Increased duration of mechanical ventilation is associated with decreased diaphragmatic force

Introduction

Respiratory muscle weakness is an important risk factor for prolonged mechanical ventilation, and may be part of critical illness related polyneuropathy and myopathy. Animal data also strongly point to atrophy and weakness of the diaphragm due to mechanical ventilation itself, called ventilator-induced diaphragmatic dysfunction. Recently, measuring transdiaphragmatic pressure following magnetic stimulation (TwPdi BAMPS) was introduced in the ICU to evaluate diaphragm function [1, 2]. We aimed to evaluate reproducibility of twitch TwPdi BAMPS in critically ill, mechanically ventilated patients. We also aimed to describe the relationship between TwPdi and duration of mechanical ventilation.

Methods

Prospective observational study in a medical ICU of a university hospital. TwPdi BAMPS was measured in critically ill and mechanically ventilated patients. Briefly, the phrenic nerves were stimulated bilaterally from the anterior approach, at the posterior border of the sternocleidomastoid muscle, at the level of the cricoids using two figure-of-eight 45 mm magnetic coils (Magstim, Dyfed, Wales) and a bistim (Magstim, Dyfed, Wales). A custom-built occlusion valve was used to create isometric conditions during stimulation. Oesophageal and abdominal pressure changes were measured using balloon catheters (UK Medical, Sheffield, UK) inserted through the nose after local anaesthesia.

Results

Nineteen measurements were made in a total of 10 patients at various intervals after starting mechanical ventilation. In seven patients, measurements were made on at least two occasions with a minimal interval of 24 hours. The between-occasion coefficient of variation of TwPdi was 9.7%, which is comparable with data from healthy volunteers. Increasing duration of mechanical ventilation was associated with a logarithmic decline in TwPdi (R = 0.69, P = 0.038). This association was also found when cumulative time on pressure control ventilation (R = 0.71, P = 0.03) and pressure support ventilation (P = 0.05, R = 0.66) were considered separately, as well as for cumulative dose of propofol (R = 0.66, P = 0.05) and piritramide (R = 0.79, P = 0.01).

Conclusions

Increased duration of mechanical ventilation is associated with a logarithmic decline in diaphragmatic force. These findings are compatible with the concept of ventilator-induced diaphragmatic dysfunction. The observed decline may also be due to the cumulative dose of sedatives/analgesics or other co-factors, such as sepsis.