- Understand the principles of Ohm’s Law in relation to Cardiac Output, Systemic Vascular Resistance and Blood Pressure
- Describe how Preload, Contractility & Afterload affect Stroke Volume and how these can be optimised clinically
- Recall the classification of adrenoceptors and their physiological action, especially in relation to Inotropy, Chronotropy and Vasoconstriction
- Recall the pertinent pharmacokinetic and pharmacological properties of Metaraminol and Ephedrine
- Compare and contrast the properties of these drugs and their clinical uses in anaesthetic practice
- Use this knowledge and understanding to select an appropriate Vasopressor for use perioperatively to optimise organ perfusion pressure in various clinical scenarios
Major body systems rely on adequate blood supply to function.
During an anaesthetic, there are many reasons why this blood supply to vital organs may becomes transiently (or permanently) disrupted and so it is essential you have a good understanding of circulatory physiology and how to optimise Cardiac Output in order to use vasoactive drugs safely.
In order to ensure an adequate blood flow to the vital organs, an adequate perfusion pressure is vital.
Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)
There are various factors that influence a patient’s optimal MAP, but generally, 65-75mmHg is sufficient to meet the metabolic requirements of vital organs such as the brain and kidneys.
As we have discussed, there are many reasons why a patient undergoing an operation/anaesthetic may become hypotensive. It is essential to consider the cause of the hypotension to be able to address it. In order to do so, you also need to be aware of Ohm’s Law.
Ohm’s Law governs electrical series circuits.
Potential Difference (V) = Current (I) × Resistance (R)
Potential Difference, Current and Resistance all have analogous physiological variables in the circulatory system and so the equation as applied to the body is as follows:
MAP – Central Venous Pressure = Cardiac Output × Systemic Vascular Resistance
This equation now dictates that hypotension can be caused by either:
- a reduced Cardiac Output
- or a reduced Systemic Vascular Resistance
Let’s look at each of these in a little more detail.
As we know, Cardiac Output is a product of Stroke Volume and Heart Rate.
There are 2 variables that increase Stroke Volume:
- Preload (End-Diastolic Volume)
There is 1 variable that reduces Stroke Volume:
Vasodilatation reduces the SVR.
Vasoconstriction increases the SVR.
While we can use vasopressors to induce systemic vasoconstriction, it is important not to ‘over-squeeze’ the patient with excess vasopressor – as this can actually lead to a reduction in end-organ perfusion, even though you may be normalising the blood pressure. If the cause of the hypotension is a reduction in Cardiac Output rather than a reduction in SVR, it is best to correct the Cardiac Output issue (e.g. with fluids / inotropes) rather than using vasopressors.
The α1 adrenoceptor is present in vasculature – agonists at this receptor induce vasoconstriction.