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

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

Management of mechanical ventilation in acute severe asthma: practical aspects

Background: Acute severe asthma induces marked alterations in respiratory mechanics, characterized by acritical limitation of expiratory flow and aheterogeneous and reversible increase in airway resistance, resulting in premature airway closure, lung, and chest wall dynamic hyperinflation and high intrinsic PEEP. Discussion: These abnormalities increase the work of breathing and can lead to respiratory muscle fatigue and life-threatening respiratory failure, in which case mechanical ventilation is life-saving. When instituting mechanical ventilation in this setting, amajor concern is the risk of worsening lung hyperinflation (thereby provoking barotrauma) and inducing or aggravating hemodynamic instability. Guidelines for mechanical ventilation in acute severe asthma are not supported by strong clinical evidence. Controlled hypoventilation with permissive hypercapnia may reduce morbidity and mortality compared to conventional normocapnic ventilation. Profound pathological alterations in respiratory mechanics occur during acute severe asthma, which clinicians should keep in mind when caring for ventilated asthmatics. Conclusion: We focus on the practical management of controlled hypoventilation. Particular attention must be paid to ventilator settings, monitoring of lung hyperinflation, the role of extrinsic PEEP, and administering inhaled bronchodilators. We also underline the importance of deep sedation with respiratory drive-suppressing opioids to maintain patient-ventilator synchrony while avoiding as much as can be muscle paralysis and the ensuing risk of myopathy. Finally, the role of noninvasive positive pressure ventilation for the treatment of respiratory failure during severe asthma is discusse

Hypertension and microvascular remodelling

In the present review, microvascular remodelling refers to alterations in the structure of resistance vessels contributing to elevated systemic vascular resistance in hypertension. We start with some historical aspects, underscoring the importance of Folkow's contribution made half a century ago. We then move to some basic concepts on the biomechanics of blood vessels, and explicit the definitions proposed by Mulvany for specific forms of remodelling, especially inward eutrophic and inward hypertrophic. The available evidence for the existence of remodelled resistance vessels in hypertension comes next, with relatively more weight given to human, in comparison with animal data. Mechanisms are discussed. The impact of antihypertensive drug treatment on remodelling is described, again with emphasis on human data. Some details are given on the three studies to date which point to remodelling of subcutaneous resistance arteries as an independent predictor of cardiovascular risk in hypertensive patients. We terminate by considering the potential role of remodelling in the pathogenesis of end-organ damage and in the perpetuation of hypertensio

Cardiovascular effects of fentanyl in conscious rats

Abstract.: The polymicrobial sepsis induced by cecal ligation and puncture (CLP) in the rat is widely used in shock research. For ethical reasons, narcotic analgesics are often administered in this model, with the potential risk of confounding effects. In conscious non-septic rats, we investigated the cardiovascular effects of a continuous i.v. infusion of fentanyl (20µg/kg per h) administered with fluid loading (10ml/kg per h) for 24h, a regimen commonly applied in rat CLP. Animals were randomly allocated to receive analgesia with fluid loading (Fentanyl group), or fluid loading alone (Control). All endpoints were assessed after 24h of infusion. At that time, Control animals had mild respiratory alkalosis, which was essentially abolished by fentanyl. Analgesia mildly elevated the plasma norepinephrine levels [median (interquartile range): Control 232pg/ml (0-292), Fentanyl 302pg/ml (234-676), P=0.045] but was devoid of any effect on blood pressure, heart rate, cardiac output (mean ±SD: Control 388±61ml/kg per min, Fentanyl 382±62ml/kg per min, P=0.87) and indices of left ventricular function derived from high-fidelity recordings of left ventricular pressure (dP/dt max: Control 11782±2324mmHg/s, Fentanyl 12107±2816mmHg/s, P=0.77). In ex vivo experiments carried out immediately after animal sacrifice, no differences were noted between the Control and Fentanyl groups in the sensitivity of endothelium-intact aortic rings to norepinephrine-induced vasoconstriction (-logEC50: Control 8.78±0.28, Fentanyl 8.83±0.26, P=0.52) or acetylcholine-induced vasodilatation (-logEC50: Control 7.00±0.37, Fentanyl 7.06±0.26±0.53, P=0.75). In conclusion, the present data provide no contraindication, and even some support for the ethical use of a high dose i.v. infusion of fentanyl in cardiovascular studies of conscious catheterized rats undergoing CLP or other painful procedure