Central venous catheterization and fatal cardiac tamponade.

Cardiac tamponade is a poorly recognized complication of central venous catheterization associated with a high mortality. We present a case of fatal cardiac tamponade after intra- pericardial infusion of total parenteral nutrition in a patient who had two central venous catheters. We suggest that catheter tip position should always be confirmed before use of a catheter. Tamponade should be suspected in a patient who deteriorates when a central venous catheter is used and resuscitation via the catheter should be avoided.

An evaluation of P0.1 measured in mouth and oesophagus, during carbon dioxide rebreathing in COPD.

The pressure generated 100 ms after the onset of an occluded inspiratory effort (P0.1) is advocated and used as a measure of respiratory centre drive. We have re-examined P0.1, measured simultaneously in the mouth (Pmo0.1) and the oesophagus (Poes0.1), during carbon dioxide rebreathing, in eight patients with severe chronic obstructive pulmonary disease, to see whether either indicates central respiratory drive. Pmo0.1 was identical to Poes0.1 in 4 out of 61, greater than Poes0.1 in 18 out of 61, and less than Poes0.1 in 39 out of 61 measurements (overall Poes0.1-Pmo0.1, median +0.075, range -0.175 to +1.01 kPa). Within a rebreathing run in an individual patient, there was considerable variability in the relationship Pmo0.1/Poes0.1 (0.89 +/- 0.24), coefficient of variation (CoV%) 14.4 +/- 3.7%), in the end-expiratory oesophageal pressure (0.7 +/- 0.54 kPa, CoV% 105 +/- 106%), and in the time delay between the onset of a fall in oesophageal pressure (Poes) from the end-expiratory level to the beginning of inspiration, defined as starting when mouth pressure (Pmo) fell below atmospheric pressure (129 +/- 25 ms, CoV% 22.5 +/- 5.3%). We conclude that the problem of determining the true onset of inspiratory muscle activity from pressure data, and the likelihood that breaths are taken from different lung volumes, make it unlikely that Poes0.1 accurately represents central respiratory drive during rebreathing in chronic obstructive pulmonary disease. Furthermore, Pmo0.1 differed from Poes0.1 during rebreathing, and their relationship was not constant, so that Pmo0.1 is even less likely to be a useful reflection of central nervous system output or respiratory centre drive in such patients.

Diaphragmatic dysfunction in neuralgic amyotrophy: an electrophysiologic evaluation of 16 patients presenting with dyspnea.

We report 16 adult men (age, 41 to 75 yr) with neuralgic amyotrophy (NA) who presented with dyspnea due to involvement of the diaphragm. All patients developed breathlessness after a prodrome of acute severe neck and shoulder pain. Bilateral diaphragm paralysis (BDP) was confirmed in 12 patients and unilateral diaphragm paralysis (UDP) in four by the absence of electrical and mechanical responses to percutaneous phrenic nerve stimulation. Global expiratory muscle strength was well preserved in all patients, but inspiratory muscle strength was reduced in proportion to the extent of diaphragmatic involvement. Lung function showed low lung volumes with preservation of carbon monoxide transfer coefficient in all patients. Two BDP patients were hypoxic (PaO2 = 67 and 54 mm Hg, respectively) on daytime arterial blood gas analysis; the latter patient with pre-existing chronic obstructive pulmonary disease and marked obesity also had borderline hypercapnia (PaO2 = 49 mm Hg). Overnight sleep studies in three BDP and two UDP patients showed frequent intermittent arterial oxygen desaturations apparently caused by obstructive sleep apneas, but there was no evidence of alveolar hypoventilation. Follow-up muscle studies in five BDP and four UDP patients between 2 and 4 yr after initial referral showed complete recovery of diaphragmatic function in only two UDP patients, one of whom relapsed a year later. We postulate that NA may be an important but underrecognized cause of diaphragmatic paralysis in otherwise normal patients. Diaphragmatic strength returns very slowly, if at all.

Inspiratory muscle effort during nasal intermittent positive pressure ventilation in patients with chronic obstructive airways disease.

Effective intermittent positive pressure ventilation can be achieved noninvasively using a nasal mask, but patient comfort may be compromised and respiratory effort increased unless the trigger threshold is low and the response time of the ventilator short. The effect of nasal ventilation upon inspiratory muscle effort and the functional characteristics of the trigger of a purpose-built ventilator were evaluated in five patients with chronic obstructive airways disease. A measure of inspiratory muscle effort, the average pressure time integral per minute, decreased by at least 80% in four patients and by 50% in one. Only two patients had significant numbers of triggered breaths (17% and 47% of total) during 1 h of ventilation with settings as used at home. Therefore trigger function was evaluated when the patients were made to trigger the ventilator by slowing the control rate. A high resting end-expiratory intrathoracic pressure decreased the effective trigger sensitivity so that a mean (SD) change in oesophageal pressure of 14.8 cmH2O was required to lower mask pressure by 2.4 (0.3) cmH2O and activate the trigger. Even under these conditions of lowest trigger sensitivity inspiratory muscle effort was not increased compared to spontaneous ventilation.

Maximal relaxation rate of inspiratory muscle can be effort-dependent and reflect the activation of fast-twitch fibers.

We have measured the normalized maximal relaxation rate (MRR, % pressure loss/10 ms) of esophageal and transdiaphragmatic pressures in five normal subjects who performed unoccluded shifts from FRC, with the peak pressure varying between 10 and 100% of each subject's maximum. MRR was computed as the maximal rate of decay of pressure divided by the peak pressure, with units of %pressure loss/10 ms. We observed that MRR became progressively faster as sniff peak pressure increased in amplitude above 10% maximum. In four subjects this trend was most marked for sniffs of less than 40% maximal pressure, with little change as peak pressure increased further. In a fifth subject this trend continued across the full range of pressure. Thus, MRR may be an effort-dependent variable during voluntary inspiratory maneuvers. We postulate that sniff MRR becomes faster with increasing peak pressure because of progressive activation of fast-twitch type II muscle fibers. The findings of this study suggest that erroneous conclusions about the significance of slowing of sniff MRR with fatigue may be made if MRR is determined from voluntary efforts with a peak pressure of less than 60% of control maximum, as may occur with fatigue.

Domiciliary nocturnal nasal intermittent positive pressure ventilation in COPD: mechanisms underlying changes in arterial blood gas tensions.

The improvement in arterial blood gas tensions following assisted ventilation in chronic obstructive pulmonary disease (COPD) has usually been attributed to the relief of incipient or established respiratory muscle fatigue. The contribution of changes in the load placed upon and the drive to the respiratory muscle pump have not been evaluated. We have investigated the contribution of changes in respiratory muscle strength, the ventilatory response to CO2 and ventilatory function to changes in arterial blood gas tensions in eight patients with severe COPD completing six months domiciliary nasal intermittent positive pressure ventilation. Six patients showed a reduction and two an increase in arterial carbon dioxide tension (PaCO2), median (range) for eight patients, -0.9 kPa (-1.5 to +0.4) (p less than 0.05) and seven showed an improvement in arterial oxygen tension (PaO2), +0.7 kPa (-0.4 to +1.7) (p less than 0.05) during daytime spontaneous breathing. The reduction in PaCO2 was not related to increased inspiratory muscle strength but was correlated with a decrease in gas trapping (Spearman rank correlation coefficient (r(S)) 0.85, p less than 0.05) and in the residual volume (r(s) 0.78, p less than 0.05), suggesting reduced small airway obstruction and, therefore, a reduction in load. The change in PaCO2 also correlated with the increase in ventilation at an end-tidal CO2 of 8 kPa during rebreathing (r(s) -0.76, p less than 0.05) suggesting improved chemosensitivity to CO2. Our data do not support the hypothesis that improvements were due to the relief of muscle fatigue. We suggest that the contribution of changes in load and central drive warrant further investigation.

Inspiratory muscle relaxation rate after voluntary maximal isocapnic ventilation in humans.

We have investigated whether the capacity of the inspiratory muscles to generate pressure and flow during a ventilatory load is related to changes in inspiratory muscle relaxation rate. Five highly motivated normal subjects performed voluntary maximal isocapnic ventilation (MIV) for 2 min. Minute ventilation and esophageal, gastric, and transdiaphragmatic pressures were measured breath by breath. We observed that ventilation, peak inspiratory and expiratory pressures, and inspiratory flow rate declined from the start of the run to reach a plateau at 60 s that was sustained for the remainder of the exercise. In a subsequent series of studies, MIV was performed for variable durations between 15 and 120 s. The normalized maximum relaxation rate of unoccluded inspiratory sniffs (sniff MRR, %pressure loss/10 ms) was determined immediately on stopping MIV. Sniff MRR slowed as the duration of MIV increased and paralleled the decline in inspiratory pressure and ventilation observed during the 2-min exercise. No further slowing in MRR occurred when ventilation became sustainable. We conclude that, during MIV, the progressive loss of ventilation and capacity to generate pressure is associated with the early onset and progression of a peripheral fatiguing process within the inspiratory muscles.

Sniff esophageal and nasopharyngeal pressures and maximal relaxation rates in patients with respiratory dysfunction.

Sniff esophageal pressure (Pes) and maximal relaxation rate (MRR, percent pressure loss/10 ms) are useful measurements of inspiratory muscle performance, but they require the passage of an esophageal balloon. We have examined the relationship between sniff esophageal and nasopharyngeal pressures (sniff Pes, sniff Pnp) and maximal relaxation rates (Pes MRR, Pnp MRR) in 13 patients with chronic obstructive pulmonary disease (COPD), five with intrapulmonary fibrosis (IPF), and seven with the "shrinking lung syndrome" of systemic lupus erythematosus (SLE). The ratio sniff Pnp/Pes (mean +/- SD) was 0.65 +/- 0.15 in COPD, 0.76 +/- 0.18 in IPF, and 0.91 +/- 0.03 in SLE. The ratio Pnp/Pes MRR was 1.20 +/- 0.2 in COPD, 1.14 +/- 0.12 in IPF, and 1.07 +/- 0.13 in SLE. We confirm that the transmission of pleural pressure to the upper airways during brief dynamic maneuvers is impaired in the presence of airway obstruction and lung fibrosis. We conclude that measurements of sniff Pnp and Pnp MRR are of limited value in patients with abnormal lung mechanics.

The effect of posture and abdominal binding on respiratory pressures.

We examined the effect of posture on the generation of respiratory pressures in 6 highly trained subjects. Transdiaphragmatic pressure was measured at FRC during bilateral percutaneous phrenic nerve stimulation (twitch Pdi) and maximal sniffs (sniff Pdi), with the abdomen bound and unbound. Maximum static inspiratory (PImax) and expiratory (PEmax) mouth pressures were measured with the abdomen unbound. Three postures were examined: seated (Se), semi-supine (30s), and supine (Su). Changes of posture did not significantly alter twitch Pdi. By contrast, sniff Pdi and static mouth pressures were significantly reduced in the Su posture. Abdominal binding significantly increased twitch Pdi only. We conclude that voluntary respiratory manoeuvres requiring activation, recruitment and coordination of different muscle groups are performed better in the Se position. We suggest that posture be standardised for serial comparative measurements of voluntary respiratory pressures in a given subject.

Diaphragm strength in the shrinking lung syndrome of systemic lupus erythematosus.

The cause of the reduced lung volume in the 'shrinking lung' syndrome of systemic lupus erythematosus (SLE) was investigated in 12 patients with the condition. Nine patients described persistent episodes of pleuritic chest pain. Narrow section (3 mm) computed tomography of the thorax revealed no interstitial fibrosis or significant pleural disease. Assessment of diaphragmatic function using manoeuvres more reliable than the maximal occluded efforts previously used alone to assess respiratory muscle strength, showed that diaphragm strength was unequivocally normal in nine of 12 patients. In three, maximum transdiaphragmatic pressure was moderately reduced, but phrenic nerve stimulation demonstrated that this was due to incomplete activation of the diaphragm during a maximal voluntary effort, rather than to a primary abnormality of the diaphragm. Results of maximum lung recoil pressures and dynamic compliance, and analysis of the 12-s maximum voluntary ventilation, suggested a restriction in chest-wall expansion, although it was not possible to identify the underlying cause of this on the basis of our results. We conclude that the 'shrinking lung' syndrome of SLE is not explained by a primary abnormality of the diaphragm.

Maximal relaxation rates of esophageal, nose, and mouth pressures during a sniff reflect inspiratory muscle fatigue.

Maximal relaxation rate (MRR, % pressure fall/10 msec) of the inspiratory muscles is reduced with fatigue. We have investigated whether MRR of esophageal pressure (Pes) generated by voluntary sniffs is decreased by fatigue, and whether sniff nasopharyngeal (Pnp) and mouth (Pmo) MRR reflect these changes. In 10 normal subjects, control MRR of sniff Pes correlated closely to Pnp MRR (r = 0.977, p less than 0.001) and Pmo MRR (r = 0.947, p less than 0.001). To produce inspiratory muscle fatigue, four highly motivated subjects breathed to exhaustion (3 to 6 min) through a high inspiratory resistance. MRR was determined from 10 sniffs for Pes, Pnp, and Pmo before fatigue, and at intervals up to 10 min after fatigue. The subjects showed a mean decrease in sniff Pes MRR of 33% (range, 20 to 42) immediately after fatigue, which returned exponentially to control values within 3 to 4 min. The mean changes in Pes MRR were reflected by similar changes in Pnp MRR, 32% (range, 18 to 43) and Pmo MRR, 33% (range, 21 to 42). Studies were repeated in the four subjects with closely similar results. We conclude that fatigue of the inspiratory muscles reduces MRR of sniff Pes, and that this is reflected in Pnp and Pmo. Sniff Pes, Pnp, and Pmo MRR measurements may provide a useful method for detecting and monitoring fatigue; Pnp and Pmo have the advantage of being less invasive.

The measurement of inspiratory muscle strength by sniff esophageal, nasopharyngeal, and mouth pressures.

Sniff esophageal pressure (Pes) is a useful measurement of global inspiratory muscle strength, although it does require passage of an esophageal balloon. We investigated the relationship between nasopharyngeal pressure (Pnp) or pressure within the mouth (Pmo) and Pes during a maximal sniff from FRC without a noseclip. We measured Pes, Pnp, and Pmo simultaneously in 10 normal volunteers, and in 12 patients with inspiratory muscle weakness. In both groups, Pnp and Pmo were slightly less but very close to Pes. In normal volunteers, the mean ratio Pnp/Pes was 0.92 +/- 0.006 (mean +/- SE) and Pmo/Pes was 0.95 +/- 0.006. Regression analysis showed Pes = 4.57 + 1.05 Pnp (r = 0.995, p less than 0.001) and Pes = 0.74 + 1.05 Pmo (r = 0.994, p less than 0.001). Similar relationships between Pnp, Pmo, and Pes were found over a wide range of pressures generated by submaximal sniffs in normal subjects. In patients, the mean ratio Pnp/Pes was 0.90 +/- 0.02 and Pmo/Pes was 0.87 +/- 0.03. Regression analysis showed Pes = 5.12 + 1.0 Pnp (r = 0.949, p less than 0.001) and Pes = 11.2 + 0.882 Pmo (r = 0.936, p less than 0.001). We conclude that Pnp and Pmo predict Pes during a maximal sniff in both normal subjects and in patients with inspiratory muscle weakness. Sniff Pnp and/or Pmo may provide a useful and less invasive method of measuring maximal inspiratory pressures during a sniff.

Comparison of two different mouthpieces for the measurement of Pimax and Pemax in normal and weak subjects.

We investigated the effect of mouthpiece design on maximum static expiratory (PEmax) and inspiratory (PImax) mouth pressures. We measured PEmax from total lung capacity (TLC) and PImax from residual volume (RV) in 21 healthy volunteers, and in 40 patients referred for respiratory muscle testing. We compared two different mouthpieces, a semi-rigid plastic flanged type fitting inside the lips, and a 4 cm diameter rubber tube held against the lips. The tube mouthpiece gave significantly higher values for PEmax (p less than 0.02) in all subjects. PImax was also significantly higher (p less than 0.005) with the tube mouthpiece in subjects who recorded normal pressures. We conclude that maximum pressures are obtained in all normal subjects with the rubber tube mouthpiece, and that differences in quoted normal ranges of maximum static respiratory pressures reflect in part the design of the mouthpiece and the way in which it was used.