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Akca O: Optimizing the Intraoperative Optimizing the intraoperative management of carbon dioxide concentration Ozan Akc¸a Purpose of review Abbreviation This review assesses whether there is a carbon dioxide CBF cerebral blood flow concentration range that provides optimum benefit to the patient intraoperatively. It includes the physiological # 2006 Lippincott Williams & Wilkins 0952-7907 effects of carbon dioxide on various organ systems in awake and anesthetized individuals and its clinical effects in the ischemia/reperfusion setting. This review will present views on end-tidal or arterial carbon dioxide Introduction tension management in the perioperative period. The normal range of carbon dioxide tension is Recent findings 35–45 mmHg. However, there are various times, how- Hypocapnia reduces intracranial pressure and is used by ever, when, as anesthesiologists, we accept or clinically clinicians during acute traumatic brain injury, acute tolerate hypocapnia (PaCO2 < 35 mmHg) or hypercapnia intracranial hemorrhage, and acutely growing brain (PaCO2 > 45 mmHg). Intraoperatively, in neurosurgical tumors. There is mounting evidence, however, that cases when increased intracranial pressure is expected, hypercapnia improves tissue perfusion and oxygenation. hypocapnia is generally achieved by hyperventilation, Therefore, clinicians may want to induce mild-to-moderate which appears to be well tolerated. In addition, in spon- hypercapnia during reperfusion states such as major taneously breathing patients or patients undergoing vascular surgery, organ transplantation, tissue-graft laparoscopic surgery, mild intraoperative hypercapnia is surgery, and cases managed with low mean arterial a well tolerated, but unintentional, byproduct. There- pressures to control bleeding. As hypercapnia preserves fore, it is valid to ask whether there is an optimum car- cerebral blood flow even under relatively low perfusion bon dioxide pressure that should be maintained intrao- pressures, it may be beneficial during global reperfusion peratively, or whether carbon dioxide pressures outside scenarios. This hypothesis needs to be tested extensively the normal range provide better perfusion or any other before being considered for clinical applications. From a benefits to organ systems. This mini review aims to pre- different perspective, current American Heart Association sent the physiological effects of a wide range of clinical Guidelines recommend 12–15 breaths/min during carbon dioxide concentrations. Additionally, the poten- cardiopulmonary resuscitation and stress the potential tial benefits and consequences of mild-to-moderate negative role of inadvertent hyperventilation on survival hypercapnia in different clinical environments will be outcome. The importance of this concept is discussed discussed. briefly. Summary Carbon dioxide, cardiac output, tissue Overall, the benefits of managing carbon dioxide perfusion, and oxygenation concentration intraoperatively for the maintenance of Peripheral tissue perfusion and oxygenation depend on cardiac output, tissue oxygenation, perfusion, intracranial various factors, including inspired oxygen concentration, pressure, and cerebrovascular reactivity are well defined. arterial oxygen tension [1], hemoglobin concentration [2], cardiac output [3], local perfusion [4,5], and the Keywords • carbon dioxide, cardiac output, hypercapnia, hypocapnia, autonomic stress response to pain [6,7 ]. Different con- ischemia, oxygen, perfusion, reperfusion, tissue centrations of carbon dioxide are known to alter some of oxygenation these parameters and may contribute to tissue perfusion and oxygenation. Increasing arterial carbon dioxide ten- sion (PaCO2) by about 10 mmHg increases the cardiac # Curr Opin Anaesthesiol 19:19–25. 2006 Lippincott Williams & Wilkins. index by about 10–15% [8,9]. Hypercapnia causes a Department of Anesthesiology and Perioperative Medicine, OUTCOMES RESEARCH rightward shift of the oxyhemoglobin dissociation Institute, and Neuroscience and Anesthesia Intensive Care Unit, University of Louisville, Kentucky, USA curve, decreases systemic vascular resistance, and, over- all, increases oxygen availability to tissue [9]. Thus, Correspondence to Ozan Akc¸a MD, Assistant Professor, 501 East Broadway, Suite 210, Louisville, KY 40202, USA changes in carbon dioxide concentration alter tissue oxy- Tel: +1 502 852 5851; fax: +1 502 852 2610; e-mail: [email protected] genation as confirmed previously by our group [8,10] Current Opinion in Anaesthesiology 2006, 19:19–25 (Fig. 1). 19 20 Thoracic anaesthesia Increasing PaCO2 also increases cardiac output [8,9,11], Increasing carbon dioxide concentration both stimulates which appears to be directly related to both hypercapnic and depresses the cardiovascular system [8,11,13,14]. acidosis per se and to hypercapnia-induced sympathetic Potentially, the most significant effect is myocardial activation and release of catecholamines [12]. In the depression, which is associated with an increased output awake individual hypercapnia triggers sympathetic acti- [15]. Cardiac output increases gradually by about 30–35% vation with mild tachycardia; but in anesthetized within the PaCO2 range 20–60 mmHg [8,16]. Most patients it causes only mild bradycardia ([CO2] > 10%), myocardial depression occurs at CO2 concentrations which does not generally alter blood pressure [12]. greater than 10–15% (i.e., PaCO2 > 75 mmHg) [11,14]. According to the systemic vascular resistance formula, Myocardial contractility does not appear to be affected up under normal hydration status, if hypercapnia increases to a PaCO2 of 75 mmHg [14]. Hypercapnia directly cardiac output (CO) but does not change mean arterial depresses the myocardium [17,18]. Hypercapnia, how- pressure, then systemic vascular resistance has to ever, also stimulates the myocardium indirectly through decrease to maintain the equilibrium. the sympathetic nervous system activation [18,19]. In the early 1970s, Blackburn et al. [18,20] showed that CO2 had inotropic effects through β-adrenergic receptors in dogs Figure 1 Cardiac index (CI), muscle tissue oxygen saturation and human patients. They concluded that the main effect (SmO2), skin blood flow (laser doppler flow velocity, LDF), and of hypercapnia on the heart was β-adrenergic receptor- subcutaneous tissue oxygen tension (PsqO2) all increased as a mediated inotropy, which has a threshold of between 70 linear function of PaCO2 and 100 mmHg PCO2 (Table 1). Carbon dioxide and cerebral perfusion and oxygenation The cerebral circulation is well innervated by sympa- thetic, parasympathetic, and sensory nerves. Sympa- thetic stimulation causes constriction of the cortical con- ducting arteries; however, this does not appear to produce any changes in cerebral blood flow (CBF) because downstream vessels dilate, possibly as a com- pensation for the upstream constriction. The parasympa- thetic innervation is less well studied, although it has been demonstrated that stimulation of the sphenopala- tine ganglion increases CBF. Overall, the autonomic nervous system may help to determine the set point for homeostatic mechanisms [21••]. Normally, there is a relatively constant perfusion of brain tissue at perfu- sion pressures of between 50 and 150 mmHg. This auto- regulatory response may rapidly shift to the left and the right, depending on each patient’s physiology. Carbon dioxide is a very potent modulator of CBF. There is a 3-to-5% alteration in CBF for every mmHg change in PaCO2. Hypercapnia causes cerebral vessels to vasodilate, while hypocapnia causes them to constrict. The graph of the relationship between carbon dioxide Table 1 Summary of hemodynamics, oxygenation and perfusion Mild-to-moderate hypercapnia within the clinical range linearly increases cardiac index Mild-to-moderate hypercapnia improves oxygen availability to tissue by altering cardiac index, shifting the oxyhemoglobin dissociation curve, and decreasing systemic vascular resistance Therefore, it may be preferable to allow the patient to develop mild-to- P values were obtained from linear regression formula (reproduced moderate hypercapnia in order to improve peripheral tissue from [8]). perfusion and oxygenation in cases that have the potential of severe peripheral perfusion compromise Optimum intraoperative CO2 Akca 21 and CBF is sigmoid with two plateaus, one below 25 (CPR) may exacerbate brain injury [25]. During pro- mmHg and the other above 75 mmHg (Fig. 2 [22]). longed hypocapnia, there is a decrease in extracellular Within the clinical range, however, the relationship fluid bicarbonate concentration, which results in the gra- appears to be linear. As blood pressure decreases and dual return of extracellular fluid pH toward normal. In autoregulatory vasodilation occurs, there is a progressive brain tissue, this normalization of local pH also nor- reduction in carbon dioxide responsiveness. In contrast, malizes cerebral blood flow. Therefore, prolonged hypo- anesthetics, such as halothane and isoflurane, that capnia eventually causes tolerance and might even cause induce vasodilation increase the slope of the dose– a rebound effect in intracranial pressure and lead to neu- response relationship, perhaps indicating that mechan- ronal ischemia [26]. isms that alter basal tone modify the response to CO2 [21••]. It is well known that cerebrovascular responses are mediated by nitric oxide (NO) related mechanisms; Due to the skull’s bony structure, the cranial cavity is a however, there is also evidence that the effects of hyper- fixed space,
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