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Occlusion Pressure (occlusion + pressure)
Selected AbstractsNorepinephrine causes a pressure-dependent plasma volume decrease in clinical vasodilatory shockACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2010A. NYGREN Background: Recent experimental studies have shown that a norepinephrine-induced increase in blood pressure induces a loss of plasma volume, particularly under increased microvascular permeability. We studied the effects of norepinephrine-induced variations in the mean arterial pressure (MAP) on plasma volume changes and systemic haemodynamics in patients with vasodilatory shock. Methods: Twenty-one mechanically ventilated patients who required norepinephrine to maintain MAP ,70 mmHg because of septic/postcardiotomy vasodilatory shock were included. The norepinephrine dose was randomly titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, haematocrit, arterial and mixed venous oxygen content and urine flow urine were measured. Changes in the plasma volume were calculated as 100 × (Hctpre/Hctpost,1)/ (1,Hctpre), where Hctpre and Hctpost are haematocrits before and after intervention. Results: Norepinephrine doses to obtain target MAPs of 60, 75 and 90 mmHg were 0.20±0.18, 0.29±0.18 and 0.42±0.31 ,g/kg/min, respectively. From 60 to 90 mmHg, increases in the cardiac index (15%), systemic oxygen delivery index (25%), central venous pressure (CVP) (20%) and pulmonary artery occlusion pressure (33%) were seen, while the intrapulmonary shunt fraction was unaffected by norepinehrine. Plasma volume decreased by 6.5% and 9.4% (P<0.0001) when blood pressure was increased from 60 to 75 and 90 mmHg, respectively. MAP (P<0.02) independently predicted the decrease in plasma volume with norepinephrine but not CVP (P=0.19), cardiac index (P=0.73), norepinephrine dose (P=0.58) or urine flow (P=0.64). Conclusions: Norepinephrine causes a pressure-dependent decrease in the plasma volume in patients with vasodilatory shock most likely caused by transcapillary fluid extravasation. [source] Automated pre-ejection period variation predicts fluid responsiveness in low tidal volume ventilated pigsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2010S. T. VISTISEN Introduction: The respiratory variation in the pre-ejection period (,PEP) has been used to predict fluid responsiveness in mechanically ventilated patients. Recently, we automated this parameter and indexed it to tidal volume (PEPV) and showed that it was a reliable predictor for post-cardiac surgery, mainly paced, patients ventilated with low tidal volumes. The aims of the present animal study were to investigate PEPV's ability to predict fluid responsiveness under different fluid loading conditions and natural heart rates during low tidal volume ventilation (6 ml/kg) and to compare the performance of PEPV with other markers of fluid responsiveness. Methods: Eight prone, anesthetized piglets (23,27 kg) ventilated with tidal volumes of 6 ml/kg were subjected to a sequence of 25% hypovolemia, normovolemia, and 25% and 50% hypervolemia. PEPV, ,PEP, pulse pressure variation (PPV), central venous pressure (CVP), and pulmonary artery occlusion pressure (PAOP) were measured before each volume expansion. Results: Sensitivity was 89% and specificity was 93% for PEPV, 78% and 93% for ,PEP, 89% and 100% for PPV, 78% and 93% for CVP, and 89% and 87% for PAOP. Conclusion: PEPV predicts fluid responsiveness in low tidal volume ventilated piglets. [source] Affective modulation of inspiratory motor drivePSYCHOPHYSIOLOGY, Issue 1 2009Ilse Van Diest Abstract The present study aimed to explore inspiratory motor drive as measured by inspiratory occlusion pressure (P100) during affective picture viewing. P100 is the decrease in mouth pressure that develops 100 ms after an inspiratory effort against a closed breathing circuit. The P100 is a measure of the "central respiratory drive." Seventy-eight healthy women viewed four pictures series (160 s) varying in content: neutral, positive, threat, or pain. They also rated each picture series on pleasantness and arousal. An occlusion was applied at the onset of inspiration in 33% of the breaths. The threat and the pain picture series were associated with an increased P100 and were rated as most unpleasant and highest in arousal. We conclude that inspiratory motor drive is affectively modulated and is a measure of the respiratory response to threatful stimuli. [source] Mechanisms by which systemic salbutamol increases ventilationRESPIROLOGY, Issue 2 2006Antony E. TOBIN Background and objective: Salbutamol (SAL) has systemic effects that may adversely influence ventilation in asthmatic patients. The authors sought to determine the magnitude of this effect and mechanisms by which i.v. SAL affects ventilation. Methods: A prospective study of nine healthy subjects (eight men, one woman; age 23 ± 1.4 years (SD)) was undertaken. Each subject received i.v. SAL at 5, 10 and 20 µg/min each for 30 min at each dose and was observed for 1 h post infusion. Minute ventilation (V,E), oxygen consumption (V,O2), CO2 production (V,CO2), occlusion pressure (P0.1), heart rate, blood pressure, respiratory rate, glucose, arterial blood gases, lactate and potassium (K+) were recorded at baseline and at 30-min intervals. The effect of 100% oxygen on V,E and P0.1 during SAL infusion at 20 µg/min was observed. Results are expressed as mean ± SEM. Results: V,E was significantly increased at 20 µg/min SAL (37.8 ± 12.1%, P = 0.01), as were V,O2 (22.5 ± 5.1%, P < 0.01) and V,CO2 (40.9 ± 10.6%, P < 0.01). Ventilation was in excess of metabolic needs as demonstrated by a rise in the respiratory exchange ratio (0.87 ± 0.03 to 0.99 ± 0.04, P < 0.05). Serum lactate rose by 124 ± 30.4% from baseline to 20 µg/min (1.1 ± 0.1 to 2.3 ± 0.25 mmol/L, P < 0.01) and base excess decreased (0.89 ± 0.56 to vs. ,1.75 ± 0.52 mmol/L, P < 0.01) consistent with a lactic acidosis contributing to the excess ventilation. There was no significant differences in V,E or P0.1 with FIO2 = 1.0, suggesting peripheral chemoreceptor stimulation was not responsible for the rise in V,E. At 20 µg/min SAL, K+ fell significantly from baseline (3.8 ± 0.06 to 2.8 ± 0.09 mmol/L, P < 0.001). Conclusion: Systemic SAL imposes ventilatory demands by increasing metabolic rate and serum lactate. This may adversely affect patients with severe asthma with limited ventilatory reserve. [source] Diagnosing acute lung injury in the critically ill: a national survey among critical care physiciansACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009A. P. J. VLAAR Background: Incidence reports on acute lung injury (ALI) vary widely. An insight into the diagnostic preferences of critical care physicians when diagnosing ALI may improve identification of the ALI patient population. Methods: Critical care physicians in the Netherlands were surveyed using vignettes involving hypothetical patients and a questionnaire. The vignettes varied in seven diagnostic determinants based on the North American European Consensus Conference and the lung injury score. Preferences were analyzed using a mixed-effects logistic regression model and presented as an odds ratio (OR) with a 95% confidence interval. Results: From 243 surveys sent to 30 hospitals, 101 were returned (42%). ORs were as follows: chest X-ray consistent with ALI: OR 1.7 (1.3,2.3), high positive end-expiratory pressure (PEEP) (15 cmH2O): OR 5.0 (3.9,6.6), low pulmonary artery occlusion pressures (PAOP) (<18 mmHg): OR 4.7 (3.6,6.1), low compliance (30 ml/cmH2O): OR 0.7 (0.5,0.9), low PaO2/FiO2 (<250 mmHg): OR 9.2 (6.9,12.3), absence of heart failure: OR 1.2 (0.9,1.5), presence of a risk factor for ALI (sepsis): OR 1.0 (0.8,1.3). The questionnaire revealed that critical care physicians with an anesthesiology background differed from physicians with an internal medicine background with regard to hemodynamic variables when considering an ALI diagnosis (P<0.05). Conclusions: Dutch critical care physicians consider the PEEP level, but not the presence of a risk factor for ALI, as an important factor to diagnose ALI. Background specialty of critical care physicians influences diagnostic preferences and may account for variance in the reported incidence of ALI. [source] | ||||||||||