Category: Diagnosis

I was shocked to find out that medical students, entering their clinical years, have not been taught the proper method and interpretation of blood pressure measurement. The current approach almost invariably uses electronic sphygmomanometers and, while convenient, it is often not performed well and misses important information which simply cannot be gleaned from an electronic sphygmomanometer.

First, and foremost, the patient must be comfortably seated with their back supported and their feet planted on the ground or supportive surface. The patient is to have rested for at least five minutes and not have had any caffeine to drink in the previous hour.

The bladder of the cuff should encircle at least 80% of the patient’s arm and the width to length ratio of the cuff should be at least 40%.

I would recommend that the systolic pressure be estimated first by palpation. One does this by reasonably rapidly inflating the cuff to 80 mmHg while palpating the radial pulse. If the pulse remains palpable, slowly increase the cuff pressure (approximately 10 mm Hg every 2 to 3 seconds) until it disappears.  Note at what pressure the pulse is obliterated. Next release the pressure of the cuff completely and raise the patient’s arm above their head (especially if he or she is obese) for at least ten seconds so as to help drain any excess venous blood that had accumulated in the arm as that has may muffle Karotkoff sounds.

Next while supporting the patient’s relaxed arm at heart level, pump up the cuff to 20 mm Hg above the previously estimated systolic blood pressure. Slowly deflate the cuff at no more than 2 mm every second while listening for Karotkoff sounds. The appearance of Karotkoff sounds (stage I) signals the patient’s systolic blood pressure. Continue to deflate the cuff paying attention to a time when Karotkoff sounds become muffled or disappear (stage II). This stage is not always present. Continue to deflate the cuff listening for the recurrence of Karotkoff sounds, if they had disappeared, or an increase in their intensity if they had only been muffled (stage III). Continue to deflate the cuff until Karotkoff sounds muffle again (stage IV). Continue to deflate the cuff until Karotkoff sounds disappear completely (stage V). True diastolic blood pressure is found between stages IV and stage V. However, if those stages occur within a narrow range, the disappearance of Karotkoff sounds identifies the diastolic blood pressure. Persistence of Karotkoff sounds well beyond phase IV is termed “systolic persistence” and, in such a case, I would record the blood pressure with three digits – systolic, phase IV and phase V readings

I would also strongly recommend that blood pressure be tested in both arms. A difference of 10 mm Hg or more can indicate, amongst other things, arteriosclerotic vascular disease and has been correlated with an increased risk of cardiovascular events.

A very prominent auscultatory gap (i.e., stage II) in which there is disappearance of Kartkoff sounds also correlates with an increased risk of cardiovascular events.²

In patients over the age of 60, those with “resistant hypertension”, diabetics and/or patients with chronic kidney disease check for evidence of possible pseudohypertension. To do so, determine if the radial artery is still palpable after the blood pressure cuff has been inflated to above systolic. If so, this signifies stiffening of the radial artery due to Monckeberg’s medial sclerosis. This procedure is known as “Osler’s maneuver”. Such a finding carries significant ramifications.³

1. Williams, J. S., Brown, S. M., & Conlin, P. R. (2009). Blood-pressure measurement. N Engl J Med, 360(5), e6.

2. Cavallini, M. C., Roman, M. J., Blank, S. G., Pini, R., Pickering, T. G., & Devereux, R. B. (1996). Association of the auscultatory gap with vascular disease in hypertensive patients. Annals of internal medicine, 124(10), 877-883.

3. Mishriki YY. Resistant hypertension: A stepwise approach. Cleveland Clinic Journal of Medicine May 2023, 90 (5) 273-274; DOI: https://doi.org/10.3949/ccjm.90c.05001

“Remember, diseases don’t read books.”
Yousri Youssef Mishriki, MD

“Uncommon manifestations of common diseases are more common than common manifestations of uncommon diseases.”
Yehia Yousri Mishriki, MD

Why can diagnosis in medicine, at times, be so difficult?

Here is a paraphrase of a typical sentence in my internal medicine textbook when I was a student/resident – “In disease x, one finds an elevated white blood cell count. At times, however, the white blood cell count can be normal or low.”

It would not suffice to know the breadth and depth of medicine, which is impossible, to always correctly diagnose one’s patients but one must also be aware of the variability of presentation of all those diseases. Sir William Osler knew as much when he wrote his epic book, ‘The Principles and Practice of Medicine’ in 1892 wherein he described the various ways in which typhoid can present and cautioning that, “This diversified symptomatology has led to many clinical errors…”. The more modern medical literature also describes the varieties of ways diseases can present atypically. For example, Cushing syndrome, due to excess cortisol production, has occasionally been described as “cyclical” rather than continuous, with variable other presentations such as periodic hormonogenesis, unpredictable hypersecretion of cortisol, fluctuating cortisol excretion or intermittent Cushing syndrome. Even in monogenetic illnesses, where one would expect a stereotypical presentation, there can be a variability of presentation due to environmental effects and exposures, post-zygotic mutations, and epigenetic influences.

In his book, ‘Thinking Fast and Slow’, Daniel Kahneman described two methods of thinking when making decisions. In the fast pathway, pattern recognition is fast, intuitive, and often driven by heuristics (cognitive shortcuts for reaching immediate solutions to a problem) and is primarily subconscious. In the slow, analytic pathway, thinking is deliberate, effortful and under conscious control. Physicians toggle back and forth between these two methods depending on the details of the cases they are analyzing, their experience and knowledge and their whim. Tversky and Kahneman posited that most inferential errors produced by heuristics and biases were due to “faulty probabilistic reasoning”. However, Jain did not agree that the diagnostic process was probabilistic, and I believe that he is, at least partially, correct. Nevertheless, once an initial diagnosis comes to mind as a result of a heuristic, biases are bound to arise, particularly anchoring and confirmation biases which interfere with one’s ability to objectively proceed with the evaluation. Furthermore, one must simultaneously avoid the diametrically opposed biases of representativeness restraint, a tendency of looking for typical manifestations of a disease while ignoring atypical variants (“when you hear hoof beats, think of horses and not zebras”) and aggregate bias, a belief that general population data do not apply to one’s patient. A setting for cognitive dissonance, if ever there was one.

What are clinicians to do? Those in the know recommend cognitive bias mitigation which involves “deliberate switching” from intuitive to analytical processing and the use of “debiasing strategies”, what I term ‘metacognition’ or thinking about one’s thinking. After one has generated an initial possible diagnosis or diagnoses, one must step back and carefully question oneself as to whether one has fallen prey to some of the more common biases. Needless to say, this is time consuming, and time is a very rare but critical commodity in accurately diagnosing one’s patients.