Central respiratory drive in acute respiratory failure of patients with chronic obstructive pulmonary disease

Control of breathing was studied in patients with chronic obstructive pulmonary disease, both in the chronic state and during acute respiratory failure. The results were compared to those in a group of age-matched normal subjects. In patients breathing air, minute ventilation was not different during acute and chronic states, and was similar to that in normal subjects. The pattern of breathing, however, was different: acutely ill patients took shorter and smaller breaths, with a breathing frequency higher than that of normal subjects. The pattern of the chronic group was intermediate between that of acutely ill patients and that of normal subjects. Mouth occlusion pressure, an index of neuromuscular respiratory drive, was 5 times greater in acutely ill patients than in normal subjects. Administration of O2 at a flow of 5 L/min caused a small (14%), bus significant, decrease in minute ventilation due to decreased respiratory frequency. The tidal volume did not change, so the decrease in minute ventilation was the result of decreased inspiratory flow. This was associated with a decreased mouth occlusion pressure that was still 3 times greater than that of normal subjects. The increase in arterial PCO2, observed after administration of O2 was not correlated with the decrease in ventilation, indicating that other factors must be responsible for the increase in arterial PCO2. We concluded that (1) despite the poor mechanical advantage of the respiratory muscles in acute respiratory failure, the increased drive to breathe results in high mouth occlusion pressure and inspiratory flow, and (2) the increase in arterial PCO2, observed during administration of O2 is not related solely to changes in respiratory drive.     

Physical therapy practice patterns in acute exacerbations of chronic obstructive pulmonary disease

BACKGROUND AND OBJECTIVE:

The importance of the multidisciplinary approach to the management of chronic obstructive pulmonary disease is increasingly emphasized. The present study aimed to examine the current practice patterns of physical therapists involved in the management of patients hospitalized with an acute exacerbation of chronic obstructive pulmonary disease.

METHOD:

A self-administered postal survey was distributed to the rehabilitation departments of all Canadian acute care hospitals with more than 250 beds. The survey addressed patient assessment, treatment, education and discharge planning for intensive care unit and/or ward admissions.

RESULTS:

In total, 66% of hospitals (n=109) participated in the study, with provincial representation mainly from Ontario (n=36 [33%]) and Quebec (n=36 [33%]). Assessment and treatment techniques did not differ greatly between the ward and the intensive care unit. Assessment focused on patient observation, pulse oximetry and auscultation, and was reported to be used ‘always or frequently’ by 76%, 76% and 69% of respondents, respectively. Less than 18% of respondents used a measure of functional capacity, and health-related quality of life measures were rarely used. Treatment focused on ambulatory techniques, with 78% and 75% of respondents using mobility and transfer training ‘always or frequently’, respectively. The most common educational topics were breathing exercises and positioning, which were addressed by 68% and 67% of respondents, respectively.

CONCLUSION:

Patient assessment focused on physical impairments, with little use of measures of function or health-related quality of life, whereas treatment focused on mobility, with a lesser focus on airway clearance. Further study is needed to identify the factors that impact these practice patterns.     

Mechanisms of hypertension in patients with chronic obstructive pulmonary disease and acute respiratory failure

PURPOSE: To investigate the effects of hypoxemia, hypercapnia, and cardiovascular hormones (norepinephrine, endothelin-1, and atrial natriuretic factor) on blood pressure during acute respiratory failure. PATIENTS AND METHODS: Patients with chronic obstructive pulmonary disease and acute respiratory failure were divided into four groups of 10 patients each: hypoxemia-normocapnia, hypoxemia-hypercapnia, hypoxemia-hypocapnia, and normoxemia-hypercapnia. Plasma norepinephrine levels were determined by high-performance liquid chromatography with electrochemical detection. Plasma endothelin-1 and atrial natriuretic factor levels were radioimmunoassayed after chromatographic preextraction.RESULTS: Systolic blood pressure and cardiovascular hormone levels were greater in patients with hypercapnia (whether or not they also had hypoxemia) than in those with normocapnia and hypoxemia. For example, in patients with hypercapnia and normoxemia, the mean (+/- SD) systolic blood pressure was 183+/-31 mm Hg and the mean norepinephrine level was 494+/-107 pg/mL, as compared with 150+/- 6 mm Hg and 243+/-58 pg/mL in those with normocapnia and hypoxemia (both P<0.05). Similar results were seen for endothelin-1 and atrial natriuretic factor levels, and for the comparisons of hypoxemic patients who were hypercapnic with those who were normocapnic. CONCLUSIONS: These results suggest that blood carbon dioxide levels, rather than oxygen levels, are responsible for hypertension during acute respiratory failure, perhaps as a result of enhanced sympatho-adrenergic activity.     

Differences in patients with chronic pulmonary embolism and primary pulmonary hypertension

Chronic pulmonary embolism is a rare disease which can occur at first with pulmonary hypertension. In these cases it may be difficult to distinguish between primary pulmonary hypertension. We examined nine patients with Chronic Pulmonary Embolism (CPE) (three females and six males, mean age 45 +/- 13 years, range 21-67 years) and ten patients with Primary Pulmonary Hypertension (PPH) (seven females and three males, mean age 35 +/- 13 years, range 10-56 years) who came to our attention during the years 1973-1986 (mean follow up 3 years). All patients had an electrocardiogram, chest x-ray, echocardiogram, cardiac catheterization with pulmonary angiography; seven patients with CPE and eight with PPH had perfusion lung scans. Progressive dyspnoea was the main feature in all the patients; four out of nine with CPE and none of the ones with PPH had a previous history of thrombophlebitis. In all the patients the electrocardiogram, chest x-ray and echocardiogram showed signs of pulmonary hypertension, so that a clear distinction between the two groups was not possible. Cardiac catheterization showed pulmonary pressure values higher in patients with PPH as compared to the ones with CPE (systolic pressure 96 mmHg vs 70 mmHg, diastolic pressure 49 mmHg vs 31 mmHg, mean pressure 65 mmHg vs 45 mmHg). Pulmonary angiography in more than half of the patients with CPE showed a "cut off" of two or more lobar branches of the pulmonary arteries. In the patients with PPH pulmonary angiography showed a dilatation of the main pulmonary artery and a diffuse bilateral hypoperfusion. Perfusion lung scan in all the cases of CPE showed zonal perfusion defects, while in all cases of PPH, with the exception of one, it was largely normal. Venograms in the districts of the inferior vena cava demonstrated thrombosis in two out of six patients with CPE. Negative venograms were found in the five patients with PPH who had this investigation performed. One patient with CPE had a surgical embolectomy, the other eight had anticoagulant oral treatment. During the follow-up period three patients with CPE and five with PPH died within five years and within fifteen months respectively, of the diagnosis.(ABSTRACT TRUNCATED AT 400 WORDS)     

Work of breathing in patients with chronic obstructive pulmonary disease in acute respiratory failure

In 11 spontaneously breathing patients with chronic obstructive pulmonary disease (COPD) in acute ventilatory failure, we measured the total inspiratory (WItot) and total resistive (WI + Eres) work rate of breathing, together with lung mechanics (dynamic pulmonary elastance and inspiratory and expiratory pulmonary flow resistance). All variables were markedly increased compared with those in normal subjects. No significant correlation was found between WItot and WI + Eres with lung mechanics data. However, when WItot and WI + Eres were expressed per liter of ventilation, a significant positive correlation was found with all lung mechanics data. These results indicate that although in patients acutely ill with COPD, work rate and work per liter of ventilation are increased, only the latter is related to the severity of pulmonary mechanical impairment, and it could be used as one of the criteria for extubation. In addition, our results indicate that at end-expiration the alveolar pressure was positive (range, 6 to 13 cm H2O) in all patients (intrinsic PEEP), a fact that must necessarily affect hemodynamics; furthermore, it imposes an extra burden on the inspiratory muscles.     

Incidence and risk factors of chronic thromboembolic pulmonary hypertension in patients after acute pulmonary embolism

Background

Early identification and treatment of chronic thromboembolic pulmonary hypertension (CTEPH) are critical to prevent disease progression. We determined the incidence and risk factors for CTEPH in patients with a first episode of acute pulmonary embolism (PE).

Methods

In this study, consecutive patients with first-episode acute PE were followed for ≤5 years. Pulmonary hypertension (PH) was screened for by echocardiography. Suspected cases were evaluated by right heart catheterization (RHC) and pulmonary angiography (PA). If invasive procedures were not permitted, PH was diagnosed by systolic pulmonary artery pressure (SPAP) >50 mmHg. Diagnosis of CTEPH was confirmed by PA, ventilation/perfusion (V/Q) lung scan, or computed tomography (CT) PA (CTPA).

Results

Overall, 614 patients with acute PE were included (median follow-up, 3.3 years). Ten patients were diagnosed with CTEPH: cumulative incidence 0.8% [95% confidence interval (CI), 0.0-1.6%] at 1 year, 1.3% (95% CI, 0.3-2.3%) at 2 years, and 1.7% (95% CI, 0.7-2.7%) at 3 years. No cases of CTEPH developed after 3 years. History of lower-limb varicose veins [hazard ratio (HR), 4.3; 95% CI, 1.2-15.4; P=0.024], SPAP >50 mmHg at initial PE episode (HR, 23.5; 95% CI, 2.7-207.6; P=0.005), intermediate-risk PE (HR, 1.2; 95% CI, 1.0-1.4; P=0.030), and CT obstruction index over 30% at 3 months after acute PE (HR, 42.5; 95% CI, 4.4-409.8; P=0.001) were associated with increased risk of CTEPH.

Conclusions

CTEPH was not rare after acute PE in this Chinese population, especially within 3 years of diagnosis. Lower-limb varicose veins, intermediate-risk PE with elevated SPAP in the acute phase, and residual emboli during follow-up might increase the risk of CTEPH.     

Influence of acute respiratory failure on renal function in advanced chronic obstructive pulmonary disease and chronic cor pulmonale

Renal function was assessed in 89 patients with advanced chronic obstructive pulmonary disease and chronic cor pulmonale, 62 of them had respiratory failure, 18 health aged served as control. The results showed that the creatinine clearance and the free water clearance were decreased in 82.3% and 69.5% of patients with respiratory failure respectively. The renal function was impaired in case of hypoxia, PaO2 less than or equal to 6.0 kPa (45 mmHg), mean 5.33 kPa (40 mmHg). Hypercapnia was one of the most important factors that effected the renal function. There was a clinical threshold which effected the renal function, i.e. PaCO2 equals more than 8.67 kPa (65 mmHg). Renal function was greatly impaired if hypercapnia and hypoxia exist at the same time. The impairment of renal function was further marked when right heart failure and acidosis developed. The causes and effects of the abnormality of renal function were preliminarily discussed.     

双水平气道正压通气治疗慢性阻塞性肺疾病合并急性呼吸衰竭的临床研究

目的探讨经鼻面罩双水平气道正压(BiPAP)通气在慢性阻塞性肺疾病(COPD)合并急性呼吸衰竭早期的应用价值。方法将80例COPD合并急性呼衰患者分为2组,每组40例,在进行抗感染、对症等常规治疗的同时,分别给予持续静滴可拉明及经鼻面罩BiPAP通气治疗6小时,判断两组之间治疗前后生命体症及血气分析变化。结果两组治疗6小时后,机械通气组在血压、心率、呼吸频率方面改善均显著优于对照组(P<0.01);对照组pH值无改善,而机械通气组pH值显著改善,与对照组相比有显著差异(P<0.01);机械通气组和对照组治疗后均有PaO2上升和PaCO2下降,但机械通气组改善更明显,与对照组相比有显著差异(P<0.01)。结论经鼻面罩BiPAP通气适合治疗COPD合并急性呼衰患者,其在改善临床症状和动脉血气指标方面均优于常规治疗,值得临床推广。     

双水平气道正压通气治疗慢性阻塞性肺疾病合并急性呼吸衰竭的临床研究

目的探讨经鼻面罩双水平气道正压（BiPAP）通气在慢性阻塞性肺疾病（COPD）合并急性呼吸衰竭早期的应用价值。方法将80例COPD合并急性呼衰患者分为2组，每组40例，在进行抗感染、对症等常规治疗的同时，分别给予持续静滴可拉明及经鼻面罩BiPAP通气治疗6小时，判断两组之间治疗前后生命体症及血气分析变化。结果两组治疗6小时后，机械通气组在血压、心率、呼吸频率方面改善均显著优于对照组（P〈0．01）；对照组pH值无改善，而机械通气组pH值显著改善，与对照组相比有显著差异（P〈0．01）；机械通气组和对照组治疗后均有PaO2上升和PaCO2下降，但机械通气组改善更明显，与对照组相比有显著差异（P〈0．01）。结论经鼻面罩BiPAP通气适合治疗COPD合并急性呼衰患者，其在改善临床症状和动脉血气指标方面均优于常规治疗，值得临床推广。     

Dopamine effects on diaphragmatic strength during acute respiratory failure in chronic obstructive pulmonary disease

STUDY OBJECTIVE: To assess the effects of dopamine, which has an inotropic effect on the myocardium and increases renal and splanchnic blood flow, on diaphragmatic contraction. DESIGN AND PATIENTS: We studied the changes in transdiaphragmatic pressure during electrical bilateral supramaximal stimulation of the phrenic nerves in eight patients with chronic obstructive pulmonary disease during acute respiratory failure. In three patients, changes in diaphragmatic blood flow were also evaluated. METHODS: All patients were intubated and artificially ventilated. Stimulated transdiaphragmatic pressure, cardiac output, evaluated with a Swan Ganz catheter, and diaphragmatic blood flow, evaluated by timed volume collections of left phrenic venous effluent (a catheter was introduced into the right femoral vein and advanced into the left inferior phrenic vein) were measured before dopamine infusion, every 10 minutes after the onset of dopamine infusion (10 micrograms/kg body weight.min during 30 minutes) and 15 minutes after the end of dopamine infusion. Arterial blood gases and pH were measured before and at the end of dopamine infusion. MEASUREMENTS AND MAIN RESULTS: Arterial blood gases and pH were maintained within normal range by mechanical ventilation throughout the study. With dopamine infusion, heart rate increased by 17% (P less than 0.001) and cardiac output by 40% (P less than 0.001) on the average. The increase in cardiac output was accompanied by a marked increase in diaphragmatic blood flow (30% on the average) in the three patients in whom it was measured (P less than 0.001). Diaphragmatic strength also increased significantly during dopamine administration. Transdiaphragmatic pressure for an identical phrenic stimulation increased by 30% (P less than 0.001) on the average. The changes in cardiac output, diaphragmatic blood flow, and transdiaphragmatic pressure persisted throughout the infusion period; all values returned to control values 15 minutes after the end of dopamine administration. CONCLUSIONS: Dopamine has a potent effect on diaphragmatic strength generation and diaphragmatic blood flow in patients with chronic obstructive pulmonary disease during acute respiratory failure. It is possible to improve diaphragmatic contraction in these patients by administering pharmacologic agents that augment diaphragmatic blood flow.     

Variability in physician estimates of survival for acute respiratory failure in chronic obstructive pulmonary disease

Physician estimates of patient survival often influence clinical decisions. I studied physician estimates of survival for a patient with acute respiratory failure and underlying chronic obstructive pulmonary disease to identify the factors that may influence these estimates. Physicians (n = 205) completed the same patient management problem and estimated the length of survival for the hypothetical patient. Physician estimates of survival were quite variable, ranging from one month to five years. Shorter estimates of survival were associated with acquisition of select case information: subjective information from family members and a professional colleague, and physiologic and functional data previously demonstrated to be predictive of survival. The study suggests that estimates of survival for the same patient may vary among physicians because of different considerations of social and physiologic case information. Physician estimates of patient survival and treatment recommendations may become more uniform with additional education or decision aids regarding the prognostication of survival.     

Controlled oxygen administration in acute respiratory failure in chronic obstructive pulmonary disease: A reappraisal

Controlled oxygen therapy may aggravate carbon dioxide retention during acute exacerbations of chronic obstructive pulmonary disease (COPD). Of 50 consecutive patients with COPD and acute respiratory failure, 13 required intubation because of carbon dioxide narcosis. With discriminant analysis of their arterial oxygen tension (PaO₂) and pH on admission, a diagram separated patients into those at high risk and those at low risk for carbon dioxide narcosis. This diagram was then used to predict carbon dioxide narcosis in 73 patients with COPD and acute respiratory failure who were treated with controlled oxygen. In 16 of these patients carbon dioxide narcosis developed. Thirteen (81 per cent) were predicted by the diagram to be at high risk for this complication. Only two (4 per cent) patients judged by the diagram to be at low risk for carbon dioxide narcosis required mechanical ventilation. Utilizing an oxygen tension (PO₂), carbon dioxide tension (PCO₂) diagram a patient's ventilatory response was compared to that of ambulatory patients with COPD. These data suggest that hypoxemia and acidosis are more discriminatory for “carbon dioxide narcosis” than hypercapnia.     

Differences in prostaglandin metabolism in cultured aortic and pulmonary arterial endothelial cells exposed to acute and chronic hypoxia

In vivo, a marked difference in blood oxygen tension exists between the pulmonary artery and the aorta. Responses of vascular endothelial cells from these vessels to changes in ambient oxygen might be influenced by the oxygen tension to which they are continuously exposed in vivo or by their anatomic site. To explore this hypothesis, we initially studied the production of the cyclooxygenase metabolites prostacyclin and thromboxane in bovine aortic and main pulmonary arterial endothelial cells grown in 21% O2 and exposed to different degrees of acute hypoxia over a wide range of times. We found that short-term hypoxia (3% or 0% O2) rapidly and transiently activates the cyclooxygenase pathway in both cell types, with a more rapid response in bovine aortic endothelial cells. To determine whether culture in an oxygen tension similar to that to which main pulmonary arterial endothelial cells are exposed in vivo alters this response, we evaluated these cyclooxygenase metabolites in bovine aortic and main pulmonary arterial endothelial cells cultured long-term in 3% O2, both at baseline and after exposure to acute anoxia (0% O2). In both cell types, we found a decrease in prostacyclin and thromboxane synthesis at baseline and evidence of an increase in the Vmax of thromboxane synthetase following stimulation with exogenous arachidonic acid. In chronically hypoxic cells exposed to acute anoxia, there were marked differences in enzyme activity compared with that in endothelial cells maintained in 21% O2 with differences depending on the origin of the endothelial cells. In bovine aortic endothelial cells, production of neither cyclooxygenase metabolite increased; in bovine main pulmonary arterial endothelial cells, only thromboxane production increased, suggesting isolated activation of the cyclooxygenase-thromboxane synthetase pathway. These studies demonstrate that acute and chronic hypoxia have profound effects on endothelial cell cyclooxygenase metabolism and that these effects depend on the duration and degree of the hypoxic exposure and the vascular bed from which the endothelial cells are derived.