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Should screening for occlusive coelic axis disease be included in goal-directed therapy?
Maximizing Cardiac Output In Severely Hypoxic Patients With ARDS – A Proposed Strategy To Improve Ar
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Richard G Fiddian-Green, FRCS, FACS None
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richardfg{at}hotmail.com Richard G Fiddian-Green
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Of the 35 septic patients studied by Friedman et al (1) 23 (66%) patients had an increased lactate concentration (> 2 mEq/L) and 26 (74%) had a low intramucosal pH (< 7.32). The authors concluded that, "Both lactate concentrations and intramucosal pH represent reliable prognostic indicators in severe sepsis, and their combination improves the prognostic assessment in these patients. Both variables are better prognostic indicators than oxygen-derived variables". Might the rise in lactate be predictive of poor outcome because the ability to shuttle lactate to the liver to sustain ATP needs by anaerobic glycolosis is compromised by the limits imposed by the capacity for oxidative phosphorylation in the liver? If so that capacity might be severely impaired by the presence of a coeliac axis stenosis and outcome improved by angioplastic dilatation and stenting of the offending vascular pathology (2). Approximately 25% of the cardiac output passes through the liver. The blood flow to the liver is derived from two different sources, the hepatic artery and the portal vein. The hepatic artery accounts for only 25-30% of total hepatic blood flow, but it in normal circumstances provides up to 50% of the oxygen supply to the liver. The portal vein is rich in nutrients including lactate. Lactate can be expected to be the preferred substrate for intrahepatic oxidative phosphorylation in sepsis because of the increase in efficiency of ATP resynthesis provided by limiting the need for ATP consumption in the intermediary metabolic steps in glycolysis. Portal venous blood is, however, partially deoxygenated and so its contribution to the hepatic oxygen supply is unlikely to exceed 50-55% in the best of circumstances. In sepsis its contribution to oxidative phosporylation must be greatly reduced especially when accompanied by a gastric intramucosal acidosis. The burden of disposing lactate being shuttled to the liver in septic patients is likely, therefore, to be met largely if not wholly by the oxygen being delivered in hepatic arterial blood. If this is compromised myocardial workload may also be greatly increased because of the need to increase blood flow to accomodate a greatly added demand for nutrient delivery (3). It should be very easy to screen by non-invasive means ICU patients for the presence of haemodynamically significant occlusive disease in the coelic axis. It is these patients who are most likely to benefit from angioplastic angioplastic dilatation and stenting. If there is one lesson gastric tonometry has taught us it is that the earlier effective measures are taken to reverse a intramucosal acidosis the more likely a favourable outcome. The inference is that to benefit from this apporach patients will have to be screened on admission to the ICU and preferably at the onset of their sepsis. Coeliac axis stenosis is likely to be a common finding in our ageing ICU populations. 1. Friedman G, Berlot G, Kahn RJ, Vincent JL. Combined measurements of blood lactate concentrations and gastric intramucosal pH in patients with severe sepsis. Crit Care Med. 1995 Jul;23(7):1184-93. 2. Richard G Fiddian-Green Coeliac axis stenosis: risk factor for adverse outcome from acute myocardial infarction? http://www.heartjnl.com/cgi/eletters/92/2/162#918, 7 Feb 2006 3. Richard G Fiddian-Green Anaerobic glycolysis in acute liver failure http://www.postgradmedj.com/cgi/eletters/81/953/148#249, 6 Mar 2005 |
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Mphamad Abdelsalam Abdelkader, Riyadh Care Hospital ICU Department
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mohamadabdelsalam{at}hotmail.com Mphamad Abdelsalam Abdelkader
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Over the last few years, there has been an interest in augmenting cardiac output (CO) and oxygen delivery (DO2) to supranormal values in an attempt to reduce the risk of multi-organ failure and death among critically ill patients. However, so far, no controlled clinical trial has been conducted to evaluate the effect of supranormal CO, aimed at maintaining a normal (not supranormal) DO2, on clinical outcome of critically ill patients with hypoxemia. Arterial hypoxemia can compromise DO2 and lead to tissue hypoxia, especially when accompanied by a low cardiac output, decreased hemoglobin concentration, or increased metabolic demands of the body. However, since DO2 is a function of CO, oxygen saturation (SaO2) and hemoglobin level, it can be hypothesized that maximizing CO can maintain a relatively normal DO2 despite a significant reduction of SaO2. The physiologic rationale for this hypothesis is based on the observation that CO is often increased in response to acute hypoxemia. Supranormal CO may, therefore, be considered a physiologic adaptation that can ensure adequate DO2 for hypoxic patients in whom oxygen content (CaO2) is often reduced. In theory, increased CO can compensate for a decrease in CaO2 to maintain a relatively normal DO2. DO2 = CaO2 x CO CaO2 = 1.34 x Hb x SaO2 DO2 = 1.34 x Hb x SaO2 x CO A number of studies have shown that CO increases significantly in normal subjects during acute hypoxemia,1, 2 a finding that may explain the observation that hypoxemia is well tolerated by normal individuals. For example, climbers in the Alps have oxygen saturations as low as 78%, and those who have reached the summit of Mount Everest have partial pressure of arterial oxygen (PaO2) less than 30 mm Hg.3 Possibly, these well trained athletes could have tolerated profound hypoxemia because of their ability to achieve high levels of cardiac output to ensure adequate oxygen supply to the tissues. It is not clear however, if increased CO, as a consequence of hypoxemia, can minimize the risk of tissue hypoxia in critically ill patients as well. In addition to improving DO2 and alleviating tissue hypoxia, supranormal CO can also improve arterial oxygenation. How could a high CO increase SaO2 of severely hypoxic patients? Firstly, improved DO2 is often associated with decreased oxygen extraction ratio, increased mixed venous oxygen saturation (SvO2) and hence, increased SaO2. This is particularly true in ARDS patients who cannot fully oxygenate blood because of underlying abnormality of ventilation/perfusion (V/Q) ratio, and in whom arterial oxygenation can be further compromised by severe desaturation of mixed venous blood. Secondly, augmenting CO will increase total pulmonary blood flow. However, as alveolar capillaries surrounding collapsed and consolidated alveoli have been constricted by the vasospastic effect of regional hypoxia, increased pulmonary perfusion is selectively diverted to the patent capillaries that supply functioning lung units. Such a selective increase in blood flow to ventilated alveoli can improve V/Q matching, optimize gas exchange and increase SaO2 (similar to the action of inhaled nitric oxide). However, probably the most important benefit of improved oxygenation is to allow reduction of inspired oxygen fraction (FiO2), positive-end expiratory pressure (PEEP), and airway pressures, thereby reducing the risk of oxygen toxicity, volutrauma, biotrauma and multi-organ failure. It must be emphasized however, that avoidance of ventilator-induced lung injury is probably more important for patients` survival than increasing SaO2. This concept was supported by the ARDS Network trial 4 which has demonstrated that clinical outcome of ARDS is improved by protective strategies that prevent further lung injury rather than improve oxygenation. In conclusion, I may hypothesize that maximizing CO can improve arterial oxygenation and maintain a relatively normal oxygen delivery to patients who have profound hypoxemia. Supranormal CO can also reduce the risk of ventilator-induced lung injury by allowing the amount of ventilatory support to be reduced. This is especially helpful for patients with ARDS who are more prone to develop lung damage when high levels of FiO2 and PEEP are used to correct hypoxemia. However, further studies are required to evaluate the therapeutic implication of supranormal CO in patients with ARDS and other diseases characterized by severe hypoxemia. References 1. Philips, BA, McConnell, JW, Smith, MD. The effects of hypoxemia on cardiac output. A dose-response curve. Chest 1988; 93:471. 2. Cargill, RI, Kiely, DG, Lipworth, BJ. Left ventricular systolic performance during acute hypoxemia. Chest 1995; 108: 899. 3. West, JB. Human limits for hypoxia. The physiological challenge of climbing Mt. Everest. Ann N Y Acad Sci 2000; 899:15. 4. The ARDS Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301. |
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