Pressure Waveforms and Cardiac Output

Take home messages

• When asked to draw a graph, listen carefully to which parameters are on the x and y axis
• Draw and talk at the same time, and practise this lots before the exam

We're clinical physiologists

I challenge you to find another specialty that tinkers with more unfettered raw physiology than anaesthetics.

We pride ourselves on our understanding of physiology, and have been known to reply to other specialties with unapologetically nerdy phrases such as:

• "Well we want to increase stroke volume don't we..."
• "This is all atelectasis and we probably just need to recruit the bases..."
• "You can give metaraminol if you want, but I'd go for a spot of inotropy.."
• "Yeah it's that Monroe-Kelly thing isn't it?"

You get the idea.

As with all things in anaesthetics, it's generally a good idea not to overcomplicate where possible, and when it comes to cardiac physiology and understanding the pressure waveforms - take it slow and steady.

• The heart is two pumps in parallel
• The right side is a low pressure, high flow pulmonary system
• The left side is a high pressure (and also high flow) systemic system
• Cardiac output is the rate of blood flow out of the heart, expressed in litres per minute
• The cardiac cycle is everything that happens over the course of a single, complete heartbeat

The first graph you need to know

"Can you draw a graph of the cardiac cycle, highlighting the relevant phases and pressure waveforms?"

This can be a gift of an SOE/OSCE question if you're prepared.

Yeah it's a busy picture - and there's no way round it - you just need to practice drawing it while talking about it until it becomes vaguely comfortable.

The cardiac cycle involves the regular process of relaxation and filling of the heart with blood (diastole), followed by contraction and ejection of blood into the great vessels (systole).

They might also be really mean and ask you avout the CVP (or JVP) waveform.

Can you draw and explain the left ventricular volume/time graph?

This is the other weird one they might get you to draw.

We should probably mention LaPlace's law

The FRCA examiners love an equation, and LaPlace's law is no exception.

As the radius of a vessel increases, or the thickness of the wall decreases, the tension experienced by the wall increases.

This is why dilated bowel is so fragile and the surgeons get seriously worried by a caecum larger than 9cm.

For the heart, it demonstrates how hard a dilated, thin walled, cardiomyopathic heart has to work to squeeze any blood into the aorta - the wall tension that the overstretched myocytes have to overcome is enormous.

Look at this balloon dog's tail

The proximal half of it is fairly well inflated, and the wall tension is squeaky high, but the end of the tail is almost completely flat, with very little wall tension at all, making it all floppy.

The pressure inside each bit is equal (otherwise gas would be flowing from one bit to another)

It is the increased radius that means the pressure is exerting a much higher wall tension across the proximal part than the distal section.

That's probably enough of that for now.

Can you explain the Frank-Starling mechanism in relation to the heart?

The Frank-Starling mechanism, or Starling’s law refers to the ability of the heart to adjust the force of contraction in response to changes in preload

• Increased preload causes stretching of the sarcomeres, and increases the number of overlapping actin and myosin binding sites
• It also sensitises the myocardium to calcium

• As demonstrated on the graph, increasing preload causing the stroke volume to increase in a linear fashion until a plateau is reached
• Positive inotropy shifts the curve to the left
• Negative inotropy shifts it to the right

What does this graph look like in heart failure?

• The graph is shifted to the left and significantly flattened, reducing the maximal attainable stroke volume
• The graph also does not plateau as normal, rather increasing ventricular filling causing a decrease in stroke volume, as is classically seen in congestive heart failure
• This is because the myocardial sarcomeres are now overdistended, reducing the number of overlapping myosin and actin binding sites and therefore reducing the force of contraction
• This distension is usually a chronic problem, because the stiff pericardium usually prevents the heart from overfilling, however over time will distend itself and allow overdistension to occur

What pressures do I need to know?

Mainly the ones in this image.

You don't necessarily need to be able to reproduce this image in major detail, but you need to be able to suggest sensible numbers for each of the relevant chambers and major blood vessels, especially if the examiner starts talking about a pulmonary artery catheter.

This gets examined a lot given we don't really use PA catheters all that much any more - they're particularly keen on the old 'here are the pressures, where is the tip of the catheter' style MCQ questions.

Useful Tweets

References and Further Reading

The Cardiac Cycle

This chapter is basically a set of long, enormously elaborate footnotes to the Wiggers Diagram, which describes the timing of pressure and volume changes in the chambers of the heart. In short, the cardiac cycle can be split into seven fairly predictable phases, each with their clearly defined boundaries, containing well described events which are a favourite of the CICM examiners.

Deranged PhysiologyAlex Yartsev

Primary FRCA Toolkit

Members receive 60% discount off the FRCA Primary Toolkit. If you have previously purchased a toolkit at full price, please email anaestheasier@gmail.com for a retrospective discount.

Discount is applied as 6 months free membership - please don't hesitate to email Anaestheasier@gmail.com if you have any questions!

Just a quick reminder that all information posted on Anaestheasier.com is for educational purposes only, and it does not constitute medical or clinical advice.