1. Hemodynamic monitoring
Magdy M Khalil, MD, EDIC

2. CO = (SV x HR) x {(Hb x 1.39 x SaO2) + (0.003 x PaO2)}
Tissue perfusion
Oxygen delivery = CO x arterial oxygen content
CO = (SV x HR) x {(Hb x 1.39 x SaO2) + (0.003 x PaO2)}
Arterial pressure (AP) = CO x SVR

3. Diagnosis of tissue malperfusion
Clinical assessment
Basic monitoring
Preload monitoring
Minimally invasive cardiac output/cardiac contractility assessment
Invasive; pulmonary artery catheter
Assessment of tissue perfusion
Haemodynamic monitoring is necessary for assessing global and regional tissue perfusion. Timely and adequate correction of instability and tissue hypoperfusion is essential to prevent progression to MODS and reduce mortality.
At the bedside, haemodynamic stability and tissue perfusion are monitored by a combination of clinical examination, monitoring devices and laboratory results
At the bedside, haemodynamic monitoring can be approached in a series of steps aimed at assessing global and regional perfusion:

4. Clinical assessment Thirst, Cold mottled extremities,
Poor peripheral pulses,
Impaired capillary refill,
Tachypnoea,
Tachycardia,
Altered mentation, or
Oliguria.

5. Basic monitoring Electrocardiography (ECG),
Arterial blood pressure (AP),
Pulse oximetry (SpO2) monitoring,
Baseline serum lactate.
All critically ill patients should have electrocardiographic (ECG), arterial blood pressure (AP) and pulse oximetry (SpO2) monitoring. Baseline serum lactate measurements and biochemical variables should be measured.
ECG monitoring
CO = SV x HR
AP = CO x SVR
Blood pressure may be measured non-invasively with a cuff placed around a limb and attached to a sphygmomanometer or an oscillometric device, or invasively using an indwelling catheter in an artery
Blood pressure monitoring
Measuring arterial blood pressure (AP) is a cornerstone of haemodynamic assessment. The definition of low AP is patient specific and interpreted in the context of the patient's usual AP. Mean arterial blood pressure (MAP) is an approximation of organ perfusion pressure. When stroke volume falls, MAP can initially be maintained by increasing heart rate or peripheral vasomotor tone. Elevated AP, especially if acute, is associated with increased vascular resistance and may be associated with tissue malperfusion e.g. hypertensive encephalopathy or acute renal failure.

6. Arterial blood pressure
Measurement
Non-invasive
Invasive
Indications for invasive arterial pressure monitoring:
Labile blood pressure
Severe hypotension
Use of rapidly acting vasoactive drugs
Frequent sampling of arterial blood.
Relative indications :
Severe hypertension
Presence of an intra-aortic balloon pump
Morbid obesity.
non-invasively with a cuff placed around a limb and attached to a sphygmomanometer or an oscillometric device, or
invasively using an indwelling catheter in an artery
Labile blood pressure or anticipation of labile blood pressure
Use of rapidly acting vasoactive drugs; vasodilators, vasopressors, inotropes

7. SpO2 monitoring
The SpO2 signal is often inaccurate in the presence of altered skin perfusion
Raised serum lactate levels may represent poor tissue perfusion. The association of increased lactate levels with circulatory failure, anaerobic metabolism and the presence of tissue hypoxia has led to its utility as a monitor of tissue perfusion in critically ill patients. Hb is haemoglobin concentration and 1.39 is the volume of oxygen (ml) that combines with 1 gram of haemoglobin. SaO2 is the percentage of Hb in arterial blood saturated with O2 (normally 97% ± 2%). Arterial O2 content consists mainly of O2 combined with Hb. A very small additional amount of O2 is carried independently of Hb in physical solution. This is of the order times the arterial oxygen tension (PaO2); normally 95 ± 5 mmHg (12 ± 1.3 kPa) in toto.

8. Serum lactate Normal level in resting humans 1 mmol/l (0.7- 1.3).
Same in venous or arterial blood
Factors affecting serum lactate level:
The normal serum lactate level in resting humans is approximately 1 mmol/l ( ).
The value is the same whether measured in venous or arterial blood (in the absence of a tourniquet).
If tissue malperfusion is suspected, measure haemoglobin and oxygen (PaO2) levels and treat if necessary.

9. Venous oxygen saturation
Cardiac output
hypoxia and
anaemia also affect the ScvO2.
pain, shivering and increased work of breathing can also affect the ScvO2 value.
carbon monoxide poisoning, cyanide poisoning, and intra-cardiac shunt
The normal range of ScvO2 in critically ill patients is 70-75%
Global perfusion: ScvO2Insertion of a central venous catheter for CVP assessment also allows measurement of ScvO2, the oxygen saturation of blood in the superior vena cava. ScvO2 is a global indicator of tissue oxygenation. Cardiac output is the single most important determinant of ScvO2; as CO falls, oxygen delivery decreases and oxygen extraction increases. Other factors that decrease oxygen delivery, such as hypoxia and anaemia also affect the ScvO2. Likewise factors that increase oxygen delivery such as pain, shivering and increased work of breathing can also affect the ScvO2 value.
The normal range of ScvO2 in critically ill patients is 70-75% Less common conditions which may affect the ScvO2 include carbon monoxide poisoning, cyanide poisoning, and intra-cardiac shunt

10. Preload monitoring Examination of the right internal jugular vein
Central venous pressure (CVP).
Catheter in SVC
An elevated intracardiac pressure may be due to an elevated volume or an elevated resistance (Acute heart failure, cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, tricuspid stenosis or regurgitation)
Estimated from respiratory motion of IVC (SB).
End-diastolic volumes (TTE /TOE)
When the patient is lying at 45 °, the peak of the jugular venous pulsation should not be >3 cm above the base of the neck.
2-Central venous pressure (CVP)
Clinical evidence of tissue hypoperfusion (e.g. cold mottled extremities, altered mentation or oliguria), hypotension or elevated serum lactate concentrations indicate a need to move to the next step in haemodynamic monitoring; preload and global perfusion assessment.
Preload abnormalities are commonly involved in tissue hypoperfusion. One can separate right ventricular (RV) and left ventricular (LV) preload. At the bedside, right atrial pressure or jugular venous pressure (RAP/JVP) is used as a surrogate of RV preload
The Frank–Starling principle states that forcefulness of ventricular contraction is determined by myocardial fibre length at end diastoleentral venous pressure
The most frequent method of assessing RAP is by measuring central venous pressure (CVP). Examination of the right internal jugular vein provides an estimate of CVP. When the patient is lying at 45 °, the peak of the jugular venous pulsation should not be >3 cm above the base of the neck. However, JVP may be difficult to evaluate in a critically ill patient.
Left ventricular stroke volume is a function of 3 variables: preload, afterload and contractility
CVP can be measured directly by placing a catheter in the superior vena cava. The normal mean CVP in a spontaneously breathing patient is 0-5 mmHg, while 10 mmHg is the upper limit of normal during mechanical ventilation. An elevated CVP (>15 mmHg) suggests volume overload and/or RV failure.
CVP is at best a general guide to preload with greater emphasis on dynamic values (monitoring trends in CVP over time) rather than single measurements. For example, continuous hypotension in a patient with a CVP <5 mmHg indicates the need for fluid therapy, whereas values in the 5-15 mmHg range are less useful because other conditions may increase the CVP and, therefore, do not necessarily represent the patient's volume status. An elevated CVP, by itself, should not prevent a fluid challenge.
Pressure = flow x resistance. An elevated intracardiac pressure may be due to an elevated volume or an elevated resistance
List four other causes of an elevated CVP.
Acute heart failure, cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, tricuspid stenosis or regurgitation.
CVP can be estimated in a spontaneously breathing patient by observing the respiratory motion of the inferior vena cava (IVC) on echocardiography. In mechanically ventilated patients limitations apply to this technique
End-diastolic volumes
Right and left ventricular end-diastolic volumes have been used to define right and left ventricular preload. Although both transthoracic (TTE) and transoesophageal (TOE) echocardiography have been used to measure right and left ventricular end-diastolic dimensions, conflicting results have been reported regarding their utility to predict preload dependence/fluid responsiveness
Normal values: CVP in a spontaneously breathing patient is 0-5 mmHg, while 10 mmHg is the upper limit of normal during mechanical ventilation
An elevated CVP (>15 mmHg) suggests volume overload and/or RV failure. with greater emphasis on dynamic values (monitoring trends in CVP over time) rather than single measurements.
CVP can be estimated in a spontaneously breathing patient by observing the respiratory motion of the inferior vena cava (IVC) on echocardiography. In mechanically ventilated patients limitations apply to this technique.

11. Predicting fluid responsiveness
Change in CO in response to a change in preload
Fluid challenge while monitoring:
AP,
heart rate,
CVP and
urine output.
Fluid responsiveness is a dynamic parameter that is defined as the On the ascending limb of the Frank–Starling ventricular function curve, increasing preload will result in an increase in CO, whereas on the plateau phase vigorous fluid resuscitation may cause pulmonary oedema and/or right ventricular dysfunction with no improvement in CO.

12. Predicting fluid responsiveness
Static parametersGEDV is the volume of blood contained in the four chambers of the heart at end diastole. ITBV is the volume of blood in the four chambers and the blood volume in the pulmonary vessels at end diastole
Dynamic parameters
pulse pressure variation (PPV) ≥13% ,
systolic pressure variation (SPV) greater than 10 mmHg on MVand
stroke volume variation (SVV).
The normal healthy heart is fluid responsive. The demonstration of fluid responsiveness is not an indication, by itself, to administer fluids
On the ascending limb of the Frank–Starling ventricular function curve, increasing preload will result in an increase in CO, whereas on the plateau phase vigorous fluid resuscitation may cause pulmonary oedema and/or right ventricular dysfunction with no improvement in CO. Methods of predicting an individual patient's preload responsiveness are useful. Fluid responsiveness is a dynamic parameter that is defined as the change in CO in response to a change in preload
The static parameters are more useful when their values are high or low; they are less helpful when they are in the intermediate range
Positive pressure mechanical ventilation produces pronounced, cyclical changes in ventricular stroke volume and systolic blood pressure. The exaggerated respiratory variation observed in the arterial pressure waveform has been used to assess preload responsiveness and has been validated in mechanically ventilated patients. A PPV of ≥13% in septic patients has been shown to be a specific and sensitive indicator of preload responsiveness. Exaggerated SPV greater than 10 mmHg during a respiratory cycle of a patient receiving positive pressure mechanical ventilation has also been shown to be useful for this assessment. SVV can be calculated using pulse contour analysis or oesophageal Doppler and has been shown to predict fluid responsiveness. More recently, methods of predicting fluid responsiveness in spontaneously breathing patients have been reported. The normal healthy heart is fluid responsive. The demonstration of fluid responsiveness is not an indication, by itself, to administer fluids

13. Minimally invasive CO/CC assessment
Indications
Hypotension despite fluid resuscitation, or
Continued evidence of global tissue hypoperfusion
Low CO + elevated measures of preload=ventricular failure.
High CO+ tissue hypoperfusion, e.g. septic shock.
Cardiac output is adequate if there is no evidence of tissue hypoperfusion
Continued evidence of global tissue hypoperfusion (e.g. oliguria, elevated serum lactate, ScvO2 <65%).
Direct measurement of CO should be considered when a patient remains hypotensive despite fluid resuscitation or there is continued evidence of global tissue hypoperfusion (e.g. oliguria, elevated serum lactate, ScvO2 <65%). The measurement may provide information specific to disease states, e.g. a low CO, combined with elevated measures of preload, may confirm ventricular failure. The adequacy of CO is assessed in terms of any evidence of tissue hypoperfusion. For many years CO was measured in critically ill patients using a pulmonary artery catheter. New emerging technologies allow measurement of CO in less invasive ways.
Note Cardiac output may be elevated in the presence of tissue hypoperfusion, e.g. septic shock.

14. Minimally invasive methods of CO measurement
Echocardiography (EF >55%)
Pulse contour analysis: measuries SV on a beat-to-beat basis from the arterial pulse pressure waveform.
Oesophageal Doppler: measures blood flow velocity) in the descending aorta (70% of total CO)
Methods using the Fick principle (Patient on MV)
Contraindications to oesophageal Doppler :
Unexplained history of dysphagia
Oesophageal pathology e.g. varices, stricture, oesophagitis
Oropharyngeal pathology
Unstable cervical spine injury
Echocardiography: cardiac contractility
exclude a cardiac cause of shock
. Assessment of cardiac contractility in terms of ejection fraction (EF). The EF is the percentage of LV diastolic volume ejected with each heart beat (normal >55%).
include cardiac tamponade, acute mitral regurgitation and aortic dissection
Pulse contour analysis
measuring stroke volume (and thus CO) on a beat-to-beat basis from the arterial pulse pressure waveform. PiCCO®, PULSECO/LiDCO™ and Vigileo/Flotrac™.
Oesophageal Doppler
Oesophageal Doppler measures blood flow velocity (70% of total CO) in the descending aorta by using a Doppler transduce
Dvantage: continuous monitoring
Contraindications and relative contraindications to oesophageal Doppler or transoesophageal echocardiography:
Unexplained history of dysphagia
Oesophageal pathology e.g. varices, stricture, oesophagitis
Oropharyngeal pathology
Unstable cervical spine injur r
Methods using the Fick principle
The Fick principle can be applied to any gas diffusing through the lungs. The NICO® monitor (Respironics) is based on application of the Fick principle using carbon dioxide. in patients receiving mechanical ventilatory support, inaccurate when dead space is significantly increased.
Any gas diffusing through the lungs e.g. CO2 (NICO®)
Cardiac index is cardiac output divided by body surface areaStroke volume is a more specific indicator of cardiac function than cardiac output as it is independent of heart rate
Techniques currently used in clinical practice are
Methods using the Fick principle.
Cardiac index is cardiac output divided by body surface area
Arterial pulse contour analysis is a technique of measuring stroke volume (and thus CO) on a beat-to-beat basis from the arterial pulse pressure waveform. There are now three commercially available systems: PiCCO®, PULSECO/LiDCO™ and Vigileo/Flotrac™. An initial CO value is estimated, based on the arterial pressure waveform and the patient's age and sex. This is then calibrated using a direct measurement of CO via trans-cardiopulmonary dilution (PiCCO®) or lithium chloride dilution (LiDCO). The Vigileo™ transducer does not use calibration with a known CO measurement; rather it tracks the shape of the arterial waveform and compares it against historical control. The compliance is then identified from the shape of the arterial waveform. Potential inaccuracies may arise from this method of calibration.
Stroke volume is a more specific indicator of cardiac function than cardiac output as it is independent of heart rate
Oesophageal Doppler measures blood flow velocity in the descending aorta by using a Doppler transducer at the tip of a probe (approximately the size of a standard oesophageal stethoscope). The device measures aortic blood flow representing about 70% of total CO
The Fick principle can be applied to any gas diffusing through the lungs. The NICO® monitor (Respironics) is based on application of the Fick principle using carbon dioxide. The technique can only be used in patients receiving mechanical ventilatory support, and the measurements become inaccurate when dead space is significantly increased.
Echocardiography can also provide accurate quantification of CO, although not on a continuous basis. Assessment of cardiac contractility is an alternative measure of LV function and is defined in terms of ejection fraction (EF). The EF is the percentage of LV diastolic volume ejected with each heart beat (normal >55%). The utility of echocardiography as a haemodynamic monitor is far greater than assessment of LV function. It is the test of choice in critically ill hypotensive patients to identify or exclude a cardiac cause of shock as it is portable to the bedside, safe and can provide an immediate diagnosis. Examples of life-threatening conditions that may be diagnosed by echocardiography include cardiac tamponade, acute mitral regurgitation and aortic dissection
List the contraindications to oesophageal Doppler and transoesophageal echocardiography.

15. Transpulmonary thermodilution; cardiac output and volumetric parameters
Global end-diastolic volume (GEDV): ITTV – PTV ( ml/m 2)
Intrathoracic thermal blood volume (ITBV): 1.25 x GEDV ( ml/m 2)
Pulmonary blood volume (PBV): ITBV – GEDV
Extravascular lung water (EVLW): ITTV – ITBV ( ml/kg).
Pulmonary vascular permeability index (PVPI) ( ): EVLW /PBV reflects the permeability of the alveolar–capillary barrier.
PVPI is higher in ALI/ARDS
EVLW is the amount of water in the lungs and is a bedside quantification of the degree of pulmonary oedema.GEDV may be a more useful measure of fluid responsiveness than CVP.
The volumetric parameter may more accurately reflect the position on the slope of the Frank–Starling curve, and thus the change in SV in response to fluidinjection site of fluid bolus (central catheter) and the temperature measurement site (arterial catheter).
This in turn allows calculation ofThe transpulmonary thermodilution technique (PiCCO® system) generates a series of volumetric parameters that have been shown to assess cardiac preload, predict fluid responsiveness and are very useful in quantification and determination of the aetiology of pulmonary oedema. The technique also allows measurement of SV and CO as above.
The underlying principle considers the intrathoracic compartments as a series of 'mixing chambers' between the injection site of fluid bolus (central catheter) and the temperature measurement site (arterial catheter). The total series of compartments comprise the intrathoracic thermal volume (ITTV) which is made up of right heart chambers, pulmonary thermal volume (PTV) and left heart chambers
This in turn allows calculation of Global end-diastolic volume (GEDV): ITTV – PTV Intrathoracic thermal blood volume (ITBV): 1.25 x GEDV Pulmonary blood volume (PBV): ITBV – GEDV Extravascular lung water (EVLW): ITTV – ITBVGEDV may be a more useful measure of fluid responsiveness than CVP. The volumetric parameter may more accurately reflect the position on the slope of the Frank–Starling curve, and thus the change in SV in response to fluid.
EVLW is the amount of water in the lungs and is a bedside quantification of the degree of pulmonary oedema.
The ratio between EVLW and PBV is called the pulmonary vascular permeability index (PVPI) and reflects the permeability of the alveolar–capillary barrier. Thus PVPI is higher in ALI/ARDS (meaning that EVLW is high compared to PBV) than in hydrostatic pulmonary oedema.
Normal volumetric parameters indexed to BSA: GEDV ml/m 2 ITBV ml/m 2 EVLW ml/kg PVPI

16. Pulmonary artery catheter
Continuous monitoring of :
RAP
PAP
PAOP (5-12 mmHg) CO
SvO2.
Indications:
Circulatory shock with evidence of tissue hypoperfusion not responding to therapy.
Management of severe pulmonary oedema.
Difficulty evaluating right and left ventricular preload in the presence of oliguria.
PAOP is. A PAOP of mmHg is generally required before hydrostatic (e.g. left heart failure) pulmonary oedema develops. When pulmonary oedema results from increased pulmonary capillary permeability (e.g. ARDS) the PAOP should be <18 mmHg
Insertion of a pulmonary artery catheter (PAC) is the most invasive monitoring step described so far. In the context of altered tissue perfusion, a PAC is considered primarily in three clinical scenarios:
Circulatory shock with evidence of tissue hypoperfusion (lactic acidosis, tachycardia, oliguria) not responding to therapy.
Management of severe pulmonary oedema.
Difficulty evaluating right and left ventricular preload in the presence of oliguria.
A valuable instrument for the diagnosis of severe mitral valve regurgitation, pulmonary hypertension, right ventricular failure, intra-cardiac shunt, high and low output failure and pericardial tamponade
The normal range for PAOP is 5-12 mmHg. A PAOP of mmHg is generally required before hydrostatic (e.g. left heart failure) pulmonary oedema develops. When pulmonary oedema results from increased pulmonary capillary permeability (e.g. ARDS) the PAOP should be <18 mmHg
The PAC enables continuous monitoring of right atrial and intrapulmonary vascular pressures, cardiac output and mixed venous oxygen saturation (SvO2). There is overlap between data obtained from a PAC and some of the monitors described above. For example, cardiac output may be estimated non-invasively and ScvO2 can serve as a surrogate marker of SvO2 in the early phase of septic shock. However, continuous monitoring of intrapulmonary vascular pressures is most readily available from a PAC. Measurement of pulmonary artery systolic pressure and pulmonary artery occlusion pressure (PAOP) estimated from echo are operator-dependent and not available on a continuous basis. PAOP approximates left atrial pressure and in the absence of mitral valve pathology reflects left ventricular end-diastolic pressure. PAOP measurement is useful to determine the cause of pulmonary oedema.

17. Interpreting haemodynamic data
Is there evidence of tissue hypoperfusion?
Is there a reduction in arterial oxygen content?
Is there a question regarding optimal preload?
Is there a question regarding stroke volume/cardiac contractility?
Is there a need for PAC?