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International consensus
Oesophageal Doppler
Figure 3
Table 1
Table 2
Table 3
Table 4
Table 5
Table 7
Table 8
Table 9

Haemodynamic monitoring

Non-invasive monitoring


  • logical to use a specific lead to view an area known to result in ischaemic changes on the 12 lead ECG but for routine use, use of the CM5 lead gives >80% detection of LV ischaemia (monitors anterior and lateral left ventricle) and causes few problems with the diagnosis of a dysrhythmia. Attach RA lead to manubrium, LA to V5 position and LL to usual position. Set monitor to lead I.
  • MCL1 (modified chest lead)is useful in patients with rhythm disturbances as atrial activity and conduction defects are easily seen. Attach LA lead to left subclavian position, LL to V1 and RA as ground; set monitor to lead III.

Blood pressure

  • most automated devices use an oscillotonometric technique and as a result the most accurate pressure is the mean arterial pressure.
  • tend to overestimate at low pressure and underestimate high pressure but the 95% confidence limits are +/- 15 mmHg over the normotensive range
  • give erroneous results in patients in AF or with other arrhythmias
  • cuff width most important determinant of the accuracy of the pressure reading. Should be 40% of mid-circumference of limb (the length should be twice the width). Cuffs which are too narrow tend to overestimate BP while those which are too wide tend to underestimate
  • complications include: ulnar nerve injury (usually associated with cuff being placed too low on upper arm), oedema of the limb, petechiae and bruising, friction blisters, failure to cycle and drip failure.

Urine output

  • although strictly speaking this is a monitor of renal perfusion only, urine output is often used as a guide to adequacy of cardiac output as the kidney receives 25% of cardiac output. When renal perfusion is adequate urine output will exceed 0.5 ml/kg/h.
  • use of diuretics such as frusemide and dopamine abolishes its usefulness as a haemodynamic monitor.

Thoracic electrical bioimpedence

  • non-invasive method of estimating cardiac output continuously
  • considerable doubt as to whether it does so accurately. A very recent study of a new system found that the mean relative error of the system compared to thermodilution cardiac output measurement was only 16.6%, however this was associated with a large standard deviation of 12.9%, indicating that in some patients it is grossly inaccurate.
  • recent data suggests that at least one device is adversely affected by the increase in lung water seen in critically ill patients

Oesophageal Doppler monitor

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Transoesophageal echocardiography

  • can be used to estimate end-diastolic volume and cardiac output
  • accurate but has a number of disadvantages
    • expensive equipment
    • specialist training required
    • short term use only
    • risk of dislodgement of ETT, NGT
    • risk of oesophageal injury

Arterial pressure monitoring

  • invasive measurement may result in an overestimate of systolic pressure due to systolic overshoot. Result of the physical properties of the system and can be eliminated by increasing the damping of the system (eg by using smaller gauge tubing) thus reducing the resonant frequency of the system. However increasing the damping reduces the sensitivity of the system. To prevent systolic overshoot the system should have a resonant frequency of > 30 Hz for heart rates up to 180/min and > 20 Hz for rates up to 120/min while retaining sufficient sensitivity. A method of determining the resonant frequency and damping coefficient of the system is given in table 1. Mean arterial pressure is accurately monitored even if the system does not meet the criteria above. The tubing connecting the arterial cannula to the transducer should be non-compliant and < 1 m in length
  • arterial pressure trace can also be used to give an indication of adequacy of preload. In mechanically ventilated patients the effect of positive intrathoracic pressure during inspiration is to increase left ventricular output and systolic arterial pressure early in inspiration, followed a few heart-beats later by a fall. This variation in arterial pressure is exaggerated in the presence of reduced preload and a significant correlation has been demonstrated between the systolic arterial pressure variations and end diastolic area estimated with transoesophageal echocardiography.
  • Systolic pressure variation can be quantified by establishing a baseline during a period of apnoea and then measuring the maximum subsequent upward (d up) and downward (d down) variation (figure 1).
    • d down:
      • normal: 5-6 mmHg
      • in one study shown to provide be a better predictor of responsiveness to fluid loading than PAOP and LV end-diastolic area
      • due to a a transient fall in venous return
      • directly affected by magnitude of tidal volume and can be greatly exaggerated in presence of air trapping or fall in chest wall compliance
    • d up:
      • normal: 2-4 mmHg
      • occurs in early inspiration
      • due to augmentation of stroke volume due to increase in L sided preload. In patient with impaired LV contractility may also reflect afterload reducing effect of positive intrathoracic pressure
  • Systolic pressure variation cannot be interpreted in presence of irregular arrhythmias and can only be used in controlled ventilation

Figure 1.

  • complications associated with invasive arterial pressure monitoring are listed in table 2. The morbidity associated with arterial cannulation is less than that associated with 5 or more arterial punctures.

 Central Venous Pressure (CVP)

  • can be monitored using catheters inserted via the internal jugular, subclavian and femoral veins.
  • correct placement should be confirmed by observation of a change in pressure in different phases of respiration, free aspiration of blood through the catheter and radiological confirmation of the position of the tip of the catheter in the superior vena cava (internal jugular and subclavian catheters)
  • femoral vein pressure can be used reliably as a guide to central venous pressure in ventilated patients who do not have excessively high intra-abdominal pressure
  • used as a guide to right ventricular filling. However, right ventricular preload is determined by end-diastolic volume not pressure and therefore, without knowledge of the ventricular compliance, an isolated CVP reading is of limited value. Compliance not only varies from patient to patient but varies with time in the same patient. Thus dynamic changes in CVP are more useful than absolute values. If the CVP rises > 7 mmHg in response to a fluid challenge (eg 50-200 ml of colloid over 10 mins) then the patient is probably maximally filled and any further filling will result in development of pulmonary oedema. If, however, the CVP returns to within 3 mmHg of its original value within 10 mins then the risk of pulmonary oedema is only moderate; nevertheless no further filling is required. If the CVP rises less than 3 mmHg the patient is probably underfilled.
  • in most patients LV filling will be adequate if RV filling is adequate but in those patients with impaired RV function (eg some patients with inferior myocardihal infarction, patients with severe sepsis) or lung disease leading to pulmonary hypertension this may not be the case. In addition left sided pressures may be abnormally high despite normal right sided pressures in patients with left ventricular dysfunction
  • analysis of waveform may yield further information (table 3). a wave is due to atrial contraction and follows p wave of ECG. c wave results from tricuspid valve closure. x descent is due to combination of atrial relaxation and downward displacement of AV junction during early part of ventricular systole. v wave corresponds to flow of blood into atrium against a closed tricuspid valve. y descent due to rapid flow of blood from atrium into ventricle in early ventricular diastole
  • complications are listed in table 4.

Pulmonary artery catheters

  • although the pulmonary artery catheter has become a standard part of haemodynamic monitoring in critically ill patients there is no conclusive evidence that its use leads to decreased mortality and it may instead increase mortality.
  • waveforms seen as the catheter passes through the heart and pulmonary artery to the wedged position are illustrated in figure 2
  • normal pressures are given in table 5.

Pulmonary artery occlusion pressure (PAOP)

  • approximates to LA pressure (LAP), which approximates to left ventricular end-diastolic pressure (LVEDP). The relationship between LVEDP and left ventricular end-diastolic volume is illustrated in figure 3.
  • in a number of conditions PAOP may not reflect LVEDP. These conditions are listed in table 6.
  • chest radiographs are not reliable means of detecting the fact that the catheter tip is outside zone III because of the effect of lung disease on West’s zones. However the following characteristics suggest the tip is outside zone III: a smooth-looking PAOP tracing, PADP < PAOP, increase in PAOP > 50% of change in alveolar pressure and a decrease in PAOP > 50% of the reduction in PEEP.
  • should be easy to aspirate blood from the tip of the PA catheter with the catheter "wedged" and the blood should be arterialized.
  • in patients with a markedly reduced vascular bed "wedging" the balloon may reduce venous return sufficiently to to result in an underestimate of both LAP and LVEDP.
  • LVEDV is determined by LV compliance and the transmural pressure. The transmural pressure can be obtained by subtracting the pressure surrounding the heart (approximately equal to the intrapleural pressure) from the LVEDP. Intrapleural pressure is closest to zero at end expiration and thus LVEDP most closely approximates to transmural pressure at end expiration.
  • analysis of the waveform may give some indication of cardiac pathology. Both constrictive pericarditis and pericardial tamponade cause the same abnormalities in the PAOP trace as in the CVP trace but the changes are seen more clearly in the CVP trace. Mitral regurgitation may cause a large v wave in the PAOP trace, which may cause it to 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 within the T wave of the ECG while the v wave occurs after the T wave. Large v waves may also be present in association with mitral stenosis, congestive heart failure or ventricular septal defect.

Pulmonary artery diastolic pressure (PADP)

  • PADP is closely related to PAWP except when the patient has pulmonary hypertension or is tachycardic. When the heart rate is > 120 beats/min there is insufficient time during diastole for venous run-off so PADP is spuriously high.

Thermodilution cardiac output measurement

  • injection of cold injectate into the right atrium causes a fall in temperature monitored in the pulmonary artery.
  • fall in temperature will be greater the lower the degree of dilution of the injectate.
  • the lower the cardiac output the lower the degree of dilution as the injectate is injected.
  • fall in temperature also depends on the temperature and the volume of the injectate. The relationship of these factors to the cardiac output is given by the Stewart-Hamilton equation:
        • Q = V(TB - TI)K1K2

    where Q = cardiac output, V = volume injected, TB = blood temperature, TI = injectate temperature, K1 and K2 = computational constants, and TB(t)dt = change in blood temperature as a function of time.

  • the colder the injectate the greater the signal-to-noise ratio and the better the accuracy and precision. However in most clinical situations 10 ml of injectate at room temperature provides an acceptable measurement.
  • smaller volume of injectate can be used in situations where volume overload is a concern without significantly affecting the results.
  • careful filling of syringes is necessary to avoid error due to variable injectate volumes.
  • respiration affects cardiac output as well as pulmonary artery blood temperature so, ideally, measurements should be made in the same phase of respiration. However it is difficult to synchronize injection with respiration and in practice an average of 3 evenly spaced measurements with variation of <10% between measurements gives an accurate estimation of cardiac output
  • causes of inaccuracy in measurements are listed in table 7. The cardiac index is the cardiac output divided by the body surface area. The latter is obtained from nomograms using the patient’s height and weight.

Derived values

  • formulae used to calculate these values and their normal ranges are given in table 8.
  • systemic vascular resistance is used as a guide to left ventricular afterload and left ventricular stroke work as a measure of contractility. Note that a change in preload can increase left ventricular stroke work without an increase in contractility and therefore preload must remain constant in order for stroke work to be used as a direct estimate of contractility. An alternative is to plot stroke work against an estimate of preload (eg PAOP) and compare that with a normal range; a shift to the left and up is interpreted as an improvement in ventricular function while a shift to the right and down is thought to reflect deterioration.
  • note that oxygen delivery is actually a measure of oxygen leaving the left ventricle and not oxygen delivery to tissue.
  • pulmonary vascular resistance calculated according to the formula given may not be the most sensitive indicator of intrinsic pulmonary vascular disease because it is highly dependent on the cardiac index and therefore to a large extent reflects ventricular function. The PAEDP-PAOP gradient may be a better indicator.

Mixed venous oxygen saturation (Sv'O2)

  • has been used as a measure of adequacy of tissue perfusion.
  • varies directly with cardiac ouput, Hb and arterial saturation and inversely with metabolic rate.
  • normal is approximately 75% but falls when oxygen delivery falls or tissue oxygen demand increases. When it falls as low as 30% oxygen delivery is insufficient to meet tissue oxygen demand and there is an increased potential for anaerobic metabolism and lactic acidosis.
  • situations with increased mixed venous oxygen saturations are more difficult to interpret; sepsis, A-V fistulae, cirrhosis, left-to-right cardiac shunts, cyanide poisoning, hypothermia and unintentional PA catheter wedging have all been reported as being associated with increased values. Increased values of Sv'O2 in sepsis may reflect a failure of cells to take up and utilise oxygen.
  • the relatively common occurrence of sepsis and of more than one medical problem in a patient means that Sv'O2 cannot be used in isolation to monitor adequacy of tissue perfusion. A normal value may simply reflect a combination of low cardiac output and sepsis.
  • can be measured either continuously using a fibre-optic Swan-Ganz catheter or by taking blood samples from the distal lumen of the Swan-Ganz catheter and measuring the saturation in a co-oximeter. At the low PvO2 in mixed venous blood the calculated saturations produced by blood gas machines are not accurate.

Right ventricular ejection fraction pulmonary artery catheter

  • utilises a PA catheter with a rapid response thermistor and an injection port that is designed to ensure uniform mixing of the iced injectate in the right atrium.
  • mean residual fraction (MRF) is calculated over time by dividing the temperature change by the R-R interval. The ejection fraction (RVEF) = 1 - MRF.
  • EDV can then be calculated from the stroke volume (CO/HR) divided by RVEF.
  • reasonable estimates of RVEF can be obtained provided that there is no valve regurgitation or arrhythmias.

Continuous thermodilution cardiac output

This uses infusion of heat from a filament in the right atrium rather than an injection of cold saline and stochastic system identification to enhance the signal-to-noise ratio. The monitor gives the average cardiac output over the previous 3-6 minutes updated every 30 seconds. Results appear to agree well with those obtained by bolus thermodilution.

Pulmonary capillary pressure (PCP)

  • major determinant in the formation of pulmonary oedema.
  • in patients with normal lungs it can be calculated from the the sum of PAOP and 40% of the difference between MPAP and PAOP. Based on the assumption that the ratio of pulmonary venous resistance to the total pulmonary vascular resistance is 0.4. In patients with lung disease or injury this may not be the case.
  • when the pulmonary artery is occluded the pressure distal to the balloon falls from pulmonary artery pressure to PAOP. The fall is characterised by first a fast and then a slow phase. The fast phase results from the cessation of pulmonary artery blood flow distal to the occlusion while the second phase results from the release of blood stored in the pulmonary capacitance vessels. The level to which the pressure falls purely as a result of cessation of pulmonary artery flow is PCP. Thus PCP can be calculated by extrapolating the slow phase back to the time of occlusion. This, however, requires knowledge of the precise time of occlusion. By using a double-port pulmonary artery catheter which has a pulmonary artery port both at the tip of the catheter and 1 cm proximal to the balloon it is possible to determine the precise time of occlusion from the time at which the two pulmonary artery pressure curves abruptly diverge


  • listed in table 9.
  • in one study of 6245 catheter insertions use of the pulmonary artery catheter was associated with death in 1 case, pulmonary infarction in 4, intrapulmonary haemorrhage in 4, permanent right bundle branch block in 3, complete heart block in 1 and ventricular ectopics requiring treatment in 193
  • if catheter appears to be knotted on CXR remember that it may not be actually knotted. Pull out other catheters in reverse order in which they were inserted and then repeat CXR. If there is a true knot: pull catheter back until it is at end of sheath. Pull hard and knot will usually enter sheath. Then remove whole apparatus. If there is no sheath pull back as far as possible then cut down to vein under local anaesthesia. If the catheter still cannot be removed (only 0.5% of knots) refer to vascular surgeons/interventional radiologists/cardiologists.
  • risk factors for major morbidity (with PA rupture being the most important) include pulmonary hypertension, anticoagulation, catheter in position for >3 days.

Cardiac output using the Fick method

  • Application of the Fick principle to oxygen uptake in the lungs can be used to measure cardiac output.
  • This method has traditionally been considered to be the "gold standard" of cardiac output measurement. However the preconditions for accurate measurement of cardiac output using the oxygen Fick method are not met in most ICU patients.
  • Use of modified carbon dioxide Fick methods result in greater agreement with thermodilution cardiac output measurement. Not widely applied and relies on controlled ventilation and steady state CO2 metabolism


  • less invasive than a pulmonary artery catheter and utilizes any available central venous line and a product specific thermodilution catheter placed in an artery (e.g. femoral or axillary). Various catheter sizes are available allowing the technique to be used in paediatric patients
  • works by a combination of pulse contour analysis and intermittent transpulmonary thermodilution. Following three cold saline bolus injections via the CVP line detected by the thermodilution catheter the device software can integrate this information with the arterial waveform to give a continuous display of cardiac output (response time 12sec). CO obtained using the PiCCO correlate well with those obtained using a PAC. Additional information includes BP, heart rate, stroke volume, systemic vascular resistance, stroke volume variation (SVV) and pulse pressure variation (PPV). SSV and PPV can be used to estimate volume responsiveness in mechanically ventilated patients as described in the arterial pressure monitoring section.
  • the transpulmonary thermodilution also allows calculation of a number of parameters with potential clinical application including global end-diastolic volume (GEDV) and intrathoracic blood volume (ITBV) that reflect cardiac preload, and extra vascular lung water (EVLW) that may correlate with degree of acute lung injury.
  • complications include those of arterial and central venous cannulation.


Regional blood flow

Jugular bulb oxygen saturation (SjO2)

  • proposed as a method of identifying those patients in whom cerebral metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF) are mismatched
  • has become widely used as a clinical monitor in neurosurgical intensive care units
  • use is based on the Fick principle, according to which cerebral arterial-mixed venous oxygen difference (AVDO2) is related to CMRO2 and CBF in the following way:

    Assuming that arterial saturation, haemoglobin concentration and the affinity of haemoglobin for oxygen remain constant, the ratio of CMRO2:CBF is proportional to the cerebral mixed venous oxygen saturation. SjO2 is assumed to be equal to cerebral mixed venous oxygen saturation.
  • two major limitations:
    • reflects adequacy of global cerebral oxygen delivery and gives no indication of adequacy of regional cerebral oxygen delivery. Thus a normal SjO2 is compatible with critical ischaemia in some parts of the brain with simultaneous luxury perfusion in others.
    • results become difficult to interpret when increased oxygen extraction can no longer compensate for reductions in oxygen delivery. In this situation CMRO2 falls and thus the SjO2 remains unchanged despite a fall in cerebral oxygen delivery.

Further reading

Gomersall CD, Oh TE. Haemodynamic monitoring. In Oh TE (ed), Intensive Care Manual, 4th ed. Oxford: Butterworth Heinemann, 1997, pp 831-8

Perel, A. Assessing fluid responsiveness by the systolic pressure variation in mechanically ventilated patients. Systolic pressure variation as a guide to fluid therapy in patients with sepsis-induced hypotension. Anesthesiology 89(6), 1998.


© Charles Gomersall July 1999, Charles Gomersall & Sarah Ramsay December 2002


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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