Hemodynamic Monitoring

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74 Hemodynamic Monitoring

Andrew Rhodes, R. Michael Grounds, E. David Bennett

Hemodynamic monitoring is the intermittent or continuous observation of normal or altered physiologic parameters pertaining to the circulatory system, with a view to the early detection of need for therapeutic intervention. It also consists in observing how the cardiovascular system responds to illness, injury, and therapeutic intervention. Invasive hemodynamic monitoring has traditionally been within the realm of the intensive care unit (ICU) or operating theater, but attempts are now being made to improve noninvasive techniques and validate their use in other clinical settings. The main function of the hemodynamic forces that are measured is to transport substrates to, and clear metabolites from, the cells in order to allow adequate cellular function. Assessment of hemodynamics must therefore also take into account the metabolic status of the cells in particular relation to the supply of oxygen.

Techniques for hemodynamic monitoring have continued to evolve, and some of the technologies have markedly improved over the last decade. There are a number of different types of equipment utilizing a variety of different physical principles available for use in the ICU. Use of a particular method of monitoring should be adapted to the type of patient and is largely dependent on available technical expertise, cost effectiveness, and individual preference in each unit.

The primary objective of hemodynamic monitoring is to ensure that the patient is achieving an optimal tissue perfusion and oxygen delivery while maintaining adequate mean arterial pressure. Identification and correction of tissue hypoxia remains one of the central tenets of every protocol that aims to resuscitate patients from shock conditions. When monitoring circulation, it is imperative therefore that an estimate is made of the adequacy of circulation with respect to the likelihood of there being underlying tissue hypoxia. The monitors that are currently available in routine clinical practice are unable to assess tissue hypoxia at either a local or a cellular level. An extrapolation is therefore made from a number of globally measured variables that provides an estimate of the likelihood of underlying disturbance. This information can then be used to direct therapeutic decisions to benefit patients.¹^–¹¹ Ideally, targeting such goals should lead to significant reductions in morbidity and mortality. There is now evidence to show that such interventions can lead to reduced morbidity and mortality in some groups of patients.¹^–³ ¹¹

The key concepts of invasive monitoring revolve around two main principles: (1) the measurement of the physiologic variable can be achieved accurately and reproducibly, and the information obtained cannot be obtained by a less invasive method of measurement; and (2) the knowledge of this variable when used correctly can improve the outcome for that patient.^12,¹³

It must be remembered that no monitoring therapy will improve patient outcome on its own. It must be linked to a clinical protocol or therapeutic target that has been proven to improve outcome. The type of monitoring is governed by the environment in which it is likely to be used. Above all, it is incumbent on us as clinicians to ensure the monitoring systems used do not harm the patient and should not add to the burden of complications or even death that may befall him or her.

Arterial Pressure Monitoring

Noninvasive measurement of blood pressure is one of the most widely undertaken procedures in clinical medicine. Invasive techniques are more commonly employed in intensive care patients for several reasons. Most importantly, the accuracy provided by intraarterial lines is vital to assess the mean arterial pressure in critically ill patients when they are hemodynamically unstable. In addition, continuous surveillance of arterial pressure is of paramount importance when vasoactive agents are used. Furthermore, frequent noninvasive arterial pressure monitoring adds to the discomfort of the patient. Finally, an arterial line also permits frequent arterial blood gas estimations. Historically it has been relatively easy to measure pressure in the major peripheral arteries. Reliance has therefore been put on the maintenance of systemic pressure under the assumption that adequate pressure will also provide adequate flow and thus adequate tissue perfusion.

Studies in intensive care patients where the focus has been the maintenance of blood pressure have not been particularly fruitful.⁴ Hypotension is defined as a systolic pressure less than 90 mm Hg or a mean pressure less than 65 mm Hg. Most intensivists accept that pressure needs to be kept at a level that allows adequate tissue perfusion, particularly of the major organs, but that maintenance of blood flow through these organs is paramount.

Interpretation of the changes seen in the arterial waveform in relation to changes in intrathoracic pressure can now also give information about whether the patient is likely to respond to a fluid challenge (Box 74-1).^6,¹⁴ A greater than 10% or 12% variability of systolic pressure, pulse pressure, and/or stroke volume caused by the regular and consistent positive pressure associated with positive-pressure inspiration indicates that the patient is probably hypovolemic and is likely to respond to fluid resuscitation. It should be stressed, however, that this technique can only be used in sedated and ventilated patients in whom there is no spontaneous breathing. This is an important technological development because occult hypovolemia is probably not uncommon in critically ill patients and if unrecognized is likely to contribute to an increase in both morbidity and mortality.

Central Venous Pressure

Central venous pressure (CVP) is the intravascular pressure in the great thoracic veins, measured relative to atmospheric pressure. It is conventionally measured at the junction of the superior vena cava and the right atrium and provides an estimate of the right atrial pressure. The CVP is often used as a marker of volemic status or preload, although the ability of this measurement to provide this information is limited.

The CVP is influenced by the volume of blood in the central venous compartment and also the compliance of that compartment (Box 74-2). Starling¹⁵ demonstrated the relationships between CVP and ventricular contraction and Guyton the relationship between venous return and CVP. By plotting the two relationships on the same set of axes, it can be seen that the “ventricular function curve” and the “venous return curve” intersect at only one point, demonstrating that if all other factors remain constant in an individual patient, a given CVP can, at equilibrium, be associated with only one possible cardiac output (Figure 74-1). Both curves can of course be affected by a number of factors: total blood volume and distribution of that blood volume between the different vascular compartments (determined by vascular tone). The inotropic state of the right ventricle will affect the shape of the ventricular function curve. When any one of these factors is altered, there will be an imbalance between cardiac output and venous return that will persist for a short time until a new equilibrium is reached at a new central venous blood volume and/or an altered central venous vascular tone.

Figure 74-1 Ventricular function and venous return curves.

Normal CVP exhibits a complex waveform, illustrated in Figure 74-2. The a wave corresponds to atrial contraction and the x descent to atrial relaxation. The c wave that punctuates the x descent is caused by the closure of the tricuspid valve at the start of ventricular systole and the bulging of its leaflets back into the atrium. The v wave is due to continued venous return in the presence of a closed tricuspid valve. The y descent occurs at the end of ventricular systole when the tricuspid valve opens and blood once again flows from the atrium into the ventricle. This normal CVP waveform may be modified by a number of pathologic processes (Box 74-3).

Figure 74-2 Central venous pressure waveform from a ventilated patient (bottom), with time-synchronized electrocardiogram (ECG) trace (top). The a wave represents atrial contraction and occurs immediately after atrial depolarization, as represented by the p wave on the ECG. The c wave represents bulging of the tricuspid valve in early ventricular systole and is followed by the v wave, caused by atrial filling during ventricular systole.

Box 74-3

Disease States that Modify the Central Venous Pressure Waveform

In atrial fibrillation, the a wave is lost and the c wave may become more prominent.

In the presence of atrioventricular dissociation or junctional rhythm, when atrial contraction may occur during ventricular systole, extremely tall cannon a waves occur due to atrial contraction against a closed tricuspid valve.

In tricuspid regurgitation, blood is ejected backward during ventricular systole from the right ventricle into the right atrium. This produces a large fused c-v wave on the central venous pressure trace.

In tricuspid stenosis, forward movement of blood from the right atrium into the ventricle occurs against a greater than normal resistance, leading to an accentuated a wave and an attenuated y descent.

With pericardial constriction, a short steep y descent will also be seen that allows differentiation from cardiac tamponade, where the central venous pressure will be monophasic with a single x descent.

If the CVP is to be used as an index of cardiac preload, the end-diastolic pressure at end expiration must be identified. The c wave marks the closure of the tricuspid valve at the beginning of ventricular systole, and immediately before its onset, the measured pressure should be equivalent to the right ventricular end-diastolic pressure (except in the case of tricuspid stenosis, in which a pressure gradient will always exist between the two chambers). Where no c wave is clearly visible, it is conventional to take the average pressure during the a wave. Where no a wave is visible (e.g., in atrial fibrillation), the pressure at the Z point (that point on the CVP waveform that corresponds with the end of the QRS complex on the electrocardiogram) should be used.

Taking all these factors into account, it is perhaps not surprising that the CVP will not provide a reliable estimate of preload in critically ill patients. The CVP correlates poorly with overall volemic status, right ventricular end-diastolic volume, stroke index, or an individual patient’s response to a fluid challenge.¹⁶ It is perhaps best used in non–critically ill patients when it can provide an estimate of the components to right ventricular filling and venous return because their vasculature is behaving in a normal physiologic manner.

Pulmonary Artery Catheter

Continuous, reliable, and accurate pressure and flow monitoring of cardiac performance helps in the early initiation of appropriate therapy toward precise hemodynamic goals. The pulmonary artery catheter with its measured and derived parameters (Boxes 74-4 and 74-5) helps direct therapy in the critically ill who balance their physiology precariously. The first double-lumen, balloon-tipped, flow-directed catheter was designed by Swan and Ganz in 1970.¹⁷ Thereafter, there have been several modifications to the pulmonary artery catheter, which now enables continuous monitoring of cardiac output from a thermodilution technique, of intravascular pressures, and of mixed venous oxygen saturation (SvO₂).

Box 74-4

Parameters Measured Using the Pulmonary Artery Catheter

Pulmonary artery pressure

Central venous pressure

Cardiac output

Pulmonary artery saturation

Mixed venous oxygen saturation

Core temperature

Box 74-5

Parameters Calculated Using the Pulmonary Artery Catheter

Systemic vascular resistance

Stroke volume

Oxygen delivery

Oxygen consumption

Pulmonary vascular resistance

Left ventricular stroke work index

Right ventricular stroke work index

The pulmonary artery catheter is used to gain a comprehensive overview of the circulation. Information can be obtained about the preload, contractility, and afterload of the heart. Modern pulmonary artery catheters also measure the mixed venous oxygen saturation, enabling the clinician to make a judgment about the balance between the oxygen supply and demand. With this information, therapy can be tailored to the individual patient’s requirements. Once correctly positioned, the balloon tip is inflated, temporarily occluding the pulmonary artery. Transducing the catheter port just distal to the balloon provides the pulmonary capillary occlusion pressure. The pressure in the left atrium becomes the main determinant of pressure distal to the inflated balloon because a static column of blood links the two points across the pulmonary capillary bed. This occlusion pressure therefore can provide an estimate of left ventricular preload. Accurate recognition of the waveform indicating the occlusion pressure is vital; however, the ability of clinicians to recognize this waveform is poor.¹⁸^–²⁰ The catheter must be in the correct position and the point at the end of expiration must be identified to exclude interference from extravascular intrathoracic pressures.

For the pulmonary capillary occlusion pressure to give an accurate estimation of left ventricular preload, a number of criteria must be met:

• No impedance to flow across the pulmonary capillary beds

• No disease of the mitral valve

• A linear relationship between pressure and volume (compliance) in the left ventricle

Many of these criteria are not valid in the critically ill, and thus much like with the CVP, pulmonary capillary occlusion pressure represents only a poor marker of systemic preload.

Appropriate use of the pulmonary artery catheter relies on the user achieving an adequate level of cardiac output for any given situation. Cardiac output can be increased by increasing the preload of the heart (Table 74-1) and then by manipulation of either the right ventricular or left ventricular afterload. The adequacy of the cardiac output can be assessed in relationship to the body’s overall energy balance by a coordinated assessment of cardiac output and SvO₂.

TABLE 74-1 Normal Values of Cardiac Pressures Obtained from a Pulmonary Artery Catheter in a Spontaneously Breathing Patient

	Mean (mm Hg)	Range (mm Hg)
Right atrium	4	3-6
Right ventricle
Systolic	25	20-30
Diastolic	4	2-8
Pulmonary artery
Systolic	25	20-30
Diastolic	10	5-15
Mean	15	10-20
Pulmonary artery occlusion pressure	10	5-14

The SvO₂ is the venous saturation of oxygen in the pulmonary artery. It enables a quantification to be made of the overall oxygen extraction of the blood. The normal value for this is in the region of 70% to 75%. Any decrease in this variable is due to either a decrease in oxygen delivery or an increase in oxygen utilization. A thorough understanding of the factors that derive these variables therefore enables a complete understanding of the circulatory dysfunction for any given patient. In recent years, use of the pulmonary artery catheter has been surrounded by controversy (Table 74-2) after the publication of a large observational study linking it with a poor outcome.²¹ There have been suggestions²²^–²⁴ that use of the pulmonary artery catheter may not improve outcome, and there have been studies where use of the pulmonary artery catheter led to a worse outcome despite the fact that its use was restricted to sicker patients.^25,²⁶ A further study started to resolve this confusion was stopped early.²⁷ Larger prospective randomized controlled trials have now been performed and have refuted earlier suggestions of harm with this tool.^28,²⁹ What is clear from most of these studies is that if the pulmonary artery catheter is used without a clear protocol for treatment, then benefit is never demonstrated. With an appropriate protocol in the correct group of patients, however, improved outcomes can be shown.^1,^2,^30,³¹

TABLE 74-2 Complications Associated with the Pulmonary Artery Catheter

Complications Associated with Catheter Insertion
Minor arrhythmias	48%
Sustained arrhythmias	Uncommon
Arterial puncture	1%
Pneumothorax	1%
Complications When Catheter Is in Place
Infection of insertion site	0%-22%
Catheter-related sepsis	2%
Mural thrombus	28%-61%
Pulmonary infarction	0.1%-7%
Rupture of pulmonary artery	<0.1%
Death	<0.1%

Pulse Contour Analysis

Analysis of the arterial pulse pressure wave obtained from an intraarterial line can provide a great deal of information over and above just the value of arterial pressure. This has led to development of technologies for continuous monitoring of cardiac output obtained by analyzing the pulse wave contour obtained from intraarterial catheters placed in either the radial or femoral arteries. 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. The concept is not new. Otto Frank developed the Windkessel model to simulate the heart-vessels interaction in 1899.³² By 1904 Elanger and Hooker had proposed a correlation between stroke volume and change in arterial pressure and suggested there was a correlation between cardiac output and the arterial pulse contour.³³ This eventually led to the development of algorithms relating the arterial pressure contour and cardiac output, and with recent advances in computer technology, this has led to the development of the principle to the point where it can be used in clinical practice. These technologies offer the ability to monitor stroke volume (and therefore cardiac output) on a near real-time basis. This has several advantages over existing technologies, because the majority of critically ill patients already have arterial pressure lines in situ, thus allowing the technology to be deemed relatively noninvasive. Fluctuations of blood pressure around a mean value are caused by the volume of blood (the stroke volume) forced into the arterial conduit by each systole. The magnitude of this change in pressure—known as the pulse pressure—is a function of the magnitude of the stroke volume.

A number of factors exist that have made the transition of this concept into clinical reality technically challenging:

• Compliance of the aorta is not a linear relationship between pressure and volume. This nonlinearity prevents any simple approach for estimating volumes from the pressure change. There needs to be correction for this nonlinearity for any individual patient.³⁴

• Wave reflection. The pulse pressure measured from an arterial trace is actually the combination of an incident pressure wave ejected from the heart and a reflected pressure wave from the periphery. To calculate stroke volume, these two waves have to be recognized and separated. This is further complicated by the fact that the reflected waves change in size, depending on the proximity of the sampling site to the heart and also the patient’s age.

• Damping. As the change in pressure around a mean value describes the stroke volume, accurate pressure measurements are imperative. Unfortunately, pressure transducer systems used in routine clinical practice often suffer from being either underdamped or overdamped, leading to imperfect waveforms and measurements.

• Aortic flow during systole. Although the filling of the aorta is on an intermittent pulsatile basis, outflow tends to be more continuous.

The systems require constant reappraisal during use, and the need for recalibration is paramount.³⁵^–³⁷ Taking all these problems into consideration, the ideal algorithm for arterial pulse contour analysis should contain the following features:

• The algorithm must work independently of whichever artery the blood pressure is being measured from—despite the known fact that the pressure waveform shape and pressure itself are changed by transmission through the arterial tree to the various peripheries.

• It must correct for known aortic nonlinearity and would need to be calibrated to take account of any individual’s variation in aortic characteristics and therefore be able to measure individual stroke volume.

• It should not be affected by changes in systemic vascular resistance causing changes in reflected wave augmentation of the peripheral arterial pressure.

• It must not rely on identifying details of wave morphology.

• It must not be affected by any form of damping or distortion of the arterial cannulae and lines.

In recent years, a number of companies have developed systems to measure stroke volume from pulse pressure analysis techniques. Many of the companies developed methods for calibrating the pulse contour changes for individual patients. This compensated for the inability to determine arterial compliance. This has been achieved with either transpulmonary thermodilution (PiCCO),³⁴ lithium dilution (LiDCO),³⁸ or an internal “autocalibration” by the Vigileo system. With an accurate and precise calibration, the data obtained by these devices are as reliable as the pulmonary artery catheter. Many questions remain unanswered, however. For instance, when are the devices likely not to provide robust information, how are the algorithms affected by significant changes in vasomotor tone, and how frequently should the recalibration be performed? Recent data have shown that the devices can be used to titrate therapy in surgical patients, with resulting improvements in outcome.³⁹

Esophageal Doppler

The 19th-century physicist Christian Doppler described the effect that bears his name, demonstrating that the shift in frequency emitted by, or reflected off, a moving object is proportional to the relative velocity between object and observer. Doppler derived a formula that related frequency shift to velocity, which included the variables that might distort this observation (such as the angulation of the point of observation to the path of the moving object and the speed sound). This observation has been widely used for measuring the speed of moving objects, ranging from stars to cars to red blood cells. Transcutaneous Doppler ultrasound has been in general clinical use for measuring blood velocity in both peripheral and central veins and arteries for a considerable time. In 1969, Light ⁴⁰ demonstrated that it could be used to measure the velocity of blood in the human aorta. This has since been further developed and improved such that blood velocity can now be measured in the descending aorta, from which cardiac output can be calculated. The two most commonly used commercially systems both use a flexible probe which is inserted down into the esophagus to a length of approximately 40 cm from the mouth. One system (Deltex CardioQ⁴¹) has a piezoelectric crystal mounted at 45 degrees on the tip of the disposable probe which produces ultrasound at a continuous frequency of 4 MHz. The probe tip is adjusted to lie in the esophagus at a point alongside the descending aorta. The ultrasonic beam is transmitted into the lumen of the aorta, insonating the moving red cells. Some of the ultrasound is reflected back to the crystal at a frequency proportional to the velocity of the moving red cells. This shifted frequency is converted to a velocity using the Doppler equation:

where V = velocity of blood in cm/sec, f = Doppler shifted frequency, Fo = transmitted frequency, C = acoustic velocity in blood, and Q = angle of Doppler beam to blood vessel. The velocity of the red blood cells thus obtained is converted to flow using a propriety algorithm which assumes the cross-sectional diameter of the descending aorta based on a number of factors including age, gender, height, and weight. Because this measurement is made on the descending aorta, it does not take into account flow to head and arms, which is assumed to be a constant 30% of the total cardiac output. Beat-by-beat values for cardiac output and stroke volume are calculated, and these values have been shown to correlate well with cardiac output measured by thermodilution.²⁵ In contrast, the other commercially available product (Arrow Hemosonics⁴²) uses a nondisposable probe over which is placed a disposable sheath; the whole device is then inserted into the esophagus. The pulsed Doppler transducer measures descending aortic red blood cell velocity. This is converted to flow by the continuous measurement of descending aortic diameter, which is obtained from an M-mode echo signal provided by a separate transducer incorporated in the probe. Good correlation with independent measurements of cardiac output have also been obtained with this device. This technique allows cardiac output and stroke volume to be measured rapidly and relatively noninvasively and requires less training than required for use of the pulmonary artery catheter. Most studies find a similar agreement with the values for cardiac output measured with this technique as compared to the pulmonary artery thermodilution catheter.⁴²^–⁴⁶ Operator experience is frequently cited as the cause of any inaccuracy. It can be difficult to ensure that the Doppler probe is correctly positioned in the esophagus to ensure that the probe tip is accurately measuring the maximal blood flow at the center of the aorta.⁴⁵ This technique has been used to improve the outcome of surgical patients by titrating fluid challenges to achieve a maximal stroke volume in the intraoperative setting.

Electrical Impedance Cardiography Technology

Electrical impedance cardiography technology measures the basal chest electrical impedance or resistance to flow in ohms.⁴⁷ The change of impedance across the chest wall is related to the change of flow of blood throughout the chest cavity. The impedance dz/dt (dz = change in impedance, dt = change in time) is produced by change in blood flow and volumes in the ascending aorta. In devices using baseline impedance, large amounts of thoracic fluid such as severe pulmonary edema may interfere with the impedance signal and dampen the waveform. The latest methods are baseline impedance independent. They provide continuous trends of heart rate and stroke volume and give derived cardiac output and index using stroke waveform morphology. Recent models of electrical impedance cardiography use advanced waveform morphology analysis to measure a filling index, the trend of which may be useful in monitoring response to therapy. Unfortunately, in view of its major limitations, its reliability in critically ill patients is very limited. Recent advancements in this technology use the concept of frequency amplification as opposed to amplitude modification (FM rather than AM), which leads to a much more robust signal-to-noise ratio. This is now known as bioreactance. Early data from this technique appear promising, although further validation is required.