Diaphragmatic relaxation rate after voluntary contractions and uni- and bilateral phrenic stimulation

We compared the rate of relaxation of the diaphragm (RRdi) after unilateral phrenic nerve stimulation, bilateral phrenic nerve stimulations, and short sharp voluntary contractions (sniffs). RRdi was measured as the maximum rate of decline in transdiaphragmatic pressure (Pdi) corrected for the change in Pdi [maximum relaxation rate (MRR)/delta Pdi], the time constant (tau) of the later exponential decline in Pdi, and the time to half relaxation (1/2 RT). In five subjects there was no difference in mean RRdi apart from a smaller MRR/delta Pdi (P less than 0.05) for left unilateral compared with either right unilateral or bilateral needle stimulation. However, RRdi varied unpredictably between unilateral and bilateral stimulation of the phrenic nerve in individual subjects. In the same five subjects, sniffs were found to have a slower RRdi than bilateral stimulations (MRR/delta Pdi 0.0064 +/- 0.0007 vs. 0.0074 +/- 0.0018/ms, tau 57.2 +/- 8.7 vs. 48.2 +/- 7.4 ms, 1/2 RT 108.9 +/- 10.9 vs. 73.9 +/- 6.0 ms; all P less than 0.05). The application and inflation of an abdominal binder to an external pressure of 60 mmHg resulted in a decrease in functional residual capacity (-710 +/- 70 ml), but there was no effect on relaxation parameters. Our findings suggest that in the evaluation of RRdi 1) unilateral hemidiaphragmatic stimulations may not accurately reflect the in vivo contractile properties of the diaphragm, 2) sniff maneuvers are not voluntary equivalents of phrenic nerve stimulations, and 3) RRdi is not affected by abdominal binder inflation up to 60 mmHg.     

Effects of phrenic nerve cooling on diaphragmatic function

The effects of phrenic nerve cooling at 0 degrees C on the nerve and diaphragmatic function were evaluated in dogs. Eleven dogs, anesthetized and mechanically ventilated, were studied. Left diaphragmatic function was assessed by recording the transdiaphragmatic pressure (Pdi) generated during electrical stimulation of the left phrenic nerve at different frequencies (0.5, 30, and 100 Hz). Phrenic nerve stimulations were achieved either directly by electrodes placed around the phrenic nerve above its pericardial course or by intramuscular electrodes placed close to the phrenic nerve endings. Electrical activity of the hemidiaphragm (Edi) was recorded and phrenic nerve conduction time (PNCT) was measured during direct phrenic stimulation. A transpericardial cooling of the nerve, at 0 degrees C, on a length of 1 cm, was performed during 30 min (group A, n = 7) or 5 min (group B, n = 4). After the cooling period, phrenic and diaphragmatic functions were assessed hourly for 4 h (H1-H4). Cooling the phrenic nerve produced a complete phrenic nerve conduction block in all dogs, 100 +/- 10 s after the onset of cold exposure. Conduction recovery time was longer in group A (11 +/- 7 min) than in group B (2 +/- 0.5 min) and PNCT remained increased throughout the study in group A. Furthermore, in group A, Pdi and Edi during direct phrenic stimulation were markedly depressed from H1 to H4. No change in these parameters was noted until H3 during intramuscular stimulation, time at which a significant decrease occurred. By contrast, Pdi and Edi from direct and intramuscular stimulations remained unchanged throughout the study in group B.(ABSTRACT TRUNCATED AT 250 WORDS)     

Attenuation of phrenic motor discharge by phrenic nerve afferents

Short latency phrenic motor responses to phrenic nerve stimulation were studied in anesthetized, paralyzed cats. Electrical stimulation (0.2 ms, 0.01-10 mA, 2 Hz) of the right C5 phrenic rootlet during inspiration consistently elicited a transient reduction in the phrenic motor discharge. This attenuation occurred bilaterally with an onset latency of 8-12 ms and a duration of 8-30 ms. Section of the ipsilateral C4-C6 dorsal roots abolished the response to stimulation, thereby confirming the involvement of phrenic nerve afferent activity. Stimulation of the left C5 phrenic rootlet or the right thoracic phrenic nerve usually elicited similar inhibitory responses. The difference in onset latency of responses to cervical vs. thoracic phrenic nerve stimulation indicates activation of group III afferents with a peripheral conduction velocity of approximately 10 m/s. A much shorter latency response (5 ms) was evoked ipsilaterally by thoracic phrenic nerve stimulation. Section of either the C5 or C6 dorsal root altered the ipsilateral response so that it resembled the longer latency contralateral response. The low-stimulus threshold and short latency for the ipsilateral response to thoracic phrenic nerve stimulation suggest that it involves larger diameter fibers. Decerebration, decerebellation, and transection of the dorsal columns at C2 do not abolish the inhibitory phrenic-to-phrenic reflex.     

Bilateral phrenic stimulation: a simple technique to assess diaphragmatic fatigue in humans

Transdiaphragmatic pressure (Pdi) and the rate of relaxation of the diaphragm (tau) were measured at functional residual capacity (FRC) in six normal seated subjects during single-twitch stimulation of both phrenic nerves. The latter were stimulated supramaximally with needle electrodes with square-wave impulses of 0.1-ms duration at 1 Hz before and after diaphragmatic fatigue produced by resistive loaded breathing. Constancy of chest wall configuration was achieved by monitoring the diameter of the abdomen and the rib cage with a respiratory inductive plethysmograph system. During control the peak Pdi generated during the phrenic stimulation amounted to 34.4 +/- 4.2 (SE) cmH2O and represented in each subject a fixed fraction (17%) of its maximal transdiaphragmatic pressure. After diaphragmatic fatigue the peak Pdi decreased by an average of 45%, amounting to 18.1 +/- 2.7 cmH2O 5 min after the fatigue run, and tau increased from 55.2 +/- 9 ms during control to 77 +/- 8 ms 5 min after the fatigue run. The decrease in peak Pdi and the increase in tau observed after the fatigue run persisted throughout the 30 min of the recovery period studied, the peak Pdi amounting to 18.4 +/- 2.8 and 18.9 +/- 3.3 cmH2O and tau to 81.3 +/- 5.7 and 88.7 +/- 10 ms at 15 and 30 min after the end of the fatigue run, respectively. It is concluded that diaphragmatic fatigue can be detected in man by bilateral phrenic stimulation with needle electrodes without any discomfort for the subject and that the decrease in diaphragmatic strength after fatigue is long lasting.     

Changes in rate of relaxation of sniffs with diaphragmatic fatigue in humans

The rate of relaxation of the diaphragm after stimulated (4 subjects) and voluntary (8 subjects) contractions was compared in normal young men. Stimulated contractions were induced by supramaximal unilateral phrenic nerve stimulation and voluntary contractions by short, sharp sniffs of varying tensions against an occluded airway. The rate of relaxation of the diaphragm was calculated from the rate of decline of transdiaphragmatic pressure (Pdi). In both conditions the maximum relaxation rate (MRR) was proportional to the peak transdiaphragmatic pressure (Pdi), whereas the time constant (tau) of the later exponential decline in Pdi was independent of Pdi. The mean +/- SE rate constant of relaxation (MRR/Pdi) was 0.0078 +/- 0.0002 ms-1 and the mean tau was 57 +/- 3.8 ms for stimulated contractions. The rate of relaxation after sniffs was not different, and it was not affected by either the lung volume at which occluded sniffs were performed (in the range of residual volume to functional residual capacity + 1 liter) or by the relative contribution gastric pressure made to Pdi. After diaphragmatic fatigue was induced by inspiring against a high alinear resistance there was a decrease in relaxation rate. In the 1st min postfatigue MRR/Pdi decreased (0.0063 +/- 0.0003 ms-1; P less than 0.005) and tau increased (83 +/- 5 ms; P less than 0.005). Both values returned to prefatigue levels within 5 min of the end of the studies. We conclude that the sniff may prove to be clinically useful in the detection of diaphragmatic fatigue.     

Cardiovascular failure and apnea in shock

A model of shock was developed in anesthetized dogs by limiting venous return with a balloon inflated in the right atrium. The change in ventilation (VE) in response to a sustained decrease in arterial pressure (Pa) to 50-60 Torr was studied by recording transdiaphragmatic pressure (Pdi) and diaphragm (Edi) and parasternal intercostal (Eic) electrical activity. Four dogs died of cardiac arrest after 20-60 min. In 11 dogs, VE, after an initial increase, decreased progressively until apnea occurred after 103 +/- 24 min, after 60% reductions in breathing frequency, Pdi, and Eic and a 30% fall in Edi. No decrease in diaphragm contractility was found in response to artificial phrenic nerve stimulation. The cardiocirculatory function deteriorated during shock until it became irreversible at apneic time. No recovery from apnea occurred without a recovery of Pa. We conclude that the fall in VE and ensuing apnea in this model resulted from a decrease in central respiratory neural output associated with a progressive deterioration of the cardiocirculatory function.     

Relationship among EMG and contractile responses of the diaphragm elicited by hypotension

In a canine model, we investigated the effects of severe hypotension on the indexes of diaphragmatic failure. We measured 1) the transdiaphragmatic pressure obtained in response to 20- and 100-Hz stimulation of phrenic nerves (Pdi20 and Pdi100), 2) the power spectrum of diaphragmatic electromyogram (EMG), 3) the ratio of integrated diaphragmatic EMG to Pdi (Edi/Pdi), and 4) the rate of relaxation of Pdi100 and Pdi20. Arterial blood pressure (Pa) was reduced to 40-50 mmHg by a balloon inflated in the inferior vena cava and was maintained at this level until Pdi100 declined to 75% of the control value (100% shock time, ST). A recovery period of 60 min at normal Pa was allowed. During hypotension, Pdi100 and Pdi20 declined only at 100% ST [95.0 +/- 13.0 (SE) min]; however, only Pdi100 recovered within 15 min. The power spectrum shifted to low frequencies early and progressively during shock period. Edi/Pdi rose significantly at 80 and 100% ST and recovered within 15 min. The relaxation rate of Pdi20 and Pdi100 increased significantly at 100% ST only. We conclude that 1) diaphragmatic contractility is depressed during severe hypotension, 2) changes in the power spectrum occurred first in the shock state, followed by alterations in Edi/Pdi, and subsequently both changes in the frequency-pressure curve and relaxation rate occurred last.     

Contractile properties of the human diaphragm in vivo

The mechanical properties of the human diaphragm have been studied at fractional residual capacity in normal seated subjects with closed glottis. The transdiaphragmatic pressure (Pdi) developed in response to single shocks or to trains of stimuli at increasing frequency was approximately 3 times greater during bilateral than unilateral stimulation. During unilateral phrenic nerve stimulation the Pdi twitches increased as the interval (0-200 ms) of a preceding conditioning stimulus to the contralateral phrenic nerve was decreased suggesting that the two hemidiaphragms are mechanically coupled in series. The contraction time and half-relaxation time of single bilateral twitches as well as the Pdi-frequency relationship (5-35 Hz) during bilateral tetanic stimulation indicate that the contractile properties of the human diaphragm are intermediate between those of fast- and slow-twitch muscle fibers. The results suggest that the contractile properties of the human diaphragm are well illustrated by single bilateral twitches recorded from the relaxed muscle, but that the responses to unilateral stimulation are misleading due to distortion by abnormal changes in the muscle geometry.     

Cervical magnetic stimulation: a new painless method for bilateral phrenic nerve stimulation in conscious humans

Assessing diaphragmatic contractility is a common goal in various situations. This assessment is mainly based on static or dynamic maximal voluntary maneuvers and twitch transdiaphragmatic pressures (Pdi) obtained by stimulation of the phrenic nerves (PS). PS eliminates the central components of diaphragmatic activation, but the available techniques of PS remain subject to some limitations. Transcutaneous PS is painful, and needle PS is potentially dangerous. Time-varying magnetic fields can stimulate nervous structures without pain and without adverse effects. In six subjects, we have studied cervical magnetic stimulation (CMS) as a method of PS. We have compared the stimulated Pdi (Pdistim) with the maximal Pdi obtained during static combined expulsive-Mueller maneuver (Pdimax) and with the Pdi generated during a sniff test (Pdisniff). CMS produced twitch Pdi averaging 33.4 +/- 9.7 cmH2O. Pdistim/Pdimax and Pdistim/Pdisniff were 24 +/- 6 and 41 +/- 14%, respectively. These values are comparable to those obtained in other studies with transcutaneous PS. They were highly reproducible in all the subjects. Electromyographic data provided evidence of bilateral maximal stimulation. CMS is a nonspecific method and may stimulate various nervous structures. However, diaphragmatic contraction was elicited by stimulation of the phrenic trunk, since the phrenicodiaphragmatic latencies (less than 7 ms) were in the range of values reported with direct stimulation of the trunk. Cocontraction of neck muscles, including the sternomastoid, was present, but its influence in the CMS-induced Pdi seems minimal. We conclude that magnetic stimulation is an easy, well-tolerated, reproducible safe, and valuable method to assess phrenic conduction and diaphragmatic twitch response.     

Validation of improved recording site to measure phrenic conduction from surface electrodes in humans.

Phrenic nerve stimulation, electrical (ES) or from cervical magnetic stimulation (CMS), allows one to assess the diaphragm contractile properties and the conduction time of the phrenic nerve (PNCT) through recording of an electromyographic response, traditionally by using surface electrodes. Because of the coactivation of extradiaphragmatic muscles, signal contamination can jeopardize the determination of surface PNCTs. To address this, we compared PNCTs with ES and CMS from surface and needle diaphragm electrodes in five subjects (10 phrenic nerves). At a modified recording site, lower and more anterior than usual (lowest accessible intercostal space, costochondral junction) with electrodes 2 cm apart, surface and needle PNCTs were similar (CMS: 6.0 +/- 0.25 ms surface vs. 6.2 +/- 0.13 ms needle, not significant). Electrodes recording the activity of the most likely sources of signal contamination, i.e., the serratus anterior and pectoralis major, showed distinct responses from that of the diaphragm, their earlier occurrence strongly arguing against contamination. With ES and CMS, apparently uncontaminated signals could be consistently recorded from surface electrodes.     

Electrical activity of phrenic nerve and diaphragm in utero.

Phrenic nerve activity, diaphragmatic EMG, and tracheal or pleural pressure changes were recorded in a chronic fetal sheep preparation. Three patterns of fetal phrenic nerve activity were observed: 1) a single burst; 2) irregular nonrhythmic bursts; and 3) prolonged rhythmic activity, seen only prior to fetal death. The total recording time was 54.53 h and the total duration of phrenic nerve activity was 65.34 min (2.16%). When an inactive period was defined as the absence of phrenic nerve activity for 60 s or more, active periods occupied 44.7% of the total time. Phrenic nerve activity was present in all fetuses and 97.5% of the time was coupled with diaphragmatic EMG. Both diaphragmatic EMG and intrapulmonary pressure changes occurred in the absence of phrenic nerve activity. In three fetal animals both phrenic nerves were transected. Tracheal pressure changes were seen which were not coupled with corresponding intrauterine pressure changes. Thus, changes in fetal tracheal pressure or diaphragmatic EMG do not necessarily represent the output of the fetal respiratory center. This study suggests that the fetal respiratory center is active in utero, but this activity is minimal and has a different pattern that that present after birth.     

Vagal effects on sinoatrial and atrial conduction studied with epicardial mapping in dogs: the influence of pacemaker shifts on the measurement of sinoatrial conduction time

The influence of pacemaker shifts on sinoatrial conduction time (SACT) was studied by investigating the effects of vagal stimulation on SACT and atrial conduction in anesthetized open-chest dogs. Isochronal maps were drawn from unipolar electrograms simultaneously recorded at 60 epicardial sites on the right atrial free wall and the inferior and superior vena cava. Vagal stimulation caused atrial conduction velocity to increase from 0.99 +/- 0.10 m/s (mean +/- SD) to 1.23 +/- 0.23 m/s (p less than 0.01), and the pacemaker to shift to lower positions along the superior vena cava - right atrial junction. As a result of the changes, the distances and the atrial conduction times from the stimulating and recording electrodes to the pacemaker site varied, and hence, the SACT values obtained indirectly by premature atrial stimulation varied. The isochronal maps were used to measure the atrial conduction times from stimulating to recording electrodes (a), from stimulating electrode to pacemaker site (b), and from pacemaker site to recording electrode (c). Indirect SACT was lengthened by vagal stimulation from 43 +/- 16 to 64 +/- 22 ms (p less than 0.02). After correcting by subtracting the atrial conduction time (b + c - a), these values became 26 +/- 6 ms (control) and 40 +/- 11 ms (vagal stimulation) (p less than 0.01). SACT values measured directly from the electrograms were 27 +/- 7 ms (control) and 42 +/- 10 ms (vagal stimulation) (p less than 0.01). Corrected indirect SACTs were closer to direct SACTs than were the uncorrected indirect SACTs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of hypocalcemia on diaphragmatic strength generation

We studied the effects of hypocalcemia on diaphragmatic force and diaphragm blood flow (Qdi) in 12 anesthetized dogs. The diaphragm was electrically stimulated with intramuscular electrodes surgically implanted in the ventral surface of each hemidiaphragm. The transdiaphragmatic pressure (Pdi) during supramaximal (50 V) 2-s stimulations applied over a frequency range of 10-100 Hz was measured with balloon catheters during tracheal occlusion at functional residual capacity. A catheter was placed via the femoral vein into the left inferior phrenic vein, and Qdi was measured by timed volume collections of left inferior venous effluent. A catheter was introduced in a femoral artery to monitor blood pressure (BP). In five additional dogs, the force generated by the sartorius muscle during electrical stimulation was also studied concomitantly to diaphragmatic force. The animals were mechanically ventilated throughout the experiment, and the arterial blood gases and pH were maintained constant. Hypocalcemia was induced by a continuous infusion of EGTA (70 mg X kg-1 X h-1), which led to a progressive decrease (P less than 0.0001) of ionized calcium plasmatic level from 2.21 +/- 0.4 meq/1 during control to 1.69 +/- 0.06, 1.25 +/- 0.5, and 1.07 +/- 0.5 meq/1 after 30, 60, and 120 min, respectively. Hypocalcemia decreased progressively Pdi, which amounted to 84 +/- 3 (P less than 0.001) and 98 +/- 2% of control values for the low frequencies (10 and 20 Hz) and the high frequencies (50 and 100 Hz), respectively, after 30 min of EGTA infusion and to 74 +/- 5 and 79 +/- 6% for the low and high frequencies, respectively, after 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Aminophylline and human diaphragm strength in vivo

The transdiaphragmatic pressure (Pdi) twitch response to single shocks from supramaximal bilateral phrenic nerve stimulation was studied before and after acute intravenous infusions of aminophylline [14.9 +/- 3.1 (SD) micrograms/ml] in nine normal subjects. Stimulation was performed with subjects in the sitting position against an occluded airway from end expiration. Baseline gastric pressure and abdominal and rib cage configuration were kept constant. There was no significant difference in peak twitch Pdi from the relaxed diaphragm between control (38.8 +/- 3.3 cmH2O) and aminophylline (40.2 +/- 5.2 cmH2O) experiments. Other twitch characteristics including contraction time, half-relaxation time, and maximum relaxation rate were also unchanged. The Pdi-twitch amplitude at different levels of voluntary Pdi was measured with the twitch occlusion technique, and this relationship was found to be similar under control conditions and after aminophylline. With this technique, maximum Pdi (Pdimax) was calculated as the Pdi at which stimulation would result in no Pdi twitch because all motor units are already maximally activated. No significant change was found in mean calculated Pdimax between control (146.9 +/- 27.0 cmH2O) and aminophylline (149.2 +/- 26.0 cmH2O) experiments. We conclude from this study that the acute administration of aminophylline at therapeutic concentrations does not significantly affect contractility or maximum strength of the normal human diaphragm in vivo.     

Changes in relaxation rate with diaphragmatic fatigue in humans

Maximum relaxation rate (MRR) and the time constant of relaxation (tau) of transdiaphragmatic pressure (Pdi) was measured in four male subjects and compared with the high-to-low frequency ratio (H/L) of the diaphragmatic electromyogram (EMG) as a predictor of diaphragmatic fatigue. Pdi and inspiratory time-to-total breath duration ratios (TI/TT) were varied, and TT and tidal volume were held constant; inspiratory resistances were used to increase Pdi. Studies were performed at various tension-time indices (TTdi = Pdi/Pdimax X TI/TT). Base-line MRR/Pdi was 0.0100 +/- 0.0004 (SE) ms-1, and baseline tau was 53.2 +/- 3.2 ms. At TTdi greater than 0.20, MRR and H/L decreased and tau increased, with maximum changes at the highest TTdi. At TTdi less than 0.20, there was no change in H/L, MRR, or tau. The time course of changes in H/L correlated with those of MRR and tau under fatiguing conditions. In this experimental setting, change in relaxation rate was as useful a predictor of diaphragmatic fatigue as fall in H/L of the diaphragmatic EMG.     

Diaphragmatic contractility after upper abdominal surgery

Postoperative dysfunction of the diaphragm has been reported after upper abdominal surgery. This study was designed to determine whether an impairment in diaphragmatic contractility was involved in the genesis of the diaphragmatic dysfunction observed after upper abdominal surgery. Five patients undergoing upper abdominal surgery were studied. The following measurements were performed before and 4 h after surgery: vital capacity (VC), functional residual capacity (FRC), and forced expiratory volume in 1 s. Diaphragmatic function was also assessed using the ratio of changes in gastric pressure (delta Pga) over changes in transdiaphragmatic pressure (delta Pdi). Finally contractility of the diaphragm was determined by measuring the change in delta Pdi generated during bilateral electrical stimulation of the phrenic nerves (Pdi stim). Diaphragmatic dysfunction occurred in all the patients after upper abdominal surgery as assessed by a marked decrease in delta Pga/delta Pdi from 0.480 +/- 0.040 to -0.097 +/- 0.152 (P less than 0.01) 4 h after surgery compared with preoperative values. VC also markedly decreased after upper abdominal surgery from 3,900 +/- 630 to 2,060 +/- 520 ml (P less than 0.01) 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after upper abdominal surgery compared with the preoperative values. We conclude that contractility of the diaphragm is not altered after upper abdominal surgery, and diaphragmatic dysfunction is secondary to other mechanisms such as possible reflexes arising from the periphery (chest wall and/or peritoneum), which could inhibit the phrenic nerve output.     

Effects of diaphragmatic ischemia on the inspiratory motor drive.

To assess the effect of diaphragmatic ischemia on the inspiratory motor drive, we studied the in situ isolated and innervated left diaphragm in anesthetized, vagotomized, and mechanically ventilated dogs. The arterial and venous vessels of the left diaphragm were catheterized and isolated from the systemic circulation. Inspiratory muscle activation was assessed by recording the integrated electromyographic (EMG) activity of the left and right costal diaphragms and parasternal intercostal and alae nasi muscles. Tension generated by the left diaphragm during spontaneous breathing attempts was also measured. In eight animals, left diaphragmatic ischemia was induced by occluding the phrenic artery for 20 min, followed by 10 min of reperfusion. This elicited a progressive increase in EMG activity of the left and right diaphragms and parasternal and alae nasi muscles to 170, 157, 152, and 128% of baseline values, respectively, an increase in the frequency of breathing efforts, and no change in left diaphragmatic spontaneous tension. Thus the ratio of left diaphragmatic EMG to tension rose progressively during ischemia. During reperfusion, only the frequency of breathing efforts and alae nasi EMG recovered completely. In four additional animals, left diaphragmatic ischemia was induced after the left phrenic nerve was sectioned. Neither EMG activity of inspiratory muscles nor respiratory timing changed significantly during ischemia. In conclusion, diaphragmatic ischemia increases inspiratory motor drive through activation of phrenic afferents. The changes in alae nasi activity and respiratory timing indicate that this influence is achieved through supraspinal pathways.     

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

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 cmH(2)O. 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 cmH(2)O 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 cmH(2)O x 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.     

Influence of acute lung volume change on contractile properties of human diaphragm

The effect of stimulus frequency on thein vivo pressure generating capacity of the human diaphragm is unknownat lung volumes other than functional residual capacity. Thetransdiaphragmatic pressure (Pdi) produced by a pair of phrenic nervestimuli may be viewed as the sum of the Pdi elicited by the first (T1Pdi) and second (T2 Pdi) stimuli. We used bilateral anteriorsupramaximal magnetic phrenic nerve stimulation and a digitalsubtraction technique to obtain the T2 Pdi at interstimulus intervalsof 999, 100, 50, 33, and 10 ms in eight normal subjects at lung volumesbetween residual volume and total lung capacity. The reduction in T2Pdi that we observed as lung volume increased was greatest at long interstimulus intervals, whereas the T2 Pdi obtained with short interstimulus intervals remained relatively stable over the 50% ofvital capacity around functional residual capacity. For all interstimulus intervals, the total pressure produced by the pair decreased as a function of increasing lung volume. These data demonstrate that, in the human diaphragm, hyperinflation has a disproportionately severe effect on the summation of pressure responseselicited by low-frequency stimulations; this effect isdistinct from and additional to the known length-tension relationship.

     

Phrenic nerve injury after catheter ablation of atrial fibrillation

Phrenic Nerve Injury (PNI) has been well studied by cardiac surgeons. More recently it has been recognized as a potential complication of catheter ablation with a prevalence of 0.11 to 0.48 % after atrial fibrillation (AF) ablation. This review will focus on PNI after AF ablation. Anatomical studies have shown a close relationship between the right phrenic nerve and it's proximity to the superior vena cava (SVC), and the antero-inferior part of the right superior pulmonary vein (RSPV). In addition, the proximity of the left phrenic nerve to the left atrial appendage has been well established. Independent of the type of ablation catheter (4 mm, 8 mm, irrigated tip, balloon) or energy source used (radiofrequency (RF), ultrasound, cryothermia, and laser); the risk of PNI exists during ablation at the critical areas listed above. Although up to thirty-one percent of patients with PNI after AF ablation remain asymptomatic, dyspnea remain the cardinal symptom and is present in all symptomatic patients. Despite the theoretical risk for significant adverse effect on functional status and quality of life, short-term outcomes from published studies appear favorable with 81% of patients with PNI having a complete recovery after 7 +/- 7 months. CONCLUSION: Existing studies have described PNI as an uncommon but avoidable complication in patients undergoing pulmonary vein isolation for AF. Prior to ablation at the SVC, antero-inferior RSPV ostium or the left atrial appendage, pacing should be performed before energy delivery. If phrenic nerve capture is documented, energy delivery should be avoided at this site. Electrophysiologist's vigilance as well as pacing prior to ablation at high risk sites in close proximity to the phrenic nerve are the currently available tools to avoid the complication of PNI.