Interactions between respiration and systemic hemodynamics. Part II: practical implications in critical care

In Part I of this review, we have covered basic concepts regarding cardiorespiratory interactions. Here, we put this theoretical framework to practical use. We describe mechanisms underlying Kussmaul's sign and pulsus paradoxus. We review the literature on the use of respiratory variations of blood pressure to evaluate volume status. We show the possibilities of attaining the latter aim by investigating with ultrasonography how the geometry of great veins fluctuates with respiration. We provide a Guytonian analysis of the effects of PEEP on cardiac output. We terminate with some remarks on the potential of positive pressure breathing to induce acute cor pulmonale, and on the cardiovascular mechanisms that at times may underly the failure to wean a patient from the ventilato

Interactions between respiration and systemic hemodynamics. Part I: basic concepts

The topic of cardiorespiratory interactions is of extreme importance to the practicing intensivist. It also has a reputation for being intellectually challenging, due in part to the enormous volume of relevant, at times contradictory literature. Another source of difficulty is the need to simultaneously consider the interrelated functioning of several organ systems (not necessarily limited to the heart and lung), in other words, to adopt a systemic (as opposed to analytic) point of view. We believe that the proper understanding of a few simple physiological concepts is of great help in organizing knowledge in this field. The first part of this review will be devoted to demonstrating this point. The second part, to be published in a coming issue of Intensive Care Medicine, will apply these concepts to clinical situations. We hope that this text will be of some use, especially to intensivists in training, to demystify a field that many find intimidatin

Saint-Gervais-les-Bains – Château de Hautecour

Les investigations préliminaires, menées durant l’été 2006 sur les élévations de l’édifice, ont permis de dénombrer sept étapes de construction, qui se développent entre la seconde moitié du xiiie s. et la fin du xviiie s. Un premier grand bâtiment composé de deux corps de logis est édifié vers 1268. Il n’en subsiste que quelques vestiges identifiés dans l’élévation du bâtiment actuel. Vers 1458, il est modifié et en partie remplacé par une nouvelle construction, composée de deux parties égal..

P-210: Beta-blockade with nebivolol enhances the acetylcholine-induced vasodilation in the cutaneaous vascular bed of normotensive volunteers

This study was undertaken to assess whether the beta1-adrenoceptor blocker nebivolol(N) increases the vasodilatory response to acetylcholine(Ach) when administered orally to healthy subjects. To this end 12 volunteers were randomly allocated to a 8-day treatment with nebivolol (n), 5 mg once a day, and atenolol(A),50 mg once a day, according to a cross-over design, with a 1 week wash-out period between the two treatment phases. The forearm skin blood flow(SBF) response to Ach applied by iontophoresis was determined using a laser-Doppler scanner imaging system before(T0) and 3 hours(T3) after N or A dosing, both on the first (Day 1) and the last day (Day 8) of treatment. The following Table shows the responses of SBF (perfusion units) (means±SD; *p<0.05 versus T0): Day 1 Day 8 T0 T3 T0 T3 Nebivolol 98±93 441±109* 393±110 426±105* Atenolol 396±97 410±99 380±109 394±98 Iontophoresis of 0.09% NaCl had no effect on SBF. These data indicate that nebivolol (administered at a dose commonly used in clinical practice), but not atenolol, enhances in humans the vasorelaxant activity of Ach in the skin vascular bed, which is compatible with a facilitation by this beta-blocker of the endothelium-dependent vasodilatio

P-101: Blunted vasodilatory responses in the cutaneous microcirculation of cigarette smokers

Background: To assess the vasodilatory response to acetylcholine (Ach, endothelium-dependent vasodilator) and Na nitroprusside (SNP, endothelium-independent vasodilator) in the skin microcirculation of habitual cigarette smokers. Methods: Male healthy habitual smokers taking no medication acting on the cardiovascular system were included. They were divided in younger (Group 1, n = 10, age: 18 to 35 years; mean = 7 pack-years) and older (Group 2, n = 10, age: 40 to 60 years; mean =30 pack-years). Younger (Group 3, n = 10) and older controls (Group 4, n = 10) consisted of age-matched non-smokers. On the day of the experiment the subjects of Groups 1 and 2 were asked to smoke at least 15 cigarettes starting in the morning. At 4 p.m. they had to smoke within 5 min a filter cigarette containing 1 mg nicotine. Subjects of Groups 3 and 4 had a sham-smoking session at 4 p.m. Ach, 1%, and SNP, 0.1%, were administered transcutaneously for 7 min on the volar face of the right forearm using iontophoresis. This was done 15 min and 40 min after the end of the smoking session for Ach and SNP, respectively. The skin blood flow responses were evaluated using a laser-Doppler flowmeter allowing to scan the surface of Ach and SNP application (circular area, 1 cm diameter). Results: The following Table shows the peak changes induced by Ach and SNP (perfusion units, means±SD): Younger Older Ach SNP Ach SNP Non-smokers 505±65 425±99 473±91 392±71 Smokers 466±102 416±59 302±50** 301±104* *p<0.05; **p<0.01, Smokers versus Non-smokers Conclusion: These data show that the vasodilatory response of the skin microvasculature is impaired in subjects having smoked cigarettes for many years. This abnormality involves both the Ach and the SNP responses, which implies a diminished relaxant capacity of vascular smooth muscle cells, even if an underlying endothelial dysfunction cannot be ruled ou

Impact of body tilt on the central aortic pressure pulse.

The present work was undertaken to investigate, in young healthy volunteers, the relationships between the forward propagation times of arterial pressure waves and the timing of reflected waves observable on the aortic pulse, in the course of rapid changes in body position. 20 young healthy subjects, 10 men, and 10 women, were examined on a tilt table at two different tilt angles, -10° (Head-down) and + 45° (Head-up). In each position, carotid-femoral (Tcf) and carotid-tibial forward propagation times (Tct) were measured with the Complior device. In each position also, the central aortic pressure pulse was recorded with radial tonometry, using the SphygmoCor device and a generalized transfer function, so as to evaluate the timing of reflected waves reaching the aorta in systole (onset of systolic reflected wave, sT1r) and diastole (mean transit time of diastolic reflected wave, dMTT). The position shift from Head-up to Head-down caused a massive increase in both Tct (women from 130 ± 10 to 185 ± 18 msec P &lt; 0.001, men from 136 ± 9 to 204 ± 18 msec P &lt; 0.001) and dMTT (women from 364 ± 35 to 499 ± 33 msec P &lt; 0.001, men from 406 ± 22 to 553 ± 21 msec P &lt; 0.001). Mixed model regression showed that the changes in Tct and dMTT observed between Head-up and Head-down were tightly coupled (regression coefficient 2.1, 95% confidence interval 1.9-2.3, P &lt; 0.001). These results strongly suggest that the diastolic waves observed on central aortic pulses reconstructed from radial tonometric correspond at least in part to reflections generated in the lower limbs

Moderate hypercapnia exerts beneficial effects on splanchnic energy metabolism during endotoxemia

Purpose: Low tidal volume ventilation and permissive hypercapnia are required in patients with sepsis complicated by ARDS. The effects of hypercapnia on tissue oxidative metabolism in this setting are unknown. We therefore determined the effects of moderate hypercapnia on markers of systemic and splanchnic oxidative metabolism in an animal model of endotoxemia. Methods: Anesthetized rats maintained at a PaCO2 of 30, 40 or 60mmHg were challenged with endotoxin. A control group (PaCO2 40mmHg) received isotonic saline. Hemodynamic variables, arterial lactate, pyruvate, and ketone bodies were measured at baseline and after 4h. Tissue adenosine triphosphate (ATP) and lactate were measured in the small intestine and the liver after 4h. Results: Endotoxin resulted in low cardiac output, increased lactate/pyruvate ratio and decreased ketone body ratio. These changes were not influenced by hypercapnia, but were more severe with hypocapnia. In the liver, ATP decreased and lactate increased independently from PaCO2 after endotoxin. In contrast, the drop of ATP and the rise in lactate triggered by endotoxin in the intestine were prevented by hypercapnia. Conclusions: During endotoxemia in rats, moderate hypercapnia prevents the deterioration of tissue energetics in the intestin