Fetal body MRI for fetal and perinatal management.

Fetal magnetic resonance imaging (MRI) has become a valuable adjunct to ultrasound (US) in diagnosing fetal abnormalities. This review is intended to highlight the contribution of MRI in parental counselling and perinatal treatment. A state-of-the-art fetal MRI protocol with experts of maternal-fetal medicine present in the MRI suite allows emphasis on patient-centred care and maximises therapeutic options.

Fetal MRI of CNS abnormalities.

Ultrasound (US) is currently the standard approach for the initial evaluation of fetal anatomy and maternal conditions during pregnancy; however, fetal magnetic resonance imaging (MRI) has now become a valuable adjunct to US in confirming/excluding suspected abnormalities and in the detection of additional abnormalities, thus changing the outcome of pregnancy and optimising perinatal management. MRI is a non-invasive diagnostic examination that does not involve ionising radiation and has no known associated negative side effects or reported delayed sequela according to the Safety Committee of the Society for MRI. The main drawback of MRI is fetal motion. The development of fast MRI sequences has significantly decreased fetal motion artefacts allowing the evaluation of the highly mobile fetus. Single-shot fast spin-echo (SSFSE) T2-weighted imaging is a standard sequence. T1-weighted sequences are primarily used to demonstrate haemorrhage, fat, and calcification. Balanced steady-state free-precession (SSFP) sequences are beneficial in demonstrating fetal structures as well as the heart and vessels. Diffusion-weighted imaging (DWI) and magnetic resonance spectroscopy (MRS) have important applications in fetal brain imaging. In this review, we illustrate a spectrum of structural abnormalities affecting the central nervous system and the spine. The aim of this article is to provide a practical approach for radiologists and clinicians to fetal MRI performance and interpretation.

MRI of the small-bowel: how to differentiate primary neoplasms and mimickers.

MRI of the gastrointestinal tract is gaining clinical acceptance and is increasingly used to evaluate patients with suspected small-bowel diseases. MRI may be performed with enterography or enteroclysis, both of which combine the advantages of cross-sectional imaging with those of conventional enteroclysis. In this paper, MRI features of primary small-bowel neoplasms, the most important signs for differential diagnosis and the diseases that can be considered as mimickers of small-bowel neoplasms, are discussed.

Auto-PEEP in respiratory failure.

Intrinsic positive end-expiratory pressure (auto-PEEP) is a common occurrence in patients with acute respiratory failure requiring mechanical ventilation. Auto-PEEP can cause severe respiratory and hemodynamic compromise. The presence of auto-PEEP should be suspected when airflow at end-exhalation is not zero. In patients receiving controlled mechanical ventilation, auto-PEEP can be estimated measuring the rise in airway pressure during an end-expiratory occlusion maneuver. In patients who trigger the ventilator or who are not connected to a ventilator, auto-PEEP can be estimated by simultaneous recordings of airflow and airway and esophageal pressure, respectively. The best technique to accurately measure auto-PEEP in patients who actively recruit their expiratory muscle remains controversial. Strategies that may reduce auto-PEEP include reduction of minute ventilation, use of small tidal volumes and prolongation of the time available for exhalation. In patients in whom auto-PEEP is caused by expiratory flow limitation, the application of low-levels of external PEEP can reduce dyspnea, reduce work of breathing, improve patient-ventilator interaction and cardiac function, all without worsening hyperinflation. Neurally adjusted ventilatory assist, a novel strategy of ventilatory assist, may improve patient-ventilator interaction in patients with auto-PEEP.

Indeterminate, subcentimetric focal liver lesions in cancer patients: additional role of contrast-enhanced ultrasound.

PURPOSE: To evaluate whether the use of contrast-enhanced ultrasound (CEUS) could improve the characterization of indeterminate subcentimetric focal liver lesions (FLLs) seen with multidetector computed tomography (MDCT) in cancer patients. MATERIALS AND METHODS: For 12 months all patients with extrahepatic tumors showing small (< 10 mm), indeterminate focal liver lesions on whole-body or abdominal computed tomography (CT) underwent immediate, targeted ultrasound (US) to rule out a cystic lesion. Whenever unenhanced US demonstrated a non-cystic lesion or failed to recognize any focal abnormality within the suspected area, CEUS was carried out. During the arterial phase, CEUS was focused on the area reflecting the CT finding, while the entire organ was explored during the portal-sinusoidal phase. RESULTS: Among the 132 patients with MDCT evidence of indeterminate, subcentimetric focal liver lesions (206 lesions), US proved the cystic nature of 138 lesions in 87 patients. In 45 cases US failed to recognize any abnormality or cystic image and these subjects underwent CEUS. The CEUS results were confirmed by further assessment or follow-up for 43 / 45 patients (3 cysts, 8 hemangiomas, 47 metastases, 2 areas of focal steatosis, 2 eosinophilic necroses, 1 granuloma, 1 abscess, 1 fistula). CEUS failed to detect 3 lesions (1 metastasis and 2 benign lesions). In 8 cases CEUS recognized additional liver metastases. CONCLUSION: CEUS can be helpful in demonstrating or excluding metastases in cancer patients with MDCT evidence of subcentimetric, indeterminate focal liver lesions.

Endocrinological derangements in COPD.

Chronic obstructive pulmonary disease (COPD) is no longer considered to affect only the lungs and airways but also the rest of the body. The systemic manifestations of COPD include a number of endocrine disorders, such as those involving the pituitary, the thyroid, the gonads, the adrenals and the pancreas. The mechanisms by which COPD alters endocrine function are incompletely understood but likely involve hypoxaemia, hypercapnia, systemic inflammation and glucocorticoid administration. Altered endocrine function can worsen the clinical manifestations of COPD through several mechanisms, including decreased protein anabolism, increased protein catabolism, nonenzymatic glycosylation and activation of the rennin-angiotensin-aldosterone system. Systemic effects of endocrine disorders include abnormalities in control of breathing, decreases in respiratory and limb-muscle mass and function, worsening of respiratory mechanics, impairment of cardiac function and disorders of fluid balance. Research on endocrine manifestations of COPD embraces techniques of molecular biology, integrative physiology and controlled clinical trials. A sound understanding of the various disorders of endocrine function associated with COPD is prudent for every physician who practices pulmonary medicine.

A comparison of minimally invasive techniques in percutaneous treatment of lumbar herniated discs. A review.

Low back pain is the commonest spine disease causing absence from work in developed countries. Low back pain with classical irradiation along the course of the nerve root affected is more frequently due to disc disease. In 60-80% of patients with herniated disc, radicular symptoms disappear with conservative treatment after about six weeks, the remainder are treated surgically with a 2-6% of incidence of true recurrence of herniation post-intervention and with failed back surgery syndrome in 15% of cases. Recently minimally invasive techniques have developed as "alternative" treatments to surgical intervention. This review aimed to assess the pathogenesis of low back pain caused by lumbar disc hernia as a basis for action of minimally invasive techniques; to illustrate the techniques already used or currently in use, to compare them in technical guidance, indications and complications, exposing for each of them the inclusion/exclusion criteria in enrolling patients and the imaging guide technique of choice. Minimally invasive techniques can be a valuable alternative to traditional surgery with low cost, low risk of complications, easy feasibility, and in the event of failure they do not exclude subsequent surgery.

Leucemia linfoide aguda a importancia do laboratorio de liquor para o sucesso do tratamento / Acute lymphoblastic leukemia: the importance of cerebrospinal fluid laboratory for successful treatament

A Leucemia Linfoide Aguda (LLA) e uma doenca caracterizada pelo acumulo de linfoblastos em numerosos orgaos e tecidos, notadamente na medula ossea. Entretanto as celulas malignas da LLA tem uma predisposicao de infiltrar o Sistema Nervoso Central (SNC) e os testiculos, sendo estes, considerados ¡°santuarios¡±. A importancia ao diagnostico da avaliacao citologica do liquido cefalorraqueano(Liquor) tornou-se fundamental para adequacao do tratamento, prognostico e para o monitoramento de eventuais recaidas. Citologicamente pode-se determinar um ¡°STATUS¡±, sendo que a avaliacao mais aceita atualmente ao diagnostico deve seguir os seguintes criterios: Status 1: puncao nao traumatica com ausencia de blastos apos citocentrifugacao. Status 2: puncao nao traumatica com presenca de blastos apos citocentrifugacao e leucocitos ¡Ü5/mm3. Status 3: puncao nao traumatica com presenca de blastosapos citocentrifugacao e leucocitos ¡Ý5/mm3 . A puncao traumatica deve ser classificada como risco, pois pode haver a infiltracao na hora da puncao. O objetivo deste trabalho e definir criteriosamente a importancia da atuacao do Farmaceutico Bioquimico no Laboratorio de Liquor auxiliando o clinico na avaliacao de conduta terapeutica baseado na avaliacao citologica do liquido cefalorraqueano.

Acute Lymphoblastic Leukemia (ALL) is an illness characterized for the accumulation of blasts in numerous organ and tissue, essential in the blone marrow. However the malignant cells of the ALL have a predisposition to infiltrate central nervous system(CNS) and the testicules, being been these, considered "sanctuaries". The importance to the diagnosis of the cytological evaluation of the cerebrospinal fluid (CSF), became basic for adequacy of the treatment, prognostic and for the involvement of eventual fallen again. Cytologically a "STATUS" can be determined, being most accepted currently to the diagnosis must follow the following criteria:CNS1 (puncture nontraumatic without leukemic blasts after ytocentrifugation), CNS2 (puncture nontraumatic, ¡Ü5 WBC/mm3 CSF with identifiable blasts after cytocentrifugation), CNS3 (puncture nontraumatic, ¡Ý5 WBC/mm3 CSF with identifiable blasts aftercytocentrifugation). TLP(+) ¨C puncture traumatic with blasts, and TLP(-) ¨C puncture traumatic without blasts. The traumatic puncture must be classified as risk therefore it can have infiltration in the hour puncture. The objective of this work is reintensification to define the importance of the performance of the Pharmaceutical Biochemist in the Cerebrospinal Fluid Laboratory assisting the physician in the based evaluation of therapeutical behavior in the cytological evaluation of the Cerebrospinal Fluid.

Can diaphragmatic contractility be assessed by airway twitch pressure in mechanically ventilated patients?

BACKGROUND: In critically ill patients inspiratory muscle function may be assessed by measurements of maximal inspiratory airway pressure and the response of twitch transdiaphragmatic pressure (Pdi tw) to bilateral phrenic nerve stimulation. The first is limited by its total dependence on patient cooperation. Although the second approach is independent of patient volition, it is impractical because it requires oesophageal and gastric balloons. Because airway pressure is easily and non-invasively recorded in patients with artificial airways, we hypothesised that twitch airway pressure (Paw tw) reliably predicts Pdi tw and twitch oesophageal pressure (Poes tw) in mechanically ventilated patients. METHODS: Thirteen mechanically ventilated patients recovering from an episode of acute respiratory failure received phrenic nerve stimulation at end exhalation. The rapid occlusion technique was used to record respiratory system mechanics. RESULTS: Stimulations were well tolerated. Mean (SE) Paw tw at end exhalation was -8.2 (1.2) cm H(2)O and Poes tw and Pdi tw were -7.3 (1.1) and 10.4 (1.8) cm H(2)O, respectively. Stimulations produced a good correlation between Paw tw and Pdi tw (p<0.001), although the limits of agreement were wide. The results were similar for Poes tw. No relationship was found between the Paw tw/Poes tw ratio and respiratory system compliance or airway resistance. Paw tw reproducibility was excellent (mean coefficient of variation 6%, range 3-9%). CONCLUSIONS: Despite a good correlation between Paw tw and Poes tw, Paw tw did not reliably predict Poes tw or Pdi tw in mechanically ventilated patients. Nevertheless, the excellent reproducibility of Paw tw suggests that it may be a useful means of monitoring inspiratory muscle contractility in the routine care of mechanically ventilated patients.

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD.

How do the respiratory centres of patients with chronic obstructive pulmonary disease (COPD) and hypercapnia respond to acute increases in inspiratory load? A depressed respiratory motor output has long been postulated, but studies on this issue have yielded inconsistent results, partly due to limitations of investigative techniques. Many of these limitations can be overcome by the twitch interpolation technique, which is capable of accurately quantifying the degree of diaphragmatic activation, termed the voluntary drive to breathe. The hypothesis that patients with COPD and hypercapnia compensate for an acute increase in mechanical load on the inspiratory muscles with a lower voluntary drive to breathe than is the case with normocapnic patients was tested. Measurements were obtained in 15 patients with COPD, six of whom displayed hypercapnia and nine normocapnia. The maximum degree of diaphragmatic activation, expressed as a voluntary activation index (mean +/- SEM), was higher in hypercapnic than in normocapnic patients (98.7 +/- 0.7 versus 94.5 +/- 0.9% (p = 0.006)), as was the mean value (94.5 +/- 0.7 versus 88.5 +/- 1.9% (p = 0.01)). Within-patient values of the index were also less variable in the hypercapnic patients (coefficients of variation, 3.4 +/- 0.3 versus 6.1 +/- 0.9%, p = 0.01). Multiple regression analysis revealed the ratio of dynamic elastance to maximum transdiaphragmatic pressure, an index of inspiratory muscle loading, and pH as the only variables that correlated with maximum voluntary activation index (r2 = 0.69, p = 0.02 for each variable). Contrary to the hypothesis, it was concluded that voluntary activation of the diaphragm was greater and less variable in hypercapnic patients than normocapnic patients with severe chronic obstructive pulmonary disease during an acute increase in inspiratory mechanical load. Whether greater diaphragmatic recruitment during episodes of a severe exacerbation of chronic obstructive pulmonary disease provides a survival advantage for hypercapnic patients with chronic obstructive pulmonary disease remains to be determined.

Effect of imposed inflation time on respiratory frequency and hyperinflation in patients with chronic obstructive pulmonary disease.

Decreases in ventilator inflation time (TI,vent) can cause tachypnea, probably as a response to lung inflation. The response may differ in chronic obstructive pulmonary disease (COPD) because time-constant inhomogeneities could foster overdistention of some lung units during early inflation, causing neural inspiratory time to be shorter than in healthy subjects. We tested the hypothesis that a decrease in TI,vent causes tachypnea, prolongation of exhalation, and a decrease in intrinsic positive end-expiratory pressure (PEEP(i)). Ten patients with stable COPD received assist-control ventilation through a mouthpiece. Decreases in TI,vent, achieved through increases in flow from 30 to 90 L/min, increased frequency, from 16.1 +/- 1.0 (SE) to 20.8 +/- 1.5 breaths/min (p < 0.001), time for exhalation, from 2.1 +/- 0.2 to 2.3 +/- 0.2 s (p < 0.025), and decreased PEEP(i), from 7.0 +/- 1.3 to 6.4 +/- 1.1 cm H(2)O (p < 0.01). Decreases in TI,vent, achieved by decreasing inspiratory pause from 2 to 0 s, increased frequency, from 12.9 +/- 0.8 to 18.1 +/- 1.6 breaths/min (p < 0.001), time for exhalation, from 2.0 +/- 0.2 to 2.6 +/- 0.3 s (p < 0.001), and decreased PEEP(i), from 6.4 +/- 1.1 to 5.5 +/- 0.9 cm H(2)O (p < 0.01). In both experiments, decreases in TI,vent reduced inspiratory effort (p < 0.01). In conclusion, strategies to reduce TI,vent in patients with COPD caused tachypnea, yet prolonged the time for exhalation with consequent decrease in PEEP(i).

Autosomal-dominant giant platelet syndromes: a hint of the same genetic defect as in Fechtner syndrome owing to a similar genetic linkage to chromosome 22q11-13.

Families with 3 different syndromes characterized by autosomal dominant inheritance of low platelet count and giant platelets were studied. Fechtner syndrome is an autosomal-dominant variant of Alport syndrome manifested by nephritis, sensorineural hearing loss, and cataract formation in addition to macrothrombocytopenia and polymorphonuclear inclusion bodies. Sebastian platelet syndrome is an autosomal-dominant macrothrombocytopenia combined with neutrophil inclusions that differ from those found in May-Hegglin syndrome or Chediak-Higashi syndrome or the Dohle bodies described in patients with sepsis. These inclusions are, however, similar to those described in Fechtner syndrome. Other features of Alport syndrome, though, including deafness, cataracts, and nephritis, are absent in Sebastian platelet syndrome. Epstein syndrome is characterized by macrothrombocytopenia without neutrophil inclusions, in addition to the classical Alport manifestations-deafness, cataracts, and nephritis-and it is also inherited in an autosomal-dominant mode. We mapped the disease-causing gene to the long arm of chromosome 22 in an Italian family with Fechtner syndrome, 2 German families with the Sebastian platelet syndrome, and an American family with the Epstein syndrome. Four markers on chromosome 22q yielded an LOD score greater than 2.76. A maximal 2-point LOD score of 3.41 was obtained with the marker D22S683 at a recombination fraction of 0.00. Recombination analysis placed the disease-causing gene in a 3.37-Mb interval between the markers D22S284 and D22S693. The disease-causing gene interval in these 3 syndromes is similar to the interval described recently in an Israeli family with a slightly different Fechtner syndrome than the one described here. Recombination analysis of these 3 syndromes refines the interval containing the disease-causing gene from 5.5 Mb to 3.37 Mb. The clinical likeness and the similar interval containing the disease-causing gene suggest that the 3 different syndromes may arise from a similar genetic defect.

Does inhaled albuterol improve diaphragmatic contractility in patients with chronic obstructive pulmonary disease?

We tested the hypothesis that the decrease in dyspnea in patients with COPD with inhaled albuterol is in part due to increased diaphragmatic contractility. Eleven patients with COPD inhaled albuterol or placebo in a double-blind randomized manner. Subsequently, dyspnea was measured while patients breathed through inspiratory resistors, and diaphragmatic contractility was quantified during maximal inspiratory efforts and after twitch stimulation of the phrenic nerves. Albuterol produced a decrease in dyspnea (5 +/- 2 to 4 +/- 2 [SD] Borg units, p < 0.01), and increases in maximal transdiaphragmatic pressure (92.4 +/- 37.2 to 102.8 +/- 37.2 cm H(2)O, p < 0.03) and potentiated twitch transdiaphragmatic pressures (21.6 +/- 7.1 to 25.2 +/- 7.6 cm H(2)O, p < 0.02). The decrease in dyspnea correlated with the increases in maximal and twitch transdiaphragmatic pressures: r = -0.64 (p = 0. 04) and r = -0.65 (p = 0.04), respectively. Compared with placebo, albuterol produced an increase in inspiratory capacity (1.87 +/- 0. 71 to 2.26 +/- 0.74 L, p = 0.002), which accounted for the increases in maximal and twitch transdiaphragmatic pressures. The decrease in dyspnea correlated with the increase in inspiratory capacity (r = -0. 62, p = 0.04), but not with the increase in FEV(1) (r = -0.13, p = 0. 72). In conclusion, albuterol relieves dyspnea and enhances respiratory muscle output in patients with COPD primarily by improving the length-tension relationship of the diaphragm rather than by improving its contractility.

Influence of ventilator settings in determining respiratory frequency during mechanical ventilation.

During mechanical ventilation, changes in inspiratory flow and tidal volume (VT) have been shown to alter respiratory frequency (f ). However, the changes in flow and VT have been accompanied by alteration in ventilator inspiratory time (TI,(vent)), and it is not clear which variable is the primary determinant. To address this issue, we employed four protocols in 15 healthy volunteers receiving assist-control ventilation. When VT was fixed and flow was delivered at 30, 60, and 90 L/min, f increased as a function of the increase in flow and the decrease in TI,(vent). When flow was held constant and VT was changed among 0.5, 1.0, and 1.5 L, f increased as a function of the decreases in VT and TI,(vent). When flow was increased from 60 to 90 L/min and these changes were balanced with VT settings of 1.0 and 1.5 L to maintain a constant TI,(vent), f did not change. When flow and VT were held constant and TI,(vent) was varied by the application of inspiratory pauses (0 to 2 s), f decreased as a function of the increase in TI,(vent) (p < 0.001). In conclusion, the imposed ventilator inspiratory time during mechanical ventilation can determine f independently of delivered inspiratory flow and VT.

Can diaphragmatic contractility be assessed by twitch airway pressures in patients with chronic obstructive pulmonary disease?

In healthy subjects and in patients without lung diseases, twitch airway pressure (Paw(tw)) responses to phrenic nerve stimulation can be used to predict twitch esophageal pressure (Pes(tw)) and twitch transdiaphragmatic pressure (Pdi(tw)), thus overcoming the need for placement of esophageal and gastric balloons. The aim of this study was to determine whether measurements of Paw(tw) combined with simple maneuvers could be used to predict Pes(tw), and possibly Pdi(tw), in patients with severe chronic obstructive pulmonary disease (COPD) (n = 12). Stimulations delivered at relaxed FRC produced a correlation coefficient (r) between Paw(tw) and Pes(tw) of 0.44 (p < 0.001) and of 0.62 (p < 0.001) during stimulations while patients performed a gentle exhalation from FRC. Stimulations performed during a gentle inhalation produced a good correlation between Paw(tw) and Pes(tw) (r = 0.92, p < 0.001); however, the limits of agreement between Paw(tw) and Pes(tw) were wide. Correlations between Paw(tw) and Pdi(tw) during the three experimental conditions were weak. In conclusion, during a gentle inspiratory effort in patients with severe COPD the correlation between Paw(tw) and Pdi(tw) was weak, whereas the correlation between Paw(tw) and Pes(tw) was good, but it was not sufficient to allow the prediction of Pes(tw) from Paw(tw) in all patients.

Does resistive loading decrease diaphragmatic contractility before task failure?

While sustaining a load that leads to task failure, it is unclear whether diaphragmatic fatigue develops progressively or occurs only at task failure. We hypothesized that incremental loading produces a progressive decrease in diaphragmatic contractility ever before task failure. Ten subjects generated 60% of maximal transdiaphragmatic pressure (Pdimax) for 2 min, 4 min, and until task failure. Before loading, 20 min after each period of loading, and approximately 20 h after the last period of loading, Pdimax, nonpotentiated and potentiated Pdi twitch pressure (Pditw), and the pattern of respiratory muscle recruitment during a CO2 challenge were recorded. Sensation of inspiratory effort at the 4th min of the task-failure protocol was greater than at the same time in the preceding 4-min protocol. Surprisingly, potentiated Pditw and Pdimax were reduced after 2 min of loading and decreased further after 4 min of loading and after task failure; nonpotentiated Pditw was reduced after 4 min of loading and after task failure. The gastric pressure contribution to tidal breathing during a CO2 challenge decreased progressively in relation to duration of the preceding loading period, whereas expiratory muscle recruitment progressively increased. A rest period of approximately 20 h after task failure was not sufficient to normalize these alterations in respiratory muscle recruitment or fatigue-induced changes in diaphragmatic contractility. In conclusion, while sustaining a mechanical load, the diaphragm progressively fatigued, ever before task failure, and when challenged the rib cage-to-diaphragmatic contribution to tidal breathing and recruitment of the expiratory muscles increased pari passu with duration of the preceding loading.

Partitioning of lung and chest-wall mechanics before and after lung-volume-reduction surgery.

In the study reported here, we partitioned the mechanics of the respiratory system into lung and chest-wall components, using the rapid occlusion technique in seven patients with severe emphysema before lung-volume-reduction surgery and 3 mo later. Patients showed improvements in 6-min walk (p < 0.01) and dyspnea (p < 0.05). The resistances of the respiratory system and chest wall were not altered by surgery. Ohmic airway resistance did not change, but the component of lung resistance (DeltaRL) due to viscoelastic behavior (stress relaxation) and time-constant inhomogeneities (pendelluft) decreased in six patients (p < 0.03). Dynamic elastance of the lung (Edyn,L) decreased after surgery (p < 0.02), whereas dynamic elastance of the chest wall did not change. The ratio of dynamic intrinsic positive end-expiratory pressure (PEEPi) to static PEEPi, which also reflects viscoelastic properties and time-constant inhomogeneities, increased after surgery (p < 0.05). The decrease in dyspnea was related to the decrease in Edyn,L (r = 0.81, p = 0.03), and tended to be related to the decrease in DeltaRL (r = 0.71, p = 0. 07). In conclusion, lung-volume-reduction surgery decreased dynamic pressure dissipations caused by stress relaxation and time-constant inhomogeneities within lung tissue, and it had no effect on the static mechanical properties of the chest wall.

Respiratory muscle dysfunction in mechanically-ventilated patients.

The interaction between a patient and a ventilator is the major determinant of the amount of respiratory muscle rest achieved by the machine. We are beginning to acquire a better understanding of the mechanisms that underlie this complex interaction, but this information has yet to be integrated into the routine clinical management of ventilator-supported patients. To achieve that goal, we need better techniques of detecting and monitoring patient-ventilation asynchrony, and the development of simple algorithms that can minimize its occurrence. Finally, research is needed to determine the occurrence and importance of respiratory muscle fatigue during failed weaning attempts so as to better guide the timing and pace of the weaning process in problematic patients.