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R Kuhlen

Publications and source records attributed to R Kuhlen.

64 records · Page 4Linked to original sources

Nitroglycerin versus epoprostenol: effects on hemodynamics, oxygen delivery, and hepatic venous oxygenation after liver transplantation.

Our objective was to determine the effects of vasodilatory treatment with epoprostenol (PGI2) and nitroglycerin (NTG) on systemic oxygen delivery index (DO2) and hepatic venous oxygen saturation (SvhO2) after liver transplantation. This prospective study used repeated-measures design. Fifteen adult patients undergoing orthotopic liver transplantation (OLT) were enrolled. Postoperatively, a fiberoptic pulmonary artery catheter was inserted into the right hepatic vein and a timed infusion of PGI2 and NTG was sequentially performed in random order at the following rates: PGI2 at 5 ng/kg/minute and NTG at 0.1 microgram/kg/minute. Each step in each sequence lasted 45 minutes, followed by a control interval of 45 minutes. Measurements were taken at the end of each period when hemodynamic function was stable. Systemic hemodynamics, DO2, oxygen uptake index (VO2), mixed venous oxygen saturation (SvO2), and SvhO2 were assessed. We found that PGI2 induced an increase of cardiac index (+18%, p < .05); DO2 (+16%, p < .05); and SvhO2 (+11%, p < .05). Mean arterial pressure was decreased during PGI2 infusion (-9%, p < .05), as well as during infusion of NTG (-10%, p < .05). NTG significantly decreased DO2 (-6%, p < .05) and SvhO2 (-4%, p < .05). Neither drug affected VO2. We conclude that PGI2 induced vasodilation and increased systemic oxygen delivery in parallel with SvhO2, suggesting a corresponding increase of hepatic oxygen supply. NTG induced systemic vasodilation and significantly impaired hepatic venous oxygen saturation and DO2. Thus, if vasodilatory therapy is indicated in the patient after liver transplantation, PGI2 appears to be better than NTG in improving DO2 without impairing splanchnic oxygenation.

Adult↗

[Clinical aspects of acute lung failure in adults (ARDS)].

Acute respiratory distress syndrome (ARDS) is rare but beset with a high mortality rate. In recent years, however, a trend towards higher survival rates has been observed. High inspiratory oxygen concentrations, large tidal volumes, and high peak inspiratory airway pressures applied during mechanical ventilation have been identified as harmful to the lung and can contribute to the progression of ARDS. This had led to reconsideration of the sequelae of ventilatory therapy. Mechanical ventilation and other adjunctive strategies in ARDS have changed from the conventional approach aiming at normalisation of physiological ventilatory parameters to an elaborated approach that intends to protect the ventilated lung, prevent oxygen toxicity, recruit the infiltrated atelectatic and consolidated lung and reduce the anatomical and alveolar dead space. This new approach consists of various forms of pressure-controlled mechanical ventilation with PEEP and permissive hypercapnia, body position changes, and inhalation of nitric oxide. Should these procedures fail to improve impaired gas exchange, extracorporeal membrane oxygenation is an additional therapeutic option. None of these therapeutic procedures, however, has been tested against traditional standard treatment in a classical randomised controlled trial. The following review focuses on the latest insights into the pathophysiology, diagnosis, and treatment of ARDS.

Combined Modality Therapy↗

Validation and clinical application of a continuous P0.1 measurement using standard respiratory equipment.

The airway occlusion pressure, P0.1, is the negative airway pressure generated during the first 100 msec of an occluded inspiration. P0.1 is a parameter for the neuro-muscular activation of the respiratory system, which is an important determinant for the work of breathing. It has been shown to be a good predictor for successful weaning from mechanical ventilation. Standard P0.1 measurement techniques are based on a total occlusion of the inspiration for more than 100 msec. These measurements are technically complex and therefore not useful for clinical purposes. Furthermore, a significant breath-by-breath variability has been shown for P0.1, which is neglected by any single point measurement technique. Therefore, we have developed a continuous on-line measurement for breath-by-breath determination of P0.1 using the Siemens Servo 900C respirator. In triggered mechanical ventilation the delay time between the onset of the patient's inspiration and flow delivery from the respiratory is more than 100 msec for this respirator. During that time the inspiration is occluded. Therefore, the trigger effort was proposed to be a good estimate of P0.1. Based on this, we calculated P0.1 as follows: airway pressure (Paw) was registered at the endotracheal tube site of the respiratory tubing, digitized and acquired by a personal computer at 100 Hz. The recorder output of the Servo 900C was connected to the same computer, delivering the electronical signal for the inspiratory valve to open when the inspiratory effort has exceeded the trigger threshold, which needs a minimal delay time of 80 msec. Around 20 msec after this signal flow is delivered from the respirator. The computer runs an algorithm, which recognizes this signal and calculates P0.1 (Servo P0.1) as the slope of the pressure drop during this 100 msec. Paw tracings and the calculated P0.1 values were displayed on the computer screen and stored on disk. This method was validated by comparing it to the standard technique, using a Hans-Rudolph valve for inspiratory occlusion and calculating P0.1 from Paw tracings during the occluded inspiration. For validation we used a mechanical lung model which generated P0.1 values ranging between 1.1-10.3 mbar. For a given adjustment of the lung model two standard measurements (standard P0.1) were made and compared to the Servo P0.1. In a total of 21 measurements the mean Servo P0.1 was 4.9 +/- 2.9 mbar; the mean standard P0.1 was 4.3 +/- 2.5 mbar. The mean difference between Servo P0.1 and standard P0.1 was 0.6 +/- 0.6 mbar (range: -0.3-1.8 mbar). The regression equation for linear regression analysis was: Servo P0.1 = 1.15* standard P0.1-0.05. This correlation was significant (r = 0.99, p < 0.01). From these data we conclude that the described method for continuous P0.1 measurement provides reliable values with the advantage of a maneuver-free, breath-by-breath measurement technique. It thereby opens the possibility for monitoring the neuro-muscular activation of the respiratory system at the bedside, which is shown as an example for a patient during weaning from mechanical ventilation.

Adult↗

A new method for P0.1 measurement using standard respiratory equipment.

The airway occlusion pressure, P0.1, is an index for the neuro-muscular activation of the respiratory system. It has been shown to be a very useful indicator for the ability of patients receiving ventilatory support to be weaned from mechanical ventilation. Since the standard measurement technique for P0.1 determination is technically complex, it is not widely available for clinical purposes. For that reason a P0.1 measurement technique was developed as an integrated function in a standard respirator (Evita, Dräger, Lübeck, Germany). This technique is easy to use and does not need any further equipment. We validated this new technique by comparing it to standard P0.1 measurements in a mechanical lung model as well as in ventilated patients. In the lung model we found a correlation between the Evita measurement and standard measurements of r = 0.99. In 6 ventilated patients the correlation was r = 0.78. Since the Evita P0.1 and the standard measurement had to be performed during two different breaths, this little poorer correlation in patients may be due to a significant breath-by-breath variability in P0.1. Comparing the Evita P0.1 and the standard measurement within one breath resulted in a clearly better correlation (r = 0.89). We conclude that this new measurement technique provides an easy and accurate P0.1 measurement using standard respiratory equipment when tested in a lung model. In patient measurements the method is less precise, which is probably due to the variable waveforms of the inspiratory driving pressure seen in patients, for example when intrinsic PEEP is present.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗

Preliminary evaluation of a new continuous intra-arterial blood gas monitoring device.

Continuous intra-arterial blood gas monitoring is a new technique, possibly offering therapeutic advantages through improved monitoring in patients prone to hypoxaemia, hypercapnia and/or respiratory acidosis. Therefore, we studied the clinical applicability, reliability, precision and side effect of long-term continuous intra-arterial blood gas monitoring in patients suffering from severe acute respiratory distress syndrome. In 10 patients continuous intra-arterial blood gas monitoring based on fluorescent optodes technique was performed. At 4 h intervals, arterial blood samples for in vitro blood gas analyses were drawn, stored in ice, and analysed within 3 min. Evaluation of data retrieved from the continuous intra-arterial blood gas monitoring and in vitro blood gas analysis was based on 596 data points using 10 catheters. Average length of insertion was 281 +/- 215 h, max. lengths of stay was 750 h. Arterial blood gas data obtained in vivo were compared to the mean of in vivo and in vitro arterial blood gases. Inter-catheter bias, expressed as percent difference between continuous intra-arterial blood gas and mean in vitro blood gas analysis was 0.19 +/- 0.23% for pH. 1.1 +/- 5.2% for PaCO2 and 1.6 +/- 5.7% for PaO2. No significant gas partial pressure dependent change in precision was demonstrable. There was no significant time dependent drift in sensor precision over the study period. No negative side-effects related to IABG monitoring were observed. We conclude that long-term use of this new device is possible in patients and represents a reliable alternative to conventional in vitro arterial blood gas analysis, when continuous monitoring of blood gases and/or acid-base balance is critical.

Acid-Base Equilibrium↗

Incidence, severity, and mortality of acute respiratory failure in Berlin, Germany.

A prospective multicenter study was carried out from October 1 to November 30, 1991, to determine the incidence, severity, and mortality of acute respiratory failure (ARF) in Berlin, Germany, a metropolis with a population of 3.44 million. Adult patients from 72 intensive care units (ICUs) were evaluated. ARF was defined as: (1) intubation and mechanical ventilation (I+MV) > or = 24 h; age > or = 14 yr. Incidence of ARF was assessed as the number of patients fulfilling ARF criteria within the 2-mo study period. Severity of ARF was defined as "no lung injury" (NLI), "mild-to-moderate lung injury" (MMLI), and "severe lung injury" (SLI) according to Murray and coworkers' proposals. Mortality was assessed as number of patients with ARF dying during ICU stay. During the study period, 508 patients were diagnosed as having ARF, representing an incidence of ARF of 88.6 per 100,000/yr. Twenty-four h after I+MV, MMLI occurred in 94% and SLI in 3.6% of the ARF patients. Overall mortality rate was 42.7%. Mortality rate in the NLI group was 36.4%; in patients with MMLI, 40.8%; and in patients with SLI, 58.8%. Our data offer novel information on incidence, severity, and mortality of ARF in a major urban population.

Adult↗

Interactions of physiological and pharmacological concentrations of ANP and angiotensin II in conscious dogs.

This study in conscious, chronically instrumented dogs investigated the effects of human atrial natriuretic peptide [hANP-(99-126)] at physiological (5 ng.kg-1.min-1) and pharmacological (5-900 ng.kg-1.min-1) doses on angiotensin II (ANG II)-mediated effects on hemodynamics, renal excretion, and aldosterone release. Five female beagle dogs kept chronically on a dietary sodium intake of 2.5 mmol Na.kg body wt-1.day-1 received an intravenous infusion of 1, 4, 10, 20, and 50 ng.kg-1.min-1 ANG II (20-min periods) without (protocol 1) or with (protocol 2) simultaneous intravenous infusion of 5 ng.kg-1.min-1 hANP-(99-126). In protocol 1, glomerular filtration rate (means +/- SD) decreased from 4.0 +/- 0.6 to 2.8 +/- 0.5 ml.kg-1.min-1, renal sodium excretion (UNaV) decreased from 2.8 +/- 1.6 to 0.4 +/- 0.2 mumol.kg-1.min-1, and urine volume (V) decreased from 45 +/- 23 to 6 +/- 8 microliters.kg-1.min-1. There were no differences in the values between protocol 1 and protocol 2. Mean arterial blood pressure (MABP) increased similarly from 118 +/- 16 to 166 +/- 9 mmHg in protocol 1 and from 109 +/- 11 to 162 +/- 7 mmHg in protocol 2. Maximal aldosterone secretion was stimulated less in protocol 2 (481 +/- 92 vs. 362 +/- 158 pg/ml; P less than 0.05). In ANG II-pretreated (20 ng.kg-1.min-1) dogs (n = 4; protocol 3), intravenous hANP-(99-126) doses of 300-900 ng.kg-1.min-1 decreased MABP and central venous pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗