1-5 Common reasons for impaired oxygenation requiring mechanical ventilation include pneumonia, cardiogenic pulmonary edema, and acute respiratory distress syndrome (ARDS). Impaired ventilation, or the inability to eliminate carbon dioxide through the lungs, can be seen as a result of an impaired ventilatory drive secondary to intracranial disease, neuromuscular disease, or as a sequela to respiratory fatigue from increased work of breathing or severe pulmonary disease.

Two of the most common causes of respiratory failure requiring mechanical ventilation in human medicine are ARDS and acute lung injury (ALI). ARDS represents a diffuse, inflammatory pulmonary disorder resulting from a wide variety of clinical conditions, both intrapulmonary and systemic, and is clinically characterized by a sudden onset, bilateral alveolar infiltrates, an arterial-to-inspired oxygen tension ratio (PaO₂-to-FiO₂) under 200 mm Hg, and the absence of left-sided heart failure. ALI describes a similar clinical scenario, however pulmonary dysfunction is marginally better, with PaO₂-to-FiO₂ ratios of 200 to 300 mm Hg. These syndromes have been recognized in both dogs and cats with naturally occurring disease (see Chapter 24, Acute Lung Injury and Acute Respiratory Distress Syndrome).^6-8 Although mechanical ventilation is vital for the support of respiratory function in patients with ARDS and other causes of respiratory failure, mechanical ventilation itself can potentiate or even induce lung injury.

VENTILATOR-INDUCED LUNG INJURY AND VENTILATOR-ASSOCIATED LUNG INJURY

Ventilator-induced lung injury (VILI) is characterized by increased capillary permeability, pulmonary edema, cellular injury, and diffuse structural damage to alveoli that is clinically indistinguishable from the damage that occurs in ARDS. For this reason, the term VILI is often restricted to describe pulmonary changes as a result of mechanical ventilation in experimental animal models. Ventilator-associated lung injury (VALI) describes a lung injury resembling ARDS that develops or worsens during the course of mechanical ventilation in clinical patients—this injury can only be associated with ventilation, rather than saying that it is definitively caused by ventilation, because the underlying disease process may be responsible for progression of lung injury.⁹ During the past decade, positive-pressure ventilation strategies have evolved based on experimental evidence of VILI and clinical trials studying the effects of ventilator management on VALI.

The role that positive-pressure ventilation plays in perpetuating lung injury is easiest to appreciate in studies of human patients who do not have ALI or ARDS at the onset of therapy. One study evaluated 332 human patients who did not fit the criteria for ALI prior to the onset of more than 48 hours of mechanical ventilation. In this study, 24% of these patients went on to develop ALI during the course of mechanical ventilation. Two of the risk factors identified for VALI in this study included larger day 1 tidal volumes (above 6 ml/kg) and a history of restrictive pulmonary disease which would result in reduced pulmonary compliance. Interestingly, larger tidal volumes were more likely to be used in presumed lower risk patients: those who were ventilated postoperatively, had lower predicted mortality rates, or had better gas exchange and pulmonary mechanics.¹⁰ This emphasizes that ventilation, be it manual or mechanical, and the risk for VALI should never be taken lightly in any patient population.

PRIMARY CAUSES OF VALI

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