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Basic standards for monitoring have been established by the ASA (Table 77-4) and should be used for the critically ill patient.29 The patient's systemic oxygenation (SpO2), ventilation (ETCO2), circulation (blood pressure and heart rate), and core temperature should be continuously monitored and evaluated during each anesthetic procedure.
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An oxygen analyzer to measure the oxygen concentration in the patient breathing system and a quantitative assessment of systemic blood oxygenation (eg, SpO2 via pulse oximetry) should be used to monitor adequate oxygenation. Ventilation should also be evaluated by clinical signs (eg, chest or abdominal excursion and auscultation of breath sounds) as well as quantitative continuous monitoring of the level of expired carbon dioxide. Monitoring the tidal volume of expired gas is strongly encouraged. There should be a rapid audible alarm if any of the components of the breathing system are disconnected.
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Each critically ill patient should have their electrocardiogram (ECG) continuously displayed, and blood pressure and heart rate should be determined and assessed every 5 minutes at a minimum. To ensure the adequacy of the patient's circulatory function, the patient should be continuously evaluated by either palpation of an arterial pulse (at a minimum), auscultation of heart sounds, observing the trace of intraarterial systemic pressure, ultrasound peripheral pulse velocity monitoring, pulse plethysmography, or oximetry.
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Core temperature monitoring should be used when clinically significant changes of body temperature are likely.
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Because of possibly rapid changes of hemodynamic status occurring during anesthesia, there must be qualified anesthesia personnel to monitor the patient and provide care throughout all general and/or regional anesthetics and during monitored anesthesia care.
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Additional monitors may be needed to provide an accurate picture of the patient's hemodynamic status and to guide therapy to optimize the patient's condition. However, there are limitations to each monitor and some risk to the patient when using invasive monitors. Thus the anesthesiologist must be cognizant of these limitations and weigh the risks and benefits of invasive monitoring to choose appropriate monitors for each critically ill patient (Table 77-5).
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Invasive Arterial Pressure Monitoring
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Because shock represents failure of the circulatory system to maintain adequate delivery of blood flow to tissues, and the goal of hemodynamic therapy is to restore adequate tissue perfusion, systemic pressure measurement is the most frequently used parameter to indirectly assess perfusion.
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In healthy individuals, blood pressure as determined by noninvasive blood pressure (NIBP) monitors is, on average, within 5 mm Hg of measurements obtained by direct arterial pressure monitoring. Sources of error in NIBP measurements include using the incorrect cuff size or highly irregular or rapid cardiac rhythms. However, in shock states, NIBP measurements are often inaccurate. Therefore, inserting an arterial catheter provides a more accurate and reproducible measurement of systemic arterial pressure. Invasive arterial monitoring allows beat-to-beat display so decisions regarding therapy can be based on continuous blood pressure analysis.
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Blood pressure does not directly equate to tissue blood flow, and the level of mean arterial pressure (MAP) to aim for is not necessarily the same in all patients. Below a MAP of 60 mm Hg, autoregulation of the coronary, renal, and central nervous system vascular beds is compromised and organ flow becomes linearly dependent on pressure. Thus in adults, maintenance of a MAP 65 mm Hg or higher is recommended to maintain and optimize flow.4 However, because the loss of autoregulation may occur at different levels in different organs, some patients require higher blood pressures to maintain adequate tissue perfusion. Furthermore, the degree to which flow autoregulation remains intact in septic patients is uncertain. Thus it may be necessary at times to supplement blood pressure measurement with other means of assessing regional and global perfusion (eg, urine output; see section on downstream monitoring).
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The invasive arterial pressure waveform can also be used to estimate blood volume status and assess fluid responsiveness in mechanically ventilated patients. A positive pressure breath reduces venous return and decreases left ventricular filling resulting in a decreased stroke volume, CO, and blood pressure. This effect can be especially marked in hypovolemic patients. Marked variations in pulse pressure, which is proportional to stroke volume, and systolic pressure tracing variations usually predict that an increase in CO will occur with volume loading.30,31
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Central Venous Pressure Catheter
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Systemic hypotension is the most common reason to initiate invasive central hemodynamic monitoring in the critically ill patient. The central venous pressure (CVP) reflects pressure in the large systemic veins. Although the CVP also reflects intravascular volume, it does not measure blood volume directly and is influenced by right-heart function, venous return, right-heart compliance, intrathoracic pressure, and the patient's positioning. Consequently, the CVP level should be interpreted with other measures of cardiac function and circulating volume (eg, pulse, blood pressure, urine output). A single CVP value may not be as important as serial CVP measurements or their change with therapy.
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Measurement of the CVP may provide useful information in patients with normal cardiac function who are hypotensive because of blood loss or widespread vasodilatation because a decreased venous return will result in a falling right atrial pressure and CVP. A central venous catheter (CVC) should be inserted when an infusion of vasopressors or inotropes is planned.
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Pulmonary Artery Catheter
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In addition to the CVP, a flow-directed pulmonary artery catheter (PAC) allows measurement of the pulmonary artery pressure, the pulmonary artery occlusion pressure (PAOP), the CO, and the mixed-venous oxygen saturation (SVO2). The PAOP reflects the pulmonary venous pressure and the left atrial and left ventricular end-diastolic pressure and therefore can provide a crude indirect estimate of left ventricular end-diastolic volume (LVEDV). Indications for placing a pulmonary artery catheter are related to the planned procedure and the patient's state of health (Table 77-6). The pulmonary artery catheter may provide useful information in any procedure associated with acute, severe changes of preload, afterload, or myocardial contractile state. For example, procedures where blood loss may be massive or where partial or complete caval occlusion might occur can cause acute changes of cardiac preload. Similarly, proximal aortic cross-clamping can cause a rapid increase of left ventricular afterload. Patient factors that can lead to the insertion of a PAC include septic shock or other significant cardiac, respiratory, or renal disease. In septic shock, both hypovolemia and myocardial dysfunction may contribute to impaired tissue perfusion. Pulmonary artery catheter placement can be used both to monitor CO and assess ventricular stroke volume.
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Unjustified use of the pulmonary artery catheter has been suppressed by the publication of an observational study demonstrating an increased mortality associated with the use of the pulmonary artery catheter in critically ill patients during the first 24 hours of intensive care as compared with case-matched controls.32 Multiple randomized controlled trials evaluating the use of the PAC in many different patient populations have not demonstrated a decreased overall mortality or obvious benefit.33-35 In all of these studies, the PAC has proven primarily to be a diagnostic tool. The studies also highlight our lack of consensus and data about our therapeutic interventions that will improve the outcome of the critically ill patient in shock.
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A major pitfall of central pressure monitoring occurs when pressure alone is used to estimate volume. Important variables in addition to the volume of the systemic and pulmonary circulations can affect the central pressure measurement. The relationship between pressure and volume is controlled by the compliance of the chamber. In patients with an abnormal left ventricular compliance, the PAOP may over- or underestimate the LVEDV. Right ventricular (RV) dysfunction is common in critically ill patients and can result from pulmonary embolism, severe acute respiratory distress syndrome (ARDS), or other conditions that increase RV afterload, such as high levels of PEEP or an increased pulmonary vascular resistance as a consequence of other vascular, cardiac, metabolic, or pulmonary causes. Because the right and left ventricles are both enclosed within the relatively stiff pericardium, pressure and volume overload of the RV can lead to abnormal motion of the interventricular septum and will impair left ventricular (LV) relaxation. In this situation, the pressure–volume relationship of the left ventricle is altered, and information obtained from the PAC may be misleading. Other factors that can affect the ability of central pressures to reflect ventricular filling volumes include increased intrathoracic pressures and valvular lesions. Increased intrathoracic pressure caused by positive pressure ventilation or increased intra-abdominal pressures can also elevate central vascular pressures. Stenotic lesions of the atrioventricular valves can also elevate central vascular pressures.
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Other potential pitfalls include problems with the transducer system (eg, improper transducer placement or reference level zeroing), improper interpretation of waveforms, and erroneous thermodilution CO measurements due to errors of injectate volume or temperature. The presence of marked tricuspid valve regurgitation, which can occur in the critically ill patient as a consequence of high pulmonary artery pressures, can also produce erroneous CO measurements. Mixed venous blood gas tensions and saturation measurements may be invalid if the blood gas analysis is inaccurate or if the pulmonary artery specimen is "arterialized" by being withdrawn from a wedged or partially wedged PAC.
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There are major but uncommon complications associated with the presence of a PAC. Rupture of the pulmonary artery is a rare occurrence (<1%) but a potentially catastrophic one with a mortality rate approaching 50%. Patients who have pulmonary hypertension, are older than 60 years, or are receiving anticoagulation therapy are at greater risk. The sudden onset of hemoptysis (especially after inflation of the pulmonary artery catheter balloon) is a sign of possible pulmonary artery rupture. Immediate management includes lateral decubitus positioning the bleeding side down, intubation with a double-lumen endotracheal tube, and increasing PEEP. Embolization via angiography, or even a lobectomy, may become necessary if pulmonary bleeding continues or is massive. The incidence of pulmonary infarction associated with the use of the pulmonary artery catheter is less than 7% and usually caused by unintentional distal migration of the PAC tip. Catheter-related thrombi may also cause pulmonary infarction. Infection related to the PAC is fairly common with a risk for clinical sepsis of less than 0.5% per day of catheter use.
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Thus hemodynamic measurements obtained from a PAC should be interpreted with the full knowledge of possible confounding factors. It may often be more appropriate to respond to trends of change in central hemodynamic measurement (eg, a slowly falling pulmonary capillary wedge pressure or CVP) rather than to the absolute values themselves.
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In view of the risks and benefits of pulmonary artery catheterization, other noninvasive methods for improving monitoring and resuscitation have been developed and evaluated. Echocardiography has been used in the operating room since the 1970s. Transesophageal echocardiography (TEE) is preferred in the operating room because the acoustic images of transthoracic echocardiography (TTE) are generally poorer than those of TEE.36 Furthermore, factors such as patient positioning, the surgical field, and surgical equipment, drapes, or other monitors may block access to the chest, limiting the usefulness of TTE.
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There are some important limitations to TEE.36 Some regions of the heart and great vessels cannot be well visualized. Insertion and manipulation of the TEE probe can produce pharyngeal and/or laryngeal trauma, dental injuries, esophageal trauma, arrhythmias, and hemodynamic effects. The inaccurate interpretation of TEE images may result in improper clinical decisions by the anesthesiologist or surgeon. The performance of TEE will require the anesthesiologists' time and attention and may thus detract from other intraoperative responsibilities or delay other important interventions.
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Nevertheless, the role of TEE is expanding both in the operating room and the ICU. Current indications for the use of intraoperative TEE include the diagnosis of myocardial ischemia, confirmation of the adequacy of valve reconstruction and other surgical repairs, and determining the causes of hemodynamic instability and other intraoperative complications.36 TEE can readily provide information on biventricular volumes and contractility, and valvular and wall-motion abnormalities.
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The perioperative period is a time of increased risk of myocardial ischemia as a result of hemodynamic and other physiologic stresses associated with anesthesia and surgery. Wall-motion abnormalities generally precede ECG changes during myocardial ischemia37 and may allow earlier detection of ischemia. The incidence of regional ventricular dysfunction detected by TEE ranges from 10% to 60% in various surgical populations.36 Intraoperative TEE detection of ischemia may permit corrective interventions such as altering surgery and/or anesthetic management, initiating infusions, and postoperative triage, which may prevent perioperative complications. There is a lack of studies demonstrating that the detection and treatment of regional ventricular dysfunction or other TEE evidence of ischemia can improve perioperative clinical outcome or increase long-term survival.
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Perioperative TEE is often used emergently to determine the cause of acute persistent, life-threatening hemodynamic disturbances. However, elective use of the TEE should be considered in the care of the critically ill surgical patient. TEE has become a useful tool for assessing hemodynamic function qualitatively and for imaging the heart (eg, to diagnose a hemopericardium or cardiac tamponade). It provides an assessment of LV function and an indirect measurement of CO, contractility, and left, and often right, ventricular volume. Because of the limitations in using catheter-derived pressure data to estimate LVEDV, TEE may determine the precise causes of hemodynamic instability (eg, a low CO) in patients with left ventricular dysfunction in a more useful fashion than the PAC.
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Esophageal Doppler monitoring measures aortic flow velocity in the thoracic aorta. A fixed relationship between aortic blood flow and CO is assumed, and thus CO can be calculated using this relationship. The esophageal Doppler is smaller than an ordinary transesophageal echocardiographic probe and thus less invasive. There have been no case reports of esophageal perforation and only reports of minor complications such as mucosal trauma and endobronchial placement. However, proper positioning of the probe is necessary to get an optimal waveform. Although the correlation between CO measured by esophageal Doppler and PAC is modest, there is an excellent correlation with the change in CO with therapeutic interventions.38 One meta-analysis found that use of the esophageal Doppler to guide intraoperative fluid management resulted in an increase of the amount of fluid administered and a reduced length of hospital stay, time to resume full oral diet, and postoperative morbidity or complications.39
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Downstream Markers of Organ Perfusion
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Derangement of blood flow at the capillary and tissue level is one of the critical pathogenic events in sepsis and is associated with multiorgan failure and mortality.40 The relationship between global hemodynamics as measured by blood pressure, CVP, and CO and microcirculatory blood flow is incompletely understood. Thus, although practice parameters suggest maintaining a MAP of 65 mm Hg or more,4 it is unclear this pressure ensures adequate tissue perfusion. In practice, indices of organ function, such as ECG evidence of myocardial ischemia, urine output, chemical measurements of blood urea nitrogen and creatinine, and liver function tests, are used to indirectly assess the adequacy of regional perfusion.
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Blood lactate levels are a product of anaerobic metabolism and an indirect marker of tissue perfusion and the adequacy of resuscitation. An elevated blood lactate concentration (>4 mEq/L) is associated with a high risk of death, and the rate of blood lactate clearance is a good marker of outcome.38 Because lactate clearance lags therapeutic interventions, lactate levels are not suited for immediate assessment of resuscitation. A recent multi-institutional study reported no survival difference in patients with severe sepsis who were resuscitated to normalize CVP, MAP, and either a lactate clearance of 10% or a normalized central venous oxygen saturation (ScVO2).41
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Gastric tonometry is a method used to assess regional perfusion of the gut. A balloon is placed in the stomach to measure the intramucosal partial pressure of carbon dioxide (Pco2). This in turn is used to indirectly determine gastrointestinal mucosal pH (pHim). Hypoperfusion causes mucosal carbon dioxide (CO2) to increase and produces gut tissue acidosis. Because CO2 readily diffuses across membranes, the PCO2 in the gut lumen leads to an increase in the gradient between arterial and luminal PCO2. Tonometry provides an indicator of the gut's blood flow-to-CO2 production ratio because a decreased pHim may arise as a result of either decreased blood flow or increased CO2 production. A low gastric pHim and increased gastric luminal PCO2 are highly predictive of postoperative complications.42 Although tonometry is a reasonably good predictor of mortality in critically ill patients,43 its usefulness as a therapeutic guide in patients with sepsis and septic shock has not been proven.
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Mixed venous oxygen saturation (SVO2) is measured either in the pulmonary artery with a PAC or estimated via the right atrium with a CVC. It can be used as an end point for therapeutic interventions.10 A low SVO2 may be due to increased oxygen consumption or a decreased hemoglobin, CO, or arterial oxygen saturation. Its major disadvantage is that it is a global measurement, and thus blood from vital organs with low tissue PO2 will be diluted by blood from organs with lower metabolic requirements and a higher PO2. Furthermore, in sepsis, there may be organ or tissue shunting at the microcirculatory level resulting in a higher SVO2.