The measurement of cardiac output has an important place in anaesthesia and critical care, although the actual benefit to patients is debatable. The concept is that there is a relationship between cardiac output and tissue oxygen delivery, and thus a subsequent impact on important clinical outcomes. The assessment can be used alongside other methods of CVS assessment, such as fluid status, to guide the treatment approach.
Some approaches may also be used to infer features of cardiac output by the assessment of related values:
Venous saturation measurements
Clinical assessment is also clearly and essential part of such an assessment. Clinical features that may be useful include:
A more detailed review of cardiovascular physiology is available elsewhere, but understanding the key components is essential.
Cardiac output is the volume of blood pumped by the heart per unit time. This is usually set as the left ventricle blood flow per minute, as the left and right flow should be essentially identical in the normal circulation. It is often corrected to the patient’s size (body surface area) to give the cardiac index.
Cardiac output = stroke volume x heart rate
The factors that impact on stroke volume are:
Cardiac output is related to blood pressure, but BP is not a surrogate of it.
BP = CO x SVR
This demonstrates how BP may not reliably be used as a marker of CO, and thus why assessment of CO is important.
The relationship between CO and oxygen delivery (DO2) is perhaps the main point of interest for clinicians. DO2 = CO x CaO2
CaO2 refers to the arterial oxygen content. CaO2 = (1.34 x Hb x SpO2) + (PaO2 x 0.0225) So, as can be appreciated in the equation, CO and the oxygen saturation are the key factors that impact on tissue oxygen delivery.
Pulmonary Artery Catheter
The PAC (a.k.a. Swan-Ganz catheter) is currently described as the ‘gold standard’ of cardiac output monitoring, although perhaps more by historical default than by clinical justification. It was first introduced in 1970, but the risk vs benefit profile has seen its use decline in more recent times.
The PAC involves the insertion of a CVC (requiring a special introducer). The next step involves ‘flotation’ of catheter into the correct location, within a pulmonary artery. A balloon at the tip of the inserted catheter is filled with air, and the flow of blood theoretically carries this balloon (and the catheter) through the right side of the heart and into a pulmonary artery. Observation of the waveform, transmitted from the tip of the catheter, can identify its locations at different steps. Once in the pulmonary artery the balloon would then be deflated.
Essentially, if a change in concentration from a known intervention can be measured, then the flow can be inferred. The traditional ‘known intervention’ became a fixed volume of cold saline (at a known temperature), with the subsequent change in temperature measured downstream of the injection, at the tip of the catheter. The degree of dilution would be dependent on the volume of what it is being diluted into. The measurement of this dilution over time would therefore demonstrate flow and the cardiac output could therefore be measured. The Stewart-Hamilton equation is used to calculate this. The average of several injections is usually employed to reduce error. Dye dilution was previously employed, using indocyanine green, but accumulation was a problem for repeated testing.
Additional measurements can also be obtained which may be of use in CVS assessment:
Pulmonary artery pressures
Right heart pressures
Mixed venous saturations
Wedge pressure refers to the measurement of the pressure measured when the catheter is wedged. The balloon is inflated and thus the artery that the catheter is sat in is occluded. There is therefore, in theory, a continuous column of blood between the tip of the catheter and the left atrium. Measurement of the pressure here can be used to infer left ventricular preload.
The Fick Principle can also be used to determine cardiac output. This is a manipulation of the physiological equations above. If we know the difference between the arterial and venous side of the circulation, and we know the VO2 (from oxygen utlisation), we can derive the cardiac output.
VO2 = CO x (CaO2-CvO2) Therefore: CO=VO2/(CaO2-CvO2)
Inaccuracy can arise from a number of conditions though:
Abnormal respiratory patterns
Pulmonary vessel rupture
There are also the complications associated with CVC insertion itself e.g. pneumothorax, arterial injury.
As noted, part of the reduction in PAC use arose from the concerns of harm alongside the absence of clear benefit.
These devices utilise the theory that the arterial waveform (specifically the pulse pressure), being produced by the contraction of the LV, has a relationship to the stroke volume. This can then be analysed to infer the cardiac output, and because of the impact of the vasculature, the SVR too. An algorithm is used to translate the shape of the arterial waveform into desired CVS parameters, including SV, CO, CI, and other useful values such as SVV. They have been well studied and generally show good correlation with the PAC 'gold standard'. They are however subject to error, some of which may be mitigated. Several use a form of calibration to increase their accuracy.
There are a number of commercially available devices utilising this approach, with slightly different methods:
This utilises a thermistor tipped arterial catheter located in a proximal artery e.g. femoral. The catheter is calibrated using transpulmonary thermodilution. Cold saline is injected into a CVC, and the subsequent temperature change is used to infer the cardiac output, in much the same way as the PAC but more distantly. After calibration, the arterial waveform itself can be used to derive the desired CVS indices.
The use of transpulmonary thermodilution allows some additional useful values to be obtained, including:
Global end-diastolic volume (or index)
Extravascular lung water
Error from this method may arise due to the extra distance that the injectate has to travel before reaching the thermistor, and the interference that may arise en route. This includes:
Pulmonary oedema - loss of injectate
Shunting (intra-cardiac or intra-pulmonary)
The technique here is very similar to those already described, but using the dilution of lithium rather than thermal energy. It also uses pulse power analysis rather than pulse contour analysis to interpret the arterial waveform. A defined volume (0.5-2ml, max 20ml) of lithium chloride 0.15mmol/L is injected on the venous side of the circulation (peripheral or central). Arterial blood is then steadily aspirated at 4ml/min through a lithium sensitive electrode, producing a similar lithium concentration vs time curve as described for temperature already. Some mathematical manipulation is needed to account for the sodium level, and to convert the plasma flow (as is just the plasma that is measured) into blood flow (which is desired).
Current lithium use
First trimester of pregnancy
Weight < 40kg
Arterial trace problems
Lithium therapy elevates the background levels, making analysis difficult. Muscle relaxants interact with lithium and can also affect accuracy when they are being used at high doses.
This approach is most commonly based on assessment of the descending aorta by a probe in the oesophagus. There is a technique that used the same principle to image the LVOT through the chest wall (the USCOM) device. It uses the doppler principle to derive the velocity of blood in the aorta - this velocity is plotted against time in the graphical representation of this. By integrating the velocity of the blood with respect to time, a stroke distance can be calculated i.e. how far the blood moves along the aorta per beat. When this is multiplied by the cross sectional area of the aorta, a stroke volume is calculated. This cross sectional area is usually estimated based on the demographics of the patient (age, height and weight). Some more advanced application may involve actual measurement of the aorta. There must also be correction to compensate for the fact that it is only the blood in the descending aorta that is being measured; about 70% of total cardiac output.
Turbulent aortic flow (the equations assume laminar)
Estimated cross-sectional area values
Problems may therefore arise from:
Aortic pathology (aneurysm, coarctation)
Lower limb vasodilatation (regional anaesthesia)
The descending aorta is measured from the oesophagus, which runs parallel and adjacent to it at a distance of about 35-40cm from the teeth. This is generally the best location for it to be used. The probe must be well lubricated before insertion, both to aid insertion and optimise sonographic contact. Manipulation of the position will be needed after insertion to achieve the optimal waveform. This is the waveform with the clearest signal and highest velocity. There should be minimal/no flow in diastole (not the case for example when imaging the celiac artery), and the flow moving away from the probe. Once this image is achieved, the analysis process can be commenced (e.g. ‘run’ mode). This will automatically trace the profile of the waveform and calculate the derived indices.
As well as providing values on cardiac output, additional components of the doppler waveform can be useful in helping to understand the CVS picture. The values provided include:
Cardiac output (CO)
Stroke volume (SV)
Flow time corrected (FTc)
Peak velocity (PV)
Cardiac Output This is simply calculated from the derived stroke volume and the measured heart rate. A cardiac index (CO adjusted to body surface area) can also be calculated based on the input patient demographics. The normal cardiac index is 2.5-3.6 L/min/m^2
Stroke Volume The stroke distance is the area under the velocity-time waveform. This is converted into a volume by the application of the aortic cross-sectional area as previously described. This is usually averaged over several beats due to beat to beat variation, the number of beats being termed the cycle length (which can be increased in cases of severe irregularity e.g. AF).
Flow time corrected The flow time is the time that the blood is flowing forward in each cycle. This varies according to heart rate, and so is corrected to the standard of 60 beats/min, a bit like is done for the QT interval. This is affected by the LV filling and by resistance to LV outflow The normal FTc is 330-360ms. A reduced FTc may be seen in:
It may be prolonged with peripheral vasodilatation e.g. anaesthesia, where ip to 400 may be considered to be normal.
Peak Velocity This is what it says, and graphically is represented by the height of the waveform. It is correlated with myocardial contractility. It is also affected by preload and afterload, rising with an (appropriately) increased preload and with a reduction in afterload. PV varies with age, giving a falling ‘normal range’ in older patients:
Age 20 - 90-120 cm/s
Age 70 - 50-80 cm/s
Mean Acceleration This is the angle of the upstroke of the doppler waveform. Again, this provides information on contractility.
Assessment of these features can give typical patterns in certain clinical conditions.
Improvement with fluid challenge
Vasodilatation e.g. sepsis
Reversal of flow in diastole
Fluid Challenge The response to a fluid challenge can be assessed using oesophageal doppler to assess whether a patient is fluid responsive. A positive response would include:
A threshold of 10% increase in SV is often used to differentiate.
Critical Care A 2004 meta-analysis by Dark and Singer suggested that it was a useful monitor for assessing changes in CVS indices, although less useful for providing absolute values when compared to the gold standard of a PAC.
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Reisner, A. Academic assessment of arterial pulse contour analysis: missing the forest for the trees? BJA. 2016. 116(6):733-736.
Dark, P. Singer, M. The validity of trans-esophageal Doppler ultrasonography as a measure of cardiac output in critically ill adults. Intensive Care Med. 2004. 30(11): 2060-6. https://www.ncbi.nlm.nih.gov/pubmed/15368037
Al Shaikh, B. Central venous and pulmonary artery catheters. e-LFH. 2012.
Avery, S. Jonas, M. Cardiac output monitoring 1. e-LFH. 2016.