Principles of Surgery, Companion Handbook

Chapter 12 Physiologic Monitoring of the Surgical Patient

Principles of Surgery Companion Handbook

HEMODYNAMIC MONITORING

The traditional clinical evaluation often is unreliable in critically ill patients because there may be major changes in cardiovascular function that are not accompanied by obvious clinical findings. Invasive hemodynamic monitoring at the bedside provides information about cardiorespiratory performance and guides therapy.

Arterial Catheterization

Arterial catheterization is indicated whenever there is a need for continuous monitoring of blood pressure and/or frequent sampling of arterial blood. States in which precise and continuous blood pressure data are necessary include shock of any etiology, acute hypertensive crisis, use of potent vasoactive or inotropic drugs, high levels of respiratory support, high-risk patients undergoing extensive operations, controlled hypotensive anesthesia, and any situation in which any of the factors affecting cardiac function is rapidly changing. This is particularly true in patients with shock, because indirect measurement of blood pressure by a cuff has been proved inaccurate. Inserting arterial lines is a relatively safe and inexpensive procedure. There are no absolute contraindications to arterial catheterization, although bleeding diathesis and anticoagulant therapy may increase the risk of hemorrhagic complications. Severe occlusive arterial disease with distal ischemia, the presence of a vascular prosthesis, and local infection are contraindications to specific sites of catheterization.

With an indwelling arterial catheter and monitoring system, the systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) can be displayed continuously. The pulse rate can be calculated from the arterial tracing when the electrocardiogram (ECG) is not available.

Many anatomic sites have been used to access the arterial circulation for continuous monitoring, i.e., the superficial temporal, axillary, brachial, radial, ulnar, femoral, and dorsalis pedis arteries. The dual blood supply to the hand and the superficial location of the vessel make the radial artery the most commonly used site for arterial catheterization. Cannulation is technically easy, as is securing the catheter in place; there is a low incidence of complications. The mean and end-diastolic radial pressures usually are accurate estimates of the corresponding aortic pressures. Most authors recommend assessing the adequacy of the collateral circulation before cannulation of the radial artery. The axillary artery has been recommended as suitable for long-term direct arterial pressure monitoring, with relatively few complications and no reported permanent sequelae. The major advantages include its larger size, freedom for the patient's hand, and close proximity to the aorta so that there is better representation of the aortic pressure waveform and minimal systolic pressure overshoot. Because of the extensive collateral circulation that exists between the thyrocervical trunk of the subclavian artery and the subscapular artery (which is a branch of the distal axillary artery), thrombosis of the axillary artery will not lead to compromised flow in the distal arm. Major disadvantages are its deep location and mobility, which increase the technical difficulty for insertion, and its location within the neurovascular sheath, which may increase the possibility of neurologic compromise if hematoma occurs.

The femoral artery also has been used for continuous blood pressure monitoring. Major advantages are its superficial location and large size, allowing easier localization and cannulation when the pulses over more distal vessels are absent. The major disadvantages are the presence of atherosclerotic occlusive disease in older patients and the problems associated with maintaining a clean dressing in the presence of draining abdominal wounds and ostomies in surgical patients. Despite some disadvantages, studies have failed to demonstrate a higher complication rate in patients with femoral artery catheters. The dorsalis pedis artery has no significant cannulation hazards if collateral flow can be demonstrated to the remainder of the foot through the posterior tibial artery. Major disadvantages are its relatively small size and overestimation of systolic pressure at this level. The superficial temporal artery has been used extensively in infants and in some adults for continuous pressure monitoring. Because of its small size and tortuosity, however, surgical exposure is required for cannulation. A small incidence of neurologic complications as a result of cerebral embolization has been reported in infants. The brachial artery is not used often because of the high complication rate associated with its use for cardiac catheterization. This artery has been used successfully for short-term monitoring, but there are little data to support the use of prolonged brachial artery monitoring. If the collateral circulation is inadequate, obstruction of the brachial artery may be catastrophic, leading to loss of the forearm and hand. Other problems include the difficulty in maintaining the site in awake, active patients and the possibility of hematoma formation in anticoagulated patients.

Central Venous Catheterization

The most common indications for central venous catheterization are to secure access for fluid therapy, drug infusions, or parenteral nutrition and for central venous pressure (CVP) monitoring. There are no absolute contraindications for CVP catheter placement, although bleeding diatheses may increase the risk of hemorrhagic complications. Vessel thrombosis, local infection or inflammation, and distortion by trauma or previous surgery are considered contraindications to specific sites of catheterization.

While central venous lines are placed primarily for venous access, useful information occasionally can be obtained by measuring the CVP. The CVP may be useful in a hypotensive trauma patient to differentiate a pericardial tamponade from hypovolemia. A properly placed catheter can be used to measure right atrial pressure, which, in the absence of tricuspid valve disease, will reflect the right ventricular end-diastolic pressure. CVP, which can give information about the relationship between intravascular volume and right ventricular function but cannot be used to assess either of these factors independently, cannot be used to assess left ventricular function in critically ill patients because ventricular disparity and independence of right and left atrial pressures have been confirmed repeatedly in these patients.

The most commonly chosen sites include the subclavian, internal jugular, external jugular, femoral, and brachiocephalic veins. The subclavian vein can be cannulated with a high rate of success and may be the easiest to cannulate in situations of profound volume depletion. Disadvantages include the higher risk of pneumothorax and the inability to compress the vessel if bleeding occurs. The internal jugular vein has been cannulated with success rates similar to those of the subclavian approach. The major advantages of internal jugular vein catheterization are the lower risk of pneumothorax and the ability to compress the insertion site if bleeding occurs.

Complications can be divided into technical or mechanical complications, usually occurring during catheter placement, and long-term complications related to the length of time the catheter remains in place. The list of technical or mechanical complications is as follows: catheter malposition, dysrhythmias, embolization (air or catheter fragments), vascular injury (hematoma, vessel laceration, false aneurysm, or arteriovenous fistula), cardiac injury (atrial or ventricular perforation or cardiac tamponade), pleural injury (pneumothorax, hemothorax, or hydrothorax), mediastinal injury (hydromediastinum or hemomediastinum), neurologic injury (phrenic nerve, brachial plexus, or recurrent laryngeal nerve injury), and injury to other structures (trachea, thyroid, or thoracic duct). Pneumothorax is the most frequently reported immediate complication of subclavian vein catheterization, and arterial puncture is the most common immediate complication of internal jugular vein cannulation. Surface-modified central venous catheters have been developed to reduce catheter-related infection. Catheters impregnated with silver sulfadiazine and chlorhexidine resist bacterial adherence and biofilm formation. At least three types of thrombi can develop in patients with central venous catheters: mural thrombus, catheter thrombus, and “fibrin sleeve” or sleeve thrombus.

Pulmonary Artery Catheterization

Several studies in critically ill patients have shown that clinical assessment is inaccurate in predicting cardiac output, pulmonary artery occlusion pressure, and systemic vascular resistance and that the information obtained from pulmonary artery catheterization prompts a change in therapy in 40–60 percent of patients. A pulmonary artery catheter usually is indicated whenever the data obtained will improve therapeutic decision making without unnecessary risk.

The pulmonary artery catheter has provided a “quantum leap” in physiologic information available for the management of critically ill patients. The information that can be obtained includes CVP, pulmonary artery diastolic pressure (PADP), pulmonary arterial systolic pressure (PASP), mean pulmonary artery pressure (MPAP), pulmonary artery occlusion (“wedge”) pressure (PAOP), cardiac output (CO) by thermodilution, mixed venous blood gases by intermittent sampling, and continuous mixed venous oximetry. On the basis of this information, a multitude of derived parameters also can be obtained.

The PAOP represents the left atrial pressure (LAP) as long as the column of blood distal to the pulmonary artery catheter tip is patent to the left atrium. This may not be so if the catheter is positioned in an area of the lung where the alveolar pressure exceeds pulmonary venous pressure (zone 2, as described by West) (Fig. 12-1) or both pulmonary artery and venous pressures (West's zone 1), causing intermittent or continuous collapse of the pulmonary capillaries. The PAOP may then reflect alveolar pressure and not LAP. This is particularly important if patients have low pulmonary vascular pressures (i.e., hypovolemia) and/or are treated with high levels of positive end-expiratory pressure (PEEP). Because the pulmonary artery catheter is flow-directed, it is most likely to pass into dependent areas of the lung where blood flow is high and both pulmonary artery and venous pressures exceed alveolar pressure (West's zone 3). In this location, the continuous column of blood between the distal lumen of the catheter and the left atrium will remain patent, and the PAOP will reflect LAP. Raising intrathoracic pressure introduces an artifact that affects all intrathoracic vascular pressures to an extent that depends on the state of pulmonary compliance. In patients with acute respiratory insufficiency, compliance often is diminished, and the “stiff” lungs do not transmit alveolar pressure as readily to the pulmonary circulation. In these patients, the PEEP artifact on the PAOP measurement usually should not exceed 1 mmHg for every 5 cmH₂O of PEEP applied.

FIGURE 12-1 Model to explain the uneven distribution of blood flow in the lung based on the pressures affecting the capillaries. In zone 1, alveolar pressure (Pa) exceeds pulmonary artery (Pa) and venous (Pv) pressures so that the collapsible vessels are held closed and there is no flow. In zone 2, pulmonary arterial pressure exceeds alveolar pressure, but alveolar pressure exceeds venous pressure. Under these conditions, there is a constriction at the downstream end of each collapsible vessel. In zone 3, pulmonary arterial and venous pressures exceed alveolar pressure, and the colapsible vessels are held open. (From: West JB, Dollery CT, Naimark A: Distribution of blood flow in isolated lung: Relation to vascular and alveolar pressures. J Appl Physiol 19: 713, 1964, with permission.)

Another method of evaluation is to observe the decrement in PAOP when PEEP is briefly removed. Because intravascular pressure measurements are affected by the intrathoracic pressure changes during respiration, they should be performed at end-expiration and obtained from a calibrated strip-chart recorder or oscilloscope rather than from a digital display.

The cardiac output is measured by the thermodilution technique, which correlates well with the Fick and the dye-dilution methods. Pitfalls in cardiac output measurement include injectate temperature different from the temperature used to determine the computer constant or that of the fluid being monitored by the reference probe, delivered volume less than the one entered in the computation constant, incorrect computer constant, rapid infusion of intravenous fluids during measurements, electrical noise created by electrocautery, faulty catheter lumens, improperly positioned catheter (e.g., if the catheter is in the wedge position or if the proximal lumen is above the atrium or within the introducer sheath), and presence of intracardiac shunts or tricuspid regurgitation. A continuous thermodilution technique is available for measuring CO. Pulmonary artery catheters are modified to locate a 10-cm thermal filament in the right ventricle during use.

Access to the central venous circulation for insertion of a pulmonary artery catheter is the same as for placement of a CVP catheter. Once an introducer sheath is in place, the pulmonary artery catheter is inserted and advanced until the tip reaches an intrathoracic vein (as evidenced by respiratory variations on the pressure tracing). The balloon is inflated with 1.5 mL of air and the catheter advanced while the operator observes the pressure waveform and the ECG tracing. After the right atrium is entered, the catheter is advanced through the right ventricle and into the pulmonary artery until a PAOP tracing is obtained (Fig. 12-2). Maneuvers often used to facilitate passage through the pulmonary valve include elevation of the head of the bed, turning the patient into the right lateral decubitus position, performance of the Valsalva maneuver, and increasing ventricular ejection in low-output states by the administration of inotropic drugs. To determine if the catheter is in the wedge position, the waveform needs to be inspected. The mean PAOP should be lower than the MPAP and lower than or equal to the PADP.

FIGURE 12-2 Normal pressure waveforms from the right side of the heart and pulmonary artery. sys = systolic; ed = end-diastolic. (From: Grossman W, Barry WH: Cardiac catheterization, in Braunwald E (ed): Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, WB Saunders, 1988, p 250, with permission.)

There are risks to pulmonary artery catheterization; they are infrequent and usually not life-threatening. In addition to the complications attributed to central venous cannulation, complications can occur during passage or after the catheter is in place. The most common complication during passage of the pulmonary artery catheter is the development of dysrhythmias. They can occur in up to 50 percent of patients, but less than 1 percent of these are serious. Transient right bundle branch block (RBBB) has been reported in 3–6 percent of catheterizations. Complications that can occur after the catheter is in place include infections, thromboembolism, and rupture of the pulmonary artery. Infections from pulmonary artery catheters are directly related to the length and severity of illness. Pulmonary infarction can result from emboli, distal migration of the pulmonary artery catheter tip, or prolonged balloon inflation occluding distal blood flow in the pulmonary artery. Pulmonary artery rupture and hemorrhage are the most serious of all the pulmonary artery catheter complications and are more likely in patients with pulmonary hypertension and in the elderly. Complications related to peripheral migration of the catheter tip can be limited by continuous monitoring of the pulmonary artery tracing, avoiding prolonged balloon inflation, ensuring proximal catheter placement by review of daily x-rays, and the use of continuous heparin flush systems.

In addition to the information directly provided by arterial and pulmonary artery catheterization, many parameters can be calculated. The derived hemodynamic parameters (Table 12-1) aid the clinician by quantitating the relationships among heart rate, filling pressures, resistance, contractility, and cardiac output. Cardiac output (CO) is the sum of all stroke volumes ejected in a given time. It usually is represented as the product of average stroke volume and heart rate (beats per minute), where stroke volume is the amount of blood ejected by the heart with each contraction. The primary determinants of stroke volume are the ventricular preload, afterload, and contractility. If there is no change in ventricular compliance (the relationship between pressure and volume), left ventricular end-diastolic volume (LVEDV) is proportional to left ventricular end-diastolic pressure (LVEDP). The second determinant of stroke volume is afterload. Afterload is the sum of all the loads against which the myocardial fibers must shorten during systole, including aortic impedance, arterial wall resistance, peripheral vascular resistance, the mass of blood in the aorta and great arteries, the viscosity of the blood, and the end-diastolic volume of the ventricle. Contractility, the final determinant of stroke volume, may be estimated in the laboratory by the maximum velocity of contraction of the cardiac muscle fibers.

TABLE 12-1 MEASURED AND DERIVED HEMODYNAMIC PARAMETERS

The level of PAOP that corresponds to optimal left ventricular preload can be determined only by sequentially assessing the effects of acute hemodynamic interventions on cardiac function and may vary. Fluid can be administered rapidly in predetermined increments while changes in PAOP and in the indices of cardiac performance are monitored. A major increase in PAOP during infusion suggests poor ventricular compliance, exhausted preload reserve, and increased risk of pulmonary edema with further volume loading. If the PAOP rises modestly, if indices of cardiac performance improve, and if PAOP returns to within several millimeters of mercury of the original value within 10 min of stopping the infusion, additional fluid can be given without high risk of exacerbating pulmonary venous congestion.

RESPIRATORY MONITORING

Monitoring ventilation and gas exchange in critically ill surgical patients is of particular importance in deciding if mechanical ventilation is indicated, assessing response to therapy, optimizing ventilator management, and deciding if a weaning trial is indicated. In addition, gas monitoring permits an assessment of the adequacy of oxygen transport and calculation of derived parameters.

Ventilation Monitoring

Lung Volumes Several lung volume measurements are useful for monitoring ventilatory function in the operating room and intensive care unit. These include tidal volume, vital capacity, minute volume, and dead space. Tidal volume (V_T) is defined as the volume of air moved in or out of the lungs in any single breath. If the tidal volume is depressed, the patient may have difficulty in both oxygenation and ventilation. V_T can be measured at the bedside using a hand-held spirometer (Wright respirometer). Vital capacity (VC) is defined as the maximal expiration after a maximal inspiration. It can be measured at the bedside in a manner similar to the one used for V_T. VC is reduced in diseases involving the respiratory muscles or their neural pathways, in obstructive and restrictive ventilatory impairment, and in patients who fail to cooperate fully. VC is normally 65–75 mL/kg. Minute volume (or total ventilation) (_E) is the total volume of air leaving the lung each minute (product of V_T and ¦). Many ventilators display _E, or it can be measured with a Wright spirometer. An increase in the minute volume required to maintain a normal arterial blood carbon dioxide tension (PaCO₂) suggests an increased dead space relative to V_T or an abnormally high carbon dioxide (CO₂) production. A resting _E of less than 10 L and the ability to double the resting _E on command have been associated with successful weaning from mechanical ventilation.

Pulmonary Mechanics Various respiratory mechanical parameters also can be monitored in the operating room and intensive care unit. These include maximal inspiratory pressure, static compliance, dynamic characteristic, and work of breathing. Inspiratory force is measured as the maximal pressure below atmospheric that a patient can exert against an occluded airway. The measurement requires a connector to an endotracheal or tracheostomy tube and a manometer capable of registering negative pressure. A maximal inspiratory pressure (PI_max) value that is more negative than –20 to 25 cmH₂O is one of the clinical parameters used to confirm recovery from neuromuscular block after general anesthesia. PI_max values more negative than –30 cmH₂O have been used to predict successful weaning from mechanical ventilation. Compliance, a measure of the elastic properties of the lung and chest wall, is expressed as a change in volume divided by a change in pressure (DV/DP). In patients receiving mechanical ventilation, a rough measure of total thoracic compliance (both the lungs and chest wall) can be obtained by dividing the delivered V_T by the inflation pressure displayed on the ventilator gauge during conditions of zero gas flow. These can be achieved by using the “inspiratory hold” option on the ventilator, during which period the airway pressure falls to a plateau. If the patient is receiving PEEP, this must first be subtracted from the plateau pressure before calculating static thoracic compliance, that is,

The usual range for adult patients receiving mechanical ventilation is 60–100 mL/cmH₂O. Decreased values are observed with disorders of the thoracic cage or a reduction in the number of functioning lung units (resection, bronchial intubation, pneumothorax, pneumonia, atelectasis, or pulmonary edema). When the static compliance is less than 25 mL/cmH₂O, as in severe respiratory failure, difficulties in weaning are common because of the increased work of breathing (see below).The dynamic characteristic is calculated by dividing the volume delivered by the peak (rather than the plateau) airway pressure minus PEEP. It is not correct to call this value dynamic compliance because it is actually an impedance measurement and includes compliance and resistance components. The dynamic characteristic is normally about 50–80 mL/cmH₂O. It may be decreased by disorders of the airways, lung parenchyma, or chest wall; if it decreases to a greater extent than the static compliance, it suggests an increase in airway resistance (e.g., bronchospasm, mucous plugging, kinking of the endotracheal tube) or an excessive flow rate. Work of breathing, which relates to the product of the change in pressure and volume, is a measure of the process of overcoming the elastic and frictional forces of the lung and chest wall. The work of breathing in the critically ill patient who requires ventilatory support (WOB_Pt) can be divided into three components: normal physiologic work (WOB_Phys), work to overcome the pathophysiologic changes in the lung and chest wall (WOB_Dis), and work to overcome the imposed work of breathing (WOB_Imp) created by our methods of ventilatory support. Finally, the patient must do additional work to breathe spontaneously against a breathing apparatus that consists of the ventilator itself, demand valve, tubing, exhalation valves, and most important, the endotracheal tube. Poor demand system sensitivity, ventilator dyssynchrony, malfunctioning demand valves, and inadequate inspiratory flows also are contributing factors. The goal of ventilatory support is to carefully titrate the ventilator's contribution to minute ventilation so that the patient's effort remains a nonfatiguing work load. Failure to do so by supplying too much or too little ventilatory support can result in unsuccessful weaning trials and increase the duration of mechanical ventilation. Normal range for WOB_Pt is 0.3–0.6 J/L.

Gas Monitoring

Blood-Gas Analysis Blood-gas measurements provide information about the efficiency of gas exchange, the adequacy of alveolar ventilation, and the acid-base status. Blood gas values usually are reported in terms of directly measured partial pressures (PO₂ or PCO₂) and calculated hemoglobin oxygen saturations (SO₂). Calculated SO₂ values are derived from the measured partial pressure and a nomogram of the oxyhemoglobin dissociation curve usually corrected for blood temperature, pH, and perhaps other factors. Because these assumptions may not be accurate in critically ill patients, actual measurements of SO₂ by co-oximetry are preferred. SO₂ also can be measured continuously by using pulse oximeters or pulmonary artery catheters that incorporate oximetric fibers (see below). Alveolar gas tensions depend on the mixture of inspired gas, ventilation, and blood flow in the lungs, the matching of ventilation and perfusion, and the composition of mixed venous blood gases. Pathophysiologic causes of arterial hypoxemia include ventilation-perfusion inequality or venous admixture from regional alveolar hypoventilation, true intrapulmonary or intracardiac shunt, and decreased mixed venous oxygen content. A decreasing PaO₂ without a change in PaCO₂ suggests that blood oxygenation is deteriorating despite constant alveolar ventilation. In the acutely ill patient, this finding usually is attributable to ventilation-perfusion imbalance or intrapulmonary shunting. An important feature of shunting is that as it increases, supplemental oxygen has progressively less effect on PaO₂ because shunted blood bypasses ventilated alveoli.

The PaCO₂ directly reflects the adequacy with which alveolar ventilation meets metabolic demands for CO₂ excretion. An increased PaCO₂ (hypercapnia) reflects the failure of the ventilatory system to eliminate the CO₂ produced during metabolism. This “ventilatory failure” traditionally is described as respiratory acidosis. Hypercapnia can occur because of hypoventilation (i.e., CNS depression), increased CO₂ production (e.g., hyperthermia, hyperthyroidism), or increased physiologic dead space resulting in inadequate alveolar ventilation. The mechanisms of hypocapnia are the reverse of those which produce hypercapnia, the most common being hyperventilation (respiratory alkalosis). In critically ill patients, sampling of mixed venous blood can be performed accurately only in the pulmonary artery.

The oxygen content of the blood is equal to the amount of oxygen bound to hemoglobin plus the amount dissolved in plasma. The amount of bound oxygen is directly related to the concentration of hemoglobin and to how saturated this hemoglobin is with oxygen (i.e., SaO₂ or SO₂). The amount of oxygen dissolved in plasma depends on the oxygen tension (i.e., PaO₂ or PvO₂). Oxygen delivery (O₂) is the volume of oxygen delivered from the heart each minute and is calculated as the product of cardiac output and arterial oxygen content (CaO₂). Oxygen consumption (O₂) is the amount of oxygen that diffuses from the capillaries into all tissues and can be calculated according to the Fick principle as the product of CO and arteriovenous oxygen content difference [C(a – )O₂]. The oxygen use coefficient or extraction ratio (O₂UC), relates oxygen consumption and oxygen delivery (O₂/O₂). The adequacy of oxygen transport also must be assessed in relation to oxygen demand, which is the amount of oxygen required by the body tissues to use aerobic metabolism. Although oxygen demand cannot be measured clinically, the relative balance between consumption and demand is best indicated by the presence of excess lactate in the blood. Lactic acidosis means that demand exceeds consumption and anaerobic metabolism is present. If oxygen delivery or consumption is low, if use is high, or if lactic acidosis is present, arterial oxygen content might be augmented by increasing hemoglobin concentration or oxygen saturation, or cardiac output might be increased by manipulation of preload, afterload, or contractility. A response might be considered beneficial if oxygen consumption increases, if use returns to the normal range, or if lactic acidosis resolves.

Capnography Capnography is the graphic display of CO₂ concentration as a waveform. It should not be confused with capnometry, which refers to only the numerical presentation of concentration without a waveform. Currently available systems for CO₂ analysis include infrared spectroscopy, mass spectrometry, and Raman scattering. In addition, a disposable, noninvasive, and inexpensive colorimetric device is available. This device permits a semiquantitative measurement of the end-tidal CO₂ concentration when it is attached between an endotracheal tube and a resuscitation bag. In the majority of stand-alone capnographs, the CO₂ concentration is measured by infrared spectroscopy. A beam of infrared light is passed through the sampled gas. CO₂ molecules in the light path absorb some of the infrared energy. The capnograph compares the amount of infrared light absorbed by the patient gas in the sample cell with the amount absorbed either by gas in a reference cell or by the sample cell during a time of known zero-gas concentration. Normally, there is a fairly predictable relationship between the peak exhaled or end-tidal CO₂ (PETCO₂) and the PaCO₂. In healthy subjects with normal lungs, the PaCO₂ is 4–6 mmHg higher than the PETCO₂. Patients with chronic obstructive lung disease (and other derangements associated with increased dead space) have an increased arterial to end-tidal CO₂ gradient [P(a – ET)CO₂]. This difference occurs because the exhaled gas from the alveolar dead space, which contains little or no CO₂, dilutes the CO₂-containing gas from the normally ventilated and perfused alveoli. PETCO₂ measurement is at present perhaps one of the most reliable means of determining proper endotracheal tube placement. PETCO₂ monitoring is extremely useful as a diagnostic tool in several situations unique to the operating room. These include the detection of air emboli during neurosurgical procedures requiring the sitting position, the detection of increased CO₂ production in malignant hyperthermia, and the detection of disconnection or malfunction of the anesthesia breathing circuit.

Pulse Oximetry Pulse oximetry provides a reliable real-time estimation of arterial hemoglobin oxygen saturation. This noninvasive monitoring technique has gained clinical acceptance in the operating room, recovery room, and intensive care unit. Pulse oximeters estimate arterial hemoglobin saturation by measuring the absorbance of light transmitted through well-perfused tissue, such as the finger or ear. The light absorbance is measured at two wavelengths—660 (red) and 940 nm (infrared)—to distinguish between two species of hemoglobin—oxyhemoglobin and deoxyhemoglobin. Oxyhemoglobin absorbs less red light than deoxyhemoglobin, accounting for its red color; at infrared wavelengths, the opposite is true. Light absorbances at both wavelengths have two components: the pulsatile (or ac) component, which is attributed to the pulsating arterial blood, and the baseline (or dc) component, which represents the absorbances of the tissue bed, including venous blood, capillary blood, and nonpulsatile arterial blood. The pulse oximeter first determines the ac components of absorbance at each wavelength and divides this by the corresponding dc component to obtain a pulse-added absorbance that is independent of the incident light intensity. It then calculates the ratio (R) of these pulse-added absorbances:

The ratio of the pulse-added absorbances at the two wavelengths is used to generate the oximeter's estimate of arterial saturation (SpO₂). The relationship between this ratio and SpO₂ is empirical. Although pulse oximetry may provide erroneous measurements when SaO₂ is less than 70 percent, these values rarely occur. SaO₂ values in the range of perhaps 70–95 percent will reflect changes in PaO₂; it is in this range that pulse oximetry finds great value in monitoring cardiorespiratory disease and directing therapy. Various physiologic and environmental factors interfere with the accuracy of pulse oximetry. These include decreased amplitude of peripheral pulses (hypovolemia, hypotension, hypothermia, vasoconstrictor infusions), motion artifact, electrosurgical interference, backscatter from ambient light, and dyshemoglobinemias. The pulse oximeter can only distinguish oxyhemoglobin and deoxyhemoglobin. If other hemoglobin species are present, an error is introduced. Laboratory co-oximeters, on the other hand, generally use more than two wavelengths and often can quantify other hemoglobin species directly. Intravenously administered dyes, particularly methylene blue and indocyanine green, can temporarily induce artifactually low saturation readings.

Continuous Mixed Venous Oximetry Measurement of the oxygen saturation of mixed venous hemoglobin (SO₂) is helpful in the assessment of the oxygen supply-demand relationship in critically ill patients. The use of improved fiberoptic oximetry systems in conventional pulmonary artery catheters has permitted continuous monitoring of SvO₂. The normal range for SO₂ in healthy subjects is 0.65–0.80, with an average value of 0.75 corresponding to a PO₂ of 40 mmHg at a normal pH of 7.4. A rapid or prolonged fall from the normal range is indicative of a significant deterioration in the patient's clinical condition. Values below the normal range may be associated with increased oxygen consumption due to fever, shivering, seizures, exercise, and agitation or associated with decreased oxygen delivery because of low cardiac output, anemia, or arterial hemoglobin desaturation. Values above the normal range indicate an increase in oxygen delivery relative to consumption and are associated with the hyperdynamic phase of sepsis, cirrhosis, peripheral left-to-right shunting, general anesthesia, cellular poisoning such as cyanide toxicity, marked arterial hyperoxia, or a technical malfunction of the system (e.g., wedged catheter). Pulmonary artery catheter oximetry differs from pulse oximetry in several ways. First, the pulmonary artery catheter measures reflected rather than transmitted light. Second, being immersed in blood, the pulmonary artery catheter has no need for the pulse-added signal analysis used by the pulse oximeter. Continuous SO₂ monitoring serves three major functions. First, it serves as an indicator of the adequacy of the oxygen supply-demand balance of perfused tissues. In clinically stable patients, a normal and stable SO₂ may be considered an additional assurance of cardiopulmonary stability. Additional assessments of cardiac output and arterial and mixed venous blood gas analyses are not necessary. Second, continuously measured SO₂ may function as an early warning signal of untoward events. In this situation, the cause of the change in SO₂ is not necessarily clear because the change in SO₂ is sensitive but not specific. It may be necessary to measure cardiac output, SaO₂, and hemoglobin (Hb) in this setting to identify the etiology of the SO₂ change. Third, continuously monitored SO₂ may improve the efficiency of the delivery of critical care by providing immediate feedback as to the effectiveness of therapeutic interventions aimed at improving oxygen transport balance.

GASTRIC TONOMETRY

Hemodynamic and oxygen-transport variables document the severity of tissue hypoxia and oxygen debt. Gastric tonometry has been proposed as a relatively noninvasive monitor of the adequacy of aerobic metabolism in organs whose superficial mucosal lining is vulnerable to low flow and hypoxemia. The gastrointestinal (GI) tract will display metabolic changes before other indices of oxygen use. In the anoxic cell, uncompensated adenosine triphosphate (ATP) hydrolysis is associated with the intracellular accumulation of adenosine diphosphate (ADP), inorganic phosphate, and hydrogen ions with resulting intracellular acidosis. These hydrogen ions lead to tissue acidosis, with unbound hydrogen ions combining with interstitial bicarbonate to form the weak acid carbonic acid that dissociates to produce CO₂ and water.

A tonometer is comprised of a semipermeable balloon connected to a sampling tube. A tonometer in combination with a standard vented gastric sump is available. The annealed balloon allows CO₂ generated in the superficial layers of the mucosa to equilibrate within the saline instilled into the balloon.

Incomplete splanchnic cellular resuscitation has been associated with the development of multiple organ system failure, more frequent septic complications, and increased mortality in the critically ill patient. In critically ill patients, gastric tonometry has been used as a predictor of both organ dysfunction and mortality and has been shown to be a better predictor of mortality than base deficit, lactate, oxygen delivery, and oxygen consumption.

RENAL MONITORING

The primary reasons for monitoring renal function is that the kidney serves as an excellent monitor of the adequacy of perfusion and to prevent acute parenchymal failure. Renal function monitoring is helpful in predicting drug clearance and proper dose management. Urine output frequently is monitored but may be misleading. Although very low urine outputs, less than 0.5 mL/kg/h, are consistently associated with low glomerular filtration rate (GFR) values, levels greater than this also can be associated with low GFR values.

The value of plasma creatinine as a measure of renal function far exceeds the value of the blood urea nitrogen (BUN). The serum creatinine level is directly proportional to the level of creatinine production and inversely related to the GFR. In contrast to BUN concentration, plasma creatinine levels are not influenced by protein metabolism or the rate of fluid flow through the renal tubules. Acute reductions in the GFR are not immediately reflected because it takes 24–72 h for equilibration to occur. Creatinine production is directly proportional to muscle mass and its metabolism. Only with measurement of creatinine clearance can the severity of such renal function loss be determined. Serial determinations of creatinine clearance are the most reliable method for clinically assessing GFR and the most sensitive test for predicting the onset of perioperative renal dysfunction. Although measurements traditionally are performed using a 24-h urine collection, measurements using a 2-h collection are reasonably accurate and easier to perform.

Tests that measure the concentrating ability of the renal tubules are used primarily in the differential diagnosis of oliguria to differentiate a prerenal cause unresponsive to judicious fluid therapy from intrinsic renal failure as a result of tubular dysfunction. Tubular function tests are useful in oliguric patients (urine output < 500 mL/day) because nonoliguric individuals typically have less severe tubular damage and their laboratory findings are likely to show more overlap with the values of patients with prerenal azotemia. The fractional excretion of sodium (FE_Na) is the most reliable of the laboratory tests for distinguishing prerenal azotemia from acute tubular necrosis. This test requires simultaneously collected “spot” urine and blood samples. FE_Na can be calculated as follows:

where U_Na is the urinary sodium concentration (in mEq/L), and P_Na is the plasma sodium concentration (in mEq/L).The FE_Na value normally is less than 1–2 percent. In an oliguric patient, a value of less than 1 percent usually is because of a prerenal cause. A value greater than 2–3 percent in this setting suggests compromised tubular function. When the value ranges between 1 and 3 percent, the test is not discriminating.

NEUROLOGIC MONITORING

Monitoring the function of the central nervous system (CNS) can permit early recognition of cerebral dysfunction and facilitate prompt intervention in situations in which aggressive early treatment favorably influences outcome. In the perioperative and trauma settings, several methods have been used to evaluate brain function and the effects of therapy. These include intracranial pressure monitoring, electrophysiologic monitoring, transcranial Doppler ultrasound, and jugular venous oximetry.

Physical findings often are unreliable to ascertain the presence of increased intracranial pressure (ICP). The direct assessment of ICP is obtained by measurement. Measuring ICP permits calculation of cerebral perfusion pressure (CPP), which is defined as the difference between the MAP and ICP. Formerly, one of the end points of CNS monitoring was believed to be the control of ICP within safe levels; emphasis has shifted to following CPP itself. Maintaining cerebral blood flow requires using an elevated minimal CPP threshold when treating the injured brain. A CPP level of at least 70 mmHg is suggested. The most common indication for ICP monitoring is severe head injury. Patients with a Glasgow Coma Scale (GCS; see Table 40-1) score of 8 or less or a GCS motor score of 5 or less should be strongly considered for ICP monitoring. Other conditions for which ICP monitoring has been recommended include subarachnoid hemorrhage, hydrocephalus, postcraniotomy, and Reye's syndrome. Several methods of ICP measurement are available (Fig. 12-3). A ventricular catheter connected to a standard strain-gauge transducer via fluid-filled lines offers excellent waveform characteristics and permits withdrawal of cerebrospinal fluid (CSF). This catheter can be difficult to insert when cerebral edema or hematoma causes shifting or collapse of the lateral ventricle system. A subarachnoid bolt is easily inserted, although at times it may give erroneous readings, depending on its placement relative to the site of injury. Epidural bolts have a lower risk of complications but are less accurate than ventricular catheters or subarachnoid bolts and do not permit withdrawal of CSF. Complications of ICP devices include infection, hemorrhage, malfunction, obstruction, and malposition. Bacterial colonization of ICP devices increases significantly after 5 days of implantation; significant intracranial infections are uncommon.

FIGURE 12-3 Diagram illustrating intraventricular catheters, epidural bolts, subarachnoid bolts, and fiberoptic catheters for ICP measurement. (Adapted from: Doyle DJ, Mark PWS: Analysis of intracranial pressure. J Clin Monit 8:81, 1992, with permission.)

The electroencephalogram (EEG) reflects spontaneous and ongoing electrical activity recorded on the surface of the scalp. Intraoperative EEG recording has been used primarily for monitoring the adequacy of cerebral perfusion during carotid endarterectomy. The compressed spectral array (CSA) is the most commonly used method of visually displaying processed EEG information. Sensory-evoked potentials (SEPs) are minute electrophysiologic responses elicited by a stimulus and extracted from an ongoing EEG by signal averaging. They reflect the functional integrity of specific sensory pathways and serve to some extent as more general indicators of function in adjacent structures. Somatosensory evoked potentials (SSEPs) reflect the integrity of the dorsal spinal columns and the sensory cortex and can be useful for monitoring during resection of spinal cord tumors, spine instrumentation, carotid endarterectomy, and aortic surgery. Brain stem auditory-evoked potentials (BAEPs) reflect the integrity of the eighth cranial nerve and the auditory pathways above the pons and are used for monitoring of the posterior fossa during surgery. Visual evoked potentials (VEPs) may be used to monitor the optic nerve and upper brain stem during resections of large pituitary tumors.

Jugular venous oximetry is an invasive method of continuously monitoring jugular venous bulb oxyhemoglobin saturation (SjvO₂). Changes in SjvO₂ provide a measure of the relationship between total cerebral blood flow and total cerebral oxygen consumption. When arterial oxygenation remains constant, a decrease in SjvO₂ from control values reflects a decrease in cerebral blood flow or an increase in cerebral metabolic oxygen consumption unmatched by an increase in flow. The range of SjvO₂ in normal subjects is 55–71 percent. In head-injured patients, the range is considerably wider, but most investigators agree that a sustained desaturation of 50–55 percent warrants evaluation. SjvO₂ levels below 50 percent are indicative of cerebral ischemia.

METABOLIC MONITORING

Energy requirements depend on a number of factors including the body surface area, age, and sex. Basal energy expenditure (BEE) can be predicted with reasonable accuracy (±5 percent) by the Harris-Benedict equation:

where W is body weight (in kilograms), H is height (in centimeters), and A is age (in years). Resting energy expenditure (REE) can be approximated from the BEE by increasing it by 10 percent. The stress of illness, the change in hormonal milieu relating to the stress state, alterations in substrate utilization, and fever all can be predicted to increase REE. While early studies emphasized increases of 25 percent for multiple-trauma patients and 50 percent for burn patients, even an increase of 60 percent above BEE would only result in a need for 40 kcal/kg/day, or less than 3000 kcal in a 70-kg patient. Excessive caloric administration potentially is detrimental.

Oxygen delivery or cardiac output times arterial oxygen content and oxygen consumption (normally about 150 mL/min/m²) assess oxidative metabolism. CO₂ production is a measure of a by-product of oxidative metabolism. The ratio of CO₂ production to oxygen consumption is termed the respiratory quotient (RQ). During normal oral dietary intake, carbohydrates, protein, and fat are ingested, giving an average RQ of approximately 0.8. During prolonged starvation, the body adapts to fat metabolism, and the RQ may fall to as low as 0.6–0.7. Conversely, during excessive carbohydrate administration, the transformation into fat releases additional CO₂, and the RQ rises above 1.0. Thus monitoring oxygen consumption and CO₂ production and calculating the RQ provide inferences into the adequacy of total calories as well as the mixture of substrates.

The classic Fick equation relates oxygen consumption to the product of cardiac output and arterial venous oxygen content difference. Repeated cardiac output determinations have an accuracy in the range of ±5 percent but are not as important as variability in the patient's physiology, in which changes may exceed ±10 percent in a short time. Pulse oximetry and mixed venous oximetry show that minute-to-minute variations in these values also occur. These factors result in a 10 percent variation between measurements and lower total values compared with validated spirometric techniques. This latter difference reflects the oxygen consumption of the lung, which is included in the spirometric method but not in the reverse Fick technique.

TEMPERATURE MONITORING

Temperature, along with heart rate, blood pressure, and respiratory rate, is one of the traditional four cardinal vital signs. Temperature usually is taken rectally in ill patients or orally when significant elevations are not expected. It is recommended that deeper core temperatures be taken in the critically ill. Core temperature can be measured by placing a thermistor probe into the esophagus or the rectum. Esophageal wires are uncomfortable and invasive and are used exclusively in patients under general anesthesia. Rectal probes are used commonly in the operating room and intensive care unit but may be extruded from the rectum and have a recognized risk of bowel wall perforation. Three devices are available for bedside measurement of core temperature in intensive care unit patients: pulmonary artery thermistor catheters, urinary bladder thermistor catheters, and infrared auditory canal probes. Measurement of pulmonary artery blood temperature by the pulmonary artery thermistor catheter has been used increasingly as a reliable indicator of core temperature. The need for a catheter is an obvious disadvantage of this approach. Urinary bladder catheters have the advantage of giving both exact measurements of urine output and continuous urine temperature. Infrared probes noninvasively measure tissue temperature in the ear canal; their measurements have more variability than bladder readings.

For a more detailed discussion, see Varon AJ, Kirton OC, and Civetta JM: Physiologic Monitoring of the Surgical Patient, chap. 12 in Principles of Surgery, 7th ed.

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Copyright © 1998 McGraw-Hill

Seymour I. Schwartz

Principles of Surgery Companion Handbook