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).
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
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|
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
|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.
|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||
|Marked respiratory swing||
|Slow systolic time||
Normal ranges for haemodynamic variables
|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.
West's zone 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:
|PAOP Low||PAOP High|
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
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:
Right and left ventricular output may differ in the presence of a cardiac shunt.
Tricuspid or pulmonary valve regurgitation can cause underestimation of cardiac output.
Variations in blood temperature affect measurements, e.g. after cardiopulmonary bypass, intravenous fluid administration.
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.
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.
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.
The product of CO x MTt represents the total volume traversed by the indicator i.e. total volume between site of injection and detection. The greater the volume the bolus has to travel through the longer it will take.
The product of CO x DSt represents the largest individual mixing volume in a series of indicator mixing chambers.
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...
PTV = Pulmonary thermal volume (equivalent to the volume V3 in the above example) i.e. derived from DSt.
ITTV = Intra thoracic thermal volume and is the sum of RAEDV + RVEDV + PTV + LAEDV + LVEDV i.e. derived from MTt.
If we subtract PTV from ITTV then we get the Global End Diastolic Volume = GEDV
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?
The pulmonary thermal volume comprises of the volume in the heart and lungs (the cardiopulmonary AKA intrathoracic blood volume, ITBV) and whatever volume is present within the chest but is extra vascular = the extra vascular lung water (EVLW).
In experimental studies the intrathoracic blood volume is related to the GEDV in a linear fashion. It is 1.25 times the GEDV.
ITTV = CO * MTt
Intra thoracic volume determined from the mean transit time
PTV = CO * Dst
Pulmonary Thermal Volume determined from the exponential downslope time
GEDV = ITTV - PTV
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)
EVLW = ITTV - ITBV
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:
The GEDV measurements are linearly related to stroke volume according to the Frank Starling model. i.e. GEDV is an accurate indicator of preload. The relationship is much better than either the CVP or the PAOP.
The ITBV is the sum of the GEDV and the pulmonary thermal volume (or pulmonary blood volume). The calculations assume that there are no volumes present in the thorax that might interfere, such as space occupying lesions, pulmonary effusions, large pulmonary emboli. The ITBV is indexed to weight to give the ITBVI
How thoracic pathologies affect the PiCCO readings: space
occupying lesions... more here. Pulmonary effusions and large pulmonary emboli
should not affect measurements as they do not take part in the pulmonary thermal
The Extravascular lung water (EVLW) pathiophysiologically relates to pulmonary oedema, either from increased intravascular filtration pressure (say from LVF or volume overload) or from increased pulmonary vascular permeability (say from endotoxic shock, pneumonia, burns, sepsis). EVLW is usually indexed to BSA and is known as EVLWI. It is the only way of measuring the lung water and is considered (by pulsion at least) to be superior to CXR appearances, Blood gases, PFTs or lung compliance/stiffness. It can be used to guide treatment (when to use high frequency ventilation for ARDS, it correlates with the severity of ARDS and the mortality.) and has been shown to reduce length of mechanical ventilation and ITU stay.
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|
|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...
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.
PVPI = EVLW / PBV
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!
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.
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)
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.
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.
|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|
|Cardiac output (CO)||5.0-7.0||l/min|
|Cardiac index (CI)||3.0-5.0||l/min/m2|
|Degree of pulmonary oedema (EVLWI)||3.0-7.0||ml/kg|
|Cardiac Function Index (CFI)||4.5-6.5||/min|
|Global Ejection Fraction (GEF)||25-35||%|
|Pulmonary Vascular Permeability Index (PVPI)||1.0-3.0|
|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|
|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||%|
|Systemic Vascular resistance (SVR)||900-1400||dyn/s/cm-5|
|Systemic Vascular resistance index (SVRI)||1200-2400||dyn/s/cm-5/m2|
|Pulmonary Vascular resistance (PVR)||150-250||dyn/s/cm-5|
|Pulmonary Vascular resistance index (PVRI)||250-400||dyn/s/cm-5/m2|
|Oxygen delivery DO2 = Oxygen
content of blood x CO
= (Hb x SaO2 x 1.34) + (PaO2 x 0.23) X CO
|Oxygen delivery index DO2I = DO2 / BSA||500-600||ml/min/m2|