Week 4 – Haemodynamic monitoring

Hemodynamic monitoring is the active assessment of cardiopulmonary status by the use of biosensors that assess physiologic outputs.
The simplest form of monitoring is the individual health care professional, inspecting the patient for consciousness, agitation or distress,
breathing regular or labored, the presence or absence of central and peripheral cyanosis; touching of the skin of a patient to note if it is
cool and moist, and if capillary refill is rapid or not; palpation of the central and peripheral pulses to note rate and firmness.
Although well established and important as bedside diagnostic tools, these simple “human-instrument” measures can be greatly expanded
by the use of pulse oximetry to estimate arterial oxygen saturation (Spo2), and the sphygmomanometer and auscultation to note systolic
and diastolic blood pressure and identify pulsus paradoxus. These classic measures of hemodynamics, often referred to as routine vital
signs, are central to the assessment of cardiorespiratory sufficiency and much of diagnostic bedside medicine is rooted in these important
However, with some exceptions, these simple and inexpensive measures do not have the discriminatory value in identifying patients as
being stable or unstable when compensatory processes mask instability or when changes in physiologic state occur rapidly. Furthermore,
they predict poorly who are at an early stage of an instability process, such as hypovolemia or heart failure, but compensating. Within the
context of circulatory shock, tachycardia may or may not develop early and even if it is present, it is nonspecific. However, these simple
measures can be markedly helped in their sensitivity to detect effective hypovolemia by making these same measures before and during
an orthostatic challenge.
For example, measuring blood pressure and pulse rate changes between lying supine, sitting, and standing markedly increase the
diagnostic capability of the measures to identify functional hypovolemia. If heart rate increases and/or blood pressure decreases with
sitting or standing, it is reasonable to presume that some degree of compatible hypovolemia exists. However, the other important concept
in making these observations is that the measures themselves do not change, but their measured values change in response to a defined
physiologic challenge: this is an example of functional hemodynamic monitoring. Functional hemodynamic monitoring is the use of a
defined physiologic stressor to access the physiologic reserve of the system.
Both invasive and non invasive hemodynamic monitoring is used extensively in critical care practice. Invasive monitoring is used to obtain
continuous pressure measurements in the central and systemic circulation. These parameters are used to estimate physiological variable
such as cardiac output and volume status.
Learning outcomes for this section
Upon successful completion of this section, you should be able to:
discuss the theoretical principles of haemodynamics
safely action haemodynamic monitoring procedures and protocols
interpret hemodynamic monitoring output
relate hemodynamic monitoring parameters to physiology of critically ill patients
realise the contribution hemodynamic monitoring makes as part of continuous patient assessment.
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The material discussed in this section requires an appreciation of the factors which are related to cardiac output.
Revise the following and list the normal values for each:
cardiac output
cardiac index
stroke volume
stroke volume index
systemic vascular resistance
pulmonary vascular resistance
Cardiac Cycle animation
Blood Pressure Animation
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Suggested readings
Core text reading
Aitken, A, Marshall, A, & Chaboyer, W.,2015, ACCCN’s critical care nursing, 3nd edn, Elsevier, Australia, Chapter 9, pp. 248-260.
Other readings are highlighted through-out this module
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Concepts of haemodynamics
Heart Lung.org – great resource – Click Here
Pressure and flow
Pressure is the force applied per unit area. In haemodynamics we always think of pressure in terms of a pressure difference. The
pressure difference along the axis, or pressure gradient, is the pressure that causes the flow of blood. The pressure difference
between the inside and outside of a vessel or the heart, which is often called transmural pressure, and causes the wall distension.
It is important to remember that even though pressure is measured with various endpoints that are manipulated and responded to
clinically; we can lose the focus of blood flow or perfusion which is the only hemodynamic concept that is associated with improved patient
Blood flow is represented by cardiac output (Q).
Cardiac Output (Q) = Stroke Volume x Heart Rate
The stroke volumes for each ventricle are generally equal, both being approximately 70-85 ml. Stroke volume is the difference between
end diastolic volume and end systolic volume.
Interesting, Q has no pressure measurement in the above formula yet pressure is what we measure regularly as volume is far more
difficult to measure. However,
Stroke volume = Pulse pressure x 2
(Pulse pressure is the difference between systolic and diastolic pressure)
Hence we have difference in pressure as explained above and it is used to calculate stroke volume which is related to flow (Q) once we
add a driving force of heart rate. Invisible to this assumption is that heart contractility and elastance determine the filling, stroke volume
and driving force contraction of the heart and must not be forgotten.
The vascular beds are a dynamic and connected part of the circulatory system against which the heart must pump to transport the blood.
Q is influenced by the resistance of the vascular bed against which the heart is pumping. For the right heart this is the pulmonary vascular
bed, creating Pulmonary Vascular Resistance (PVR), while for the systemic circulation this is the systemic vascular bed, creating Systemic
Vascular Resistance in dynes-sec-cm (SVR).
Put simply, increasing resistance decreases Q; conversely, decreasing resistance increases Q.
By simplifying Darcy’s (and Ohm’s)Law, we get the equation that
Flow = Pressure/Resistance
When applied to the circulatory system, we get:
Q = Mean Arterial Pressure/Systemic Vascular Resistance
Much of the focus clinically on haemodynamics is the Mean Arterial Pressure (MAP) but as you can see it is related to Q or blood flow only
when Systemic Vascular Resistance (SVR) is added to the equation. Hence a patient may have MAP that is matching a prescribed
endpoint of 75 mmHg, but if the SVR is high the Q will be reduced to below the cell’s metabolic need for oxygen and nutrients and the
patient will struggle to survive.
So it is worthwhile to assess SVR in conjunction with MAP.
SVR can be measured through various haemodynamic devices and can be assessed clinically as peripheral coolness and capillary return.
However as you can see in the equation below, the SVR can be calculated with simple monitoring.
Q = (HR × SV) = MAP / SVR
Calculate the HR and the SV; then you can calculate the Q or cardiac output. As you are measuring the MAP with monitoring and it is
easily accessed, you can divide the MAP by Q to get an approximation of the SVR in dynes-sec-cm by multiplying MAP in mmHg by 80.
SVR = 80 x MAP/Q
Ohm’s Law and Hemodynamics (Fluid …
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Cardiac Output and Respiration
Q is affected by the phase of respiration with intra-thoracic pressure changes influencing diastolic heart filling and therefore Q. Breathing in
reduces intra-thoracic pressure, filling the heart and increasing Q, while breathing out increases intra-thoracic pressure, reduces heart
filing and Q. This respiratory response is called stroke volume variation and can be used as an indicator of cardiovascular status and fluid
These respiratory changes are important, particularly during mechanical ventilation, and Q (as well as arterial and central venous
pressure) should therefore be measured at a defined phase of the respiratory cycle, usually end-expiration.
Calculate the Cardiac output (HR & SV), SVR and MAP for your allocated patients this week. Consider:

  1. The clinical assessment of the patient compared with their haemodynamic values.
  2. Medications that the patient is receiving that modulate SVR, HR, or cardiac output (contractility and/or stroke
  3. The relationship between the MAP and the SVR and how cardiac output is affected.
    Viscosity and Poiseuille’s Law (Fluid M…
    How Does Respiratory Pump Affect Ve…
    Hemodynamic Principles
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    Arterial Pressure Monitoring
    Fluid filled monitoring devices are used extensively to evaluate pressures in various cardiovascular compartments. These work on the
    assumption that any change in pressure at any point in an unobstructed fluid filled system results in a similar change in pressure at all
    other points in the system. In most invasive monitoring systems this involves a fluid filled intravascular catheter attached to a pressure
    transducer which converts the pressure of the fluid into an electrical signal. This depends upon the fluid filled system to be unobstructed
    by air bubbles or kinks and low compliance semi rigid tubing used.
    A flush system consisting of a bag of normal saline to which heparin may or may not be added is used to maintain patency of the fluid
    filled monitoring device.
    Read the relevant section in your text book and answer the following questions.
  4. Describe briefly how a waveform is displayed on the monitor. [You will need to understand the relationship
    between monitor, transducer and patient parameters to answer this question correctly.]
  5. Describe the square wave form test and the effect of dampening on the pressure measurement system.
    What can cause a dampened response?
  6. Why is it important that non-distensible tubing be used on pressure monitoring lines?
  7. Describe the meaning of the systolic, diastolic and mean arterial pressures? If these are abnormal, (high or
    low) what does it mean for the patient? How is the mean calculated?
  8. Draw an intra-arterial waveform. What does the dicrotic notch signify?
  9. Where and how are arterial catheters inserted?
  10. What is the Allen test and when is this performed?
  11. What are the complications of intra-arterial catheter monitoring? What nursing observations are necessary to
    detect these?
  12. Why are transducers calibrated and zeroed?
  13. What is the purpose of levelling the transducer? Locate the phlebostatic axis.
  14. Discuss the infection control risk with venous access devices. Research the protocols in place in your
    department to minimise the risk of infection.
    CVP and Arterial Line Waveform Interp…
  15. Arterial Pressure Monitoring, Chapter 4 in Hemodynamic Monitoring Made Incredibly Visual! 2nd Edition. Lippincott Williams & Wilkins. Web. – Click Here
  16. 1. Quick guide to cardipulmonary care booklet – Click Here
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    Central venous pressure monitoring
    The central venous pressure gives a direct measurement of right atrial pressure and indirectly reflects the preload of the right ventricle or
    right ventricular end diastolic pressure. The measurement of end diastolic pressure gives an estimation of end diastolic volume. Volume
    estimations are used to titrate fluid therapy and increase cardiac output by optimising preload. This is based on the Frank Starling Law of
    the heart which states that the greater the end diastolic fiber stretch the greater the force of contraction. Overfilling can result in a
    decrease in stroke volume and cardiac output.
    Central venous access is frequently necessary for both measurement of central venous pressure and access for fluids and infusions.
  17. Magder, S 2015, ‘Understanding central venous pressure: not a preload index?’, Current Opinion in Critical Care, vol. 21, no.
    5 pp 369-375. Click Here
    2 De Backer, D. & Vincent, J.-L. 2018. Should we measure the central venous pressure to guide fluid management? Ten
    answers to 10 questions. Critical Care, 22, 43. Click Here
  18. Explain how central venous pressure can represent blood flow?
  19. What are the possible sites of insertion of a central venous catheter?
  20. What factors may influence the decision of insertion site?
  21. Familiarise yourself with the markings on the catheter which indicate insertion length. What is the usual
    insertion length for in each site of insertion?
  22. Describe the seldinger technique of insertion of central venous catheters.
  23. Why is it important to place the patient in a slightly head down position during insertion or disconnection of a
    central venous line?
  24. What is the normal CVP and what factors may affect it?
  25. Describe the effect of the respiratory cycle on the central venous pressure and how this affects the
    measurement which is recorded. How does this differ if the patient is mechanically ventilated?
  26. Source the procedure in your unit for extraction of a CV blood sample for a Central Venous Oxygen
    Saturation (ScvO2) measurement.
  27. List five possible complications when using a central venous catheter?
  28. Central venous catheters are available in different brands, with different numbers of access ports, designed
    for different sites and different length of insertion times. They also have different coatings for infection control
    reasons. Make a list of the various central venous catheters available in your unit and their particular
    characteristics. Explain in what situation their use would be applicable and why?
    Central Line Procedure
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    Pulmonary artery pressure monitoring
    This section is for critical care specialists
    The pulmonary artery catheter has been used extensively since the 1970s to evaluate filling pressures of the left ventricle by way of
    measuring the pulmonary artery occlusion pressure. This gives an estimation of the left ventricular preload. The pulmonary artery catheter
    is also used to calculate cardiac output by way of thermodilution, and blood gas analysis of samples taken from the catheter tip give an
    accurate measurement of mixed venous oxygenation. It’s popularity has reduced in the last few years with other less invasive technologies
    being used.
  29. List the ports and the function of each commonly found on a pulmonary artery catheter.
  30. Familiarise yourself with the insertion measurements on the pulmonary artery catheter. What is the likely
    insertion length of pulmonary artery in the most common insertion sites?
  31. Describe the insertion technique for the pulmonary artery catheter. Familiarise yourself with the waveform
    characteristics at each stage of the insertion process.
  32. Make a list of the possible complications of pulmonary artery catheter both during the insertion process and
    while insitu. Include the routine assessments performed to detect these and the precautions which are taken
    to prevent these occurring.
  33. How is a pulmonary capillary occlusion pressure (PCOP) or ‘wedge’ pressure obtained?
  34. What does the PCWP (PCOP) indicate and what could be considered normal, optimal and fluid overloaded
    values? Explain why you see these as such and in what clinical circumstances.
  35. How can you tell if the PCWP value is accurate?
  36. Why is the mixed venous sample taken from the PA port?
  37. How should pulmonary catheter balloon rupture be prevented and treated? Describe your nursing actions of
    treatment using an ABC process
  38. What is microshock and how do we prevent it?
    Pulmonary Arterial Catheterization
    12 Measuring Wedge Pressure
  39. Pulmonary Artery Pressure Monitoring, Chapter 6 in Hemodynamic Monitoring Made Incredibly Visual! 2nd Edition. Lippincott Williams & Wilkins. Web. – Click Her
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    Cardiac output measurement
    Invasive hemodynamic monitoring is used to monitor cardiac output in critically ill patients. This parameter allows the practitioner to
    calculate other derived indices of cardiovascular function. The pulmonary artery catheter has long been considered the gold standard
    method of measuring cardiac output in critically ill patients. More recently other techniques have been employed for cardiac output
    estimation. The pulmonary artery catheter provides a measurement of cardiac output by means of thermodilution. Here a bolus of a known
    volume of crystalloid solution into the right atrial or CVP port. A calculation of stroke volume is made based on the resulting temperature
    changes at the tip of the pulmonary artery catheter. Like measurements of PCWP and CVP the measurement of cardiac output is affected
    by breathing and must be taken at the same part of the respiratory cycle, normally at end expiration.
    Calculations of other indices of cardiovascular function are made using these values along with the PCWP and CVP measurement. These
    values are converted to indices by the hemodynamic calculator available on most modern monitors. Here, the height and weight of the
    patient are used to index the value to body surface area. These include systemic vascular resistance index which gives an estimation of
    left ventricular afterload, and pulmonary vascular resistance which gives an estimation of right ventricular afterload. Contractility is
    measured by calculation of the stroke work indices of the right and left ventricle.
    In recent years the use of the pulmonary artery catheter has decreased in some critical care units in favour of less invasive methods of
    monitoring cardiac output. These include the techniques of transpulmonary thermodilution and pulse contour analysis as used by PiCCO
    technology and trans-oesophageal Doppler measurement. A recent systematic review by the Cochrane Collaboration (Harvey et al 2006)
    concluded that the use of pulmonary artery catheters do not improve survival or hospital length of stay, but do contribute to the cost of
    treatment. The study did also comment that the use of alternative methods of cardiac output analysis requires careful scrutiny before they
    are widely adopted into general practice.
    Read the relevant section in your text book and answer the following questions.
  40. Why do we need to perform at least three measurements before calculating our results and what are you
    observing about them?
  41. Define cardiac index.
  42. Why is 5% dextrose the fluid of choice in cardiac output measurement?
  43. Cardiac output can be measured in many different ways: the most commonly used method is by
    thermodilution. Describe other ways of obtaining cardiac output measurement (describe three, one must
    include PICCO or NICCO).
    Swan-Ganz Thermodilution Pulmonary …
  44. Cardiac Output Monitoring, Chapter 7 in Hemodynamic Monitoring Made Incredibly Visual! 2nd Edition. Lippincott Williams & Wilkins. Web. – Click Here
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    Pulse contour analysis—continuous cardiac output
    Pulse Contour Analysis uses the concept of Frank Starling to calculate stroke volume and cardiac output of the left heart by analysing the
    aortic pulse contour. This method involves the calculation of the area under the systolic portion of the arterial pressure waveform, which,
    divided by aortic impedance, allows the estimation of the left ventricular stroke volume. Various different monitoring devices use arterial
    pulse contour analysis for continuous cardiac output monitoring, for example, the PiCCO© or the PulseCO©. So called dynamic
    parameters, such as the systolic pressure variation (SPV), the pulse pressure variation (PPV), and the stroke volume variation (SVV), all
    based on respiratory—induced changes in the interactions of heart and lungs have been evaluated by different groups to improve the
    assessment of fluid responsiveness, and by that to optimise fluid therapy in mechanically ventilated patients the method of arterial pulse
    contour analysis seems to be indeed a useful carrier to transfer clinically relevant, direct information on systemic blood flow in an
    automated and continuous mode, and most importantly without any time delay at the patient’s bed side.
  45. How can haemodynamic monitoring be used to predict the response of a patient to intravenous fluid?
  46. What other clinical indicators can you use in your assessment of patient fluid volume status?
    13 Measuring Cardiac Output
    Fluid Responsiveness
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    Recognising deterioration with haemodynamic monitoring
    When a patient is admitted to hospital with an acute medical illness, their safety is a prime concern for healthcare professionals. However,
    a number of studies published over the last two decades have demonstrated that significant unintentional harm is caused to patients
    through nurses’ failure to recognise the signs of clinical deterioration. Changes in the patient’s physical condition result in haemodynamic
    instability as the critical bodily functions start to fail and may be detected through observation and recording of the patient’s physiological
    vital signs of respiratory rate, heart rate, blood pressure and temperature, and other haemodynamic parameters which gradually become
    more abnormal with the progression of deterioration. The effective nursing observation of patients is therefore crucial to patient safety and
    outcome since this is the first step in identifying signs of clinical concern. Despite significant attention given to the observation of patients
    and the publication of national guidance to clinical staff, the issue of unrecognised clinical deterioration of patients continues to be a
    significant problem.
    Early recognition of deterioration
    It is difficult to identify patients early on in the course of circulatory shock because normal sympathetically medicated compensatory reflex
    mechanisms express themselves so as to sustain a relatively normal organ perfusion pressure and blood flow. For example, the normal
    response of the body to hypovolemia or impaired ventricular pump function is to attempt to maintain an adequate mean arterial pressure
    (MAP) by increasing sympathetic tone causing vasoconstriction, decreasing unstressed vascular volume, increased contractility, and
    tachycardia. In a healthy athlete early on in hypovolemic shock, tachycardia may not present, and in the elderly and those with
    dysautonomia tachycardia may not develop at all. Because these reflex sympathetic feedback mechanisms aim to sustain MAP above a
    minimal value to maintain cerebral and coronary blood flow, and because vascular capacitance is reduced to sustain cardiac output,
    hypotension not only occurs late but must be associated with tissue hypoperfusion. Hypotension in the setting of circulatory shock must
    also reflect failure of compensatory mechanisms to sustain normal homeostasis.
    Thus, hypotension is a medical emergency not only because it must be associated with tissue hypoperfusion but also because it
    signals loss of intrinsic mechanisms to sustain effective blood flow.
    Furthermore, restoring MAP by the use of vasopressors improves tissue oxygenation in septic patients. Thus, the immediate restoration of
    MAP while other flow-directed resuscitation efforts are under way is essential in minimizing ongoing tissue hypoperfusion.
    Using the principles described herein, it is possible for the bedside clinician to answer four interrelated important questions of their
    Are they compensating?
    Are they volume responsive?
    Is arterial tone increased, normal or decreased?
    Is their heart able to sustain flow without high filling pressures (ie high CVP)?
    Haemodynamic protocol
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    Haemodynamic Simulation-H.264 for V…
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    Lifespan considerations
    Lifespan considerations
    Paediatric Focus
    The key principles of haemodynamic monitoring are similar to that of adults. It is however beneficial to be aware of some major differe
    The major key point is that placement of invasive lines is technically more difficult and time consuming than placing them in adults.
    This will alter the risk:benefit ratio and there may often be a higher threshold for the insertion of invasive lines in paediatric patients com
    In paediatrics, the best method of monitoring is frequent observation and clinical assessment.
    Like adults, end organ perfusion can be assessed by monitoring level of consciousness, capillary refill time, urine output, and lacta
    Insertion of invasive lines will almost always necessitate a degree of sedation, especially the insertion of central lines as children m
    Sedation must always be administered with caution in children as it may cause them to lose their sympathetic drive which may resu
    Sampling anaemia can be a significant problem due to the low total blood volume of paediatric patients compared with adults.
    Fluid infusions to maintain line patency are a significant contributor to total fluid intake, necessitating absolute diligence when moni
    Paediatric BASIC (2014). Basic assessment and Support in Paediatric Intensive Care.
    Figure: Paediatric arterial line insertion and dressing in an infant
    Older Adult Focus
    The older adult has more subtle compensatory responses and the signs and symptoms may be easily missed. This is the result of agin
    Increased dysrhythmias
    increased atrial size and irritability
    left ventricular myocardial thickening leading to decreased compliance
    lower ejection fraction,
    thickened heart valves that interfere with forward flow
    decreased response to sympathetic nervous system
    decreased sensitivity of baroreceptors;
    generalised stiffening of arterial vessels, including aorta.

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