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Hung yu Huang
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Lindsay Dong
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Huang, H.;  Huang, C.;  Li, L. Prolonged Mechanical Ventilation: Outcomes and Management. Encyclopedia. Available online: https://encyclopedia.pub/entry/24390 (accessed on 17 May 2024).
Huang H,  Huang C,  Li L. Prolonged Mechanical Ventilation: Outcomes and Management. Encyclopedia. Available at: https://encyclopedia.pub/entry/24390. Accessed May 17, 2024.
Huang, Hung-Yu, Chih-Yu Huang, Li-Fu Li. "Prolonged Mechanical Ventilation: Outcomes and Management" Encyclopedia, https://encyclopedia.pub/entry/24390 (accessed May 17, 2024).
Huang, H.,  Huang, C., & Li, L. (2022, June 23). Prolonged Mechanical Ventilation: Outcomes and Management. In Encyclopedia. https://encyclopedia.pub/entry/24390
Huang, Hung-Yu, et al. "Prolonged Mechanical Ventilation: Outcomes and Management." Encyclopedia. Web. 23 June, 2022.
Prolonged Mechanical Ventilation: Outcomes and Management
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This entry is adapted from the peer-reviewed paper 10.3390/jcm11092451

Prolonged mechanical ventilation (PMV) is defined as successful extubation after more than three spontaneous breathing trials or taking more than 14 days. The pathophysiology of PMV includes the presence of an abnormal respiratory drive or ventilator-induced diaphragm dysfunction. Numerous studies have demonstrated that ventilator-induced diaphragm dysfunction is related to increases in in-hospital deaths, nosocomial pneumonia, oxidative stress, lung tissue hypoxia, ventilator dependence, and costs.

prolonged mechanical ventilation reactive oxygen species respiratory drive ventilator-induced diaphragm dysfunction

1. Introduction

A percentage of critically ill patients experience chronic respiratory failure and require prolonged mechanical ventilation (PMV) [1]. PMV is defined as successful extubation after more than three spontaneous breathing trials or taking more than 14 days [1], although some studies have used different definitions, especially studies in the United Kingdom and Europe [2]. Approximately 5–13% of patients with acute respiratory failure require PMV, and a trend of increasing PMV exists worldwide [3].

Patients receiving PMV may experience complications, including limb muscle atrophy, impaired functional status, and diaphragm dysfunction [4]. Moreover, the basal respiratory drive levels may be altered in patients with PMV, depending on the pulmonary disease present and the cause of respiratory failure [5][6][7]. Brain stem lesions may impair the central and low respiratory drives, causing abnormal respiratory function, hypoventilation, or respiratory acidosis, any of which may lead to ventilator dependence [7].

2. Respiratory Drive

The brain stem responds to levels of O2, CO2, and pH in the blood and cerebrospinal fluid through chemoreceptive neurons and initiates automatic respiration [8]. Airway occlusion pressure (P0.1) or hypercapnic ventilatory response can be used to measure respiratory drive [5][7][9]. P0.1 is defined as the negative airway pressure generated during the first 100 ms of an occluded inspiration measured by a ventilator [9]. The hypercapnic challenge test is performed with the modified Read rebreathing method, and the hypercapnic challenge with CO2 induces an increase in the ventilatory drive and the level of P0.1 recorded by bedside capnograph and pneumotachograph [9]. The hypercapnic ventilatory response is used as a predictor of weaning outcomes in patients with short- or long-term use of MV; old age, comorbidities, and muscle weakness, which may lead to a low hypercapnic ventilatory response [7][10][11][12]. In patients receiving PMV with brainstem lesions (brain stem infarction, brain tumor, traumatic intracerebral hemorrhage), high P0.1 responses to a hypercapnic challenge are associated with higher rates of successful weaning from MV, and an increase in P0.1 of more than 6 cmH2O after the hypercapnic challenge is a predictor of weaning success [7].
Mechanical power is the energy transferred to the respiratory system per unit of time, which is the product of respiratory rate, tidal volume, and the airway pressure during pressure-controlled ventilation [13][14]. Higher mechanical power is associated with ventilator-induced lung injury and worse clinical outcomes [15]. Mechanical power is a novel concept to guide mechanical ventilator adjustments for acute respiratory distress syndrome [16]. For patients with PMV, mechanical power may be a tool used as respiratory drive to assess ventilator weaning and needs further investigation.

3. Ventilator-Induced Diaphragm Dysfunction

The diaphragm is the primary skeletal muscle responsible for effective lung expansion [17]. The diaphragm is a thin, dome-shaped muscular and central membranous tendon structure that separates the thoracic and abdominal cavities. Under normal conditions, contraction of the diaphragm increases the internal height of the chest cavity and causes the inspiration of air. Relaxation of the diaphragm and the thoracic cage leads to expiration. The diaphragm strength is measured by the transdiaphragmatic pressure (Pdi) derived from the difference between the pressure in the stomach (gastric pressure, Pga) and the esophageal pressure (Pes, as an indicator of pleural pressure): Pdi = Pga − Pes. The gold standard in patients who cannot cooperate in the test is to calculate the Pdi via twitch magnetic stimulation of the phrenic nerves (Pdi,tw). Maximal inspiratory pressure (MIP) is recorded following a maximum inspiratory effort against an occluded airway [18][19][20]. PMV may induce the rapid debilitation of diaphragmatic strength and endurance and lead to a reliance on ICU ventilators or long-term facilities; Petrof and Vassilopoulos refer to this as ventilator-induced diaphragm dysfunction (VIDD) [21][22][23][24]. Demoule et al. revealed that approximately 80% of ICU patients receiving MV exhibit an altered pattern of ICU-acquired diaphragm weakness after the first use of MV [24]. Numerous studies have demonstrated that VIDD is associated with increases in in-hospital deaths, nosocomial pneumonia, oxidative stress, lung tissue hypoxia, ventilator dependence, and costs [18][19][24], suggesting that diaphragmatic weakness with a reduced capacity of the diaphragm to produce inspiratory pressure may be considered as an example of unacknowledged organ failure in patients with a critical illness. Respiratory muscle abnormalities in critically ill patients may arise from tissue hypoxia, abnormally high diaphragm activity, neuromyopathies, hypercapnic respiratory failure, sepsis, medications (sedatives, steroids, and neuromuscular blocking reagents), MV duration, and malnutrition [20][25]. Sepsis is linked to diaphragm dysfunction in more than half of the ICU patients with PMV [20][26]. Tissue hypoxia is frequently associated with inflammation in patients with sepsis, which is induced by several mechanisms, including microvascular hypoperfusion, microthrombi formation, and regional arteriolar vasoconstriction related to hypercoagulability and leucosequestration [20][26]. Previous animal and brain-dead human studies have revealed that the onset of diaphragm injury was rapid, occurring within 6 to 18 h after MV and the magnitude of impairment of diaphragmatic contraction increased with the time spent on the ventilator [19][20][21][22]. Because of the high medical care expenses and poor prognosis associated with delayed extubation and a prolonged hospital stay of PMV patients, it is, therefore, an important objective to assist ventilator-dependent patients in early weaning from ventilators. Although the specific etiology of PMV is unclear, long-term use of MV may result in the rapid development of VIDD because of concurrent critical ill neuromyopathy, severe infection, excessive or low-pressure support, and patient-ventilator asynchrony [19][20][21][22]. The underlying pathophysiological mechanisms posited for the decrease in diaphragm muscle contractility and endurance are thought to result from elevated oxidative stress, muscle proteolysis (arising from ubiquitin–proteasome system activation, calpain, caspase-3, and the autophagy–lysosomal pathway), and mitochondrial injuries within the diaphragm muscle fibers [20][22]. Figure 1 illustrates the signaling pathway implicated in VIDD development.
/media/item_content/202206/62b50a870de95jcm-11-02451-g001.png
Figure 1. Schematic figure illustrating the signaling pathway implicated in VIDD development. Endotoxin-induced augmentation of mechanical stretch-mediated ROS generation and diaphragm injury are associated with diaphragm proteolysis, mitochondrial dysfunction, autophagy, as well as activation of the caspase-3, calpain, and ubiquitin–proteasome pathways. Diaphragm weakness can be attenuated by administering antioxidants, enoxaparin, or through partial support for mechanical ventilation or pulmonary rehabilitation. Akt = serine/threonine kinase/protein kinase B; ETC = electron transport chain; FoxO1 = Class O of forkhead box1; HIF = hypoxia-inducible factor; LC3 = light chain 3; LMWH = low-molecular-weight heparin; LPS = lipopolysaccharide; mtDNA = mitochondrial DNA; mTOR = mammalian target of rapamycin; MuRF-1 = muscle ring finger-1; NF-κB = nuclear factor κappa B; PI3-K = phosphoinositide 3-OH kinase; ROS = reactive oxygen species; TLR4 = toll-like receptor 4; VIDD = ventilator-induced diaphragm dysfunction.
Reactive oxygen species (ROS), which are produced in mitochondria, sarcoplasmic reticula, sarcolemma, and transverse tubes, are the major oxidants and upstream regulators of proteolysis and mitochondrial dysfunction in the diaphragm [27][28]. Caspase-3 is a cysteine protease-evoking skeletal muscle proteolysis, which is initiated by class O of forkhead box 1 (FoxO1) and the oxidative load in VIDD [29][30][31]. When proteolysis is initiated, caspase-3 can disassemble actin and myosin complexes from the myofibrillar lattice and trigger the release of dissociated myofibrillar proteins which are susceptible to degeneration through the ubiquitin–proteasome system. Calpains are reported to be responsible for the occurrence of VIDD, and their primary function is to support myofibrillar protein turnover by releasing sarcomeric proteins for degradation by caspase-3 [25][32].
An MV-induced oxidative load may impair diaphragm contractility, which is vital for increased proteolytic pathway expression [33][34][35]. The principal proteases in skeletal muscles comprise the ubiquitin–proteasome system and lysosomal enzymes [20][36]. The upregulation of the diaphragm muscle-specific ubiquitin E3 ligases, atrogin-1 and RING-finger proteins-1, is crucial for the proteolysis of monomeric myofibrillar proteins in the diaphragms of patients and animals receiving MV [35][36][37]. Mitochondria are major resources of diaphragmatic ROS and serve as an essential upstream modulator that mediates molecular pathways, promoting diaphragm muscle atrophy during endotoxemia or MV [38][39]. Reduced mitochondrial biogenesis and cytochrome-c oxidase enzyme activity, but increased mitochondrial DNA activity and lipid accumulation were identified in the diaphragm of brain-dead patients receiving MV [40]. The respiratory chain complexes II, III, and IV, and the ratio of state 3 to 4 (respiratory control ratio) are reduced in mitochondria isolated from rodent diaphragms [39][41]. Elevated levels of autophagosomes also occur in MV-mediated diaphragmatic inactivity, as reflected in an increase in the autophagic marker microtubule-associated protein light chain 3 [25][42][43].
Nuclear factor-κB (NF-κB) activation has been implicated in diaphragm injury and atrophy through measurements of the maximal twitch airway pressure after magnetic stimulation of the phrenic nerve of patients receiving MV [25][32][44]. An oxidative load triggered by mediators produced from inflammatory cells may react with redox-sensitive NF-κB, leading to the progression of coagulation and inflammation, which are related to the pathogenesis of VIDD or sepsis [45][46].
The current approach to reducing VIDD is to avoid controlled MV and the use of unnecessary neuromuscular blocking agents. Notably, low-molecular-weight heparin (LMWH) can reduce lipopolysaccharide-induced acute lung injury and systemic inflammation in animal models of endotoxemia [47][48].

4. Clinical Impact and Multiple Comorbidities

50% of patients (95% confidence interval [CI]: 47–53) were successfully weaned from MV, in-hospital mortality was 29% (95% CI: 26–32), and only 19% (95% CI: 16–24) of patients were discharged home [1]. Recognized factors of weaning failure are underlying respiratory diseases, previous ICU admissions, a high acute physiology and chronic health evaluation (APACHE II) score, and pneumonia [49][50][51][52]. Other factors related to unsuccessful weaning are elevated blood urea nitrogen levels, low Glasgow coma scale (GCS) scores, low serum albumin, and low maximal inspiratory pressure levels [53].

The prognosis for patients requiring PMV is poor. Among 29 studies of PMV, the pooled mortality rate was 62% at year 1 [1]. In a cohort study in the United States, 53.7% of patients requiring PMV were successfully weaned from ventilation at discharge, and 66.9% of these patients were still alive at year 1 [54]. However, the survival rate of patients with ventilator dependence was only 16.4% at post-discharge year 1 [54].

Comorbidities exacerbate diseases and have a severe impact on the outcomes of patients requiring PMV. Chronic obstructive pulmonary disease (COPD), cardiac disease, cerebral vascular or neuromuscular disease, end-stage renal disease, and malignancy are common comorbidities in patients requiring PMV [53][55][56][57][58].

Patients requiring PMV often experience long-term immobilization complications, including limb muscle atrophy, diaphragm dysfunction, pressure ulcers, joint contracture, and deconditioning [59][60]. Muscle-strengthening activities aim to progressively improve mobility and functional activity [61]. Pulmonary rehabilitation has been used to improve physical capacity and the quality of life in patients with chronic pulmonary diseases [62][63][64][65]. For patients requiring PMV, pulmonary rehabilitation could provide clinical benefits [61][66][67][68][69].

A comprehensive physical exercise program includes cardiopulmonary endurance exercises and peripheral muscle training. Upper and lower limb exercises include passive leg raising, weighted resistance, and stationary cycle ergometry training [61][70][71]. Respiratory muscle training consists of placing a sandbag on the abdomen during breathing, using a threshold device, or performing diaphragmatic breathing control [61][69][70][71][72][73][74]. The goal is for the patient to increase their mobility and functional activity and gradually recover from being bedridden to sitting, standing, and walking [67][70][73][74]. The benefits of physical exercise programs for patients requiring PMV include functional improvement, increased weaning rates, shorter duration of hospitalization, and reduced mortality [67][70][73][74]. Notably, Dong et al. showed that early rehabilitation training lessened the diaphragm dysfunction during ventilator use, increased weaning rates from the ventilator, and shortened the intubation duration in patients with MV in the ICU [70].

In patients requiring PMV, immobility and long-term ventilator use result in complications, such as the atrophy of respiratory muscles, decreased lung volume, and atelectasis [4]. When performing rehabilitation exercises, patients requiring PMV may experience respiratory muscle fatigue and intolerance to exercise because of the increased ventilatory demand [66]. Intermittent positive pressure breathing (IPPB) can increase the delivery of inspiratory positive pressure to the airway to achieve homogeneous gas distribution, recruit collapsed alveoli, and facilitate lung expansion [75]. During the weaning process, IPPB and positive end-expiratory pressure (PEEP) may increase lung volume and reduce the work of breathing during the expiratory phase, thus helping patients requiring PMV to tolerate the rehabilitation program [76]. 

Electrical muscle stimulation triggers muscle contraction and could be used to recover muscle atrophy and improve muscle strength after prolonged bed rest [77][78][79][80]. The majority of patients requiring PMV have increased muscle catabolism and decreased muscle mass synthesis after prolonged bed rest, particularly in the lower limbs [81][82].
Malnutrition is common in PMV patients and associated with poor outcomes, including difficult wound healing, nosocomial infections, and increased mortality [83]. Nutritional support is important, however, there is no standardized protocol regarding the administration route, type of nutrients and timing of nutrition support.

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Subjects: Critical Care Medicine
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Hung-Yu Huang
,
Chih-Yu Huang
,
Li-Fu Li
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Update Date: 24 Jun 2022
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