Advanced Haemodynamic Monitoring and support

Part 1: Monitoring

Contents

6. Monitoring Perfusion – Gastric Tonometry

7. Monitoring Oxygen Consumption – Mixed Venous Saturation

8. Summary

1. Introduction

2. What is haemodynamic monitoring?

3. Advanced haemodynamic monitoring

4. Central Venous Pressure Monitoring

5. Cardiac Output Measurementa) Introduction

b) Derived parameters from cardiac output

c) Cardiac Output using CO2

d) Cardiac output using dilution technique

e) Pulmonary Artery Catheters

f) Transpulmonary Thermodilution

g) Lithium dilution

h) Stroke Volume / Pulse Pressure Variation

i) Oesophageal Doppler

j) Echocardiography

k) Thoracic bioimpedance

l) Indications for monitoring cardiac output

m) Clinical applications

n) Evidence to support cardiac output monitoring

Introduction

• Monitoring is one of the fundamental aspects of intensive care

• We monitor several physiological parameters regularly:

– ECG, heart rate, SpO2, arterial blood pressure in real time

– Other parameters such as temperature, urine output, respiration rate, GCS and blood sugars are monitored at frequent, but regular intervals

• We monitor these parameters:

– To alert us of deterioration or potential deterioration of patient’s state

– To intervene when there are signs pointing to a deterioration

– To assess response to treatment

‘Not everything that counts can be counted and not everything that can be counted counts’ . . . Albert Einstein

What is haemodynamic monitoring?

• Haemodynamic monitoring focuses on the circulatory system, its adequacy and end organ perfusion

• Markers such as blood pressure and heart rate give an indirect measure of the circulatory system

• Tachycardia and hypotension may thus indicate either a decreased preload or impaired myocardial contractility

• They are not accurate:

– The heart rate is influenced by many other factors

– Tachycardia may be the result of pain, anxiety, drugs or arrhythmias and not necessarily a reduced preload or decreased cardiac output

– Similarly, a low blood pressure may be secondary to drugs, postural effects or vasodilatation

– A ‘normal’ blood pressure in a hypertensive patient may actually indicate a shocked state!

What is haemodynamic monitoring?

• Surrogate markers of organ perfusion include:

– Skin perfusion - measured by capillary refill

– Urine output

– Mental state – usually assessed by the GCS

• These may do not accurately measure perfusion:

– Capillary refill may be affected by other factors including ambient temperature

– Urine output may be vary in the setting of previous renal dysfunction

– Mental alertness may not be assessable in the intubated patient; delirium may contribute to a decreased GCS

• Other indirect markers of perfusion including serum lactate are not exclusive to poor perfusion and are elevated in other medical conditions as well

Advanced haemodynamic monitoring

• The ‘regular’ monitoring of the haemodynamic status provides sufficient information in most situations

• There are situations where this may not sufficient to make decisions

• Advanced haemodynamic monitoring involves monitoring the circulatory system and the components that affect it :

– Preload

– Myocardial contractility

– Afterload

• It also involves monitoring oxygen consumption and end organ perfusion

Central Venous Pressure Monitoring

Central Venous Pressure

• The pressure measured in the superior and inferior venacava

• Reflects right atrial pressure

• Usually measured through a catheter inserted into the internal jugular or subclavian veins as well as through peripherally inserted central venous catheters

• The pressure in the femoral veins also reflects central venous pressure, although increased abdominal pressure may modify this sufficiently to render it inaccurate

• The right atrial pressure may be directly measured using the pulmonary artery catheter (see section on PA catheters)

• CVP pressure monitoring is common - catheters in the central veins are inserted frequently for administration of vasoactive agents or hypertonic solutions and for long-term venous access

History

• First described in patients undergoing thoracic surgery

• Hughes and Magovern1 described a fall in CVP with blood loss and a rise in CVP with transfusion in 1959

• CVP was initially used as a guide for fluid resuscitation and monitoring in cardiac and thoracic surgery and later on was used in major operative procedures

• This practice then spilled over to the Intensive Care Units and now forms a common modality of haemodynamic monitoring in critically ill patients

1. Hughes RE, Magovern GJ. The Relationship Between Right Atrial Pressure and Blood Volume. Arch Surg. 1959;79: 238-243.

Central Venous Pressure

• Used as a surrogate marker for cardiac filling pressures - rise in CVP indicates better cardiac filling

• Frank- Starling principle states that the force of cardiac contraction is proportional to the end-diastolic length of the fibre

• This muscle length is proportional to the volume of blood at the end of diastole: the preload

• Thus, preload is one of the determinants of cardiac output

• Increased preload results in proportionately increased stroke volume

• In clinical practice, it is not possible to measure the end diastolic volume of the right ventricle to determine the preload

• End diastolic right ventricular pressure is reflected in the CVP which is therefore used as a surrogate marker of preload

Central Venous Pressure

• The relationship between ventricular end diastolic volume and pressure is not linear but curvilinear (see figure)

• When the ventricle is operating in the flat portion of the curve, there is little change in pressure with end diastolic volume

• In the steep area of the curve, small changes of volume results in greater changes in pressure

• Decreased ventricular compliance causes greater pressure changes with volume

• Ventricular compliance is influenced by relaxation, geometry and the mechanical characteristics of the ventricle

Decreased compliance

Normal

Increased compliance

Left ventricular volumeLe

ft v

entr

icul

ar

pre

ssu

re

End diastolic pressure

End diastolic pressure

End diastolic pressure

Factors affecting CVP• Normal CVP in a healthy adult: 0 -7 mm Hg

• CVP of 0 may be normal in a healthy person - central veins are capacitance veins, potentially able to hold large volumes of blood without appreciable changes in pressure

• Higher CVP may reflect poor ventricular compliance than good filling pressures

• Changes in the transmural pressure - difference in the pressure between the cardiac chamber and the juxtacardiac pressure – also affects CVP

• Juxtacardiac pressure is affected by pericardial and pleural pressures

• In a ventilated patient, pleural pressures are affected by the compliance of the lung, pressures exerted by the ventilator, and PEEP

• These pressure changes are complex and do not affect the CVP in a linear fashion. The practice of subtracting PEEP pressure to the CVP may not always reflect actual CVP

• Pressures in the right atria may also be affected by changes in the ventricles or the atria:

– Valvular abnormalities of the tricuspid and rarely, the pulmonary valves

– Pulmonary hypertension

Factors affecting CVP… • The pressures are affected by changes in the respiratory cycle:

– Decreased intra-thoracic pressure at the beginning of spontaneous ventilation decreases the CVP

– The onset of positive pressure ventilation causes an increase in CVP • The CVP is usually measured at the end of expiration when

juxtacardiac pressures approach atmospheric pressure• Technical issues may also affect the actual CVP measurement,

including:– Improper position of the catheter – abutment against a vessel wall– Thrombus in the catheter– Improper zeroing or placement of the transducer – Simultaneous rapid Infusion of fluids1 (rates > 50 ml/hour tends to

increase the CVP) 1. Ho AM-H, Dion PW, Karmakar MK and Jenkins CR. Accuracy of central venous pressure monitoring during simultaneous continuous infusion through the same catheter. Anaesthesia, 2005; 60: 1027–1030

CVP waveform

• Waveform has a characteristic trace coinciding with changes in the cardiac cycle:

– Prominent positive a wave - atrial contraction

– Smaller, positive c wave – closure of tricuspid valve during isovolumetric contraction

• Atrial relaxation decreases in atrial pressure (x descent)

• Filling of the atrium causes pressures to rise again (v wave)

• This is followed by the y descent, a negative waveform reflecting ventricular filling as the tricuspid valve opens

Monitoring with CVP

• Used both in resuscitation and as a guide to fluid therapy

• Low CVP in a haemodynamically unstable patient reflects decreased preload and may be an indication for additional fluids

• Its use to guide fluid resuscitation is recommended and in several guidelines including management of septic shock

• Evidence to support this is however not convincing

• In a systematic review, Marik1 found no correlation between CVP and blood volume

• This review also found that CVP, or a change in CVP did not predict fluid responsiveness

• The CVP should not be used in isolation and the pressure measured is a composite of a number of factors affecting the right atrial pressure

• Trends in the change in the CVP and using the CVP in conjunction with other haemodynamic parameters helps overcome some of these barriers

1. Marik PE, Baram B, Vahid B. Does Central Venous Pressure Predict Fluid Responsiveness? Chest, 2008; 134: 172 - 178

Cardiac Output Measurement

Introduction

• Assessment of cardiac output is an important part of monitoring haemodynamically unstable patients

• Until recently, the measurement of cardiac output was considered essential:

– To characterize the type of shock

– To monitor response to therapeutic interventions

– To optimise factors that influence cardiac output

– To optimise oxygen delivery

Definitions

• Cardiac output (CO): amount of blood pumped by the heart per unit time

• Measured as the output in litres per minute – normal: 4 - 8 l/ minute

• Varies with body habitus; usually indexed to the body surface area (BSA):

(litres/ minute/ m2) – normal 2.5 – 4 L/min/m2

• A wide variety of parameters may be derived in addition to cardiac output

• These, along with their normal values, are given in the following tables

• Together, they provide us with a better understanding of the haemodynamic status of a patient

• This information may be used to direct therapy – for example, using an inotrope to improve cardiac index or using a vasopressor to increase systemic vascular resistance

Derived parameters from cardiac output

Parameter Calculation Normal values

Stroke Volume (index)(using cardiac index will give the stroke volume index)

60 – 100 ml/ beat(33 - 47 ml/m2/beat)

Systemic Vascular Resistance (index)

1000 -1500 dyne s/ cm5

(1970 - 2390 dyne s/cm5/m2)

Pulmonary Vascular Resistance(index)

<250 dyne s/cm5 (255 - 285 dyne s/cm5/m2)

Left Ventricular Stroke Work (index)

58 - 104 gm-m/beat(50 - 62 gm-m/m2/beat)

Right Ventricular Stroke Work(index)

8 - 16 gm-m/beat(5 - 10 gm-m/m2/beat)

MAP= mean arterial pressure; RAP = right atrial pressure ( or CVP); PAWP = pulmonary artery wedge pressure; MPAP = mean pulmonary artery pressure (pulmonary systolic pressure +(2 x pulmonary diastolic pressure)/ 3); 80 and 0.10136 are the numbers required for conversion to the units of measurement

Derived parameters…

Parameter Calculation Normal values

Coronary Artery Perfusion pressure

Diastolic BP-PAWP 60 - 80 mmHg

Oxygen Delivery (index) CaO2 x Cardiac Output (CI) 950 - 1150 ml/min(500 - 600 ml/min/m2)

Oxygen Consumption (index) (C(a - v)O2) x CO (CI) 200 - 250 ml/min(120 - 160 ml/min/m2)

CaO2= oxygen content of arterial blood ({1.34 x Hb/L x SaO2} + {0.0031 x PaO2}); (C(a - v)O2) = difference between arterial and venous oxygen content;

Cardiac output measurement: Fick Principle

• Adolf Fick, in 1870, first measured cardiac output after describing the principles behind it

• The blood flow to an organ (body) per unit time may be calculated by the ratio of a marker’s consumption by that organ (body) to the difference between arterial and venous contents of that marker

• Fick used oxygen as a marker and calculated cardiac output as:

– VO2 = oxygen consumption; CaO2 = arterial oxygen content; CvO2 = venous oxygen content

• The accuracy of this measurement relies on several assumptions:

– Flow through the pulmonary vessels are constant

– There are no shunts in the pulmonary vasculature – shunts underestimates cardiac output

– That oxygen uptake in the lungs is minimal

• Using this method in the critically ill patient is not practical:

– It is not possible to exclude oxygen uptake in inflamed lungs

– The method can be challenging in patients requiring high FIO2

– There may be shunting of blood

Cardiac Output using CO2

Cardiac output using CO2

• To overcome the difficulty of using oxygen consumption to estimate cardiac output, investigators focussed on using carbon dioxide production (VCO2)

• Two main techniques have been described:

• One method is to calculate VO2 using VCO2 and the respiratory quotient (R):

VO2 =

– Oxygen content (CaCO2) is measured using oxygen saturation and Haemoglobin concentration: CaCO2 = 13.4 x Hb x SaO2

– Rearranging: CO =

– The drawbacks of using this method include measuring mixed venous saturation and determination of R

Cardiac output measurement using CO2

• An alternative method using partial rebreathing of CO2 has been described

• It uses the Fick Principle :

CO =

• A rebreathing circuit with a CO2 and airflow sensor is placed between the endotracheal tube and the ventilator

• Data is collected before and after a period of rebreathing

• VCO2 is calculated using the CO2 detected in the circuit and airflow

• Assuming that cardiac output and mixed venous content remained constant between baseline and the end of rebreathing, Cardiac output may be calculated:

CO =

• CaCO2 can also be estimated from the end-tidal carbon dioxide (etCO2) and the CO2 disassociation curve (S)

• Using this: CO =

Cardiac output measurement using CO2

• The potential benefits using this technique include its non-invasive nature and its ability to be repeated at relatively frequent intervals

• It can be only done in intubated and ventilated patients; large gas leaks in non-invasive ventilation preclude its use

• It has not shown consistent correlation with other techniques of measurement of CO

• Its measurement is unreliable in several clinical situations:

– Large intra pulmonary shunts

– Where tidal volumes vary (spontaneously breathing patient) or when ventilator settings may alter dead space

– Chronic lung disease, where ventilator- perfusion mismatch can occur

– The postoperative cardiac patient where increased pulmonary dead space and shunts may occur

– Acute lung injury (ALI) and ARDS where the heterogeneous nature of the injury causes a wide variation of gas exchange. End tidal CO2 may be a poor estimate of CaCO2

Cardiac output using dilution technique

Cardiac output measurement: Indicator-dilution

• Described initially by Stewart, later by Hamilton

• When an indicator is injected into the blood stream, its concentration at a downstream sampling site initially increases and then falls proportional to blood flow

• As the indicator re-circulates, its concentration rises briefly and then reaches a steady state if it is not excreted

• The area under the extrapolated primary decay curve (coloured area in the figure) is equal to blood flow (cardiac output):

Q =

Q = cardiac output; I = amount of indicator; C idt: integral of indicator concentration over time

Time (secondsC

on

cen

tra

tion

of

ind

ica

tor

Injection

Transit time

Re-circulation

Extrapolated primary decay

curve

Cardiac output measurement: Thermodilution

• The initial indicators used to measure cardiac output included indocyanine green and radioactive isotopes

• The indicator dilution principle can also be applied using cold saline as an indicator and measuring the change of temperature of blood

• Cold saline is injected into the proximal port of a catheter while a thermistor records the temperature distally

• The mean decrease in temperature (integral of the time versus temperature curve) is inversely proportional to the cardiac output

• A modification of the Stewart - Hamilton equation is used:Q =

TB = temperature of blood; TI = temperature of injectate; K = computation constant; VI = volume of injectate; = integral of temperature change over time

Cardiac output with thermodilution• Major advantages of using the thermodilution technique include:

– Non-toxic and can be repeated

– Repeated measurements, performed correctly, show very low coefficients of variance

– There is no recirculation

– Shows good agreement with other indicator dilution methods including indocyanine green

– Has now become the ‘gold standard’ for clinical measurement of cardiac output

• The values obtained using thermodilution have some limitations:

– Requires placement of a pulmonary artery catheter

– Inaccurate in low-output states, tricuspid regurgitation, atrial and ventricular septal defects

– There must be a variation of ~15% between the means of 2 measurements to interpret changes as significant

– Cold saline may cause bradycardia, decreasing cardiac output. This limitation may be overcome by using saline at room temperature, compromising on precision. Measurements using this may vary if the patient is hypothermic

Pulmonary Artery Catheters

History• Bradley, along with Branthwaite, described pulmonary artery catheterisation,

using a rigid thermistor tipped catheter placed under fluoroscopy in the pulmonary artery with a second catheter for injection in the right atrium1. Cardiac output was measured by thermodilution

• Advances in technology have kept pace with the development of the catheter with addition of more lumens and the use of better materials

• There are now dedicated monitors available with software to calculate a broad range of haemodynamic parameters

• Incorporation of a heating element proximally has eliminated the need for injecting cold solutions

Jeremy Swan and William Ganz

• Jeremy Swan conceived and developed a balloon tipped catheter that could be floated into the pulmonary artery. William Ganz added a thermistor to the tip to the device, enabling measurement of cardiac output thermodilution

1. Chatterjee K. The Swan-Ganz Catheters: Past, Present, and Future. Circulation. 2009;119:147-152

Principles • The pulmonary artery (PA) catheter allows measurement of the pulmonary

pressures - systolic, diastolic and wedged• Enables measurement of cardiac output using the thermodilution method• Allows measurement of mixed venous oxygen saturation, from which

oxygen consumption can be calculated• Together, these haemodynamic parameters provide a better understanding

of preload, myocardial contractility and afterload• Information from these parameters may be used to guide fluid and

vasoactive medication therapy

Principles

• The balloon at the end of the PA catheter is inflated to wedge the catheter in the pulmonary artery and isolate it from upstream pressures

• The pressure measured at the tip of the catheter reflects the pressure of a distal static column of blood which ends at the junction of the pulmonary vein with the left atrium

• As the resistance of the pulmonary venous system is negligible, this pressure reflects pulmonary venous and left atrial pressure – a measure of the left ventricular filling pressure

• Sometimes the pulmonary artery diastolic pressure is used as a measure of left atrial pressure instead of the wedged pressure

• This is acceptable in normal circumstances because at the end of diastole, the pulmonary artery pressure equilibrates with the downstream capillary and venous pressures

RV LV

Pulmonary artery

RV LV

Pulmonary artery

wedged

West’s Zones and pulmonary vascular pressures

Levitzky M G. Advances in Physiology Education 2006;30:5-8

©2006 by American Physiological Society

• Catheters placed in West’s zones 1 and 2 are more likely to reflect alveolar (PA) than venous pressures (PV). Catheters placed in zone 3 are not influenced by the alveolar pressures and are more likely to reflect true venous pressures.

• In mechanically ventilated patients, PA is affected by PEEP and this may influence wedge pressures

• The pressure within the capillaries are subject to the pressure in the alveoli and may influence the wedged pressure

• West described the interaction of the alveoli and capillary pressures and grouped them into three zones: see figure

Normal waveforms

• The pressure waveforms in the wedged position resembles a damped CVP waveform with ‘a’, ‘c’ and ‘v’ waves along with an ‘x’ and ‘y’ descents

• When the catheter is not wedged, it displays the pulmonary artery waveform

• There is a phase delay in the waveform compared to the ECG trace

• the peak of the a wave follows the P wave of the ECG by about 240 milliseconds; the v wave follows the T wave of the ECG; the v wave is larger than the a wave

pres

sure

Right atrium Right ventricle Pulmonary artery wedged

10

20

av

va

Normal Values

Right atrial pressure 2 – 6 mm Hg

Right ventricular systolic pressure 15 – 25 mm Hg

Right ventricular diastolic pressure 0 – 8 mm Hg

Pulmonary artery systolic pressure 15 – 25 mm Hg

Pulmonary artery diastolic pressure 8 – 15 mm Hg

Mean Pulmonary artery pressure()

10-20 mm Hg

Pulmonary artery wedged pressure 6 – 12 mm Hg

Inaccuracies with thermodilution

• Catheter malposition:

– Thermistor wedged against a vessel wall

– Coiling of the catheter - thermistor close to the injectate port

• Injection/ technique:

– Incorrect recording of injectate temperature

– Slow injection - underestimates cardiac output (see figure)

– Large volume – underestimates; small volume over estimates cardiac output

• Cardiac:

– Cardiac dysrhythmias

– Extremes of cardiac output

• Others:

– Abnormal respiratory patterns – respirations cause fluctuations in cardiac output

– Rapid infusion of IV fluids at the same time

– Abnormal haematocrit – will affect K value

Artefacts in thermodilution caused by improper injection

Normal curve

Prolonged injection time

Uneven injection

Uneven injection

Semicontinuous thermodilution cardiac output

• Thermodilution technique requires a injection of cold saline every time one needs to measure cardiac output

• Limits its use as a continuous monitoring tool – particularly in conditions where haemodynamic changes can potentially occur rapidly

• One way to overcome this challenge is to use heat instead of cold as an indicator

• Achieved by using a heating filament on the proximal portion of the catheter with a thermistor distally to measure temperature

• Heating filament generates low power pulses of heat; decay of heat is measured by the thermistor and cardiac output computed

• Shows good correlation with the Fick and thermodilution techniques

• Potential disadvantages include:

– Inaccuracy when cold fluid is boloused through the same line

– Incompatibility with Magnetic Resonance Imaging

– Interference from electro-diathermy

– Inability to detect sudden changes in cardiac output

Transpulmonary Thermodilution

Cardiac Output : Transpulmonary thermodilution

• Transpulmonary thermodilution technique is a variation of the traditional thermodilution technique

• Does not require a pulmonary artery catheter - a central venous catheter and an arterial line, preferably placed in the femoral vein is required

• Allows calculation of additional parameters: intra thoracic blood volume, global end diastolic volume and extra vascular lung water that may be help in the management of complex haemodynamic states

• Commercially available packages also uses the arterial pulse waveform (pulse contour analysis), referenced to the thermodilution curve, to give a beat by beat analysis of cardiac output

• This allows calculation of additional parameters such as pulse pressure variation and stroke volume variation that can aid in determining fluid status

Transpulmonary thermodilution - principles

• Following central venous injection, cold saline / dye passes through the right heart, the lung, the left heart and the aorta as far as the detection site

• The individual cardiac chambers and the lung, with the extravascular lung water, are the mixing chambers for the cold bolus

• When a dye bound to albumin is used, it will mix only within the heart chambers and pulmonary circulation

LA LVRA RVPulmonary

blood volume

Injection of cold saline into a central vein

Temperature changes recorded from a peripheral

artery

Extra vascular lung water

Right heartlungs

Left heart

Transpulmonary dilution - principles

• If a cold injectate is used, the chambers of the heart and the lung become the mixing chamber. The volume of this mixing chamber is the intrathoracic thermal volume (ITTV)

• The lungs, along with the extravascular lung water (EVLW) is the largest mixing chamber and its the volume is the pulmonary thermal volume (PTV)

LA LVRA RVPulmonary

blood volume

Intrathoracic thermal volume

Pulmonary thermal volume

Transpulmonary dilution - principles

• Indicators bound to albumin (like indocyanine green) do not leave the circulation

• It mixes within the chambers of the heart and the pulmonary circulation

• The volume within the chambers of the heart and the pulmonary circulation is the intrathoracic blood volume (ITBV)

• The volume of blood within the lung is the pulmonary blood volume (PBV)

LA LVRA RVPulmonary

blood volume

Intrathoracic blood volume

Pulmonary blood volume

Measurement of cardiac output• Cold saline / dye is injected into a central vein and the change in temperature or

concentration of dye is measured distally in an artery

• Cardiac output is calculated applying the Stewart – Hamilton formula

• Mean transit time (MTt) is the mean time taken for the indicator to be detected

• It is measured as the period between the start of the injection, and the point where the decay in the curve has dropped to 75% of its maximum

• Down slope time (DSt) represents the mixing behaviour of the indicator within the pulmonary circulation - the largest mixing chamber

• It is measured as the time taken for the curve to drop from 75% to 25% of its maximum

injection

Mean transit timeDownslope time

Time - seconds

Measurement of cardiac output

• If cold saline is used as the indicator, MTt is proportional to the ITTV:ITTV = MTtthermal x Cardiac Output

• When a dye bound to albumin is used, MTt is proportional ITBV – an indicator of preload:

ITBV

• With cold saline, the DSt is proportional to the pulmonary thermal volume (PTV):

PTV = DStthermal x Cardiac Output

• If a dye is used, DSt will be proportional to the pulmonary blood volume (PBV):

PBV = DStdye x Cardiac Output

injection

Mean transit timeDownslope time

Time - seconds

Cardiac output using double indicators

• A second indicator bound to albumin, usually a dye such indocyanine green, in addition cold saline can be also used to to obtain a cardiac output

• This indicator remains confined to the intravascular compartment

• Using the MTt for both indicators, ITBV and ITTV can be computed:ITBV = MTtdye x cardiac outputITTV = MTtthermal x cardiac outputExtravascular lung water (EVLW) = ITTV - ITBV• EVLW represents the interstitial mixing compartment and has been shown to

correlate with severity of illness1. It may be used as a guide to reduce positive fluid balance

injection

Mean transit timeDownslope time

Time - seconds

1. Sakka SG, Klein M, Reinhart K, Meier-Hellmann A. Prognostic value of extravascular lung water in critically ill patients. Chest. 2002; 122: 2080- 2086.

Single indicator technique

• The single indicator technique retains the same approach but uses only cold saline as the indicator

• The advantage is convenience and decreased costs

• It allows calculation of the same parameters as the double indicator technique and correlates well with both the double indicator technique and thermodilution technique

• It also allows referencing cardiac output to the pulse waveform, and using proprietary algorithms, to provide a continuous cardiac output using pulse contour analysis

Cardiac output – derived values

• Subtracting PTV from ITTV gives the volume of the four chambers of the heart: the global end diastolic volume (GEDV):GEDV = ITTV - PTV

• ITBV has been demonstrated to have a linear relationship with GEDV1:

ITBV = (GEDV x 1.25) – 28.4 ml • Extravascular lung water can be calculated by subtracting ITTV from ITBVEVLW = ITTV - ITBV • Both GEDV and ITBV are indicators of preload. Being volumetric measurements,

they are better than pressure based measurements

• They do not differentiate between right and left cardiac volumes and can be unreliable in right heart failure

LA LVRA RVPulmonary

blood volume1. Genahr A, McLuckie A. Transpulmonary

thermodilution in the critically ill. British J Intensive Care 2004: 6 - 10

Lithium dilution

• Lithium is used as the indicator: cardiac output is measured using the transpulmonary technique

• Lithium is non toxic in small doses and is measured using an ion sensitive electrode

• Shows good agreement with thermodilution techniques

• Advantages of using this technique:

– Lithium can be injected peripherally

– Blood can be sampled from a peripherally placed arterial line

• Limitations include:

– Inability to use it in patients on Lithium therapy

– The need to sample blood and its disposal

Stroke Volume / Pulse Pressure Variation

Principles

Maximum pulse pressure

Minimum pulse pressure

Stroke volume maxStroke volume min

• Both techniques rely on the principle that raised intrathoracic pressures in the inspiratory cycle of mechanical ventilators decreases venous return and therefore, cardiac output

• This decrease is determined by calculating cardiac output (area under the arterial waveform in systole) during inspiration (decreases) and expiration (SVV)

• The calculated cardiac output is usually referenced to a previous measurement of cardiac output using a transpulmonary dilution technique

• The Flo trac™ system developed by Edwards Life Sciences uses a proprietary algorithm to calculate cardiac output using pulse waveform analysis without the need for calibration

• The difference between pulse pressures (PPV) or the systolic pressures (SPV) is also used as a surrogate marker, obviating the need for cardiac output measurement

inspiration expiration

Application

• Pulse pressure variation and stroke volume variation is calculated as the difference between the maximum and minimum systolic pressure / stroke volume during the inspiratory cycle

• The variation is usually expressed as a percentage of the mean pulse pressure/ stroke volume

• Larger variations have been shown to correlate with fluid responsiveness, indicating that the heart is operating on the steep side of the Frank-Starling curve

• In a meta-analysis1, variations between over 11 % appeared to correlate well with fluid responsiveness in mechanically ventilated patients

• Robust data on spontaneously breathing patients is awaited

1. Marik PE, Cavallazzi R, VasuT , Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: A systematic review of the literature. Crit Care Med 2009; 37: 2642 - 2647

Oesophageal Doppler

Oesophageal Doppler

• The Doppler effect describes a change in frequency (f) of sound that occurs due to relative motion between a wave source, the wave receiver and a wave reflector

• The ultrasound transducer is wave source and receiver while red cells reflect the waves

• The magnitude of Doppler shift is proportional to the velocity of blood flow

• The velocity of blood flow (V – m/sec), is calculated from the Doppler equation: = aortaoesophagus

f transmitted

f received

Dop

pler

pro

be

Δf = ft - fr

ft = transmitted frequencyc = velocity of sound in tissue (1540 m/s)cos θ = incident angle between the ultrasound beam and blood flow direction (if the probe is parallel to the aorta, θ = 0° and cos θ = 1)

Oesophageal Doppler

• Multiplying the flow velocity by the cross-sectional area of the aorta and the ejection time gives an estimate of the stroke volume

• Depending on the equipment used, the cross-sectional area of the aorta is estimated either from a normogram based on patient height, weight and age or, from direct estimates using the ultrasound

• A correctional factor is applied to account for that proportion of stroke volume distributed to the coronary, carotid and subclavian arteries

• Cardiac output is calculated by multiplying the stroke volume with the heart rate

• In addition to cardiac output, the system also gives information about the preload and contractility of the heart by analysing the waveform

Oesophageal Doppler – waveform analysis

• Waveform of velocity against time is shown below

• The base of the triangle represents the systolic ejection time, also called the flow time. Because this is dependent on the heart rate, it is corrected using a modification of Bazett’s equation for correction of QT interval in the ECG

• The corrected flow time (FTc) is the systolic ejection time corrected to one cardiac cycle per second

• The area under the curve (shaded orange) is the stroke distance: the distance the column of blood has moved forward in the aorta during systole

• Multiplying the stroke distance with the cross-sectional area of the aorta (direct measurement or normogram) gives the stroke volume. A correction is applied to account for blood flow to the branches of the aortic arch and coronaries

Time

velo

city

peak velocity

flow time

AUC = Stroke

distance

Oesophageal Doppler – waveform analysis

• In addition to measuring stroke volume and cardiac output, analysis of the Doppler waveform gives information about preload and contractility

• FTc and peak velocity are the parameters used to indicate preload

• A shortened FTc with a normal or moderately reduced peak velocity (waveform with narrow base and near normal amplitude) is seen in hypovolemic states

• A shortened FTc with a markedly reduced peak velocity (waveform with a narrow base and decreased amplitude) reflects increased afterload

• Reduced amplitude with a more shallow slope and rounded apex is seen with left ventricular failure

• Peak velocity and mean acceleration reflect contractility

Time

velo

city

peak velocity

flow time

AUC = Stroke

distance

mea

n ac

cele

ratio

n

Oesophageal Doppler – waveform analysis

• The waveform is also used to see response to therapy such as fluid boluses or inotropes – see figure

• While this does look promising, there are limited number of studies1 that have validated oesophageal Doppler as a monitoring tool

• Most of the studies have been done in a peri-operative setting and its applicability to a general ICU setting is not clear

Hypovolemia - ↓ FTc, stroke volume, normal peak velocity

Response to fluids

SV=47 PV=63 SV=64 PV=63.5

SV=42 PV=42 FTc= 232 SV=72 PV=65 FTc= 345

Increased afterload - ↓ SV, PV and FTc

Response to vasodilators

SV=42 PV=45.5 SV=59 PV=63

Left ventricular failure - ↓ SV, PV and normal FTc

Response to inotropes

1. Ospina-Tascón GA, Cordioli RL Vincent J-L. What type of monitoring has been shown to improve outcomes in acutely ill patients? Intensive Care Med. 2008; 34: 800–820

Oesophageal Doppler - limitations

• The measurements assume that flow in the aorta is laminar. This may not always be the case and the values may not be accurate in:

– Coarction of aorta or aortic stenosis

– Aneurysms or dissection

– When balloon pump counter pulsation is used

• Deviations from the assumed angle of insonation (θ, the angle at which the Doppler signals are sent) will result in erroneous velocity values

• The cross sectional area of the aorta is assumed to be a perfect circle. This may not be true, especially if there are aortic plaques or compliance is poor

• Estimation of cardiac output assumes that a fixed proportion of blood goes to the coronaries and the branches of the aortic arch. This may not always be true. Shock states result in redistribution of cardiac output

Echocardiography

• Provides accurate assessment of stroke volume and chamber pressures

• Also enables estimation of myocardial function / dysfunction including diastolic dysfunction

• Severity of valvular dysfunction can be assessed

• Disadvantages:

– Requires trained personnel

– Equipment costs

– Operator dependent

– Body habitus, ventilation and position of the patient may preclude obtaining good images

– Examination takes considerable time; real time imaging is not possible – can be overcome to a certain extent by limiting assessment to fixed protocols

Thoracic bioimpedance

• Measures thoracic impedance to a high frequency, low magnitude current applied between electrodes in the neck and thorax

High frequency low magnitude

current

Thoracic Bioimpedance

and ECG sensing

• Bioimpedance of the thorax is influenced by the amount of fluid in the thorax

• Fluid in the thorax (mainly blood in the venacavae and aorta) changes with cardiac cycle – causing changes in bioimpedance

• Bioimpedance is inversely proportional to the amount of fluid in the thorax

• Stroke volume and cardiac output is computed after filtering electric noise caused by other fluid movement

• Results using thoracic bioimpedance have been mixed - some studies have shown good correlation with invasive methods currently used, others have not

• Acute lung injury, pleural effusions, pneumonia and obesity interfere with bioimpedance and result in inaccurate measurements

Indications for monitoring cardiac output

Diagnostic• Differential diagnosis of shock

– Cardiogenic– Septic– Hypovolemic

• Evaluation of pulmonary oedema– Cardiogenic from non cardiogenic

• Evaluation of cardiac failure– Tamponade

• Evaluation of cardiac structures– Valvular disease and intracardiac

shunts

• Others– Shock in acute myocardial infarction– Pulmonary hypertension

Therapeutic• Guide therapy in shock

– Fluid management– Vasopressor / inotropes

• Guide therapy peri-operatively• Guide therapy in cardiac failure• Ventilator management• Multi - organ failure

Clinical applications

• Assessment of fluid status:

– CVP/ Right atrial pressure – non specific, low pressures may be due to venous dilatation; high pressures may be reflective of pulmonary/ intra cardiac pathology

– Right ventricular end diastolic volume – estimated by echo and thermodilution – more accurate measurement of preload

– Global end diastolic volume – transpulmonary thermodilution

– Decreased peak velocity and FTc on oesophageal Doppler

– Increased pulse pressure / stroke volume variation in mechanically ventilated patients

• Assessment of contractility:

– Direct measurement of ejection fraction, systolic and diastolic function on echo

– cardiac output / index; stroke volume / index using thermodilution, transpulmonary dilution or Doppler

– Left or right ventricular stroke work index

• Assessment of afterload:

– Systemic vascular resistance / index

Evidence to support cardiac output monitoring

• Most of the evidence comes from the use of PA catheters

• Several reports published1 - suggesting harm from the use of PA catheters

• More recent randomized control studies and several meta analyses2 have not shown harm from their use

• These studies also failed to show a proven benefit (mortality or length of ICU/ hospital stay) of using PA catheters compared with standard care3

• Paucity of studies on the efficacy of other forms of cardiac output monitoring; however they are likely to reflect data from PA catheters

• Routine use of cardiac output monitoring may not be beneficial

• There may be may be some conditions where it may provide additional data aiding in diagnosis and therapy

1. Connors AF, Speroff T, Dawson NV, Thomas CT, Harrell FE, Wagner D et al.The Effectiveness of Right Heart Catheterization in the Initial Care of Critically III Patients. JAMA. 1996; 276: 889-8972. Shah MR, Hasselblad V, Stevenson LW, Binanay C, O’Connor CM, Sopko G et al. Impact of the Pulmonary Artery Catheter in Critically Ill Patients. JAMA. 2005; 294: 1664-16703. Harvey S, Young D, BramptonW, Cooper A,Doig GS, SibbaldW, Rowan K. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database of Systematic Reviews 2006, Issue 3.

Monitoring Perfusion – Gastric Tonometry

Introduction

• The goal of haemodynamic monitoring and support - ensure organs are adequately perfused

• Assessment of the mental state and urine output are important clinical markers of organ perfusion in the brain and kidney

• Often, these organs become involved in the disease process or cannot be assessed because of sedation / existing disease

• Gastric tonometry is one technique used to assess regional perfusion

Gastric tonometry

• Assesses splanchnic perfusion based on stomach’s mucosal pH by measuring gastric luminal PCO2

using a fluid filled balloon permeable to gases

• The balloon is attached to a nasogastric tube and allowed to equilibrate with the luminal carbon dioxide. Luminal CO2 reflects intramucosal CO2

• PCO2 is measured along with a simultaneous arterial blood gas and the luminal

pH is calculated

• Several limitations to using gastric tonometry routinely:

– takes about 90 minutes for CO2 to equilibrate between the balloon and the lumen

– Luminal CO2 may be affected by acid secretion (or lack of it if the patient is on acid suppressing agents) and feeding

– No convincing evidence1 to support its routine use in the intensive care as several trials have failed to show benefit in using this form of monitoring

1. Holley A, Lukin W, Paratz J, Hawkins T, Boots R Lipman J. Review article: Part two: Goal-directed resuscitation – Which goals? Perfusion targets. Emergency Medicine Australasia (2012) 24, 127–135

Monitoring Oxygen Consumption – Mixed Venous Saturation

Mixed venous saturation

• Oxygen content of venous blood (CvO2) in the pulmonary artery (mixed venous blood) is used to estimate oxygen consumption (VO2), using the Fick equation

• Indicative of the global metabolic requirements of the body

• Relationship between oxygen delivery (DO2) and VO2 is linear – DO2 increases to keep up VO2 - up to a point (critical DO2). Beyond this, consumption exceeds supply, forces cells to revert to anaerobic metabolism

• The point at which critical DO2 occurs is not the same for all organs; it also changes with disease states like sepsis

• Low CvO2 reflects inadequate DO2 or increased consumption with greater oxygen extraction

• Saturation of mixed venous blood (SvO2) can be used instead of CvO2

• The normal SvO2 is > 75%

• The central venous saturation (ScvO2) of the superior venacava is used instead of SvO2 ; there is some evidence that changes parallel that of SvO2

• SvO2 is usually lower than ScvO2 by 2-5 %; this can reverse in shocked states

Clinical utility

• ScvO2 is one of the clinical monitoring tools used to guide fluid resuscitation as part of the bundle in ‘early goal-directed therapy’ of septic shock1, 2

• A ScvO2 < 70 % was used as a trigger to increase DO2 by increasing cardiac output or increasing haemoglobin once fluid resuscitation resulted in a target CVP of 8 -12

• Using this bundle, Rivers demonstrated a decrease in mortality; we await results of more recent studies

• Several studies have used SvO2 monitoring in the perioperative setting3. Most of the studies involving vascular patients do not demonstrate a mortality benefit or reduced length of ICU / hospital stay though there is some evidence to support its use in cardiac surgery

1. Holley A, Lukin W, Paratz J, Hawkins T, Boots R, Lipman J. Review article: Part one: Goal-directed resuscitation – Which goals? Haemodynamic targets. Emergency Medicine Australasia (2012) 24, 14–22

2. Rhodes A, Bennett DE. Early goal-directed therapy: An evidence-based review. Crit Care Med 2004; 32: S448 -4503. Shepherd SJ, Pearse R. Role of Central and Mixed Venous Oxygen Saturation Measurement in Perioperative Care.

Anesthesiology 2009; 111: 649 - 656

Summary

• Advanced haemodynamic monitoring is useful in critically ill patients with haemodynamic instability

• It provides more information about the circulatory state of the patient including

– Preload– Myocardial contractility– Afterload– Perfusion and oxygen consumption

• Cardiac output monitoring provides information about all these parameters• There are several modalities of monitoring to choose from • Decisions on which modality is best depends on the clinical situation,

available resources and institutional preference• There is no clear evidence that cardiac output monitoring improves outcomes

– but information from it can be used in clinical decision making• Mixed venous saturation is useful to monitor oxygen consumption and is one

of the parameters used to titrate therapy in septic shock