Chapter 32: Hemodynamic Monitoring

Hemodynamic monitoring can identify cardiovascular insufficiency and ensure optimal treatment of the critically ill. Advanced techniques help identify and prioritize various causes of hemodynamic instability and can enable tailored interventions.

Hemodynamic monitoring changes therapeutic decisions in more than 50% of patients and can detect cryptic cardiovascular compromise. We will focus on techniques applicable to the ED: blood pressure monitoring, central venous pressure (CVP) monitoring, cardiac output (CO) monitoring, and blood oxygenation and organ perfusion monitoring (Table 32-1). Use of any technology must be associated with a therapy and a response to therapy—functional hemodynamic monitoring. Applying a technology without a therapeutic strategy limits any potential benefit. In practice, it is best to use more than one approach and monitor therapeutic responses (Table 32-2).¹

Blood pressure is the force exerted by the circulating blood through a blood vessel. Assessing arterial pressure is very important, as hypotension implies tissue hypoperfusion; shock is a state of organ hypoperfusion but is not always associated with hypotension. Hypotension is always pathologic and reflects a failure of normal circulatory homeostatic mechanisms, whereas normotension does not necessarily indicate cardiovascular stability. Normal blood pressure can occur in the setting of profound circulatory shock in the face of significant vasoconstriction or in a patient with antecedent high arterial pressure. For example, a patient in cardiogenic or hypovolemic shock may remain normotensive because of a marked increase in vascular resistance.

OPTIMAL BLOOD PRESSURE

Arterial pressure is the input pressure for organ perfusion and is a function of peripheral vascular resistance and blood flow. There is no absolute level of normal CO in the unstable, metabolically active patient because CO is proportional to metabolic demand. However, organ perfusion pressure becomes compromised as mean arterial pressure (MAP) decreases below 60 mm Hg and/or cardiac index (CO/body surface area) decreases below 2.0 L/min/m².

Optimal MAP varies depending on the underlying cause of hemodynamic instability. In distributive shock, such as refractory septic shock, increasing MAP >65 mm Hg with fluids and vasopressors increases oxygen delivery but does not improve outcome, indices of organ perfusion, or survival.²

The American College of Cardiology/American Heart Association guidelines in 2004 recommend targeting a systolic pressure of at least 80 mm Hg in patients with acute myocardial infarction. In traumatic brain injury, a systolic pressure <90 mm Hg is an independent predictor for increased morbidity and mortality. A higher blood pressure may be required to maintain optimal cerebral perfusion pressure of 50 to 70 mm Hg (cerebral perfusion pressure = MAP – intracranial pressure), such that MAP <80 mm Hg may be an independent predictor of worse outcome.³ In patients with hemorrhagic shock, delayed fluid resuscitation and toleration of a MAP of 40 mm Hg until definitive surgical intervention may improve survival.⁴ The International Consensus Conference recommends a target MAP of 40 mm Hg in uncontrolled hemorrhage due to trauma, a MAP of 90 mm Hg for traumatic brain injury, and a MAP >65 mm Hg for other forms of shock.⁵

Blood pressure varies with each heartbeat. The systolic pressure is the maximum pressure during ventricular ejection, and the diastolic pressure is the lowest pressure in the blood vessels between heartbeats during ventricular filling. Because the vascular circuit is elastic, both systolic and diastolic pressures vary throughout the vascular system. Systolic pressure can increase by up to 20 mm Hg, while the diastolic pressure similarly decreases as the pressure wave moves peripherally from the aorta. However, MAP (Formula 1) varies by only 1 to 2 mm Hg, whether measured centrally or peripherally; in practice, estimate MAP using the sum of the diastolic pressure and one third of the pulse pressure (Formula 1).⁶

PALPATION

Ability to palpate the radial, femoral, or carotid pulse in an emergency situation is traditionally thought to represent a minimum systolic pressure of 80, 70, or 60 mm Hg, respectively. However, confirmatory data are lacking, and these estimates may overestimate systolic pressure when compared to invasive measurements in patients with hypovolemic shock.

SPHYGMOMANOMETRY

Auscultation for blood pressure began with the invention of the sphygmomanometer by Scipione Riva-Rocci in 1896 and was later refined by Nicolai Korotkoff in 1905. To auscultate for blood pressure, place a cuff around the upper arm. Hold the bell of the stethoscope over the brachial artery as the cuff is gradually inflated to at least 30 mm Hg above the point at which the radial pulse disappears. Next, deflate the cuff at a rate of 2 to 3 mm Hg per second. The appearance of tapping sounds (Korotkoff sounds) corresponds to the systolic pressure. The diastolic pressure corresponds to the disappearance of Korotkoff sounds. Appropriate cuff size, cuff placement, proper placement of the stethoscope bell, appropriate cuff deflation rate, auscultation of Korotkoff sounds, dysrhythmia, observer bias, and faulty equipment all contribute to variability in the auscultatory method. Ideal cuff sizes are noted in Table 32-3.

An inappropriately small cuff for the size of the arm results in falsely elevated blood pressure measurements. A cuff too large for the size of the arm results in falsely low measurements.

Sphygmomanometric measurements of blood pressure often report slightly higher systolic pressure and lower diastolic pressure than those reported from simultaneous direct measurement using an intra-arterial catheter. This is because the reflected pressure waves summate with cuff inflation and increase systolic pressure, whereas the ischemic vasodilation downstream from the occluded cuff decreases cuff opening diastolic pressure.

OSCILLOMETRY

Most clinical blood pressure monitors use oscillometry. The amplitude of the fluctuations (or oscillations) in blood pressure in a sphygmomanometer cuff is analyzed and converted to pressure measurements by a computer device without the need for auscultation with the stethoscope. With gradual deflation of the cuff, oscillations begin above systolic pressure. The point of maximum oscillation corresponds to MAP. The systolic and diastolic pressures are estimated by an empiric algorithm. Despite widespread use, controversy exists regarding the accuracy of oscillometric blood pressure monitors. When in doubt, use manual sphygmomanometric measurement of blood pressure.

PHOTOPLETHYSMOGRAPHY

To measure the beat-to-beat blood pressure and thus provide continuous blood pressure monitoring, Penaz developed a technique with a small finger cuff containing a photoplethysmograph.⁷ This device estimates blood volume in the finger with a light source on one side of the cuff and an infrared detector on the opposite side. The pressure in the blood vessels is proportional to the pressure in the cuff required to keep the blood volume constant. Special proprietary algorithms adjust for potential measurement errors caused by cold temperature or vasoactive agents.

In the vasoconstricted patient, noninvasive blood pressure measurements can underestimate systolic pressure by more than 30 mm Hg. MAP, however, is generally similar, whether measured noninvasively or invasively.⁸

The arterial catheter can be used for measuring MAP and pulse pressure, for estimating CO, and for repeated blood sampling. The International Consensus Conference for Hemodynamic Monitoring in Shock recommends invasive blood pressure monitoring for patients with refractory shock receiving vasoactive agents.⁵ Uses for arterial catheterization are described in Table 32-4.

The radial artery is used most frequently for arterial catheterization. The femoral artery is an alternative in emergent situations, and often easier to access than the radial artery, especially in hypotensive patients. Other potential sites include the axillary, brachial, dorsalis pedis, ulnar, tibialis posterior, and temporal arteries, although these sites are rarely used (see chapter 31, "Vascular Access.")

In the presence of vasoconstriction, femoral arterial blood pressure measurements are more accurate than radial artery measurements. The risk for infection and limb ischemia is similar between radial and femoral artery cannulation (Table 32-5).⁹ The primary risk of emergent femoral arterial catheterization is trauma to the artery during catheter insertion, with potential development of a pseudoaneurysm or retroperitoneal hematoma.

Placement of an intra-arterial catheter requires knowledge of the anatomic landmarks of the selected site. US guidance may be used.

The catheter can be inserted directly over a needle or by using the Seldinger technique over a guidewire. The Allen test, used to confirm collateral blood flow before radial artery catheterization, is inaccurate in predicting postcatheterization hand ischemia. In patients with profound hypotension, a cutdown may be required to cannulate the artery. After successful arterial catheterization, connection of the catheter to the pressure transducer should reveal an arterial waveform. The square wave flush test is applied to determine if artifacts in the tubing and recording system are damping the pressure measurements. See Figure 32-1 for the square wave flush test with intra-arterial blood pressure measurement.

An overdamped system suggests that trapped air bubbles in the tubing are falsely lowering pressure measurements. An underdamped system will overestimate systolic pressure and underestimate diastolic pressure. Of note, in both situations, MAP is the most accurate measure. Flushing the system should remove the air bubbles. If this does not fix the problem, replace the tubing.

By definition, CVP is the back pressure to systemic venous return, with high values indicating larger than normal volume returning to the heart from the systemic circulation. A number of factors contribute to the CVP value (Table 32-6). The use of CVP monitoring as a guide to resuscitation in critically ill patients is a subject of debate.

OPTIMAL CENTRAL VENOUS PRESSURE

CVP measurements range from 2 to 8 mm Hg in normal healthy individuals and are affected by multiple factors (Table 32-6).¹⁰ A single absolute CVP value helps most when very low (such as to exclude right heart failure in a patient with a normal MAP) or very high (such as to suggest right heart failure and/or volume overload). In general, a CVP <4 mm Hg in the critically ill patient should prompt fluid resuscitation with careful monitoring.⁵ However, CVP measures do not correlate with circulating blood volume or changes in blood volume.

Volume expansion in a healthy volunteer with normal diastolic compliance will immediately increase blood volume, whereas the CVP remains relatively normal. On the contrary, the same volume expansion in an elderly patient with cardiomyopathy, decreased diastolic compliance, and low circulating volume will elevate CVP (Figure 32-2).

Despite the limitations of CVP as a measure of blood volume, the classic "5-2 rule" can still provide a rapid estimation in the ED of volume status.¹¹ After initial CVP measurement, infuse 250 mL normal saline IV over 15 minutes (10 to 20 mL/min bolus). An increase in CVP >5 mm Hg indicates volume overload and discontinuation of fluid. An increase in CVP of ≤2 mm Hg indicates hypovolemia and justifies additional fluid challenge. "Volume responsiveness" is the best use of CVP in resuscitation. A target CVP of 8 to 12 mm Hg during resuscitation of the critically ill patient has been advocated, but the relative response will better guide therapy than any target alone.¹²

Always measure CVP at end-expiration in both spontaneously breathing and mechanically ventilated patients. During spontaneous inspiration, the decreased intrathoracic pressure decreases transmural pressure in the heart, resulting in a decreased CVP. Conversely, intrathoracic pressure increases during an inspiratory breath of mechanical ventilation, resulting in an increase in CVP. Significant variation in inspiratory and expiratory CVP measurements suggests a compliant heart wall that will most likely respond to volume infusion. Conversely, the lack of respiratory variation in CVP may indicate that the heart is on the flat part of the cardiac function curve and will no longer respond to fluids.

JUGULAR VENOUS PULSATION

Observing internal jugular venous pulsation is a method to estimate right atrial pressure. The sternal angle is roughly 5 cm above the center of the right atrium regardless of the patient's position. With the patient sitting at a 45-degree angle, add 5 cm (distance from the sternal angle to the right atrium) to the vertical distance between the jugular pulsation and the sternal angle to estimate CVP in cm of water (cm H₂O). A pulsation >4.5 cm vertically above the sternal angle when the patient is sitting at 45 degrees indicates a CVP of >9.5 cm H₂O (Figure 32-3). In patients with heart failure, an elevated jugular venous pressure is independently associated with adverse outcomes, such as hospitalization and death.¹³ Visualization of the internal jugular vein pulsation by physical examination is not always possible in the ED in obese or uncooperative patients.

ULTRASONOGRAPHY

US is a valuable tool to visualize the neck veins for central venous catheterization. It can also be used to determine elevated jugular venous pressure and provide a noninvasive method for measuring CVP. The right jugular vein is examined using a high-frequency linear transducer (7 to 9 MHz). The jugular venous pulse is the site where the vein tapers, resembling the neck of a wine bottle (Figure 32-4). Measure the vertical distance in centimeters between this point of vein collapse and the sternal angle and add 5 cm to obtain a CVP measurement in cm H₂O.

If the jugular vein is distended and larger than the adjacent common carotid artery when viewed in the transverse plane with the patient in a semi-upright position, then the CVP is >10 cm H₂O.

A nearly collapsed internal jugular vein on the transverse view in the supine position indicates a very low CVP. Correlation between US and echocardiogram is very good at high measurements.¹⁴ Bedside US interpretations agree with formal echocardiographic estimates, with 83% for high, 67% for moderate, and 20% for low CVP measurements.

Traditionally, CVP is monitored with a fluid-filled catheter inserted in the internal jugular or subclavian vein proximal to the right atrium. The distal tip sits in the superior vena cava. Indications for central venous catheterization include fluid and vasopressor administration, unsuccessful or inadequate peripheral venous access, central venous oxygenation (ScvO₂) measurement, pulmonary artery catheterization, and transvenous pacemaker placement. Further details regarding central venous cannulation are provided in chapter 31.

After successful catheter insertion and radiographic verification, connect the catheter to a manometer or a pressure transducer of a monitor for continuous CVP waveform display. Place the transducer at the level of the right atrium, approximately 5 cm below the sternal angle. An acceptable CVP waveform is needed to accurately interpret the measured values (Figure 32-5). The c-wave represents bulging of the tricuspid valve into the right atrium and occurs at the onset of systole. The base of the c-wave is used to determine a CVP value because it is the final pressure in the ventricle before the onset of contraction, reflecting preload.

Measurement of CVP from the internal jugular or subclavian vein is ideal. However, at times, measurement using femoral vein catheterization is required, such as in patients with coagulopathy, patients in whom subclavian and/or internal jugular vein catheterization is unsuccessful or has resulted in a complication, or when immediate central venous access is required. While not preferred, femoral CVP measurements are reliable.¹⁵

Oxygen delivery is a function of arterial oxygen content and CO. Perfusion pressure is the most important driving force determining regional blood flow, which in the aggregate defines CO. Because the primary goal of resuscitation from shock is to reverse tissue hypoperfusion, CO is often considered the ideal indicator of perfusion and oxygen delivery.

OPTIMAL CARDIAC OUTPUT AND DETERMINING FLUID RESPONSIVENESS

Traditionally, Starling's law (Figure 32-6) guided resuscitation care, with an increase in CO of greater than 15% after a fluid challenge considered the standard for assessing ideal fluid replacement. The most important contributor to increasing CO is increasing preload by successive fluid challenges.

VOLUME RESPONSIVENESS IN MECHANICALLY VENTILATED PATIENTS

Respiratory variations in blood pressure may aid in assessing volume status in the mechanically ventilated patient. Positive-pressure mechanical ventilation alters venous return and induces several predictable cyclic changes in vena caval diameters, pulmonary blood flow, and left ventricular output (Figure 32-7). In the volume-responsive patient, increasing intrathoracic pressure during positive-pressure inspiration will decrease venous return by decreasing the pressure gradient, which causes superior and inferior vena cava narrowing, decreased pulmonary blood flow, and a three- to four-beat phase lag decrease in left ventricular stroke volume and arterial pulse pressure.¹⁶ A pulse pressure variation >13% predicts a >15% increase in CO in response to a 500-mL crystalloid bolus.¹⁷

Continuing fluid administration until the pulse pressure variation between inspiration and expiration decreases to <10% improves outcomes.¹⁸ Because arterial pressure is directly proportional to stroke volume, stroke volume variation strongly predicts fluid responsiveness, with a sensitivity of 81% and specificity of 80%.¹⁹ A disadvantage of this technique is that the patient must be fully in synchrony with the positive-pressure mechanical breaths and without vigorous spontaneous breathing or dysrhythmia for stroke volume variation to be accurate. Nonetheless, this technique is useful to assess volume responsiveness in the sedated and ventilated patient.

VOLUME RESPONSIVENESS IN SPONTANEOUSLY BREATHING PATIENTS

Volume responsiveness in spontaneously breathing patients and those with dysrhythmias may be assessed by passive leg raising. Postural changes transiently increase venous return when the legs are raised to 30 degrees above the chest and held for 1 minute. This maneuver approximates giving a 300-mL blood bolus to a 70-kg patient. Changes in heart rate, blood pressure, CVP, or CO persist for approximately 2 to 3 minutes after passive leg raising. The dynamic increases in CO induced by passive leg raising are as sensitive and specific to predicting volume responsiveness as pulse pressure variation during positive-pressure mechanical ventilation.²⁰

Minimally invasive or noninvasive hemodynamic monitoring techniques to measure CO in the ED setting include thoracic electrical bioimpedance/bioreactance, esophageal Doppler US, transcutaneous Doppler US, and pulse pressure waveform analysis.

THORACIC ELECTRICAL BIOIMPEDANCE AND BIOREACTANCE

Thoracic electrical bioimpedance measures total blood flow within the aorta (or CO). Current is applied between the outer electrodes. The inner electrodes measure impedance to current flow through the thorax. Maximal current flow is along the path of least resistance (i.e., the great vessels). The change in impedance is proportional to change in volume and CO (Figure 32-8).²¹

Thoracic electrical bioimpedance was first used clinically to monitor CO in astronauts. CO measured with thoracic electrical bioimpedance correlates well with invasive measurements. It can also be used to differentiate cardiac from noncardiac causes of dyspnea and guide treatment in the ED.²² A limit of this technique is that patient movement decreases signal reliability and accuracy.

Bioreactance is a modification of bioimpedance. Bioreactance applies a signal filter to analyze frequency shifts traversing the thoracic cavity creating a greater signal-to-noise ratio than bioimpedance. It is less sensitive to patient movement and external interference, although the accuracy in measuring CO is debated.²³

ESOPHAGEAL DOPPLER US

Esophageal Doppler US measures instantaneous blood flow velocity in the descending aorta to determine stroke volume and CO (i.e., CO = stroke volume × heart rate). A Doppler transducer probe is inserted through the mouth or nose into the esophagus until its tip is at the midthoracic level. The probe is then rotated until the transducer faces the aorta to detect the characteristic aortic velocity signal profile (Figure 32-9).

Esophageal Doppler US CO readings correlate well with pulmonary artery catheter measurements.²⁴ However, this technique is operator dependent and often not well tolerated in awake patients, limiting ED use.

TRANSCUTANEOUS DOPPLER US

Transcutaneous Doppler US uses the same principles to measure CO as esophageal Doppler US. Measurements are obtained by applying the Doppler US probe at the sternal notch, with the US beam aimed at the ascending aorta. Significant operator training is required, again limiting the ED utility.²⁵

PULSE PRESSURE WAVEFORM ANALYSIS

Pulse pressure waveform analysis uses an indwelling intra-arterial catheter to measure CO. Proprietary algorithms use arterial pressure waveform (or the pulse contour) and arterial vascular compliance to derive CO. Depending on the manufacturer, the measured CO may have to be regularly calibrated with another reference standard, such as lithium. Other systems may require the patient's specific physical characteristics for calibration. This technology has not yet been tested within a treatment protocol for the ED setting.

CO is most commonly measured invasively with pulmonary artery catheterization using the thermodilution method. The benefit of using the pulmonary artery catheter for hemodynamic monitoring in the ED setting has not been investigated. Current expert consensus does not recommend the routine use of the pulmonary artery catheter in the management of the critically ill patient.^5,26 Given all this, pulmonary artery catheterization is usually avoided in the ED.

Blood pressure, CVP, and CO serve as macro-hemodynamic parameters. To assess tissue oxygenation or perfusion, venous oxygen saturation, serum lactate level, and tissue oxygenation provide further guidance during resuscitation.

CENTRAL VENOUS OXYGEN SATURATION

Venous oxygen saturation monitoring is a method to assess the relationship between tissue oxygen extraction, oxygen delivery, and oxygen consumption. A normal oxygen extraction ratio of 25% to 35% results in a venous oxygen delivery (reflected in venous oxygen saturation) of approximately 70% of arterial oxygen delivery. Venous oxygen saturation (SVO₂₎ is ideally measured in the pulmonary artery as a mixed venous sample (SmVO₂); this access point is generally not practical in the ED. Clinically, venous oxygen saturation reflects the balance between oxygen delivery and oxygen consumption, with low values reflecting inadequate delivery and/or excessive consumption.

Central venous oxygen saturation (ScVO₂) measurement only requires placement of a central venous catheter in the jugular or subclavian vein, making it an attractive alternative to SmvO₂. ScvO₂ can be easily measured by drawing a standard venous blood gas from the distal port of the central line and obtaining a measured oxygen saturation. Also, a special catheter allows continuous measurement if desired.

In healthy individuals, ScvO₂ is 2% to 3% less than SmvO_2; in shock states, ScvO₂ is typically 5% to 10% higher than SmvO₂ as blood flow is redistributed from the abdominal vascular beds to the cerebral and coronary circulation.²⁷ Although absolute values of ScvO₂ and SmvO₂ may be different, low values of either measurement reflect an imbalance in oxygen transport and portend worse outcomes. Most important, the two measures typically change in parallel and thus trends in SCVO₂ closely reflect trends in SmvO₂.²⁸

Clinical Use of Central Venous Oxygen Saturation

The principal value of ScvO₂ is its ability to detect occult inadequate oxygen delivery. During initial management, low ScvO₂ points to global tissue hypoxia despite normal vital signs and urine output. Left untreated, tissue hypoxia can lead to organ failure and death. Thus, regardless of the underlying pathophysiologic state (e.g., heart failure, septic shock, trauma), a low ScvO₂ value represents inadequate oxygen delivery relative to oxygen consumption. Troubleshooting a low ScvO₂ then focuses on the determinants of oxygen delivery (Is the patient hypoxic? Anemic? Is CO impaired, and if so, why? For example, low contractility, hypovolemia, or tamponade.). On the demand side, is oxygen consumption increased due to heightened metabolic demand such as from fever, pain, or seizure (Table 32-7)? Clinically, hypoxia and anemia are generally easily diagnosed and treated. A low ScvO₂ can detect occult low CO, prompting further investigation and therapy.

Normal (approximately 70%) or high ScvO₂ values do not necessarily mean that the patient is hemodynamically stable. ScvO₂ is a global measure of oxygen transport, and regional areas of tissue hypoperfusion can be present even with normal ScvO₂ values, particularly in the lower half of the body. In several disease states (e.g., hypothermia, terminal shock, cyanide poisoning), the ability of the tissues to extract oxygen from the blood is impaired, leading to "arterialization" of the venous blood with high ScvO₂.

Using ScvO₂ monitoring in a treatment protocol—targeting CVP 8 to 12 mm Hg, MAP >65 mm Hg, and ScvO₂ >70%—for septic shock patients early after arrival to the ED (or early goal-directed therapy) decreased mortality in single-center studies.^{12,29,30,31,32} However, new data showed this invasive approach had no improved outcome compared to usual care in a multicenter study enrolling patients after early recognition, fluid boluses, and antibiotics have occured.³³ These results show that CVP and ScvO₂-guided care may be an appropriate option in patients where shock is failing to resolve despite efforts to identify.

LACTATE

In critical illness, an oxygen debt develops when oxygen delivery is inadequate to meet tissue oxygen demand and compensatory mechanisms are exhausted. This results in global tissue hypoxia, anaerobic metabolism, and lactate production. High lactate is a well-established prognostic marker in critically ill patients with various forms of shock, a fact identified in the 1800s.³⁴

In addition to shock, causes of elevated lactate include seizure, diabetic ketoacidosis, malignancy, thiamine deficiency, malaria, human immunodeficiency virus infection, carbon monoxide or cyanide poisoning, and mitochondrial myopathies. Commonly used drugs, such as metformin, simvastatin, lactulose, antiretrovirals, niacin, isoniazid, and linezolid, can also cause a lactate elevation.³⁵

Blood lactate concentrations also reflect the interaction between its production and elimination. During critical illness, a patient with hepatic dysfunction may have a higher lactate level compared with another patient without liver disease due to impaired hepatic clearance. However, lactate elevation in a patient with chronic liver disease still portends a poor prognosis, because patients with liver disease do not commonly have a high lactate level in the absence of shock.³⁶

Clinical Use of Lactate

Hyperlactatemia is not always accompanied by hypotension or a low bicarbonate level and/or elevated anion gap; thus, the lactate level must be separately measured. Venous lactate levels correlate well with arterial lactate levels.³⁷ However, repeat any elevated venous lactate level if inconsistent with the clinical condition, preferably with an arterial measurement.

A lactate level ≥4 mmol/L in normotensive patients requires further attention, because this cutoff is associated with increased intensive care unit admission rates and mortality. Furthermore, persistent elevation in lactate for >24 hours is associated with increased mortality as high as 90%.³⁸ Lactate clearance (or the ability to decrease serum lactate levels) as early as 6 hours in patients with septic shock improves 60-day survival.³⁹ When included in a treatment protocol, lactate clearance is noninferior to ScvO₂-guided care in the ED.⁴⁰ However, targeting both lactate clearance and optimal ScvO₂ may result in better outcomes than either alone.⁴¹

TISSUE OXYGEN SATURATION

Tissue oxygen saturation (StO₂) can be measured by near-infrared spectroscopy, a noninvasive technique capable of continuous measurement using the varying light absorption properties of deoxygenated and oxygenated blood. Near-infrared light (680 to 800 nm) is largely transparent to biologic tissue, absorbed primarily by hemoglobin, and minimally affected by skin blood flow. Importantly, the near-infrared spectroscopy signal primarily reflects hemoglobin in the small end vessels and approximates the oxygen saturation of venous blood. Near-infrared spectroscopy StO₂ measurements correlate and trend with SmvO₂ and ScvO₂ and can detect occult regional hypoxia even when SmvO₂ and vital signs have normalized.⁴² However, darkly pigmented skin may impair measurement accuracy.

Clinical Use of Tissue Oxygen Saturation

StO₂ values reflect resuscitation adequacy and the magnitude of traumatic injury, as well as organ failure in critically ill patients.⁴³ An StO₂ <75% measured at the thenar eminence distinguishes severe shock patients from healthy volunteers. Dynamic measurements using a brief vascular occlusion test to measure changes in StO₂ may offer greater value than static StO₂ measurements.⁴⁴

Changes in StO₂ during the vascular occlusion test are associated with the need for emergency operation or transfusion within the first 24 hours of hospitalization in trauma patients.⁴⁵ However, StO₂ as a hemodynamic goal incorporated in an ED treatment protocol is still investigative.