Chapter 6 _ Hemodynamic Monitoring | Chapter6 121 Hemodynamic Monitoring Michael R. Pinsky, MD, CM, Dr h.c., FCCP, MCCM cardiovascular function, minimally invasive, | monitoring, pulmonary artery catheter, shock, | thermodiution | Key words: haan mnitrig, | | Disclosures: The author has consulted for and received honoraria/speaking fees from Eduvards Lifesciences, LiDCO Lid, and Cheetah Medical. He holds stock options in LIDCO Lid. and Cheetah. He has received or applied for patents 6776764 and 11/388861. This work was supported in part by NIH grant HL67181 ‘The purposes of hemodynamic monitoring are to characterize the cardiovascular state of the individual, identify cardiovascular insufficiency and its most probable ses, and monitor response to targeted therapies aimed a restoring cardiovascular sufficiency. The previous shock. It chapters outlined the various forms of circulator is within this physiological framework that interpretation of data derived from hemodynamic monitoring arises. shock and systemic hypotension are medical sustained, even for a short time, they will result in end-organ dysfunction and increased sand mortality. The basic tenet of resuscitation is to provide adequate oxygen (O.) delivery (DO,) to ‘meet metabolic demand and reverse any existing tissue hypoperfusion. Accordingly, the choice of monitoring technique must be individualized for each patient. In general, noninvasive continuous monitoring, if available and accurate, is preferred to invasive intermittent monitoring, In realty, some degree of inv ness ‘of monitoring is often required to accurately assess the physiological data in a continuous fashion in the monitoring and management of the critically ill patient, ‘The principal hemodynamic monitoring biomarkers discussed in this chapter are arterial pressure, central venous pressure, pulmonary artery pressure and its, occlusion pressure, estimates of cardiac output (CO), and the various ways of ass ing oxygenation, Like all vascular monitoring using fluid-filled catheters connected to electronic pressure transclucers, hemodynamic monitoring122 Chapter & | Comprehensive Critical Care: Adult requires an open tubing system without obstruction atthe tip (often due to blood clots). climination of air bubbles in the hing that dampen the signal, and hydrosta ic zeroing to the isosbestie point (S em below the manubrium stern) in order to measure dynamic and mean pressure and arterial pressure-derived estimates of (CO, However, unlike other vascular pressure measures, arterial pressure has large pressure swings associated with rapid acceleration and deceleration, and these demand ‘hat stiff and short tubing be used to connect the intra- arterial catheter to the pressure transducer.‘ The technical aspects of measuring pressures and pressure-derived CO are beyond the scope of this chapter. Similarly, measures 0f CO by indicator dilution require complete indicator mixing, no early recirculation (eg, intracardiac shunts), and an appropriate sensor. All commercially available indicator curate Sensors, so most dilution devices have sulficiently ‘measurement errors come {rom incomplete indication mixing or early recirculation artifacts ARTERIAL BLOOD PRESSURE Arterial blood pressure isthe primary force driving blood into the tissues. Thus hypotension is a medical emergency because it not only causes tissue hypoperfusion but also cffeetively abolishes normal autoregulation of blood flow distribution. Furthermore, owing to baroreceptor feedback and the inereased use of Badrenergic blocking ‘often neither tachycardia nor hypotension occurs in shock. agents, tumtil the final terminal stages* Blood pressure varies phasically with each heartbeat. Systolic pressure is the maximum pressure during ventricular ejection, and diastolic pressure isthe Lowest pressure in the blood vessels between heartbeats during ventricular filling as the stored arterial blood runs off into the periphery. The systolic to diastolic pressure Uitference is called the pulve pressure and is determined by lelt ventricular (LV) stroke volun arterial n extent the rate of LV cent capacitance, and to a cert ejection. Since the arterial circuit is elastic and funetions as both a resistor to prevent pacitor for the ejected blood and an outtlow pid decreases in arterial pressure in diastole, both systolic and diastole pressures vary across the vascular tree. Systolic pressure usually increases from central to peripheral sites whereas diastolic pressure decreases slightly. Mean arterial pressure (MAP), ‘estimated as the sum of diastolic pressure plus one-third ‘of the pulse pressure, is the primary driving pressure for cerebral and peripheral organ perfusion. Coronary perfusion is primarily determined by diastolic arterial pressure because cardiac contraction during systole otherwise stops intramyocardial blood flow. Importantly, MAP throughout the large to medium-sized arteries is, constant because these central arteries have almost no ‘measurable resistance, Noninvasive Measures of Arterial Pressure The most common way of measuring arterial pressure is with a sphygmomanometer.’ This is often automated using an oscillatory algorithm that senses flow. There is inction between the automatic blood fundamental dis pressure measures (eg, Dynamat) and auscultation-defined measures of blood pressure using Korotkoif sounds In an unstable patient, one should not rely on noninvasive ‘automatic measures of blood pressure, because the oscillatory sensing algorithm degrades, but rather should ‘measure blood pressure manually using a stethoscope."? Sphygmomanometric measurements of blood pressure often give slightly higher systolic pressure and lower diastolic pressure than those reported from simultaneous dinect measul ment using an intra-arterial catheter. This is because with culf inflation the reflected pressure waves summiate, ine: vasodilation downstream from the occluded cuff decreases x systolie pressure, whereas the ischemic cutf-opening diastolic pressure. Invasive Measures of Arterial Pressure Intra-arterial catheterization isthe reference method for bloox! pressure measurement and should be used inall hemodynamically unstable patients in whom accurate and continuous measures of arterial pressure are required, The reason for this statement, which may be at ‘odds with prior recommendations. is that intra-arterial catheterization provides instantaneous measures of MAP,arterial pulse pressure, pulse pressure variation, and CO) with newer transducer technologies. The arterial catheter allows easily repeated blood sampling for chemistries and blood gas analysis The most frequently used site for arterial catheterization is the tery, Femoral artery ion is also used and can be easier to perform catheter in hypotensive patients although it is associated with more complications when the catheter is left in place. Still in the profoundly vasoconstricted patient, radi arterial pressure can underestimate central arterial pressure measured more proximally.’ Arterial Pressure Targets ‘Once one measures arterial pressure, the major question is the target range of pressures to be maintained in order to sustain organ perfusion without exeessively increasing LV afterload. Hypotension decreases organ perfusion pressure and blood flow, stimulating a sympathetic response to, increase vasomotor tone, heart rate, and contractility. The ‘change in local vasomotor tone in response to decreased arterial pressure forms the basis of autoregulation to maintain constant blood flow. Cardiac output is important to sustain an adequate and changing blood flow to match changes in vasomotor tone such that arterial pressure to the organ remains optimal. Since CO is proportional to metabolic demand, which itself can vary 3-fold in a ‘matter of minutes, there is essentially no normal CO in the critically il patient, However, as MAP decreases below 65 mm Hg in a previously nonhypertensive patient, organ perfusion becomes compromised. Thus a reasonable arterial pressure target is a MAP between 90 and 60 mm Hg." although the optimal MAP will vary depending ‘on the underlying cause of hemodynamic instability." To assess the adequacy of MAP to sustain peripheral perfusion, the bedside clinician needs to assess additional ‘measures of organ perfusion, such as mixed venous O, saturation (Svo,).central venous O, saturation (Seve, lac ‘acid levels, urine output, capillary blood flow, or gastric mucosal Pco, The fist 2 of these parameters are, discussed further subsequently. Finally, cerebral perfusion isa function of MAP relative to intracranial pressure. Thus, in the setting of neurotrauma cerebral perfusion pressure ‘must be measured. As a general rule one should target a Hemodynamic Monitoring | Chapter 123 MAP of 90 mm Hg for traumatic brain injury" and a MAP. greater than 65 mm He for other forms of shock, CENTRAL VENOUS PRESSURE Although central venous access is often used as a secure ¢ for infusion of fluids and vasoactive venous acces drugs as well as sampling of blood for various things including Sevo, its use in assessing intravascular volume status is poor. Central venous pressure (CVP) is not a ‘measure of central blood volume nor can its values be used to determine whether a patient will be volume responsive. Still, dynamic decreases in CVP of greater than 2 mm Hg during spontaneous inspiration appear to identify those patients who are volume responsive independent of the absolute CVP value." CVP is the back pressure to systemic venous return; thus, high CVP (12 mm Hg) indicate a larger than normal mean systemic pressure allowing an adequate perfusion pressure gradient to sustain venous return.* However, CVP in and of itself does not reflect blood volume status. From the perspective of patient safety, the insertion of a central venous catheter using ultrasound guidance for internal jugular vein insertion has also become part of standard care and has markedly reduced complications.” Noninvasive Measures of CVP Central venous pressure can be estimated noninvasively by inspection of jugular venous pulsation. With the patient sitting at 45°, the height of the jugular venous distention fabout S em above the stimate CVP® Potentially, this approach is most useful in documenting sin JVD® on phasic increases in JVD (IVD) above the sternal angle center of the right atrium) can be used to sustained incre with spontaneous inspiration, suggesting cor pulmonale or pulmon: in atrial fibrillation, y hypertension, and periodic cannon waves seen Invasive Measures of CVP Although CVP is usually measured from the internal jugular or subclavian vein via an indwelling catheter, it can ‘be estimated from a femoral venous site as long as there124 Chapter | Comprehensive Critical Care: Adult intra-abdominal pressure <12 mm Hg). Using the femoral site for a central is no intra-abdominal hypertension (i venous catheter is also associated with a greater incidence of complications The effects of the respiratory eyele on al intrathoracic vascular pressures must be considered when ‘examining a continuous CVP measurement. To minimize the pressure artifact induced by respiratory pressure changes, I intrathoracic vascular pressures should be ‘measured at end-expiration. In the dyspneie patient ora patient who is fighting the ventilator, determination of end- expiration can be very difficult, it not impossible, Extreme caution needs to be used when estimating CVP under these conditions, PULMONARY ARTERY PRESSURE AND PULMONARY ARTERY OCCLUSION PRESSURE Bedside balloon flotation insertion of a pulmonary artery of right atrial, pulmonary arterial, and pulmonary artery occlusion pressure (Ppao) plus CO and mixed venous ©, saturation defined hemodynamic monitoring in critica than 40 years" Pulmonary artery pressure is measured from the tip of a nonoccluded pulmonary artery catheter catheter and subsequent measure care for more once this catheter has been floated past the pulmonic valves into the main pulmonary arteries Mean pulmonary artery pressure measures can be calculated similarly to MARoas described previously, with the proviso that they are measured at endhexpiration. Thus, one can measure tery systolic, diastolic, and mean pressures. pulmonary Mean pulmonary artery pressure is usually used to assess input pulmonary vascular pressure for calculating, pulmonary vascular resistance (PVR), whereas systolic pulmonary artery pressure reflects the afterload against which the right ventricle ejects, By balloon inflation and migration of the ea a medium-sized pulmonary arte heter tip into where itis occluded,one ean measure Ppao, Pulmonary artery oeclusion pressure is used most often to asess PVR, pulmonary edema, intravascular volume status and LV pretoad, and LV performance.” Pulmonary Hypertension and Pulmonary Vascular Resistance Increased pulmonary arterial pressure impedes right ventricular (RV) ejection, causing RV dilation and ‘a decreased CO. If pulmonary hypertension occurs rapidly. as with massive pulmonary embolism or marked hyperinflation, aeute cor pulmonale and cardiovascular collapse occur. Pulmonary hypertension can be duc to aan increase in pulmonary vasomotor tone, pulmonary cular obstruction, or passive increases in Ppao due to LY failure. The pulmonary circulation normally has a low resistance, with pulmonary arterial diastolic pressure yer than Ppao. By measuring pulmonary artery pressure, Ppao, and CO, one can calculate PVR as the ratio of the pressure gradient divided by flow: (mean pulmonary artery pressure ~ Ppao)(CO. If PVR is increased, then therapies to reduce pulmonary only slightly artery pressure are needed (eg, O,, inhaled ri intravenous pulmonary vasodilator therapy), Patients with pulmonary hypertension who have inereased PVR that is not responsive to vasodilator therapy usually have cither vascular obstruction (eg, pulmonary embolism), or ‘vascular loss (eg, emphysema). If pulmonary hyperter is associated with a normal PVR, then LV failure is its probable ca Unfortunately, PVR isa poor measure of pulmonary vasomotor tone, Pulmonary vascular pressure can istention, vary across lung regions because of lung, structural damage and acute inflammatory processes (cg, hyperinflation, emphysema, pulmonary fibrosis, pulmonary emboli, and acute lung injury). Thus, measuring, PVR cannot idemtfy local injury or explain why PVR levated. Furthermore, with nonhomogeneous lung pulmonary blood flow will preferentially go to ince, thus masking lung dis those regions with the lowest resis abnormalities, Pulmonary Edema Pulmonary edema can be caused by elevations of pulmonary capillary pressure (hydrostatic or secondary pulmonary edema), increased capillary or alveolar permeability (primary pulmonary edema), epitheli iterated ntheor a combination of both. If pulmonary capillary pressure increas above 20 mm He, hydrostatic vascular forces promote increased fluid flux across the capillary membrane, flooding the alveoli. However, if capillary or alveolar cel injury is present, as in acute lung injury, alveolar flooding can oceur at much lower pulmonary capillary pressures. Clinicians usually use Ppao as a surrogate of pulmonary capillary pressure, and if pulmonary venous resistance is not increased, this assumption is valid, Measures of absolute Ppao are used todetermine the cause of pulmonary edema, Inthe setting edeme, Ppa values less than about 18 mm Hg suggest capillary leak, whereas values greater than of pulmonary this suggest heart failure, However, these are not hard values, For example, transient severe LV dysfunetion can transiently increase Ppao during upper airway obstruction with vigorou ir inspiratory efforts piratory stridor, obstructive sleep apnea), unstable angina (reversible ischemia), and arrhythmias Increased pulmonary capillary pressure increases pulmonary venous resistance (cg, intracerebral an occur when massive sympathetic di hemorrhage and heroin overdose), which reverses quickly while the pulmonary edema remains Furthermore, persistently elevated pulmonary capillary pressures can coexist with normal Ppao values if pulmonary venous resistance is increased and CO is also iner the case in high altitude pulmonary edema and end-stage acute lung injury. wed, ass often Left Ventricular Preload and Volume Status Pulmonary artery occlusion pressure is often used, erroneously to assess intravascular volume status and LY preload. Regrettably, neither absolute Ppao values; nor their change in response to fluid infusion trends preload or volume responsiveness The reasons for this st.although inereases in LV end volume will inerease CO in volume-responsive patients, the relation between Ppao and LV end-diastolic volume is curvilinear and may be very different among subjects are multiple, solic and within subjects as RV volumes, intrathoracic pressure, and myocardial ischemia vary. Second, Ppao is not the distending pressure for LV filling but is only an estimate Hemodynamic Monitoring | Chapter 125 of LY intraluminal pressure, whereas pericardial pressure and LV diastolic compliance can vary widely and not be indicated by this or other measures Hyperinflation, tamponade, and active inspiratory and expiratory muscle activity can rapidly alter pericardial pressure. Myocardial ischemia, arrhythmias, and acute RV dilation can alter LV diastolic compliance and can occur over a few heartbeats “Thus itis not surprising that Ppao is a very poor predictor of preload responsiveness. The use of Ppao as a measure of LY end-diastolic volume and preload responsiveness is not recommended. Assessment of Left Ventricular Performance “The assessment of LV performance is central to invasive hemodynamic monitoring. The primary determinants of LY performance are preload (LV end-diastolic volume), afterload (LY wall stress, which is itself the product of LV end-diastolic volume and diastolic arterial pressure), heart rate, and contractility. Since LV end-diastolic volume isa fundamental determinant of stroke volume and LV stroke work, Ppao is often used as a surrogate for LV ‘end-diastolic volume and for the calculation of stroke ‘work, which is the product of the difference between MAP to Ppao and stroke volume. Thus, Ppao can be used to construct Starling curves that plot Ppao versus LY stroke work. With this approach, patients with heart failure can be classified by their Ppao and cardiac index values using a Ppao of 18 mm Hg and a cardiac index of 2.2 Limin/m’ as cutotf values. Low cardiac indices and, high Ppao reflect heart failure, and low Ppuo reflects hypovolemia, whereas high cardiac indices and high Ppao reflect volume overloaded and low Ppao reflects increased sympathetic tone, ‘These constructs are probably too simplistic, as many a clinical study has documented. Still in the patient without Jung or pericardial disease, tamponade, or pulmonary embolism, the relation between Ppao and LV stroke work ‘can be used to assess LV performance.126 Chapteré | Comprehensive Critical Care: Adult CARDIAC OUTPUT Shock reflects an inadequate DO, to mect the body's metabolic demand, and CO isa primary determinant of DO,, Indeed, except for extreme hypoxemia and anemia, ‘most of the increase in DO, that occurs with resuscitation ‘and normal biological adaptation is attributable to increasing CO.A vast array of devices, both invasive and noninvasive, are available tha ical Uevision making. measure CO accurately enough to drive el Noninvasive Measures of Cardiac Output Cardiac output can be reliably measured noninvasively using a variety of techniques including ultrasound, plethysmographic pressure profile analysis, and bioreuctance. The most commonly used noninvasive techniques are ultrasound based and include echocardiography, pulsed esophageal Doppler, and ve suprastemal notch ultrasound. continuous-w: Echocardiography ‘To conduct transthoracic echocardiographie analysis of the aortic root flow, the clinician places the echo probe along the short axis of the aorta using pulse Doppler to m probe from the suprasternal notch looking through the aortic value to measure aortic velocity using continuous- this procedure requires training sure the aortic value diameter and then positions the wave Doppler. Althoug ‘and measures only a single point in time, it can reliably estimate CO. The accuracy of the measure inereases with transesophageal echocardiography, but so does in aortic low tion to predict volume Recent consensus conferences of multiple professional so have stated that basic expertise in ultrasound techniques its invasiveness. One can use ch during positive pressure ve responsiveness. as described subsequently should bea central part of all critical care medicine training, However, since the transthoracic measures of CO are highly dependent on the expertise of the operator and cannot be measured continuously, this important method will not be discussed further. Esophageal Doppler Ultrasound Esophageal Doppler ultrasound uses an esophageal probe simi descending aortic flow as it parallels the esophagus, A Doppler transducer probe is inserted orally or nasally size toa nasogastric tube ton ure {to midthoracic level and rotated until the probe senses a characteristic aortie velocity signal profile.” This technique can be taught to bedside murses and can be used to drive resuscitation algorithms to improve patient outcomes in patients undergoing high-risk surgery.” Several studies have documented that esophageal Doppler estimates of CO and its change can be made accurately after minimal taining." Similarly, dynamic increases in CO assessed by esophageal Doppler in response to a passive leg-rai {est predict volume responsiveness" The only drawback to this technology is that nasogastric insertion is dificult, necessitating oral insertion, so this is not the preferred technique in the awake nonintubated patient. However, \when compared with standard therapy in randomized clinical trials, the use of esophageal Doppler ultrasound to achieve targeted DO, levels in high-risk perioperative patients resulted in decreased hospital length of stay and. ed postoperative complications." Furthermore, deer complications with the use of esophageal Doppler measures are very rare. Transcutaneous Doppler Ultrasound This modification of the esophageal Doppler technique uses a handheld probe placed at the suprasternal notch with the transducer aimed downward at the aortic valve, This technique is easy to learn and gives accurate measures of LV stroke volume and CO,“ However, like echocardiographie techniques, ranscutaneous ultrasound cannot be used continuously. Th device can he used asa decision support tool to identify e and to calibrate accurate, noninvasive patients who are volume respor minimally invasive devices (discussed later). Potentially, transcutaneous ultrasound will be most readily aecepted in transport.” the emergency department,* during medics ‘and on the general medical floor to rapidly identify cardiovaseu y.* Still, no clinical trials have been published using this promising technology to guide resuscitationThoracic Electrical Bioreactance Thoracic electrical bioimpedance has been around for decades and is accurate only in highly shielded environments because electrical interference makes the ‘measures of CO unreliable.” However, using the frequency modulation component of the thoracic impedance signal ina process called bioreactance markedly eliminates this artifact and increases the accuracy of the estimates of CO and its change.” Both bioimpedance and bioreactanee rely ‘ona derivation of Ohm's law, which states that the flow of an electrical current is equal to the voltage drop between 2ends of a circuit, divided by the resistance or impedance tocurrent flow. Since most of current low through the thorax occurs in the aorta and vena cava, changes in impedance reflect changes in volume and CO, Validation studies comparing bioreactance and pulmonary artery catheter thermodilution CO conclude that bioreactance has acceptable accuracy." Furthermore, the dynamic responsiveness of the bioreactance signal allows it 1o be used in combination with a passive leg-raising maneuver to assess fluid responsiveness, However, although clinical trials using bioreactance technology to guide resuscitation are ongoing, no clinical studies have yet been published using this promising technology. Invasive Measures of Cardiac Output Thermodilution Using the Pulmonary Artery Catheter Invasive measurement of CO using the pulmonary artery catheter remains the most common method used linicaly, although this trend is rapidly changing." The pulmonary artery catheter has a thermistor located 4em from the tip and a proximal port located 30cm from the tip Cardiac output is measured by injecting cold fuid through the proximal port. Under normal conditions once the pulmonary artery catheter is placed, the proximal port resides at or above the right atrium such that bolus injections of cold (thermal) fluid are mixed in the contracting right ventricle. The thermistor records the dynamic change in blood temperature. The thermoditution- estimated CO is inversely proportional to the area under, the temperature versus time curve. Subsequently, Hemodynamic Monitoring | Chapter6 127 thermal (heat) signal using an induetion coil in the RV region of the pulmonary artery catheter permits the clinician to estimate CO continuously, albeit less accurately measuring dynamic changes in ow. Importantly measures of stroke volume and CO when coupled with other measured hemodynamic variables allow for the calculation of various important parameters, ike LY stroke work and both systemic DO, and consumption. Although the clinical utility and outcome benefit of pulmonary artery catheterization have been debated for many years* no study has used pulmonary artery catheter-specific measures to drive resuscitation algorithms and compared outcomes with those of other patients not having such information. Given the present climate in critical eare ‘medicine itis highly doubtful that such a study will be undertaken. Similar to the pulmonary artery catheter is the transthoracic thermodilution method of estimating CO, the only difference being that the measure of thermal change is made in a central artery instead of the pulmonary artery. This approach does not require pulmonary artery catheter insertion but has a major limitation in that the arte sensor, since the thermal sample needs tobe of a flow-by signal must pass by the sensor to report its change, thus req artery. 2 insertion of the thermistor probe into a femoral Arterial Pulse Pressure Waveform Analysis is is also referred to as Pulse pressure waveform analy minimally invasive monitoring because it requires only the insertion of an arterial catheter. Several commercially available devices use proprietary algorithms that analyze the arterial pressure waveform (or the pulse contour). Each estimates central arterial compliance differently, and the techniques that require a standard external measure of CO for their calibration are the most accurate.* Since we varies depending on the patient's blood pressure, age, sex, and height, these devices usually need to be recalibrated on a regular basis. The 2. common arterial comy reference standards for calibration are transthoracic lithium dilution” and thermodilution.»’ Recent algorithms have been developed that do not require external128 Chapter 6 | Comprehensive Critical Care: Adult calibration with a CO reference standard." Recent head to-heud comparisons of all the invasive and minimally invasive devices demonstrated significant intradevice variability.® suggesting that if one uses these devices it is best to stick with only 1 or 2 devices and learn to use them well rather than use several over time in the sa patient. A list of the available devices commonly used to estimate CO is given in Table 1 on page 128, In gene minimally invasive device should be externally validated using an independent means if possible, and this should be one often if the cardiovascular tone of the patient varies rapidly. a ‘A central question in the resuscitation of hemodynamically ‘unstable patients is whether they need increased blood. fow to the tissues A patient who isin circulatory shock will need increased DO, Accordingly, efforts to rapidly increase blood flow are important to minimize tissue ischemia and organ dysfunction, Traditionally, an increase in CO of greater than 15% alter a fluid challenge has been considered the gold standard reflecting fluid responsiveness If CO does not increase in response t0 fluid challenge, then the presumptive diagnosis of impaired cardiac contractility is made and inotropes are given to increase blood flow. Importantly, there is no absolute CO target that should be taken as optimal. The focus during resuscitation from circulator shock should be a relative change in CO in response to therapy and the associated ‘change in organ perfusion. Over the past 15 years, numerous studies have validated that either arterial pulse pressure or stroke volume, referred to as pulse pressure variation (PPV) and stroke volume variation (SVV),** respectively, induced by positive pressure ventilation can accurately identify patients who are volume responsive and those who are not.” A threshold value of either PPV or SVV greater than 15% defines volume responsiveness when patients are ventilated witha tidal volume of § mL/kg or more. ‘These parameters are not accurate during arrhythmias ancl spontaneous breathing because of varying R-R intervals and ventricular interdependence-induced changes in LY diastolic compliance, respectively. In those eases. one can perform a passive leg-raising maneuver and note the transient inerease in CO. Postural changes such as passive leg raising have been used for many years to Table 1. Commercially Available Devices to Estimate Cardiac Output at the Bedside [ Noninvasive Echocardiography Various manufacturers Transcutaneous ultrasound USCOM (USCOM Ltd) Esophageal Doppler Cardio (Deltex Medical) Bioimpedance BioZ SonoSite) Bioreactance: NICOM (Cheetah Medical) Plethysmographic Nexfin (BMEYE) Invasive Minimally invasive (external calibration) PiCCO pls (Pulsion Ltc) LIDCO plus (LIDCO Le) Minimally invasive (slfcalibrating) FloTrac (Edwards Lifesciences) DCO rapid (LOCO Ltd) Pulmonary artery catheter Bolus thermodilution (Edwards Lifesciences) & Continuous thermodilutiontransiently increase venous return. The legs are raised to 30° above the ches increase in CO is recorded. This maneuver approximates 2300-mL blood bolus in 2 70-kg patient that persists for approximately 2 to 3 minutes Changes in heart rate, blood pressure, CVP,or CO are then observed after and held for | minute,and the maximal passive leg raising (PLR). The dynamic increases in CO induced by passive leg raising are as sensitive and specific in predicting volume responsiveness as is PPV during, positive pressure mechanical ventilation using any of the lly available, minimally inv devices. Importantly, one cannot use the pulmonary artery catheter because neither bolus nor continuous CO ive monitoring ‘measures by this device are rapid enough in their sensing to detect these small and short-lived changes in CO. OXYGENATION AND TISSUE PERFUSION Since there is no specific CO that is considered normal, only one that is adequate or inadequate to meet the metabolic demands of the body, other measures of cardiovascular sufficiency need to be made to assess the adequacy of blood flow. Importantly, maintenance of a normal blood pressure does not equate to adequate tissue blood flow because vasomotor tone varies to keep arterial pressure in an acceptable range, Furthermore, targeting, a defined supranormal level of DO, does not ensure metabolic demand. To assess the adequate flow to mi adequacy of O, delivery,one needs to measure arterial and venous blood O, saturations and surrogate measures of tissue hypoxia, such as serum lactate levels and tissue O, saturation. Pulmonary artery catheterization indes true mixed venous O, saturation (Svo,), whereas Sevo, taken via a central venous catheter mostly reflects the degree of O, extraction from the brain and the upper part of the body. Pulse Oximetry Continuous monitoring of arterial blood O, saturation (Sa0,) using pulse oximetry is universally used in the ICU although clinical data of its usefulness are lacking despite 129 Hemodynamic Monitoring | Chapter 6 impressive clinical trials attempting to demonstrate a bene! ity of pulse oximetry re arterial blood ‘gas analysis. Pulse oximeters estimate Sao, saturation ial effect. The greatest u is in reducing the need for repeti by measuring the tissue light absorption at 2 specifi wavelengths, 660 nm (red) and 940 nm (infrared). The absorption ratios, based on calibration against known Sao, values, allow for the continuous measurement of Sao,, Importantly, nonphasic O, absorption also occurs, so the devices presume that dynamic changes in the density of| absorption must reflect the arterial pulse, hence the name pulse oximetry. Accordingly, if no arterial pulsatlity is seen from the plethysmographie waveform, Suo, cannot be calculated using these devices Since they actually measure the pulsed O, saturation, they are referred to as pulse O. saturation (Spo), whi ipproximates Sao, well? n practi Detection of Hypoxemia ‘The most commonly used application of Spo, is the detection of hypoxemia. Hypoxemia is usually defined 1 Spo, less than 90%. Titration of Fio, and other v tilatory maneuvers to keep Spo, ereater than 90% is ‘common goa! in most critically ill patients. However, there is litte additional benefit in increasing Spo, above 95% hecause of the shape of the oxyhemoglobin dissociation curve limits O,-carrying capacity. Taking the usually stated 95% confidence limits of 4%, an oximeter reading of 95% could represent a Pao, between 60 mm Hg (Sao, > 91%) and 160 mm Hy (Sao, > 99%). Thus, decisions on ventilatory therapy should not be determined solely by Spo, values, Detection of Volume Responsiveness Another novel us plethysmographic waveform analysis. Variation in plethysmographic density from beat to beat reflects of pulse oximetry is the paired variations in arterial pulse pressure, thus making plethysmographie variability another method of a volume res essing, onsiveness in the ventilator-dependent patient, as discussed earlier."130 Chapter 6 | Comprehensive Critical Care: Adult Venous Oximetry and the Physiology of Svo, and Scvo, The DO, describes whole-body O, supply without reference to blood flow distribution or O, uptake. DO, is ‘equal to the product of CO and arterial O, content (Ca0,). Arterial O, content is the sum of O, bound to hemoglobin (Hb) (product of Hb concentration Sao, and dissolved , (Pao,). The formula is Cao, = Hb x 1.36 x Sao, x Pao, x (0.0031. Thus, dissolved O, in the plasma has minimal etfect ‘on overall Cao, Clinically, DO, only has relevance to O, demand estimate by whole-body O, consumption (VO.). Since VO, must equal the difference in DO, and the amount of O, remaining in mixed venous blood, VO, can be expressed by the Fick principle as the product of CO and arteriovenous, , content difference (Cao, ~ Cvo,): VO, = CO (Cao, where mixed venous O, content (Cvo,) like Cao, is Cvo, = Hb x 1.36 x Svo, x Puo, x 0.0031. By simple algebraic transposition, Cvo, = Cao, ~(VO/CO). Thus, Cvo, reflects the relationship between whole-body VO, and CO under conditions of a constant Cao, Importantly, $vo, is the most important factor to determine Cvo, since, like in arterial blood, the dissolved O, can be neglected and Hb is usually constant over short time intervals. Thus, S¥0, correlates well with the O, supply-to-demand ratior® Trending Svo, and Scvo, to Assess Circulatory Sufficiency A decrease in Svo, and Sevo, usually represents an. increased metabolic stress Factors that deerease Sv, include low CO or anemia (decreasing DO.) exervise (increasing VO.), and hypoxemia. In the sedated patient not actively bleeding and in whom Sao, is greater than 90%, Svo, and CO covary. Importantly, the normal cardiovascular response of increasing VO, (exercise) is nd CO. Thus, Svo, normally ing DO. Therefore, a decrease in Svo, oF Sevo, does not necessarily to increase O, extraction decreases during exercise despite i ‘mean that tissue hypoxia vecurs Only if Svo, decreases tess than 50% can one be sure some degree of tissue hypoxia has occurred.” Conversely, a normal Svo, (eg, oT: i saturation) does not ensure that some vascular beds are not underperfused. In summary, $vo, can iggesting i ¢ in DO, (¢g, anemia, hypoxia, hypovolemia, failure) or increased VO, (eg, fever, pain, stres, shivering). creasing cardiovascular stress due Since central venous catheterization is commonly performed for a variety of reasons in critically ill patients, rect access to central venous blood is also commonly available in most critically ill patients. Thus, Sevo, is often Used as a surrogate for Svo,,Since most central venous, catheters have their distal tip in the superior vena cava, Sevo, reflects the venous blood of the upper body but neglects venous drainage from the lower body (ie, intra- abdominal organs). Accordingly, Sevo, is usually lower than Svo, by 2% to 3% because the lower body extracts less O, than the upper body, making inferior vena caval O, saturation higher.**The primary cause of the lower inferior vena caval O, extraction isthe oxidative phosphorylation blood flow (eg, renal blood flow, portal flow, hepatic blood flow), Importantly, however, Svo, and Sevo, change parallel when the ratio of whole-body O, supply and (©, demand is altered Still the difference between the absolute values of Sevo, and Svo, changes under conditions of shock. In septic shock, for example, Scvo, often exceeds much as 8%, and the opposite can occur with hypovolemic and cardiogenic shock. During cardiogenic ‘or hypovolemic shock, mesenteric and renal blood flow decreases, which for the same level of metabolic demand tion.” In septic shock, splanchnie increases local O, extr O, consumption increases, thus increasing local O, extraction despite increased CO" Thus Sevo, cannot be used as surrogate for Svo, under conditions of circulatory shock, As rule, ifSevo, is less than 65% then inadequate DO, probably exists but if Sevo, is greater than 70% it has no prognostic utility Near-Infrared Spectroscopy to Measure Tissue O, Saturation Neat-infrared spectroscopy (NIRS) is a noninvasive technique capable of continuous measurement that uses the varying light absorption properties of deoxygenated and oxygenated blood to determine tissue O, }saturation (Sto,). Near infrared light (680-800 nm) is, largely transparent to biological tissue and is absorbed primarily by Hb, and absorption is minimally affected by skin blood flow. The Sto, signal primarily reflects, ‘oxygenation in the small end-vessels and, unlike pulse ‘oximetry, approximates the venous O, saturation, Although different devices have different penetration levels and sensitivities to changes in Hb concentrations several studies showed that Sto, can vary independently of Spo, and Sevo,, Regional Sto, asurements can detect occult regional hypoxia even, lized, making, it a valuable (ool in the assessment of compartment when Svo, and vital signs have norm syndromes” Tissue O, saturation values greater than 85% also reflect resuscitation adequacy, whereas in trauma patients persistent Sto, values less than 60% reflect a poor outcome.” Dynamic Sto, measurements using brief vessel occlusion challenges, referred to as a vascular ‘occlusion test, can define initial blood flow distribution: decreased deoxygenating slope suggests misdistribution of microcirculatory flow whereas a reduced reoxygenation slope suggests inadequate CO.” This dynamic technique has been used to assess circulatory sufficiency in patients with trauma and sepsis and during weaning from mechanical ventilation. FUNCTIONAL HEMODYNAMIC MONITORING The primary utility of hemodynamic monitoring is to identify cardiovascular instability, help determine causal factors, and guide therapy.*'A fundamental assumption ‘underpinning these methods is that the rapid identification of tissue hypoperfusion and its correction will improve patient outcomes Functional hemodynamic monitoring uses defined physiological perturbations to stress the cardiovascular system and reveal resultant changes in arterial pressure and COS These methods include the assessment of volume responsiveness and the detection of occult tissue hypoperfusion, Hemodynamic Monitoring | Chapter6 131 Preload Responsiveness ‘The use of positive pressure breathing-induced PPV ind SVV (discussed earlier) and passive leg-raising- induced changes in CO* accurately predicts volume responsiveness Similarly, one can measure inferior vena caval diameter decreases during inspiration,*™ superior vena caval decreases during inspiration’™ and aortic low velocity changes and plethysmographic pulse oximetry change to predict volume responsiveness. Using a simple SWV minimization can markedly reduce intra-operative protocol hospital length of stay. Occult Circulatory Shock B reoxygenation during a vascular occlusion test reveals, isdistribution of blood flow and occult circulatory shock, jon and camining the changes in Sto, deoxyger respectively andthe Sto, changes induced by a vascular occlusion test Goal-Directed Therapy Initial studies suggested that the nonspecific inerea in DO, to supranormal levels in cri ly ill patients improved survival” Subsequent studies using aggressive resuscitation to inerease DO, to supranormal levels in patients with existing organ failure to document survival benefit reported that if anything this procedure increased mortality.” In essence, the benefit o « 88 However, snot be realized by already dead tissue carly aggressive resuscitation driven by hemodynamic monitoring if done before the onset of organ injury survival, whether done uniformly improves carly goal-directed therapy in septic patients presenting to ‘and as preoptimization an emergency department,” therapy for high-risk surgical patients)" but ess so in postoptimization therapy for postoperative patients with difficult intraoperative courses, suggesting that early ‘agaressive resuscitation is most useful in the intraoperative arena but sil shows benefit in the ICU, although to a lesser degree132 Chapter 8 | Comprehensive Critical Care: Adult SUMMARY Hemodynamic monitoring is done to determine whether a subject is physiologically stable, to determine whether blood flow to the periphery is adequate to meet metabolic demands, to diagnose specific causes of circulatory shock, to determine specific therapies. and to indicate when cardiorespiratory sufficiency has been reestablished. 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