Purpose
During neurally adjusted ventilatory assist (NAVA) the ventilator is driven by the patients electrical activation of the diaphragm (EAdi), detected by a special esophageal catheter. A reliable positioning of the EAdi-catheter is mandatory to trace a representative EAdi signal. We aimed to determine whether a formula that is based on the measurement from nose to ear lobe to xiphoid process of the sternum (NEX distance) modified for EAdi-catheter placement (NEX
mod
) is sufficient for predicting the accurate catheter position.
Methods
Twenty-six patients were enrolled in this study. The optimal EAdi-catheter position (OPT) was defined by: (1) stable EAdi signal, (2) electrical activity highlighted in central leads of the catheter positioning tool, and (3) absence of p-wave in distal lead. Afterwards NEX
mod
was calculated and compared to the OPT finding.
Results
At NEX
mod
the EAdi signal was suitable for running NAVA in 18 out of 25 patients (72%). NEX
mod
was identical with OPT in four patients (16%). NAVA was possible in all patients at OPT. Median OPT position was 2 cm caudal of the NEX
mod
ranging from 3 cm too cranial to a position 12 cm too caudal (
P
< 0.01). In one patient excluded from further analysis EAdi-catheter placement led to the diagnosis of bilateral injury of the phrenic nerves.
Conclusions
EAdi-catheter placement based on the NEX
mod
formula allows running NAVA in about two-thirds of all patients. The additional tools provided are efficient and facilitate the correct positioning of the EAdi-catheter for neurally adjusted ventilatory assist.
Nine patients with heterozygous familial hypercholesterolaemia were treated for eight weeks with either 40 mg pravastatin or placebo under double blind conditions. Six patients received pravastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. Treatment with pravastatin resulted in a significant decrease in plasma cholesterol caused by a decrease in low density lipoprotein cholesterol (LDL-c) of 30% (p<0.005). We determined the effect of this medication on the lithogenicity of bile. Cholesterol saturation index of fasting gall bladder bile decreased with 23% (p<0-01) from 1-06 to 075 during treatment with pravastatin. A reduction of 24% (p<0-01) in molar percentage of biliary cholesterol was seen. After treatment the total bile acid excretion in faeces and the molar percentage of biliary bile acids were not significantly changed, suggesting that pravastatin does not influence bile acid biosynthesis to a significant extent. These findings indicate that treatment with pravastatin can decrease the incidence and complications of cholesterol gail stones.
The ventilator mode NAVA seems to be well tolerated in a heterogeneous group of critically ill patients. Pre-setting of the NAVA level during PSV can result in an overestimation of the required ventilator support. An additional titration of the NAVA level ads valuable information although difficult to interpret in some cases.
The relation between carnitine palmitoyltransferase (CPT) activity and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity was investigated. Rats were treated with aminocarnitine or 1-carnitine overnight. In rats, in which CPT activity was inhibited by aminocarnitine, plasma and hepatic triacylglycerol contents were increased 5- to 6-fold. The plasma cholesterol concentration was unchanged, while the hepatic cholesterol content was lowered (-16%). Hepatic cholesterol synthesis, determined by following the incorporation of 14C-acetate and 3H2O into digitonin-precipitable sterols, in liver slices was increased 5- to 7-fold. HMG-CoA reductase activity in liver microsomes was increased to the same extent.
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