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Maximizing Cardiac Output In Severely Hypoxic Patients With ARDS – A Proposed Strategy To Improve Ar
- Mohamad Abdelsalam Abdelkader (7 June 2006)
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Biologically Variable Ventilation and Alveolar Recruitment
- W. Alan C. Mutch (26 January 2006)
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Mohamad Abdelsalam Abdelkader, Riyadh Care Hospital ICU Department
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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. Conflict of Interest:None declared |
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W. Alan C. Mutch, Professor, Department of Anesthesia University of Manitoba
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The recent review article by Mols, Priebe and Guttman on alveolar recruitment in acute lung injury is timely and comprehensive(1). I thank the authors for their commentary on the potential of "biologically variable ventilation", to facilitate recruitment as discussed in their article on page 158 in "future ventilatory strategies". At the end of this section the authors state that to date "...it has not been evaluated clinically". In fact, this ventilator has been used clinically and the findings reported in Anesthesiology(2). In this study, in patients undergoing abdominal aortic aneurysmectomy, variable ventilation resulted in improved oxygenation, better carbon dioxide clearance, lower dead space ventilation, increased respiratory system compliance and lower peak inspiratory pressures compared to conventional control mode ventilation, when examined over the perioperative period. 1. Mols G, Priebe H-J, Guttman J. Alveolar recruitment in acute lung injury. Br J Anaesth 2006; 96: 156-66. 2. Boker A, Haberman CJ, Girling LG, Guzman RP, Louridas G, Tanner JR, Cheang M, Maycher BW, Bell DD,Doak GJ. Variable ventilation improves perioperative lung function in patients undergoing abdominal aortic aneursymectomy. Anesthesiology 2004; 100: 608-16. Sincerely; W.A.C. Mutch, MD, FRCPC, Professor, Department of Anesthesia, University of Manitoba, Winnipeg, CANADA Conflict of Interest:WACM is co-founder of Biovar Life Support Inc. developer of the biologically variable ventilator discussed in this e-letter. World wide exclusive rights to the ventilator have been ceded to Respironics Inc. |
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