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
techniques.
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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4/9/2020 Study plan: Week 4 – Haemodynamic monitoring
https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585802 4/15
Review
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
preload
afterload
systemic vascular resistance
pulmonary vascular resistance
contractility.
Cardiac Cycle animation
Blood Pressure Animation
4/9/2020 Study plan: Week 4 – Haemodynamic monitoring
https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585802 5/15
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
4/9/2020 Study plan: Week 4 – Haemodynamic monitoring
https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585802 6/15
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
survival.
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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