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
• Invasive Arterial Pressure
• Pulmonary Artery catheter and PAOP
• CO with PAC thermodilution
• PiCCO:     transpulmonary thermodilution, pulse contour analysis
• LiDCO
• COLD
• Oesophageal doppler
• Derived variables
• Complete list of cardiovascular variables

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

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):

• COPD or any chronic pulmonary disease that might cause pulmonary hypertension
• Valvular heart disease, particularly MS
• Pulmonary oedema, whether of cardiogenic or non-cardiogenic origin.

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

• RV failure in Acute Inferior MI or Posterior MI. In acute RV infarction the RV fails and the CVP rises. However you need to volume load to maintain cardiac output... More here.

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:

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

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

Figure 1

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

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

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

Normal ranges for haemodynamic variables

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.

Assumptions:

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:

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!

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

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:

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

PiCCO

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.

They diagrammatically represent this journey like this:

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.

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.

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.

In summary:

	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 volume.
     

• 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.

Summary

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

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.

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.

Note

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