ARTERIAL BLOOD PRESSURE

The systemic pulse wave propagates from the aortic valve at 6–10 m/s. During its passage into the peripheral vasculature there is a progressive increase in systolic (SBP) and reduction in diastolic blood pressures (DBP), as standing and reflected waves become incorporated into the waveform, a process known as distal pulse amplification. Consequently, systemic arterial pressure measurements vary according to the site of measurement.

Mean arterial pressure (MAP) is arguably a more relevant index to monitor than either SBP or DBP for three reasons:

In the absence of sophisticated waveform analysis, arterial pressure is poorly correlated with cardiac output. Hence clinical estimation of cardiac output from arterial pressure and heart rate is unreliable until extreme hypotension occurs.²

CENTRAL VENOUS CATHETERISATION (CVC)

CVC is indicated for monitoring of central venous pressure (CVP) and administration of certain drugs and parenteral nutrition. Modified catheters are also available which continuously monitor central venous oxygen saturation (S_cvO₂). Contraindications to CVC are relative and reflect potential complications of the procedure (Table 12.3). These should be considered in selecting the site for catheter insertion. Particular attention should be paid to the coagulation profile and factors which affect coagulation such as thrombolysis and activated protein C therapy.

Table 12.3 Complications of central venous catheterisation, with preventive and treatment options⁶²

Traditionally, puncture of the central vein is performed by passing a needle along the anticipated line of the vein with reference to surface anatomical landmarks (landmark method). Catheterisation is usually achieved via the subclavian, internal jugular or external jugular veins into the superior vena cava.¹² The median cubital and basilic veins are used less commonly. Access to the subclavian vein is usually via the infraclavicular approach, but the supraclavicular approach is safe and reliable in experienced hands.

The use of ultrasound has been advocated to optimise the success rate of CVC insertion and minimise complications.¹³ Two-dimensional imaging can be used to localise the vein and define anatomy prior to placement of a CVC by standard landmark techniques. Ultrasound can also provide real-time, two-dimensional guidance during CVC insertion. Alternatively, audio-guided Doppler ultrasound can aid localisation of the vein and differentiate it from its companion artery during CVC insertion.

In 2002, the UK National Institute for Clinical Excellence issued guidelines recommending the use of ultrasound for elective catheterisation of the internal jugular vein, and consideration of ultrasound guidance in most clinical situations.¹⁴ These recommendations for ultrasound-guided internal jugular catheterisation are supported by meta-analysis.¹⁵ However, there are limited data supporting its use for subclavian and femoral veins.

The right tracheobronchial angle and carina are common radiological markers of insertion depth. In an attempt to reduce further the incidence of venous erosion (which is rare but potentially catastrophic), some practitioners place the catheter tip lower in superior vena cava or even in the upper right atrium, ensuring that the catheter is parallel to the long axis of the vein so that the tip does not abut the vein or heart wall end-on.¹⁶

Femoral venous catheterisation with radiological positioning of the tip close to the right atrium produces pressure measurements in good agreement with the subclavian CVP.¹⁷

PULMONARY ARTERY CATHETER

Right-heart catheterisation using a flow-directed balloon-tipped catheter was introduced by Swan and Ganz in 1970.²³ The ability to monitor sophisticated haemodynamic and gas exchange variables at the bedside appealed to clinicians, and the PAC was rapidly accepted into routine critical care.

In 1996 a non-randomised cohort study of PAC use in American teaching hospitals appeared to show that, in any of nine major disease categories, PAC in the first 24 hours increased 30-day mortality (odds ratio 1.24, 95% confidence interval (CI) 1.03–1.49), mean length of stay and mean cost per hospital stay.²⁴ A simultaneous editorial called for a moratorium on PAC use, and for a prospective multicentre trial.²⁵

A subsequent Cochrane database systematic review of PAC monitoring in adult ICU patients incorporated data from two recent multicentre trials and 10 other studies.²⁶ The pooled mortality odds ratio for studies of general ICU patients was 1.05 (95% CI 0.87–1.26) and for studies of high-risk surgery patients was 0.99 (95% CI 0.73–1.24). PAC monitoring had no impact on ICU or hospital length of stay (where reported). A recent multicentre trial incorporating protocolised haemodynamic management of patients with acute lung injury compared PAC-guided with CVC-guided therapy.²⁷ There were no significant differences in 60-day mortality or organ function between groups. Overall, these data suggest that PAC monitoring in critically ill patients is not associated with increased mortality or with survival benefit.

On the other hand, recent data suggest a differential association between PAC use and mortality dependent upon severity of illness. Logistic regression analyses of data from a tertiary-care university teaching hospital²⁸ and from the National Trauma Data Bank (American College of Surgeons)²⁹ suggest that PAC use may be associated with survival benefit in the most severely ill/injured patients.

Overall, the PAC still finds application as a haemodynamic monitoring tool in the ICU and the operating room. However, its role is under increasing scrutiny, and continues to decline in favour of less invasive alternatives. It could be argued that future PAC use should be guided by studies to determine optimal management protocols and appropriate patient groups.²⁶

Traditional indications for PAC monitoring have been to:

Contraindications for insertion reflect those for CVC. If known in advance, atypical cardiac or vascular anatomy, either congenital or secondary to trauma or surgery, should also be considered. Less invasive monitoring might provide the data that are sought. Also, PAC monitoring does not exclude simultaneous recourse to other monitoring techniques.

CATHETER INSERTION³⁰

A 7.5–9 F 15-cm introducer sheath is first inserted by the Seldinger technique. The subclavian and internal jugular veins are most commonly used. Access is feasible with the 110-cm catheter via the median cubital, basilic and femoral veins. The external jugular veins can also be used, although difficulty may be encountered passing the introducer both into the vein and then subsequently below the clavicle into the subclavian vein.

Balloon volume is 1.5 ml. The balloon should be tested prior to insertion into the sheath. Deflation should always occur passively to minimise the risk of balloon damage. Before passage through the heart the balloon should be inflated to assist flow guidance and protect against myocardial injury and dysrhythmias. Inflation should not be forced, and should not alter the waveform prior to wedging. The right atrium is reached at 15–20 cm from the internal jugular vein, 10–15 cm from the subclavian vein, 30–40 cm from the femoral vein and 40 and 50 cm respectively from the right and left basilic veins. The right ventricle and pulmonary artery (PA) are then entered at additional 10-cm intervals, with a further 10 cm to PA occlusion.³¹ Waveforms seen as the catheter floats to the wedged position are shown in Figure 12.1.

Figure 12.1 Pressure tracings and electrocardiogram (ECG) trace obtained on insertion of a pulmonary artery catheter. The snap flush test confirms an appropriate frequency response and degree of damping. RA, right atrial trace; RV, right ventricular trace (note simultaneous premature ventricular contractions during RV passage of the catheter); PA, pulmonary artery trace (note dichrotic notch and elevated diastolic pressure); PW, pulmonary wedge trace (note respiratory variation).

(Reproduced with permission from Leatherman JW, Marini JJ. Pulmonary artery catheterization: interpretation of pressure recordings. In: Tobin MJ (ed.) Principles and Practice of Intensive Care Monitoring. New York: McGraw Hill; 1998: 822.)

MEASURED VARIABLES

The PAC remains unique in its ability to measure right ventricular and pulmonary arterial pressures directly at the bedside. In acute respiratory distress syndrome (ARDS), where pulmonary hypertension and increased right ventricular afterload are linked to excess mortality,³² a PAC can assist in the titration of afterload-reducing therapies such as inhaled prostacyclin or nitric oxide.

In this context echocardiography might be considered as a less invasive alternative, since it provides a qualitative assessment of right ventricular loading³³ and can estimate PA pressures via Doppler techniques.³⁴ However, these are largely confined to intermittent ‘snapshot’ assessments, and can be challenging in mechanically ventilated patients.

Normal pressures are given in Table 12.5.

Table 12.5 Measured and derived variables from pulmonary artery catheter

Site	mmHg	kPa
Right atrium: mean	−1–7	0.13–0.93
Right ventricle: systolic	15–25	2.0–3.3
Right ventricle: diastolic	0–8	0–1.1
Pulmonary artery: systolic	15–25	2.0–3.3
Pulmonary artery: diastolic	8–15	1.1–2.0
Pulmonary artery: mean	10–20	1.3–2.6
Pulmonary artery occlusion pressure	6–15	0.8–2.0

PULMONARY ARTERY OCCLUSION PRESSURE

Measurements of PAOP should be performed by slow injection of air into the balloon while watching the PA waveform. Overwedging can lead to falsely high occlusion pressures or pulmonary arterial rupture. Less than 1.5 ml air may be required. Deflation after PAOP measurement should re-establish the normal pulmonary arterial waveform. If not, distal migration has occurred and the catheter should be withdrawn until the waveform is re-established.

PAOP should be measured during end-expiration and ideally in end-diastole, using the electrocardiogram (ECG) P-wave as a marker. PAOP has been termed the back-pressure to pulmonary blood flow,³⁵ and is also a key determinant of pulmonary capillary pressure (see below) and hence extravascular lung water. When the catheter wedges in a branch of the PA it creates a static column of blood which equilibrates with downstream pressure at the site where it rejoins the flowing pulmonary venous system (the j point). Here the blood is very near the left atrium. PAOP therefore closely approximates left atrial pressure (LAP), which approximates left ventricular end-diastolic pressure (LVEDP). The validity of PAOP as a surrogate of preload depends on a number of assumptions (Figure 12.2). These assumptions are often incorrect in critically ill patients and the use of PAOP to reflect preload has been questioned.³⁶

Figure 12.2 Factors affecting the accuracy of pulmonary artery occlusion pressure (PAOP) as a measure of preload in critically ill patients. Clinically, left ventricular end-diastolic volume (LVEDV) is usually accepted as a surrogate of preload. LAP, left atrial pressure; LVEDP, left ventricular end-diastolic pressure.

Zone 3 or not?³⁷

The catheter tip usually floats to a level at or below the left atrium. To maintain a column of fluid between the pressure transducer and the LAP, the tip should be in West’s zone 3 (alveolar pressure < pulmonary venous pressure). Factors which increase the likelihood of wedging in zones 1 and 2 include high intrathoracic pressures when there is normal or increased lung compliance (e.g. obstructive pulmonary disease and high intrinsic positive end-expiratory pressure (PEEP)) and low cardiac output states. Here, rotating the relevant lung down maximises the likelihood of zone 3 positioning.

At the bedside, tests which suggest appropriate zone 3 catheter tip positioning include:

• tip of the catheter at or below the left atrium on lateral supine chest radiograph

• clearly delineated atrial waveforms

• respiratory variation of PAOP is ≤ 50% static airway pressure (peak – plateau)

• PAOP alters by < 50% of PEEP alterations

Waveform analysis

As with CVP, analysis of the PAOP waveform may give some indication of cardiac pathology. Constrictive pericarditis and pericardial tamponade show the same abnormalities (but less clearly) as in the CVP trace. Mitral regurgitation may cause a large v-wave, which may be confused with the PA waveform. The two can be distinguished by examining the timing of the waves relative to the T-wave of the ECG. The peak of the PA systolic wave occurs before and the v-wave occurs after the T-wave. Large v-waves may also be associated with mitral stenosis, congestive heart failure or ventricular septal defect.

Potential substitutes for PAOP

Measurement of PAOP requires wedging, which is associated with a number of risks (Table 12.6). The normal PA diastolic pressure (PADP) to PAOP gradient is < 5 mmHg, so that PADP may normally be used as a close approximation for PAOP. However, tachycardia (> 120 beats/min) and conditions that increase pulmonary vascular resistance (such as ARDS, chronic obstructive pulmonary disease and pulmonary embolism) variably increase this gradient, invalidating direct substitution of PADP for PAOP. The relationship between PADP and PAOP tends to be stable over hours. Once this is determined, PADP can be used to track PAOP in the short term without repeated wedge manoeuvres.

Table 12.6 Complications encountered with the pulmonary artery catheter (PAC) with proposed measures for prevention and treatment⁶³

Complications	Prevention	Treatment
During insertion
Damage to adjacent structures	As for central venous cannulation	As for central venous cannulation
Perforation of pulmonary artery	Ensure balloon inflated throughout insertion. Continuously monitor pulmonary artery waveform. Avoid distal PAC tip position	As for pulmonary artery rupture below
Air embolism	Raise venous pressure prior to insertion. Always occlude open ends during insertion. Use sheaths with pneumatic valve. Periodically check and tighten all connections. Remove air from fluid bag and tubing. Dress site with occlusive dressing after removal	Left lateral Trendelenburg position. Administer 100% oxygen and ventilatory support. If PAC in place, tighten all connections and attempt to aspirate air from right atrium or right ventricle. Basic/advanced life support if necessary
Dysrhythmia	Keep balloon inflated during passage from RA to PA. Minimise insertion time	For sustained ventricular tachycardia, remove PAC from right ventricle. For ventricular fibrillation, remove PAC and defibrillate
Right bundle branch block/complete heart block	Avoid PAC insertion in patients with left bundle branch block (LBBB) if possible. Insert PAC with pacing electrodes in patients with LBBB	Use pacing equipment as required
Catheter knotting/kinking	Minimise insertion time. Do not advance catheter against resistance. Check for waveform change from RA to RV or RV to PA after advancing 15 cm; if not, withdraw catheter	Check chest X-ray. Pull knot back then remove the sheath and catheter. If no sheath used, a cut-down to vein under local anaesthesia may be required. Exploration by a vascular surgeon is indicated if unsuccessful (5% of occasions)
Valve damage	Ensure balloon is inflated during forward passage through the heart and deflated prior to any retraction	Cardiothoracic consultation
During maintenance
Dysrhythmia (37%)	Remove PAC when no longer required	See above
Thrombosis	As for central venous cannulation	As for central venous cannulation
Pulmonary artery rupture (0.2%)	Risk factors include pulmonary hypertension, anticoagulation and in situ duration > 3 days. Maintain high level of suspicion. Avoid distal PAC tip position. Minimise wedge procedures. Continuously monitor pulmonary artery waveform – withdraw PAC if spontaneous wedging occurs, inflate with only enough air to change PA to PAOP waveform. Withdraw PAC if PAOP obtained with < 1.25 ml air	Check PAC position on chest X-ray, deflate and pull back. If applicable, stop anticoagulation therapy. Lateral position, affected side down. Selective bronchial intubation. PEEP. Surgical repair
Pulmonary infarction	As for pulmonary artery rupture	Check PAC position on chest X-ray, deflate and pull back. Observe
Infection – including endocarditis	As for central venous cannulation	As for central venous cannulation
Air embolism	High suspicion of balloon rupture. Avoid repeating failed attempts to inflate	See above

RA, right atrial; PA, pulmonary artery; RV, right ventricular; PEEP, positive end-expiratory pressure; PAOP, pulmonary artery occlusion pressure.

Echocardiographic (non-invasive) estimation of PAOP has recently been described in critically ill patients.³⁸

PULMONARY CAPILLARY HYDROSTATIC PRESSURE (P_cap)³⁹

P_cap tends to force fluid out of the pulmonary capillaries into the interstitium, and when elevated can contribute to the development of pulmonary oedema. In critical illness such as ARDS and sepsis, variability in the distribution of the precapillary and postcapillary resistance alters the relationship between P_cap and PAOP. Because of this, a normal PAOP may substantially underestimate the tendency for fluid leakage from the pulmonary capillaries. Although it can be challenging, measurement of P_cap can be performed at the bedside by analysis of a pressure transient after an acute PA occlusion (Figure 12.3).

Figure 12.3 Capillary pressure (P_cap) has been estimated from the pulmonary artery pressure decay following occlusion with balloon inflation. For better visualisation the occlusion trace is superimposed on a non-occluded trace, both recorded during an expiratory hold during mechanical ventilation. An additional trace using 20 data point moving average smoothing of the original trace (collected at 100 Hz) is superimposed on the curves. This further facilitates the visual estimation of the capillary pressure by defining more exactly the point of divergence of the occluded and non-occluded curves. In addition, an exponential curve has been fitted on the curve 0.3–2 s after occlusion. This fitted curve has then been extrapolated to the time of occlusion to provide the capillary pressure.

(Reproduced from Takala J. Pulmonary capillary pressure. Intens Care Med 2003; 29: 890–3, Figure 1, with kind permission of Springer Science and Business Media.)

MIXED VENOUS OXYGEN TENSION AND SATURATION

See Chapter 14.

BOLUS THERMODILUTION CARDIAC OUTPUT

A bolus injection into the right atrium of cold injectate (usually 5% dextrose) transiently decreases blood temperature in the PA (monitored by a thermistor proximal to the balloon). The mean decrease in temperature (calculated by integrating temperature over time) is inversely proportional to the cardiac output, which can be determined by a modification of the Stewart–Hamilton equation:

where Q = cardiac output; V = volume injected; Tb = blood temperature; Ti = injectate temperature; K1 and K2 = corrections for specific heat and density of injectate and for blood and dead space volumes; and Tb(t)dt = change in blood temperature as a function of time.

This is an indicator dilution method, using temperature change instead of indocyanine green dye, radioisotopes or chemicals such as sodium thiocyanate and hypertonic saline. Advantages are:

• The indicator is non-toxic.

• It does not recirculate. Repeat measurements are limited only by volume constraints and the time to regain temperature stability between injections.

• The method shows good agreement with the Fick and indocyanine green methods. However, there is considerable variability. A clinically significant change in cardiac output cannot be diagnosed with certainty unless there is a difference of approximately 15% between the mean of three cardiac output determinations and the previous mean.⁴⁰

Too much or too little injectate will respectively underestimate and overestimate cardiac output. Cold injectate (preferably 0–4° C, but up to 12° C is usually accepted) improves the signal-to-noise ratio, but causes a brief decrease in heart rate, reducing cardiac output while it is being measured. Room temperature injectate introduces a small decrement in bias and precision, but has acceptable accuracy. However, the accuracy using room temperature injectate is further degraded at extremes of cardiac index, high ambient temperatures (and thus injectate temperature) or in patient hypothermia.²⁹

Respiration causes fluctuations in cardiac output and PA temperature. Reproducibility is improved by taking measurements in expiration, though this may not reflect cardiac output throughout the respiratory cycle. Timing can be difficult and in practice an average of three evenly spaced measurements is taken. Causes of inaccurate measurements are listed in Table 12.7.

Table 12.7 Causes of inaccurate bolus thermodilution cardiac output measurements

Catheter malposition

Wedge position

Thermistor impinging on vessel wall

Abnormal respiratory pattern

Intracardiac shunts

Tricuspid regurgitation (common in mechanically ventilated patients)

Cardiac dysrhythmias

Incorrect recording of injectate temperature (minimised by siting thermistor on injection port)

Rapid intravenous infusions, especially if administered via the introducer sheath

Injectate port close to or within introducer sheath

Abnormal haematocrit values (affecting K2 value)

Extremes of cardiac output (room temperature injectate)

Poor technique

Slow injection (> 4 s)

Incorrect injectate volume

SEMICONTINUOUS THERMODILUTION CARDIAC OUTPUT⁴¹

This method uses the same principles as bolus thermodilution, but allows semicontinuous measurement by employing a thermal filament wrapped around the right ventricular segment of the catheter. This transmits low-power pulses of heat. ‘On–off’ heat pulses in pseudo-random binary code are delivered in cycles. The downstream thermistor detects the heat pulses, which are then cross-correlated with the input sequence and power (to allow differentiation of thermal signal from noise).

The method shows good experimental agreement with the Fick and bolus thermodilution methods, with bias and precision in the ranges of –0.08 to +0.35 and 0.5–1.2 l/min respectively.

Drawbacks of the technique are:

• inaccuracy during thermal disequilibrium,⁴² such as rapid infusions of cool fluids or after cardiac bypass

• delay in detecting sudden changes in cardiac output⁴²

• magnetic resonance imaging is contraindicated (it can melt the thermal filament)

• electrocautery can interfere with measurements

TRANSPULMONARY INDICATOR DILUTION

With this technique, thermal and other indicators injected into a central vein are detected in a systemic artery. Because the indicators pass through all chambers of the heart as well as the entire pulmonary circulation, information additional to cardiac output can be gained. In particular, central blood volumes and indices of extravascular lung water can be quantified (Figure 12.4).

Figure 12.4 Diagrammatic representation of the mixing chambers of the cardiopulmonary system. CV, central venous; EVLW, extravascular lung water; LAEDV, left atrial end-diastolic volume; LVEDV, left ventricular end-diastolic volume; PBV, pulmonary blood volume; RAEDV, right atrial end-diastolic volume; RVEDV, right ventricular end-diastolic volume; TD, thermodilution. ITTV is the whole volume between the points of injection and detection, including the EVLW. Pulmonary thermal volume (PTV) is the sum of PBV + EVLW. ITBV is the sum of RAEDV + RVEDV + PBV + LAEDV + LVEDV. EVLW = ITTV – ITBV. GEDV is the sum of RAEDV + RVEDV + LAEDV + LVEDV.

(Reproduced from Hudson ERGN, Beale RF. Lung water and blood volume measurements in the critically ill. Curr Opin Crit Care 2000; 6: 222–6.)

ULTRASOUND

Two approaches are available to measure stroke volume (and thereby, cardiac output) using sound waves. The first involves the use of echocardiography to measure systolic and diastolic left ventricular volumes. Stroke volume is calculated as the difference between these two volumes. Access to expensive echocardiographic equipment and trained personnel limits the usefulness of this technique for haemodynamic monitoring. The second method uses Doppler techniques to measure stroke volume (Figure 12.5).⁵² This approach is less dependent on image quality and shows better agreement with thermodilution.⁵³ Although ultrasonic measurements tend to be operator-dependent, Doppler measurement of aortic blood flow demonstrates good reproducibility (intraobserver, interobserver and day-to-day variability 3.2 ± 2.9%, 5.4 ± 3.4% and 3.3 ± 3.1%, respectively).⁵⁴

Figure 12.5 Doppler stroke volume calculation. The cross-sectional area (CSA) of flow is calculated as a circle from echocardiographic measurements or nomogram-based estimations. Velocity–time integral (VTI) is the integral of Doppler velocity with regard to time. Stroke volume (SV) is calculated as the product of CSA and VTI (ml/s in this example). Cardiac output is calculated from the product and SV and heart rate. Peak velocity of flow (V_peak) is also indicated.

The Doppler principle states that the frequency of reflected sound is altered by a moving target, such as red blood cells. Continuous and pulsed-wave Doppler are the main techniques employed to measure flow. Physical principles for the two techniques are similar. Pulsed-wave Doppler allows the site (depth) of sampling to be specified; the target sample is usually central laminar flow. With continuous-wave Doppler, a piezoelectric crystal transmits the ultrasound beam while another measures the frequency ofreflected waves. The velocities of all the red blood cells moving along the path of the ultrasound beam are recorded. As a result, a continuous-wave Doppler recording consists of a full spectral envelope with the outer border corresponding to the fastest-moving blood cells. The flow velocity (V) of red cells can be determined from the Doppler shift in the frequency of reflected waves.

where C is the speed of ultrasound in tissue (1540 m/s), ΔF is the frequency shift, F₀ is the emitted ultrasound frequency, and θ is the angle of incidence. The most accurate results are obtained when the ultrasound beam is parallel to flow (θ = 0°, cos θ = 1; θ =180°, cos θ = –1). However, angles up to 20° still yield acceptable results (θ = 20°, cos θ = 0.94).

In addition to measuring stroke volume, Doppler assessment of aortic blood flow can provide additional haemodynamic information. For instance, the duration of the aortic velocity signal corrected for heart rate (corrected flow time: FT_c) is inversely related to the systemic vascular resistance; hence, it is a marker of left ventricular afterload. A decrease in left ventricular preload can be associated with an increase in afterload (low FT_c). Other causes include excessive vasopressor doses, heart failure and hypothermia (all produce a low FT_c).⁵⁵ The peak velocity of aortic blood flow (V_peak) has been proposed as an index of contractility. Also, respiratory variation in V_peak (ΔV_peak) has been described as a predictor of increased cardiac output in response to fluid challenge.⁵⁶

PARTIAL REBREATHING OF CO₂^8,10,51

The Fick principle is an extension of the law of conservation of mass and states that the amount of a substance taken up by an organ (or the whole body) per unit time is the product of the arteriovenous concentration difference by the blood flow to the organ (or body). Historically it has been used to determine cardiac output by analysing oxygen uptake from the lungs (direct Fick method). This method requires PA catheterisation to sample mixed venous blood. Traditionally, it has been considered the ‘gold standard’, but in most ICU patients the stringent preconditions for accuracy are not met. Further error is introduced by the elevated oxygen consumption of inflamed lungs. Use is therefore mainly confined to cardiac laboratories.

The Fick principle can be applied to indicators other than oxygen. The indirect Fick method employs CO₂ as an alternative. The indirect Fick method can be represented mathematically by the formula:

where VCO₂ is whole-body CO₂ elimination, and CaCO₂ and CvCO₂ are the CO₂ contents of arterial and mixed venous blood respectively.

A partial rebreathing technique can be used to eliminate the need to measure CvCO₂ directly. The rebreathing values are obtained by introducing an additional 150 ml of dead space into the ventilator circuit (disposable rebreathing loop) and taking measurements once a new equilibrium has been established. Cardiac output can be measured at 3-minute intervals. Assuming that the CvCO₂ concentration does not change significantly throughout the rebreathing period, the terms associated with CvCO₂ cancel each other out and are not needed to calculate cardiac output.

The CO₂ concentration and airflow during a breathing cycle are measured by a mainstream infrared and airflow sensor. VCO₂ is obtained by multiplying airflow by CO₂ concentration. CaCO₂ is derived from end-tidal CO₂ (etCO₂) and the slope of the CO₂ dissociation curve (S). This is represented mathematically as:

Partial CO₂ rebreathing really measures non-shunted pulmonary capillary blood flow rather than total cardiac output. Therefore a correction for venous admixture is added based on FiO₂ and SaO₂ (measured by pulse oximetry).

THORACIC ELECTRICAL BIOIMPEDANCE^8,10

An alternating electrical current (high-frequency, very low magnitude) is passed through the thorax. Current is kept constant and fluctuations in electrical impedance are measured. Six electrodes are usually attached (two in the upper thorax/neck region and four in the lower thorax). These electrodes detect changes in bioimpedance and monitor cardiac electrical signals. The technique is very sensitive to any alteration in position or contact of the electrodes to the patient.

The change in aortic blood flow due to myocardial contraction (stroke volume) is measured from the changes in thoracic bioimpedance through the cardiac cycle. Other factors that contribute to a change in overall thoracic bioimpedance include changes in tissue fluid volume and changes in venous and pulmonary blood volume induced by respiration. Respiratory artefact is eliminated by averaging values over several cardiac cycles using the R-R interval as a synchronising signal.

Measuring whole-body rather than truncal impedance by placing electrodes on wrists and ankles also appears successful.

Inaccuracies can arise from numerous sources. These include motion artefact, electrical interference, dysrhythmias (including frequent premature atrial contractions and atrial fibrillation) and acute change in tissue water content (such as pulmonary oedema, pleural effusions or expansion of interstitial fluid). Despite these limitations, it is clinically appealing due to its non-invasive nature. Recent studies of second-generation technology have shown improved reliability of this technique.

FUNCTIONAL HAEMODYNAMIC MONITORING

The recently coined term, functional haemodynamic monitoring, implies a therapeutic application, independent of diagnosis.⁶⁰ It has been posed in response to the observation that, although stated in physiological terms, haemodynamic questions must be practical and concrete in order to address clinical problems. Arguably the most relevant functional haemodynamic question is: ‘Will stroke volume (or consequently cardiac output) increase with volume loading?’ This question can help guide the resuscitation of haemodynamically unstable patients and defines the clinical usefulness of predicting fluid responsiveness. This is an area of increasing research and clinical interest beyond the scope of this chapter. For reference, variables that have been described as indices of preload or predictors of fluid responsiveness in critically ill patients are presented in Table 12.9.

Table 12.9 Variables described as indices of cardiac preload or fluid responsiveness in critically ill patients

Variables have been divided into static and dynamic categories. Static variables are estimates of ventricular preload at a point in time, usually end-expiration. Dynamic variables are characterised by measurement of variation in haemodynamic measurements in response to changes in cardiac loading conditions.^{47,49,56,64–69}