Handbook of Clinical Anesthesia

Chapter 27

Standard Monitoring Techniques

Monitoring represents the process by which anesthesiologists recognize and evaluate potential physiologic problems by identifying prognostic trends in patients in a timely manner (Greenberg SB, Murphy GS, Vender JS: Standard monitoring techniques. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 695–714). Effective monitoring decreases the potential for poor outcomes that may occur after anesthesia by identifying derangements before they result in serious or irreversible injury. Monitoring devices increase the specificity and precision of clinical judgments. Standards for Basic Anesthesia Monitoring have been adopted by the American Society of Anesthesiologists (ASA).

  1. Inspiratory and Expired Gas Monitoring

The concentration of oxygen in the anesthetic circuit must be measured. Manufacturers of gas machines place oxygen (O2) sensors on the inspired limb of the anesthesia circuit to ensure that hypoxic gas mixtures are not delivered to patients. Monitoring inspired O2 concentration does not guarantee the adequacy of arterial oxygenation.

  1. Monitoring of Expired Gases
  2. Carbon Dioxide
  3. Monitoring of expiratory CO2(end-tidal CO2 or PETCO2) has evolved as an important physiologic and safety procedure for identifying placement of the endotracheal tube (this does not confirm placement above the carina) and for assessing variables such as

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ventilation (PaCO2), rebreathing, cardiac output, distribution of blood flow, and metabolic activity.

 

Figure 27-1. The capnogram is divided into four distinct phases. The first phase (A–B) represents the initial stage of expiration (gas from anatomic dead space) and is usually devoid of CO2. At point B, CO2-containing gas is present at the sampling site, and a sharp upstroke (B–C) is seen in the capnogram. Phase C–D represents the ventilation-weighted average concentration of CO2 in alveolar gas. Point D is the highest value and is designated as the end-tidal CO2 concentration. At point D, the patient begins to inspire CO2-free gas, and there is a steep downstroke (D–E) back to baseline. Normally, unless rebreathing of CO2 occurs, the baseline approaches zero.

  1. Capnometryis the measurement and numeric representation of the CO2 concentration (in millimeters of mercury [mm Hg]).
  2. capnogramis a continuous concentration–time display of the CO2 concentration (divided into four distinct phases) sampled at the patient's airway during ventilation (Fig. 27-1).
  3. Capnographyis the continuous monitoring of the patient's capnogram.
  4. The end-tidal CO2concentration provides a clinical estimate of the PaCO2, assuming ventilation and perfusion in the lungs are appropriately matched (normal gradient, 5–10 mm Hg) and no sampling errors occur during measurement. (Sidestream analyzers may dilute a patient's tidal breath with fresh gas, especially when tidal volume is small, as in young patients. Loose connections and system leaks also dilute end-tidal CO2.)
  5. Dead space(ventilation without perfusion) and a resulting increase in the difference between the PaCO2 and the end-tidal CO2 (dead space gases containing little or no CO2greatly dilute the end-tidal CO2 concentration) may reflect

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hypoperfusion states, chronic obstructive pulmonary disease, and embolic phenomena (thrombus, air).

Table 27-1 Reasons for Changes in the End-Tidal Carbon Dioxide Concentration

Increases

Decreases

Hypoventilation

Hyperventilation

Hyperthermia

Hypothermia

Sepsis

Hypoperfusion

Malignant hyperthermia

Pulmonary embolism

Rebreathing

Slowed metabolism

Increased skeletal muscle activity

 

  1. Shunt(perfusion without ventilation) causes minimal changes in the gradient between PaCO2 and end-tidal CO2.
  2. Capnography has decreased the potential for unrecognized accidental esophageal intubation.
  3. Because the esophageal or gastric gas concentration is primarily composed of inspired gas, it should contain exceedingly small amounts of CO2. After an accidental esophageal intubation, the first one or two “breaths” may contain some CO2, but the concentration should approach zero after four or five “breaths.”
  4. A continuous stable CO2waveform ensures the presence of alveolar ventilation (tube in the trachea) but does not necessarily indicate that the endotracheal tube is properly positioned above the carina.
  5. Common causes of gradual increases or decreases in end-tidal CO2reflect changes in CO2 production or changes in CO2 elimination (Table 27-1).

Table 27-2 Explanations for Abrupt Decreases in the End-Tidal Carbon Dioxide Concentration

Malposition of the tracheal tube into the pharynx or esophagus
Disruption of airway integrity (disconnection or obstruction)
Disruption of the sampling line
Pulmonary embolism
Low cardiac output
Cardiac arrest

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Table 27-3 Information derived from the capnogram waveform

Slow Rate of Rise of Upstroke
Chronic obstructive pulmonary disease
Acute airway obstruction
Normally Shaped but Increased End-Tidal CO2 Concentration
Alveolar hypoventilation
Increased CO2 production
Transient Increases in End-Tidal CO2 Concentration
Tourniquet release or aortic unclamping
Administration of bicarbonate
Insufflation of CO2 during laparoscopy
Failure of the Baseline to Return to Zero
Rebreathing

  1. A sudden decrease in end-tidal CO2to near zero requires a rapid assessment of possible causes (Table 27-2).
  2. The adequacy of cardiopulmonary resuscitation can be assessed by capnography, as reflected by a reappearance or an increase in end-tidal CO2with restoration of pulmonary blood flow.
  3. The size and shape of the capnogram waveform may be informative (Table 27-3).
  4. Multiple Expired Gas Analysis.Many critical events may be detected by analysis of respiratory and anesthetic gases (Table 27-4). Nitrogen (N2) monitoring provides quantification of washout during preoxygenation. A sudden increase in the N2 concentration in the exhaled gas indicates either introduction of air from leaks in the anesthesia delivery system or venous air embolism.

III. Arterial Oxygenation Monitoring

  1. Pulse Oximetry
  2. Measurement of the peripheral O2saturation of hemoglobin (SpO2) on a continual basis is the standard of care for measuring oxygenation during anesthesia and in the postanesthesia care unit.

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Table 27-4 Gas Analysis and the Detection of Critical Events

Event

Monitored Gas

Error in gas delivery system

Oxygen
Carbon dioxide
Nitrogen
Inhaled anesthetic

Anesthesia machine malfunction

Oxygen
Carbon dioxide
Nitrogen
Inhaled anesthetic

Disconnection

Carbon dioxide
Oxygen
Inhaled anesthetic

Vaporizer malfunction or contamination

Volatile anesthetic

Anesthesia circuit leaks

Nitrogen
Carbon dioxide

Tracheal tube cuff leaks

Nitrogen
Carbon dioxide

Poor mask fit

Nitrogen
Carbon dioxide

Air embolism

Nitrogen
Carbon dioxide

Hypoventilation

Carbon dioxide

Airway obstruction

Carbon dioxide

Malignant hyperthermia

Carbon dioxide

Circuit hypoxia

Oxygen

  1. Overwhelming evidence supports the capability of pulse oximetry for detecting desaturation before it is clinically apparent.
  2. No definitive data demonstrate a decrease in morbidity and mortality associated with the use of pulse oximetry.
  3. The absence of a pulsatile waveform limits the ability of a pulse oximeter to calculate the SpO2.
  4. A relationship exists between hemoglobin saturation and O2tension (in mm Hg) as depicted by the oxyhemoglobin dissociation curve (Fig. 27-2).
  5. The SpO2measured by pulse oximetry is not the same as the arterial O2 saturation (SaO2) measured by a laboratory co-oximeter. In clinical circumstances when other hemoglobin moieties (methemoglobin, carboxyhemoglobin) are present in low

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concentrations, the SpO2 value is higher than the SaO2 reported by the blood gas laboratory.

 

Figure 27-2. The relationship between arterial hemoglobin saturation with oxygen (%) and PO2 is represented by the sigmoid-shaped oxyhemoglobin dissociation curve.

  1. Many factors may influence the accuracy or ability of a pulse oximeter to calculate SpO2(Table 27-5).
  2. Blood Pressure Monitoring

Intraoperative measurements and recordings of arterial blood pressure (at least every 5 minutes) are important indicators of the adequacy of circulation.

  1. Indirect Measurement of Arterial Blood Pressure
  2. The simplest method of blood pressure determination estimates systolic blood pressure by palpating the return of the arterial pulse or Doppler sounds while an occluding cuff is deflated.
  3. Auscultationof Korotkoff sounds (which result from turbulent flow within an artery in response to the mechanical deformation from the blood pressure cuff) is a common method of blood pressure measurement.
  4. Systolic blood pressure is considered to be equivalent to the appearance of the first Korotkoff sound, and disappearance of the sounds or a muffled tone is considered to be equivalent to the diastolic

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blood pressure. Mean arterial pressure (MAP) is calculated as the diastolic blood pressure plus one third of the pulse pressure (systolic blood pressure minus diastolic blood pressure).

Table 27-5 Factors That Influence the Accuracy of Pulse Oximetry

Absence of a Pulsatile Waveform
Hypothermia
Hypotension
Altered vascular resistance (vasoactive drugs)
Factitiously High SpO2
Increased carboxyhemoglobin concentration
Increased methemoglobin concentration (SpO2 tends to be 85% regardless of the actual SaO2 or PaO2)
Motion
Awake patient
Shivering
Extraneous Light Sources
Factitiously Low SpO2
Methylene blue
Fingernail polish

PaO2= arterial oxygen partial pressure; SaO2 = arterial oxygen saturation;
SpO2 = peripheral oxygen saturation of hemoglobin.

  1. The detection of sound changes is subjective, requires pulsatile flow (unreliable during low flow), and is prone to mechanical errors (Table 27-6).

Table 27-6 Mechanical Errors Associated with Auscultatory Measurement of Blood Pressure

Falsely High Estimates of Blood Pressure
The cuff is too small (bladder width should approximate 40% of the circumference of the extremity)
The cuff is applied too loosely
Uneven compression of the underlying artery
The extremity is below heart level
Falsely Low Estimates of Blood Pressure
The cuff is too large
Cuff deflation is at a rate more rapid than 3 mm Hg per second
The extremity is above heart level

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Table 27-7 Problems Associated with Noninvasive Automatic Cycled Cuff-Based Blood Pressure Monitoring Systems

Edema of the extremity
Petechiae formation
Ulnar neuropathy (an encircling cuff should be applied proximal to the ulnar groove)
Interference with timing of intravenous drug administration when the access site is located in the same extremity as the monitoring system
Hydrostatic effect (this should be corrected by adding or subtracting 0.7 mm Hg for every centimeter the cuff is above or below the level of the heart)

  1. Automated oscillometryhas replaced auscultatory and palpatory techniques for routine intraoperative blood pressure monitoring.
  2. Oscillometry accurately measures systolic blood pressure, diastolic blood pressure, and MAP (discrepancy with centrally placed arterial line <5 mm Hg).
  3. A variety of cuff sizes makes it possible to use oscillometry in patients of all ages.
  4. Problems with Noninvasive Blood Pressure Monitoring.Complications may accompany repeated inflations of automatically cycled blood pressure cuffs placed on the upper extremity (Table 27-7).
  5. Invasive Measurement of Vascular (Arterial Blood) Pressure
  6. Indwelling arterial cannulation not only offers anesthesiologists the opportunity to monitor beat-to-beat changes in arterial blood pressure but also provides vascular access for arterial blood sampling.
  7. Intra-arterial measurement of blood pressure is subject to many sources of error based on the physical properties of fluid motion and the performance of the catheter–transducer–amplification system used to sense, process, and display the pressure pulse wave. Ideally, the catheter and tubing are stiff, the volume of fluid in the connecting tubing is small, the number of stopcocks is limited, and the connecting tubing length is not excessive.

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  1. Because many therapeutic decisions are based on changes in arterial blood pressure, it is imperative that anesthesiologists understand the physical limitations imposed by fluid-filled pressure transducer systems.
  2. In clinical practice, underdamped catheter–transducer systems tend to overestimate systolic blood pressure by 15 to 30 mm Hg and to amplify artifact (“catheter whip”).
  3. Air bubbles cause overdamping and underestimation of systolic blood pressure.
  4. MAP is accurately measured even in the presence of overdamping or underdamping.
  5. In clinical practice, it is sufficient to calibrate the transducer to atmospheric pressure, usually with the transducer located at the level of the right atrium.
  6. Arterial Cannulation
  7. The radial artery remains the most popular site for cannulation because of its accessibility and the presence of a collateral blood supply (Fig. 27-3).
  8. The prognostic value of the Allen test in assessing the adequacy of the ulnar collateral circulation has not been confirmed.
 

Figure 27-3. Technique for radial artery cannulation.

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  1. Complications of Invasive Arterial Monitoring(Table 27-8)
  2. Traumatic cannulation has been associated with median nerve dysfunction, hematoma formation, and thrombosis.
  3. Abnormal radial artery blood flow after the removal of an arterial catheter (a nontapered 20- to 22-gauge Teflon catheter is recommended) occurs frequently (presumably because of radial artery thrombosis), with normalization of blood flow usually occurring in 3 to 7 days.
  4. Direct arterial pressure monitoring requires constant vigilance and correlation of the measured blood pressure with other clinical parameters before therapeutic interventions are initiated.

Table 27-8 Cannulation Sites for Direct Arterial Blood Pressure Monitoring

Site

Clinical Points

Radial artery

Preferred cannulation site
Ischemia most likely reflects arterial thrombosis
Aneurysm formation
Arteriovenous fistula formation
Infection
Fluid overload in neonates from continuous flush techniques (3–6 mL/hr)

Ulnar artery

Complications similar to those of radial artery
Principal source of blood flow to the hand

Brachial artery

Insertion site medial to biceps tendon
Median nerve damage

Axillary artery

Insertion site at junction of pectoralis major and deltoid muscles

Femoral artery

Easy access in low-flow states
Potential for local and retroperitoneal hemorrhage
Catheter with increased length preferred

Dorsalis pedis artery

Collateral circulation via posteriortibial artery
Higher systolic blood pressure

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  2. Sudden increases or decreases in blood pressure may represent a hydrostatic error when the position of the transducer is not adjusted after changes in the position of the operating room table.
  3. A sudden decrease in blood pressure may be caused by a damped tracing from a partially occluded or kinked arterial catheter.
  4. Before initiating therapy based on a change in blood pressure, the calibration of the transducer system and the patency of the arterial cannula should be verified.
  5. Central Venous and Pulmonary Artery Monitoring

The right internal jugular vein is the most common site for cannulation (Table 27-9 and Figs. 27-4, 27-5 and 27-6). Ultrasound-guided placement of the right internal jugular vein venous catheter may decrease complications and improve first attempt success rates.

  1. Central Venous Pressure Monitoring
  2. Central venous pressure is essentially equivalent to right atrial pressure, and the normal waveform consists of three peaks (a, c, and v waves) and two descents (x, y) (Table 27-10 and Fig. 27-7).
  3. The possibility of venous air embolism is decreased by positioning the patient in a head-down position during placement or removal of the central venous catheter.
  4. Central venous catheter placement is an important source of nosocomial infection and sepsis, emphasizing the importance of sterile technique during catheter placement and of the application of appropriate dressings (Table 27-11).
  5. Pulmonary Artery Monitoring
  6. Indicationsfor placement of a pulmonary artery catheter are broadly defined. (Intracardiac pressures, thermodilution cardiac output, and mixed venous O2 saturations should be measured, and derived hemodynamic indices should be calculated.) The measured and derived information is used to help define the clinical problem, monitor the progression of hemodynamic dysfunction, and guide the response to therapy.

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Table 27-9 Central Venous Pressure Cannulation Sites

Site

Advantages

Disadvantages

Right internal jugular vein

Accessible from head of operating room table
Predictable anatomy
High success rate in both adults and children
Good landmarks

Carotid artery puncture
Trauma to the brachial plexus
Pneumothorax

Left internal jugular vein

Same as for right internal jugular vein

Damage to thoracic duct
Difficulty in maneuvering the catheter through the jugular–subclavian junction
Carotid artery puncture and embolization of the left dominant cerebral hemisphere

External jugular vein

Superficial location Safety

Lower success rate
Kinks at the subclavian vein

Subclavian vein

Accessible
Good landmarks

Pneumothorax
Hemothorax
Chylothorax
Pleural effusion

Antecubital vein

Few complications

Lowest success rate
Thrombosis
Thrombophlebitis

Femoral vein

High success rate
Thrombophlebitis

Catheter sepsis

  1. Pulmonary artery catheter monitoring may decrease perioperative complications if its use is tailored to the clinical condition of the patient as it changes with time.
  2. The ASA has developed Practice Guidelines for Pulmonary Artery Catheterization.
  3. Correct placement of a pulmonary artery catheter is most often guided by observing changes in vascular waveforms (Fig. 27-8).

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Figure 27-4. Three anatomic approaches for placement of a catheter in the internal jugular vein. The patient is placed head down with the head turned away from the intended venipuncture site. A 22-gauge locator needle may be inserted initially to identify the vein and thus minimize the likelihood of accidental carotid artery puncture when the larger needle is placed. Return of desaturated blood or transduction of the catheter (venous pressure) confirms entry into the internal jugular vein. SCM = sternocleidomastoid.

  1. Pulmonary capillary wedge pressure is used to indirectly assess left ventricular end-diastolic volume by reflecting changes in left ventricular end-diastolic pressure. Right-sided filling pressures often are poor indicators of left ventricular filling, either as absolute numbers or in terms of direction of change in response to therapy.
  2. Factors Affecting the Accuracy of Pulmonary Artery Catheter Data(Table 27-12)

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Figure 27-5. Placement of a catheter in the external jugular vein. SCM = sternocleidomastoid.

  1. Complications of Pulmonary Artery Catheter Monitoring(Tables 27-13 and 27-14)
  2. Mixed Venous Oximetry
  3. Advances in fiberoptic technology have led to the development of pulmonary artery catheters that can continuously measure mixed venousO2 saturation (SvO2).
  4. SvO2varies directly with cardiac output, hemoglobin concentration, and SaO2 and inversely with minute O2 consumption.
  5. When all other variables are constant, SvO2reflects corresponding changes in cardiac output.
  6. The normal SvO2is 75%, and anaerobic metabolism occurs when SvO2 is below 30%.

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Figure 27-6. Placement of a catheter (infraclavicular approach) in the subclavian vein. The patient is placed head down with the head turned away from the intended venipuncture site. Placing a roll between the scapulas opens the space between the clavicle and first rib. The needle is inserted 1 cm below the midpoint of the clavicle and advanced toward the anesthesiologist's finger in the suprasternal notch, keeping close to the posterior surface of the clavicle. Return of desaturated blood or transduction of the catheter (venous pressure) confirms entry into the subclavian vein.

  1. Central Venous Oxygen and Its Relation to Mixed Venous Oxygen
  2. Central venous O2(ScvO2) represents O2 extraction from the upper body and brain but may serve as a surrogate measure of SvO2.
  3. ScvO2may not reflect SvO2 in the presence of septic shock.

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Table 27-10 Diagnostic Value of Central Venous Pressure Waveforms

Waveform

Associated Conditions

Large a waves

Tricuspid stenosis
Pulmonic stenosis
Pulmonary hypertension
Decreased right ventricular compliance

Large v waves

Tricuspid regurgitation
Right ventricular papillary muscle ischemia or right ventricular failure
Constrictive pericarditis
Cardiac tamponade

 

Figure 27-7. Central venous pressure (CVP) waveforms in relation to electrical events on the electrocardiogram (ECG).

Table 27-11 Complications Common to All Central Venous Pressure Catheter Placement Techniques

Accidental arterial puncture (hematoma, false aneurysm, arteriovenous fistula)
Poor positioning of the catheter during placement (vascular orcardiac chamber perforation, cardiac dysrhythmias)
Injury to surrounding structures
Clot and fibrinous sleeve formation
Thrombosis of the vein (embolus)
Catheter-related sepsis (see guidelines for prevention ofcatheter-related infections developed by the Centers for Disease Control and Prevention)
Bleeding

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Figure 27-8. Pressure tracing observed during flotation of a pulmonary artery catheter through the right atrium (RA), right ventricle (RV), and pulmonary artery (PA) and into a pulmonary capillary wedge (PCW) position.

  1. Clinical Benefits of Pulmonary Artery Monitoring.Perioperative outcomes have been reported to be improved, worsened, or unchanged by pulmonary artery catheter usage. Several recent articles have illustrated insufficient

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evidence for an outcome benefit from the use of a pulmonary artery catheter.

Table 27-12 Factors Affecting the Accuracy of Pulmonary Artery Catheter Data

Pulmonary vascular resistance (any disease- or drug-induced increase alters the relationship between pulmonary capillary wedge pressure and pulmonary artery end-diastolic pressure)
Alveolar–pulmonary artery pressure relationships (flow-directed pulmonary artery catheters usually advance to gravity-dependent areas of highest pulmonary blood flow; the location of the catheter should be confirmed with lateral chest radiography)
Intracardiac factors (mitral stenosis interferes with validity of left atrial pressure as a reflection of left ventricular end-diastolic pressure; decreased left ventricular compliance interferes with the validity of pulmonary capillary wedge pressure as a reflection of left ventricular end-diastolic pressure)

Table 27-13 Complications of Pulmonary Artery Catheter Passage

Cardiac dysrhythmias (this is the most common complication; it is usually transient)
Catheter knotting, kinking, or coiling
Cardiac valve damage
Heart block
Perforation of the pulmonary artery, right atrium, or right ventricle
Trauma to the right ventricular endocardium

  1. Temperature Monitoring
  2. The potential for accidental heat loss or the risk of triggering malignant hyperthermia requires the continued observation of temperature changes.
  3. Perioperative hypothermiacommonly results from anesthetic-induced inhibition of thermoregulation as well as a cold ambient environment in the operating room and heat loss owing to surgical exposure of tissues.
  4. Anesthetized patients often behave like poikilotherms until the core temperature approaches a new set point for thermoregulation.
  5. Patients at greatest risk for perioperative hypothermia include elderly patients, burn patients, neonates, and patients with spinal cord injuries.

Table 27-14 Complications of Pulmonary Artery Catheter Presence

Thrombosis
Pulmonary infarction
Pulmonary artery rupture
Thrombocytopenia
Sepsis or infection
Cardiac valve damage
Endocarditis
Thromboembolism
Balloon rupture
Cardiac dysrhythmias
Trauma to the right ventricular endocardium

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  1. Perioperative hyperthermiaoccurs rarely, and potential explanations other than malignant hyperthermia include exposure to endogenous pyrogens, increases in metabolic rate secondary to thyrotoxicosis or pheochromocytoma, and anticholinergic blockade of sweating.
  2. Central temperature is customarily measured using temperature probes placed in the nasopharynx, esophagus, blood (pulmonary artery catheter), bladder, or rectum.
  3. During routine noncardiac surgery, temperature differences between these sites are small.
  4. During and after cardiopulmonary bypass or deliberate hypothermia, gradients between these sites are predictable.
  5. During cooling in anesthetized patients, changes in rectal temperature often lag behind changes in central (core) temperature.
  6. During rewarming, probe locations residing in regions of high blood flow often reflect blood temperature rather than central temperature, emphasizing that the adequacy of rewarming is best judged by measuring temperature at more than one location.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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