Clinical Aspects of Respiratory Muscle Dysfunction in the Critically Ill

The aim of the present study was to investigate the electrophysiology of the phrenic nerve and the diaphragm muscle during sepsis.In total, 26 rats underwent either sham laparotomy or caecal ligation and puncture (CLP). Electrophysiology was evaluated via a phrenic nerve conduction study and needle electromyography of the diaphragm, prior to CLP, 6 and 24 h post-CLP and on day 7. The histopathology of the diaphragm muscle and phrenic nerve was also examined on day 7.In the sepsis group, the phrenic nerve conduction study showed decreased amplitude of compound action potential (CMAP), and prolongation in the duration and the latency of CMAP. The diaphragmatic needle electromyography showed decreased amplitude and frequency of the motor unit action potential (MUP), and prolongation in the duration of MUP, at all time points, compared with the pre-CLP values. The electrophysiological abnormalities were consistent with axonal and demyelinating phrenic nerve neuropathy. Electrophysiological abnormalities were present at 6 h with worsening at 24 h and on day 7. Histopathological examination showed normal muscular fibres and focally slight myelin degenerations of the phrenic nerve fibres.In conclusion, sepsis induced phrenic nerve neuropathy as early as the 6th h in rats.

Section: Discussionmentioning

confidence: 99%

Sepsis induces early phrenic nerve neuropathy in rats

Naycı

Atış²,

Çömelekoğlu³

et al. 2005

“…Patients with ICUAW often have abnormal nerve conduction (more typically axonal loss than prolonged conduction time [71]) and the disease was originally postulated as ''critical illness neuropathy'' [72]. The effect of denervation of muscle is complex because nervous stimulation is required for the maintenance of muscle phenotype as well for contraction.…”

Section: Neuropathy and Nerve Activitymentioning

confidence: 99%

Molecular mechanisms of intensive care unit-acquired weakness

Bloch¹,

Polkey²,

Griffiths³

et al. 2011

Intensive care unit-acquired weakness (ICUAW) is an increasingly recognised and important clinical consequence of critical illness. It is associated with significant morbidity and mortality. The aetiology of this disease is not well understood. The purpose of this article is to review our understanding of the molecular pathogenesis of ICUAW in the context of current knowledge of clinical risk factors and aetiology.Key features of the disease are loss of muscle mass resulting from a shift in the dynamic balance of muscle protein synthesis and breakdown and a reduction in force-generating capacity. These alternations are secondary to neuropathy, disruption of the myofilament structure and function, a disrupted sarcoplasmic reticulum, electrical inexcitability and bioenergenetic failure.As knowledge and understanding of ICUAW grows, potential therapeutic targets will be identified, hopefully leading to multiple strategies for prevention and treatment of this important condition.

“…Viewed in this light, the ability to nonvolitionally assess muscle strength with magnetic stimulation appears to be particularly valuable on the ICU. Respiratory muscle function and critical illness neuromuscular abnormalities in the ICU have recently been reviewed [95,96], and the focus of discussion here will be confined to the use (present and potential) of magnetic stimulation.…”

Section: Critical Illnessmentioning

confidence: 99%

Magnetic stimulation for the measurement of respiratory and skeletal muscle function

Man¹

2004

118

Respiratory and skeletal muscle function is of interest in many areas of pulmonary and critical care medicine. The capacity of the respiratory muscle pump to respond to the load imposed by disease is the basis of an understanding of ventilatory failure. Over the last four decades, considerable progress has been made in quantifying the capacity of the respiratory muscles, in terms of strength, endurance and fatigue. With the development of magnetic stimulation, it has recently become possible to nonvolitionally assess the respiratory muscles in a clinically acceptable way. This is of particular interest in the investigation of patients receiving critical care, those with neuromuscular disease, and in children where volitional efforts are either not possible or likely to be sub-maximal. Furthermore, the adaptation of these techniques to quantify the strength of peripheral muscles, such as the quadriceps, has allowed the effects of muscle training or rehabilitation, uninfluenced by learning effect, to be assessed. This article focuses on the physiological basis of magnetic nerve stimulation, and reviews how the technique has been applied to measure muscle strength and fatigue, with particular emphasis upon the diaphragm. The translation of magnetic stimulation into a clinical tool is described, and how it may be of diagnostic, prognostic and therapeutic value in several areas of pulmonary medicine. In particular, the use of magnetic stimulation in neuromuscular disease, the intensive care setting, chronic obstructive pulmonary disease and paediatrics will be discussed. The nonvolitional assessment of skeletal musclesFor routine muscle strength measurements, the force generated from a maximum voluntary contraction (MVC) is often used. However volitional, effort-dependent manoeuvres for measuring strength are not always suitable for patients as the ability to perform a true MVC relies upon subject motivation and cooperation. This is particularly so in patients on intensive care units (ICU), children, patients with cognitive difficulties, and those patients prevented from performing a true MVC by pain (for example, following surgery). However, even in well-motivated subjects, sub-maximal muscle activation is common in routine clinical practice [1]. As volitional manoeuvres are influenced by a learning effect, the value of MVC is also limited in studies of training or rehabilitation. Consequently, there has been a need for nonvolitional methods to assess muscle strength. Skeletal muscle physiologySkeletal muscle is controlled by electrical impulses conducted by motor neurones that lead to the release of acetylcholine from the motor end plate, thus depolarising the muscle cell membrane. The force generated by muscle contraction is dependent upon a number of factors, including the number of muscle fibres stimulated, muscle length at the time of stimulation and the frequency of stimulation. The force-frequency curve of a muscle is of particular relevance in the understanding of nonvolitional techniques to asse...