The Latin verb monere, which means “to warn, or advise” is the origin for the English word monitor. In modern medical practice, patients undergo monitoring to detect pathologic variations in physiologic parameters, providing advanced warning of impending deterioration in the status of one or more organ systems. The intended goal of this endeavor is to allow the clinician to take appropriate actions in a timely fashion to prevent or ameliorate the physiologic derangement. Furthermore, physiologic monitoring is used not only to warn, but also to titrate therapeutic interventions, such as fluid resuscitation or the infusion of vasoactive or inotropic drugs. The intensive care unit (ICU) and operating room are the two locations where the most advanced monitoring capabilities routinely are employed in the care of critically ill patients.
In the broadest sense, physiologic monitoring encompasses a spectrum of endeavors, ranging in complexity from the routine and intermittent measurement of the classic vital signs (i.e., temperature, heart rate, arterial blood pressure, and respiratory rate) to the continuous recording of the oxidation state of cytochrome oxidase, the terminal element in the mitochondrial electron transport chain. The ability to assess clinically relevant parameters of tissue and organ status and employ this knowledge to improve patient outcomes represents the “holy grail” of critical care medicine. Unfortunately, consensus often is lacking regarding the most appropriate parameters to monitor in order to achieve this goal. Furthermore, making an inappropriate therapeutic decision due to inaccurate physiologic data or misinterpretation of good data can lead to a worse outcome than having no data at all. Of the highest importance is the integration of physiologic data obtained from monitoring into a coherent and evidenced-based treatment plan. Current technologies available to assist the clinician in this endeavor are summarized in this chapter. Also presented is a brief look at emerging techniques that may soon enter into clinical practice.
In essence, the goal of hemodynamic monitoring is to ensure that the flow of oxygenated blood through the microcirculation is sufficient to support aerobic metabolism at the cellular level. In general, mammalian cells cannot store oxygen for subsequent use in oxidative metabolism, although a relatively tiny amount is stored in muscle tissue as oxidized myoglobin. Thus, aerobic synthesis of adenosine triphosphate (ATP), the energy “currency” of cells, requires the continuous delivery of oxygen by diffusion from hemoglobin in red blood cells to the oxidative machinery within mitochondria. Delivery of oxygen to mitochondria may be insufficient for several reasons. For example, cardiac output, hemoglobin concentration of blood, or the oxygen content of arterial blood each can be inadequate for independent reasons. Alternatively, despite adequate cardiac output, perfusion of capillary networks can be impaired as a consequence of dysregulation of arteriolar tone, microvascular thrombosis, or obstruction of nutritive vessels by sequestered leukocytes or platelets. Hemodynamic monitoring that does not take into account all of these factors will portray an incomplete and perhaps misleading picture of cellular physiology.
Under normal conditions when the supply of oxygen is plentiful, aerobic metabolism is determined by factors other than the availability of oxygen. These factors include the hormonal milieu and mechanical workload of contractile tissues. However, in pathologic circumstances when oxygen availability is inadequate, oxygen utilization (VO2) becomes dependent upon oxygen delivery (DO2). The relationship of VO2 to DO2 over a broad range of DO2 values is commonly represented as two intersecting straight lines. In the region of higher DO2 values, the slope of the line is approximately zero, indicating that VO2 is largely independent of DO2. In contrast, in the region of low DO2 values, the slope of the line is nonzero and positive, indicating that VO2 is supplydependent. The region where the two lines intersect is called the point of critical oxygen delivery (DO2crit), and represents the transition from supply-independent to supply-dependent oxygen uptake. Below a critical threshold of oxygen delivery, increased oxygen extraction cannot compensate for the delivery deficit; hence, oxygen consumption begins to decrease. The slope of the supply-dependent region of the plot reflects the maximal oxygen extraction capability of the vascular bed being evaluated.
The subsequent sections will describe the techniques and utility of monitoring various physiologic parameters.
The pressure exerted by blood in the systemic arterial system, commonly referred to as “blood pressure,” is a cardinal parameter measured as part of the hemodynamic monitoring of patients. Extremes in blood pressure are either intrinsically deleterious or are indicative of a serious perturbation in normal physiology. Arterial blood pressure is a complex function of both cardiac output and vascular input impedance. Thus, inexperienced clinicians may assume that the presence of a normal blood pressure is evidence that cardiac output and tissue perfusion are adequate. This assumption frequently is incorrect and is the reason why some critically ill patients may benefit from forms of hemodynamic monitoring in addition to measurement of arterial pressure.
Blood pressure can be determined directly by measuring the pressure within the arterial lumen or indirectly using a cuff around an extremity. When the equipment is properly set up and calibrated, direct intra-arterial monitoring of blood pressure provides accurate and continuous data. Additionally, intra-arterial catheters provide a convenient way to obtain samples of blood for measurements of arterial blood gases and other laboratory studies. Despite these advantages, intra-arterial catheters are invasive devices and occasionally are associated with serious complications.
Noninvasive Measurement of Arterial Blood Pressure
Both manual and automated means for the noninvasive determination of blood pressure use an inflatable sphygmomanometer cuff to increase pressure around an extremity, and a means for detecting the presence or absence of arterial pulsations. Several methods exist for this purpose. The time-honored approach is the auscultation of the Korotkoff sounds, which are heard over an artery distal to the cuff as the cuff is deflated from a pressure higher than systolic pressure to one less than diastolic pressure. Systolic pressure is defined as the pressure in the cuff when tapping sounds are first audible. Diastolic pressure is the pressure in the cuff when audible pulsations first disappear.
Another means for pulse detection when measuring blood pressure noninvasively depends upon the detection of oscillations in the pressure within the bladder of the cuff. This approach is simple, and unlike auscultation, can be performed even in a noisy environment (e.g., a busy emergency room). Unfortunately, this approach is neither accurate nor reliable. Other methods, however, can be used to reliably detect the reappearance of a pulse distal to the cuff and thereby estimate systolic blood pressure. Two excellent and widely available approaches for pulse detection are use of a Doppler stethoscope (reappearance of the pulse produces an audible amplified signal) or a pulse oximeter (reappearance of the pulse is indicated by flashing of a light-emitting diode).
A number of automated devices are capable of repetitively measuring blood pressure noninvasively. Some of these devices measure pressure oscillations in the inflatable bladder encircling the extremity to detect arterial pulsations as pressure in the cuff is gradually lowered from greater than systolic to less than diastolic pressure. Other automated noninvasive devices use a piezoelectric crystal positioned over the brachial artery as a pulse detector. The accuracy of these devices is variable, and often dependent on the size mismatch between the arm circumference and the cuff size.1 If the cuff is too narrow (relative to the extremity), the measured pressure will be artifactually elevated. Therefore, the width of the cuff should be approximately 40% of its circumference.
Another noninvasive approach for measuring blood pressure relies on a technique called photoplethysmography. This method is capable of providing continuous information, since systolic and diastolic blood pressures are recorded on a beat-to-beat basis. Photoplethysmography uses the transmission of infrared light to estimate the amount of hemoglobin (directly related to the volume of blood) in a finger placed under a servo-controlled inflatable cuff. A feedback loop controlled by a microprocessor continually adjusts the pressure in the cuff to maintain the blood volume of the finger constant. Under these conditions, the pressure in the cuff reflects the pressure in the digital artery. The measurements obtained using photoplethysmography generally agree closely with those obtained by invasive monitoring of blood pressure.2 However, these readings may be less accurate in patients with hypotension or hypothermia.
Invasive Monitoring of Arterial Blood Pressure
Direct and continuous monitoring of arterial pressure in critically ill patients may be performed by using fluid-filled tubing to connect an intra-arterial catheter to an external strain-gauge transducer. The signal generated by the transducer is electronically amplified and displayed as a continuous waveform by an oscilloscope. Digital values for systolic and diastolic pressure also are displayed. Mean pressure, calculated by electronically averaging the amplitude of the pressure waveform, also can be displayed. The fidelity of the catheter-tubing-transducer system is determined by numerous factors, including the compliance of the tubing, the surface area of the transducer diaphragm, and the compliance of the diaphragm. If the system is underdamped, then the inertia of the system, which is a function of the mass of the fluid in the tubing and the mass of the diaphragm, causes overshoot of the points of maximum positive and negative displacement of the diaphragm during systole and diastole, respectively. Thus, in an underdamped system, systolic pressure will be overestimated and diastolic pressure will be underestimated. In an overdamped system, displacement of the diaphragm fails to track the rapidly changing pressure waveform, and systolic pressure will be underestimated and diastolic pressure will be overestimated. It is important to note that even in an underdamped or over-damped system, mean pressure will be accurately recorded, provided the system has been properly calibrated. For these reasons, when using direct measurement of intra-arterial pressure to monitor patients, clinicians should make clinical decisions based primarily on the measured mean arterial blood pressure.
The radial artery at the wrist is the site most commonly used for intra-arterial pressure monitoring. Other sites include the femoral and axillary artery. It is important to recognize, however, that measured arterial pressure is determined in part by the site where the pressure is monitored. Central (i.e., aortic) and peripheral (e.g., radial artery) pressures typically are different as a result of the impedance and inductance of the arterial tree. Systolic pressures typically are higher and diastolic pressures are lower in the periphery, whereas mean pressure is approximately the same in the aorta and more distal sites.
Distal ischemia is an uncommon complication of intra-arterial catheterization. The incidence of thrombosis is increased when larger-caliber catheters are employed and when catheters are left in place for an extended period of time. The incidence of thrombosis can be minimized by using a 20-gauge (or smaller) catheter in the radial artery and removing the catheter as soon as feasible. The risk of distal ischemic injury can be reduced by ensuring that adequate collateral flow is present prior to catheter insertion. At the wrist, adequate collateral flow can be documented by performing a modified version of the Allen test, wherein the artery to be cannulated is digitally compressed while using a Doppler stethoscope to listen for perfusion in the palmar arch vessels.
Another potential complication of intra-arterial monitoring is retrograde embolization of air bubbles or thrombi into the intracranial circulation. In order to minimize this risk, care should be taken to avoid flushing arterial lines when air is present in the system, and only small volumes of fluid (less than 5 mL) should be employed for this purpose. Catheter-related infections can occur with any intravascular monitoring device. However, catheter-related bloodstream infection is a relatively uncommon complication of intra-arterial lines used for monitoring, occurring in 0.4% to 0.7% of catheterizations.3 The incidence increases with longer duration of arterial catheterization.
The electrocardiogram (ECG) records the electrical activity associated with cardiac contraction by detecting voltages on the body surface. A standard 3-lead ECG is obtained by placing electrodes that correspond to the left arm (LA), right arm (RA), and left leg (LL). The limb leads are defined as lead I (LA-RA), lead II (LL-RA), and lead III (LL-LA). The ECG waveforms can be continuously displayed on a monitor, and the devices can be set to sound an alarm if an abnormality of rate or rhythm is detected. Continuous ECG monitoring is widely available and applied to critically ill and perioperative patients. Monitoring of the ECG waveform is essential in patients with acute coronary syndromes or blunt myocardial injury, because dysrhythmias are the most common lethal complication. In patients with shock or sepsis, dysrhythmias can occur as a consequence of inadequate myocardial oxygen delivery or as a complication of vasoactive or inotropic drugs used to support blood pressure and cardiac output. Dysrhythmias can be detected by continuously monitoring the ECG tracing, and timely intervention may prevent serious complications. With appropriate computing hardware and software, continuous ST-segment analysis also can be performed to detect ischemia or infarction.
Additional information can be obtained from a 12-lead ECG, which is essential for patients with potential myocardial ischemia or to rule out cardiac complications in other acutely ill patients. Continuous monitoring of the 12-lead ECG is now available and is proving to be beneficial in certain patient populations. In a study of 185 vascular surgical patients, continuous 12-lead ECG monitoring was able to detect transient myocardial ischemic episodes in 20.5% of the patients.4 This study demonstrated that the precordial lead V4, which is not routinely monitored on a standard 3-lead ECG, is the most sensitive for detecting perioperative ischemia and infarction. To detect 95% of the ischemic episodes, two or more precordial leads were necessary. Thus, continuous 12-lead ECG monitoring may provide greater sensitivity than 3-lead ECG for the detection of perioperative myocardial ischemia, and may become standard for monitoring high-risk surgical patients.
Currently, there is considerable interest in using computerized approaches to analyze ECG waveforms and patterns to uncover hidden information that can be used to predict sudden cardiac death or the development of serious dysrhythmias. ECG patterns of interest include repetitive changes in the morphology of the T-wave [T-wave alternans (TWA)]5and heart rate variability.6
Integrated monitoring systems employ software that integrates vital signs to produce a single-parameter index which allows early detection of physiologic perturbations. The input variables include noninvasive measurements of heart rate, respiratory rate, blood pressure, blood oxygen saturation via pulse oximetry (SpO2), and temperature. The software uses sophisticated algorithms refined in an iterative fashion to develop a probabilistic model of normality, previously developed from a representative sample patient training set. Variance from these data set are used to evaluate the probability that the patient-derived vital signs are within the normal range. An abnormal index can occur while no single vital sign parameter is outside the range of normal if their combined patterns are consistent with known instability patterns. Employing such an integrated monitoring system in step-down unit patients has been shown to be a sensitive method to detect early physiologic abnormalities that may precede hemodynamic instability.7
Cardiac Output and Related Parameters
Bedside catheterization of the pulmonary artery was introduced into clinical practice in the 1970s. Although the pulmonary artery catheter (PAC) initially was used primarily to manage patients with cardiogenic shock and other acute cardiac diseases, indications for this form of invasive hemodynamic monitoring gradually expanded to encompass a wide variety of clinical conditions. Clearly, many clinicians believe that information valuable for the management of critically ill patients is afforded by having a PAC in place. However, unambiguous data in support of this view are scarce, and several studies suggest that bedside PAC may not benefit most critically ill patients, and in fact lead to some serious complications (see next).
Determinants of Cardiac Performance
Starling’s law of the heart states that the force of muscle contraction depends on the initial length of the cardiac fibers. Using terminology that derives from early experiments using isolated cardiac muscle preparations, preload is the stretch of ventricular myocardial tissue just prior to the next contraction. Thus, cardiac preload is determined by end-diastolic volume (EDV). For the right ventricle, central venous pressure (CVP) approximates right ventricular end-diastolic pressure (EDP). For the left ventricle, pulmonary artery occlusion pressure (PAOP), which is measured by transiently inflating a balloon at the end of a pressure monitoring catheter positioned in a small branch of the pulmonary artery, approximates left ventricular end-diastolic pressure. The presence of atrioventricular valvular stenosis may alter this relationship.
Clinicians frequently use EDP as a surrogate for EDV, but EDP is determined not only by volume but also by the diastolic compliance of the ventricular chamber. Ventricular compliance is altered by various pathologic conditions and pharmacologic agents. Furthermore, the relationship between EDP and true preload is not linear, but rather is exponential.
Afterload is another term derived from in vitro experiments using isolated strips of cardiac muscle, and is defined as the force resisting fiber shortening once systole begins. Several factors comprise the in vivo correlate of ventricular afterload, including ventricular intracavitary pressure, wall thickness, chamber radius, and chamber geometry. Since these factors are difficult to assess clinically, afterload is commonly approximated by calculating systemic vascular resistance, defined as mean arterial pressure (MAP) divided by cardiac output.
Contractility is defined as the inotropic state of the myocardium. Contractility is said to increase when the force of ventricular contraction increases at constant preload and afterload. Clinically, contractility is difficult to quantify, because virtually all of the available measures are dependent to a certain degree on preload and afterload. If pressure-volume loops are constructed for each cardiac cycle, small changes in preload and/or afterload will result in shifts of the point defining the end of systole. These end-systolic points on the pressure vs. volume diagram describe a straight line, known as the end-systolic pressure-volume line. A steeper slope of this line indicates greater contractility.
Placement of the Pulmonary Artery Catheter
In its simplest form, the pulmonary artery catheter (PAC) has four channels. One channel terminates in a balloon at the tip of the catheter. The proximal end of this channel is connected to a syringe to permit inflation of the balloon with air (saline should never be used). Prior to insertion of the PAC, the integrity of the balloon should be verified by inflating it. In order to minimize the risk of vascular or ventricular perforation by the relatively inflexible catheter, it also is important to verify that the inflated balloon extends just beyond the tip of the device. A second channel in the catheter contains wires that are connected to a thermistor located near the tip of the catheter. At the proximal end of the PAC, the wires terminate in a fitting that permits connection to appropriate hardware for the calculation of cardiac output using the thermodilution technique (see next). The final two channels are used for pressure monitoring and the injection of the thermal indicator for determinations of cardiac output. One of these channels terminates at the tip of the catheter. The other terminates 20 cm proximal to the tip.
Placement of a PAC requires access to the central venous circulation. Such access can be obtained at a variety of sites, including the antecubital, femoral, jugular, and subclavian veins. Percutaneous placement through either the jugular or subclavian vein generally is preferred. Right internal jugular vein cannulation carries the lowest risk of complications, and the path of the catheter from this site into the right atrium is straight. In the event of inadvertent arterial puncture, local pressure is significantly more effective in controlling bleeding from the carotid artery compared to the subclavian artery. Nevertheless, it is more difficult to keep occlusive dressings in place on the neck than in the subclavian fossa. Furthermore, the anatomic landmarks in the subclavian position are quite constant, even in patients with anasarca or massive obesity; the subclavian vein always is attached to the deep (concave) surface of the clavicle. In contrast, the appropriate landmarks to guide jugular venous cannulation are sometimes difficult to discern in obese or very edematous patients. However, ultrasonic guidance, which should be used routinely, has been shown to facilitate bedside jugular venipuncture.8
Cannulation of the vein normally is performed percutaneously, using the Seldinger technique. A small-bore needle is inserted through the skin and subcutaneous tissue into the vein. After documenting return of venous blood, a guidewire with a flexible tip is inserted through the needle into the vein and the needle is withdrawn. A dilator/introducer sheath is passed over the wire, and the wire and the dilator are removed. The proximal terminus of the distal port of the PAC is connected through low-compliance tubing to a strain-gauge transducer, and the tubing-catheter system is flushed with fluid. While constantly observing the pressure tracing on an oscilloscope, the PAC is advanced with the balloon deflated until respiratory excursions are observed. The balloon is then inflated, and the catheter advanced further (“floated”), while monitoring pressures sequentially in the right atrium and right ventricle en route to the pulmonary artery. The pressure waveforms for the right atrium, right ventricle, and pulmonary artery are each characteristic. The catheter is advanced out into the pulmonary artery until a damped tracing indicative of the “wedged” position is obtained. The balloon is then deflated, taking care to ensure that a normal pulmonary arterial tracing is again observed on the monitor; leaving the balloon inflated can increase the risk of pulmonary infarction or perforation of the pulmonary artery. Unnecessary measurements of the pulmonary artery occlusion pressure are discouraged as rupture of the pulmonary artery may occur.
Even in its simplest embodiment, the PAC is capable of providing clinicians with a remarkable amount of information about the hemodynamic status of patients. Additional information may be obtained if various modifications of the standard PAC are employed. By combining data obtained through use of the PAC with results obtained by other means (i.e., blood hemoglobin concentration and oxyhemoglobin saturation), derived estimates of systemic oxygen transport and utilization can be calculated. Direct and derived parameters obtainable by bedside pulmonary arterial catheterization are summarized in Table 13-1. The equations used to calculate the derived parameters are summarized in Table 13-2. The approximate normal ranges for a number of these hemodynamic parameters (in adults) are shown in Table 13-3.
Table 13-1Directly Measured and Derived Hemodynamic Data Obtainable by Bedside Pulmonary Artery Catheterization ||Download (.pdf) Table 13-1 Directly Measured and Derived Hemodynamic Data Obtainable by Bedside Pulmonary Artery Catheterization
|STANDARD PAC || |
SV (or SVI)
QT or QT* (continuous)
SVR (or SVRI)
PVR (or PVRI)
| || |
QT or QT* (intermittent)
| || |
Table 13-2Formulas for calculation of hemodynamic parameters that can be derived by using data obtained by pulmonary artery catheterization ||Download (.pdf) Table 13-2 Formulas for calculation of hemodynamic parameters that can be derived by using data obtained by pulmonary artery catheterization
QT* (L·min–1·m–2) = QT/BSA, where BSA is body surface area (m2)
SV (mL) = QT/HR, where HR is heart rate (min–1)
SVR (dyne·sec·cm–5) = [(MAP – CVP) × 80] /QT, where MAP is mean arterial pressure (mm Hg)
SVRI (dyne·sec·cm–5m–2) = [(MAP – CVP) × 80] /QT*
PVR (dyne·sec·cm–5) = [(PAP – PAOP) × 80] /QT, where PAP is mean pulmonary artery pressure
PVRI (dyne·sec·cm–5m–2) = [(PAP – PAOP) × 80] /QT*
RVEDV (mL) = SV/RVEF
Ḋo2(mL·min–1·m–2) = QT* × Cao2 × 10, where Cao2 is arterial oxygen content (mL/dL)
⊽o2(mL·min–1·m–2) = QT* × (Cao2 – C⊽o2) × 10, where C⊽o2 is mixed venous oxygen content (mL/dL)
Cao2 = (1.36 × Hgb × Sao2) + (0.003 + Pao2), where Hgb is hemoglobin concentration (g/dL), Sao2 is fractional arterial hemoglobin saturation, and Pao2 is the partial pressure of oxygen in arterial blood
C⊽o2 = (1.36 × Hgb × S⊽o2) + (0.003 + P⊽o2), where P ⊽o2 is the partial pressure of oxygen in pulmonary arterial (mixed venous) blood
QS/QT = (Cco2 – Ca o2)/ (Cco2 – Cv o2), where Cc o2 (mL/dL) is the content of oxygen in pulmonary end capillary blood
Cco2 = (1.36 × Hgb) + (0.003 + Pao2), where Pao2 is the alveolar partial pressure of oxygen
Pao2 = [Fio2 × (PB – PH2O)] – Paco2/RQ, where Fio2 is the fractional concentration of inspired oxygen, PB is the barometric pressure (mm Hg), PH2O is the water vapor pressure (usually 47 mm Hg), Paco2 is the partial pressure of carbon dioxide in arterial blood (mm Hg), and RQ is respiratory quotient (usually assumed to be 0.8)
Table 13-3Approximate normal ranges for selected hemodynamic parameters in adults ||Download (.pdf) Table 13-3 Approximate normal ranges for selected hemodynamic parameters in adults
0–6 mm Hg
Right ventricular systolic pressure
20–30 mm Hg
Right ventricular diastolic pressure
0–6 mm Hg
6–12 mm Hg
Systolic arterial pressure
100–130 mm Hg
Diastolic arterial pressure
60–90 mm Hg
75–100 mm Hg
~15 mL 02 dL blood
|Ḋo2 || |
|⊽o2 || |
Measurement of Cardiac Output by Thermodilution
Before the development of the PAC, determining cardiac output (QT) at the bedside required careful measurements of oxygen consumption (Fick method) or spectrophotometric determination of indocyanine green dye dilution curves. Measurements of QT using the thermodilution technique are simple and reasonably accurate. The measurements can be performed repetitively and the principle is straightforward. If a bolus of an indicator is rapidly and thoroughly mixed with a moving fluid upstream from a detector, then the concentration of the indicator at the detector will increase sharply and then exponentially diminish back to zero. The area under the resulting time-concentration curve is a function of the volume of indicator injected and the flow rate of the moving stream of fluid. Larger volumes of indicator result in greater areas under the curve, and faster flow rates of the mixing fluid result in smaller areas under the curve. When QT is measured by thermodilution, the indicator is heat and the detector is a temperature-sensing thermistor at the distal end of the PAC. The relationship used for calculating QT is called the Stewart-Hamilton equation:
QT = [V × (TB – TI) × K1 × K2] /∫TB(t)dt
where V is the volume of the indicator injected, TB is the temperature of blood (i.e., core body temperature), TI is the temperature of the indicator, K1 is a constant that is the function of the specific heats of blood and the indicator, K2 is an empirically derived constant that accounts for several factors (the dead space volume of the catheter, heat lost from the indicator as it traverses the catheter, and the injection rate of the indicator), and ∫TB(t)dt is the area under the time-temperature curve. In clinical practice, the Stewart-Hamilton equation is solved by a microprocessor.
Determination of cardiac output by the thermodilution method is generally quite accurate, although it tends to systematically overestimate QT at low values. Changes in blood temperature and QT during the respiratory cycle can influence the measurement. Therefore, results generally should be recorded as the mean of two or three determinations obtained at random points in the respiratory cycle. Using cold injectate widens the difference between TB and TI and thereby increases signal-to-noise ratio. Nevertheless, most authorities recommend using room temperature injectate (normal saline or 5% dextrose in water) to minimize errors resulting from warming of the fluid as it transferred from its reservoir to a syringe for injection.
Technologic innovations have been introduced that permit continuous measurement of QT by thermodilution. In this approach, thermal transients are not generated by injecting a bolus of a cold indicator, but rather by heating the blood with a tiny filament located on the PAC upstream from the thermistor. By correlating the amount of current supplied to the heating element with the downstream temperature of the blood, it is possible to estimate the average blood flow across the filament and thereby calculate QT. Based upon the results of several studies, continuous determinations of QT using this approach agree well with data generated by conventional measurements using bolus injections of a cold indicator.9 Information is lacking regarding the clinical value of being able to monitor QT continuously.
The Fick equation can be written as QT = VO2/(Cao2 – CVO2), where Cao2 is the content of oxygen in arterial blood and CVO2 is the content of oxygen in mixed venous blood. The Fick equation can be rearranged as follows: CVO2 = Cao2 – VO2/QT. If the small contribution of dissolved oxygen to CVO2 and Cao2 is ignored, the rearranged equation can be rewritten as SVO2 = Sao2 – VO2/(QT × Hgb × 1.36), where SVO2 is the fractional saturation of hemoglobin in mixed venous blood, Sao2 is the fractional saturation of hemoglobin in arterial blood, and Hgb is the concentration of hemoglobin in blood. Thus it can be seen that SVO2 is a function of VO2 (i.e., metabolic rate), QT, Sao2, and Hgb. Accordingly, subnormal values of SVO2 can be caused by a decrease in QT (due, for example, to heart failure or hypovolemia), a decrease in Sao2 (due, for example, to intrinsic pulmonary disease), a decrease in Hgb (i.e., anemia), or an increase in metabolic rate (due, for example, to seizures or fever). With a conventional PAC, measurements of SVO2 require aspirating a sample of blood from the distal (i.e., pulmonary arterial) port of the catheter and injecting the sample into a blood gas analyzer. Therefore for practical purposes, measurements of SVO2 can be performed only intermittently.
By adding a fifth channel to the PAC, it has become possible to monitor SVO2 continuously. The fifth channel contains two fiber-optic bundles, which are used to transmit and receive light of the appropriate wavelengths to permit measurements of hemoglobin saturation by reflectance spectrophotometry. Continuous SVO2 devices provide measurements of SVO2 that agree quite closely with those obtained by conventional analyses of blood aspirated from the pulmonary artery. Despite the theoretical value of being able to monitor SVO2 continuously, data are lacking to show that this capability favorably improves outcomes. In a prospective, observational study of 3265 patients undergoing cardiac surgery with either a standard PAC or a PAC with continuous SVO2 monitoring, the oximetric catheter was associated with fewer arterial blood gas and thermodilution cardiac output determinations, but no difference in patient outcome.10 Since pulmonary artery catheters that permit continuous monitoring of SVO2 are more expensive than conventional PACs, the routine use of these devices cannot be recommended.
The saturation of oxygen in the right atrium or superior vena cava (ScVO2) correlates closely with SVO2 over a wide range of conditions,11 although the correlation between ScVO2 and SVO2 has been questioned under certain conditions (e.g., septic shock).12 Since measurement of ScVO2 requires placement of a central venous catheter rather than a PAC, it is somewhat less invasive and easier to carry out. By using a central venous catheter equipped to permit fiber-optic monitoring of ScVO2, it may be possible to titrate the resuscitation of patients with shock using a less invasive device than the PAC.11,13 The Surviving Sepsis Campaign international guidelines for the management of severe sepsis and septic shock recommends that during the first 6 hours of resuscitation, the goals of initial resuscitation of sepsis-induced hypoperfusion should include all of the following: CVP 8–12 mm Hg, MAP ≥ 65 mm Hg, urine output ≥ 0.5 mL/kg/h. ScVO2 of 70% or SVO2of 65%.14
Effect of Pulmonary Artery Catheterization on Outcome
Despite initial enthusiasm for using the PAC in the management of critically-ill patients, several studies have failed to show improved outcomes with their use. Connors and colleagues reported results of a major observational study evaluating the value of PAC in critically ill patients.15 These researchers compared two groups of patients: those who did and those who did not undergo placement of a PAC during their first 24 hours of ICU care. The investigators recognized that the value of their intended analysis was completely dependent on the robustness of their methodology for case-matching, because sicker patients (i.e., those at greater risk of mortality based upon the severity of their illness) were presumably more likely to undergo pulmonary artery catheterization. Accordingly, the authors used sophisticated statistical methods for generating a cohort of study (i.e., PAC) patients, each one having a paired control matched carefully for severity of illness. Connors et al concluded that placement of a pulmonary artery catheter during the first 24 hours of stay in an ICU is associated with a significant increase in the risk of mortality, even when statistical methods are used to account for severity of illness.15
A number of prospective, randomized controlled trials of PAC are summarized in Table 13-4. The study by Pearson et al was underpowered with only 226 patients enrolled.16 In addition, the attending anesthesiologists were permitted to exclude patients from the CVP group at their discretion; thus, randomization was compromised. The study by Tuman et al was large (1094 patients were enrolled), but different anesthesiologists were assigned to the different groups.17 Furthermore, 39 patients in the CVP group underwent placement of a PAC because of hemodynamic complications. All of the individual single-institution studies of vascular surgery patients were relatively underpowered, and all excluded at least certain categories of patients (e.g., those with a history of recent myocardial infarction).18,19
Table 13-4Summary of randomized, prospective clinical trials comparing pulmonary artery catheter with central venous pressure monitoring ||Download (.pdf) Table 13-4 Summary of randomized, prospective clinical trials comparing pulmonary artery catheter with central venous pressure monitoring
Pearson et al16
“Low risk” patients undergoing cardiac or vascular surgery
CVP catheter (group 1); PAC (group 2); PAC with continuous S⊽o2 readout (group 3)
No differences among groups for mortality or length of ICU stay; significant differences in costs (group 1 < group 2 < group 3)
Tuman et al17
Cardiac surgical patients
No differences between groups for mortality, length of ICU stay, or significant noncardiac complications
Bender et al18
Vascular surgery patients
No differences between groups for mortality, length of ICU stay, or length of hospital stay
Valentine et al19
Aortic surgery patients
PAC + hemodynamic optimization in ICU night before surgery; CVP
No differences between groups for mortality or length of ICU stay; significantly higher incidence of postoperative complications in PAC group
Sandham et al20
“High risk” major surgery
No differences between groups for mortality, length of ICU stay; increased incidence of pulmonary embolism in PAC group
Harvey S, et al21
Medical and surgical ICU patients
PAC vs. no PAC, with option for alternative CO measuring device in non-PAC group
No differences in hospital mortality between the 2 groups, increased incidence of complications in the PAC group
Binanay, et al23
Patients with CHF
PAC vs. no PAC
No difference in hospital mortality between the 2 groups, increased incidence of adverse events in the PAC group
Wheeler, et al24
Patients with ALI
PAC vs. CVC with a fluid and inotropic management protocol
No difference in ICU or hospital mortality, or incidence of organ failure between the 2 groups; increased incidence of adverse events in the PAC group
In the largest randomized controlled trial of the PAC, Sandham et al randomized nearly 2000 American Society of Anesthesiologists (ASAs) class III and IV patients undergoing major thoracic, abdominal, or orthopedic surgery to placement of a PAC or CVP catheter.20 In the patients assigned to receive a PAC, physiologic goal-directed therapy was implemented by protocol. There were no differences in mortality at 30 days, 6 months, or 12 months between the two groups, and ICU length of stay was similar. There was a significantly higher rate of pulmonary emboli in the PAC group (0.9% vs. 0%). This study has been criticized because most of the patients enrolled were not in the highest risk category.
In the “PAC-Man” trial, a multicenter, randomized trial in 65 United Kingdom hospitals, over 1000 ICU patients were managed with or without a PAC.21 The specifics of the clinical management were then left up to the treating clinicians. There was no difference in hospital mortality between the 2 groups (with PAC 68% vs. without PAC 66%, p = 0.39). However, a 9.5% complication rate was associated with the insertion or use of the PAC, although none of these complications were fatal. Clearly, these were critically ill patients, as noted by the high hospital mortality rates. Supporters of the PAC use cite methodology problems with this study, such as loose inclusion criteria and the lack of a defined treatment protocol.
A meta-analysis of 13 randomized studies of the PAC included over 5000 patients was published in 2005.22 A broad spectrum of critically ill patients was included in these heterogeneous trials, and the hemodynamic goals and treatment strategies varied. While the use of the PAC was associated with an increased use of inotropes and vasodilators, there were no differences in mortality or hospital length of stay between the patients managed with a PAC and those managed without a PAC.
The ESCAPE trial (which was one of the studies included in the previous meta-analysis)23 evaluated 433 patients with severe or recurrent congestive heart failure (CHF) admitted to the ICU. Patients were randomized to management by clinical assessment and a PAC or clinical assessment without a PAC. The goal in both groups was resolution of CHF, with additional PAC targets of a pulmonary capillary occlusion pressure of 15 mm Hg and a right atrial pressure of 8 mm Hg. There was no formal treatment protocol, but inotropic support was discouraged. Substantial reduction in symptoms, jugular venous pressure, and edema was noted in both groups. There was no significant difference in the primary end point of days alive and out of the hospital during the first 6 months, or hospital mortality (PAC 10%; vs. without PAC 9%). Adverse events were more common among patients in the PAC group (21.9% vs.11.5%; P = 0.04).
Finally, the Fluids and Catheters Treatment Trial (FACTT) conducted by the Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network was published in 2006.24 The risks and benefits of PAC compared with central venous catheters (CVC) were evaluated in 1000 patients with acute lung injury. Patients were randomly assigned to receive either a PAC or a CVC to guide management for 7 days via an explicit protocol. Patients also were randomly assigned to a conservative or liberal fluid strategy in a 2 × 2 factorial design (outcomes based on the fluid management strategy were published separately). Mortality during the first 60 days was similar in the PAC and CVC groups (27% and 26%, respectively; P= 0.69). The duration of mechanical ventilation and ICU length of stay also were not influenced by the type of catheter used. The type of catheter employed did not affect the incidence of shock, respiratory or renal failure, ventilator settings, or requirement for hemodialysis or vasopressors. There was a 1% rate of crossover from CVC-guided therapy to PAC-guided therapy. The type of catheter used did not affect the administration of fluids or diuretics, and the net fluid balance was similar in the two groups. The PAC group had approximately twice as many catheter-related adverse events (mainly arrhythmias).
Few subjects in critical care medicine have historically generated more emotional responses among experts in the field than the use of the PAC. As these studies demonstrate, it is not possible to show that therapy directed by use of the PAC saves lives when it is evaluated in a large population of patients. Certainly, given the available evidence, routine use of the PAC cannot be justified. Whether selective use of the device in a few relatively uncommon clinical situations is warranted or valuable remains a controversial issue. Consequently, a marked decline in the use of the PAC from 5.66 per 1000 medical admissions in 1993 to 1.99 per 1000 medical admissions in 2004 has been seen.25 Based upon the results and exclusion criteria in these prospective randomized trials, reasonable criteria for perioperative monitoring without use of a PAC are presented in Table 13-5.
Table 13-5Suggested criteria for perioperative monitoring without use of a pulmonary artery catheter in patients undergoing cardiac or major vascular surgical procedures ||Download (.pdf) Table 13-5 Suggested criteria for perioperative monitoring without use of a pulmonary artery catheter in patients undergoing cardiac or major vascular surgical procedures
No anticipated need for suprarenal or supraceliac aortic cross-clamping
No history of myocardial infarction during 3 months prior to operation
No history of poorly compensated congestive heart failure
No history of coronary artery bypass graft surgery during 6 weeks prior to operation
No history of ongoing symptomatic mitral or aortic valvular heart disease
No history of ongoing unstable angina pectoris
One of the reasons for using a PAC to monitor critically ill patients is to optimize cardiac output and systemic oxygen delivery. Defining what constitutes the optimum cardiac output, however, has proven to be difficult. A number of randomized trials evaluating the effect on outcome of goal-directed compared to conventional hemodynamic resuscitation have been published. Some studies provide support for the notion that interventions designed to achieve supraphysiologic goals for DO2, VO2, and QT improve outcome.26,27 However, other published studies do not support this view, and a meta-analysis concluded that interventions designed to achieve supraphysiological goals for oxygen transport do not significantly reduce mortality rates in critically ill patients.28,29 At this time, supraphysiological resuscitation of patients in shock cannot be endorsed.
There is no simple explanation for the apparent lack of effectiveness of pulmonary artery catheterization, although several concurrent possibilities exist. First, even though bedside pulmonary artery catheterization is quite safe, the procedure is associated with a finite incidence of serious complications, including ventricular arrhythmias, catheter-related sepsis, central venous thrombosis, pulmonary arterial perforation, and pulmonary embolism.20 The adverse effects of these complications on outcome may equal or even outweigh any benefits associated with using a PAC to guide therapy. Second, the data generated by the PAC may be inaccurate, leading to inappropriate therapeutic interventions. Third, the measurements, even if accurate, may often be misinterpreted.29 Furthermore, the current state of understanding is primitive when it comes to deciding what is the best management for certain hemodynamic disturbances, particularly those associated with sepsis or septic shock. Taking all of this into consideration, it may be that interventions prompted by measurements obtained with a PAC are actually harmful to patients. As a result, the marginal benefit now available by placing a PAC may be quite small. Less invasive modalities are available that may provide clinically useful hemodynamic information.
It may be true that aggressive hemodynamic resuscitation of patients, guided by various forms of monitoring, is valuable only during certain critical periods, such as the first few hours after presentation with septic shock or during surgery. For example, Rivers and colleagues reported that survival of patients with septic shock is significantly improved when resuscitation in the emergency department is guided by a protocol that seeks to keep ScVO2 greater than 70%.13 Similarly, a study using an ultrasound-based device (see Doppler Ultrasonography below) to assess cardiac filling and SV showed that maximizing SV intraoperatively results in fewer postoperative complications and shorter hospital length of stay.30
Minimally Invasive Alternatives to the Pulmonary Artery Catheter
Because of the cost, risks and questionable benefit associated with bedside pulmonary artery catheterization, there has been interest in the development of practical means for less invasive monitoring of hemodynamic parameters. Several approaches have been developed, which have achieved variable degrees of success. None of these methods render the standard thermodilution technique of the pulmonary artery catheter obsolete. However, these strategies may contribute to improvements in the hemodynamic monitoring of critically ill patients.
When ultrasonic sound waves are reflected by moving erythrocytes in the bloodstream, the frequency of the reflected signal is increased or decreased, depending on whether the cells are moving toward or away from the ultrasonic source. This change in frequency is called the Doppler shift, and its magnitude is determined by the velocity of the moving red blood cells. Therefore, measurements of the Doppler shift can be used to calculate red blood cell velocity. With knowledge of both the cross-sectional area of a vessel and the mean red blood cell velocity of the blood flowing through it, one can calculate blood flow rate. If the vessel in question is the aorta, then QT can be calculated as:
where A is the cross-sectional area of the aorta and ∫V(t)dt is the red blood cell velocity integrated over the cardiac cycle.
Two approaches have been developed for using Doppler ultrasonography to estimate QT. The first approach uses an ultrasonic transducer, which is positioned manually in the suprasternal notch and focused on the root of the aorta. Aortic cross-sectional area can be estimated using a nomogram, which factors in age, height, and weight, back-calculated if an independent measure of QT is available, or by using two-dimensional transthoracic or transesophageal ultrasonography. While this approach is completely noninvasive, it requires a highly-skilled operator in order to obtain meaningful results, and is laborintensive. Moreover, unless QT measured using thermodilution is used to back-calculate aortic diameter, accuracy using the suprasternal notch approach is not acceptable. Accordingly, this method is useful only for obtaining very intermittent estimates of QT, and has not been widely adopted by clinicians.
A second more promising, albeit more invasive, approach has been introduced. In this method blood flow velocity is continuously monitored in the descending thoracic aorta using a continuous-wave Doppler transducer introduced into the esophagus. The probe is connected to a monitor, which continuously displays the blood flow velocity profile in the descending aorta as well as the calculated QT. In order to maximize the accuracy of the device, the probe position must be adjusted to obtain the peak velocity in the aorta. In order to transform blood flow in the descending aorta into QT, a correction factor is applied that is based on the assumption that only 70% of the flow at the root of the aorta is still present in the descending thoracic aorta. A meta-analysis of the available data show a good correlation between cardiac output estimates obtained by trans-esophageal Doppler and PAC in critically-ill patients.31 The ultrasonic device also calculates a derived parameter termed flow time corrected (FTc), which is the systolic flow time in the descending aorta corrected for heart rate. FTc is a function of preload, contractility, and vascular input impedance. Although it is not a pure measure of preload, Doppler-based estimates of SV and FTc have been used successfully to guide volume resuscitation in high-risk surgical patients undergoing major operations.30
The impedance to flow of alternating electrical current in regions of the body is commonly called bioimpedance. In the thorax, changes in the volume and velocity of blood in the thoracic aorta lead to detectable changes in bioimpedance. The first derivative of the oscillating component of thoracic bioimpedance (dZ/dt) is linearly related to aortic blood flow. On the basis of this relationship, empirically derived formulas have been developed to estimate SV, and subsequently QT, noninvasively. This methodology is called impedance cardiography. The approach is attractive because it is noninvasive, provides a continuous readout of QT, and does not require extensive training. Despite these advantages, measurements of QT obtained by impedance cardiography are not sufficiently reliable to be used for clinical decision making and have poor correlation with thermodilution.32
Because of the limitations of bioimpedance devices, a newer approach for processing the impedance signal was developed and commercialized. This approach is based on the recognition that the impedance signal has two components: amplitude and phase. Whereas the amplitude of the thoracic impedance signal is determined by all of the components of the thoracic cavity (bone, blood, muscle and other soft tissues), phase shifts are determined entirely by pulsatile flow. The vast majority of pulsatile flow is related to blood moving within the aorta. Therefore, the “bioreactance” signal correlates closely with aortic flow, and cardiac output determined using this approach agrees closely with cardiac output measured using conventional indicator dilution techniques.33
Another method for determining cardiac output is an approach called pulse contour analysis for estimating SV on a beat-to-beat basis. The mechanical properties of the arterial tree and SV determine the shape of the arterial pulse waveform. The pulse contour method of estimating QT uses the arterial pressure waveform as an input for a model of the systemic circulation in order to determine beat-to-beat flow through the circulatory system. The parameters of resistance, compliance, and impedance are initially estimated based on the patient’s age and sex, and subsequently can be refined by using a reference standard measurement of QT. The reference standard estimation of QT is obtained periodically using the indicator dilution approach by injecting the indicator into a central venous catheter and detecting the transient increase in indicator concentration in the blood using an arterial catheter. In one commercially available embodiment of this approach, the lithium ion (Li+) is the indicator used for the periodic calibrations of the device. The lithium carbonate indicator can be injected into a peripheral vein, and the doses do not exert pharmacologically relevant effects in adult patients. The Li+ indicator dilution method has shown to be at least as reliable as other thermodilution methods over a broad range of CO in a variety of patients.33 In another commercially available system, a conventional bolus of cold fluid is used as the indicator for calibration. The thermodilution-based calibration requires central venous catheterization, although the temperature change is detected in a transpulmonary fashion (i.e., in a peripheral artery).
Measurements of QT based on pulse contour monitoring using these two approaches are comparable in accuracy to standard PAC thermodilution methods, but are less invasive since transcardiac catheterization is not needed.34 Using on-line pressure waveform analysis, the computerized algorithms can calculate SV, QT, systemic vascular resistance, and an estimate of myocardial contractility, (i.e., the rate of rise of the arterial systolic pressure [dP/dT]). The use of pulse contour analysis has been applied using noninvasive photoplethysmographic measurements of arterial pressure. However, the accuracy of this technique has been questioned and its clinical utility remains to be determined.35
One commercially available device, which can be used for estimating cardiac output, does not require external calibration. Instead, the relationship between pulse pressure and stroke volume is determined using a proprietary algorithm that uses biometric data, such as age, gender, and height, as inputs. Although this methodology is gaining fairly wide acceptance in critical care medicine, reported accuracy (in comparison to “gold standard” approaches) is not very good.33
Partial Carbon Dioxide Rebreathing
Partial carbon dioxide (CO2) rebreathing uses the Fick principle to estimate QT noninvasively. By intermittently altering the dead space within the ventilator circuit via a rebreathing valve, changes in CO2 production (Vco2) and end-tidal CO2 (ETco2) are used to determine cardiac output using a modified Fick equation (QT = ΔVco2/ΔETco2). Commercially available devices use this Fick principle to calculate QT using intermittent partial CO2 rebreathing through a disposable rebreathing loop. These devices consist of a CO2 sensor based on infrared light absorption, an airflow sensor, and a pulse oximeter. Changes in intrapulmonary shunt and hemodynamic instability impair the accuracy of QT estimated by partial CO2 rebreathing. Continuous in-line pulse oximetry and inspired fraction of inspired O2 (Fio2) are used to estimate shunt fraction to correct QT.
Some studies of the partial CO2 rebreathing approach suggest that this technique is not as accurate as thermodilution, the gold standard for measuring QT.34,36 However, other studies suggest that the partial CO2 rebreathing method for determination of QT compares favorably to measurements made using a PAC in critically ill patients.37
Transesophageal echocardiography (TEE) has made the transition from operating room to intensive care unit. TEE requires that the patient be sedated and usually intubated for airway protection. Using this powerful technology, global assessments of LV and RV function can be made, including determinations of ventricular volume, EF, and QT. Segmental wall motion abnormalities, pericardial effusions, and tamponade can be readily identified with TEE. Doppler techniques allow estimation of atrial filling pressures. The technique is somewhat cumbersome and requires considerable training and skill in order to obtain reliable results. Recently, a TEE probe has been introduced into practice that is small enough in diameter that it can be left in place for as long as 72 hours. While only limited data are currently available with this probe, it seems like it will be a useful cardiac monitoring tool for use in selected, patients with complex problems.
Assessing Preload Responsiveness
Although pulse contour analysis or partial CO2 rebreathing may be able to provide estimates of SV and QT, these approaches alone can offer little or no information about the adequacy of preload. Thus, if QT is low, some other means must be employed to estimate preload. Many clinicians assess the adequacy of cardiac preload by determining CVP or PAOP. However, neither CVP nor PAOP correlate well with the true parameter of interest, left ventricular end-diastolic volume (LVEDV).38 Extremely high or low CVP or PAOP results are informative, but readings in a large middle zone (i.e., 5–20 mm Hg) are less useful. Furthermore, changes in CVP or PAOP fail to correlate well with changes in stroke volume.37,39 Echocardiography can be used to estimate LVEDV, but this approach is dependent on the skill and training of the individual using it, and isolated measurements of LVEDV fail to predict the hemodynamic response to alterations in preload.40
When intrathoracic pressure increases during the application of positive airway pressure in mechanically ventilated patients, venous return decreases, and as a consequence, left ventricular stroke volume (LVSV) also decreases. Therefore, pulse pressure variation (PPV) during a positive pressure episode can be used to predict the responsiveness of cardiac output to changes in preload.39,41 PPV is defined as the difference between the maximal pulse pressure and the minimum pulse pressure divided by the average of these two pressures. This approach has been validated by comparing PPV, CVP, PAOP, and systolic pressure variation as predictors of preload responsiveness in a cohort of critically ill patients. Patients were classified as being “preload responsive” if their cardiac index [QT/Body Surface Area (BSA)] increased by at least 15% after rapid infusion of a standard volume of intravenous fluid.42 Receiver-operating characteristic (ROC) curves demonstrated that PPV was the best predictor of preload responsiveness. Although atrial arrhythmias can interfere with the usefulness of this technique, PPV remains a useful approach for assessing preload responsiveness in most patients because of its simplicity and reliability.40
Near-infrared Spectroscopic Measurement of Tissue Hemoglobin Oxygen Saturation
Near-infrared spectroscopy (NIRS) allows continuous, noninvasive measurement of tissue hemoglobin oxygen saturation (StO2) using near-infrared wavelengths of light (700–1000 nm). This technology is based on Beer’s law, which states that the transmission of light through a solution with a dissolved solute decreases exponentially as the concentration of the solute increases. In mammalian tissue, three compounds change their absorption pattern when oxygenated: cytochrome aa3, myoglobin, and hemoglobin. Because of the distinct absorption spectra of oxyhemoglobin and deoxyhemoglobin, Beer’s law can be used to detect their relative concentrations within tissue. Thus, the relative concentrations of the types of hemoglobin can be determined by measuring the change in light intensity as it passes through the tissue. Since about 20% of blood volume is intra-arterial and the StO2 measurements are taken without regard to systole or diastole, spectroscopic measurements are primarily indicative of the venous oxyhemoglobin concentration.
NIRS has been evaluated to assess the severity of traumatic shock in animal models and in trauma patients. Studies have shown that peripheral muscle StO2, as determined by NIRS, is as accurate as other end points of resuscitation (i.e., base deficit, mixed venous oxygen saturation) in a porcine model of hemorrhagic shock.43 Continuously-measured StO2 has been evaluated in blunt trauma patients as a predictor of the development of multiple organ dysfunction syndrome (MODS) and mortality.44 Exactly 383 patients were studied at seven level 1 trauma centers. StO2was monitored for 24 hours after admission along with vital signs and other endpoints of resuscitation, such as base deficit (BD). Minimum StO2(using a minimum StO2≤ 75% as a cutoff) had a similar sensitivity and specificity in predicting the development of MODS as BD ≥ 6 mEq/L. StO2 and BD were also comparable in predicting mortality. Thus, NIRS-derived muscle StO2 measurements perform similarly to BD in identifying poor perfusion and predicting the development of MODS or death after severe torso trauma, yet have the additional advantages of being continuous and noninvasive. Ongoing prospective studies will help determine the clinical utility of continuous monitoring of StO2 in clinical scenarios such as trauma, hemorrhagic shock, and sepsis.
The ability to monitor various parameters of respiratory function is of utmost importance in critically ill patients. Many of these patients require mechanical ventilation. Monitoring of their respiratory physiology is necessary to assess the adequacy of oxygenation and ventilation, guide weaning and liberation from mechanical ventilation, and detect adverse events associated with respiratory failure and mechanical ventilation. These parameters include gas exchange, neuromuscular activity, respiratory mechanics, and patient effort.
Blood gas analysis may provide useful information when caring for patients with respiratory failure. However, even in the absence of respiratory failure or the need for mechanical ventilation, blood gas determinations also can be valuable to detect alterations in acid-base balance due to low QT, sepsis, renal failure, severe trauma, medication or drug overdose, or altered mental status. Arterial blood can be analyzed for pH, Po2, Pco2, HCO3– concentration and calculated base deficit. When indicated, carboxyhemoglobin and methemoglobin levels also can be measured. In recent years, efforts have been made to decrease the unnecessary use of arterial blood gas analysis. Serial arterial blood gas determinations are not necessary for routine weaning from mechanical ventilation in the majority of postoperative patients.
Most bedside blood gas analyses still involve removal of an aliquot of blood from the patient, although continuous bedside arterial blood gas determinations are now possible without sampling via an indwelling arterial catheter that contains a biosensor. In studies comparing the accuracy of continuous arterial blood gas and pH monitoring with a conventional laboratory blood gas analyzer, excellent agreement between the two methods has been demonstrated.45 Continuous monitoring can reduce the volume of blood loss due to phlebotomy and dramatically decrease the time necessary to obtain blood gas results. Continuous monitoring, however, is expensive and is not widely employed.
Determinants of Oxygen Delivery
The primary goal of the cardiovascular and respiratory systems is to deliver oxygenated blood to the tissues. DO2 is dependent to a greater degree on the oxygen saturation of hemoglobin (Hgb) in arterial blood (Sao2) than on the partial pressure of oxygen in arterial blood (Pao2). DO2 also is dependent on QT and Hgb. Dissolved oxygen in blood, which is proportional to the PaO2, makes only a negligible contribution to DO2, as is apparent from the equation:
DO2 = QT × [(Hgb × Sao2 × 1.36) + (Pao2 × 0.0031)]
Sao2 in mechanically ventilated patients depends on the mean airway pressure, the fraction of inspired oxygen (Fio2),and SVO2. Thus, when Sao2 is low, the clinician has only a limited number of ways to improve this parameter. The clinician can increase mean airway pressure by increasing positive-end expiratory pressure (PEEP) or inspiratory time. Fio2 can be increased to a maximum of 1.0 by decreasing the amount of room air mixed with the oxygen supplied to the ventilator. SVO2 can be increased by increasing Hgb or QT or decreasing oxygen utilization (e.g., by administering a muscle relaxant and sedation).
Peak and Plateau Airway Pressure
Airway pressures routinely are monitored in mechanically ventilated patients. The peak airway pressure measured at the end of inspiration (Ppeak) is a function of the tidal volume, the resistance of the airways, lung/chest wall compliance, and peak inspiratory flow. The airway pressure measured at the end of inspiration when the inhaled volume is held in the lungs by briefly closing the expiratory valve is termed the plateau airway pressure (Pplateau). As a static parameter, plateau airway pressure is independent of the airway resistance and peak airway flow, and is related to the lung/chest wall compliance and delivered tidal volume. Mechanical ventilators monitor Ppeak with each breath and can be set to trigger an alarm if the Ppeak exceeds a predetermined threshold. Pplateau is not measured routinely with each delivered tidal volume, but rather is measured intermittently by setting the ventilator to close the exhalation circuit briefly at the end of inspiration and record the airway pressure when airflow is zero.
If both Ppeak and Pplateau are increased (and tidal volume is not excessive), then the underlying problem is a decrease in the compliance in the lung/chest wall unit. Common causes of this problem include pneumothorax, hemothorax, lobar atelectasis, pulmonary edema, pneumonia, acute respiratory distress syndrome (ARDS), active contraction of the chest wall or diaphragmatic muscles, abdominal distention, and intrinsic PEEP, such as occurs in patients with bronchospasm and insufficient expiratory times. When Ppeak is increased but Pplateau is relatively normal, the primary problem is an increase in airway resistance, such as occurs with bronchospasm, use of a small-caliber endotracheal tube, or kinking or obstruction of the endotracheal tube. A low Ppeak also should trigger an alarm, as it suggests a discontinuity in the airway circuit involving the patient and the ventilator.
Ventilator-induced lung injury (VILI) is now an established clinical entity of great relevance to the care of critically ill patients. Excessive airway pressure and tidal volume adversely affect pulmonary and possibly systemic responses to critical illness. Subjecting the lung parenchyma to excessive pressure, known as barotrauma, can result in parenchymal lung injury, diffuse alveolar damage similar to ARDS, and pneumothorax, and can impair venous return and therefore limit cardiac output. Lung-protective ventilation strategies have been developed to prevent the development of VILI and improve patient outcomes. In a large, multicenter randomized trial of patients with ARDS from a variety of etiologies, limiting plateau airway pressure to less than 30 cm H2O and tidal volume to less than 6 mL/kg of ideal body weight reduced 28-day mortality by 22% relative to a ventilator strategy that used a tidal volume of 12 mL/kg.46 For this reason, monitoring of plateau pressure and using a low tidal volume strategy in patients with ARDS is now the standard of care. Recent data also suggest that a lung-protective ventilation strategy is associated with improved clinical outcomes in ventilated patients without ARDS.47
The pulse oximeter is a microprocessor-based device that integrates oximetry and plethysmography to provide continuous noninvasive monitoring of the oxygen saturation of arterial blood (Sao2). It is considered one of the most important and useful technologic advances in patient monitoring. Continuous, noninvasive monitoring of arterial oxygen saturation is possible using light-emitting diodes and sensors placed on the skin. Pulse oximetry employs two wavelengths of light (i.e., 660 nm and 940 nm) to analyze the pulsatile component of blood flow between the light source and sensor. Because oxyhemoglobin and deoxyhemoglobin have different absorption spectra, differential absorption of light at these two wavelengths can be used to calculate the fraction of oxygen saturation of hemoglobin. Under normal circumstances, the contributions of carboxyhemoglobin and methemoglobin are minimal. However, if carboxyhemoglobin levels are elevated, the pulse oximeter will incorrectly interpret carboxyhemoglobin as oxyhemoglobin and the arterial saturation displayed will be falsely elevated. When the concentration of methemoglobin is markedly increased, the Sao2 will be displayed as 85%, regardless of the true arterial saturation.48 The accuracy of pulse oximetry begins to decline at Sao2 values less than 92%, and tends to be unreliable for values less than 85%.49
Several studies have assessed the frequency of arterial oxygen desaturation in hospitalized patients and its effect on outcome. Monitoring pulse oximetry in surgical patients is associated with a reduction in unrecognized deterioration, rescue events and transfers to the ICU.50 Because of its clinical relevance, ease of use, noninvasive nature, and cost-effectiveness, pulse oximetry has become a routine monitoring strategy in patients with respiratory disease, intubated patients, and those undergoing surgical intervention under sedation or general anesthesia. Pulse oximetry is especially useful in the titration of Fio2 and PEEP for patients receiving mechanical ventilation, and during weaning from mechanical ventilation. The widespread use of pulse oximetry has decreased the need for arterial blood gas determinations in critically ill patients.
Capnometry is the measurement of carbon dioxide in the airway throughout the respiratory cycle. Capnometry is most commonly measured by infrared light absorption. CO2 absorbs infrared light at a peak wavelength of approximately 4.27 μm. Capnometry works by passing infrared light through a sample chamber to a detector on the opposite side. More infrared light passing through the sample chamber (i.e., less CO2) causes a larger signal in the detector relative to the infrared light passing through a reference cell. Capnometric determination of the partial pressure of CO2 in end-tidal exhaled gas (Petco2) is used as a surrogate for the partial pressure of CO2 in arterial blood (Paco2) during mechanical ventilation. In healthy subjects, Petco2 is about 1 to 5 mm Hg less than Paco2.51 Thus, Petco2 can be used to estimate Paco2 without the need for blood gas determination. However, changes in Petco2 may not correlate with changes in Paco2 during a number of pathologic conditions (see next).
Capnography allows the confirmation of endotracheal intubation and continuous assessment of ventilation, integrity of the airway, operation of the ventilator, and cardiopulmonary function. Capnometers are configured with either an in-line sensor or a sidestream sensor. The sidestream systems are lighter and easy to use, but the thin tubing that samples the gas from the ventilator circuit can become clogged with secretions or condensed water, preventing accurate measurements. The in-line devices are bulky and heavier, but are less likely to become clogged. Continuous monitoring with capnography has become routine during surgery under general anesthesia and for some intensive care patients. A number of situations can be promptly detected with continuous capnography. A sudden reduction in Petco2 suggests either obstruction of the sampling tubing with water or secretions, or a catastrophic event such as loss of the airway, airway disconnection or obstruction, ventilator malfunction, or a marked decrease in QT. If the airway is connected and patent and the ventilator is functioning properly, then a sudden decrease in Petco2 should prompt efforts to rule out cardiac arrest, massive pulmonary embolism, or cardiogenic shock. Petco2 can be persistently low during hyperventilation or with an increase in dead space such as occurs with pulmonary embolization (even in the absence of a change in QT). Causes of an increase in Petco2 include reduced minute ventilation or increased metabolic rate.