Relationship_Between_Inhalation_Anesthetics_and_Intravenous_Propofol_on_the_Incidence_of_Intraoperative_Hypothermia

Research Paper The Relationship between Inhalation Anesthetics and Intravenous Propofol on the Incidence of Intraoperative Hypothermia Submitted in partial fulfillment of the Requirements for the degree of Master of Science Table of Contents Abstract………………………………………………………………………………….....4 Introduction……………………………………………………………………………….. 5 Literature Review………………………………………………………………………......6 Discussion and Recommendations………………………………………………………..17 References………………………………………………………………………………...20 Abstract Hypothermia during general anesthesia is common and may be associated with intraoperative complications such as myocardial morbidity and postoperative chills. Understanding how anesthetic agents aaffect intraoperative temperature regulation could lead to improvements in the quality of anesthetic care provided to patients. This literature review investigated how inhalation anesthetic agents and total intravenous anesthesia (TIVA) aeffect intraoperative temperature regulation. Researchers demonstrated Wwhen measuring blood pressure response to cold-induced vasoconstriction with and without inhalation anesthetic agents (desflurane and isoflurane) researchers found that, the rise in mean arterial pressure was similar. Researchers also demonstrated that the incidence of postoperative chills in patients undergoing lumber disk surgery was not statistically significant when comparing isoflurane inhalation anesthesia and TIVA (remifentanil and propofol). When comparing texamining the use of Sevoflurane inhalation anesthesia toand TIVA (propofol) on the thermoregulatory responses in patients undergoing transsphenoidal pituitary surgery, researchers demonstrated that the response was similar. [ In the previous sentence, do you mean to say that the result of both studies was similar, i.e., that neither technique demonstrated a statistically significant result'] Lastly, researchers’ demonstrated lipid-emulsion propofol attenuated the thermoregulatory response to hypothermia better than sevoflurane or micro-emulsion propofol when providing anesthesia in the elderly. Introduction Thermoregulation is the homeostatic process of to maintaining body temperature within a certain range. Maintenance of body temperature is accomplished by thermoregulatory defense mechanisms such as vasoconstriction and shivering (responses to cold) or vasodilatation and diaphoresis (responses to warmth) (Sessler, 1997). Thermoregulation consists of three characteristics: threshold, gain, and maximum response intensity. Threshold is the temperature at which the thermoregulatory mechanisms are triggered. Gain is the rate of change of response with a given change in temperature (the slope of the response curve). Maximum response intensity is the upper limit of the response (Sessler, 2009). Temperature regulation in the human body is controlled by the autonomic nervous system. Positive and negative feedback mechanisms maintain normal body temperature. The ability to regulate temperature occurs via the skin’s thermal input. During exposure to hot or cold environments, thermal sensors send temperature information to central regulatory centers in the anterior hypothalamus which have certain temperature thresholds (Satinoff, 1978). General anesthesia disrupts the thermoregulatory mechanisms by significantly decreasing the threshold temperatures of vasoconstriction and shivering (Kurz, Sessler, Schroeder, & Kurz, 1993). The thermoregulatory responses to cold (vasoconstriction and shivering) are not triggered until the core body temperature reaches the decreased threshold temperature. Consequently, the core body temperature drops more than normal temperature (~37 degree Celsius) during general anesthesia. [New paragraph]There are three phasesstates of core body temperature change. First, core body temperature decreases rapidly due to the body heat redistribution from the core area to the peripheral area (Matsukawa et al., 1995). Second, core body temperature decreases slowly with a linear pattern because heat production is less than heat loss (Hynson & Sessler, 1992). Last, core body temperature remains almost constant as heat production equals heat loss (Sessler, Olofsson & Rubinstein, 1988). The almost constant temperature state occurs when patients are maintained relatively warm or they have peripheral vasoconstriction triggered by core temperatures of 33-35 degree Celsius (Belani et al., 1993). Generally, hypothermia is defined as a core body temperature less than 35 degree Celsius (source for this definition', or state something like “In the realm of medicine, a core body temperature less than 35 degrees Celsius is accepted definition of hypothermia”). Hypothermia can be utilized for therapeutic reasons. , Hhowever, when hypothermia is eployed therapeuticallyused during general anesthesia, there is an increased risk of postoperative wound infection, intraoperative bleeding and transfusion requirements, postoperative morbid cardiac events, and recovery and hospitalization (Frank et al., 1997; Kurz, Sessler, & Lenhardt, 1996; Smied, Kurz, Sessler, Kozek, & Reiter, 1996). Hypothermia can also cause significant discomfort during the postoperative period. (By what mechanism' I.e., incisional pain plus shivering = an increased perception of pain on behalf of the patient, or cite a study whereby patients who were shivering post-op reported higher pain ). Prevention of hypothermia during anesthesia is very important and an understanding of the thermoregulatory effects of anesthetic agents utilized in current practice is necessary for anesthesia providers. Inhalation agents, such as Sevoflurane, Isoflurane, Desflurane, and the intravenous agent, Propofol, are widely used in the maintenance of general anesthesia and possess similar but individually uniquedifferent thermoregulatory characteristics. Understanding general thermal characteristics of each agent is critical to improve warming efforts. This literature review aims to identify the relationship between inhalation anesthetics and intravenous propofol on the incidence of hypothermia intraoperatively. Literature Review One of the leading causes of perioperative death is adverse cardiac outcomes (Source'). Peripheral and central vasoconstriction triggered by hypothermia increases arterial pressure and increases the risk of myocardial morbidity (Mangano, 1990). The risk of myocardial morbidity increases three fold, even with mild hypothermia (Frank et al., 1995). Greif, Laciny, Rajek, Doufas, and Sessler (2003) investigated the effects of cold-induced vasoconstriction on arterial pressure with and without volatile anesthesia. The purpose of the research was to determine if the hypertensive response to hypothermia was blunted by the utilization of isoflurane or desflurane. Data were collected from three independent prospective studies and analyzed retrospectively. Treatments for each study were randomized and the primary endpoint was arterial pressure. The research received IRB approval and participant written consent. To control for physiologic or disease states that may confound results, tThe researchers chose participants were healthy male volunteers who were neitherot obese, taking medication, nor did they havehad a history of thyroid disease, dysautonomia, or Reynaud's syndrome. Participants were minimally clothed and ambient temperature was kept at 22-23 degree Celsius during the investigation. To induce anesthesia, 3-5 mg/kg of propofol was utilized and maintained with an inhalation agent. Circadian thermoregulatory fluctuation was minimized by starting studies in the morning thus maintaining triggered responses at similar times during the day. Ten participants were included in the first study were and anesthetized with 2.8 volume percentage of desflurane post-induction. Participants were paralyzed, mechanically ventilated, and turned to the left-lateral position. By putting padding under the rib cage, the brachial artery compression and the restriction of flow to the dependent arm were avoided. The second study included nine participants who took part in the study on three separate days. During the first day, no anesthesia was administered as this was the baseline control group day. During the second and third day, participants received end-tidal desflurane concentrations of 3.5% and 5.6% respectively. All participants maintained spontaneous ventilation. The third study was composed of eight participants who took part in the study on four separate days. Participants received end-tidal isoflurane concentrations 0.6%, 0.7%, 0.8%, and 1.0% each study day, respectively. On the third day, the participants were initially evaluated without anesthesia (baseline/control) followed by the administration of anesthesia. All participants maintained spontaneous ventilation. To induce thermoregulatory vasoconstriction mean-skin temperature was reduced to 31 degree Celsius using a circulating water mattress and forced air cooler. The mean skin-surface temperature was calculated from measurements at 15 sites by assigning the following regional percentages to each area: head, 6%; upper arms, 9%; forearms, 6%; hands, 2.5%; fingers, 2%; back, 19%; chest, 9.5%; abdomen, 9.5%; medial thigh, 6%; lateral thigh, 6%; posterior thigh, 7%; anterior calves, 7.5%; posterior calves, 4%; feet, 4%; and toes, 2%. The core body temperature was taken from the tympanic membrane at one minute intervals. (Perhaps a comment about the reliability of various thermoregulatory devices is in order here – or somewhere in this paper; just a bullet statement that presents the reliability of esophageal, rectl probe, tympanis or skin thermometers).Cold induced vasoconstriction and peripheral vasodilation were measured by calculating forearm-minus-fingertip skin temperature gradient; if the gradient was greater than +2 degree Celsius it was considered vasoconstriction and if the gradient was less than -2 degree Celsius it was considered vasodilation. Heart rate and arterial pressure were measured at five minute intervals oscillometrically. Laser doppler flowmetry and perfusion index estimated vascular tone and were measured at one minute intervals. All measures were compared using two-tailed, paired t-tests. Differences in the measures were compared using two-tailed, unpaired t-tests with Bonferroni correction; statistical significance was P