[Algorithms for oxygenation and difficult intubations in resuscitation].
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Algorithms↗
Biomedical subjects
J C Chevrolet
Publications and source records attributed to J C Chevrolet.
Effects of the prone position on gas exchange and hemodynamics in severe acute respiratory distress syndrome.
OBJECTIVES: To address the following issues regarding the use of prone position ventilation in patients with severe acute respiratory distress syndrome (ARDS): a) response rate; b) magnitude and duration of improved oxygenation in responders during a 12-hr trial and the consequences of returning to the supine position; c) effects of the prone position on gas exchange and hemodynamics; d) consequences of oxygenation in nonresponders; and e) effects of repeated prone position trials. DESIGN: Prospective, nonrandomized interventional study. SETTING: Medical intensive care unit, university tertiary care center. PATIENTS: Nineteen consecutive, mechanically ventilated patients (age 45+/-20 yrs, mean+/-SD) with ARDS and severe hypoxemia, defined as PaO2/FiO2 of < or = 150 with FiO2 of > or = 0.6 persisting for < or =24 hrs, and a pulmonary artery occlusion pressure of <18 mm Hg. INTERVENTIONS: Patients were turned prone for 2 hrs. Nonresponders were returned supine, but responders were maintained prone for 12 hrs before being returned to the supine position. The procedure was repeated on a daily basis in all patients, until inclusion criteria were no longer met or the patients died. MEASUREMENTS AND MAIN RESULTS: Hemodynamic, blood gas, and gas exchange measurements were performed at the following time points: a) baseline supine; b) after 30 mins prone; and c) after 120 mins prone. Additional measurements for nonresponders were taken after 30 mins supine. For responders, additional measurements were taken after 12 hrs prone and 30 mins supine. Patients were considered responders if an increase in PaO2 of > or = 10 torr (> or =1.3 kPa), or increase in the PaO2/FiO2 ratio of >20 occurred within 120 mins. Eleven (57%) patients responded to the prone position. There was no difference in initial baseline parameters between responders and nonresponders. After 30 mins, the prone position in responders increased PaO2 and decreased calculated venous admixture (Qva/Qt). This improvement was the maximal obtained, and was maintained throughout the 12-hr prone period. After 12 hrs prone, mean FiO2 had been lowered from 0.85+/-0.16 to 0.66+/-0.18 (p < .05). Thirty minutes after the patients were returned supine, PaO2, PaO2/FiO2, and Qva/Qt were not different from 12-hr prone values, and were improved in comparison with baseline supine values. There was no worsening of gas exchange or hemodynamics in nonresponders. After the initial trial, a total of 28 additional episodes of prone position ventilation were performed in nine of the 19 patients. Of the 24 additional episodes in the responders, there was a response in 17 (71%) of 24 episodes. In the four additional episodes in nonresponders, there was a response in only one (25%) of four episodes. Response was accompanied by the same beneficial effects on gas exchange and Qva/Qt and absence of effect on hemodynamics as in the initial trial. There was no worsening in gas exchange or hemodynamics in nonresponder trials. CONCLUSIONS: Based on the data from this study, the prone position can improve oxygenation in severely hypoxemic ARDS patients without deleterious effects on hemodynamics. This beneficial effect does not immediately disappear on return to the supine position. In our patients, an absence of response to this technique was not accompanied by worsening hypoxemia or hemodynamic instability. Repeated daily trials in the prone position should be considered in the management of ARDS patients with severe hypoxemia.
Adolescent↗
Activation of human macrophages by mechanical ventilation in vitro.
Positive-pressure mechanical ventilation supports gas exchange in patients with respiratory failure but is also responsible for significant lung injury. In this study, we have developed an in vitro model in which isolated lung cells can be submitted to a prolonged cyclic pressure-stretching strain resembling that of conventional mechanical ventilation. In this model, cells cultured on a Silastic membrane were elongated up to 7% of their initial diameter, corresponding to a 12% increase in cell surface. The lung macrophage was identified as the main cellular source for critical inflammatory mediators such as tumor necrosis factor-alpha, the chemokines interleukin (IL)-8 and -6, and matrix metalloproteinase-9 in this model system of mechanical ventilation. These mediators were measured in supernatants from ventilated alveolar macrophages, monocyte-derived macrophages, and promonocytic THP-1 cells. Nuclear factor-kappaB was found to be activated in ventilated macrophages. Synergistic proinflammatory effects of mechanical stress and molecules such as bacterial endotoxin were observed, suggesting that mechanical ventilation might be particularly deleterious in preinjured or infected lungs. Dexamethasone prevented IL-8 and tumor necrosis factor-alpha secretion in ventilated macrophages. Mechanical ventilation induced low levels of IL-8 secretion by alveolar type II-like cells. Other lung cell types such as endothelial cells, bronchial cells, and fibroblasts failed to produce IL-8 in response to a prolonged cyclic pressure-stretching load. This model is of particular value for exploring physical stress-induced signaling pathways, as well as for testing the effects of novel ventilatory strategies or adjunctive substances aimed at modulating cell activation induced by mechanical ventilation.
Cytokines↗
Transcutaneous PCO2 to monitor noninvasive mechanical ventilation in adults: assessment of a new transcutaneous PCO2 device.
UNLABELLED: The present study was designed to analyze the usability of a commercially available, transcutaneous PCO2 (TcPCO2) sensor for monitoring noninvasive positive pressure ventilation (NPPV). Twenty-six hemodynamically stable patients with intra-arterial radial catheters were assessed. After stabilization of TcPCO2, arterial blood was analyzed and results were compared with TcPCO2 at time of sampling. To evaluate the drift of the signal, samples were taken hourly in five patients for 4 h while continuously recording TcPCO2. Finally, to assess for the response of the sensor to changes in PaCO2, six patients underwent continuous TcPCO2 recording while initiating or interrupting NPPV; arterial samples were analyzed before the event, and 1, 3, 5, 7, 9, and 20 min afterwards. RESULTS: TcPCO2 and PaCO2 were tested over a range of 26 to 71 mm Hg, and were found to be closely correlated (r=0.968, p<0.0001); mean bias was 0.75 mm Hg. There was no significant drift of TcPCO2 as compared with PaCO2 over 4 h. The time of response of TcPCO2 to initiation or interruption of NPPV was <60 s. An estimation of the lag time averaged 5+/-3 min (range, 1 to 9 min). CONCLUSION: TcPCO2 in hemodynamically stable adults was in excellent agreement with arterial measurements. The time of response to a change in ventilation was compatible with the aim of clinical monitoring of patients under NPPV.
Aged↗
[Thrombolysis in acute myocardial infarct in everyday clinical practice].
We prospectively included in a database all thrombolyzed acute transmural myocardial infarction patients admitted to our hospital from November 1986 to September 1995. Six hundred and twenty-seven patients (497 males) with a mean age of 61 +/- 12 years (range 26-88 years) were included. 87% were having their first acute myocardial infarction. Different thrombolytic regimens were applied in the emergency room but the vast majority (92%) received t-PA. The median delay between the onset of pain and admission was 2 h 0 min (10 min-22 h). The median admission to treatment time was 40 min (5 min-6 h 20 min). The latter has been shortened (median 55 min from 1986 to 1989 versus 35 min from 1990 to 1995, p < 0.05) during the study period. The rate of intracerebral hemorrhage was 2.4% (confidence interval 1.1-3.5%) and no significant predictor could be found, although patients with cerebral bleeding tended to be slightly older (66 +/- 9 years vs 61 +/- 13 years, p = ns). The rate of false diagnosis was only 4.6%, even when patients with a final diagnosis of unstable angina and/or aborted acute myocardial infarction were included. The in-hospital mortality was 8.8%, a rate similar to those reported in the literature. Using multivariate analysis, negative prognostic factors were higher age (p < 0.001), advanced Killip class at admission (p < 0.001) and elevated peak CPK levels (p < 0.001). These results confirm that thrombolysis for acute myocardial infarction in the emergency room can be done with a short admission-to-treatment time and with an acceptably low rate of false diagnosis. However, our intracerebral hemorrhage rate was clearly higher than generally reported in the literature and may be explained by a different patient selection from that in large randomized studies.
Adult↗
[Noninvasive ventilation in intensive care].
Non-invasive ventilation has been in use for many years to provide long-term home ventilatory support to patients with chronic respiratory failure. In recent years, it has emerged on the intensive care scene as a means of avoiding intubation in acute respiratory failure. The results of several studies indicate that such an approach can lead to a reduction in mortality and duration of hospital stay compared to conventional mechanical ventilation with endotracheal intubation. The purpose of this article is to explore the various ventilatory techniques available, the choice of respirator and ventilatory mode in various clinical conditions, and to discuss some of the logistics involved in the optimal use of this technique.
Acute Disease↗
Effects of inhaled salmeterol and salbutamol (albuterol) on morning dips compared in intensive care patients recovering from an acute severe asthma attack.
OBJECTIVE: To assess the effect of a long-acting inhaled beta 2-agonist, salmeterol (SM), compared to a short-acting inhaled beta 2-agonist, salbutamol (or albuterol, SB) on the occurrence of morning dip (MD) in patients recovering from an acute severe asthma attack (ASA). DESIGN: Prospective study. SETTING: 18-bed, medical intensive care unit (ICU) in a university hospital. PATIENTS: 19 patients suffering from an ASA. INTERVENTIONS: Serial measurements of the peak expiratory flow rate (PEFR), arterial blood gases, vital capacity and forced expiratory volume in one second (FEV1) were performed from admission. All patients were first treated with i.v. methyl prednisolone and i.v. SB. Once the PEFR was stable and > 35% of predicted value, i.v. SB was stopped while i.v. steroids were maintained, and patients were randomised to either inhaled SB (9 patients, 400 micrograms every 4 h) or inhaled SM (10 patients, 100 micrograms every 12 h). RESULTS: The mean admission PEFR was 26.1 +/- 11.7% of the predicted value and was not different between the two groups. MD was more frequent with SB (6/9 patients) than with SM (4/10). The severity of MD, expressed in l/min fall in PEFR, was higher in SB than in SM (106 +/- 25 vs 55 +/- 37; p < 0.05). DISCUSSION: MD is frequent in ASA. In ASA, SM appears to reduce the frequency and the severity of MD more than SB. The clinical implications of this observation, particularly a lowering of mortality and a shortening of the ICU stay, remain to be investigated.
Acute Disease↗
Additive beneficial effects of the prone position, nitric oxide, and almitrine bismesylate on gas exchange and oxygen transport in acute respiratory distress syndrome.
OBJECTIVE: To test the hypothesis that prone position ventilation, nitric oxide, and almitrine bismesylate, each acting by a different mechanism to improve arterial oxygenation, could exert additive beneficial effects when used in combination in patients with severe acute respiratory distress syndrome (ARDS). DESIGN: Prospective, nonrandomized, interventional study. SETTING: Medical and surgical intensive care units at a university tertiary care center. PATIENTS: Twelve patients with ARDS and severe hypoxemia, defined as PaO2/FIO2 of < or = 150 and FIO2 of > or = 0.6, with pulmonary artery occlusion pressure of < 18 mm Hg. INTERVENTIONS: Inhaled nitric oxide (20 parts per million for 15 mins) in the supine and prone position, and intravenous almitrine bismesylate while prone (1 mg/kg/hr for 60 mins), alone or combined with nitric oxide. MEASUREMENTS AND MAIN RESULTS: Hemodynamic, blood gas, and gas exchange measurements were performed at sequential time points as follows: a) baseline supine; b) nitric oxide in the supine position; c) after return to baseline supine; d) after 30 mins prone; e) after 120 mins prone; f) nitric oxide while prone; g) after return to baseline prone; h) almitrine bismesylate prone; and i) nitric oxide and almitrine bismesylate combined, for 15 mins prone. Patients were considered responders to the prone position if a gain in PaO2 of > or = 10 torr (> or = 1.3 kPa) or a gain in the PaO2/FIO2 ratio of > or = 20 was observed. Seven patients (58%) responded to being turned prone. Compared with supine baseline conditions, nitric oxide and supine position increased arterial oxygen saturation from 89 +/- 1 (SD)% to 92 +/- 3% (p < .05) and nitric oxide plus prone position increased arterial oxygen saturation (94 +/- 3% vs. 89 +/- 4%, p < .05) and decreased the alveolar-arterial oxygen difference from 406 +/- 124 torr (54 +/- 15 kPa) to 387 +/- 108 torr (51 +/- 14 kPa) (p < .05). Almitrine bismesylate increased PaO2/FIO2 vs. baseline (122 +/- 58 vs. 84 +/- 21, p < .05). Almitrine bismesylate decreased the alveolar-arterial oxygen difference vs. baseline from 406 +/- 124 torr (53.9 +/- 16.5 kPa) to 386 +/- 112 torr (51.3 +/- 14.8 kPa) and vs. nitric oxide and supine position from 406 +/- 111 torr (53.9 +/- 14.7 kPa) to 386 +/- 112 torr (51.3 +/- 14.8 kPa) (p < .05). Prone position alone did not improve oxygenation. However, the combination of nitric oxide and almitrine bismesylate increased PaO2/FIO2 vs. nitric oxide supine and nitric oxide prone conditions (147 +/- 69 vs. 84 +/- 25 and 91 +/- 18, respectively; p < .05). In patients responding to the prone position (n = 7), combining nitric oxide and almitrine bismesylate led to further improvement in PaO2 compared with the prone position alone, with PaO2 increasing from 78 +/- 12 torr (10.3 +/- 1.6 kPa) to 111 +/- 55 torr (14.7 +/- 7.3 kPa) (p < .05), which was not the case when either nitric oxide or almitrine bismesylate was added separately. Heart rate and cardiac output were increased by almitrine bismesylate compared with all other measurements. Mean pulmonary arterial pressure was decreased by nitric oxide (27 +/- 7 vs. 30 +/- 7 mm Hg nitric oxide supine vs. baseline supine and 29 +/- 7 vs. 33 +/- 8 mm Hg nitric oxide prone vs. baseline prone, p < .05) and increased by almitrine bismesylate (36 +/- 9 vs. 30 +/- 7 mm Hg baseline supine, 27 +/- 7 mm Hg nitric oxide supine, 33 +/- 8 mm Hg baseline prone, and 29 +/- 7 mm Hg nitric oxide prone; p < .05). The increase in mean pulmonary arterial pressure was totally abolished by nitric oxide (31 +/- 5 vs. 36 +/- 9 mm Hg, p < .05). Minute ventilation, respiratory system compliance, physiologic deadspace, and PaCO2 remained unchanged. CONCLUSION: In ARDS patients with severe hypoxemia, arterial oxygenation can be improved by combining the prone position, nitric oxide, and almitrine bismesylate, without deleterious effects.
APACHE↗
Nitric oxide and prostacyclin as test agents of vasoreactivity in severe precapillary pulmonary hypertension: predictive ability and consequences on haemodynamics and gas exchange.
BACKGROUND: In patients with primary pulmonary hypertension who respond to vasodilators acutely, survival can be improved by the long term use of calcium channel blockers. However, testing for such a response with calcium channel blockers or prostacyclin (PGI2) may cause hypotension and adversely affect gas exchange. Nitric oxide (NO), which does not have these effects, could be a better test agent. METHODS: NO (10, 20, and 40 ppm for 15 minutes), PGI2 (1-->10 ng/kg/min), and oral nifedipine (10 mg, then 20 mg/h) were administered sequentially to 10 patients after determination of the 24 hour spontaneous variability of their pulmonary and systemic mean arterial pressures. Patients were considered responders if the mean pulmonary artery pressure or pulmonary vascular resistance decreased by 20% or more. RESULTS: Six patients (60%) responded to all three agents, and three to none of the agents. One patient responded to PGI2 only. In those who responded to vasodilators, NO had no major effect on gas exchange or systemic haemodynamics, while PGI2 and nifedipine both induced systemic hypotension (mean (SD) systemic arterial pressure 72 (14) versus 89 (19) mm Hg with PGI2 and 72 (15) versus 86 (17) mm Hg with nifedipine, p < 0.05) and hypoxaemia (PaO2 8.7 (1.4) versus 10.8 (1.0) kPa with PGI2 and 8.6 (1.4) versus 10.2 (1.5) kPa with nifedipine, p < 0.05) and increased venous admixture (28 (9) versus 14 (4)% with PGI2 and 22 (9) versus 13 (5)% with nifedipine, p < 0.05). CONCLUSIONS: NO inhalation can accurately predict a vasodilator response to nifedipine in patients with severe pulmonary hypertension without adverse effects on systemic haemodynamics and gas exchange. This absence of side effects may make it a more appropriate agent for testing the vasodilator response.
Antihypertensive Agents↗
Haemodynamic and endocrinological effects of noninvasive mechanical ventilation in respiratory failure.
The aim of this study was to investigate the haemodynamic and endocrinological effects of noninvasive positive pressure ventilation (NIPPV). Eleven patients with oedema and recent hypercapnic and hypoxaemic worsening of a chronic respiratory insufficiency were included. Echocardiography, cardiac radionuclide assessment, blood catecholamines, salt and water handling hormones were measured at admission and discharge (long study (LS)). To discriminate between the action of NIPPV and other treatments, measurements were performed on the fourth day, for 4 h without NIPPV and 4 h with NIPPV (short study (SS)). NIPPV entailed a correction of P(a,CO2) and an increase of P(a,O2) in LS and SS. Oedema disappeared. Body weight decreased (from 85+/-42 to 81+/-40 kg) during LS. Systolic and mean pulmonary arterial pressure decreased in LS and SS. Right ventricular ejection fraction increased in LS. Left ventricular ejection fraction did not change. Cardiac index was normal on admission and then decreased. Natriuretic peptides and catecholamines were increased on admission, whereas plasma renin activity, aldosterone and vasopressin were normal. We suggest that in these patients, oedema can occur independently of renin-angiotensin-aldosterone-vasopressin and with a normal cardiac output. Noninvasive positive pressure ventilation allowed a correction of blood gases, associated with the resolution of oedema, a decrease in pulmonary arterial pressures and an increase in right ventricular ejection fraction.
Atrial Natriuretic Factor↗
[Ventilation in the prone position in acute respiratory distress syndrome (ARDS)].
Prone position mechanical ventilation (PPV) secures an improvement in gas exchange in approximately two-thirds of ARDS patients. Recent experimental and clinical data suggest that PPV acts mainly by recruiting alveoli situated in the dorsal dependent regions which are collapsed under the superimposed weight of the overlying edema-laden lungs. The purpose of this article is to provide an overview of the basic pathophysiological mechanisms underlying PPV as well as to underscore the promising clinical results so far obtained with this technique. In spite of these results the place of PPV among the other ventilatory and pharmacological approaches in the supportive treatment of ARDS, and the possible beneficial or deleterious consequences of associating PPV with one or more of these therapeutic modalities, remains to be determined.
Animals↗
[Acute decompensation in chronic obstructive respiratory insufficiency. Pathogenesis of edema and role of noninvasive mechanical ventilation].
Chronic obstructive pulmonary disease (COPD) is rather common. It is nearly always associated with excessive smoking. In advanced stages of COPD, patients have severe obstruction of airways and develop often acute episodes of respiratory failure, commonly due to broncho-pulmonary infections. This review addresses nonpharmacological treatment of these episodes of acute decompensation. The value of mechanical ventilation is discussed in view of two recent advances: noninvasive ventilation by face or nose mask as alternative to tracheal intubation and improved notions about the pathogenesis of fluids and salt retention as causes of occasionally occurring edema.
Acute Disease↗
Relationship between pulmonary oxygen consumption, lung inflammation, and calculated venous admixture in patients with acute lung injury.
OBJECTIVE: To determine in patients with acute lung injury whether increased pulmonary oxygen consumption (VO2pulm), computed as the difference between oxygen consumption measured by indirect calorimetry (VO2meas) and calculated by the reverse Fick method (VO2Fick), would: (1) correlate with the degree of lung inflammation assessed by bronchoalveolar lavage (BAL); (2) lead to an overestimation of calculated venous admixture (Qva/Qt). DESIGN: Prospective study. SETTING: University hospital, medical intensive care unit. INTERVENTION: None. MEASUREMENTS AND RESULTS: In nine mechanically ventilated patients with acute lung injury (Apache II 12 +/- 5, lung injury score 2 +/- 0.6, mean +/- SD), whole-body VO2 (VO2wb) was determined simultaneously by indirect calorimetry and the reverse Fick technique, after which BAL was immediately performed. VO2meas was significantly higher than VO2Fick (128 +/- 24 and 102 +/- 18 ml/min per m2, respectively, p < 0.001). Median VO2pulm was 25.3 ml/min per m2 (range 1.98-51.5), thus representing 19 +/- 11% of VO2wb. Total BAL cellularity was increased in all patients (median 47, range 24-200 x 10(4)/ml), as was the total polymorphonuclear (PMN) count (median 78 range 5-93 x 10(4)/ml). Macrophage counts were in the normal range. There were raised BAL levels of interleukin-6 (IL-6) (median 945, range 23-1800 ng/ml) and elastase (median 391, range 5-949 ng/ml). Median protein levels were 270 micrograms/ml (range 50-505). There was no correlation between VO2pulm and BAL cellularity, PMNs, elastase, IL-6, or protein. Qva/Qt was 31.7 +/- 8%. Qva/Qt, corrected for the presence of VO2pulm, (Qva/Qtcorr), was 30.3 +/- 8% (P < 0.01 vs Qva/Qt), a 4.2% overestimation due to VO2plum. There was no correlation between Qva/Qt or Qva/Qtcorr and VO2pulm. CONCLUSIONS: In mechanically ventilated patients with acute lung injury, VO2pulm was increased and led to a 19% underestimation of VO2wb determined by the reverse Fick method, as well as to a 4.2% overestimation of calculated Qva/Qt. Lung inflammatory activity was increased, as assessed by BAL cellularity, IL-6 and elastase levels. However, there was no correlation between VO2pulm and the intensity of pulmonary inflammation.
Adult↗
Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome.
OBJECTIVE: To measure the effects of rapid permissive hypercapnia on hemodynamics and gas exchange in patients with acute respiratory distress syndrome (ARDS). DESIGN: Prospective study. SETTING: 18-bed, medical intensive care unit, university hospital. PATIENTS: 11 mechanically ventilated ARDS patients. INTERVENTION: Patients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30-60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P50 increased by 7.5 mmHg. Settings were then maintained for 2 h. RESULTS: Minute ventilation was reduced from 13.5 +/- 6.1 to 8.2 +/- 4.1 l/min (mean +/- SD), PaCO2 increased (40.3 +/- 6.6 to 59.3 +/- 7.2 mmHg), pH decreased (7.40 +/- 0.05 to 7.26 +/- 0.05), and P50 increased (26.3 +/- 2.02 to 31.1 +/- 2.2 mmHg) (p < 0.05). Systemic vascular resistance decreased (865 +/- 454 to 648 +/- 265 dyne.s.cm-5, and cardiac index (CI) increased (4 +/- 2.4 to 4.7 +/- 2.4 l/min/m2) (p < 0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29 +/- 5 to 32 +/- 6 mmHg, p < 0.05). PaO2 remained unchanged, while saturation decreased (93 +/- 3 to 90 +/- 3%, p < 0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO2 > 90%. PvO2 increased (36.5 +/- 5.7 to 43.2 +/- 6.1 mmHg, p < 0.05), while saturation was unmodified. The arteriovenous O2 content difference was unaltered. Oxygen transport (DO2) increased (545 +/- 240 to 621 +/- 274 ml/min/m2, p < 0.05), while the O2 consumption and extraction ratio did not change significantly. Venous admixture (Qva/Qt) increased (26.3 +/- 12.3 to 32.8 +/- 13.2, p < 0.05). CONCLUSIONS: These data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Qva/Qt, CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.
Adult↗
Quadriparesia following permissive hypercapnia and inhalational anesthesia in a patient with severe status asthmaticus.
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Adult↗
Lack of effects of recombinant growth hormone on muscle function in patients requiring prolonged mechanical ventilation: a prospective, randomized, controlled study.
OBJECTIVE: To evaluate the benefit of recombinant human growth hormone administration on muscle strength and duration of weaning in critically ill patients undergoing prolonged mechanical ventilation. DESIGN: Prospective, randomized, controlled, single-blind study. SETTING: Intensive care unit. PATIENTS: Twenty patients requiring > or = 7 days of mechanical ventilation for acute respiratory failure. INTERVENTION: Random assignment to receive either 0.43 IU (approximately 0.14 mg) recombinant growth hormone/kg body weight/day (treated group), or saline (nontreated group) for 12 days. MEASUREMENTS AND MAIN RESULTS: Nutritional support was guided by indirect calorimetry. Cumulative nitrogen balance was positive throughout the study period in the treated group 17.3 (44.9 +/- 17.3[SEM] g/12 days) vs. the nontreated group (-65.8 +/- 11.8 g/12 days) (p<.0001). Despite similar initial plasma concentrations, recombinant growth hormone supplementation resulted in marked increases in growth hormone, insulin like growth factor-1, and insulin concentrations (p<.05, .02, and .0001, respectively, vs. nontreated group). Body impedance determined net fat-free mass increased in the treated group (0.8 +/- 0.6 kg) vs. the nontreated group (-1.1 +/- O.5 kg) (p<.03). Initial peripheral muscle function, assessed by computer-controlled electrical stimulation of the adductor pollicis, was similarly lower in treated and nontreated groups than sex and age-matched normal controls, and decreased further during the study period. Arterial blood gases, cumulative total mechanical ventilation time, and number of hrs/day of mechanical ventilation during weaning were similar in both patient groups. Only three of the ten patients in each group were weaned from mechanical ventilation by day 12. CONCLUSIONS: Daily administration of recombinant growth hormone in mechanically ventilated patients with acute respiratory failure promotes a marked nitrogen retention. However, this reaction is accompanied neither by an improvement in muscle strength nor by a shorter duration of ventilatory supports.
Acute Disease↗
Impact of a public campaign on pre-hospital delay in patients reporting chest pain.
OBJECTIVE: To decrease pre-hospital delay in patients with chest pain. DESIGN: Population based, prospective observational study. SETTING: A province of Switzerland with 380000 inhabitants. SUBJECTS: All 1337 patients who presented with chest pain to the emergency department of the Hôpital Cantonal Universitaire of Geneva during the 12 months of a multimedia public campaign, and the 1140 patients who came with similar symptoms during the 12 months before the campaign started. MAIN OUTCOME MEASURES: Pre-hospital time delay and number of patients admitted to the hospital for acute myocardial infarction (AMI) and unstable angina. RESULTS: Mean pre-hospital delay decreased from 7h 50 min before the campaign to 4 h 54 min during it, and median delay from 180 min to 155 min (P < 0.001). For patients with a final diagnosis of AMI, mean delay decreased from 9 h 10 min to 5 h 10 min and median delay from 195 min to 155 min (P < 0.002). Emergency department visits per week for AMI and unstable angina increased from 11.2 before the campaign to 13.2 during it (P < 0.02), with an increase to 27 (P < 0.01) during the first week of the campaign; visits per week for non-cardiac chest pain increased from 7.6 to 8.1 (P = NS) during the campaign, with an increase to 17 (P < 0.05) during its first week. CONCLUSIONS: Public campaigns may significantly reduce pre-hospital delay in patients with chest pain. Despite transient increases in emergency department visits for non-cardiac chest pain, such campaigns may significantly increase hospital visits for AMI and unstable angina and thus be cost effective.
Angina, Unstable↗
Recombinant human growth hormone in chronic and acute respiratory insufficiency.
Chronic respiratory insufficiency leads to protein-calorie malnutrition (PCM). PCM results in increased morbidity (e.g., infection), which in turn promotes further body wasting. The latter leads to respiratory muscle dysfunction and acute respiratory failure. Nutritional support alone is generally insufficient to counterbalance this hypoxemic and stress-related muscle catabolism. Recombinant human growth hormone (rhGH) can preserve or replenish nitrogen reserves, mostly contained in body muscle mass. It was hypothesized that rhGH, through its ability to improve muscle mass and function, could be a valuable therapeutic adjunct in both chronic and acute respiratory insufficiency. The results are controversial, and the beneficial effects of rhGH in patients with chronic and acute respiratory insufficiency, in terms of improvement of respiratory function, morbidity, and quality of life, remain to be shown. Well-designed studies, specifically targeting these end points as well as cost-effectiveness, are needed to better define the place of rhGH in the nutritional support of these patients.
Acute Disease↗