Hemodynamic changes in acute adrenal insufficiency

Objective Acute adrenocortical insufficiency is an unusual cause of isolated shock. The purpose of this study is to describe the cardiovascular changes in 6 patients with acute adrenal insufficiency presenting with hemodynamic instability.Design Retrospective and prospective studySetting Medical intensive care unit in a university hospital.Patients 6 patients studied by right cardiac catheterization.Measurements and results Results before glucocorticoid treatment show two possible hemodynamic states: 1) myocardial depression with hypovolemia in 3 patients, and 2) hyperdynamic shock with high cardiac output and diminished systemic arterial resistance in 3 other patients. The 3 patients presenting hyperdynamic shock were all given intravenous fluid therapy of over 20 ml/kg before the first hemodynamic measurement. For 2 other patients with low cardiac index and high systemic arterial resistance studied prospectively, 20 ml/kg intravenous fluid therapy transformed the hemodynamic state to hyperdynamic shock. The cardiovascular effect of glucocorticoid treatment studied in 4 patients was resulted in an improvement in the left ventricular systolic work index.Conclusions Diagnosis of acute adrenocortical insufficiency must be considered if clinical manifestations are present suggesting septic shock without any obvious infectious cause in patients having undergone considerable intravenous fluid therapy as an initial course of treatment.     

Hemodynamic effects of vasodilators on pulmonary hypertension in decompensated chronic obstructive pulmonary disease

Vasodilators have been reported to improve the hemodynamic status of some patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD). We investigated the effects of sodium nitroprusside (50 micrograms/min) and hydralazine (25 mg) on pulmonary hemodynamics in 12 patients during acute exacerbation of COPD. Apart from its known systemic effects, nitroprusside decreased significantly mean pulmonary artery pressure (MPAP) from 36 +/- 10 to 31 +/- 12 mm Hg (p less than .04), decreased slightly pulmonary vascular resistance, and did not change cardiac index. Except for a slight but significant increase in MPAP from 35 +/- 5 to 38 +/- 5 mm Hg (p less than .002), hydralazine produced no significant hemodynamic changes. These results suggest that vasodilator therapy with sodium nitroprusside and hydralazine for pulmonary hypertension secondary to acute COPD is probably not helpful.     

Mechanisms of acute exacerbation of respiratory symptoms in chronic obstructive pulmonary disease

Exacerbations of chronic obstructive respiratory disease (ECOPD) are acute events characterized by worsening of the patient's respiratory symptoms, particularly dyspnoea, leading to change in medical treatment and/or hospitalisation. AECOP are considered respiratory diseases, with reference to the respiratory nature of symptoms and to the involvement of airways and lung. Indeed respiratory infections and/or air pollution are the main causes of ECOPD. They cause an acute inflammation of the airways and the lung on top of the chronic inflammation that is associated with COPD. This acute inflammation is responsible of the development of acute respiratory symptoms (in these cases the term ECOPD is appropriate). However, the acute inflammation caused by infections/pollutants is almost associated with systemic inflammation, that may cause acute respiratory symptoms through decompensation of concomitant chronic diseases (eg acute heart failure, thromboembolism, etc) almost invariably associated with COPD. Most concomitant chronic diseases share with COPD not only the underlying chronic inflammation of the target organs (i.e. lungs, myocardium, vessels, adipose tissue), but also clinical manifestations like fatigue and dyspnoea. For this reason, in patients with multi‐morbidity (eg COPD with chronic heart failure and hypertension, etc), the exacerbation of respiratory symptoms may be particularly difficult to investigate, as it may be caused by exacerbation of COPD and/or ≥ comorbidity, (e.g. decompensated heart failure, arrhythmias, thromboembolisms) without necessarily involving the airways and lung. In these cases the term ECOPD is inappropriate and misleading.     

Managing acute respiratory failure during exacerbation of chronic obstructive pulmonary disease

Exacerbations of chronic obstructive pulmonary disease (COPD) are a major health problem, causing more than half a million hospital admissions per year in the United States. Although overall mortality is low, it is substantially higher with severe exacerbations that require intensive care and mechanical ventilation. The majority of COPD exacerbations result from infection, with typical bacterial organisms most commonly identified. Numerous randomized controlled trials and meta-analyses have documented the benefits of antibiotics, low-flow oxygen, and systemic corticosteroids, and the therapeutic equivalency of the major classes of bronchodilators (short-acting beta-agonist and anticholinergics). Randomized controlled trials also demonstrate that noninvasive ventilation can decrease the incidence of intubation, shorten stay, reduce infectious complications, and improve survival. Although patients who require intubation have the worst prognosis, the vast majority of them can be successfully liberated from mechanical ventilation. For invasively ventilated patients the clinical emphasis should be on improving patient-ventilator interaction and avoiding dynamic hyperinflation (intrinsic positive end-expiratory pressure).     

Short-term effects of prone position in chronic obstructive pulmonary disease patients with severe acute hypoxemic and hypercapnic respiratory failure

Objective To assess the short-term effects of prone positioning (PP) in chronic obstructive pulmonary disease (COPD) patients with severe hypoxemic and hypercapnic respiratory failure requiring invasive mechanical ventilation.Design and setting Prospective observational study in the general intensive care unit of a university-affiliated hospital.Patients 11 consecutive COPD patients with persistent hypoxemia (PaO₂/FIO₂ 200 mmHg with FIO₂ 0.6) and hypercapnia requiring invasive mechanical ventilation. Patients with adult respiratory distress syndrome or left ventricular failure were excluded. Mean age was 73±11 years, mean weight 86±31 kg, mean SAPS II 53±10, and ICU mortality 36%.Interventions Patients were turned every 6 h.Measurements and results A response to PP (20% or greater PaO₂/FIO₂ increase) was noted in 9 (83%) patients. Blood gases were measured in the PP and supine (SP) positions 3 h after each turn, for 36 h, yielding six measurement sets (SP1, PP1, SP2, PP2, SP3, and PP3). PaO₂/FIO₂ was significantly better in PP: 190±26 vs. 113±9 mmHg for PP1/SP1, 175±22 vs. 135±16 mmHg for PP2/SP2, and 199±24 vs. 151±13 mmHg for PP3/SP3. After PP1 PaO₂/FIO₂ remained significantly improved, and the PaO₂/FIO₂ improvement from SP1 to SP2 was linearly related to PaO₂/FIO₂ during PP1 (r=0.8). The tracheal aspirate volume improved significantly from SP1 to PP1. PaCO₂ was not significantly affected by position.Conclusions PP was effective in treating severe hypoxemia in COPD patients. The first turn in PP was associated with increased tracheal aspirate.This article refers to the editorial     

Gradual versus abrupt weaning from respiratory support in acute respiratory failure and advanced chronic obstructive lung disease

Two methods of weaning from mechanical ventilation were compared in 18 instances of acute respiratory failure requiring mechanical ventilation for more than 30 days in patients with advanced chronic obstructive lung disease. All patients were ventilated using intermittent mandatory ventilation. Abrupt weaning (AW) consisted of abruptly discontinuing mechanical ventilation when the patients were considered ready for unassisted breathing. Gradual weaning (GW) involved a gradual reduction in the rate of intermittent mandatory ventilation before starting unassisted breathing. Gradual or abrupt weaning alone was used for weaning in five and four instances, respectively. Both methods were used in nine other instances. In the 14 instances when GW was tried, weaning was successful in three. In the 13 instances when AW was tried, weaning was successful in nine. The time in which mechanical ventilation was required was 64 +/- 31 (SD) days with GW and 42 +/- 12 (SD) days with AW. There was no difference in age, pulmonary function, or arterial blood gas results between the patients being weaned by the different methods. I conclude that GW offers no advantage over AW in weaning patients with advanced chronic obstructive lung disease requiring prolonged mechanical ventilation.     

无创通气治疗慢性阻塞性肺疾病急性发作伴呼吸衰竭的临床研究

目的 探讨无创通气在慢性阻塞性肺疾病(COPD)急性发作伴呼吸衰竭中的应用.方法 将50例COPD急性加重合并Ⅱ型呼吸衰竭患者随机分为对照组和实验组,每组25例.对照组用常规药物治疗,实验组用常规药物加无创正压通气治疗.结果 两组患者治疗前的基础情况和血气指标差异无统计学意义(P＞0.05).治疗后实验组呼吸频率(RR)、心率(HR)、动脉血pH、氧分压(PaO2)、二氧化碳分压(PaCO2)均明显改善(P＜0.05),但实验组与对照组比较,治疗后PaO2上升更明显(P＜0.01),PaCO2下降更明显(P＜0.01).治疗48h后,实验组和对照组呼吸困难明显缓解的人数分别为22例和13例(P＜0.05).实验组和对照组平均住院日分别为(12±5)d和(18±6)d(P＜0.01).结论 无创通气治疗COPD急性发作伴呼吸衰竭较仅用常规药物治疗能更快地缓解临床症状,提高PaO2和降低PaCO2.     

Physiologic effects of early administered mask proportional assist ventilation in patients with chronic obstructive pulmonary disease and acute respiratory failure

OBJECTIVE: To evaluate the physiologic short-term effects of noninvasive proportional assist ventilation (PAV) in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD). DESIGN: Prospective, physiologic study. SETTING: Respiratory intermediate intensive care unit. PATIENTS: Seven patients with acute respiratory failure requiring noninvasive mechanical ventilation because of exacerbation of COPD. INTERVENTIONS: PAV was administered by nasal mask as first ventilatory intervention. The setting of PAV involved a procedure to adjust volume assist and flow assist to levels corresponding to patient comfort. Volume assist was also set by means of the "run-away" procedure. Continuous positive airway pressure (CPAP) amounting to 2 cm H2O was always set by the ventilator. This setting of assistance (PAV) was applied for 45 mins. Thereafter, CPAP was increased to 5 cm H2O (PAV + CPAP-5) without any change in the PAV setting and was administered for 20 mins. Oxygen was delivered through a port of the mask in the attempt to maintain a target SaO2 >90%. MEASUREMENTS AND MAIN RESULTS: Arterial blood gases, breathing pattern, and inspiratory effort were measured during unsupported breathing and at the end of PAV, and breathing pattern and inspiratory effort were measured after 20 mins of PAV + CPAP-5. PAV determined a significant increase in tidal volume and minute ventilation (+64% and +25% on average, respectively) with unchanged breathing frequency and a significant improvement in arterial blood gases (PaO2 with the same oxygen supply, from 65 +/- 15 torr to 97 +/- 36 torr; PaCO2, from 80 +/- 11 torr to 76 +/- 13 torr; pH, from 7.30 +/- 0.02 to 7.32 +/- 0.03). The pressure-time product calculated over a period of 1 min (from 318 +/- 87 to 205 +/- 145 cm H2O x sec x min(-1)) was significantly reduced. PAV + CPAP-5 resulted in a further although not significant decrease in the pressure-time product calculated over a period of 1 min (to 183 +/- 110 cm H2O x sec x min(-1)), without additional changes in the breathing pattern. CONCLUSIONS: Noninvasive PAV is able to improve arterial blood gases while unloading inspiratory muscles in patients with acute exacerbation of COPD.     

Membrane oxygenators for acute respiratory insufficiency

Extracorporeal circulation with a membrane oxygenator (ECMO) was used in 11 patients with acute respiratory insufficiency who did not respond to conventional treatment. By pass was veno-arterial in every case, seven times with femoral artery return, three times with axillary artery return, and once with both femoral and axillary return. Five patients died on ECMO. Six patients were taken off ECMO and two of them are long-term survivors. In nine cases ECMO allowed short-term control of respiratory failure. The respective roles of oxygen supply from ECMO and the haemodynamic changes incurred by its use are discussed. Although use of ECMO for long periods seems less hazardous now, present results are restricted by the lack of therapy for the underlying pulmonary lesions.     

Hemodynamic and gas exchange responses to inhalation of nitric oxide in patients with the acute respiratory distress syndrome and in hypoxemic patients with chronic obstructive pulmonary disease

Objective: Inhalation of nitric oxide (NO) can improve oxygenation and decrease mean pulmonary artery pressure (MPAP) in patients with the acute respiratory distress syndrome (ARDS). It is not known whether inhaled NO exerts a similar effect in hypoxemic patients with chronic obstructive pulmonary disease (COPD). Design: Prospective clinical study. Setting: General intensive care unit in Sabadell, Spain. Patients: Nine mechanically ventilated COPD patients (mean age 72±2 years; forced expiratory volume in 1 s 0.91±0.11 l) and nine ARDS patients (mean age 57±6 years; mean lung injury score 2.8±0.1) Measurements and results: We measured hemodynamic and gas exchange parameters before NO inhalation (basal 1), during inhalation of 10 ppm NO (NO-10), and 20 min after NO was discontinued (in basal 2) in the ARDS group. In the COPD group, these parameters were measured before NO inhalation (basal 1), during different doses of inhaled NO (10, 20, and 30 ppm), and 20 min after NO was discontinued (basal 2). A positive response to NO was defined as a 20% increment in basal arterial partial pressure of oxygen (PaO₂). MPAP and pulmonary vascular resistance (PVR) decreased significantly, while other hemodynamic parameters remained unchanged after NO-10 in both groups. Basal oxygenation was higher in the COPD group (PaO₂/FIO₂ (fractional inspired oxygen) 190±18 mmHg) than in the ARDS group (PaO₂/FIO₂ 98±12 mmHg), (p<0.01). After NO-10, PaO₂/FIO₂ increased (to 141±17 mmHg, p<0.01) and Qva/Qt decreased (39±3 to 34±3%, p<0.01) in the ARDS group. There were no changes in PaO₂/FIO₂ and Qva/Qt when the NO concentration was increased to 30 ppm in the COPD group. In both groups, a correlation was found between basal MPAP and basal PVR, and between the NO-induced decrease in MPAP and in PVR. The NO-induced increase in PaO₂/FIO₂ was not correlated with basal PaO₂/FIO₂. In the ARDS group, six of the nine patients (66%) responded to NO and in the COPD group, two of nine (22%) (p=0.05). Conclusions: NO inhalation had similar effects on hemodynamics but not on gas exchange in ARDS and COPD patients, and this response probably depends on the underlying disease. Received: 19 December 1995 Accepted: 28 September 1996     

Physiological effects of noninvasive positive ventilation during acute moderate hypercapnic respiratory insufficiency in children

Introduction  A prospective physiological study was performed in 12 paediatric patients with acute moderate hypercapnic respiratory insufficiency to assess the ability of noninvasive positive pressure ventilation (NPPV) to unload the respiratory muscles and improve gas exchange. Materials and methods  Breathing pattern, gas exchange, and inspiratory muscle effort were measured during spontaneous breathing and NPPV. Results  NPPV was associated with a significant improvement in breathing pattern, gas exchange and respiratory muscle output. Tidal volume and minute ventilation increased by 33 and 17%, and oesophageal and diaphragmatic pressure time product decreased by 49 and 56%, respectively. This improvement in alveolar ventilation translated into a reduction in mean partial pressure in carbon dioxide from 48 to 40 mmHg (P = 0.01) and in respiratory rate from 48 to 41 breaths/min (P = 0.01). No difference between a clinical setting and a physiological setting of NPPV was observed. In conclusion, this study shows that NPPV is able to unload the respiratory muscles and improve clinical outcome in young patients admitted to the paediatric intensive care unit for acute moderate hypercapnic respiratory insufficiency. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.