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Background: Stable severe chronic obstructive pulmonary disease (COPD) patients with chronic hypercapnic respiratory failure treated by nocturnal bi-level positive pressure non-invasive ventilation (NIV) may experience severe morning deventilation dyspnea. We hypothesised that in these patients, progressive hyperinflation, resulting from inappropriate ventilator settings, leads to patient-ventilator asynchrony (PVA) with a high rate of unrewarded inspiratory efforts and morning discomfort. Methods: Polysomnography (PSG), diaphragm electromyogram and transcutaneous capnography (PtcCO2) under NIV during two consecutive nights using baseline ventilator settings on the first night, then, during the second night, adjustment of ventilator parameters under PSG with assessment of impact of settings changes on sleep, patient-ventilator synchronisation, morning arterial blood gases and morning dyspnea. Results: Eight patients (61 ± 8 years, FEV1 30 ± 8% predicted, residual volume 210 ± 30% predicted) were included. In all patients, pressure support was decreased during setting adjustments, as well as tidal volume, while respiratory rate increased without any deleterious effect on nocturnal PtcCO2 or morning PaCO 2. PVA index, initially high (40 ± 30%) during the baseline night, decreased significantly after adjusting ventilator settings (p = 0.0009), as well as subjective perception of PVA leaks, and morning dyspnea while quality of sleep improved. Conclusion: The subgroup of COPD patients treated by home NIV, who present marked deventilation dyspnea and unrewarded efforts may benefit from adjustment of ventilator settings under PSG or polygraphy

Udgivelsesdato: 2010-Apr-12, Objective. Terlipressin (TP) is a potent vasoconstrictor, which is widely used in the treatment of bleeding esophageal varices and the hepatorenal syndrome. Side effects to TP are often related to skin hypoxaemia. The aim of the study was to investigate the transcutaneous oxygen pressures (TcPO(2) mmHg) after administration of 2 mg of TP. Patients and methods. Nineteen patients with cirrhosis and ascites were included. TcPO(2) mmHg were measured continuously measured at the chest, abdominal wall and at the lower extremity at baseline and after 2 mg TP in 15 patients and placebo in 4 patients. Results. The mean whole body TcPO(2) decreased after TP by 34% (p < 0.005). The decrease was even more pronounced in the lower extremity: above knee -33% (50 vs. 33 mmHg, p = 0.01) and below knee -52% (52 vs. 26 mmHg, p = 0.001). Levels below 30 mmHg, were found in 60% of the patients after TP compared to 0% in the placebo group, p = 0.005. There were no significant changes in TcPO(2) after placebo. The baseline leg TcPO(2) correlated inversely with the MELD score (r = -0.64 and p < 0.003) and the increase in MAP after TP correlated inversely with TcPO(2) at the thorax (r = -0.60, p = 0.009). Conclusions. Sixty percent of patients with decompensated cirrhosis develop hypoxaemia in the lower limb after one dose of TP.

Udgivelsesdato: 2010-Apr-12, Objective. Terlipressin (TP) is a potent vasoconstrictor, which is widely used in the treatment of bleeding esophageal varices and the hepatorenal syndrome. Side effects to TP are often related to skin hypoxaemia. The aim of the study was to investigate the transcutaneous oxygen pressures (TcPO(2) mmHg) after administration of 2 mg of TP. Patients and methods. Nineteen patients with cirrhosis and ascites were included. TcPO(2) mmHg were measured continuously measured at the chest, abdominal wall and at the lower extremity at baseline and after 2 mg TP in 15 patients and placebo in 4 patients. Results. The mean whole body TcPO(2) decreased after TP by 34% (p < 0.005). The decrease was even more pronounced in the lower extremity: above knee -33% (50 vs. 33 mmHg, p = 0.01) and below knee -52% (52 vs. 26 mmHg, p = 0.001). Levels below 30 mmHg, were found in 60% of the patients after TP compared to 0% in the placebo group, p = 0.005. There were no significant changes in TcPO(2) after placebo. The baseline leg TcPO(2) correlated inversely with the MELD score (r = -0.64 and p < 0.003) and the increase in MAP after TP correlated inversely with TcPO(2) at the thorax (r = -0.60, p = 0.009). Conclusions. Sixty percent of patients with decompensated cirrhosis develop hypoxaemia in the lower limb after one dose of TP.

Purpose: We studied the effect of intracavernous oxygen tension on the alteration of cavernous smooth muscle fibers in potent and impotent men. Materials and Methods: Intracavernous oxygen tension (mm. Hg) was measured during flaccidity and 10 minutes after intracavernous prostaglandin E1 injection in psychogenic control patients, and those with venous leakage and arterial lesions. Cavernous biopsies were performed and the percent of smooth muscle fibers was analyzed objectively using immunohistochemical actin anti- actin staining. Simultaneously brachial oxygen tension (mm. Hg) was measured and the cavernous brachial oxygen tension index was then determined. Results: At flaccidity no significant difference was noted in oxygen tension values among the 3 groups of patients. After prostaglandin E1 injection cavernous oxygen tension and the cavernous brachial oxygen tension index in the control group were significantly different (p <0.01) from those of the venogenic and arteriogenic groups (p <0.01). The mean percent of cavernous smooth muscle fibers in the control group was significantly different from those of the venous leakage and arterial lesion groups (p <0.01). There was a good correlation between the percent of cavernous muscle fibers and the value of oxygen tension before (p <0.05) and after prostaglandin E1 injection (p <0.01). A similar correlation was noted between cavernous muscle fibers and cavernous brachial oxygen tension index in the different groups of patients (p <0.01). Conclusions: Reduction of the intracavernous smooth muscle fibers in impotent patients could be explained by low intracavernous oxygen tension., SCOPUS: ar.j, info:eu-repo/semantics/published

Purpose: We studied the effect of intracavernous oxygen tension on the alteration of cavernous smooth muscle fibers in potent and impotent men. Materials and Methods: Intracavernous oxygen tension (mm. Hg) was measured during flaccidity and 10 minutes after intracavernous prostaglandin E1 injection in psychogenic control patients, and those with venous leakage and arterial lesions. Cavernous biopsies were performed and the percent of smooth muscle fibers was analyzed objectively using immunohistochemical actin anti- actin staining. Simultaneously brachial oxygen tension (mm. Hg) was measured and the cavernous brachial oxygen tension index was then determined. Results: At flaccidity no significant difference was noted in oxygen tension values among the 3 groups of patients. After prostaglandin E1 injection cavernous oxygen tension and the cavernous brachial oxygen tension index in the control group were significantly different (p <0.01) from those of the venogenic and arteriogenic groups (p <0.01). The mean percent of cavernous smooth muscle fibers in the control group was significantly different from those of the venous leakage and arterial lesion groups (p <0.01). There was a good correlation between the percent of cavernous muscle fibers and the value of oxygen tension before (p <0.05) and after prostaglandin E1 injection (p <0.01). A similar correlation was noted between cavernous muscle fibers and cavernous brachial oxygen tension index in the different groups of patients (p <0.01). Conclusions: Reduction of the intracavernous smooth muscle fibers in impotent patients could be explained by low intracavernous oxygen tension., SCOPUS: ar.j, info:eu-repo/semantics/published

There are few data in the EEG literature describing the time course of hyperventilation-(HV) induced changes in blood gases, despite this being a routine activating procedure. We studied changes in blood gases and EEG in nine normal adult subjects before, during, and after HV. The mean PCO2 fell 18 mm Hg from the baseline during HV and recovered in 7 min. The mean PO2 rose 7 mmHg during HV and fell to 25 mm Hg below baseline 5 min after HV. The PCO2 recovery period is longer than is usually assumed in clinical EEG. The PO2 fall to a nadir at 5 min after the end of HV suggests that close attention should be paid to this period, as is confirmed by the re-buildup seen in moyamoya disease. Despite uniform changes in blood gases, the EEG median power frequency change showed marked variability; on average, it dropped by 1 Hz during HV and returned to baseline within 2 min of resumption of normal respiration. The EEG root-mean-square power showed a 200% increase during HV and also had returned to normal within 2 min., Journal Article, info:eu-repo/semantics/published

Transcranial Doppler (TCD) examinations are increasingly being used in studies of headache pathophysiology. Because blood velocity is highly dependent on PCO2, these parameters should be measured simultaneously. The most common way of performing measurements during TCD examinations is as end-tidal pCO2 with a capnograph. When patients are nauseated and vomit, as in migraine, the mask or mouthpiece connected to the capnograph represents a problem. We therefore evaluated whether a transcutaneous pCO2 electrode was as useful as the capnograph for pCO2 measurements in TCD examinations. We conclude that this is not the case, and recommend capnographic end-tidal pCO2 measurements during TCD examinations. However, transcutaneous pCO2 measurements may represent a supplement to spot measurements of end-tidal pCO2 in stable conditions when long-term monitoring is needed, and the mask or mouthpiece of the capnograph has to be taken on and off between recordings.

Transcranial Doppler (TCD) examinations are increasingly being used in studies of headache pathophysiology. Because blood velocity is highly dependent on PCO2, these parameters should be measured simultaneously. The most common way of performing measurements during TCD examinations is as end-tidal pCO2 with a capnograph. When patients are nauseated and vomit, as in migraine, the mask or mouthpiece connected to the capnograph represents a problem. We therefore evaluated whether a transcutaneous pCO2 electrode was as useful as the capnograph for pCO2 measurements in TCD examinations. We conclude that this is not the case, and recommend capnographic end-tidal pCO2 measurements during TCD examinations. However, transcutaneous pCO2 measurements may represent a supplement to spot measurements of end-tidal pCO2 in stable conditions when long-term monitoring is needed, and the mask or mouthpiece of the capnograph has to be taken on and off between recordings.

There are few data in the EEG literature describing the time course of hyperventilation-(HV) induced changes in blood gases, despite this being a routine activating procedure. We studied changes in blood gases and EEG in nine normal adult subjects before, during, and after HV. The mean PCO2 fell 18 mm Hg from the baseline during HV and recovered in 7 min. The mean PO2 rose 7 mmHg during HV and fell to 25 mm Hg below baseline 5 min after HV. The PCO2 recovery period is longer than is usually assumed in clinical EEG. The PO2 fall to a nadir at 5 min after the end of HV suggests that close attention should be paid to this period, as is confirmed by the re-buildup seen in moyamoya disease. Despite uniform changes in blood gases, the EEG median power frequency change showed marked variability; on average, it dropped by 1 Hz during HV and returned to baseline within 2 min of resumption of normal respiration. The EEG root-mean-square power showed a 200% increase during HV and also had returned to normal within 2 min., Journal Article, info:eu-repo/semantics/published

Transcranial Doppler (TCD) examinations are increasingly being used in studies of headache pathophysiology. Because blood velocity is highly dependent on PCO2, these parameters should be measured simultaneously. The most common way of performing measurements during TCD examinations is as end-tidal pCO2 with a capnograph. When patients are nauseated and vomit, as in migraine, the mask or mouthpiece connected to the capnograph represents a problem. We therefore evaluated whether a transcutaneous pCO2 electrode was as useful as the capnograph for pCO2 measurements in TCD examinations. We conclude that this is not the case, and recommend capnographic end-tidal pCO2 measurements during TCD examinations. However, transcutaneous pCO2 measurements may represent a supplement to spot measurements of end-tidal pCO2 in stable conditions when long-term monitoring is needed, and the mask or mouthpiece of the capnograph has to be taken on and off between recordings.

The effectiveness of caffeine citrate in preventing idiopathic apnea in premature infants was evaluated. Thirty-seven preterm infants born before the 32nd week of gestation were studied. After an intravenous loading dose of 10 mg/kg of caffeine citrate, two different oral maintenance regimens were followed: 5 mg/kg in Group I and 2.5 mg/kg in Group II. A significant decrease in the number of apneic spells occurred in both treated groups as compared with a control group. In Group II, the frequency of side effects such as tachycardia and gastrointestinal intolerance was significantly lower than in Group I. Group II theophylline plasma levels were significantly lower than those of Group I. The lower Group II theophylline levels presumably explain the reduced frequency of side effects.