Franco Laghi

Loyola University, New Orleans, Louisiana, United States

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Publications (103)471.83 Total impact

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    ABSTRACT: Ultrasound measurements of diaphragm thickness (T di) and thickening (TFdi) may be useful to monitor diaphragm activity and detect diaphragm atrophy in mechanically ventilated patients. We aimed to establish the reproducibility of measurements in ventilated patients and determine whether passive inflation by the ventilator might cause thickening apart from inspiratory effort. Five observers measured T di and TFdi in 96 mechanically ventilated patients. The probe site was marked in 66 of the 96 patients. TFdi was measured at peak and end-inspiration (airway occluded and diaphragm relaxed) in nine healthy volunteers inhaling to varying lung volumes. The association with diaphragm electrical activity was quantified. Right hemidiaphragm thickness was obtained on 95 % of attempts; left hemidiaphragm measurements could not be obtained consistently. Right hemidiaphragm thickness measurements were highly reproducible (mean ± SD 2.4 ± 0.8 mm, repeatability coefficient 0.2 mm, reproducibility coefficient 0.4 mm), particularly after marking the location of the probe. TFdi measurements were only moderately reproducible (median 11 %, IQR 3-17 %, repeatability coefficient 17 %, reproducibility coefficient 16 %). TFdi and diaphragm electrical activity were positively correlated, r (2) = 0.32, p < 0.01). At inspiratory volumes below 50 % of inspiratory capacity, passive inflation did not cause diaphragm thickening. TFdi was considerably lower in patients on either partially assisted or controlled ventilation compared to healthy subjects (median 11 vs. 35 %, p < 0.001). Ultrasound measurements of right hemidiaphragm thickness are feasible and highly reproducible in ventilated patients. At clinically relevant inspiratory volumes, diaphragm thickening reflects muscular contraction and not passive inflation. This technique can be reliably employed to monitor diaphragm thickness, activity, and function during mechanical ventilation.
    Intensive Care Medicine 02/2015; 41(4). DOI:10.1007/s00134-015-3687-3 · 7.21 Impact Factor
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    ABSTRACT: Muscle-mass loss augers increased morbidity and mortality in critically ill patients. Muscle-mass loss can be assessed by wide linear-array ultrasound transducers connected to cumbersome, expensive console units. Whether cheaper, hand-carried units equipped with curved-array transducers can be used as alternatives is unknown. Accordingly, our primary aim was to investigate in 15 nondisabled subjects the validity of measurements of rectus femoris cross-sectional area by using a curved-array transducer against a linear-array transducer-the reference-standard technique. In these subjects, we also determined the reliability of measurements obtained by a novice operator versus measurements obtained by an experienced operator. Lastly, the relationship between quadriceps strength and rectus area recorded by two experienced operators with a curved-array transducer was assessed in 17 patients with chronic obstructive pulmonary disease (COPD). In nondisabled subjects, the rectus cross-sectional area measured with the curved-array transducer by the novice and experienced operators was valid (intraclass correlation coefficient [ICC]: 0.98, typical percentage error [%TE]: 3.7%) and reliable (ICC: 0.79, %TE: 9.7%). In the subjects with COPD, both reliability (ICC: 0.99) and repeatability (%TE: 7.6% and 9.8%) were high. Rectus area was related to quadriceps strength in COPD for both experienced operators (coefficient of determination: 0.67 and 0.70). In conclusion, measurements of rectus femoris cross-sectional area recorded with a curved-array transducer connected to a hand-carried unit are valid, reliable, and reproducible, leading us to contend that this technique is suitable for cross-sectional and longitudinal studies.
    The Journal of Rehabilitation Research and Development 12/2014; 51(7):1155-64. DOI:10.1682/JRRD.2013.08.0187 · 1.43 Impact Factor
  • Franco Laghi · Nausica D'Alfonso · Martin J Tobin ·

    Intensive Care Medicine 08/2014; 40(10). DOI:10.1007/s00134-014-3448-8 · 7.21 Impact Factor
  • Hameeda Shaikh · Daniel Morales · Franco Laghi ·
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    ABSTRACT: For many critically ill patients admitted to an intensive care unit, the insertion of an endotracheal tube and the initiation of mechanical ventilation (MV) can be lifesaving procedures. Subsequent patient care often requires intensivists to manage the complex interaction of multiple failing organ systems. The shift in the intensivists' focus toward the discontinuation of MV can thus occur late in the course of critical illness. The dangers of MV, however, make it imperative to wean patients at the earliest possible time. Premature weaning trials, however, trigger significant respiratory distress, which can cause setbacks in the patient's clinical course. Premature extubation is also risky. To reduce delayed weaning and premature extubation, a three-step diagnostic strategy is suggested: measurement of weaning predictors, a trial of unassisted breathing (T-tube trial), and a trial of extubation. Since each step constitutes a diagnostic test, clinicians must not only command a thorough understanding of each test but must also be aware of the principles of clinical decision making when interpreting the information generated by each step. Many difficult aspects of pulmonary pathophysiology encroach on weaning management. Accordingly, weaning commands sophisticated, individualized care. Few other responsibilities of an intensivist require a more analytical effort and carry more promise for improving patient outcome than the application of physiologic principles in the weaning of patients.
    Seminars in Respiratory and Critical Care Medicine 08/2014; 35(4):451-468. DOI:10.1055/s-0034-1381953 · 2.71 Impact Factor
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    ABSTRACT: We hypothesized that improved diaphragmatic neuromechanical coupling during inspiratory loading is not sufficient to prevent alveolar hypoventilation and task failure, and that the latter results primarily from central-output inhibition of the diaphragm and air hunger rather than contractile fatigue. Eighteen subjects underwent progressive inspiratory loading. By task failure all developed hypercapnia. Tidal transdiaphragmatic pressure (ΔPdi) and diaphragmatic electrical activity (ΔEAdi) increased during loading–the former more than the latter; thus, neuromechanical coupling (ΔPdi/ΔEAdi) increased during loading. Progressive increase in extra-diaphragmatic muscle contribution to tidal breathing, expiratory muscle recruitment, and decreased end-expiratory lung volume contributed to improved neuromechanical coupling. At task failure, subjects experienced intolerable breathing discomfort, at which point mean ΔEAdi was 74.9 ± 4.9% of maximum, indicating that the primary mechanism of hypercapnia was submaximal diaphragmatic recruitment. Contractile fatigue was an inconsistent finding. In conclusion, hypercapnia during acute loading primarily resulted from central-output inhibition of the diaphragm suggesting that acute loading responses are controlled by the cortex rather than bulbopontine centers.
    Respiratory Physiology & Neurobiology 07/2014; 198(1). DOI:10.1016/j.resp.2014.03.004 · 1.97 Impact Factor
  • Franco Laghi · Nausica D'Alfonso · Martin J Tobin ·
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    ABSTRACT: Because the diaphragm is essential for survival, we wondered if it might be less vulnerable to the long-lasting effects of fatigue than limb muscles. Using a recently introduced magnetic probe to activate the phrenic nerves, we followed the evolution of twitch transdiaphragmatic pressure after inducing fatigue in healthy volunteers. Twenty-four hours after its induction, diaphragmatic fatigue had not fully recovered. Findings from this study later served as the foundation for incorporating a once-daily, T-tube-trial arm into a randomized controlled trial of techniques for ventilator weaning in intensive care unit patients and also influenced the design of a controlled trial of the weaning of tracheostomy patients who required prolonged ventilation. The research methodology was later employed to determine whether low-frequency fatigue is responsible for weaning failure. Employing a further modification of the technique-twitch airway pressure-it became evident that respiratory muscle weakness is a greater problem than fatigue in ventilated patients. Twitch airway pressure is now being used to document the prevalence and consequences of ventilator-induced respiratory muscle weakness. Our study-which began with a circumscribed, simple question-has yielded dividends in unforeseen directions, illustrating the fruitfulness of research into basic physiological mechanisms.
    Intensive Care Medicine 05/2014; 40(9). DOI:10.1007/s00134-014-3340-6 · 7.21 Impact Factor
  • Hameeda Shaikh · Franco Laghi ·

    Critical care medicine 03/2014; 42(3):737-8. DOI:10.1097/CCM.0000000000000002 · 6.31 Impact Factor
  • Franco Laghi · Hameeda Shaikh ·

    Critical care medicine 02/2014; 42(2):492-4. DOI:10.1097/CCM.0000000000000003 · 6.31 Impact Factor
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    ABSTRACT: Breathing-retraining and helium-oxygen (heliox) have been used to improve exercise tolerance in COPD. We hypothesized that, in patients with COPD, exercise duration after exercise-training plus breathing-retraining and oxygen would be longer than after exercise-training plus heliox or after exercise-training plus oxygen alone. We also explored the short-term maintenance of gains in exercise duration after using each technique. Of 192 COPD patients recruited, 103 were randomly assigned to exercise-training plus heliox (n = 33), exercise-training plus breathing-retraining and oxygen (n = 35) and exercise-training and oxygen (n = 35). FiO2 was 0.30 during testing and training in all groups. Patients exercised on a treadmill thrice-weekly for eight weeks. Before, at completion of training, and six-weeks later, patients underwent constant-load treadmill testing. At completion of training, improvements in exercise duration in the heliox and breathing-retraining groups were not significantly different. Compared to the exercise-training plus oxygen group, exercise duration improved more in the breathing-retraining group (P = 0.008) but not in the heliox group (P = 0.142). Hyperinflation was reduced with breathing-retraining plus oxygen compared to the other two groups. Six-weeks later, improvements in exercise duration were still greater with breathing-retraining than with exercise-training (P = 0.015). In contrast, improvements in exercise duration with heliox did not differ from those in the other two groups. In moderate-to-severe COPD, exercise-training combined with either heliox or with breathing-retraining yielded not significantly different improvements in exercise duration - with only the latter being superior to exercise-training. Six-weeks after training, these improvements were still greater after exercise-training plus breathing-retraining than after exercise-training.; No.: NCT00123422.
    Respiratory medicine 11/2013; 108(2). DOI:10.1016/j.rmed.2013.10.023 · 3.09 Impact Factor
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    ABSTRACT: A 56-year-old woman with a history of paraplegia and chronic pain due to neuromyelitis optica (Devic's syndrome) was admitted to a spinal cord injury unit for management of a sacral decubitus ulcer. During the hospitalization, she required emergency transfer to the intensive care unit (ICU) because of progressive deterioration of respiratory muscle function, severe respiratory acidosis, obtundation and hypotension. Upon transfer to the ICU, arterial blood gas revealed severe acute-on-chronic respiratory acidosis (pH 7.00, PCO2 120 mm Hg, PO2 211 mm Hg). The patient was immediately intubated and mechanically ventilated. Intravenous fluid boluses of normal saline (10.5 L in about 24 h) and vasopressors were started with rapid correction of hypotension. In addition, she was given hydrocortisone. Within 40 min of initiation of mechanical ventilation, there was improvement in acute respiratory acidosis. Sixteen hours later, however, the patient developed life-threatening hypokalemia (K(+) of 2.1 mEq/L) and hypomagnesemia (Mg of 1.4 mg/dL). Despite aggressive potassium supplementation, hypokalemia continued to worsen over the next several hours (K(+) of 1.7 mEq/L). Urine studies revealed renal potassium wasting. We reason that the recalcitrant life-threatening hypokalemia was caused by several mechanisms including total body potassium depletion (chronic respiratory acidosis), a shift of potassium from the extracellular to intracellular space (rapid correction of respiratory acidosis with mechanical ventilation), increased sodium delivery to the distal nephron (normal saline resuscitation), hyperaldosteronism (secondary to hypotension plus administration of hydrocortisone) and hypomagnesemia. We conclude that rapid correction of respiratory acidosis, especially in the setting of hypotension, can lead to life-threatening hypokalemia. Serum potassium levels must be monitored closely in these patients, as failure to do so can lead to potentially lethal consequences.
    Heart & lung: the journal of critical care 05/2013; 42(4). DOI:10.1016/j.hrtlng.2013.03.004 · 1.29 Impact Factor
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    EC Goligher · F Laghi · ND Ferguson ·

    Critical Care 03/2013; 17(2). DOI:10.1186/cc12083 · 4.48 Impact Factor
  • Martin J Tobin · Franco Laghi · Amal Jubran ·
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    ABSTRACT: The development of acute ventilatory failure represents an inability of the respiratory control system to maintain a level of respiratory motor output to cope with the metabolic demands of the body. The level of respiratory motor output is also the main determinant of the degree of respiratory distress experienced by such patients. As ventilatory failure progresses and patient distress increases, mechanical ventilation is instituted to help the respiratory muscles cope with the heightened workload. While a patient is connected to a ventilator, a physician's ability to align the rhythm of the machine with the rhythm of the patient's respiratory centers becomes the primary determinant of the level of rest accorded to the respiratory muscles. Problems of alignment are manifested as failure to trigger, double triggering, an inflationary gas-flow that fails to match inspiratory demands, and an inflation phase that persists after a patient's respiratory centers have switched to expiration. With recovery from disorders that precipitated the initial bout of acute ventilatory failure, attempts are made to discontinue the ventilator (weaning). About 20% of weaning attempts fail, ultimately, because the respiratory controller is unable to sustain ventilation and this failure is signaled by development of rapid shallow breathing. Substantial advances in the medical management of acute ventilatory failure that requires ventilator assistance are most likely to result from research yielding novel insights into the operation of the respiratory control system. © 2012 American Physiological Society. Compr Physiol 2:2871-2921, 2012.
    Comprehensive Physiology 10/2012; 2(4):2871-2921. DOI:10.1002/cphy.c110030 · 4.74 Impact Factor
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    Franco Laghi · Rafael Fernandez ·

    Intensive Care Medicine 08/2012; 38(10):1583-5. DOI:10.1007/s00134-012-2680-3 · 7.21 Impact Factor
  • Franco Laghi ·

    Critical care medicine 08/2012; 40(8):2525-6. DOI:10.1097/CCM.0b013e318258ebc5 · 6.31 Impact Factor
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    ABSTRACT: Most patients with chronic obstructive pulmonary disease (COPD) are middle-aged or older, and by definition all have a chronic illness. Aging and chronic illness decrease sexual interest, sexual function, and testosterone levels. To date, researchers have not simultaneously explored prevalence, risk factors, and impact of sexual dysfunctions on quality of life and survival in men with COPD. We tested three hypotheses: First, sexual dysfunctions, including erectile dysfunction, are highly prevalent and impact negatively the quality of life of those with COPD. Second, gonadal state is a predictor of erectile dysfunction. Third, erectile dysfunction, a potential maker of systemic atherosclerosis, is a risk factor for mortality in men with COPD. In this prospective study, sexuality was assessed in 90 men with moderate-to-severe COPD (40 hypogonadal) by questionnaire. Testosterone levels, comorbidities, dyspnea, depressive symptoms, and survival (4.8 years median follow-up) were recorded. Seventy-four percent of patients had at least one sexual dysfunction, with erectile dysfunction being the most common (72 %). Most were dissatisfied with their current and expected sexual function. Severity of COPD was equivalent in patients with and without erectile dysfunction. Low testosterone, depressive symptoms, and presence of partner were independently associated with erectile dysfunction. Severity of lung disease and comorbidities, but not erectile dysfunction, were independently associated with mortality (p = 0.006). Sexual dysfunctions, including erectile dysfunction, were highly prevalent and had a negative impact on quality of life in men with COPD. In addition, gonadal state was an independent predictor of erectile dysfunction. Finally, erectile dysfunction was not associated with all-cause mortality.
    Beiträge zur Klinik der Tuberkulose 07/2012; 190(5):545-56. DOI:10.1007/s00408-012-9398-4 · 2.27 Impact Factor
  • Brian Canavan · Franco Laghi · Martin J. Tobin · Amal Jubran ·

    American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012
  • David J. McElligott · Eileen G. Collins · Franco Laghi ·

    American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012
  • Kendra Hammond · Jobby Mampilly · Franco A. Laghi · Amal Jubran · Martin J. Tobin ·

    American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012

  • American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012

  • American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California; 05/2012

Publication Stats

2k Citations
471.83 Total Impact Points


  • 2008-2014
    • Loyola University
      New Orleans, Louisiana, United States
    • University of Alberta
      Edmonton, Alberta, Canada
  • 2005-2014
    • Loyola University Chicago
      • Stritch School of Medicine
      Chicago, Illinois, United States
  • 1995-2014
    • Edward Hines, Jr. VA Hospital
      Hines, Oregon, United States
  • 2011
    • U.S. Department of Veterans Affairs
      Washington, Washington, D.C., United States
  • 2007-2010
    • Loyola University Medical Center
      • Division of Pulmonary and Critical Care Medicine
      Maywood, Illinois, United States