
Tom talks Cardiac Cycle, Coronary Perfusion and breaks down Blood pressure and the Hagen–Poiseuille Law,
There is a debrief and extra detailing at the end in very quick fire ‘words that convey you know what you’re on about’ sot of standing.
Check out VivaCast 006 for more oxygen fun, and episode 002 for how carbon dioxide gets from cell to atmosphere
Article Spring Board
What determines coronary perfusion pressure?
Coronary perfusion pressure is determined by the difference between aortic diastolic pressure and left ventricular end-diastolic pressure, influencing myocardial oxygen delivery.
What is blood pressure?
Pressure = force / area
Force exerted per unit area of vascular surface area
How does systemic vascular resistance relate to mean arterial pressure, systemic vascular resistance and cardiac output?
We know that pressure = flow x resistance. (this is Darcy’s Law)
The flow in this situation is analogous to cardiac output, pressure relates as mean arterial pressure.
[math] MAP = CO . SVR [/math]
[math] SVR = \frac{MAP – CVP}{CO} [/math]
SVR is in units of dyne/s/cm-5
1 dyne = the force required to accelerate 1 gram of material 1cm^2
Hagen-Poiseuille Laws
[math] Pressure Gradient = \frac{8.Q.\eta .l}{\pi r^4} [/math]
[math] Resistance = \frac{8.\eta .l}{\pi r^4} [/math]
- [math] \eta [/math] = Viscosity
- [math] l [/math] = Length
- [math] Q [/math] = Flow
Resistance is
- Proportional to viscosity and length
- Inversely proportional to radius to ^4
Laminar vs Turbulent Flow
Laminar is stable flow through a tube, fastest flow is in the middle as it ‘slips’ past the matter already moving next to it, slowest at edges. The shift at which a particular liquid/solution shifts from Laminar to Turbulent is guided by…
Reynolds Number
[math] Reynolds Number = \frac{v.\rho.d}{\eta} [/math]
note, Reynolds number has no dimension
- v = velocity (m/s)
- [math] \rho [/math] = density of liquid/gas (kg/m^3)
- d = Diameter (m)
- [math] \eta [/math] = Viscosity – (N/s/m^2)
- A number >2000 = odds are its going to be turbulent
Flow in a turbulent system is difficult to predict, and is a meddly of eddy currents and disorder (like the NHS?)…
Coronary Perfusion Pressure
LV Flow Systole – Negligible flow Diastole – Profound flow
RV Flow Systole – reduced but present flow Diastole – plenty of flow
This can be formalised using a formulaic approach:
Coronary Perfusion Pressure = Aortic Pressure – Intraventricular pressure
Therefore the perfusion gradient is quite significantly bigger compared to the LV, note the diastolic pressure is used in the diastolic phase.
- LV systole = 120mmHg
- LV diastole = 10mmHg (against aortic diastolic pressure)
- RV systole = 25mmHg
- RV diastole = 5mmHg (against aortic diastolic pressure)
- LV systole coronary perfusion pressure = 0 mmHg
- LV diastole coronary perfusion pressure = 70 mmHg
- RV systole coronary perfusion pressure = 95 mmHg
- RV diastole coronary perfusion pressure = 75 mmHg
Notes – this means a tachycardic heart, which spends 1/3 of its time getting no perfusion disproportionately impacts the LV The RV on the other hand, is not terribly used to any periods of underperfusion, so in situations where it dilates and strains its ischaemic pre-conditioning is non-existent and it fares poorly.
Cardiac Cycle
- Atrial Systole – Atrial kick adding 20% to cardiac output!
- Isovolumetric ventricular contraction – Pressure climbs – volume remains the same as pressure needs to ascend to the diastolic pressure in the aorta to open the valves
- Rapid ejection – as it says on the tin
- Reduced ejection – as pressure in aorta and ventricle equalise flow across the graident diminshes
- Isovolumetric relaxation – The ventricle has finished emptying what it can it relaxes, the aortic valve closes
- Rapid ventricular filling – much likele tere is a quick and slow ejection phase driven by pressure gradient the same occurs in diastole
- Reduced ventricular filling
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Transcript
Gas, Gas, Gas Episode 891: Blood Pressure, Flow, Resistance and Cardiac Cycle
Introduction and Episode Overview
00:00-01:07
Please listen carefully. Hello, and welcome to Gas, Gas, Gas, the podcast that covers the FRCA primary exam. We’re going to fit into your day and give you as much of your life back as you could possibly imagine. I’m here to make your studying easier – listen to us on your commute, in the gym, in the shower, or when you’re ironing your scrubs. Expect facts, concepts, model answers and the odd tangent. Check out the show notes for all the detail, and remember to follow the show so that you never miss an episode. Let’s get on with it.
Hello everyone, this is James at Gas Gas Gas. This is more VivaCast action with our willing victim Tom. He finds himself a way into quite a heavy session. I’ve decided to split this physiology section down into three subsets because otherwise it’s just too much to learn, I think, in one go, and you just melt your brain.
We’re going to do blood pressure, coronary perfusion pressure, flow resistance, and dip our toe into the cardiac cycle. All core stuff that you should be able to reel off the keywords for. Let’s get on with it.
Blood Pressure Definition and Governing Factors
01:07-03:28
Summary: Tom explains blood pressure fundamentals and the key factors that determine it.
Okay, Tom, we’re beavering away and we’re making excellent forward progress, and we are now an hour and a half into our viva action. The smile on your face has actually gotten bigger, not smaller. Are you ready for your physiology viva? My favourite topic, physiology. I’ve got a favourite textbook – we’ll talk about that after.
What is blood pressure and what governs it?
[Brief technical delay mentioned]
So blood pressure is a measure of pressure within your arterial system. So pressure itself is equal to force over area, and if you measure the force over the area within your arteries, it gives you an arterial blood pressure. You can also measure blood pressure in various other parts of the vasculature, such as central venous pressure, right atrial pressures and things like that.
Can you beat the question? Sorry, I think there was another section to it, other than what is blood pressure?
What is blood pressure, but what governs it?
So blood pressure is governed importantly by your cardiac output and by your systemic vascular resistance. So cardiac output is equal to stroke volume times your heart rate. So increases in heart rate and increases in stroke volume will lead to increases in blood pressure, as higher amounts of blood per unit time are ejected from the heart. And the vasoconstriction of your small vessels will be extremely important in dictating pressure within your vascular system as well, due to the Hagen-Poiseuille equation.
Flow Dynamics and the Hagen-Poiseuille Equation
03:28-05:34
Summary: Detailed discussion of laminar flow physics and the factors affecting vascular resistance.
So laminar flow, which is normal flow within arterial vessels, is equal to π times the radius of the vessel to the power of four times the pressure difference across the system divided by eight times the length of the vessel and multiplied by the viscosity, which is ν.
And could you just talk me through when you’re mentioning resistance there – increases in resistance are proportional to what or inversely proportional to what?
So as the radius of blood vessels and particularly arterioles decreases, resistance and pressure increase together. And as the radius of them increases, then conversely blood pressure decreases, as does resistance.
So as we mentioned the Hagen-Poiseuille equation before, you know, Q equals πr⁴ΔP over 8Lν, you’ll notice that the radius of the vessels is going to have a really significant effect because it’s to the fourth power, and so changes in vessel size will have a large effect on blood pressure. So, as they decrease, flow will decrease and pressure will increase, and the converse is also true.
Other things that affect blood pressure include… How does viscosity affect the resistance in the system?
So as viscosity increases, resistance also increases in direct proportion. So viscous blood, so blood with a high haematocrit or with a low temperature, will lead to increased resistance in the vascular system.
And length?
So, yeah, length – as I mentioned before, so flow is inversely proportionate to 8Lν. As length increases, resistance also increases. And if you think of multiple vessels, they can be thought of really as one longer vessel. Increased number of vessels, so increased numbers of tissues to supply will also increase resistance, such as in obese patients.
Laminar vs Turbulent Flow
05:34-07:02
Summary: Tom contrasts laminar and turbulent flow characteristics, including clinical applications like heliox therapy.
So you mentioned that this is reliant on flow in a laminar system. What’s the contrary to laminar flow?
So turbulent flow is another type of flow that occurs within certain systems and different things affect the rate of flow within a turbulent system versus a system with laminar flow. So when turbulence is an important factor, the radius of the vessels or tubing that a fluid flows through is still important, but only r² rather than r⁴, so it has a smaller impact.
Length remains important in systems with turbulent flow, but viscosity becomes less important, and the density of the fluid that’s flowing turbulently is more important. So as density decreases, flow increases within a turbulent system.
An important application of this can be the use of heliox in asthmatic patients. So as their bronchioles constrict, they develop turbulent flow within their airways, and that flow can be increased proportionally to the decreased density of the air they’re breathing. So adding helium decreases the density of the inspired gases and means they can increase flow within the small airways.
Coronary Artery Perfusion
07:02-08:21
Summary: Discussion of how cardiac cycle phases affect left and right coronary artery blood flow differently.
So moving on to thinking about flow in some particular vessels, how does flow differ between the left and right coronary arteries throughout the cardiac cycle?
The left coronary artery is more significantly impacted by ventricular systole, as the relatively large and muscular left ventricle contracts, it constricts the radius of that vessel, decreasing flow and increasing pressure within the left coronary artery.
You still have some increase in pressure and decrease in flow in the right coronary artery during ventricular systole, but to a much lesser extent due to the lower pressures in the right side of the heart and the reduced muscle wall thickness.
So it sounds like flow is dependent on whereabouts in the cardiac cycle you are?
Most flow happens to the left coronary artery during diastole, and in the right coronary artery you get proportionally – there is still more blood supply during diastole, but there is a larger proportion of blood delivered during systole.
The Cardiac Cycle
08:21-10:11
Summary: Tom works through the phases of the cardiac cycle from diastole through systole.
So you mentioned diastole and systole there. Could you break down the cardiac cycle for me into its components?
So we can begin thinking about the cardiac cycle as ventricular diastole initially, so this is the end of ventricular systole as the right and left ventricles relax, then pressure drops in the ventricles. As the pressure in the atria becomes greater than that in the ventricles, the mitral and tricuspid valves open and we get filling of the left and right ventricles.
Towards the end of their filling we have atrial systole, where the atria contract and complete the filling of the ventricles, and this is closely followed by ventricular contraction. This can be divided into several different parts of the cycle.
So initially we have – I can’t remember the terminology actually – but initially we have contraction, but prior to the pulmonary and aortic valves opening we have contraction with a constant volume.
Isovolumetric contraction, that’s what it’s called.
It is indeed. Yeah. And the muscle of the ventricular walls contracts. You get a sharp increase in pressure in the ventricles and then at some point the pressure in the ventricles exceeds the pulmonary or aortic valves respectively, and you move into the next phase, which is rapid ejection.
So here we have a large pressure difference between the left ventricle and the aorta and between the right ventricle and the pulmonary arteries, and so we have rapid ejection of blood in that part of systole. We then move into isovolumetric relaxation, which is like the converse part of the cycle.
Host Summary and Key Teaching Points
10:11-14:13
Summary: James provides a comprehensive review of the key concepts with additional clinical insights and memorable details.
Lovely. There we have it. So just so we’re all on exactly the same page, I’m going to blast through the key points.
Pressure Fundamentals
Pressure is force over area, or stress – also force over area. We know that pressure is guided by flow and resistance. This is Darcy’s law. We know that the formula for pressure in our human – calculating the mean arterial pressure in our system – is cardiac output times systemic vascular resistance.
We can work out systemic vascular resistance by subtracting the central venous pressure from the mean arterial pressure and dividing it by the cardiac output. That’s how they interrelate anyway.
Flow and Resistance – The Hagen-Poiseuille Equation
When we’re thinking about flow in a system or resistance in a system, which is what I’m more interested in really, the resistance for flow in a tube that follows most of the rules – i.e. it’s laminar – resistance equals eight times the viscosity of the liquid times the length divided by π times radius to the power of four.
So we all know that that means that resistance is inversely proportional to the radius to the power of 4. So that’s the most important thing. You can also manipulate viscosity by putting more crystalloid in someone. You can’t really alter length, really, but I suppose you could cut their limbs off, although that’s very extreme. You would reduce peripheral vascular resistance that way.
Actually, interestingly, once upon a time, for heart failure, they used to put sequential tourniquets on people’s arms and legs, allowing the legs to fill from a venous perspective, because they’d occlude the venous pressure but allow the arterial pressure to prevail. So you could fill a leg with all the fluid in a person and therefore offload their heart transiently. You can imagine that this doesn’t really work for a very long time, but it’s a cool thing to think about.
Laminar vs Turbulent Flow – Reynolds Number
Then we touched upon laminar versus turbulent flow. And the thing that helps you guide “is it going to be turbulent, is it not going to be turbulent” is Reynolds number. Reynolds number is a dimensionless number. If the number is greater than about two thousand, odds are it’s going to be turbulent.
The formula for Reynolds number is the velocity of the fluid times the density of the material, fluid, gas, whatever, times the diameter of the thing you’re running it down divided by the viscosity. So there you can infer that it’s inversely proportional to the viscosity, and proportional to the velocity, the density, and the diameter.
Coronary Perfusion Patterns
We then talked about flow in coronary arteries. The big hitters here is that the left ventricle is perfused only in diastole, whereas the right ventricle is perfused throughout systole and diastole.
This means that the right ventricle is probably less conditioned than the left ventricle when it comes to being exposed to ischaemia, because that right ventricle is having a delightful time getting oxygen throughout the whole cycle with a few shifts in flow, whereas the left ventricle only gets that delight in diastole, so it’s a bit more conditioned to tolerating a period of low perfusion. Protect the right ventricle. Hmm.
Cardiac Cycle Summary
And then we touched on cardiac cycle. This is something you just need to be able to reel off, ideally with perhaps a few little bits of extra flair alongside. I’m just going to tell you that it’s atrial systole, isovolumetric contraction, and then it’s rapid and then reduced ejection, isovolumetric relaxation and then rapid and reduced filling.
Have a look at the show notes. Thank you very much for listening, guys. Ta-ra!
Closing
14:13-14:31
Thanks for listening to the episode, guys. If you found it useful or awful, please like and subscribe and rate the show. Definitely, go check out the show notes on gasgasgas.uk. We all know that this is a bucket of content. I want you to take some time for yourself and don’t overcook it. Don’t freak out, keep studying.

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