Assessment of Cardiac Filling and Blood Flow

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Assessment of Cardiac Filling and Blood Flow

The accurate assessment and manipulation of the circulation are important parts of the management of critically ill patients. The principal objective of cardiorespiratory manipulation is to ensure optimal oxygen delivery. Adequate cellular respiration, adequate delivery of substrates and pharmaceuticals, and eventual recovery of organs and tissues are possible only when this has been achieved. This chapter deals with the physiologic principles governing the cardiovascular system and discusses interpretation of hemodynamic data in a clinical context. With the increasing number of medical devices available to monitor the circulation, this chapter also outlines the principles underlying the design and function of these devices, as well as their uses and limitations (Tables 3.1 to 3.4).

Table 3.1

Primary Measured Hemodynamic Data

Parameter/Formula Normal Range
Arterial blood pressure (BP)  
 Systolic (SBP) 90-140 mm Hg
 Diastolic (DBP) 60-90 mm Hg
Mean arterial pressure (MAP):
[SBP + (2 × DBP)]/3		 70-105 mm Hg
Right atrial pressure (RAP) 2-6 mm Hg
Right ventricular pressure (RVP)  
 Systolic (RVSP) 15-25 mm Hg
 Diastolic (RVDP) 0-8 mm Hg
Pulmonary artery pressure (PAP)  
 Systolic (PASP) 15-25 mm Hg
 Diastolic (PADP) 8-15 mm Hg
Mean pulmonary artery pressure (MPAP):
[PASP + (2 × PADP)]/3		 10-20 mm Hg
Pulmonary artery occlusion pressure (PAOP) 6-12 mm Hg
Left atrial pressure (LAP) 6-12 mm Hg
Cardiac output (CO):
HR × SV/1000		 4.0-8.0 L/min

HR, heart rate; SV, stroke volume.

Table 3.2

Derived Hemodynamic Data

Derived Parameter/Formula Normal Range
Cardiac index (CI):
CO/BSA		 2.5-4.0 L/min/m2
Stroke volume (SV):
CO/HR × 1000		 60-100 mL/beat
Stroke volume index (SVI):
CI/HR × 1000		 33-47 mL/m2/beat
Systemic vascular resistance (SVR):
80 × (MAP − RAP)/CO		 1000-1500 dyn⋅s/cm5
Systemic vascular resistance index (SVRI):
80 × (MAP − RAP)/CI		 1970-2390 dyn⋅s/cm5/m2
Pulmonary vascular resistance (PVR):
80 × (MPAP − PAOP)/CO		 <250 dyn⋅s/cm5
Pulmonary vascular resistance index (PVRI):
80 × (MPAP − PAOP)/CI		 255-285 dyn⋅s/cm5/m2

BSA, body surface area; CO, cardiac output; HR, heart rate; MAP, mean arterial pressure; MPAP, mean pulmonary artery pressure; RAP, right atrial pressure; PAOP, pulmonary artery occlusion pressure.

Cardiac Filling

One of the fundamental concepts of hemodynamic optimization of the critically ill patient is the manipulation of cardiac output as a main determinant of blood flow and oxygen delivery. Cardiac output is defined as the product of stroke volume (SV) and heart rate (HR). Although options to control heart rate are limited, clinical studies investigating hemodynamic optimization protocols have been largely focused on interventions to increase stroke volume. The stroke volume of the heart is determined by the complex interaction of three components: preload, contractility, and afterload. A thorough understanding of the physiology and pathophysiologic principles that define these components is essential for the clinician to successfully control and improve cardiovascular dynamics.

Our current understanding of the relationship between preload and contractility and their effect on stroke volume is based on the experiments of Dario Maestrini, Otto Frank, and Ernest Starling. Culminating in Starling’s “law of the heart,” which states that the force of myocardial contraction is directly proportional to the end-diastolic myocardial fiber length (or “preload”), as determined by the ventricular end-diastolic volume (EDV).1,2 It is this relationship, commonly known as the Frank-Starling mechanism that matches venous return to cardiac output (Fig. 3.1).

The most common intervention used by clinicians to improve stroke volume—the administration of fluids—is aimed at increasing venous return as a main determinant of EDV. In this regard two factors are important to consider: the position of an individual heart on the Frank-Starling curve and the expected response to fluid administration, as well as giving the right amount of fluid in order to achieve a hemodynamic response. The dynamics of venous return have been extensively described by Arthur Guyton, whose theories contribute to our current understanding of the circulation and may help to optimize venous return.3,4

Preload

Based on Ernest Starling’s observations, preload is defined as the tension developed by the stretch of the myocardial fibers: An increase in venous return leads to an increase in EDV which in turn increases myocardial sarcomere length, resulting in an increase of contractility and a rise in stroke volume and cardiac output. Conversely, a decrease in venous return will reduce EDV, resulting in a decreased stroke volume and cardiac output. This mechanism matches the mechanical activity of both ventricles under changing physiologic conditions and functions independent of nervous supply.

Preload is determined by the following factors:

• Circulating blood volume

• Venous capacitance (i.e., sympathetic stimulation resulting in venoconstriction, mechanical compression)

• Posture: The Trendelenburg position (supine, head down) increases venous return. Clinically, a passive leg raise test may be performed to assess volume responsiveness by autotransfusion of approximately 300 mL of blood from the splanchnic and lower limb compartments to the central circulation, increasing preload.

• Intracavitary pressures: Abdominal hypertension and increased intrathoracic pressures (i.e., during positive-pressure ventilation and application of positive end-expiratory pressure [PEEP]) can oppose venous return.

• Ventricular compliance: Ventricular compliance determines the relationship between EDV and end-diastolic pressure (i.e., diastolic dysfunction or impaired relaxation as in ventricular hypertrophy).

• Heart rate: The filling time influences EDV.

• Atrial contraction: Atrial contraction contributes to EDV and may be impaired (i.e., in atrial fibrillation).

Indicators of Preload

In vivo measurement of sarcomere length is not possible. To assess this variable in the clinical setting, ventricular end-diastolic pressures have been traditionally used as surrogate parameters to estimate EDV. Although EDV can be assessed by echocardiography, continuous monitoring of this parameter is currently not possible. Static indices of preload include traditional parameters assessing filling pressures or volumes as well as parameters derived from recently introduced techniques based on thermodilution (see later), which have been classified as volumetric indices of preload. Recently, parameters based on the cyclic changes in intrathoracic pressure during mechanical ventilation have been introduced as estimates of preload responsiveness under certain circumstances, although they do not measure preload per se. These dynamic indices of preload can play a role in predicting an increase of stroke volume after an increase of preload, or in other words, the “fluid responsiveness” of the ventricle.

Static Indicators of Preload

These parameters give an estimate of preload, but their ability to predict a response to fluid administration is limited. Static preload indices have been defined for both sides of the heart:

Static indices of the left side of the heart:

Static indices of the right side of the heart:

It is generally postulated that EDVs correspond to myocardial sarcomere length just prior to ventricular contraction and that end-diastolic pressures correspond with EDVs.

For the left side of the heart these relationships are as follows:

image

For the right side of the heart these relationships are as follows:

image

It is important to note that these assumptions do not hold true in most clinical conditions and all parameters are influenced by physiologic and technologic factors. Ventricular pressures and volumes both are influenced by ventricular compliance, so there is only a poor relationship between the two, and the traditional assumption that CVP, RAP, PAOP, and LAP estimate LVEDP as an indicator of LVEDV has to be questioned. PAOP reflects left ventricular function only if the vascular system between the catheter tip and the left ventricle is free from any pathologic condition that could influence the pressures detected by the catheter.

PAOP overestimates LVEDP in the following conditions:

PAOP underestimates LVEDP in the following conditions:

PAOP readings are accurate only if the tip of the pulmonary artery catheter (PAC) is appropriately wedged in West lung zone 3, corresponding to the lower third of the lung where continuous blood flow can be assumed.

The PAOP does not predict preload and bears little or no relationship to the subsequent response to a volume challenge. It is important to realize, however, that pressure is one of the driving forces responsible for edema formation in the lungs. In this regard, the PAOP may function as more of a safety limit rather than as a guide to therapy.5–7

The CVP reflects RAP and has been traditionally used as a marker of right ventricular preload and, assuming a relationship between CVP, RVEDP, and RVEDV, of left ventricular preload. However, CVP does not accurately reflect left ventricular preload and has been shown to correlate poorly with blood volume.5–7 The main clinical value of measuring CVP is to provide information about the right side of the heart, as in cases of right ventricular failure or in assessing the right ventricular response to pulmonary hypertension. A low CVP in the setting of clinical signs of tissue hypoperfusion may be predictive of a benefit from fluid administration, and a rapid significant rise of CVP during a fluid challenge may indicate that the heart is not fluid responsive.8–12

Volumetric Indicators of Preload

Based on cardiac output measurements using thermodilution and incorporating indicator passage times, volumetric preload parameters have been introduced as an alternative to conventional “static” parameters and have become available with thermodilution-based monitoring techniques such as the PAC, pulse contour continuous cardiac output (PiCCO), and EV1000 systems. The continuous end-diastolic volume index (CEDVI), derived from a modified PAC is a surrogate of RVEDV. Global end-diastolic volume index (GEDVI), intrathoracic blood volume index (ITBVI), and extravascular lung water index (EVLWI) are parameters provided by devices that require transpulmonary thermodilution for the measurement of cardiac output based on pulse pressure analysis (i.e., PiCCO and EV1000 systems, see later). GEDVI represents the total intracardiac volume, and the volume of the descending aorta has been shown to be a better indicator of preload than CVP.13,14

Dynamic Indicators of Preload (or Preload Responsiveness)

Based on the study of heart-lung-interactions a number of so-called dynamic preload indicators have been introduced. Although these parameters are not measures of preload per se, they play an important role in the prediction of the hemodynamic response (i.e., by an increased cardiac output) to an increase in preload (preload or “volume” responsiveness). Generally, these parameters are based on the observation that transient changes in preload occur during mechanical ventilation.15,16

Contractility

Ventricular contractility, or inotropy, describes the strength of ventricular contraction. It is defined as the tension developed by myocardial fibers at a given preload and afterload and the velocity of the shortening of the myocardial sarcomeres. It represents the intrinsic ability of the myocardium to generate a force independent of filamental stretch or ventricular loading conditions. Contractility is influenced by the following factors:

Factors that increase myocardial contractility:

The following factors reduce myocardial contractility:

Contractility is difficult to assess in the clinical setting. The temporal rate of change of ventricular pressure (dP/dt) and its maximum value (peak dP/dt) can be derived invasively (i.e., in the cardiac catheterization laboratory) or estimated less invasively with varying accuracy by echocardiography and some cardiac output monitoring devices. This parameter has been shown to be related to ventricular function in clinical studies. Echocardiography provides additional functional assessment of ventricular wall motion and blood velocity kinetics. Parameters such as the fractional area change (FAC) and ejection fraction (EF) are no accurate measures of contractility but are related to the contractile state of the myocardium and can be used to guide therapy.

Afterload

The afterload of the heart may be considered as the ventricular wall tension required to eject the stroke volume during systole. According to the law of LaPlace, afterload relates to the stress within the wall of the ventricle developing during systolic ejection:

image

where T = tension, P = intraventricular pressure, and r = intraventricular radius. In this equation afterload is mainly dependent on wall thickness and ventricular radius. At a given pressure, an increase in ventricular radius (i.e., dilatation of the ventricle) will increase afterload. An increase in wall thickness (i.e., ventricular hypertrophy) will reduce afterload.

Afterload for the left ventricle is increased by the following factors:

Afterload for the right ventricle is increased by the following factors:

The Anrep effect describes an intrinsic regulatory mechanism of the heart in response to an acute increase in afterload, which results in an initial reduction in stroke volume followed by an increase in EDV, which restores the stroke volume toward near-normal values.

Indicators of Afterload

SVR and PVR are the most commonly used indicators of afterload in the clinical setting for the left and right ventricle, respectively. Vascular resistance can be described as the mechanical property of the vascular system opposing flow of blood into a vascular bed. There are two main components of vascular resistance:

SVR and PVR cannot be measured directly and thus are calculated from Ohm’s law:

image

where V = voltage, I = current, and R = resistance. Applied to cardiovascular physiology this principle looks as follows:

image

in which ΔP is the pressure gradient, CO (cardiac output) is “flow,” and R is the resistance.

SVR is calculated as follows:

image

where MAP = mean arterial pressure (mm Hg), RAP = right atrial pressure (mm Hg), and CO = cardiac output. To convert from mm Hg to dyne × second/cm5 the multiplication by 80 is necessary. Normal values for SVR range from 800 to 1200 dyne × second/cm5. If standardized to body surface area, SVR is quoted as SVRI (SVR index) with normal values for SVRI ranging from 1900 to 2400 dyne × second/cm5/m2.

The following factors affect SVR:

In the same way as SVR, PVR may be calculated using the pressure differential across the pulmonary vasculature, between the mean pulmonary artery pressure (MPAP) and PAOP:

image

Values for PVR are normally below 250 dyne × second/cm5. Again, PVR is often quoted as the PVR index or PVRI with a normal range between 255 to 285 dyne × second/cm5/m2.

The following factors affect PVR:

Clinical Limitations of Systemic Vascular Resistance and Pulmonary Vascular Resistance

Although the concept of vascular resistance permits an intuitive understanding of the circulation, a number of limitations make it unreasonable to use SVR and PVR to guide therapy. First, because SVR and PVR are derived variables, errors inherent in the measurement of their components (i.e., filling pressures) are multiplied, making the derived number less accurate. Further, these calculations assume a linear relation between pressure and flow, which does not exist in vivo (Fig. 3.2). It is therefore wise to use these parameters with caution and consider their limitations in clinical practice.

Clinical Interpretation of Indicators of Preload

It has already been stressed that accurate assessment of the preload status of the heart is important because it may allow for the application of interventions resulting in an improvement of cardiovascular dynamics. However, without knowing whether the heart will actually respond to an increase of a certain status of volume or preload, this information is only of limited value. This concept—the individual response of cardiac output to a volume challenge—has become known as volume responsiveness.30 Intravascular volume expansion is often the initial intervention in patients with circulatory failure. However, only approximately 50% of patients given a fluid challenge will respond by increasing cardiac output. The ability to distinguish fluid-responsive patients from nonresponders is important to avoid inappropriate and potentially harmful fluid challenges in situations in which other interventions (i.e., inotropes or vasopressors) should be preferentially used. Consequences of inappropriate fluid therapy include pulmonary edema, deterioration in gas exchange, and cardiac failure.

There are currently a number of parameters available with different monitoring modalities that can be used as estimates of preload and may predict volume responsiveness under defined conditions.

Static Indicators of Preload

Conventional static markers of cardiac preload, such as CVP and PAOP, are poor predictors of fluid responsiveness. CVP and PAOP reflect intracavitary pressures that frequently show poor correlation with transmural pressures, which are actually related to EDV through chamber compliance. Therefore, EDV is overestimated (i.e., under the application of PEEP) or underestimated (i.e., in concentric left ventricular hypertrophy) in many clinical situations. Furthermore, static parameters do not determine the position of the heart on the “individual” Frank-Starling curve as contractile function is not taken into the account. A patient may fail to respond to a fluid challenge because of ventricular dysfunction or poor ventricular compliance (see Fig. 3.1). It is important to realize, however, that pressure is one of the driving forces responsible for edema formation in the lungs. So although the PAOP is considered to have limited utility for predicting and guiding fluid challenges, it does have a role to play in determining how much volume should be administered to patients and may be regarded as more of a safety limit, rather than as a guide to therapy.5,6

Dynamic Indicators of Preload

A number of dynamic parameters have been described that allow the clinician at the bedside to predict with some accuracy which patients will or will not respond to a fluid challenge. These parameters include the SVV, PPV, SPV, and the PVI and changes of vena cava diameters as derived by echocardiography. Generally, an SPV, PPV, SVV, or PVI variation greater than approximately 10% suggests that the patient will be volume responsive (Fig. 3.3). As stressed earlier in this chapter, these parameters require controlled mechanical ventilation and a tidal volume of at least 8 mL/kg of body weight to be maintained in order to remain reliable. Further, the presence of arrhythmias and severe tricuspid regurgitation precludes the safe use of these variables.16

The Passive Leg-Raising Test

Patients who are critically ill seldom fulfill criteria to allow for dynamic preload indices to be accurate predictors of volume responsiveness. The passive leg-raising test has been suggested to overcome these limitations: Traditionally performed by lifting the legs up at a 45-degree angle in a supine position, approximately 150 mL of blood can be recruited to increase venous return in order to predict a response of cardiac output to a noninvasive, endogenous fluid challenge. However, by starting the passive leg raising from a 45-degree semirecumbent position, a substantial increase of mobilized venous blood can be achieved by adding venous blood from the splanchnic compartment to that from the lower extremities, increasing the sensitivity of the maneuver for the prediction of fluid responsiveness. It is important to note that when performing the passive leg raising, the monitoring modality used must be able to track changes in cardiac output within a time frame of approximately 60 to 90 seconds.33–35

The Diagnostic Fluid Challenge

In the care of critically ill patients situations do exist in which the preceding parameters are not reliable and a passive leg-raising test may be contraindicated owing to technical constraints or based on the patient’s underlying illness, such as in brain injury with elevated intracranial pressure. In this scenario the clinician may rely on the administration of fluids as a diagnostic intervention to indicate a potential benefit from further fluid therapy by assessing the response of various hemodynamic parameters, with stroke volume being the parameter most widely used in studies investigating fluid responsiveness, with an increase of 10% to 20% indicating a positive response. Although the optimal volume to function as a fluid challenge has yet to be determined, it can be recommended in this situation to use the CVP as an indicator of a sufficient challenge of the right ventricle to ensure that an adequate preload has been achieved.36,37

It is important to recognize, however, that identification of a patient who is fluid responsive is not the same as saying that the patient should be given fluid without an appreciation of the clinical context. Most healthy patients will be volume responsive; however, few will benefit from volume challenges. In critically ill patients, other clinical factors need to be taken into account. Does the patient actually need a higher cardiac output? Or is cardiac output adequate, so that further increase may actually cause harm?

Hemodynamic Status and Blood Flow

Cardiac output (or blood flow) is an important variable to be considered in a critically ill patient. Although arterial pressure has been used as the target for therapy, this focus is perhaps related more to convenience in measurement than to a sound physiologic rationale. When patients become critically ill, it is extremely difficult to predict cardiac output from routine clinical assessment, so sensible and logical use of vasoactive therapy requires monitoring of both pressure and flow. Arterial blood pressure often is mistakenly used as a surrogate marker for blood flow; however, no direct relationship between pressure and flow exists. Moreover, clinical estimation of cardiac output can be difficult and inaccurate, although clinical assessment must not be ignored. Often these signs constitute the only tool that a clinician may have to estimate a patient’s hemodynamic status before admission to a critical care unit. At this stage the response of clinical assessment to simple therapeutic maneuvers can give important information. If, however, the patient fails to respond in a suitable fashion, monitoring of these variables becomes necessary in order to direct therapy.

Cardiac output is the volume of blood ejected by the left ventricle per minute. It is the product of heart rate and stroke volume. It should be borne in mind that excessive heart rates will reduce diastolic ventricular filling time, with a negative impact on stroke volume. Heart rhythm also is essential in determining cardiac output, and in general any rhythm other than sinus rhythm will result in a reduction in stroke volume. For example, the loss of atrial contribution to diastolic ventricular filling in atrial fibrillation results in a subsequent reduction in stroke volume and hence cardiac output.

Cardiac output should not be considered in isolation from other relevant variables. The concept of oxygen delivery describes the relationship between cardiac output and arterial oxygen content:

image

This variable (oxygen delivery) has been used in many studies, especially in the high-risk surgical population, as a target for resuscitation.

Measurement of Cardiac Output

The ideal method of measuring cardiac output would be noninvasive, accurate, continuous, safe, easy to use, and operator independent; would provide rapid data acquisition; and would be cost effective. None of the cardiac output monitoring devices currently available possesses all of these properties. Conventional thermodilution remains the clinical gold standard for accuracy in cardiac output measurement; however, newer, less invasive monitoring methods that provide continuous cardiac output data are establishing a role in patients’ hemodynamic management.38

The Fick Principle

Fick described the following relationship in the nineteenth century: Q = M/(A − V). That is, the uptake or release of a substance (M) by an organ is the product of the blood flow (Q) through that organ and the arteriovenous concentration difference (A − V) of the substance in question.

Applying the Fick principle to cardiac output measurement of the pulmonary blood flow over 1 minute may be achieved by measuring the arteriovenous oxygen content difference across the lungs and the rate of oxygen uptake. Oxygen uptake may be determined using spirometry by measuring the expired gas volume over a known time and calculating the difference in oxygen concentration between the expired gas and that of inspired gas. Accurate collection of the gas is difficult, unless the patient has an endotracheal tube, because of the leaks that occur around a facemask or mouthpiece. Analysis of the gas is straightforward if the inspired gas is air, but if it is oxygen-enriched air, two possible problems need to be taken into consideration: (1) the addition of oxygen may fluctuate, producing an error due to the nonconstancy of the inspired oxygen concentration, and (2) measurement of small changes in oxygen concentration at the top end of the scale is difficult. Blood oxygen content is measured via blood gas analysis. In the absence of intrapulmonary or intracardiac shunts, the pulmonary blood flow is equal to the systemic blood flow and thus cardiac output.

The technique just described based on the Fick principle may thus be used as an accurate and reliable static measure of cardiac output, but it remains a time-consuming and largely laboratory-based tool. Several variants of the basic method have been devised, but usually their accuracy is less reliable.

Thermodilution

As mentioned earlier, thermodilution from the PAC is considered to be the gold standard of cardiac output measurement for accuracy and acceptability in the clinical setting. Newer methods are routinely validated against the PAC thermodilution technique. A bolus of 5 to 10 mL of cold 0.9% NaCl or 5% dextrose is injected through the proximal port of a PAC into the right atrium. Temperature changes are measured by a distal thermistor in the pulmonary artery. A plot of temperature change against time gives a thermodilution curve from which cardiac output can be calculated from the Stewart-Hamilton equation (Fig. 3.4). Application of this equation assumes three major conditions: complete mixing of blood and indicator, no loss of indicator between place of injection and place of detection, and constant blood flow. For accurate results with this technique, it is important to ensure adherence to these conditions.

The degree of change in the temperature is inversely proportional to the cardiac output.

Modern PACs are able to provide a continuous reading of cardiac output. They contain an electrical heating coil that sits in the right atrium, which heats up the blood in a semirandom binary fashion. The pulsed heating bursts can be detected by the thermistor in the pulmonary artery, which after autocorrelation with the inputting signal can provide continuous cardiac output. It has to be noted, however, that this technique has a latency of 7 to 10 minutes.

Dye/Indicator Dilution

A number of techniques are available to measure cardiac output with the use of either a dye (indocyanine green) or an indicator (lithium). The concept is exactly the same as that for thermodilution: injection of a substance into the right side of the heart and detection of the same substance distally, either in the pulmonary artery or in the aorta. A curve is generated, which is replotted semilogarithmically to correct for recirculation of the dye. Cardiac output is calculated from the injected dose, the area under the curve (AUC), and the duration of effect (short duration indicates high cardiac output) from the Stewart-Hamilton equation:

image

Arterial Pulse Pressure Analysis

Arterial pulse pressure analysis is a technique of measuring and monitoring stroke volume on a beat-to-beat basis from the arterial pulse pressure waveform. This technique has several advantages over technologies such as the PAC, including its less invasive nature, as arterial access is available in most patients. Changes in both stroke volume and cardiac output are then shown on an almost continuous basis. A fair amount of less invasive cardiac output monitoring devices based on pulse pressure analysis are now commercially available and have resulted in a decreased use of the pulmonary catheter in most institutions (Table 3.5).

The fluctuations of blood pressure around its mean value occur as a specific volume of blood—the stroke volume—is forced into the aorta by each cardiac contraction. The magnitude of this pressure change, the pulse pressure, is a function of the magnitude of the stroke volume. On a beat-to-beat basis, the only factor that determines changes in pulse pressure is change in stroke volume, owing to the relatively slow nature of reactive vascular changes. In order to translate the pressure waveform into an accurate stroke volume, however, an estimate of the arterial compliance and resistance must be made. The greater the compliance, the less will be the vascular resistance to the pulsatile increase in the arterial pressure, and the less will be the pressure required to distend the vessel to accommodate a given stroke volume.

The need to incorporate arterial compliance and resistance into the measurement system has hindered this technology for many years. The origins of the pulse contour method for estimation of beat-to-beat stroke volume are based on the Windkessel model described by Otto Frank in 1899. Only recently have methods been described that can compensate or correct for these compliance or resistance changes to provide an accurate determination of stroke volume. Different technologies address this by different methods. Both lithium dilution and thermodilution techniques have been validated to calibrate pulse pressure tracking systems. Other devices are being marketed with the ability to self-calibrate after identifying vascular compliance and resistance directly from the pressure waveform.39

Proprietary Systems Requiring Calibration

PiCCO System

The PiCCO system40 (Pulsion Medical Systems, Munich, Germany) utilizes a pulse contour method of tracking arterial pressure to derive changes in stroke volume. This system consists of a thermistor-tipped catheter, which is placed in the femoral or brachial artery. The device identifies the systolic area by recognizing the dicrotic notch on the arterial waveform. The systolic area is divided by the aortic impedance to calculate stroke volume. Transpulmonary thermodilution, requiring a central venous line, is used to calibrate the system in order to account for individual aortic compliance. In addition to tracking cardiac output and stroke volume, this technology also can provide dynamic indicators of volume responsiveness (SVV, SPV, and PPV), as well as a number of volumetric markers of preload (GEDV, ITBV, and EVLW). This system has been shown to be interchangeable with the pulmonary catheter in terms of the accuracy of measuring cardiac output and has been validated in a broad spectrum of clinical settings.40

LiDCOplus System

The LiDCOplus41–44 (LiDCO, Cambridge, UK) tracks the power of the arterial waveform, rather than the contour, in order to track changes in stroke volume. A theoretical advantage is that the effect of reflected waves is reduced because the device does not need to identify specific parts of the arterial waveform. Because the morphologic pattern is not assessed, this technology also decreases (but does not negate) the effects of damping on the pressure system. This system can be calibrated by any independent form of cardiac output monitoring device but is sold with the proprietary lithium dilution cardiac output modality. The LiDCOplus technology also tracks the dynamic parameters of preload: SVV, SPV, and PPV.

Uncalibrated Systems

Flotrac.

The Flotrac system (Edwards Lifesciences, Irvine, CA) consists of a proprietary transducer and a separate monitor (Vigileo). The technology assesses the variance of the arterial waveform in comparison with specific demographic characteristics of the patient to identify changes in stroke volume and analyzes statistical properties of the arterial pressure waveform to account for individual vascular resistance and compliance. Recent software updates have considerably improved the response time to changes in vascular dynamics (approx. 20 seconds), although concerns remain regarding the accuracy of cardiac output measurements in acute hemodynamic changes. Nonetheless, the Flotrac/Vigileo system has been integrated into protocols of hemodynamic optimization showing an improvement in clinical outcomes.48–51

Nexfin.

The Nexfin system has been introduced recently as a totally noninvasive monitor of cardiac output. This system operates by applying a stepwise approach: An arterial pressure signal generated by combining photoelectric plethysmography with an intermittently inflated pressure cuff to maintain a constant arterial diameter. This finger arterial pressure signal is converted to a brachial arterial pressure waveform, which is used to calculate cardiac output. The current algorithm uses individualized components of a three-element Windkessel model, with age, gender, height, and weight as input parameters, incorporating the nonlinear effect of mean pressure and the influence of individual characteristics on aortic mechanical properties. Clinical studies have shown adequate correlation with cardiac output derived by thermodilution. The device offers the possibility of monitoring cardiac output at a very early clinical stage and may be instrumental in early treatment initiation.52

Transesophageal Doppler53–56

The esophageal Doppler cardiac output monitor, described in the early 1970s, provides a safe and minimally invasive means of continuously monitoring the circulation. In comparison to suprasternal probes, esophageal probes have the advantage of less positional variety due to the smooth muscle tone of the esophagus and less signal interference from bone, soft tissue, and lung due to the close proximity of the aorta to the esophagus. The esophageal Doppler monitor measures blood flow velocity in the descending thoracic aorta using a flexible ultrasound probe. When these data are combined with the aortic cross-sectional area, other hemodynamic variables including stroke volume and cardiac output can be calculated. With the currently marketed device (CardioQ, Deltex, Chichester, UK) aortic cross-sectional area is assumed, providing minimally invasive, continuous cardiac output assessment. Abrupt changes in cardiac output are much better followed with Doppler systems than with the PAC-based continuous cardiac output systems.

Despite several potential sources of error, good correlation has been observed between measures of cardiac output made simultaneously with the esophageal Doppler monitor and with conventional thermodilution. Esophageal Doppler ultrasonography has been used for intravascular volume optimization both in the perioperative period and in the critical care setting.29,32–35 One of the main advantages of the technique is the capability of rapid data acquisition after esophageal probe insertion.

Identification of the descending aortic waveform is essential for the correct use of the esophageal Doppler cardiac output monitor. Waveforms from other structures, such as the pulmonary artery, azygos vein, or celiac axis, may be encountered, leading to misinterpretation. After the characteristic descending aortic waveform is acquired, the signal is optimized before data acquisition by movement of the probe a centimeter up or down until the waveform indicates the best possible velocity and color intensities, followed by rotation of the probe to optimize the signal further if possible. The “peak velocity” display is used as a reference to the highest identified wave.

Esophageal Doppler waveform analysis has been increasingly evaluated as a method for determining optimal cardiac preload. The key preload parameter of interest is the flow time (FT)—the time required from the start of the waveform upstroke to return to baseline. FT represents the duration of left ventricular systole and makes up one third of the cardiac cycle (cycle time). Because the FT is heart rate dependent, it typically is corrected (FTC) to a rate of 60 beats per minute to compensate for the change in duration of systole. The FTC reflects the afterload status of the circulation. Decreased levels commonly are seen in hypovolemic patients, but caution in interpretation is advised because this pattern also can be seen with profound vasoconstriction. A more sensible use of this device is in following the effects of a fluid challenge. Because stroke volume can be determined on a beat-to-beat basis, it is easy to see the effects on the circulation of a small fluid bolus. Diagrammatic representations of characteristic Doppler waveform patterns are shown in Figure 3.5.

Echocardiography57,58

TTE and TEE both are evolving tools in the critical care setting, and particularly TEE has become a standard of care for intraoperative monitoring in patients undergoing cardiac valvular replacement or repair. TEE has been used for a number of years for acute hemodynamic monitoring and diagnostic purposes in the cardiothoracic critical care setting and its use in the general critical care setting is now becoming commonplace.

Echocardiography provides a dynamic assessment of cardiac function, allowing visualization of cardiac chamber dimensions, functional assessments such as estimation of ventricular ejection fractions, detection of regional and global wall motion abnormalities, detection of valvular abnormalities, and exclusion of pericardial effusion. It also can be used to derive cardiac output from measurement of blood flow velocity by recording the Doppler shift of ultrasound signals reflected from the red blood cells. The time-velocity integral, which is the integral of instantaneous blood flow velocities during one cardiac cycle, is obtained for the blood flow in the left ventricular outflow tract (other sites can be used). This is multiplied by the cross-sectional area and the heart rate to give cardiac output. The results for cardiac output measured by this device in skilled hands are comparable to those obtained with use of the PAC.

The main disadvantages of the method are that a skilled operator is needed, the probe is large and therefore heavy sedation or anesthesia is needed, the equipment is very expensive, and an expert user is needed to adjust the probe to give continuous cardiac output readings. Nonetheless, echocardiography has an important and established clinical role. The modality is covered in detail in Chapter 8.

Bioimpedance and Bioreactance

Transthoracic bioimpedance is a technique initially developed as a noninvasive method of studying cardiovascular function during space flight. The underlying principle is the occurrence of changes in electrical impedance of the thoracic cavity with ejection of blood during systole.37 In this model, the thorax is assumed to be a cylinder having electrical length between neck and xiphoid and has a basic impedance. A constant small current is passed between two outer electrodes attached to the skin (BioZ system) or an endotracheal tube (ECOM system), voltage change is sensed by two inner electrodes, and impedance is derived according to the equations described by Sramek and Bernstein.59 Impedance is recognized to change with the cardiac cycle (related to changes in blood volume). The rate of change of impedance is a reflection of cardiac output. It is thought to be useful in estimating trends in cardiac output but not for absolute measurements. Contraction of the heart produces a cyclic change in transthoracic impedance of approximately 0.5%, unfortunately giving a rather low signal-to-noise ratio. Stroke volume and cardiac output can be measured continuously and at fixed intervals using this technique. Studies suggest that transthoracic bioimpedance is accurate in healthy volunteers, but its reliability decreases in critically ill patients, including those with sepsis or increased lung water, and in persons with pacemakers. Clinical evaluation studies have so far shown conflicting results and the technique has not gained wide clinical acceptance to date.60–62

Assessment of Adequacy of the Circulation

Resuscitation of critically ill patients is a complex process. The rationale for most resuscitation maneuvers is that the delivery of oxygen to the tissues is inadequate, resulting in tissue hypoxia. Resuscitation is therefore aimed at increasing the oxygen delivery to a level at which enough oxygen is brought to the tissues to ensure efficient metabolism, so that normal cellular processes can occur. Part of this process entails measuring cardiac output and then increasing this variable to an “adequate” level. Unfortunately, this strategy is complicated as a result of the fact that all patients’ cardiac output requirements differ—no “normal” level of flow can be specified for any patient in any given situation. In order to assess adequacy of perfusion, therefore, a number of surrogate markers need to be assessed that give an estimate of the underlying metabolic status. The cardiac output then needs to be assessed in combination with these surrogate markers of metabolism in order to ensure that resuscitation is improving the clinical situation.

Clinical Assessment

The first step in the hemodynamic assessment must be a thorough clinical assessment. Pulse rate and quality, respiratory rate, skin temperature, capillary refill time, core-peripheral temperature gradient, level of consciousness, and urine output are strongly related to cardiovascular dynamics, and a change in these clinical parameters may indicate deterioration as well as a positive response to a hemodynamic intervention. Skin mottling, pallor, and diaphoresis are alarming signs that need immediate and appropriate intervention. Recent studies have shown a strong relationship between clinical and microcirculatory parameters and underline their importance in hemodynamic assessment.69–71

Mixed Venous Oxygenation72–75

image is the oxygen saturation of mixed venous blood in the pulmonary artery. It reflects the overall venous saturation after the blood has been fully mixed in the right side of the heart. image is related to the balance between oxygen delivery (DO2I) and the ability to extract oxygen, or the oxygen extraction ratio (O2ER). Under normal circumstances, oxygen consumption is independent of supply until oxygen delivery falls below the anaerobic threshold. The normal O2ER is approximately 25%, giving an image of 75%. In the face of a reduction in oxygen delivery, the tissues maintain oxygen consumption by increasing oxygen extraction, so image decreases. However, image does not necessarily vary with cardiac output. Not all patients can increase their O2ER if DO2I falls. Clinically, the response of image to an increase in cardiac output or oxygen delivery can aid hemodynamic manipulation. image can be measured by sampling blood from the distal lumen of a PAC and then measuring oxyhemoglobin saturation by means of co-oximetry, or by using an oximetric PAC that is able to continuously display image. A flow diagram of a published protocol using PAC-derived parameters is shown in Figure 3.6.

It has been suggested that image should be monitored and the key variables manipulated to keep it within the normal range (65% to 75%). In practice, this means ensuring that the hemoglobin concentration and arterial oxygen saturation are normal and then either increasing cardiac output or decreasing oxygen utilization (such as by sedation or cooling). Thus, image monitoring provides a means of assessing the adequacy of cardiac output for a given patient. This strategy has been used with success in post–cardiac surgery patients and has been suggested for use in critically ill patients.

Central Venous Oxygen Saturation

In patients without PACs in place, central venous oxygen saturation (ScvO2) may be measured by sampling from the distal lumen of a central venous line in the SVC. This variable bears some relationship to the mixed venous oxygen saturation, although because the venous blood is not totally mixed in the SVC, the relationship should be considered as representing a guide rather than reflecting reality. In practice, the central venous oxygen saturation should be used as a screening tool, rather than as an accurate marker of adequacy. If the level is very low, then the inference can be made that the circulation is inadequate; however, near-normal levels do not preclude underlying problems. The use of this variable in this fashion has proved successful in reducing mortality rates for early severe sepsis and is recommended as a target for therapy by the Surviving Sepsis Campaign.74–76

Blood Lactate

Blood lactate levels represent the balance between lactate production and lactate metabolism. The liver is responsible for the major part of lactate metabolism. Inadequate oxygen delivery and tissue hypoxia, irrespective of the underlying cause, results in increased lactate generation. In critically ill patients, high blood lactate levels develop from a combination of inadequate oxygen delivery secondary to poor perfusion (in terms of both perfusion pressure and flow), impaired cellular oxygen utilization from mitochondrial damage, and reduced hepatic clearance of lactate. A resolving lactic acidosis along with clinical signs of improved perfusion is an important indicator of improving perfusion after resuscitation. Lactate levels and lactate clearance have been shown to predict mortality risk and morbidity, and studies investigating protocols aimed at decreasing lactate levels have shown the potential role of lactate as a treatment goal.77–80

Venous-to-Arterial CO2 Difference (PCO2 Gap)

Oxygen-derived parameters, namely image and ScvO2, may falsely indicate adequate tissue perfusion in the presence of anaerobic metabolism due to microcirculatory compromise. In this situation, a decrease in oxygen consumption (VO2) may occur, either because of impaired oxygen delivery or reduced oxygen demand resulting in normal levels of image or ScvO2. In hypoxic conditions due to impaired tissue perfusion a rise in the partial pressure of CO2 (PCO2) is usually seen, widening the gap between arterial and venous PCO2. Recent clinical studies have suggested that the venous-to-arterial CO2 difference using a central venous and an arterial blood sample (P(cv − a)CO2 or PCO2 gap) may be used as a complementary tool to unmask inadequate tissue perfusion in patients who are apparently resuscitated to target goals, namely, an ScvO2 of 70%. Further prospective clinical studies will show if this parameter has the potential to function as a treatment goal in the resuscitation of critically ill patients with hemodynamic compromise.81–83

Goal-Directed Therapy

The concept of goal-directed therapy refers to the protocolized assessment and manipulation of hemodynamic variables in the resuscitation of critically ill patients. This approach became fashionable in the late 1980s and early 1990s, with a resurgence of interest in the early 2000s. Initially these protocols were relatively simple and consisted of measures to increase oxygen delivery and consumption to predefined targets. It was soon recognized that the same targets could not be used for every single group of patients undergoing different conditions and procedures, so protocols have now been refined for different patient populations.

Hemodynamic Optimization of the High-Risk Surgical Patient

Many different protocols have been used for the management of the high-risk surgical patient.84–92 Initially all such protocols targeted an oxygen delivery index of 600 mL/minute/m2 with the use of fluids and positive inotropic agents. Measurement of cardiac output was performed through a PAC. Currently, many different protocols have been devised, some targeting oxygen delivery, some the mixed venous oxygen saturation, and some ensuring adequate volume loading by targeting a maximal stroke volume. The newer protocols reflect the more modern technologies, so they typically involve less invasive strategies and techniques. Data suggesting one protocol over another are essentially lacking, so it is best to choose appropriate monitoring technologies and therapeutic end points in accordance with the particular characteristics of the patient group being treated and depending on availability of appropriate devices and trained practitioners. Two protocols for optimization are shown in Figures 3.6 and 3.7.

Early Goal-Directed Therapy of Severe Sepsis

Resuscitation of patients with severe sepsis and septic shock has been studied with an early goal-directed approach74 (Fig. 3.8). In this approach, cardiac output has not actually been measured; however, a number of surrogate markers of adequacy of the circulation have been targeted. Volume loading is instigated early in this protocol and then targeted against markers of lactate metabolism and central venous oxygen saturation. If these markers fail to fall, then oxygen utilization is decreased by sedation and mechanical ventilation, and oxygen delivery is increased with the use of red blood cell transfusion and a positive inotrope. It should be noticed that although different parameters are being used, this strategy is very similar in principle to that used in the high-risk surgical group of patients.

Conclusions

Resuscitation of critically ill patients is a complex process. Several simple steps need to be taken to ensure delivery of an appropriate level of resuscitation. First, the patient should attain an optimal level of preload. This is best achieved by identifying the group of patients who are likely to benefit from volume loading and then providing this intervention, while at the same time not giving excess intravascular volume to patients who are unlikely to benefit from it. If it is impossible to predict which patients will benefit, then the fluid should be given under tightly controlled circumstances in the form of a fluid challenge with close monitoring of the circulation. After appropriate volume resuscitation, the circulation of some patients will still be inadequate for their metabolic demands. These patients may then benefit from either a reduction in oxygen requirements or an increase in oxygen delivery. This approach necessitates the monitoring of the circulation and the metabolic status.

Key Points

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