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 ways in which the shape of the arterial waveform can be correlated with the pathology affecting the cardiovascular system. This matter has never enjoyed very much attention from the CICM examiners, and for the purposes of revision can be viewed as something apocryphal. Certainly, one would not spend the last few pre-exam hours frantically revising these waveforms. In fact it has been abundantly demonstrated that a person can cultivate a gloriously successful career in Intensive Care without any appreciation of this material.
If for whatever reason further reading is required, one should probably get a hold of the excellent Atlas of Cardiovascular Monitoring by Jonathan B. Mark. Among its many merits, the book features actual recorded arterial waveforms instead of artwork.
The waveform depicted here represents the arterial pressure wave of a hypertensive person with poorly compliant arteries, borrowed from Mills et al (2008), who in turn adapted it from Smith et al (2000). It is supposed to be an aortic pulse waveform produced by applanation tonometry of the radial artery.
The non-compliant vessels do not stretch in response to the systolic pressure, and thus the pressure rises rapidly at the beginning of systole, resulting in a steep systolic upstroke.Because of the poor compliance, a powerful reflected wave is sent back to the aortic root, which when added to the systolic effort of the ventricle makes for a high peak systolic pressure. Other reflected waves may also follow, as the pressure reverberates though the hollow woodwind arteries of this smoker.
In the elderly, the reflection wave arrives early, during systole - before the aortic valve closes- thus adding to afterload and thus to the myocardial workload; while in diastole there may be no reflection wave, which means the coronary arteries miss out on its benefit. The systolic afterload contribution from the reflected wave disappears in vasodilation, and appears with vasoconstriction.
Is this for real? Perhaps. Murgo et al (1980) were able to demonstrate that the systolic pressure (and MAP for that matter) in the aorta increases by about 10 mmHg when manual pressure occludes the femoral arteries. The authors were able to demonstrate that the main reason for this was the increase in the magnitude of the reflected wave. Their diagram (depicted on the left) was recorded from the ascending aorta using a transducer-tipped catheter introduced via the brachial artery.
The question is, does this adequately describe what happens in hypertension? All of Murgo's patients had angiography for chest pain, but none had any cardiovascular disease. It would be wonderful to have some actual "official" recorded waveforms to display, but most authors reproduce each other's sketches instead. Fortunately these sketches are occasionally accurate. In "Age, hypertension and arterial function"(2006), McEniery et al offer representative examples which are reproduced below alongside a real waveform from a patient with malignant hypertension.
On the surface, this seems to have some sort of clinical relevance. For instance, Weber et al (2006) were able to find an association between this reflected wave systolic augmentation and an increased risk of coronary artery disease. However in practice, arterial waveform analysis in hypertension would rarely yield an appreciable improvement on the impression one has already formed of the patient from their history, examination and vital signs. In other words, for the classical waveform demonstrated above, the slope of the systolic upstroke and systolic pressure augmentation by wave reflection add little useful information to the blood pressure measurement (which was 240/100 mmHg).
In their paper "Valve origin of the aortic incisura", Sabbah and Stein were able to demonstrate (using a plastic tube and some cadaveric valves) that the incisura is due to aortic valve closure, and that information regarding the aortic valve can be derived from the shape of the waveform. Though the scanned copy of their 1978 article is greatly degraded by time, one can use the tracing they produced to identify the cardinal features.
The ventricle struggles to squeeze blood though the stenosed aortic valve, and thus the systolic upstroke becomes less steep. No matter the force of contraction, the pressure rise will not be rapid. The systolic peak may also be lower, as it is difficult to generate high aortic pressures in this condition. The pulse pressure may be narrowed, but doesn't have to be (because the aortic stenosis may coexist with some aortic regurgitation). The incisura is lost. The dicrotic notch is also supposed to disappear - though this makes less sense given the real possibility that it has little to do with the closure of the aortic valve. However, authoritative sources (eg. Petzold et al in their 2013 article on pulse contour analysis) reproduce a classically notchless peripheral arterial waveform for aortic stenosis, suggesting that if this is a misconception, then it is shared by the highest echelons of medicine, and therefore probably also by the CICM examiners (should this piece of esoterica ever find its way into the SAQs).
To agin refer to Petzold et al (2013), the popular impression is that aortic regurgitation has a sharp systolic upstroke - instead of contracting isovolumetrically, pressure from early contraction of the LV is transmitted directly to the aorta. This will be followed by a steep systolic decline: pressure will drop rapidly (that's the blood regurgitating into the LV as it fills in diastole).
There should be a wide pulse pressure, as the diastolic run-off is steep and reaches a low end-diastolic value. In fact, the more incompetent the valve, the closer the systemic diastolic pressure will approach LV end-diastolic pressure, which is probably close to 5 mmHg. Conventionally, among elderly physicians this might still be remembered as Corrigan's sign.
There is supposed to be a "descendent" dicrotic notch, which is difficult to explain. If the dicrotic notch is supposed to be due to the closure of the aortic valve, then if the aortic valve doesn't close one would logically expect to lose the notch. Certainly, this is seen when you actually focus on aortic valve activity: in measuring regurgitant cadaveric valves Sabbah and Stein (1978) commented that "The magnitude of the aortic incisura diminished with an increasing severity of insufficiency". Similarly, the above waveform which was borrowed from Jenkins (2007) seems to have no dicrotic notch and a small incisura. Those were both central recordings.
One must consider that there might be a distinct dicrotic notch distally, and that it will be "descendent" because the whole dicrotic limb is lower. Alternatively, one might embrace the explanation published by Chirinos et al (2018). The authors deduced by waveform analysis that the normal forward compression wave is followed by a mid-systolic "suction wave", which is the consequence of the left ventricle relaxing to a low pressure. Such was their explanation for the appearance of a bisferiens pulse with aortic regurgitation.
Speaking of bisferiens pulse. HOCM is supposed to produce this characteristic arterial waveform, or so it is repeated throughout the textbooks. On closer inspection, there is little data in support of this, apart from an ancient case report by Goodwin et al (1959). The case report is written in a beautiful manner, characteristic of the times. It also appears to be the first time anybody suggested the term "obstructive cardiomyopathy" to describe this pathology. The authors marveled at the thickness of the myocardium. "In order to obtain a left ventricular pressure curve a 4-inch (10-cm.) needle had to be thrust in up to the hilt and even then good complexes were intermittent,the systolic peak being cut off on many".
To cut a long story short, the authors found that these patients had a bisferiens-like pulse. There was a sudden midsystolic pressure drop, as the LVOT collapsed on itself and systolic flow ceased.
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