Haemodynamic monitoring

NB: If you do any procedure, particularly ones that can have serious adverse consequences, document in the notes that you've done it and that everything went smoothly (if it did).

Central Venous Pressure (CVP)

Commonly used to assess the intravascular volume / preload. Usually placed in internal jugular or subclavian vein and tip directed towards lower end of the SVC. Measures the right atrial pressure, which is the same as RV end diastolic pressure and relates directly to RV preload. Given a few assumptions (no lung pathology that might cause pulmonary hypertension, no valvular heart disease, no isolated RV failure) this can be thought to parallel the left atrial pressure and therefore LV preload.

Reminder of the Starling curve

Frank-Starling Curve

Ventricular function curves describe the fundamental Frank-Starling relationship. - As the amount of 'stretch' (preload) on the ventricular fibres is increased in diastole, so the resulting force of contraction of the next beat is increased. Note that in the failing heart (shown in red), the curve is relatively 'flat'. Under these circumstances, increasing preload will not enhance ventricular performance. In fact, the reverse may occur because wall tension will increase with a concomitant increase in oxygen requirements of the heart. The green curve represents a heart in which contractility is increased. PAOP is plotted if you're considering the left ventricle, CVP if you're considering the right. See further down for PAOP.

The value of the CVP can be obtained using a heparin/saline filled manometer, zeroed to the midaxillary line as the reference point, or by using a pressure transducer. Normally CVP ranges between 6 and 12 mmHg.

When RAP is even less similar to LAP (and therefore is a worse indicator of preload):

What else (apart from preload) can the CVP tell you?

How does PEEP affect it: If you're ventilated on IPPV with a degree of PEEP, then the intra-thoracic pressure is artificially elevated during expiration (when you take all intra thoracic measurements) and the CVP will read higher than the value would be without the PEEP. Some people simply subtract the PEEP from the CVP reading to give the 'real' CVP - but this tends to underestimate the CVP. Excessive PEEP limits systemic venous return and therefore can dramatically decease CVP, thus RV preload and thus, cardiac output.

What are all the waves about?

A wave: During atrial systole (which is immediately before ventricular systole) the pressure in the RA increases - this is the A wave, and occurs starts just after the P wave ends and before the QRS.

Z point: During the A wave the atrial pressure is greater than the ventricular diastolic pressure. At that point, the atrium is contracted, the tricuspid is open. Therefore, the high point of the A wave closely parallels the right ventricular end diastolic pressure. Remember, when the tricuspid valve is open and the right ventricle is full, the ventricle, atrium and vena cavae are all connected. Therefore, that point is the CVP (rarely termed the Z-point)

C wave: Then the onset of (ventricular) systole - the right ventricle starts to contract and the tricuspid valve closes - this bulges back into the atrium and causes the c-wave

X descent: Then follows the x descent, which represents the fall in pressure as the right atrium relaxes

V wave: The v wave develops as the right atrium is filling from systemic venous return and the TV is closed and the RV is contracting

Y descent: The y descent represents the end of ventricular systole and the TV opens, therefore the pressure in the RA is released.

'Important' findings on the CVP trace:

Large a wave Increased resistance to RV filling such as with Pulmonary hypertension or pulmonary stenosis (may occur in tricupsid stenosis). If very large are termed "cannon a waves" and represent atrial systole against a closed TV, this happens occasionally in complete heart block, VT and nodal rhythms.
Large v waves Tricuspid regurgitation. RV contracting -> high pressure across incompetent valve --> high RA pressure


Invasive arterial blood pressure monitoring

A plastic cannula (very similar to the usual venous catheters AKA venflons) is inserted into a peripheral artery under aseptic conditions (variable). Some kits have on/off switches on them, some are inserted with a Seldinger technique. Radial artery is commonest. Should you perform an Allen's test? maybe. After radial - brachial, after that femoral. Some suture it in, some don't. If the patient is awake - always use lignocaine as LA. If they're sedated you can use lignocaine as it's supposed to stop 'vasospasm'. The line is connected to a pressure transducer and gives a real time pressure trace on the monitor. It is also commonly used to take blood from for whatever.

Interpreting the trace:

The pulse pressure and it's waveform are affected by the stroke volume output of the heart, the compliance/distensibility of the vascular tree and the character of the ejection from the heart.

The dicrotic notch (fall on the downward slope) indicates the cessation of systole and represents closure of the aortic valve and subsequent retrograde flow. The location of the dicrotic notch varies according to the timing of aortic closure in the cardiac cycle. For example, aortic closure is delayed in patients with hypovolemia. Consequently, the dicrotic notch occurs farther down on the dicrotic limb in hypovolemic patients. The dicrotic notch also appears lower on the dicrotic limb when arterial pressure is measured at more distal sites in the arterial tree. Diastolic pressure is measured just before the beginning of the next systolic upstroke.

An alternative view is the the dicrotic notch in an arterial pressure waveform does not necessarily correspond to the incisura in the aortic pressure waveform (caused by closure of the aortic valve). The dicrotic notch and the dicrotic wave that follow it are thought to be due to a reflected pressure wave.

An anacrotic notch (fall on the upstroke) is not shown here but represents a sudden decrease in the rate of acceleration of pressure and corresponds to the present of severe aortic stenosis limiting the upstroke.

'Important' types of pulse

Slow rising AS
Collapsing AR
Pulsus Alternans In severe myocardial failure - alternating strong and weak beats.
Pulsus Bigeminus Strong and weak pulses alternate when having regular ventricular ectopics (the VE impulse lacks the atrial component and thus has a smaller stroke volume)
Pulsus paradoxus Usually during inspiration the negative intrathoracic pressure causes a diminished cardiac output. In states where an exaggeratedly negative intrathoracic pressure is generated (such as severe asthma) the effect is increased.
Pulsus bisferiens Either in HOCM or severe AS with AR. Double pulse.

The shape of the arterial waveform can give qualitative data on the circulation.

Figure 1

a The rate of increase in pressure relates to myocardial contractility
b The area under pulse pressure stroke volume
c systolic time myocardial oxygen consumption
d diastolic time myocardial oxygen supply

This data is used in pulse contour analysis, see below.

Information that can be gained from the appearance of the waveform:

Short systolic time
  • Hypovolaemia
  • High systemic peripheral resistance
Marked respiratory swing
  • Hypovolaemia
  • Pericardial effusion
  • High intra-thoracic pressure
  • Airways obstruction
Slow systolic time
  • Poor myocardial contractility
  • High systemic peripheral resistance (?)

Pulmonary Artery Catheter (PAC), previously known as the Swan Ganz catheter.

Normal ranges for haemodynamic variables

    mmHg Comment
Right atrial pressure Mean 0 - 5 Same as CVP
Right ventricular pressure Systolic 20 - 30 To force blood into lungs
  Diastolic 0 - 5 To allow flow from RA in diastole
Pulmonary Artery Pressure Systolic 20 - 30 Continuous with RV
  End-Diastolic 10 - 15 Pulmonary valve closed
  Mean 10 - 20  
Pulmonary Artery Wedge Pressure (PAWP) = occlusion pressure (PAOP) Mean 6 - 12 Roughly equals LA pressure

Supervision is essential for this procedure. A special line (Swan sheath) is put into the convenient vein (L/R IJ) that allows the introduction of the PAC, it has a valve that the PAC passes through. Whilst cleverly watching the pressure tracing, looking for ventricular ectopics and remaining sterile, advance the PAC with an accomplice operating the balloon.

Once the catheter tip is in the right atrium the balloon is inflated with the recommended volume (usually <1.5ml) of air and the catheter is further advanced whilst monitoring the pressure waveforms. The catheter enters the pulmonary artery after having passed through the right ventricle. Transition from a right ventricular trace to a PA trace is confirmed by an increased diastolic pressure. Eventually, the catheter tip wedges in a small branch of the pulmonary artery causing the waveform to flatten as there is no flow across the catheter.

The stationary column of blood extending from the tip of the catheter to the left atrium is roughly equivalent to the left atrial pressure. Which is equal to the left ventricular end diastolic pressure (LVEDP). Which relates to preload and myocardial contractility.


  1   2   3   4  
  1. Pulmonary Artery Diastolic Pressure's relation to Pulmonary Artery Occlusion Pressure is affected by pulmonary hypertension
  2. Pulmonary Artery Occlusion Pressure relation to Left Atrial Pressure is affected by which West's zone you're in, see below.
  3. Is LAP a valid measure of LVEDP. Not always - In the presence of mitral stenosis or other causes of obstruction to left atrial outflow, LAP (and therefore PAOP) will overestimate LVEDP. Even if the mitral valve is normal, the presence of tachycardia may also lead to overestimation of LVEDP
  4. LV end diastolic pressure is related to LV end diastolic volume. The volume corresponds to the LV end-diastolic fibre length which is what directly affects the cardiac output. Provided that LV compliance (stiffness) does not change acutely, this is a reasonable assumption. However, we now know that reductions in ventricular compliance are an early hallmark of ventricular ischaemia and that therefore under the conditions when the PAC is most likely to be needed, the central assumption is incorrect

West's zone of the lung:

West's zones of the lung.

The lung has been divided into three principal zones on the basis of the relationship between Pulmonary Arterial (Pa), Alveolar (PA) and Pulmonary Venous (Pv) Pressures.

In Zone I of the lung alveolar pressure exceeds both arterial and venous pressure (PA > Pa > Pv). Such a zone is pure alveolar deadspace. In Zone II of the lung alveolar pressure exceeds the venous but not the arterial pressure at some stage in the respiratory cycle (Pa > PA > Pv). In Zone III alveolar pressure never exceeds either arterial or venous pressure (Pa > Pv > PA).

A catheter tip wedged in a Zone I or Zone II arterial branch will measure the alveolar rather than the pulmonary artery occlusion ("Left atrial") pressure.

In the erect position, zone III alveoli are situated in the dependant areas of the lung. Zone III alveoli are, by definition, well-perfused and therefore a flow-directed catheter naturally tends to such areas.

Other uses of the PAC:

  1. Thermodilution estimation of cardiac output (see further down page)
  2. Obtaining blood from the PA - mixed venous blood. SvO2 is useful.
  3. Some have an oximeter on the tip giving continuous SvO2.
  4. The sheath can be used for temporary pacing wires!
  • Hypovolaemia shock
  • Cardiogenic shock
  • Septic shock
  • Cardiac tamponade

Measuring Cardiac Output with a PAC

Thermodilution is in essence an 'indicator dilution' technique similar to the classical indocyanine green method except that instead of a quantity of dye, a fixed volume of cool injectate is used as the indicator. The equation used for calculating cardiac output (CO) using temperature effectively measures the area under the temperature-change curve when a known quantity of 'cool' is administered. The equation is known as the Stewart-Hamilton equation

Thermodilution curve

Figure 2.

Typical form of the fall in blood temperature which occurs in the pulmonary artery when a bolus of cold saline is injected into the central venous lumen of a pulmonary artery catheter. The change in blood temperature is detected by the thermistor which has a response time of ~ 50 msec.

Modern monitors often invert the temperature curve so that it more closely resembles the traditional dye dilution curve.

The cold bolus travels a short distance: from the SVC through the TV into the RV, through the PV into the PA and then past the thermistor at the tip of the PAC in the pulmonary artery.

The Stewart-Hamilton Equation:


A plot of temperature change DT versus time is the thermodilution curve (graph above). Cardiac output is inversely proportional to the area under the thermodilution curve (with a large cardiac output, the bolus is pumped rapidly past the thermistor, and so the area is small)

Good analogy: if you're standing on a platform looking across the tracks and a fast train comes through the station - it is only in your field of vision for a short time. If it's a slow train it stays in your field of vision for a longer time.

Problems with this approach to calculating the cardiac output:

  1. Right and left ventricular output may differ in the presence of a cardiac shunt.

  2. Tricuspid or pulmonary valve regurgitation can cause underestimation of cardiac output.

  3. Variations in blood temperature affect measurements, e.g. after cardiopulmonary bypass, intravenous fluid administration.

  4. Positive pressure ventilation produces beat-to-beat variations in right ventricular stroke volume during the respiratory cycle. Measured cardiac output will depend on the timing of the bolus injection.

The catheter is attached to a cardiac output computer (or monitoring system) that displays a curve of change in temperature against time and that calculates the cardiac output and derived indices automatically.

Continuous cardiac output measurements from PACs
It is possible to measure cardiac output 'continuously' using a specially modified PAC. These 'CCO' catheters have a heating coil built in and regularly heat up by a specific amount (this part of the catheter is in the RV) and then measure the temperature at the tip in the PA. They need to be calibrated first via the traditional method.

Derived variables from PAC... See


The PiCCO System is a relatively new device allowing intermittent cardiac output monitoring by aortic transpulmonary thermodilution technique and continuous cardiac output monitoring by pulse contour analysis. From Pulsion systems, excellent description of how it works on their website.

Transpulmonary thermodilution technique

Exactly like the PAC thermodilution technique except the cold fluid bolus travels a lot further. Into the CVP line, through the right side of the heart, the lungs, the left side of the heart and then detected in a special arterial line (with a thermistor), usually in the femoral artery.

The cardiac output is calculated from the Stewart Hamilton equation i.e. the area under the top graph. Exactly like the PAC does it. However because the cold bolus travels much further the PiCCO device can cleverly calculate other potentially useful variables.

NOTE: The way the PiCCO device works out all the clever numbers is hugely complex and confusing and not really essential to know. If you're not really interested then skip this section and go to Pulse Contour Analysis.

They diagrammatically represent this journey like this:

RAEDV Right Atrial End Diastolic Volume
RVEDV Right Ventricular End Diastolic Volume
ETV EVWL (see later)
PBV Pulmonary Blood Volume
LAEDV Left Atrial End Diastolic Volume
LVEDV Left Ventricular End Diastolic Volume

Just like in Figure 2 above you get a change in temperature vs. time graph.

Below shows the graph of change in temp (inverted) against time and then below it, the logarithm of temperature against time.

Firstly cardiac output is calculated from the Stewart Hamilton equation i.e. the area under the top graph.

You have a value for the Cardiac output in volume/per unit.

MTt Mean transit time = half the indicator has passed
DSt Downslope time = the exponential downslope time of the TD curve

Interpreting the bottom graph gives you some values (MTt and DSt) in seconds.

The product of volume/unit time x time= volume.

PiCCO claims to be able to estimate VOLUMES not just pressures.

This is an example not using the cardiopulmonary volumes, but showing that as a general physical rule the total volume can be calculated from the MTt and the volume of the largest chamber can be calculated from the DSt.

Total Volume V1 + V2 + V3 + V4 = MTt x Flow
V3 V3 = Dst x Flow

Convinced? No, me neither. If anyone has a simple and convincing way of explaining this then please let me know.

Going back to our cardiopulmonary model...

It's reasonably straightforward that from analysing the log of the change in temperature against time you can calculate the GEDV and the PTV.

How can we find out what are the constituent parts of the pulmonary thermal volume?

In summary:


Intra thoracic volume determined from the mean transit time

PTV = CO * Dst

Pulmonary Thermal Volume determined from the exponential downslope time


Global end diastolic volume.

Can also be re-arranged as GEDV = CO * (MTt-DSt)

ITBV = 1.25 * GEDV

Intra thoracic blood volume (total cardiopulmonary intra vascular fluid volume)

Can also be re-arranged as ITBV = 1.25 * CO * (MTt-DSt)


Extra vascular Lung Water = Intra thoracic blood volume

Can also be re-arranged as EVLW = ITTV - 1.25 * GEDV

Or even EVLW = [CO * MTt] - [1.25 * CO * (MTt-DSt)]

From all the complex jiggery pokery:


From taking three values from the temperature vs. time graph (CO, MTt, DSt) the PiCCO can estimate:

1 Cardiac output (CO), also indexed to BSA to cardiac index = CI. 3.0-5.0 l/min/m2
2 Preload (ITBVI) 850-1000 ml/m2
3 Degree of pulmonary oedema (EVLWI) 3.0-7.0 ml/kg

These values are only obtained at the time of doing the thermodilution measurement and are not continuously updated. These measurements need to be repeatedly as often as is necessary.

How do these measurements assist in the management of the patient?

Pulsion have produced a decision tree which may be helpful...

Derived variables...

1. Cardiac Function Index = CFI, normal range 4.5-6.5 /min

The ratio of the index of cardiac output to the index of the GEDV. A measure of how well the CO is doing in relation to it's preload.

This might be used if you've noticed a low ITBVI and given fluids but the CO has not improved. You would give inotropes in this situation but the presence of a low CFI would confirm that the heart is failing to keep on it's Frank Starling curve and needs a little help. See diagram above.

2. Global ejection fraction (GEF). A % of total blood expelled from the heart every beat to the total amount of blood estimated to be present just prior to ventricular systole.

GEF = (4 x SV) / GEDV

3. Pulmonary Vascular Permeability Index. (PVPI). This tells you how much pulmonary oedema there is in relation to how much preload there is.


These derived variables don't give you new information they just give you a number to quantify the relationship between other measured variables.


What slightly messes up thermodilution: odd placement of venous or arterial catheters.

What really messes up thermodilution: IABP and cardiopulmonary bypass!

Continuous Cardiac Output from Pulse Contour Analysis

This is infinitely simpler than the stuff above.

The arterial pulse shape depends on cardiac output and the characteristics of the arterial tree, including where you are measuring from. Pulse-Contour Continuous Cardiac Output (PCCO) can be calculated once then system has been calibrated from the thermodilution technique. As the characteristics of the vascular tree change the CCO needs to be re-calibrated reasonably often. The longer since the last calibration the less accurate the CCO and all it's derived numbers will be.

The calibration by thermodilution determines the constant 'cal' and the constant for 'aortic compliance'.

CO = HR x SV. SV is calculated from the area under the pulse pressure.

Other values from the arterial pulse analysis:

1. dPmx = Maximum dP/dt = i.e. greatest left ventricular velocity increase = equivalent to the measurement "a" in figure 1. This is an index of left ventricular contractility and is measured in mmHg/s = usual values...

2. Stroke volume variation - SVV

SVmax and SVmin are measured over 30 seconds and SV mean is calculated. The variation in stroke volume = SVmax-SVmin/SVmean. The concept behind SVV is that the lower down the Frank-Starling curve you are - the greater the variation in your SV. Adding addition EDV will decrease your SVV. The effect will be dimished as you rise up the F-Starling curve. The manfacturers claim that the SVV "... prognoses the reaction of the heart on volume loading and correspondes directly to the Frank-Starling curve".

Values: Aim for <10% SVV. If it's over 10% then volume load.

The SVV only applies in mechanically ventilated patients.

Oesophageal Doppler

Doppler probe in oesophagus measures velocity of flow in descending aorta.

You need to know the diameter of the descending aorta. You can either measure it via the name probe or work it out. Age, height, weight and sex of patient into computer and it calculates (based on statistics) the likely aortic diameter. The specific cross-sectional area (CSA).

Stroke volume is then derived from the flow velocity, ejection time and aortic cross sectional area. The velocity time integral (VTI) represents a specific distance along which the column of blood is projected during one cardiac cycle. The VTI is, therefore, directly related to systolic function of the ventricle.

Cardiac output can now be calculated as follows: VTI (cm) x CSA (cm2) = Stroke volume (cm3)

Pulse CO / LiDCO from www.lidco.com

Works in exactly the same way as the PiCCO but uses Lithium Chloride solution instead of cold saline boluses. Compares very well. LiDCO will not give you the EVLW.


The COLD-System is a haemodynamic monitoring system which was distributed by PULSION Medical Systems between 1992 and 2000. This device is not available any more. Most of the basic research studies for the development of the PiCCO was conducted with the COLD-System.

Principles of the Double-Indicator Dilution Measurement

After injection of the cold indocyanine green (ICG) solution, the thermal indicator dilution curve was recorded in the pulmonary artery by the thermistor of the PAC. In addition, the thermistor-tipped fiberoptic catheter in the descending aorta recorded the dye indicator dilution curve and the thermal indicator dilution curve.

The determination of flow and volume by this method is based on the simultaneous application of the two indicators:

Cardiac index is determined by the standard thermodilution technique. The calculation of intrathoracic volumes is performed by an analysis of the transit times of the indicators derived from the dilution curves that are recorded in the descending aorta. Mean transit time (MTt) and exponential downslope time (DSt) of the thermal and dye indicators are recorded.

By multiplying CO with the MTt of each indicator, the volume between the sites of injection and indicator detection can be calculated.

The ITBV calculation is based on the dye indicator curve, while the intrathoracic thermal volume (ITTV) is based on the thermal indicator curve.

Multiplying the CO with the DSt of the thermodilution curve results in the pulmonary thermal volume (PTV), which is the largest single mixing volume.

GEDV is obtained by subtracting the pulmonary thermal volume from the intrathoracic thermal volume.

Other Derived variables

Vascular Resistances
The resistance of the systemic and pulmonary circulations can be calculated using data derived from the CO

These calculations are analogous to Ohm's law. V=IR. Rearranged. R = V/I. Or Resistance = Voltage/Current (It helps if you remember that voltage is potential difference and that current is flow of charge). In this case it's:

Measure of Vascular resistance = (Difference in pressure from start to finish) * Constant / Flow of Blood Volume.

The systemic vascular resistance (SVR) is a measure of LV afterload and is an important determinant of the performance of the left heart. It is calculated in metric units according to the equation:

SVR = (MAP - RAP * 79.9)/CO

It is often indexed to BSA and then becomes SVRI.

The pulmonary vascular resistance (PVR) is a measure of RV afterload. It is calculated in metric units according to the equation:

PVR = (MPAP - PAOP * 79.9)/CO

Calculated vascular resistances can be converted to indices by multiplying the absolute value of resistance by the body surface area.

Note that two units of measurement of resistance are used. 'Hybrid' units and metric units - the values quoted here being in metric units. Hybrid units are measured in mmHg/min/L, and metric units in dynes/sec/cm -5. Conversion from hybrid to metric units is achieved by multiplying the hybrid value by 79.9.

The normal ratio of PVR to SVR is 0.15. In the presence of an anatomical right-to-left shunt, the balance between PVR and SVR will determine the ratio of pulmonary to systemic blood flow and hence the degree of cyanosis.

A complete list of all cardiovascular variables


Basic physiology

Right atrial pressure Mean 0 - 5 mmHg
Right ventricular pressure Systolic 20 - 30
Diastolic 0 - 5
Pulmonary Artery Pressure Systolic 20 - 30
End-Diastolic 10 - 15
Mean 10 - 20
Pulmonary Artery Wedge Pressure (PAWP) = occlusion pressure (PAOP) Mean 6 - 12

Measured data either from PAC or PiCCO

Cardiac output (CO) 5.0-7.0 l/min
Cardiac index (CI) 3.0-5.0 l/min/m2

Measured data from PiCCO/thermodilution method

Preload (ITBVI) 850-1000 ml/m2
Degree of pulmonary oedema (EVLWI) 3.0-7.0 ml/kg

Derived data from PiCCO/thermodilution method

Cardiac Function Index (CFI) 4.5-6.5 /min
Global Ejection Fraction (GEF) 25-35 %
Pulmonary Vascular Permeability Index (PVPI) 1.0-3.0  

Measured data from PiCCO/Pulse Contour Analysis

Stroke Volume (SV) 50-110 ml
Stroke Volume Index (SVI) 40-60 ml/m2
Cardiac output (PCCO) 5.0-7.0 l/min
Cardiac Index (PCCI) 3.0-5.0 l/min/m2
Heart rate 60-90 /min
Systolic (SBP), Diastolic (DBP), Mean (MAP) you know it! mmHg
dPmax = Maximum dP/dt, left ventricular contractility 1200-2000 mmHg/s
Stroke Volume Variation, SVV <10 %

Derived data from CO, MAP, CVP

Systemic Vascular resistance (SVR) 900-1400 dyn/s/cm-5
Systemic Vascular resistance index (SVRI) 1200-2400 dyn/s/cm-5/m2

Derived data only if you've got a PAC in

Pulmonary Vascular resistance (PVR) 150-250 dyn/s/cm-5
Pulmonary Vascular resistance index (PVRI) 250-400 dyn/s/cm-5/m2
PVR:SVR ratio 0.15

Other related variables

Oxygen delivery DO2 = Oxygen content of blood x CO

= (Hb x SaO2 x 1.34) + (PaO2 x 0.23) X CO

~900 ml/min
Oxygen delivery index DO2I = DO2 / BSA 500-600 ml/min/m2


Many thanks to:

The superb (and fully referenced) Australian website The 'St George' Guide To Pulmonary Artery Catheterisation by Andrew Pybus. And to Pulsion for providing a great powerpoint presentation on their website.


March 2004.