PaO2 increases with coughing in patients with chronic lung disease

We considered if the cyanosis frequently observed during a cough attack in patients with chronic lung disease was due to worsening hypoxemia. To investigate the effects of cough on PaO₂, we measured arterial blood gases before and after a voluntary coughing period of 45 sec, in 11 patients with Interstitial Lung Disease (ILD) and 14 patients with Chronic Obstructive Lung Disease (COPD). All patients significantly increased (p < 0.05) their PaO₂ (COPD: from 49 ± 2 to 60 ± 2 mmHg; ILD from 44 ± 2 to 51 ± 3 mmHg, mean ± SD) and decreased their PaCO₂. We conclude that stable patients with COPD and ILD increase their PaO₂ with coughing most likely due to hyperventilation. The cyanosis observed could be due to peripheral circulatory effects of coughing.     

Effects of continuous positive airway pressure on lung function in patients with chronic obstructive pulmonary disease and sleep disordered breathing

OBJECTIVE: Sleep disordered breathing (SDB), namely hypoventilation and obstructive sleep apnoea, occur in about 50% of patients with severe chronic obstructive pulmonary disease (COPD). Previous studies that have investigated the reversal of SDB in such patients with nasally applied intermittent positive airway pressure have reported a fall in PaCO2 but little change in airflow obstruction. We reasoned that the lack of improvement in airflow obstruction may be due to insufficient expiratory pressure. Accordingly, we sought to determine the effects of chronic nasal continuous positive airway pressure (CPAP), at highest tolerable levels, upon blood gases and airflow obstruction in patients with severe COPD and SDB. METHODOLOGY: Fourteen patients were studied, ten of whom were able to tolerate CPAP (10.2 +/- 0.9 cmH2O) for at least 3 months. RESULTS: Within the CPAP compliant group, there was a fall in PaCO2 (58.0 +/- 3.5 to 48.0 +/- 0.9 mmHg, P = 0.015) associated with a rise in PaO2 (54.8 +/- 3.8 to 63.2 +/- 1.8 mmHg, P = 0.015) and forced expiratory volume in 1 s (0.95 +/- 0.13 to 1.10 +/- 0.13 L, P < 0.005). Concurrent with these improvements was a substantial fall in hospitalization rates (from 3.85 to 0.73 admissions per annum). CONCLUSION: Improvements in gas exchange, airflow obstruction and hospitalization rates were observed in patients with COPD and SDB treated with nasal CPAP during sleep.     

Significance of pulmonary artery pressure in emphysema patients with mild-to-moderate hypoxemia

The guidelines of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) do not recommend the measurement of pulmonary artery pressure in patients with chronic obstructive pulmonary disease (COPD). This is on the basis that the mean pulmonary artery pressure (mPAP) does not provide more clinical information than measurement of the oxygen tension in arterial blood (PaO2). The mPAP correlates well with PaO2 in emphysema patients with severe hypoxemia (PaO2 < or = 7.3 kPa (55 mmHg)). However, the occurrence and significance of mPAP is unclear in patients without severe hypoxemia (PaO2 > 7.3 kPa (55 mmHg)). In order to evaluate the usefulness of measurement of mPAP in emphysema patients without severe hypoxemia, we performed right heart catheterization and investigated the pulmonary hemodynamics of 53 patients without severe hypoxemia. In addition, we identified long-term prognostic factors with a mean follow-up term of 77 months after right heart catheterization. Seventeen of 27 patients with mild-to-moderate hypoxemia exhibited pulmonary hypertension (mPAP > or = 2.7 kPa (20 mmHg)) and the classification according to severity in GOLD exhibited a greater correlation to mPAP than PaO2. Moreover, only mPAP was found to be a significant prognostic factor according to multivariate proportional hazards analysis (P = 0.01). We conclude that mPAP is more informative about the severity of emphysema than PaO2 in patients with mild-to-moderate hypoxemia.     

Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease

Sixteen patients with severe chronic obstructive pulmonary disease (COPD) (average values at the onset of O2 therapy: FEV1, 891 +/- 284 ml; PaO2, 50.2 +/- 6.6 mmHg; PaCO2, 51.0 +/- 6.4 mmHg) underwent 3 consecutive right heart catheterizations. The first was performed 47 +/- 28 months (T0) before the onset of long-term O2 therapy (LTO2). The second was performed just before the onset of LTO2 (T1). The third was performed after 31 +/- 19 months of LTO2 (T2). Oxygen therapy (15 to 18 h/day) was prescribed on the basis of usual criteria. From T0 to T1, PaO2 decreased from 59.3 +/- 9.4 to 50.2 +/- 6.6 mmHg, and mean pulmonary arterial pressure (Ppa) worsened from 23.3 +/- 6.8 to 28.0 +/- 7.4 mmHg (p less than 0.005). From T1 to T2, PaO2 was stable, whereas Ppa decreased from 28.0 +/- 7.4 to 23.9 +/- 6.6 mmHg (p less than 0.05). Pulmonary hypertension improved in 12 of the 16 patients. Before the onset of LTO2 (from T0 to T1), there was a yearly increase in Ppa of 1.47 +/- 2.3 mmHg, whereas during LTO2 a yearly decrease of 2.15 +/- 4.4 mmHg was observed, and the difference between these 2 values was highly significant. The changes in Ppa either from T0 to T1 or from T1 to T2 were not associated with concomitant changes in cardiac output or pulmonary capillary wedge pressure but were related to changes in pulmonary vascular resistance. These results suggest that LTO2 for 15 to 18 h/day can reverse the progression of pulmonary hypertension in a high percentage of patients with severe COPD, but that normalization of Ppa is rarely observed.     

Long-term effect of almitrine bismesylate in patients with hypoxemic chronic obstructive pulmonary disease

A long-term evaluation of the therapeutic efficacy and safety of oral almitrine bismesylate (AB) (50 mg twice daily) was made on 25 patients with COPD and moderate hypoxemia residing at an altitude of 1,500 m in a double-blind placebo-controlled study. Thirteen patients receiving AB (baseline PaO2, 54.3 +/- 4.9 mm Hg; mean +/- SD) and 12 patients receiving placebo (baseline PaO2, 53.0 +/- 4.1 mmHg) were periodically followed by arterial blood gas and other pulmonary function studies and plasma levels of AB. Eight patients receiving AB and nine patients receiving placebo were followed for 1 yr; all patients were followed for at least 90 days. AB administration resulted in an increase in PaO2 to 62.2 +/- 9.3 mm Hg (p less than 0.01) on Day 28. The increase was maintained until Day 360 (63.8 +/- 4.6 mm Hg; p less than 0.01). The mean plasma concentration of AB on Day 28 was approximately one-half that on Day 90 when the plasma level reached a near maximum. AB was associated with weight loss (five of 13 patients receiving AB lost more than 10% of their baseline body weight) and peripheral paresthesias of the lower extremities (three patients), both occurring at the peak plasma levels of the drug. We conclude that AB causes a long-term improvement in arterial oxygenation in hypoxemic patients with COPD residing at an altitude of 1,500 m. Our data suggest that lower doses of AB might produce the same effect on PaO2 with less adverse associated effects, and this should be tested in future studies.     

Combined inhalation of nitric oxide and oxygen in patients with moderate to severe COPD: effect on blood gases

Inhaled nitric oxide (NO) has been reported to improve oxygenation in patients with COPD if administered in combination with oxygen (O2). Little, however, is known about the variability of these effects and the potential influence of body position. Twenty-six spontaneously breathing patients with moderate to severe COPD inhaled clean air, O2(FiO2, 0.29), 5 ppm NO, 5 ppm NO+O2, 10 ppm NO+O2, 10 ppm NO, and again clean air in an upright position. Blood gas analysis from arterialized capillary blood was performed after each inhalation. Tests were repeated on different days to assess the variability of the response. Furthermore, eight patients were studied in both upright and supine position while inhaling 5 ppm NO in the presence or absence supplemental O2. As compared to clean air, NO led to a mean decrease in PaO2 of -0.9 mmHg at 5 ppm and of -2.8 mmHg at 10 ppm NO. Similarly, NO+O2 led to a dose-dependent fall in PaO2 of -1.8 and -3.6 mmHg, respectively, as compared to O2. Average within-subject variation (SD) of the effects elicited by 5 and 10 ppm NO was 2.4 and 2.3 mmHg without additional O2, and 4.7and 5.3 mmHg with O2. The effects of 5 ppm NO+O2 differed significantly between upright and supine position; as compared to O2 alone, mean (SD) changes were -3.7 +/- 5-8 vs. +1.1 +/- 4.9 mmHg, respectively. Our findings suggest thatthe addition of NO to inhaled oxygen, when given in an upright position, does not lead to an improvement of PaO2 in patients with moderate to severe COPD. Furthermore, it turned out that it was not possible to define responders and non-responders to inhaled NO on an individual basis, since the variability ofthe responses was similar to the mean     

Normocapnia during nIPPV in chronic hypercapnic COPD reduces subsequent spontaneous PaCO2

Hypercapnia has been accepted during nasal intermittent positive pressure ventilation (nIPPV) and during subsequent spontaneous breathing in patients with chronic hypercapnic respiratory failure (HRF) due to COPD. We tested the hypothesis that nIPPV aimed at normalizing PaCO2 will reduce PaCO2 during subsequent spontaneous breathing. For that purpose 14 consecutive inpatients (age 61.4 +/- 9.9 years) with chronic HRF due to COPD were established on passive pressure-controlled nIPPV in a stepwise approach. Assisted ventilation with supplemental oxygen to reach normoxemia was started followed by passive ventilation with a stepwise increment in the inspiratory pressure and finally by a stepwise increase in the respiratory rate to establish normocapnia. Baseline pulmonary function parameters were: FEV1 0.97 +/- 0.43 l, PaCO2 59.5 +/- 8.4 mmHg, PaO2 49.9 +/- 7.8 mmHg, HCO3- 35.6 +/- 5.2 mmol/l, pH 7.39 +/- 0.04. Normoxemia as well as normocapnia was thus established by decreasing PaCO2 by 19.5 +/- 7.0 mmHg during nIPPV within 8.8 +/- 3.8 days (P < 0.001) (inspiratory pressure 29.8 +/- 3.8 mmHg, respiratory rate 22.9 +/- 1.9 BPM). Spontaneous PaCO2 measured 4 h after cessation of nIPPV decreased to 46.0 +/- 5.5 mmHg (P < 0.001), and HCO3- decreased to 27.2 +/- 3.0 mmol/l (P < 0.001). At 6 months of follow-up, II patients continued nIPPV with stable blood gases and with a decrease of P0.1/Plmax from 9.4 +/- 4.3% to 5.9 +/- 2.0% (P < 0.005). In conclusion, normalization of PaCO2 by passive nIPPV in patients with HRF due to COPD is possible and leads to a significant reduction of PaCO2 during subsequent spontaneous breathing and is associated with improved parameters of respiratory muscle function.     

Effects of hydralazine on hemodynamics, ventilation, and gas exchange in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Reports on hemodynamic effects of hydralazine on pulmonary hypertension (primary or secondary) usually include cases with severe disease or with mixed varieties of pulmonary vascular disease. Serious side effects and death have been reported. Effects of this drug on ventilation and gas exchange are unknown. We investigated the short-term effects of hydralazine treatment on hemodynamics, ventilation, and gas exchange in a relatively homogeneous group of patients with severe chronic obstructive pulmonary disease and moderate exertional pulmonary hypertension (mean pulmonary artery pressure, 43 +/- 3 mmHg). Hydralazine produced significant improvement in cardiac index, total pulmonary resistance, and oxygen transport. We also observed significant improvement in alveolar ventilation (mean PaCO2, decreased from 47 +/- 2 to 40 +/- 3 mmHg at rest and from 51 +/- 3 to 43 +/- 3 mmHg during exercise). The severe exertional hypoxemia of the group (mean PaO2, 48 +/- 2 mmHg) improved significantly (mean PaO2, 57 +/- 3 mmHg). Four of 11 patients showed increased exercise tolerance after hydralazine. This change is probably related to a combined improvement in hemodynamics plus a newly observed improvement in gas exchange and ventilation. Three of 14 patients could not tolerate hydralazine because of marked tachycardia. Serious side effects were not observed in the remaining group.     

Repeated waon therapy improves pulmonary hypertension during exercise in patients with severe chronic obstructive pulmonary disease

OBJECTIVES: Repeated Waon therapy, which uses a far infrared-ray dry sauna system, improved the vascular endothelial function and the cardiac function in patients with chronic heart failure. In patients with chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH) is associated with a poor prognosis. We investigated whether repeated Waon therapy improves PH, cardiac function, exercise tolerance, and the quality of life (QOL) in patients with COPD. METHODS: Consecutive 13 patients with COPD, who met the Global Initiative for Chronic Obstructive Lung Disease criteria and had breathlessness despite receiving conventional treatments, were recruited for this study. They underwent Waon therapy at 60 degrees C in sauna for 15 min following 30 min warmth with blankets outside of the sauna room. This therapy was performed once a day, for 4 weeks. Cardiac function, exercise tolerance, and St. George's Respiratory Questionnaire (SGRQ) were assessed before and 4 weeks after Waon therapy. RESULTS: Right ventricular positive dP/dt at rest elevated significantly from 397 +/- 266 to 512 +/- 320 mmHg/s (p = 0.024) after the therapy. While the PH at rest did not significantly decrease, the PH during exercise decreased significantly from 64 +/- 18 to 51 +/- 13 mmHg (p = 0.028) after Waon therapy. Furthermore, the therapy prolonged the mean exercise time of the constant load of cycle ergometer exercise test from 360 +/- 107 to 392 +/- 97 s (p = 0.032). The total scores of SGRQ improved from 59.7 +/- 16.9 to 55.3 +/- 17.2 (p = 0.002). In addition, no adverse effects were observed related to Waon therapy. CONCLUSIONS: Repeated Waon therapy improved right ventricular positive dP/dt, PH during exercise, exercise tolerance and the QOL in patients with severe COPD.     

A comparative study of patients with chronic obstructive pulmonary disease with and without obstructive sleep apnea syndrome

We aimed to study whether the presence of obstructive sleep apnea syndrome (OSAS) in patients with chronic obstructive pulmonary disease (COPD) led to differences in clinical picture, gas exchange during awake and sleep states and mechanical ventilation, in comparison with patients with COPD alone. We enrolled 48 COPD patients. In 26 (54.1%), OSAS was ruled out (non-OSAS COPD group) by polysomnography, and in 22 (45.8%) associated OSAS was diagnosed (OSAS COPD group). Patients in the OSAS COPD group experienced greater daytime sleepiness and less dyspnea. Body mass index was not significantly difference. The OSAS COPD group had significantly lower daytime PaO2 (66.4 +/- 10.4 mmHg in the OSAS COPD group and 75.5 +/- 11.2 mmHg in the non-OSAS COPD group; p = 0.01); there were no differences in PaCO2.Pimax in the OSAS-COPD group was 70.6 +/- 23.8 cmH2O, a level that was significantly lower than in the non-OSAS COPD group (Pimax 90.5 +/- 26.1 cmH2O; p = 0.04). Patients in the non-OSAS COPD group experienced longer periods of REM sleep. Nighttime saturation parameters were significantly different in the group with OSAS. We conclude that patients with both OSAS and COPD experience greater oximetric changes than those without OSAS, during both sleep and awake states. The deterioration of respiratory muscle pressures in such patients may play an important role in the changes. The groups also present differences in the intensity of some symptoms, such as degree of daytime sleepiness and dyspnea.     

One-year non-invasive ventilation in chronic hypercapnic COPD: effect on quality of life

The data on long-term application of non-invasive ventilation (NIV) in patients with chronic respiratory failure due to COPD are contradictory. We evaluated the effect of the addition of NIV to optimal treatment for 1 year on the quality of life of stable hypercapnic COPD patients. NIV was offered to 49 of 58 initially enrolled consecutive patients, of whom 22 refused NIV and comprised the standard treatment group whereas 27 received NIV. Quality of life was assessed with the SF-36 questionnaire. Additional measurements included blood gases, pulmonary function tests, dyspnea, daytime sleepiness, exacerbations and hospitalizations. The NIV group showed a significant improvement in quality of life in the third month, both in the Physical (31+/-4 to 38+/-8, p<0.0001) and the Mental Component Summary Score (28+/-7 to 40+/-10, p=0.009), that was maintained until the twelfth month. PaCO2 decreased by the first month in the NIV group (54+/-4.5 to 44.6+/-5.6 mmHg, p<0.0001), and PaO2 rose during the sixth month (58.9+/-5.7 to 64.4+/-6.5 mmHg, p=0.004). Dyspnea and diurnal sleepiness improved significantly. No significant improvements were observed in the control group. Patients on NIV spent less days in the hospital compared to controls. NIV when added to optimal medical treatment has beneficial effects on quality of life in stable hypercapnic COPD patients, with additional improvements in arterial blood gases, dyspnea and daytime sleepiness.     

Pulmonary blood volume in patients with interstitial pneumopathy and pulmonary heart disease. Its study at rest and during exercise

Pulmonary blood volume (PBV) measurements have been reported in chronic lung disease that do not include diffuse interstitial lung disease (ILD) and cor pulmonale (CP). In this study, PBV was measured using the double injection single sampling method, at rest and at exercise in ten patients with ILD due to extrinsic allergic alveolitis (n = 6) or usual interstitial pneumonia (n = 4). Lung biopsies were obtained in 8 patients, and in none of them the stage of fibrosis was predominant over inflammation. The degree of vascular lesions was in four patients grade I and in four grade II (Heath-Edwards classification). At rest, most of the patients had elevated mean pulmonary artery pressure (PAP) and vascular resistance (PVR), (mean PAP 30 +/- 4 mmHg and 336 +/- 171 d.s. cm.-5, respectively), hypoxemia (paO2 = 48 +/- 2 mmHg) and a severely reduced PBV (53.6 +/- 11 ml.s.qm.). At exercise, pulmonary arterial hypertension worsened and, although PBV value increased significantly (rest = 53.6 +/- 11.6 ml.m2, s.qm. exercise 132 +/- 28 ml.s.qm.p less than 0.01) it remained abnormally low with respect to normal value. Comparison of the mean intravascular pressure-PBV measurements relationship in different lung diseases showed that ILD patients with CP have the greatest abnormality. Possible explanations for the severe reduction in PBV include restriction of extra-alveolar vessels as a consequence of lung volume loss, restriction of intra-alveolar vessels due to structural and functional changes imposed by the inflammation-fibrosis process and vascular restriction due to vasoactive factors (alveolar hipoxia).     

Gas exchange alterations in patients with chronic obstructive lung disease

In a series of 23 patients with COPD, Wagner et al showed three distinct patterns of VA/Q distributions and a correlation between Burrows' clinical classification and the observed distribution patterns. Using the inert gas method, we studied 51 patients suffering from severe but stable COPD (FEV1 = 0.84 +/- 0.38 L; PaO2 = 58.5 +/- 10.5 mm Hg; PaCo2 = 48 +/- 6 mmHg; Ppa = 22 +/- 8 mmHg) breathing room air in a steady state. The H pattern (high mode of VA in high VA/Q) was found in 24 cases. There was an L pattern (Q mode in low VA/Q units) in nine cases and an HL (high-low) pattern in 16 cases (two patients were assigned another group). The analysis of the distribution data confirmed that VA/Q heterogeneity was the main factor underlying gas exchange disturbances in COPD. The PaO2 of the H subjects was higher than that of both HL (p less than 0.02) and L subjects. The true shunt value in the L group was significantly lower than in the H and HL groups. However, the relationship between clinical or functional aspects and distribution was not direct. The fraction of patients of H, HL, or (H + HL) types was nearly identical in the three clinical groups. The H pattern was found to be predominant in cases of COPD.     

Cough in COPD: correlation of objective monitoring with cough challenge and subjective assessments

BACKGROUND: The relationships between objective cough rates, cough reflex sensitivity, subjective estimates of cough frequency, and cough-related quality of life in patients with COPD are poorly understood. SUBJECTS: Twenty-six patients with stable COPD who complained of cough (76.9% men; mean +/- SD age, 68.7 +/- 6.9 years; mean FEV(1), 54.2 +/- 12.0% of predicted; median smoking history, 42.4 pack-years [range, 13 to 135 pack-years]). METHODS: Subjects performed a cough challenge test, ambulatory daytime and overnight sound recordings, scored the severity of cough (0 to 5 score and visual analog scale) for each recording period, and completed a cough-specific quality of life questionnaire (CQLQ). Coughs were counted manually and quantified in terms of cough seconds per hour (cs/h): the number of seconds within the recording that contain cough. RESULTS: Overall median time spent coughing was 7.5 cs/h (range, 2.7 to 23.1 cs/h; daytime median, 12.4 cs/h [range, 3.3 to 40.4 cs/h]; overnight, 1.9 cs/h [0.0 to 19.0 cs/h]) [p = <0.01]. Median log concentration of citric acid eliciting five coughs (C5) was - 0.9 mol/L (range, - 1.5 to 0.0 mol/L). Day time but not overnight time spent coughing was significantly correlated with log C5 (log C5 r = - 0.49, p = 0.02, and r = - 0.20, p = 0.37, respectively). Subjective cough scores and visual analog scales were moderately associated with objective time spent coughing: daytime (r = 0.37, p = 0.03, and r = 0.41, p = 0.03) and overnight (r = 0.48, p = <0.01, and r = 0.5, p = 0.01), respectively. CONCLUSIONS: Subjective measures of cough and cough reflex sensitivity are statistically related to time spent coughing in patients with COPD, but with low-to-moderate levels of correlation. These measures have insufficient predictive value to substitute for objective time spent coughing; however, in conjunction with the CQLQ, they may provide a qualitative dimension to the assessment of cough.     

One year treatment with almitrine improves hypoxaemia but does not increase pulmonary artery pressure in COPD patients.

Almitrine bismesylate, a chemoreceptor agonist, improves hypoxaemia in a high percentage of chronic obstructive pulmonary disease (COPD) patients and its long-term use may thus be of interest in these patients. The course of pulmonary haemodynamics during a one year treatment was investigated in severe COPD patients (forced expiratory volume in one second FEV1 = 1,040 +/- 80 SEM ml) with persistent hypoxaemia (initial arterial oxygen tension (PaO2) in the range 6.6-8.6 kPa (50-65 mmHg]. Patients were given either almitrine (A, n = 27), 100 mg.day-1, during two consecutive months per quarter followed by a one month wash-out period (intermittent "schedule"), or placebo (P, n = 18) with the same schedule. Eleven patients in group A and 8 in group P could not complete the one year study because of lack of compliance, worsening of respiratory insufficiency, or for other reasons. In the remaining patients, PaO2 significantly increased in group A (n = 16) from 7.6 +/- 0.1 to 8.3 +/- 0.2 kPa (56.9 +/- 1.0 to 62.7 +/- 1.7 mmHg) (p less than 0.001) but not in group P (n = 10) from 7.5 +/- 0.3 to 7.9 +/- 0.3 kPa (56.1 +/- 2.3 to 59.1 +/- 2.1 mmHg). PaCO2 did not significantly change in either group. Pulmonary artery mean pressure (PAP) was stable in both groups: from 26.8 +/- 2.1 to 25.4 +/- 1.9 mmHg in group A, and from 20.6 +/- 1.1 to 20.9 +/- 1.5 mmHg in group P.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of nifedipine in patients with unstable chronic obstructive pulmonary disease

The hemodynamic and gas exchange effects of 20 mg of nifedipine (NFD), at rest and exercise were evaluated in seven patients with unstable COPD and pulmonary hypertension. The cause of instability was pulmonary infection (n = 6) and pulmonary emboli (n = 1). At rest, pulmonary hypertension (Pp = 40 +/- 3 mmHg), severe hypoxemia (PaO2 +/- 2 mmHg) and elevated pulmonary vascular resistance (Rp) = 9 +/- .6 u.sq.m, were found. At exercise, Pp raised to 52 +/- 5 mmHg with no change in cardiac index (CI), Rp or gas exchange. After NFD at rest, significant (p less than 0.05) increases in CI, oxygen transport and venous admixture occurred. Also, Rp and systemic arterial pressure and resistance decreased significantly. Pp and blood gas exchange did not vary. Rp and systemic resistance were lower at exercise after NFD than without the drug with no change in blood gas exchange. The pulmonary flow pressure relationship showed a right shift after NFD in both, rest and exercise conditions. We conclude that NFD can be of value for the management of pulmonary hypertension that aggravates COPD.     

Diagnosis of cyanosis and digital clubbing caused by liver cirrhosis

Six cases of cyanosis and digital clubbing caused by liver cirrhosis were reported. The mean levels of PaO2 and PaCO2 were 6.4 +/- 0.8 kPa (48.3 +/- 6.2 mmHg) and 3.9 +/- 0.8 kPa (29.5 +/- 6.1 mmHg) respectively. The cause of cyanosis and digital clubbing in liver cirrhosis was discussed. Abnormal intrapulmonary shunting (IPS), which was proved in 4 cases by whole-body radionuclide scanning with 99mTc-MAA, is suggested as the major cause of cyanosis in liver cirrhosis. Clinically IPS is usually associated with debilitating conditions characterized by hyperventilation, abnormality of lung diffusion and orthodeoxia or platypnea. The authors suggest that whole-body radionuclide scanning with 99mTc-MAA may be performed for establishing IPS if liver cirrhosis is highly suspected to be the cause of severe hypoxemia.     

Nocturnal cough in patients with chronic bronchitis and emphysema

Patients with respiratory disease commonly report that their sleep is disrupted by nocturnal cough. We have recorded cough during the night in 10 patients with severe chronic bronchitis and emphysema (forced expiratory volume in one second, 1.0 +/- SEM 0.1/L) who complained of nocturnal cough and correlated cough with electroencephalographic sleep stage and arterial oxygenation. Cough was recorded using a directional microphone and an auto-editing tape recorder system. Each cough was subsequently verified by a listener. There was a mean of 14.6 +/- 4.5 bouts of coughing per patient per night, each bout lasting on average 3.9 +/- 0.2 s. Eighty-five percent of coughing bouts occurred during electroencephalographically confirmed wakefulness (p less than 0.02 versus sleep), and coughs during true sleep were rare, with only 1 patient coughing during rapid eye movement sleep and none during Stages 3 and 4 sleep. Cough was only once followed by arousal. There was no correlation between cough and either apneas or hypoxemia during sleep. We conclude that spontaneous cough is suppressed during sleep and only rarely awakens patients.     

Effects of positive end-expiratory pressure ventilation and extracorporeal ultrafiltration method in patients with refractory heart failure

We studied the effects of positive end-expiratory pressure (PEEP) ventilation in ten patients with acute myocardial infarction (nine in Killip class III, one in Killip class IV; pulmonary capillary wedge pressure greater than 24 mmHg) and of extracorporeal ultrafiltration method (ECUM) in seven patients with refractory heart failure due to acute myocardial infarction and others. Application of PEEP resulted in significant increases in PaO2 and SaO2 and decrease in PaCO2. Significant reduction in mean pulmonary arterial and pulmonary capillary wedge pressures and heart rate was observed, while stroke work index increased significantly. There was a significant correlation between changes in stroke work index and PaO2 after the application of PEEP. The use of ECUM removed fluid of 1416 +/- 662 ml (680-2800 ml) with the ultrafiltration flux rate being 478 +/- 223 ml/hour. Significant decreases in mean pulmonary arterial, pulmonary capillary wedge and central venous pressures were observed, while PaO2 increased significantly. BUN and serum creatinine levels increased significantly, and total protein and serum albumin tended to increase. There was a significant correlation between fluid removed and change in PaO2 after the use of ECUM. Thus, PEEP and ECUM are beneficial for patients with refractory heart failure. The mechanism(s) are: reduction in preload due to an increased intrathoracic pressure and a decreased systemic venous return with PEEP, or due to removal of excess fluid with ECUM, and improvement of the oxygenation of the blood.