POSTOPERATIVE HYPOTHERMIA IN THE GERIATRIC PATIENT

Transcription

1 TITLE: Author: POSTOPERATIVE HYPOTHERMIA IN THE GERIATRIC PATIENT Robert N. Sladen, MD. Professor and Vice-Chair, Department of Anesthesiology; Medical Director, Cardiothoracic-Surgical ICU, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA Temperature Regulation Humans are homeotherms; that is, there is a protected central core within which temperature varies minimally (CNS, viscera, great vessels). A peripheral shell provides a large facility for altering heat gain and loss: 50% of the body mass is within 3 cm of the skin. The temperature regulating center is situated in the hypothalamus and receives signals from free nerve endings in the skin that connect to neurons in the dorsal root ganglia. The anterior hypothalamus regulates heat loss: sensitive to changes in temperature, it modulates the posterior center. The posterior hypothalamus regulates heat gain: sympathetic responses, thyroid effects. Several CNS transmitters are involved with thermoregulation: 5-hydroxytryptamine (5HT) and prostaglandins (PGE1, PGE2) mediate heat gain; catecholamines (norepinephrine) respond to heat loss. The threshold of any regulatory system is that point above or below which the control action is invoked. Any change in core temperature below or above the threshold value initiates heat production or loss. The threshold differs for different responses (e.g. shivering, panting), has diurnal variation, and is altered by CNS changes, e.g. during anesthesia. Mechanisms for heat gain include (1) increased basal metabolic rate (BMR), (2) heat conservation by peripheral vasoconstriction or piloerection, (3) shivering, (4) non-shivering thermogenesis (NST), or passive heat gain from the environment. Increase in muscle tone alone can increase heat production by 100%. Subclinical shivering precedes obvious muscle movements and is detectable by electromyography. Severe shivering can increase heat production 5-10 fold. NST is an essential mechanism of heat production in neonates. Brown fat - rich in mitochondria - is distributed over neck, back, viscera, great vessels. Norepinephrine release activates cyclic AMP, which activates lipolysis, and releases free fatty acids, which are oxidized producing heat energy. Mechanisms for heat loss include (1) vasodilation, (2) sweating and (3) passive loss to the environment. Heat production commences when the CNS temperature is less than the threshold (set point), and is maximal with skin temperature at 20 C. If the CNS temperature is greater than the threshold, it doesn't matter what the skin temperature is. Vasodilation and sweating increase dramatically when CNS temperature exceeds 36.5 C; a difference of 0.5 C triples the rate of heat loss. Physical factors and Heat Transfer Heat transfer can occur only when there is a difference in temperature between two surfaces, and involves four distinct mechanisms: (1) conduction, (2) radiation, (3) convection and (4) evaporation. Conduction implies heat transfer between two immediately adjacent bodies: there is no net movement of molecules. In patients, heat transfer depends on blood flow to the area of contact and resistance is usually high because of insulation and molecular mismatch. Radiation implies heat transfer across space from one surface to another, and depends on the difference between the temperature of the skin and the surfaces, e.g. wall of the OR and patient s skin thus, interposing blankets negates the effect of radiant heaters. Convection involves particular movement in a fluid medium; requires interface conduction to start and is increased by eddy currents. Heat transfer depends on the gradient of temperature between the skin and surrounding air (often up to 15 C), as well as air velocity. Convection losses can be curtailed by the layer of stagnant, still air at the skin, enhanced by piloerection. With severe OR draughts (2 m/sec), convection losses can reach 200 kcal/hr. In evaporation, high energy molecules are lost from liquid to gas; the mean temperature of the remaining molecules decreases and the liquid cools. Losses increase with increased temperature of the liquid, gas movement over the surface and decreased humidity of the surface gas. Examples of evaporative heat loss during anesthesia include insensible loss from the skin, pleura, peritoneum (increased by cold liquids like skin prep, irrigation, blood, tissue fluids, uo to 400 kcal/hr with air movement at 2 m/sec and 50% relative humidity); lungs (1L cold, dry air requires 15 kcal to warm and saturate it from 20 C to 37 ; and seating, which may be noticed during rapid core warming on cardiopulmonary bypass (CPB) and must be differentiated from sympathetic response to pain and stress. Change in patient body heat content during anesthesia reflects the balance between heat gain from metabolic (100 kcal/hr) and work heat production (negligible), and loss to the air-conditioned OR environment by conduction, radiation, convection or evaporation. In a thermoneutral environment the ambient temperature is such that there is no net change. Temperature Measurement Monitoring devices utilize either a thermistor or thermocouple. In a thermistor a tiny sintered, compressed bead (<0.1 mm) of a heavy metal oxide (e.g. copper, nickel) is attached to electrodes. Thermal capacity is small and the probe undergoes a large, rapid decrease in resistance as temperature increases, e.g. from 2000 to 1400 ohms at ohms at 20 C to 40 C. A thermocouple circuit consists of two dissimilar metals (e.g. copper, copper-nickel alloy) kept at constant temperature, with a reference and a measuring junction. A current is set up that is directly proportional to the temperature difference between the two junctions. Temperature sites may measure the central, intermediate or peripheral compartment. Central sites include tympanic membrane, which is closest to the core (hypothalamus) via the internal carotid artery; nasopharynx (NP), which is close to internal carotid artery but affected by the temperature of inspired gas; and pulmonary artery (via the pulmonary artery catheter).

2 2 A thermistor incorporated into a laryngeal mask airway (LMA) provides good correlation with NP temperature. Intermediate sites may become central if the core enlarges, and include the esophagus (24 cm below larynx, between left atrium and aorta); rectum; bladder (affected by urinary flow) and axilla. Skin temperature monitoring can be used to indicate temperature gradients between core and periphery (i.e., redistribution of heat), and cutaneous vascular tone (i.e. perfusion). Heat Loss During Anesthesia In air-conditioned ORs, physical and environmental factors are a primary determinant of heat loss. An ambient temperature of 21 C is the dividing line between heat gain or loss in healthy young adults, but is higher in the elderly. Most adult ORs have temperature of C. The air temperature is cold, with very low humidity, and convection currents (draughts) are created by rapid room air turnover. Radiant losses to the cold OR walls may be substantial. Losses are exacerbated by skin preparation and irrigation of wounds, cavities, bladder with cold fluids, the use of cold intravenous solutions (20 C) or blood (4 C), and prolonged surgery with exposed serosal surfaces (thoracotomy, laparotomy). The physiologic response to heat loss (and gain) is markedly impaired by anesthesia. Opioids and volatile anesthetics suppress the catecholamine response to hypothermia and alter the central hypothalamic thresholds. Volatile anesthetics and regional anesthesia induce peripheral vasodilation that suppresses thermoregulatory vasoconstriction. Neuromuscular blockade, volatile anesthetics and regional anesthesia abolish increases in muscle tone and shivering. The net effect is to lower the threshold for responses to cold (vasoconstriction, shivering) and elevate the threshold for responses to heat (vasodilation, sweating). The interthreshold range (over which there are no responses to cold or heat) is widened from less than 0.5 C to as much as 3.5 C. In this range the anesthetized patient is poikilothermic, i.e. the environment directly affects central temperature. The pattern of intraoperative hypothermia has three distinct phases. In the first hour after induction there is a rapid decrease in central temperature that reflects redistribution of heat from the warm core to the newly vasodilated periphery. Subsequently there is slower but progressive central hypothermia, dependent on heat balance in the OR. Finally, the central temperature reaches a plateau or may even rewarm, as the thermoregulatory thresholds are reached and/or external warming methods begin to take effect. During cardiopulmonary bypass (CPB) with moderate hypothermia, blood from the bypass circuit cools the central core rapidly to about 30 C. The intermediate zone (muscle, fat) cools more slowly. The blood is warmed to 37 C prior to separating from CPB, but then cools to about 35 C over the next hour or so. This afterdrop is due to redistribution of heat from the warm blood to the still-cool intermediate zone. Thus, the patient arrives in the ICU cool, with elevated systemic vascular resistance (SVR) and diminished oxygen consumption (VO2) and carbon dioxide production (VCO2). During subsequent rewarming, SVR decreases and VO2 and VCO2 both increase (see below). Effect of Advanced Age There are numerous reasons for impaired thermoregulatory responses and even failure - in the elderly patient. Responses to cold become progressively impaired. Basal metabolic rate (BMR) decreases with age, and there is a loss of resting muscle tone. The average heat production between the age of 20 and 40 years is 40 kcal/m 2 /hr; over the age of 60 years this diminishes to 30 kcal/m 2 /hr. Elderly men more than women have decreased body fat, so that there is an increased surface area:body mass ratio, and more potential for radiant heat loss. As the circulatory system ages, thermoregulatory cutaneous vasoconstriction becomes impaired, although the pressor response to cold is enhanced. The threshold and intensity of the shivering response is impaired, because of central changes and decreased muscle mass. In awake patients, the perception of cold becomes impaired as well. Coexistent diseases that induce autonomic neuropathy, notably chronic renal failure and diabetes, or vasculitides such as SLE, impair neuronal and vascular thermoregulatory responses. Similarly, responses to heat are also impaired. Cutaneous vasodilation and sweating rate are decreased, and the sweating threshold is elevated. In awake patients, the perception of heat becomes impaired as well. However, all these changes may be ameliorated by the overall state of fitness or health of the patient. Elderly patients develop more hypothermia during surgery. There is a direct relationship between age and the development of perioperative hypothermia during general and epidural anesthesia. The central temperature threshold that triggers thermoregulatory vasoconstriction is decreased about 1 C during general anesthesia; the threshold for shivering is decreased about 1 C during spinal anesthesia. During the first hour of anesthesia, when heat redistributes from the core to the newly vasodilated periphery, the central temperature decreases about 0.3 C in a 20 year-old, but as much as 1.1 C in an 80 year-old patient. Elderly patients enter the PACU with a central temperature up to 1 C colder than young patients, postoperatively shiver less and take longer to rewarm. Intraoperative Consequences of Hypothermia Mild to moderate levels of hypothermia (34-35 C) provide a remarkable degree of cerebral protection to ischemic injury (conversely, mild levels of hyperthermia markedly exacerbate cerebral ischemic injury). Inadvertent cooling may therefore be beneficial in procedures such as carotid endarterectomy and thoraco-abdominal surgery. More severe hypothermia (<34 C) has potentially adverse effects on all organ system functions. There is progressive

3 3 myocardial depression, and emergence of bradycardia, bradyarrhythmias; the appearance of Osborne waves (J-point elevation) may presage ventricular arrhythmias. The ventilatory response to hypoxemia and hypercarbia is progressively diminished, with hypopnea. During mechanical hyperventilation, decreased VCO2 predisposes to acute respiratory alkalosis. Drowsiness, confusion, stupor, coma ultimately ensue, and emergence from anesthesia is delayed. Blood viscocity is increased, leading to sludging, poor perfusion and organ ischemia. Importantly, coagulation becomes progressively impaired below 33 C; even mild hypothermia increases intraoperative blood loss and the requirement for blood products. This hypothermic coagulopathy is not reflected by standard coagulation studies, because the tested blood is warmed to 37 C. Cold induces hyperglycemia through catecholamine release, and diuresis by impairment of tubular sodium reabsorption. Volatile anesthetics are more soluble in cold blood, which decreases MAC and delays emergence. Certain neuromuscular agents (e.g. vecuronium, cisatracurium) are metabolized more slowly and have a more prolonged duration of action. Postoperative Consequences of Hypothermia Postoperative rewarming vasodilation unmasks underlying hypovolemia, and if severe may result in hypotension, tachycardia, or even myocardial ischemia. Shivering not only causes patient discomfort but dramatically increases VCO2 (increased minute ventilation, respiratory acidosis) and VO2 (cardiac output must increase or mixed venous desaturation hypoxemia, and myocardial ischemia may ensue). Shivering and chest wall rigidity interfere with ventilation and uniform gas flow; increased intrapleural pressure can cause spurious elevation of intravascular pressures (CVP, pulmonary artery pressures). The marked increase in heat production associated with persistent cutaneous vasoconstriction leads to rapid temperature elevation. Temperature overshoot to C is not uncommon (servo wobble) and starts to plateau only when peripheries vasodilate and heat loss balances heat production. Use of cooling blankets may simply trap heat by cutaneous vasoconstriction and exacerbate overshoot - and may even cause peripheral ischemia by reducing blood flow to metabolically hyperactive tissues. Mild perioperative hypothermia suppresses the mitogen-induced activation of lymphocytes and the production of protective cytokines, and it is associated with a greater incidence of postoperative surgical wound infections and longer hospital length of stay. Alpha-stat versus ph-stat The ph-stat methodology implies that arterial blood gases (ABGs), measured in the laboratory at 37 C, are corrected back to the patient's temperature. For example, a hypothermic patient (28 C) on a ventilator with a PaCO2 of 40 mmhg measured at 37 C would be reported as having a corrected PaCO2 of 25 mmhg. If the ph at 37 C were 7.4, the corrected ph would be This suggests that minute ventilation (or increase CO2 flow on cardiopulmonary bypass) should be decreased to normalize the corrected PaCO2 and ph. Herman Rahn (a German physiologist) described the neutral point of water, i.e. [H + ] = [OH - ], increases as temperature decreases. Ectotherms keep their blood ph 0.6 greater than the neutral point of water. For example, the arctic codfish, which has a blood temperature of -1.9 C, has a blood ph of 8.17! Animal studies suggest that metabolism benefits from increasing alkalosis with decreasing blood temperature, as long as the ph = 7.4 and PaCO2 = 40 mmhg when measured at 37 C. Animal studies suggest that animals kept alkalotic at low temperature have better myocardial function and higher fibrillation threshold coming off CPB. In other words, in the example cited above, the apparent respiratory alkalosis is acceptable. Since the ABGs are normal at 37 C, the PaCO2 of 25 and ph of 7.52 are appropriate at a temperature of 28 C. Normalization of the corrected ABGs would cause a relative respiratory acidosis at 28 C. The simplest approach is to use uncorrected ABGs (alpha-stat). If the PaCO2 is 40 and the ph is 7.4 when measured at 37 C, it doesn't matter what the corrected values are. Prevention of Heat Loss during Anesthesia Control of ambient temperature is essential, and most modern ORs are provided with rapidly acting heating/cooling systems. Entering a freezing OR simply adds to a patient's apprehension and sympathetic tone; in the elderly it can be disastrous. It is a very simple step to turn up the room temperature before the patient enters the OR, which will enhance patient comfort and diminish heat redistribution from the core to the skin during the first hour of anesthesia. This benefit is enhanced further if patients are prewarmed in the holding area before entry to the OR. Once the patient is insulated by the drapes the room temperature can safely be turned down. Insulation by a simple enveloping cover is the most cost-effective way to decrease heat loss in the OR. It prevents draughts from removing the stagnant air layer above the skin (convection), reflects heat back to the patient (radiation), creates 100% humidification of the air above the skin (prevents evaporation), and decreases direct contact with cold surfaces (conduction). Any impervious cover, including plastic, saran wrap, space blankets, steridrape, will do. All exposed areas should be covered. The most efficient method of conserving (or for that matter, gaining) heat in the operating room and PACU is the forced-air warming blanket, which operates on the basis of convection. Warmed air is forced through a light air-mattress placed over exposed parts of the patient's body. However, it should not be placed over an ischemic area (e.g. the lower part of the body during aortic cross-clamping) because of increased tissue VO2 and increased risk of burn injury.

4 4 Skin prep and irrigation fluids should be warmed, and warm saline pads can be placed on exposed serous surfaces to decrease major evaporative loss. Use of blood warmers for rapid administration of bank blood (4 C) is essential. At this temperature the P50 is so left-shifted that at venous PO2 hemoglobin is still 100% saturated. In other words, cold blood simply acts is an inert volume expander - it is completely unable to give up any O2 to the tissues.. Oxygen transport requires energy from the patient to warm the cold blood, further exacerbating oxygen supply:demand balance in sick patients. Rapid infusion of cold blood via a central line can cause arrhythmias. Cold blood is viscous, difficult to infuse, and worsens peripheral vasoconstriction. Although colloids and crystalloids these fluids are at room temperature (20 C), infusion of large amounts (> 4L) can contribute to hypothermia. Use blood warmers for these fluids is warranted in big cases, even if transfusion is not planned. Heated, humidified anesthetic gas prevents the body from losing energy in warming and humidifying dry gas in the trachea and may decrease pulmonary complications caused by mucosal crusting and ciliary paralysis. The artificial nose (e.g. HumidVent ) is a simple, inexpensive fine mesh filter placed in airway that traps the warmth and humidity of patient's expired air, and uses it to warm, humidify dry inspired gas. Anesthetic gas thus achieves a state similar to that induced by nasopharynx, i.e. temperature about C, 70-90% relative humidity, and a water content of 30 mgh2o/l. However, it cannot add heat to an already hypothermic patient. The electronic heater-humidifier provides full artificial heatinghumidification: temperature C, 100% relative humidity, 44 mgh2o/liter. 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