The Circulation
OXYGEN DELIVERY
Oxygen delivery to cells is vital for cell metabolic activity and constitutes the principle function of the cardiopulmonary organ system. Before discussing the cardiovascular component of oxygen delivery, a description of oxygen concentrations at the arteriolar, capillary, and cellular level as well as oxygen affinity for hemoglobin will be presented.
Blood Flow and Diffusion
Oxygen enters the arterioles at pO2 and hemoglobin saturation close to arterial levels, and the concentration thereafter usually diminishes as the distance along the arteriolar system and capillaries lengthens. The drop in pO2 and saturation is dependent upon the rate of oxygen extraction by the cells supplied by the arterioles and capillaries, but hemoglobin normally delivers oxygen to transcapillary tissues at a partial pressure of 5-30 mm Hg (1, 2, 3).
The diffusion of oxygen from the arterioles and capillaries to the cells is indirectly proportional to the distance of cells from capillaries. Therefore, an increase in the interstitial space may diminish oxygen concentration at the cellular level. Normal mitochondrial pO2 falls in the range of 4-20 mm Hg. However, mitochondria can function with a pO2 in excess of only 1 mm Hg (1). Thus, mitochondrial hypoxia is more likely a function of less oxygen reaching the arterioles and capillaries (diminished perfusion, decreased oxygen delivery to the capillaries) rather than diminished diffusion from the capillary to the cell (4).
At the capillary level, oxygen release from hemoglobin is an important aspect of oxygen transfer to the interstitium and, subsequently, to cells. The relationship between hemoglobin saturation and oxygen tension is described by the oxyhemoglobin saturation curve (Fig. 3.1). The position of the oxyhemoglobin dissociation curve along the horizontal axis is described by the P50 value, the oxygen tension necessary to saturate 50% of the hemoglobin (normal, 26.3 mm Hg; adults at sea level) (5). The shape of the curve illustrates that less oxygen is released when pO2 drops at the higher level (60-100 mm Hg), but more oxygen is released at levels that develop in the capillary circulation (30-50 mm Hg). A shift of the oxyhemoglobin curve to the right (an increase in P50) results in more oxygen release (less oxygen affinity), whereas a shift to the left results in less oxygen release.
Several factors that cause right and left shifts are listed in Table 3.1 (5). 2, 3-Diphosphoglycerate (DPG), a product of erythrocyte glycolysis, is a major determinant and indirectly proportional to hemoglobin-oxygen affinity. DPG is diminished in stored red blood cells and the transfused blood takes more than 24 hours to regain its normal level. Low serum inorganic phosphate levels also result in DPG depletion. Importantly, hypothermia and metabolic alkalosis, commonly seen in critically ill surgical patients, increase hemoglobin oxygen affinity. Therefore, the use of fresh red cells, providing inorganic phosphate intravenously, reversing hypothermia, and correcting metabolic alkalosis, may improve oxygen delivery to the cells.
CARDIOVASCULAR SYSTEM
The major function of the cardiovascular system is to deliver oxygen to the tissues and remove byproducts of metabolism to their sites of elimination (lungs, kidneys, liver). The determinants of total body oxygen delivery are listed with other commonly measured or calculated hemodynamic variables in Table 3.2 (6). As can be seen from this formula, the pulmonary component is limited to providing adequate arterial oxygen saturation (≥90% at a PaO2 of >60 mm Hg). This is usually readily achieved with modern respiratory therapy. Hemoglobin frequently increases with transfusion, but during a critical illness, concerns about the adverse effects of blood transfusion have been associated with the commonplace acceptance of hemoglobin concentrations in the range of 7-8 gm/dL. Such a reduction in oxygen content (nearly 50% of normal for some patients) is usually well tolerated, indicating that for most surgical critical illness, the delivery
of oxygen to tissues is principally linked to blood flow, that is, cardiac output, rather than blood oxygen content (6, 7, 8, 9).
of oxygen to tissues is principally linked to blood flow, that is, cardiac output, rather than blood oxygen content (6, 7, 8, 9).
 Figure 3.1 Characteristic oxyhemoglobin saturation curve. |
Table 3.1 Factors Altering Hemoglobin-Oxygen Affinity | ||||||
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The determinants of cardiac output can be organized both by the variables that affect ventricular function and those that affect venous return. Depending on clinical circumstances, the logical application of one such physiology (physio-logic) may be more suitable than the other, as described below.
Ventricular Physiology
The major determinants of ventricular performance are listed in Table 3.3. Preload represents the magnitude of myocardial muscle stretch before contraction, the stimulus described by the Frank-Starling mechanism (Fig. 3.2), whereby increased stretch leads to increased contraction until the muscle is overstretched. Preload is most appropriately measured as end-diastolic volume (EDV) (10, 11). Since volume is not easily measured clinically, the direct proportion between ventricular volume and ventricular end-diastolic pressure (EDP) allows pressure measurement to estimate volume. As described in the section on “Confounding Variables,” the pressure-volume relationship (compliance) may change and make pressure measurements difficult to interpret.
Ventricular afterload is determined primarily by the resistance to ventricular ejection present in either the pulmonary [pulmonary vascular resistance (PVR)] or systemic arterial tree [systemic vascular resistance (SVR)]. With constant preload, the increased afterload diminishes ventricular ejection, and decreased afterload augments ejection (Fig. 3.3).
Contractility represents the force of contraction under conditions of a predetermined preload and/or afterload. Factors that can increase and decrease contractility are listed in Table 3.4. A change in contractility, like a change in afterload, will result in a different cardiac function curve (Fig. 3.4).
Table 3.2 Hemodynamic and Oxygen Delivery Variables (2) | |||||||||||||||||||||||||||||||||||||||||||||
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Table 3.3 Determinants of Ventricular Function | |
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 Figure 3.2 Schematic diagram of Starling’s law of the heart. The inset demonstrates the difference between cardiac and skeletal muscle, where cardiac muscle does not decompensate as rapidly with increasing stretch. |
 Figure 3.3 The decrease in stroke volume (black line), which develops secondary to an increase in resistance (dotted line). |
Table 3.4 Factors Affecting Myocardial Contractility | ||||||||||
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 Figure 3.4 Schematic representation of the cardiac function curve with different contractility states. |
 Figure 3.5 Schematic representation of the effects of inotrope (dopamine) administration and afterload reduction (nitroprusside) on cardiac index. Note that afterload reduction also reduced preload and augmentation of preload further increased cardiac index. A, control; B, dopamine; C, dopamine and nitroprusside; D, dopamine and nitroprusside and preload restoration. |
The combined influence of increasing contractility and decreasing afterload to improve ventricular function is illustrated in Figure 3.5.
Heart rate is directly proportional to cardiac output (not cardiac muscle mechanics per se) until rapid rates diminish ventricular filling during diastole.
Right and Left Ventricular Differences
The differences in the structure and position of the right and left ventricles can influence the relative importance of each of the determinants of ventricular function listed above. The right ventricle’s initial response to increased afterload is an increase in contractility, called homeometric autoregulation. As afterload increases further, the RV can respond to endogenous catecholamines. Subsequently, the RV begins to dilate and augment function via the Frank-Starling mechanism. If this continues, the right ventricle eventually fails (output decreases as preload increases) and the left ventricle may consequently suffer from two mechanisms: diminished preload from poor right ventricular output, and diminished volume from leftward shift of the interventricular septum. Such a failure can be catastrophic (12, 13).
Vascular Resistance
The relationship between cardiac output and circulatory pressure is described by the formulae for systemic and pulmonary vascular resistance shown in Table 3.2. Resistance to flow in the systemic and pulmonary artery systems resides mostly in the arteriolar region. This is distinctly different from the venous system where resistance is primarily located in the large veins of the thorax and abdomen.
Arterial vascular resistance is the most common afterload against which the right and left ventricles must eject. Calculation and manipulation of vascular resistance are practical tools for hemodynamic assessment and management of critically ill surgical patients. Table 3.5 lists the common conditions that alter systemic and pulmonary vascular resistance. Note that disease may have variable effects upon the systemic circulation, but almost always increases pulmonary vascular resistance.
Table 3.5 Factors Affecting Vascular Resistance | ||||||||||||||||||||||||||||||||
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Venous Return
While the term venous return is used commonly, the determinants of venous return are rarely considered in clinical practice. As will be emphasized, in surgical patients, the physiol-logic of augmenting venous return can be more practical as a method of improving the circulation than the logic applied to ventricular function.
Venous return is linked to another important function of the venous system, that is, blood volume capacitance. About 70% of the blood volume is contained in the veins, with the splanchnic and cutaneous veins the largest reservoir regions. The splanchnic reservoir is the principle resource for acute mobilization of blood volume.
Total venous capacitance is the sum of the capacity of individual veins. Capacity is the volume contained in a vein at a specific distending pressure. Venous compliance is the change in volume (ΔV) of a vein secondary to a change in distending pressure (ΔP). Distending pressure (DP) is not the pressure within the lumen of the vein, but the difference between intraluminal and extraluminal pressure, such that DP is greater than zero if the pressure inside the lumen is greater than the pressure outside (14, 15).
When DP is zero, the volume in a vein is designated as unstressed (Vu). When DP is greater than zero, the volume in a vein is called stressed (Vs). Under resting conditions, about 70% of the venous blood volume is in unstressed veins that serve the reservoir function, but the venous pressure that determines venous return is governed by Vs. The relationship between Vs and Vu and venous return is illustrated in Figure 3.6 (14).
Venous return (VR) is also described by the following formula: (15)
Where, MCFP = mean circulatory filling pressure, CVP = central venous pressure [right atrial pressure (RAP)], RV = venous resistance, and RA = arterial resistance.
 Figure 3.6 Venous return stressed and unstressed volumes—the tub analogy. The water in the tub represents total venous volume and a hole in the tub divides the total volume into stressed (Vs) and unstressed (Vu) volumes. The water leaves the tub depending upon the diameter of the hole (representing venous resistance) and the height of the water above the hole (Vs). An increase in Vs results in an increase in flow. Vu does not affect flow. Moving the hole down (a relative increase in Vs compared with Vu) increases flow. This represents the effect of venoconstriction. CVP is the pressure at the end of the opening that inhibits flow through the tube. Source: From Ref. 14. |
MCFP is the pressure in small veins and venules, which must be higher in the periphery than CVP so that blood can flow from the periphery to the thorax. RV is located primarily in the large veins in the abdomen and chest. RA is located mostly in the arterioles.
The principal factor determining MCFP is Vs, a variable directly influenced by blood volume (14, 15). Additional factors that alter venous return variables are listed in Table 3.6. This list shows that surgical patients frequently have diseases or therapeutic interventions that may inhibit venous return.
Physical Exam of the Circulation
For the surgeon, examination of the cardiovascular system (observing or measuring the parameters listed in Table 3.7) is used primarily to assess total body and regional perfusion. When perfusion is inadequate, then physical exam can provide an assessment of the likely etiology.
Total Body Perfusion
Measurement of the vital signs (systolic and diastolic blood pressure, pulse, respiration, temperature) is the first step of the physical examination. As evident in the calculations in Table 3.2, blood pressure is determined by both cardiac output (flow) and resistance. Frequently, a decrease in blood pressure indicates a decrease in cardiac output (hypoperfusion), especially when the neuroendocrine response to decreased flow causes increased vascular resistance. However, blood pressure may be in the normal range or elevated in the face of hypoperfusion, with conditions such as congestive heart failure (CHF), hypothermia, and in patients with underlying hypertension with a baseline pressure above the normal range. In addition, hypotension may be present during normal or augmented perfusion, such as that occuring in severe inflammation or spinal cord injury, when the reason for a lower pressure is a lower resistance rather than lower flow. Orthostatic hypotension (>20 mm Hg drop in systolic, >10 mm Hg drop in diastolic pressure) is more specific for intravascular volume depletion, but often difficult to obtain in surgical critical care settings.
Tachycardia is a more sensitive indicator of hypoperfusion and orthostatic stress but is less specific and can be a result of various other causes (i.e., anxiety, pain, temperature elevation, delirium). Respiratory rate and depth can be increased as a response to the acidosis of decreased oxygen delivery, but is also subject to other stimuli. Core temperature can be increased in hyperdynamic circulatory states and decreased with severe hypoperfusion (see below).
Table 3.6 Factors Altering Venous Return Variables | |
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With mild-to-moderate hypoperfusion, patients often become restless and agitated, pulling at restraints, intravenous lines, and nasogastric tubes. Severe hypoperfusion can result in obtundation and coma.
Most commonly, hypoperfusion stimulates a neuroendocrine response that results in peripheral vasoconstriction and, consequently, pale to cyanotic and cool to cold extremities. Skin covering the patella is particularly sensitive to hypoperfusion and vasoconstriction here, resulting in “purple knee caps” that may be an early clinical sign of hypoperfusion. Skin temperature (cool vs. warm) may be particularly useful for identifying patients with a hyperdynamic circulation (warm extremities) (16).
Distended neck veins are consistent with impairment of cardiac function, but not always with CHF or cardiogenic shock (17). CVP elevation and neck vein distention may be secondary
to a force exerted outside the lumen of the right atrium (tension pneumothorax, pericardial tamponade, positive end-expiratory pressure (PEEP), prolonged expiration in chronic obstructive pulmonary disease (COPD)].
to a force exerted outside the lumen of the right atrium (tension pneumothorax, pericardial tamponade, positive end-expiratory pressure (PEEP), prolonged expiration in chronic obstructive pulmonary disease (COPD)].
Table 3.7 Cardiovascular Physical Exam | ||||||||
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Examination of the heart focuses on the quality of heart sounds (diminished sounds may represent pericardial fluid or shift of the mediastinum) and the presence or absence of murmurs and/or a gallop. Distinguishing an S3 gallop from an S4 may be difficult, especially with tachycardia. The distinction is important, however, since an S4 is common in patients aged 50 years and above and an S3 is quite specific but not very sensitive for a failing left ventricle (17, 18).
Urine output at least 0.5 cm3/kg/hr is usually considered an indication of adequate total body perfusion. Unfortunately, as described in the section on “Confounding Variables,” even this clinical tool must be evaluated with caution. Importantly, examination of the lungs and extremities for evidence of edema is not specific for cardiac dysfunction. As will be emphasized later, in surgical critical illness total body salt and water excess is commonly associated with, at best, a normal, but still too frequently, a decreased intravascular volume. Under these circumstances, relying on the lung or the periphery to draw conclusions about cardiac filling and function can be dangerously misleading.
Regional Perfusion
Physical examination evidence of regional hypoperfusion is limited primarily to the extremities. A painful, pale, pulseless, paralyzed, and cold extremity with paresthesia is diagnostic of acute arterial insufficiency. Chronic arterial insufficiency demonstrates loss of pulse, hair loss, dependent rubor, and sometimes loss of muscle mass. Acute venous obstruction, particularly in the iliofemoral region, may also cause decreased extremity perfusion. The lower extremity may be edematous and white (phlegmasia alba dolens) with little arterial compromise, or edematous and blue (phlegmasia cerulea dolens) with increased muscular pressure sufficient to diminish arterial circulation and cause tissue necrosis, often resulting in skin with fluid-filled bullae.
Physical examination alone is rarely sufficient to evaluate precisely other types of regional hypoperfusion (cerebral, gastrointestinal), but can contribute greatly to the overall clinical evaluation. For instance, evidence of sudden neurologic deficit consistent with middle cerebral artery occlusion or an unremarkable abdominal exam coexistent with severe abdominal pain may lead to the diagnosis of cerebral and intestinal infarction, respectively.
Hemodynamic Monitoring
The purpose of hemodynamic monitoring is to measure the cardiovascular variables that help assess the adequacy of the circulation (where is the hole?), the etiology of an inadequate
circulation (why is the hole there?), and the effect of therapeutic interventions (how do I plug the hole?). In this section, the emphasis will be on the fundamentals of commonly used and emerging hemodynamic monitors, the confounding variables that make a monitor difficult to interpret, methods of reducing confusion, complications of monitoring equipment, and selection of patients for more complex hemodynamic analysis. Except as related to confounding variables and/or complications, no technical details of monitor placement or use will be presented.
circulation (why is the hole there?), and the effect of therapeutic interventions (how do I plug the hole?). In this section, the emphasis will be on the fundamentals of commonly used and emerging hemodynamic monitors, the confounding variables that make a monitor difficult to interpret, methods of reducing confusion, complications of monitoring equipment, and selection of patients for more complex hemodynamic analysis. Except as related to confounding variables and/or complications, no technical details of monitor placement or use will be presented.
Continuous Electrocardiogram Monitoring
Continuous electrocardiogram (EKG) monitoring to record heart rate and indicate arrhythmias is the simplest and most frequently used hemodynamic monitor after standard blood pressure and pulse determinations. While arrhythmias are common in surgical critical illness, a comprehensive review of the diagnosis and management of rhythm disturbance is beyond the scope of this manual.
Measurement of Arterial Pressure
Arterial catheterization is often used to supplement blood pressure cuff measurements with constant monitoring and ease of blood sampling. Under normal conditions, the aortic pressure pulse is altered as the aortic root pressure is transmitted to the peripheral arteries, producing a small increase in systolic pressure and decrease in diastolic pressure (19). Most often the radial and femoral arteries are accessed, while more rarely the dorsalis pedis or brachial arteries. Severe vasoconstriction may impede perfusion of the radial or dorsalis pedis arteries and result in a lower pressure than the aortic root. This may be less so with femoral cannulation, but severe vasoconstriction impeding peripheral pulses is a matter of concern even if a higher pressure is recorded in a larger vessel (20).
Patients with a left ventricular volume that is placed within the upward slop range of the Frank-Starling effect are considered “volume responsive,” indicating that ventricular output will increase with greater ventricular muscle stretch and decrease with lesser ventricular muscle stretch (Fig. 3.2). Through effects on CVP and RV, positive pressure ventilation can result in a decrease in venous return and, therefore, lower cardiac output for ventricles that are volume responsive. Thus, beat-by-beat ventricular output, that is, stroke volume, can also be decreased by positive pressure ventilation in volume responsive hearts, causing a decrease in pulse pressure (ΔPP) witnessed during expiration. Therefore, techniques that monitor beat-to-beat alterations in blood pressure in patients on mechanical ventilation and in sinus rhythm can augment the analysis of intravascular volume, an emerging technology that may expand the value of arterial pressure monitoring (20, 21).
Measurement of Venous Pressures
The measurement of central venous and pulmonary venous pressure is used to estimate the right and left atrial pressure (LAP), respectively. In the absence of obstruction (e.g., superior vena cava syndrome), superior vena cava pressure (CVP) equals mean RAP which, in the absence of tricuspid valve disease, equals right ventricular end-diastolic pressure (RVEDP). Similarly, in the absence of pulmonary venous obstruction (e.g., high alveolar pressure with PEEP, pulmonary veno-occlusive disease), the pressure obtained by inflating the balloon on the end of a flow-directed pulmonary artery catheter (Fig. 3.7), referred to as the pulmonary artery occlusion pressure (PAOP) or pulmonary capillary wedge pressure (PCWP), equals mean LAP, which in the absence of mitral valve disease, equals left ventricular end diastolic pressure (LVEDP). Therefore, in most patients, CVP and PAOP measure right and left ventricular filling pressures (22). As described in section on “Ventricular Physiology,” these pressures are directly proportional to EDV, provide an indirect measure of ventricular preload and still a direct measure of the pressure within the lumen of the superior vena cava and pulmonary capillaries. Ranges of normal and representative abnormal values for CVP and PAOP are shown in Table 3.8.
 Figure 3.7 A representation of the pressure tracing as a balloon-tipped pulmonary artery catheter is passed from the right atrium, through the right ventricle, and into the pulmonary artery. Further advancement results in the “wedge” or pulmonary artery occlusion pressure wave form depicted. Note that this wave is not flat, but with atrial and ventricular contraction it exhibits an “a” and a “v” wave. Source: From Ref. 114. |
Table 3.8 Representative Values of Venous Pressures | |||||||||||||||
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In patients with normal cardiac function, CVP is a few mm Hg lower than LAP and PAOP is nearly identical to LAP. However, acute and chronic heart and pulmonary disease (Table 3.9) may not only interfere with the relationship of atrial pressure to ventricular end diastolic pressure, but can also make CVP and PAOP unequal, sometimes changing in opposite directions (22). Thus, in patients with known cardiac or pulmonary disease simultaneous measurement of the right and left ventricular filling pressure can be more useful and is usually achieved by placing the flow-directed pulmonary artery catheter percutaneously.
Blood Volume Measurement
As noted previously and described more fully in the section on “Confounding Variables,” measurement of intraluminal pressure is an imprecise monitor of vascular volume and, in particular, cardiac preload. During the last decade, the use of transpulmonary thermodilution has been applied to measure both cardiac output (see below) as well as intrathoracic blood volume (ITBV). ITBV has been shown in populations as diverse as cardiac surgery and pancreatitis patients to have the ability to provide a better indication of cardiac preload and the potential to respond to intravascular volume augmentation than either CVP and/or PAOP measurement (23, 24).
Cardiac Output Measurement
Thermodilution
Cardiac output can be easily measured using the same pulmonary artery catheter that measures pulmonary artery pressures and PAOP as well as other methods that use thermodilution. Thermodilution is based on the principle of indicator dilution with “cold” as the indicator that is injected into an unknown volume. Indicator dilution has been used for decades to measure static physiologic volumes (e.g., blood volume, extracellular fluid volume). However, since cardiac output is a time-dependent variable, time must be included in the measurement technique. For example, to measure a static volume (V) a known amount of indicator (I) can be mixed in the
volume and the concentration of I (C) measured. A good scientist will determine C many times and then calculate the mean. V then equals I/mean C. In a time-dependent system, a known amount of indicator I is mixed into a time-dependent volume Q(t) and results in a time-dependent concentration C(t). The measurement of concentration of the indicator as a function of time is depicted in Figure 3.8. To calculate Q(t), the mean of the measured concentration must be determined by the mean value theorem such that:
volume and the concentration of I (C) measured. A good scientist will determine C many times and then calculate the mean. V then equals I/mean C. In a time-dependent system, a known amount of indicator I is mixed into a time-dependent volume Q(t) and results in a time-dependent concentration C(t). The measurement of concentration of the indicator as a function of time is depicted in Figure 3.8. To calculate Q(t), the mean of the measured concentration must be determined by the mean value theorem such that:
Table 3.9 Disease Likely to Manifest an LAP Not = CVP | |
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The same concept is used with the thermodilution technique. Therefore, using an “amount” of cold injected into the right atrium that mixes with the blood in the right ventricle and pulmonary artery, the “concentration” of cold is measured by the thermistor at the end of the pulmonary artery catheter or elsewhere in the arterial system. The integration of this time-dependent concentration and division into the amount of cold is automatically accomplished by the computer supplied with the measurement equipment. The correlation between thermodilution cardiac output and indocyanine green indicator dilution is excellent (r = 0.99). The correlation of pulmonary artery catheter (PAC) thermodilution cardiac output with that obtained using the transpulmonary device (TPD) that measures ITBV is also excellent (r = 0.96) (25).
Esophageal Doppler Monitor
The esophageal Doppler probe measures the velocity of blood flow in the lumen as well as the diameter of the descending thoracic aorta. Using the shape of the velocity curve and several calculations, these data can provide information about cardiac output, preload, and systemic resistance. Placement and interpretation of data may be less challenging than PAC placement and data interpretation, but there is no information provided about pulmonary artery parameters that might influence the right heart function analysis. Several studies have supported esophageal doppler monitor (EDM) for assessing the response to intravascular volume augmentation (26, 27, 28).
Ultrasound
Echocardiography is useful for assessing ventricular function, heart valve alterations, and pericardial fluid accumulation. As a snapshot of cardiac function, echocardiography provides little assistance in the hour-to-hour, intervention-to-intervention, evaluation of response to management. Even when hemodynamic function is analyzed during the snapshot, the value of echo-cardiographic data has been questioned (28, 29).
Tissue Oxygen Measurement
Both near-infrared spectroscopy (NIRS) and transcutaneous pO2 measurement show promise for identifying peripheral tissues at risk. Evidently, when peripheral tissues are at risk, vital
organ function is also at risk despite the sacrifice of flow to less vital organs. Failure to achieve resuscitation of oxygen-related parameters as measured by either technique is associated with a poor outcome and such techniques may be more sensitive and specific than the measurement of global parameters such as cardiac index and oxygen delivery (32, 33, 34).
organ function is also at risk despite the sacrifice of flow to less vital organs. Failure to achieve resuscitation of oxygen-related parameters as measured by either technique is associated with a poor outcome and such techniques may be more sensitive and specific than the measurement of global parameters such as cardiac index and oxygen delivery (32, 33, 34).
 Figure 3.8 A typical indicator dilution curve, which can be used to calculate cardiac output. |
Measurement of Tissue pCO2
Carbon dioxide (CO2), along with ATP and heat, is a product of oxidative phosphorylation. As tissue perfusion brings oxygen to cells, it takes CO2 away. As the lungs serve to add oxygen to the blood, they serve to remove CO2. Decreased tissue perfusion results in CO2 tissue accumulation and decreased lung elimination from increased physiologic dead space (see chap. 6). Anaerobic metabolism results in lactic acid production and subsequent interaction with the bicarbonate buffer that can also increase tissue CO2 (35). Therefore, tissue CO2 accumulation and the difference between tissue pCO2 (tpCO2) and arterial pCO2 (apCO2) are markers of both perfusion and metabolic deficits in the monitored tissue.
Gastrointestinal tract (GIT) perfusion is particularly vulnerable to the neuroendocrine response to decreased cardiac output (see chap. 8) and an increase in tissue pCO2 during critical illness has been documented even in the stomach, a portion of the GIT with robust arterial supply. Data in humans support the concept that upper intestinal tissue pCO2 is a practical marker for the magnitude of shock and the response or lack of response to therapy (36, 37).
Measurement of stomach pCO2 has methodological difficulties and emerging technologies are assessing the use of pCO2 monitoring at sublingual, buccal, and urinary bladder sites (38, 39, 40). Tissues in the facial region and pelvis are usually considered less threatened by the neuroendocrine response to hypoperfusion as compared to the GIT, but sublingual and urinary bladder data suggest vulnerability equal to that in the proximal GIT (39, 40).
Measurement of Oxygen Delivery (DO2) and Consumption (VO2)
Placement of a pulmonary artery catheter not only allows measurement of cardiac output, but also of mixed venous blood gases, which along with arterial blood gases and hemoglobin, allow for calculation of DO2 and VO2 (Table 3.2). Since many disease states either diminish oxygen delivery and/or increase oxygen consumption (see chap. 2), a plot of the relationship between delivery and consumption may be a more useful indication of the need for further hemodynamic interventions than the absolute DO2 and VO2 values, per se (see Fig. 2.1). Optimization of oxygen delivery may be considered present when an increase in DO2 results in no further increase in VO2 (supply-independent oxygen consumption). This concept has resulted in considerable controversy in patient management (see below).
Measurement of Central Venous or Mixed Venous Oxygen Saturation
Measurement of DO2 and VO2 requires more invasive equipment (PAC) and/or more sophisticated oxygen monitoring (measurement of oxygen consumption in the ventilation circuit)
than are commonly used in critical care units today. Mixed venous saturation (mvO2 sat) has been shown to have a direct relationship to the ratio of DO2 to VO2 with an r value of 0.96 (41). Normal mvO2 sat is >70%, indicating that no more than 30% of DO2 is utilized in healthy, baseline states. Studies of oxygen delivery and consumption during critical illness suggest that supply independent oxygen consumption is also achieved when mvO2 sat has reached this concentration, with the implication that further efforts to improve DO2 are not warranted (see chap. 2).
than are commonly used in critical care units today. Mixed venous saturation (mvO2 sat) has been shown to have a direct relationship to the ratio of DO2 to VO2 with an r value of 0.96 (41). Normal mvO2 sat is >70%, indicating that no more than 30% of DO2 is utilized in healthy, baseline states. Studies of oxygen delivery and consumption during critical illness suggest that supply independent oxygen consumption is also achieved when mvO2 sat has reached this concentration, with the implication that further efforts to improve DO2 are not warranted (see chap. 2).
Since measurement of mvO2 sat necessitates a PAC, the use of central venous oxygen saturation (cvO2 sat) has been advocated as a surrogate for mvO2 sat, especially since this appeared to be a good indicator of successful resuscitation in severe sepsis (42). Many studies before and since the publication of this resuscitation paradigm have indicated an imperfect correlation between mvO2 sat and cvO2 sat, especially in patients with a low cardiac index (43). Typically, cvO2 sat is several percentage points higher than mvO2 sat. Although imperfect, if empiric data show that cvO2 sat >70% is associated with a reduction in morbidity and/or mortality, then the practical value of this measure of total body tissue oxygenation is evident.
Acid-Base Monitoring
Acid-base monitoring during surgical critical illness is commonly employed by measurement of arterial pH, base-deficit calculations, and measurement of lactic acid. Of these, arterial pH, which can be influenced by ventilation as well as various cellular metabolic states, is the least useful. Base deficit is more specific for metabolic alterations, but is influenced by high concentrations of chloride provided with 0.9% saline infusion (44, 45). Lactic acid, then, is the preferred monitor and, certainly, lactic acid concentrations have been linked to oxygen delivery deficits and oxygen debt (see chap. 2). Since metabolic alterations that impair pyruvate metabolism without hypoxia can also increase lactic acid concentrations, a more specific indication of anaerobic lactic acid production is an increase in the lactate-pyruvate ratio, a value that is typically unavailable in common clinical laboratories. At present, an increase in lactic acid, therefore, infers a poor prognosis and can also infer an oxygen delivery deficit, but this variable should not be the only monitor driving hemodynamic management decisions (46, 47).
CONFOUNDING VARIABLES
Each of the hemodynamic monitors described above can provide misleading information because of improper technique, inadequate experience with the device, or because of physiologic changes that make the information difficult to interpret. This section will cover the common confounding variables in hemodynamic monitoring and suggest methods to diminish confusion.
Physical Examination
In surgical critical illness, physical examination and other clinical information is often inadequate to predict measured hemodynamic variables (48). For instance, a common error is to misinterpret the physical examination information suggesting total body salt and water excess (evidence of peripheral and pulmonary edema and weight gain) as evidence that intravascular volume is in excess (i.e., that this indicates CHF). Therefore, other monitoring techniques are often used to assess the circulation. Unfortunately, just like physical examination, these tools are not immune from artifacts or misinterpretation.
Arterial Pressure Monitoring
As mentioned previously, severe peripheral vasoconstriction may lower pressures measured in the radial or dorsalis pedis arteries as compared to pressures measured in the femoral or more proximal vessels. Even if the more proximal pressure is higher, vasoconstriction of this magnitude usually denotes hypoperfusion worthy of intervention.
Such physiological reasons for a significant discrepancy between aortic pressure and more peripheral pressures are rare and a normal arterial pressure tracing is sufficiently well
understood that artifactual alterations in a pressure tracing (e.g., plugged catheter, position related dampening of the signal, etc.) are usually readily recognized by the critical care team.
understood that artifactual alterations in a pressure tracing (e.g., plugged catheter, position related dampening of the signal, etc.) are usually readily recognized by the critical care team.
Table 3.10 Confounding Variables in Venous Pressure Monitoring | ||||||||
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Venous Pressure Monitoring (Table 3.10)
In contrast to arterial pressure monitoring, venous pressure monitoring (central venous, pulmonary venous, right atrial, left atrial) is subject to many confounding variables, including the lack of recognition of proper wave form, disregard for unphysiologic relationship between monitored variables, diminished ventricular compliance, and increased intrathoracic pressure.
Lack of Recognition of Proper Wave Form
A normal right and LAP tracing demonstrates an increase in pressure corresponding to atrial contraction (A wave) followed by a second increase secondary to ventricular contraction (V wave) (Fig. 3.9). Catheters placed in the large thoracic veins and the occluded pulmonary artery should also demonstrate this picture, although commonly with some damping as compared to atrial placement. CVP, LAP, and PAOP should not be flat lines. With the loss of atrial contraction (atrial fibrillation, junctional rhythm), only the V wave, timed with ventricular contraction, will be recognized.
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