THERMOREGULATION AND OXYGEN MONITORING
| TEMPERATURE AND ITS EFFECT ON PERIOPERATIVE OUTCOMES —Daniel I. Sessler, MD, Chair, Department
of Outcomes Research, and L and S Weakley Professor of Anesthesiology, Cleveland Clinic, Cleveland, OH
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| Thermoregulation: body temperature normally tightly regulated; core temperature varies with circadian rhythm;
body temperature centrally regulated based on thermal information from entire body (eg, skin surface, deep central
organs, spinal cord, brain); thermoregulatory defenses modulate core temperature; behavior most important thermoregulatory
defense that allows humans to live in diverse environments (eg, wearing sweater, turning on air
conditioning, building house); behavioral responses not available to surgical patients; must therefore depend on autonomic
defenses; sweating, vasoconstriction, and shivering—major autonomic defenses in humans; vasoconstriction
defined as arteriovenous shunt constriction in fingers and toes; major effect on body heat content and dissipation
of heat to environment; body temperature normally between threshold (ie, triggering core temperature) for sweating
and threshold for vasoconstriction; sweating occurs when body temperature exceeds threshold (dissipates heat;
brings core temperature into interthreshold range); body temperature below threshold triggers vasoconstriction (constrains
metabolic heat to core; increases core temperature to interthreshold range); shivering occurs at 1° C below vasoconstriction
(means vasoconstriction failed); most people do not shiver routinely
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| Effects of anesthesia on temperature: study results with desflurane, alfentanil, dexmedetomidine, and propofol
show sweating essentially unaffected by anesthesia; in contrast, vasoconstriction and shivering thresholds decrease
substantially with anesthetic drugs; interthreshold range increases 2° to 4° C; body temperature control during
anesthesia 10 to 20 times worse than normal (ie, anesthetized patients poikilothermic until “quite cold”);
anesthetic-induced inhibition of thermoregulatory control results in decreased body temperature; rapid initial decrease
in core temperature (1°-1.5° C) over first hour, followed by slow linear decrease in core temperature, and
eventually core temperature plateau
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 | Initial rapid decrease in core temperature: results from internal core-to-periphery redistribution of body heat (not
heat loss to environment); core temperature not average body temperature, but temperature of trunk and head;
half of body mass (arms and legs) 2° to 4° C colder than core; thermal gradient between core and periphery maintained
by tonic thermoregulatory vasoconstriction; redistribution of heat major cause of hypothermia in most patients
(more important than exposure)
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| Second phase (slow linear decrease): results from heat loss exceeding heat production; body heat content, mean
body temperature, and core temperature all decrease; linear phenomenon (difference between heat loss and heat
production constant over time); most of loss from radiation and convection (not from conduction or evaporation)
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| Third phase (core temperature plateau): occurs when patient becomes sufficiently hypothermic to trigger thermoregulatory
vasoconstriction; occurs at 34° to 34.5° C core temperature; effectively constrains metabolic heat
to core; core temperature stays constant
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| Temperature monitoring: 4 reliable core temperature monitoring sites pulmonary artery, tympanic membrane, nasopharynx,
and distal esophagus; can be used interchangeably; rarely differ by >0.2° C, except during most rapid
warming and cooling phases of cardiopulmonary bypass; if careful, other sites can be used in most patients; important
to choose appropriate patient, position probe carefully, and use good judgment; sites include mouth, axilla, and bladder;
good indicators of core temperature (except during cardiopulmonary bypass); infrared tympanic monitors not favored
by speaker; temperature reading “nowhere near” tympanic membrane; rectal temperature also problematic;
reasonable analog of core temperature at steady state, but not helpful because of 15- to 30-min time lag
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| Consequences of hypothermia: in animals, mild hypothermia (1°-3° C) provides marked protection against ischemia
and hypoxia; 2° C of tissue hypothermia more protective against ischemia than any known drug (available
data do not support use in humans in most circumstances); hypothermia shown helpful in cardiac arrest (better
long-term neurologic outcomes); study of neonatal hypoxia also shows better outcome with hypothermia
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| Complications associated with hypothermia: randomized prospective trials; each case involves only 2° C of hypothermia;
standard of care when studies conducted was to allow hypothermia; therapeutic intervention was extra
warming; one study showed 3-fold reduction in morbid myocardial outcomes with normothermia; several reasons
to believe hypothermia would impair coagulation—mild hypothermia profoundly impairs platelet function; hypothermia
also inhibits enzymes of coagulation cascade; study of patients undergoing hip arthroplasty found hypothermic
patients lost 1 U more blood than normothermic patients; hypothermic patients also required significantly
more allogeneic blood; speaker conducting meta-analysis to show that mild hypothermia significantly increases
blood loss and transfusion requirement; healing of surgical wound infection may be impaired—due to decreased
perfusion of peripheral tissues (less O2 delivery); hypothermia directly impairs immune function—including macrophage
motility; also impairs scar formation (necessary to form barrier against further contamination); in patients
undergoing colon resection, number of infections tripled in hypothermic group, and duration of hospitalization prolonged
by 20% (even when analysis restricted to uninfected patients); other effects to consider—impairs enzymes
that degrade drugs; study found duration of action of vecuronium in patient 2° C hypothermic exceeds duration of
action of pancuronium in normothermic patient; if patient hypothermic, use nerve stimulator to avoid administering
excessive muscle relaxant; duration of recovery prolonged (substantial fraction of normal); thermal discomfort significant
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| Maintaining normothermia: passive insulator—easiest way to minimize heat loss; eg, plastic bags, paper and
cloth drapes, cotton blankets, space blankets; reduces heat loss by 30%; cover as much of patient as possible; insulation
alone not sufficient to keep most patients normothermic (due to initial core-to-periphery redistribution of
body heat); most patients require active warming system—usually forced air (least expensive safest easiest way to
keep warm); combines low cost and high degree of safety; avoid circulating water mattress because of possibility
of burns; counteract effects of redistribution by prewarming—warms peripheral tissues; ≥30 min forced-air warming
required before entering operating room (OR); fluid warming does not warm patient, but prevents fluid-induced
cooling (does not transfer heat to patient, compensate for redistribution hypothermia, or compensate for heat loss
from incisions); important secondary warming method for patient receiving large amount of fluid
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| NEW DEVELOPMENTS IN OXYGEN MONITORING —Steven J. Barker, MD, Professor and Head, Department
of Anesthesiology, University of Arizona College of Medicine, Tucson
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| Oxygen transport in humans: at rest, humans consume ≈1020 molecules of O2 per second; rather than molecular
diffusion, humans have complex cardiopulmonary system to transport O2 ; blood (containing hemoglobin [Hb])
travels through left side of heart and pumps O2 to tissues; at typical resting cardiac output (≈5 L per minute), 1 L
O2 delivered to tissues per minute; 250 mL per minute of O2 used by body; remainder stays in venous blood and
returns to right side of heart
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| Air to arterial blood: Hb designed to carry O2 at typical atmospheric pressures (≈70 mm Hg); transport curve shifted
to right, aiding O2 delivery, in situations that apply stress to body (eg, decreasing pH, increasing temperature, or increasing
CO 2 ); equation for arterial blood O2 content—CaO 2 = 1.38 x Hb (g/dL) x SaO 2 (arterial O2 saturation) +
0.003 x PaO 2 (arterial O2 tension); using typical arterial values, normal CaO 2 ≈21 mL/dL; CaO 2 in units of mL O2
per 100 mL blood (also known as vols percent)
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| Arterial blood to tissues: amount of O2 delivered to tissues by arterial blood determined by calculating CaO 2 multiplied
by flow of arterial blood (cardiac output [CO]); O2 returned to heart calculated as venous content times
flow of venous blood
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| O2 consumption by tissues (VO 2 ): difference between arterial O2 delivery and venous O2 return; factor 1.38 becomes
13.8 because Hb measured in g/dL, whereas CO measured in L/min; Fick equation given as VO 2 = 13.8 x Hb x CO x
SaO 2 - SVO 2 ÷ 100 [VO 2 = 13.8(Hb)(CO)(SaO 2 -SO 2 )/100]; substituting normal resting values, Hb = 15 g, CO = 5 L/
min, SaO 2 = 98%, SVO 2 = 75%, resting VO 2 predicted to be 240 to 250 mL/min; during exercise, CO can be rapidly
increased to ≥20 L/min and SVO 2 decreased to 40%, yielding maximum VO 2 of 2400 mL/min; same mechanisms can
be used to compensate for disease processes, eg, anemia (Hb value 2.5 g/dL; compensates by increasing CO to 15 L/
min and decreasing SVO 2 to 40%; results in normal VO 2 )
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| Oxygen monitoring in arterial blood: fiberoptic optode—measures PO2 as opposed to SO2 ; composed of long
thin optical fiber <0.5 mm in diameter; dye on tip of fiber has property known as fluorescence quenching (dye illuminated
with incident light of one color, but radiates back up fiber as fluorescent light of different color); wavelengths
measured; for specific dye, if O2 present in environment around dye, fluorescence process inhibited or
quenched; other dyes sensitive to hydrogen ions; any PO2 monitor gives early trend warning before patient in danger;
pulse oximetry does not give early warning of descending PO 2 (eg, endobronchial intubation); intra-arterial
optode—no longer used; expensive; unreliable; measures PO 2 not SO 2 ; likely to return to clinical practice in another
form; pulse oximetry—measures Hb saturation; form of spectrophotometry; measures concentration of substance
by looking at light absorbance (color); reduced Hb (RHb); has high absorbance at red wavelength and low
absorbance at infrared wavelength; oxyhemoglobin (O2 Hb) has low absorbance at red wavelength; thus, well oxygenated
patient looks pink and red (O2 Hb allowing red light to come through); 3 assumptions of conventional pulse
oximetry—1) two, and only two, light absorbers in blood (O2 Hb and RHb); 2) everything that pulsates must be arterial
blood (pulse oximetry uses 2 wavelengths; calculates pulse-added absorbance [fluctuating component divided
by fixed absorbance component] at red and infrared wavelengths; then calculates ratio of 2 pulse-added
absorbances [for each wavelength] by built-in calibration algorithm; ratio related to arterial Hb saturation); 3) one
empirical experimental calibration curve fits all humanity
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| Sources of error in pulse oximetry: examples of violated assumptions include low signal-to-noise ratio (pulsations
not detectable or overwhelmed by artifact, eg, motion artifact, venous pulsations) and additional colors (eg,
intravenous [IV] dyes, dyshemoglobins)
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| Dyshemoglobins: in experiment, dogs exposed to carbon monoxide; as carboxyhemoglobin (COHb) increased, true
saturation decreased linearly; but pulse oximetry saturation (SpO2 ) estimated at ≈90%; concluded that pulse oximetry
sees carboxyhemoglobin as if composed mostly of oxyhemoglobin; in similar experiment, increasing methemoglobin
(MetHb) concentrations (up to 60%) produced SpO2 readings that gradually decreased to ≈85%; if
either MetHb or COHb present, pulse oximetry has fewer equations than unknowns and cannot determine hemoglobin
concentration; Masimo recently announced “Rainbow Technology” pulse co-oximetry that uses 8 light
wavelengths; provides estimate of COHb, MetHb, and SaO2 simultaneously; also includes perfusion index and
low signal indicator; hand-held device; applications in field and in hospital; preliminary human volunteer data
from speaker’s laboratory encouraging
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| Failure: early studies showed ≈1% overall failure rate in OR for patients classified as American Society of Anesthesiologists
(ASA) physical status class 1; but Moller showed 7% failure rate for patients classified as ASA
physical status class 4; due to low perfusion; motion artifact causes fluctuating arterial blood and pulsating
venous blood; performance in motion and low perfusion have improved with new technology
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| Oxygen in tissue: transcutaneous O2 (Ptc O2 ) sensor; must be heated to facilitate diffusion through stratum corneum;
O2 comes from hyperemic dermis to Clark electrode; measure O2 delivery to skin; measures O2 tension, not saturation;
transcutaneous index (ratio of Ptc O 2 to PaO 2 ) reflection of perfusion (varies with cardiac output)
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| Oxygen in venous blood: venous O2 saturation (SVO 2 ) invasive continuous real-time monitor; indicates overall
health of O2 transport system; good trend monitor; used to fine tune positive end-expiratory pressure (PEEP) or
continuous positive airway pressure (CPAP) or other ventilator settings; depends on 4 variables
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| Conclusion: monitoring O2 in respired gas and arterial blood using pulse oximetry standard of care; look for new developments
in pulse oximetry; neither respired gas nor arterial blood indicates O2 delivery to tissues, cells, mitochondria,
or vital organs; look for new developments in organ-specific O2 monitoring, especially brain and heart;
venous O2 monitoring tracks overall health of O2 transport process and worth considering
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Suggested Reading
Aylott M: The neonatal energy triangle. Part 2: Thermoregulatory and respiratory adaption. Paediatr Nurs 18:38,
2006; Barker SJ et al: Comparison of three oxygen monitors in detecting endobronchial intubation. J Clin Monit
4:240, 1988; Barker SJ et al: Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology
70:112, 1989; Barker SJ et al: Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a
human volunteer study. Anesthesiology 105:892, 2006; Barker SJ: “Motion-resistant” pulse oximetry a comparison of
new and old models. Anesth Analg 95:967, 2002; Barker SJ: Standardization of the testing of pulse oximeter performance.
Anesth Analg 94:S17, 2002; Clifton GL et al: Use of moderate hypothermia during elective craniotomy. Tex
Med 88:66, 1992; De Witte J et al: Perioperative shivering: physiology and pharmacology. Anesthesiology 96:467,
2002; Frank SM et al: Increased myocardial perfusion and sympathoadrenal activation during mild core hypothermia
in awake humans. Clin Sci (Lond) 104:503, 2003; Frank SM et al: Temperature monitoring practices during regional
anesthesia. Anesth Analg 88:373, 1999; Frank SM et al: Threshold for adrenomedullary activation and increased cardiac
work during mild core hypothermia. Clin Sci (Lond) 102:119, 2002; Frank SM et al: Warmed humidified inspired
oxygen accelerates postoperative rewarming. J Clin Anesth 12:283, 2000; Hanowell L et al: Ambient light
affects pulse oximeters. Anesthesiology 67:864, 1987; Heier T et al: Impact of hypothermia on the response to neuromuscular
blocking drugs. Anesthesiology 104:1070, 2006; Insler SR et al: Perioperative thermoregulation and temperature
monitoring. Anesthesiol Clin 24:823, 2006; Lichtman AD et al: Malignant hyperthermia following systemic
rewarming after hypothermic cardiopulmonary bypass. Anesth Analg 102:372, 2006; Moller JT et al: Randomized
evaluation of pulse oximetry in 20,802 patients: I. Design, demography, pulse oximetry failure rate, and overall complication
rate. Anesthesiology 78:436, 1993; Sessler DI: Complications and treatment of mild hypothermia. Anesthesiology
95:531, 2001; Sessler DI: Perioperative heat balance. Anesthesiology 92:578, 2000; Sessler DI: Perioperative
thermoregulation and heat balance. Ann N Y Acad Sci 813:757, 1997; Siddik-Sayyid SM et al: Can we prevent malignant
hyperthermia after hypothermic cardiopulmonary bypass in a malignant hyperthermia-susceptible patient?
Anesth Analg 104:214, 2007; Todd MM et al: A comfortable hypothesis reevaluated. Cerebral metabolic depression
and brain protection during ischemia. Anesthesiology 76:161, 1992; Todd MM et al: Mild intraoperative hypothermia
during surgery for intracranial aneurysm. N Engl J Med 352:135, 2005; Welsh FA et al: Mild hypothermia prevents
ischemic injury in gerbil hippocampus. J Cereb Blood Flow Metab 10:557, 1990; Welsh FA et al: Postischemic hypothermia
fails to reduce ischemic injury in gerbil hippocampus. J Cereb Blood Flow Metab 11:617, 1991.
Educational Objectives
| The goal of this program is to positively influence perioperative outcomes by reviewing the dynamics of thermoregulatory
control and to identify new developments in oxygen monitoring. After hearing and assimilating this program,
the participant will be better able to:
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| 1. Discuss thermoregulation in the human body.
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| 2. Review the effects of anesthesia on body temperature.
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| 3. Analyze the consequences and possible complications associated with hypothermia.
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| 4. Summarize the transport of O2 from the atmosphere to the cell.
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| 5. Describe monitors that function at 4 stages of the O2 transport process.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose relevant
financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified
conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary
business or commercial interest. For this program, the following has been disclosed: Dr. Barker has received partial support
of research expenses from companies that manufacture pulse oximetry devices, including Masimo, Novametrix,
Ohmeda, and Philips.
Acknowledgements
Dr. Sessler spoke at the 60th Postgraduate Assembly in Anesthesiology, held December 8-12, 2006, in New York,
NY, and sponsored by the New York State Society of Anesthesiologists, Inc. Dr. Barker was recorded at the 80th
Clinical and Scientific Congress, held March 24-28, 2006, in San Francisco, CA, and sponsored by the International
Anesthesia Research Society. The Audio-Digest Foundation thanks the speakers, the NYSSA, and the IARS for their
cooperation in the production of this program.
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