This chapter is relevant to Section G7(iii) of the 2017 CICM Primary Syllabus, which asks the exam candidate to "describe the invasive and non-invasive measurement of blood pressure, including limitations and potential sources of error". It deals with the reasons for why the arterial pressure waveform is the shape that it is.
Generally, this topic has not been a prominent feature of the CICM Part I. In the Part II exam, trainees have occasionally been asked about the possible information which can be derived from the arterial waveform tracing (Question 30.2 from the second paper of 2013). Questions regarding the change of the waveform depending on its position in the vascular tree have also appeared (Question 11.1 from the first paper of 2010). Because of this, a brief entry on "information derived from the arterial pressure waveform" is available in the Required Reading section for the Fellowship exam, mainly as a refresher and summary for the time-poor Part II exam candidate.
The arterial pressure wave (which is what you see there) is a shockwave; it travels much faster than the actual blood which is ejected. It represents the impulse of left ventricular contraction, conducted though the aortic valve and vessels along a fluid column (of blood), then up a catheter, then up another fluid column (of hard tubing) and finally into your Wheatstone bridge transducer.
Interestingly some of the best resources for this were found in the course of reading a dissertation by Rebecca Cunningham, a biomedical engineering student qualifying from the University of Massachusetts in 2012. It turns out one really gets to understand the human arterial pulse when one is trying to simulate it mechanically for the purposes of teaching arterial line insertion. By following her references one pulls on a string which finishes in Chapter Eight, "Direct Arterial blood Pressure Monitoring: Normal Waveforms" (p. 81) of Jonathan B. Mark's Atlas of Cardiovascular Monitoring (1998). For all intents and purposes this source should be regarded with superstitious reverence. Virtually all illustrations in subsequent physiology textbooks on the subject were borrowed or adapted to some extent from this source.
The arterial pulse waveform
The arterial pulse waveform can be separated into three distinct components
- The systolic phase, characterised by a rapid increase in pressure to a peak, followed by a rapid decline. This phase begins with the opening of the aortic valve and corresponds to the left ventricular ejection
- The dicrotic notch, which represents the closure of the aortic valve
- The diastolic phase, which represents the run-off of blood into the peripheral circulation.
The waveform can be separated into an anacrotic (upstroke) and dicrotic (downstroke) limbs. The origin of the term is from Greek dikrotos, which means "beating twice" (krotos meaning "stroke"); anacrotic having been abbreviated from anadicrotic.
The peak correlates with the systolic blood pressure as measured by a normal non-invasive cuff. The trough (i.e. the lowest reading before the next pressure wave) is the diastolic pressure. The mean arterial pressure (MAP) is calculated from the area under the pressure curve, which is a more accurate way of doing it than the old "diastolic plus one third times the pulse pressure" method. That method can get you into trouble. Consider the arterial pressure waveforms below. Though with identical systolic and diastolic pressures, the area under the curve for one waveform is substantially smaller, leading to a lower MAP.
The pulse pressure waveform has several components, each invested with some sort of meaning. These components are:
- Systolic upstroke
- Systolic peak pressure
- Systolic decline
- Dicrotic notch
- Diastolic runoff
- End-diastolic pressure
The significance of these features is discussed in detail below.
Timing of arterial pulse and the ECG
The systolic upstroke does not occur immediate following the contraction of the heart. On the ECG, the electrophysiological phenomenon which signals the beginning of systole is the R wave. According to textbooks, the arterial pulse wave does not appear on the monitors until a 160-180 millisecond delay.
Most of these timing recordings are made in the cardiac cath lab, using transducer-tipped catheters in the aortic root. Thus, this delay interval is probably different in real-life situations where the patient's arterial line is connected to the pressure transducer by a length of tubing. For instance, a man armed with a smartphone camera and a calculator can easily determine that the delay is longer.
The reasons for the delay are not completely related to the measurement apparatus. After the R wave, the depolarisation wave has to spread through the left ventricle, some isovolumetric contraction needs to take place, then the aortic valve has to open, and then the aortic pressure wave needs to travel up the aorta and down the arm (at 6-10 m/s). Generally speaking, knowing about this delay is only meaningful when you make some sort of decisions on the basis of it. A classical application of such knowledge is when you try to manually set up an aortic balloon pump to a pressure trigger.
This is the ventricular ejection. Of the two forward pressure wave components, this part is generated by the fast-moving 10m/sec wave, and corresponds to the peak aortic blood flow acceleration at the opening of the aortic valve. One might correctly surmise that things which influence aortic flow rates will also influence this component of the waveform. That would be correct. The slope of this segment has some vague relationship with the rate of change in LV pressure and with the competence of the aortic valve. When the slope of this component is slurred, there may be aortic stenosis.
Though the change in pressure over time (dP/dt) of the systolic upstroke must to some extent be related to the force of the LV contraction, the utility or reliability of this relationship has never been convincingly demonstrated. Esper and Pinsky (2014) quote several conflicting studies. Realistically, the way the LV contraction influences the arterial systolic pressure upstroke must be a complex interplay of contractility, aortic valve flow, arterial peripheral resistance, diastolic pressure, the pattern of LV electrical activation, and so on.
Peak systolic pressure:
This is the maximum pressure in the central arteries, generated during the systolic ejection. The peak systolic pressure is what you bleed with. This is the pressure that blows the haemostatic thrombus plugs off the vessels you have so carefully cauterised, and stresses the wall of the fragile aneurysm. The major contributions to this variable are the LV contraction, central arterial compliance and the reflected pressure wave.
The systolic peak derives its shape from the influence of reflected waves coming back from the vascular tree. When the blood is running down the aorta, there is little resistance (it's a huge vessel) and the mean arterial pressure is relatively unaffected on its way to the radial artery. Then, down to the level of the arterioles, the resistance increases dramatically. This high resistance tends to "iron out" the pulse pressure waveform, and flow in arterioles is a lot less pulsatile than in the larger arteries. As a result of this increased resistance (think of it more as a brick wall) the pressure waves are reflected back towards the aortic valve. The point where this reflected wave makes its contribution can even produce an "anacrotic notch" along the systolic upstroke, a visible shoulder in the rate of pressure change.
The peak systolic pressure (and therefore also the pulse pressure) will be low in patients with highly compliant vessels, because there is little wave reflection and because the central arteries will distend gladly in response to LV systolic flow. An excellent example of this is a neonate. In the adult, there is usually plenty of backward wave reflection. The effect of these reflected pressure waves is usually to amplify the systolic blood pressure and to change the shape of the waveform.
As you move further down the vascular tree, the reflected wave becomes more and more prominent, and moves further into systole. This was demonstrated wonderfully by Murgo et al (1980), who recorded the pressure waveforms in the human aorta while gradually withdrawing the measuring catheter down to the iliac bifurcation.
The image is reproduced here with no permission whatsoever. Note the reflected wave in the upper aorta is a late phenomenon, whereas at the bifurcation it has merged completely with the systolic peak. Murgo and colleagues were also able to demonstrate that this amplification increases as the vascular tree becomes less compliant. When they manually occluded the femoral arteries bilaterally, the augmented pressure of the arterial waveform increased by 10mmHg.
Peripheral vascular disease, heart failure, HOCM, vasodilated shock, irregular pulse, arteriovenous malformations and what have you - all of these have some influence on the arterial pressure waveform by means of delaying, exaggerating, reducing or accelerating the pressure wave reflection. Murgo et al (1981) and O'Rourke et al (1984) offer excellent explanations of how and why these things happen, and the effect of disease states is discussed in the chapter on the interpretation of abnormal arterial pressure waveforms.
Distal systolic pulse amplification
The action of reflected waves is a well-recognised influence on the systolic pressure, and the phenomenon is called distal systolic pulse amplification. There is a famous diagram, reproduced in many textbooks, which seems to originate in Gedde's Handbook of Blood Pressure Measurement (1981). It demonstrates the change in systolic pressure which occurs as the result of moving further and further from the aortic root, stacking more and more of the accumulating reflected pressure waves on top of the systolic peak. This diagram is reproduced below in tribute to Geddes, lovingly modified to demonstrate the individual components more clearly.
Its not clear where Geddes got these waveforms, but it is likely he and his students recorded them directly (possibly directly in themselves). Alternatively it may be derived from earlier works such as Nielsen et al (1974), who demonstrated that the systolic pressure in the posterior tibial artery was about 25mmHg higher than in the brachial.
This is the rapid decline in arterial pressure as the ventricular contraction comes to an end. The fall in pressure represents a period of time during which the efflux of blood from the central arterial compartment is faster than the influx of blood from the emptying left ventricle. In fact, during this time the flow from the ventricle is minimal (Wiggers, 1952). This decline is even more rapid when there is a left ventricular outflow tract obstruction (and systole comes to an abrupt halt before the left ventricle is finished with the ejection).
Dicrotic notch and the incisura
This thing is widely believed to be the effect of the aortic valve closing. The valve closes and there is a sudden increase in pressure as the aortic blood volume suddenly discovers that it has nowhere else to go, apart from the peripheral circulation. In perfect circumstances, when measured in the aorta, this notch is very sharp and it actually does represent the closing of the aortic valve. In fact, when it is measured in the aorta the notch is called the incisura, because it cuts into the waveform. However, further down the arterial tree the incisura disappears. It is replaced by the dicrotic notch, a mutant offspring of several reflected waves, only vaguely related to the behaviour of the aortic valve.
The position and prominence of the dicrotic notch depends on many things. For one, it is one of the elements of the arterial pulse which requires the analysis of high frequency waves; consequently it is one of the first details to disappear when the transducer system is overdamped.
The relationship between the incisura and the functional status of the aortic valve was demonstrated nicely by Sabbah and Stein (1978) who made pre- and post-valve replacement recordings of aortic pressure waves in human subjects. Not satisfied with this, they created a plexiglass model of the aortic root and mounted human valves in it (ones which they obtained at autopsy). The diagram below is from their classic paper. Note the absence of a distinct dicrotic notch in the case of a severely calcified stenosis as well as regurgitation. In both circumstances the valve fails to close normally, and the normal dicrotic notch pattern is lost.
As you move further out into the peripheral circulation, the incisura ends up being slurred and softened. It is generally believed that the peripheral dicrotic notch owes more of its shape to the vascular resistance of peripheral vessels than to the closing of the aortic valve. This is best illustrated in this image, modified from O'Rourke via McDonalds Blood Flow In Arteries (6th ed).
Observe how in the ascending aorta, the incisura is distinct and sharp. That's clearly the valve doing that. As the catheter is retracted into the abdominal aorta, its sharpness and distinctness fade, and by 35-40cm it is barely a bump on the curve of the systolic decline. However, at around the same time one starts noticing the second beat of the pulse (the second stroke which gives origin to the term dicrotic). What people refer to as the dicrotic notch is the trough before this peak, and - from O'Rourke's recordings - clearly distinct from effect of the aortic valve closure.
The latency of the dicrotic notch behind the systolic peak varies with the position of the arterial line, moving further and further from the systolic peak the further you go down the arterial tree. This is probably because some component of it is still related to waves reflected off the closed aortic valve, which would take longer to arrive in the distal circulation. Again, there is a frequently reproduced diagram which demonstrates the progressive migration of the dicrotic notch (from Bedford RF: Invasive blood pressure monitoring. In Blitt CD [ed]: Monitoring in anesthesia and critical care. New York: Churchill Livingstone, 1985, p 505). This diagram is also reproduced here, after being slightly molested in Illustrator.
Diastolic run-off and the influence of arterial reservoir pressure
The diastolic run-off is the drop in pressure which occurs after the aortic valve has closed. There is no flow from the LV, but pressure does not drop suddenly - rather, it decreases gradually along an exponential curve. The reason for this is arterial "cushioning", or the reservoir effect of pumping blood into an elastic tube.
This elastic recoil of large arteries contributes as much as 40% to the stroke volume (Wang et al, 2003); after the LV systole has ceased this recoil maintains a higher pressure in early diastole, pushing blood into the peripheral circulation. This elastic recoil clearly contributes to the shape of the waveform. Davies et al (2007) were able to separate the aortic pulse pressure waveform into a forward pressure wave, a reflected bakcward pressure wave, and the arterial reservoir pressure.
The shape of this reservoir pressure plainly has some relationship with the characteristics of the reservoir. The nice supple aorta of a your person is going to perform differently to the calcified barnacle-encrusted aneurysm farm of an elderly smoker. This was demonstrated scientifically by McVeigh et al (1999) who measured the arterial waveform shapes in a group of people of different ages. Observe their Figure 4, reproduced below and modified to include the contribution from arterial reservoir pressure.
Waveform (a) represents the radial waveform of a 25 year old person, (b) is 47 years old, and (c) is 80. Now, those pink overlays are purely in the author's imagination (they weren't a part of the original image from McVeigh et al), but they illustrate the point. Nice compliant arteries of the youth produce less reservoir pressure because they distend readily in response to systolic flow. In old age, the reservoir is much less compliant, and the pressure generated by pumping blood into it will be higher, deforming the shape of the diastolic run-off.
This is the pressure exerted by the vascular tree back upon the aortic valve. Hardened non-compliant vessels will cause this pressure to be raised. Soft vasoplegic vessels of a septic patient will offer little resistance, and the diastolic pressure will be lower. A regurgitant aortic valve will cause this pressure to be lower than normal, because instead of meeting the aortic valve the pressure wave travels all the way though to the ventricle via the regurgitant jet. The diastolic pressure is what fills your coronary arteries, and should not be ignored.
A very widened pulse pressure suggests aortic regurgitation (as in diastole, the arterial pressure drops to fill the left ventricle though the regurgitating aortic valve)
A very narrow pulse pressure suggests cardiac tamponade, or any other sort of low output state (eg. severe cardiogenic shock, massive pulmonary embolism or tension pneumothorax).