scholarly journals Explorations of Unilateral Diaphragmatic Paralysis

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Alexandre Quesnel ◽  
Françoise Beuret Blanquart ◽  
Jean Paul Marie ◽  
Eric Verin
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Esophageal Pressure ◽  
Diagnostic Value ◽  
Diaphragmatic Paralysis ◽  
Inspiratory Pressure ◽  
Maximal Inspiratory Pressure ◽  
Phrenic Nerve Stimulation ◽  
Diaphragmatic Dysfunction ◽  
Chest X Ray

Objective. The aim of the present study was to evaluate sniff test, maximal inspiratory pressure, and presence of paradoxical inspiratory diaphragmatic movements and their diagnostic value in patients referred for suspicion of diaphragmatic dysfunction. Methods. Twenty-two patients (8 men and 14 women, 58±13 years) with suspected diaphragmatic dysfunction were included. Pulmonary function test was evaluated by spirometry. Diaphragm dysfunction was diagnosed with unilateral phrenic nerve stimulation. Esophageal pressure was recorded during sniff test and maximal static inspiratory movements. Detection of paradoxical diaphragmatic movement was performed with anteroposterior projection of chest X-ray fluoroscopic video. Results. Phrenic nerve stimulation enabled diagnosis of diaphragmatic paralysis in 15 of the 22 patients. The remaining 7 patients had normal explorations. Lung volumes were significantly lower in patients with diaphragmatic paralysis than in control subjects, as maximal inspiratory pressure. No patient with normal diaphragmatic exploration had paradoxical inspiratory movement. The combined diagnostic value of reduced esophageal pressure during sniff test, reduced esophageal pressure during maximal static inspiratory movements, and presence of paradoxical inspiratory movement had a sensitivity of 87% and a specificity of 71%. Conclusion. Our results suggest that, in most cases, a combination of sniff test, maximal inspiratory pressure, and paradoxical inspiratory movement could help to diagnose diaphragmatic dysfunction. Nevertheless, phrenic nerve stimulation remains the best test for assessing diaphragmatic dysfunction.

Determinants of diaphragm motion in unilateral diaphragmatic paralysis

2004 ◽  
Vol 96 (1) ◽  
pp. 96-100 ◽  
Author(s):  
Pierre Scillia ◽  
Matteo Cappello ◽  
André De Troyer
Keyword(s):  
Clinical Practice ◽  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Diaphragmatic Paralysis ◽  
Phrenic Nerve Stimulation ◽  
Anesthetized Dogs ◽  
Diaphragm Motion ◽  
Cardinal Sign ◽  
Stimulation Of

Cranial displacement of a hemidiaphragm during sniffs is a cardinal sign of unilateral diaphragmatic paralysis in clinical practice. However, we have recently observed that isolated stimulation of one phrenic nerve in dogs causes the contralateral (inactive) hemidiaphragm to move caudally. In the present study, therefore, we tested the idea that, in unilateral diaphragmatic paralysis, the pattern of inspiratory muscle contraction plays a major role in determining the motion of the inactive hemidiaphragm. We induced a hemidiaphragmatic paralysis in six anesthetized dogs and assessed the contour of the diaphragm during isolated unilateral phrenic nerve stimulation and during spontaneous inspiratory efforts. Whereas the inactive hemidiaphragm moved caudally in the first instance, it moved cranially in the second. The parasternal intercostal muscles were then severed to reduce the contribution of the rib cage muscles to inspiratory efforts and to enhance the force generated by the intact hemidiaphragm. Although the change in pleural pressure (ΔPpl) was unaltered, the cranial displacement of the paralyzed hemidiaphragm was consistently reduced. A pneumothorax was finally induced to eliminate ΔPpl during unilateral phrenic nerve stimulation, and this enhanced the caudal displacement of the inactive hemidiaphragm. These observations indicate that, in unilateral diaphragmatic paralysis, the motion of the inactive hemidiaphragm is largely determined by the balance between the force related to ΔPpl and the force generated by the intact hemidiaphragm.

scholarly journals Phrenic nerve stimulation prevents diaphragm atrophy in patients with respiratory failure on mechanical ventilation

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Michal Soták ◽  
Karel Roubík ◽  
Tomáš Henlín ◽  
Tomáš Tyll
Keyword(s):  
Mechanical Ventilation ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Intervention Group ◽  
Ventilator Weaning ◽  
Control Group ◽  
Phrenic Nerve Stimulation ◽  
Diaphragm Thickness ◽  
Diaphragmatic Dysfunction ◽  
Diaphragm Atrophy

Abstract Background Diaphragm atrophy and dysfunction is a major problem among critically ill patients on mechanical ventilation. Ventilator-induced diaphragmatic dysfunction is thought to play a major role, resulting in a failure of weaning. Stimulation of the phrenic nerves and resulting diaphragm contraction could potentially prevent or treat this atrophy. The subject of this study is to determine the effectiveness of diaphragm stimulation in preventing atrophy by measuring changes in its thickness. Methods A total of 12 patients in the intervention group and 10 patients in the control group were enrolled. Diaphragm thickness was measured by ultrasound in both groups at the beginning of study enrollment (hour 0), after 24 hours, and at study completion (hour 48). The obtained data were then statistically analyzed and both groups were compared. Results The results showed that the baseline diaphragm thickness in the interventional group was (1.98 ± 0.52) mm and after 48 hours of phrenic nerve stimulation increased to (2.20 ± 0.45) mm (p=0.001). The baseline diaphragm thickness of (2.00 ± 0.33) mm decreased in the control group after 48 hours of mechanical ventilation to (1.72 ± 0.20) mm (p<0.001). Conclusions Our study demonstrates that induced contraction of the diaphragm by pacing the phrenic nerve not only reduces the rate of its atrophy during mechanical ventilation but also leads to an increase in its thickness – the main determinant of the muscle strength required for spontaneous ventilation and successful ventilator weaning. Trial registration: The study was registered with ClinicalTrials.gov (18/06/2018, NCT03559933, https://clinicaltrials.gov/ct2/show/NCT03559933).

Negative intrathoracic pressure decreases independently left ventricular filling and emptying

1989 ◽  
Vol 257 (1) ◽  
pp. H120-H131 ◽  
Author(s):  
J. Peters ◽  
C. Fraser ◽  
R. S. Stuart ◽  
W. Baumgartner ◽  
J. L. Robotham
Keyword(s):  
Stroke Volume ◽  
Nerve Stimulation ◽  
Lung Volume ◽  
Phrenic Nerve ◽  
Intrathoracic Pressure ◽  
Esophageal Pressure ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Phrenic Nerve Stimulation

The mechanism for the fall in left ventricular (LV) stroke volume with normal and obstructed inspiration is controversial with changes proposed in LV preload and afterload. During respiration extending over several cardiac cycles, changes in both LV filling and emptying could occur, rendering demonstration of any responsible mechanism difficult. To evaluate the independent effects of negative intrathoracic pressure (NITP) on LV filling and emptying, we have analyzed the effects of NITP confined to either diastole or systole using electrocardiogram (ECG)-triggered phrenic nerve stimulation in six anesthetized closed-chest dogs. Lung volume was either maintained by completely obstructing the airway or allowed to increase during NITP. With diastolic NITP and the airway obstructed during phrenic nerve stimulation, LV filling volume (integrated mitral flow) significantly decreased (-37 +/- 6.1% SE) associated with increases in LV and right atrial filling pressures at end diastole relative to both atmospheric and esophageal pressures. Right atrial pressure relative to either atmospheric or esophageal pressure increased significantly more than left atrial pressure. The ensuing LV stroke volume (integrated ascending aortic flow) decreased significantly (-30.8 +/- 5.9%). With NITP confined to systole and at constant LV preload, LV stroke volume also decreased (-12.9 +/- 2.5%) associated with an increase in LV systolic pressure relative to esophageal pressure. Similar significant changes were observed despite a smaller fall in esophageal pressure when lung volume was allowed to increase during either diastolic or systolic NITP. We conclude that 1) NITP confined to diastole decreases LV filling and the ensuing LV stroke volume, most likely by ventricular interdependence; 2) NITP confined to systole also decreases LV stroke volume, presumptively by imposing an increased afterload on the LV; 3) both diastolic and systolic mechanisms should contribute to a decreased LV stroke volume during normal and obstructed inspiration; and 4) if the effects of intrathoracic pressure changes were to extend over several cardiac cycles, mechanisms exist to account for either increases or decreases in LV volumes.

Insulation discontinuity in a vagus nerve stimulator lead: a treatable cause of intolerable stimulation-related symptoms

2010 ◽  
Vol 112 (4) ◽  
pp. 829-831 ◽  
Author(s):  
Mark C. Spitz ◽  
Ken R. Winston ◽  
Edward H. Maa ◽  
Steven G. Ojemann
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Nerve Stimulator ◽  
Phrenic Nerve Stimulation ◽  
Diaphragmatic Dysfunction ◽  
New Device ◽  
Vagus Nerve Stimulator ◽  
Left Vagus

Discontinuity in the silicone insulation over an electrode of a left vagus nerve stimulator (VNS) allowed the aberrant leak of current to the phrenic nerve and other structures. This resulted in ipsilateral diaphragmatic dysfunction, inability to vocalize, and severe radiating pain into the jaw and upper incisor for the duration of each stimulation. The device was explanted and a new device was implanted. All stimulation-related symptoms ceased immediately. A similar discontinuity in the silicone insulation is the likely explanation for several prior reports of poorly understood pains and phrenic nerve stimulation in patients with VNSs. The findings and analysis of this case establish a rationale for consideration of replacement of the VNS lead in all similarly symptomatic patients.

Site of phrenic nerve stimulation-induced upper airway collapse: influence of expiratory time

2002 ◽  
Vol 92 (2) ◽  
pp. 665-671 ◽  
Author(s):  
F. Sériès ◽  
G. Éthier
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Emg Activity ◽  
Phrenic Nerve Stimulation ◽  
Nasal Breathing ◽  
Expiratory Time ◽  
Airway Collapse

Electrical phrenic nerve stimulation (EPNS) applied at end expiration during exclusive nasal breathing can be used to characterize upper airway (UA) dynamics during wakefulness by dissociating phasic activation of UA and respiratory muscles. The UA level responsible for the EPNS-induced increase in UA resistance is unknown. The influence of the twitch expiratory timing (200 ms and 2 s) on UA resistance was studied in nine normal awake subjects by looking at instantaneous flow, esophageal and pharyngeal pressures, and genioglossal electromyogram (EMG) activity during EPNS at baseline and at −10 cmH2O. The majority of twitches had a flow-limited pattern. Twitches realized at 200 ms and 2 s did not differ in their maximum inspiratory flows, but esophageal pressure measured at maximum inspiratory flow was significantly less negative with late twitches (−6.6 ± 2.7 and −5.0 ± 3.0 cmH2O respectively, P = 0.04). Pharyngeal resistance was higher when twitches were realized at 2 s than at 200 ms (6.4 ± 2.4 and 2.7 ± 1.1 cmH2O · l−1 · s, respectively). EMG activity significant rose at peak esophageal pressure with a greater increase for late twitches. We conclude that twitch-induced UA collapse predominantly occurs at the pharyngeal level and that UA stability assessed by EPNS depends on the expiratory time at which twitches are performed.

Assessment of neonatal diaphragmatic paralysis using magnetic phrenic nerve stimulation

1999 ◽  
Vol 27 (3) ◽  
pp. 224-226 ◽  
Author(s):  
G.F. Rafferty ◽  
A. Greenough ◽  
G. Dimitriou ◽  
M. I. Polkey ◽  
A. Long ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Diaphragmatic Paralysis ◽  
Phrenic Nerve Stimulation

Botzinger complex region role in phrenic-to-phrenic inhibitory reflex of cat

1989 ◽  
Vol 67 (4) ◽  
pp. 1364-1370 ◽  
Author(s):  
D. F. Speck
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Inhibitory Response ◽  
Phrenic Nerve Stimulation ◽  
Bötzinger Complex ◽  
Before And After ◽  
Pass Through ◽  
Bilateral Lesions ◽  
Decerebrate Cats ◽  
Inhibitory Reflex

Neuronal recordings, microstimulation, and electrolytic and chemical lesions were used to examine the involvement of the Botzinger Complex (BotC) in the bilateral phrenic-to-phrenic inhibitory reflex. Experiments were conducted in decerebrate cats that were paralyzed, ventilated, thoracotomized, and vagotomized. Microelectrode recordings within the BotC region revealed that some neurons were activated by phrenic nerve stimulation (15 of 69 expiratory units, 9 of 67 inspiratory units, and 19 nonrespiratory-modulated units) at average latencies similar to the onset latency of the phrenic-to-phrenic inhibition. In addition, microstimulation within the BotC caused a short latency transient inhibition of phrenic motor activity. In 17 cats phrenic neurogram responses to threshold and supramaximal (15 mA) stimulation of phrenic nerve afferents were recorded before and after electrolytic BotC lesions. In 15 animals the inhibitory reflex was attenuated by bilateral lesions. Because lesion of either BotC neurons or axons of passage could account for this attenuation, in eight experiments the phrenic-to-phrenic inhibitory responses were recorded before and after bilateral injections of 5 microM kainic acid (30–150 nl) into the BotC. After chemical lesions, the inhibitory response to phrenic nerve stimulation remained; however, neuronal activity typical of the BotC could not be located. These results suggest that axons important in producing the phrenic-to-phrenic reflex pass through the region of the BotC, but that BotC neurons themselves are not necessary for this reflex.

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